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Tips And Methods On How To Avoid Cancer
Being able to have a friendly and informative back-and-forth conversation with your doctor is crucial if you want to know your treatment options for a disease like cancer. visit this site right here need to be aware of the fact that there is a lot more that goes into living with and treating this disease than what a physician can tell you. Study these tips to learn more about cancer.
One of the best ways to avoid getting cancer is to avoid doing things which may cause cancer. Two of the biggest offenders when it comes to causing cancer are smoking and tanning beds. Staying away from these two things gives you a much better chance at being cancer free.
Carcinogens are known to cause cancer. A common place to find carcinogens that most people do not realize is on wooden decks and play sets. Wooden decks and play sets built before 2005 are likely to contain a coating of arsenic pesticide. This coating can stick to skin and clothes and increase the chances of causing cancer in the body.
In order to beat cancer it is important for you to stay strong and to never give up on yourself. You have to be willing to put up a fight against the cancer and not just let it win. Fighting to beat cancer means that you are emotionally strong and believe you will beat it.
If you have been diagnosed with cancer and are a smoker, you need to quit right away. The ingredients in cigarettes have been proven to have very bad side effects on the body and for someone that is battling cancer they can be very detrimental. It is important to quit as soon as possible to have a fighting chance against the cancer.
There are do alternative treatments for cancer work of individuals out there that have antiquated notions when it comes to cancer. They may fear that your disease is something that is contagious, or that you can no longer perform your job at work. Try not to hide anything, and be honest.
It's important that you work hard to deal with your feelings and emotions if you or someone you know has cancer. This is going to be a very emotional time in ways you cannot possibly understand unless you've been through it, and unchecked emotions can destroy relationships permanently and lead to a world of regret.
Because they are so rich in glutathione, avocados are a great cancer-preventing food you can eat. The reason avocados work to prevent cancer is that their powerful antioxidants wage a war against the free radicals floating around in your body. Eliminating free radicals is how you work to eliminate cancer cells.
Chaga Mushroom: Uses, Benefits and Side Effects
Chaga Mushroom: Uses, Benefits and Side Effects Chaga mushroom (Inonotus obliquus) is a type of fungus that grows mainly on the bark of birch trees in cold climates, such as Northern Europe, Siberia, Russia, Korea, Northern Canada and Alaska.
If you live alone, try to stock up on meals when you feel well. Cook up a large batch of chicken or soup and freeze it. Since there will probably be days when your cancer treatment leaves you feeling a little weak, it will be very helpful to be able to quickly heat up a meal and relax.
Staying out of the sun is key in preventing skin cancer, but most people do not listen to this advice in the wintertime. Believe it or not, the same UV rays from the sun penetrate the atmosphere in the cooler months too. You might not feel the heat, but you will receive the same radiation.
If you have been recently diagnosed with cancer or have had it for some time I would highly suggest finding and joining a cancer support group. Cancer is one of the hardest diseases to deal with emotionally because it's mortality rates. Having a support group will help you cope and enjoy your life the best you can.
Find comfort in something tangible and not something idealistic when you are battling cancer. It's a great idea to keep your eye on the prize and to envision full recovery, but it's also important that you cling to tangible results and take things one step at a time. Looking too far ahead may cause you to miss important steps in your recovery.
When you are dealing with cancer, you want to have a sufficient support group. This support group can get you through the worst of times and even the best of times, offering the support that is needed and the motivation you need to continue with your treatment and therapy measures.
For women, a mammogram is a great way to prevent breast cancer. A regularly schedule mammogram allows doctors to detect any lumps in breast tissue. Lumps in the breast tissue are a possible sign of breast cancer. Self breast exams should also be performed by women at home.
Reducing your risk of cancer is much simpler than beating it. Skin cancer can be prevented by avoiding overexposure to the sun. In any instance when you will be spending a long period in the sun, apply an adequate sunscreen product to all areas of your skin.
cancer alternative medicine of screenings are available to help prevent cancer, detect when cancer is present and identify any other problems. While it is easy to let things slip when you have a busy schedule, taking time to do cancer screenings is important enough to make time for.
If you are living on your own while going through cancer treatment, think ahead. Prepare larger amounts of food on the days that you feel well enough to cook and put the extras in containers in the freezer for the days that you do not feel much like cooking.
Keep a phone handy whenever you are home. If you need to have one installed in your bedroom, do it, otherwise take your cordless phone with you wherever you go in your home. You may need it for emergencies or you may find it to be a great social connection when you are bored.
Signs of ovarian cancer can be very subtle. It is sometimes referred to as the "silent killer" due to the lack of symptoms until the cancer has progressed. The most common symptom includes pain in the the abdominal area, pelvis or back. Increased size of the abdomen area is another symptom. The stomach appears similar to that of a pregnant woman's stomach.
One of the best ways in order to ease someone that has been diagnosed with cancer is to consciously listen to what they say. Listening to someone might sound easy but it is harder than it looks. With that said, it is important to not interrupt and listen to what they have to say with not only your ears but with your eyes and body as well.
If you are wondering what to do now, after your diagnosis, this article has given you a lot of ideas for moving forward. It is important to understand that you need to follow the advice of your doctor, but that feeling better and looking better while you go through it is possible.
Tips On How To Handle Having Cancer
Leading a fulfilling and fruitful life will require that you do everything you can to remain healthy. In other words, life is something you have to work at to enjoy. So if you ever get the news that you have cancer, remember that this isn't the end. It's only your cue to work harder. Find out how to work harder and smarter by using the tips below.
Recognize intellectually that your physical appearance will probably change after a cancer diagnosis. If you go into treatment anticipating that you will eventually look different, you will have a much better attitude when those changes actually take place. Talk to your doctor about what to expect as you prepare to begin your journey.
When facing cancer, you should remember to anticipate physical changes. Cancer and cancer treatments such as chemotherapy will cause your body to experience changes, such as hair loss. Keeping these changes in mind will help you prepare for them in advance and remove any chances of being surprised by them. Find a patient physician who is willing to spend time discussing these matters with you.
Eating a balanced diet is a solid cancer-fighting tool to keep in your arsenal. Especially with colon cancer, diets that are high in fat and cholesterol have a direct correlation to cancer, so maintain balance in your diet to fight against this. High-fiber diets aid in the fight against cancer.
One of the most important tips to remember after being diagnosed with cancer is to maintain a healthy life style. Maintaining a healthy lifestyle will give you more energy, which you will need during the treatment process. A healthy lifestyle consists of eating healthy foods and doing regular exercise.
Understand that with cancer some people are going to be awkward and nervous around you. This isn't actually a fear of you. They realize that cancer isn't contagious. They just do not know how to approach the subject. Do not take it personally if people are a bit standoffish at first.
Someone with cancer is going to want and need their time alone, so you have to know when to back off and to give a person some space. Having pride is important to everyone and sometimes, people do not want you to see them so vulnerable. Respect their request for privacy or you might be pushed away completely.
There are many new people who will enter your life if you have cancer, as you put together a team to help develop a treatment plan. This will include nurses, oncologists, specialists and support groups who can help you with treatment or aid you in your fight. People who have a good support system have higher survival rates, so welcome these people and new friends into your life and accept the help that they have to offer.
If you're outside deck or wooden play set dates prior to 2005 in its construction, then you should consider applying a seal to it. Most of the wood that is in these sets had an arsenic pesticide applied to them. Sealing them protects the kids from the cancerous chemicals.
New therapy cures cancer with just one injection
New therapy cures cancer with just one injection Current cancer therapies have terrible side effects and aren't always effective. And with things like radiotherapy and chemotherapy, the number of treatments one needs to endure makes side effects progressively worse over time. A new technique developed by researchers at Stanford University uses two agents which when combined, alert the body's immune system to the presence of cancer, in order to eliminate it.
There is Look At This that you have to live with unbearable pain as a cancer sufferer, so make sure that you are getting the right pain medication. There are dozens of pain meds out there, and if the one you're taking isn't working well, make sure you tell your doctor that you need something different.
Staying out of the sun is key in preventing skin cancer, but most people do not listen to this advice in the wintertime. Believe it or not, the same UV rays from the sun penetrate the atmosphere in the cooler months too. You might not feel the heat, but you will receive the same radiation.
When you are first diagnosed with cancer, you should immediately make an appointment with your dentist. When making your appointment, inform the receptionist of your diagnosis so they can get you in quickly. Treatment can sometimes affect your oral health. Therefore, before starting any treatment plan it is necessary to have a dental cleaning and any necessary dental work done.
In an effort to prevent cancer - stay away from tobacco products! This includes smoking and chewing tobacco. These items have been shown to increase the likelihood that you will develop lung, bladder, cervical, oral, and pancreatic as well as kidney cancer. Avoiding them will not only help reduce your risk of cancer, it will help you lead a healthier lifestyle overall.
Stay organized. You are going to have many appointments to go to and have to keep track of many different dates. Get a calendar and use it to keep track of things that are important. You can even log how you have felt on different days so you can let your doctor in on your progress.
https://medicine.wustl.edu/news/siteman-cancer-center-to-offer-newest-form-of-proton-therapy/ will put off getting a mammogram because they are afraid of the results. It is scary thinking that you may be diagnosed with cancer but it is far more scary to not have the screening done. The earlier you catch it the better your chances of beating it!
Make time to go outside and enjoy the fresh air. Your cancer treatments may make it impossible for you to exercise, but spending time outside will help you feel refreshed and rejuvenated. If you can walk or participate in a light jog do that as well. Exercise is important to the healing process.
Improving your immune system is going to help your body be able to protect itself against a number of different things. This includes cancer, diseases, and other conditions. Boosting your immune system is going to better prepare your body to fight off any cancer cells that are in your body.
Use a calendar or schedule book to log your activities. https://drive.google.com/drive/folders/0B_-u9r2Wdc94TUNVMHBzeFJyd00?usp=sharing means that you will be busier than usual with appointments, meetings and visits from your friends and family. Keeping track of all these events will help you stay organized and make your life a little less stressful.
Cancer prevention is a much wiser path than treating an avoidable cancer after the fact. Limiting exposure to the sun and using sunscreen are two great methods of avoiding skin cancer.
Having a few options out there, whether dealing with prevention or treatment, or even dealing with yourself or your loved ones, is a great way to be fully prepared should cancer ever inflict its damage upon you. Make sure you're memorizing these tips so that you can always use them to help.
Enhance Your Weight-Loss Regimen With These Ideas
If you are looking to start on your weight loss journey, then you've come to the right place. The tips below will help jump start you onto a road of shedding pounds and dropping inches. The weight loss process does not happen overnight. You need to start incorporating these ideas into your life and you will start to lose pounds.
Part of weight loss is regular elimination. The more rapidly your body can move food and liquid through your system, the less chance it will have to build up and accumulate pounds. Though chemical laxatives are generally a bad idea, a diet very high in fiber (whole-grain products, lots of fruits, vegetables, and of course, plenty of water) will keep one's digestive tract in good working order, which will assist in your weight loss efforts.
Make better choices! In https://www.diigo.com/user/vivaa2015 to lose weight, substitute more physical activities as opposed to passive ones! An example of this would be using the stairs instead of riding the elevator or escalator. Additional effort produces great benefits! Among them is extra calories burned which increases weight loss endeavors!
For effective weight-loss exercising, you should join a gym rather than attempt to do all your exercising on your own. In the long run a good gym membership will save you money by providing facilities, equipment and services you could not possibly afford to buy on their own. At read this will also find a community of fellow exercisers who can support and assist you.
To ensure that you remain committed to your weight loss plan, get everyone in your family excited about eating healthy foods. Make the same snacks and meals for each person living in your household; that way, you won't be tempted to eat one of the unhealthy foods that they are indulging in.
Downsize your plate to lose more weight. Traditional plates are bigger in diameter than is necessary to hold an appropriate amount of food. The desire to fill your plate and subsequently empty your plate is usually counterproductive to weight loss. Try using a child-sized plate, this will allow you to keep up your habits in a healthier way.
When you are trying to lose weight, avoid mindless eating. Slow down and pay attention to what you are doing when you have something to eat. Do not just sit in front of the TV eating directly out of the package and barely tasting what you are eating. You will consume much less food if you are careful to really think about it first.
If you want to maximize your body's response to your weight loss efforts, be sure to get at least eight hours of uninterrupted sleep every night. An excessively tired or fatigued body and mind lacks the endurance, strength, and fortitude needed to carry you throughout the day and help you to persevere during your fitness program. Tiredness is also a key cause of emotional eating.
The best way to accelerate weight loss is to include some sort of weight training regiment. One pound of muscle burns ten times the calories as one pound of fat, and that is just sitting idly. So next time you go to the gym don't just hit the treadmill, but hit some weights to, your waist line will thank you.
Keep https://www.marketwatch.com/story/dow-turns-negative-as-trump-announces-sweeping-changes-to-health-care-policy-2018-05-11 on good nutrition and not fad diets. Extreme diets that focus on curbing your nutritional intake might at first prompt weight loss, but will ultimately only put your health in danger. These ubiquitous diets enjoy short-term popularity, but fade just as quickly as they appear. Fad diets fade out quickly as people begin to realize that the benefits are generally short lived, and the diets themselves can be dangerous to their health.
When you are trying to lose weight, avoid mindless eating. Slow down and pay attention to what you are doing when you have something to eat. Do not just sit in front of the TV eating directly out of the package and barely tasting what you are eating. You will consume much less food if you are careful to really think about it first.
When embarking on your weight loss goals, try adding cinnamon to your diet. Not only does cinnamon have health benefits such as lowering LDL cholesterol, it has also been proven to relieve joint pain. This will give you the strength to exercise on a regular basis, which will help you drop the pounds.
Eating foods that have healthy fats such as olives, salmon and walnuts will help you to feel satisfied for a longer period of time. Eating these foods will help you to eat less throughout the day because you will not be hungry, and it will prevent you from just eating anything you can find at the moment.
Try three bean salad when you are working at losing weight. It's easy to prepare a version low in calories right at home. All you have to do is mix three cans of beans with light Italian dressing. This will make enough of this high fiber snack for you to munch on all week.
If you are used to having bacon bits all over your salads, you can have something similar that is much more healthy. Taking low fat ham and crisping it in a non-stick pan, can have the same effect as bacon. Crumble it up and sprinkle it on your salads.
A useful weight loss tip is to always have small packages or containers of low-calorie snack food on hand. Carrying carrot and celery sticks, rice cakes or some air-popped corn in your purse or briefcase, makes sensible snacking possible, at any time of the day. In this way, anyone can curb impulse food binges capable of sinking even the best-intentioned diet plans.
To help avoid weight gain during the holidays, choose foods that taste good, but are still light, and good for you. Fresh cranberry sauce is delicious and high in acidity, so it helps you avoid infections. For a boost of beta carotene and vitamin A, be sure to enjoy sweet potato, squash and pumpkin dishes. If you are preparing these yourself, experiment with reducing the sugar by half. You probably won't be able to tell the difference.
The best way to lose weight and maintain it is to treat yourself from time to time. If you are really craving something "� if you deny having it "� it will make it harder for you to stay happy with your weight loss program. Instead, eat visit my web site in moderation, and as they are meant to be eaten - as treats!
In conclusion, it was easy to get to your current weight but it is not going to be easy to lose it. Among other things you need to immediately change your diet. Hopefully the rest of the tips in this article will help you to achieve the weight loss you desire.
How To Get That Healthy Skin That You Have Always Desired
Having great looking skin is not rocket science, despite the claims of the makers of those expensive skin care products on the market today. It is simply a matter of knowing what to do to help your skin be the best it can be. Take a look at the fresh ideas in the skin care tips below.
To keep your skin looking beautiful, don't forget the sunscreen. One of the top causes of premature aging is due to sun damage. Get a light facial moisturizer that contains an SPF of at least 15. Sun damage can cause wrinkles, freckles, sun spots and dry skin. Protect your skin and don't leave the house without your sunscreen.
Cut down on fatty and sugary foods. Fried foods and foods high in sugar may taste good, but they wreak havoc on your face. Eliminate them from your diet as much as possible, and that includes soft drinks. Replace those junk foods with healthier alternatives (for example, eat yogurt instead of ice cream) and watch your skin improve.
Drinking enough water daily works wonders for your skin. It will hydrate you and flush out the toxins from your body. Your skin will look more shiny and good hydration can fight the damaging effects of sun rays. This leads to healthier looking skin.
Always use https://www.mid-day.com/articles/summer-health-care-tips-7-ways-to-keep-yourself-cool-with-smart-food-habits/19432170 or body lotion. Doing so will prevent many of the skin conditions caused by dry skin such as, itchiness, redness, peeling, and acne. Make sure that it is hypoallergenic as well as of the non-greasy type. This simple tip will make your life a lot easier as well as help to keep you looking fabulous.
If weight loss in my area is oily, sensitive, or prone to breakouts, do away with bar soaps and bar cleansers. Instead, look for cleansers that are dispensed in pump or spray bottles. The moist, exposed surface of bar soaps, combined with the humidity of an enclosed bathroom, encourages the growth of acne-causing bacteria.
If you are a mother, it is important that you keep your baby happy and healthy by moisturizing their skin daily. You must watch your child everyday, in case a dry skin area forms. If your son or daughter begins to form dry skin, you should moisturize the area immediately.
No skin care routine can truly be complete without proper maintenance. A consistent and regular regimen of cleansing (without harsh soaps), followed by moisturizing and weekly exfoliation, creates a supple and elastic quality in the skin that makes your additional skin care treatments not only easier, but in many cases, less necessary.
If you are looking to keep your skin looking healthy all the time, then you should limit your bath or shower time. Taking longer baths and showers depletes healthy oils from your skin. Additionally, if you make sure to take warm, instead of hot showers, your skin will retain a fuller brilliance.
To gain more benefit to your skin from an exfoliating treatment, extend the time you exfoliate, not the force that you use. If you scrub your skin with extra force, you'll just end up causing more damage. A longer exfoliation time will clear more of the dead skin cells and dirt, without hurting your skin.
Get plenty of exercise. Exercising frequently helps your skin maintain a healthy fresh glow by regulating the oxygen flow in your body. Make sure you avoid wearing makeup while you exercise because your it can trap your sweat within your pores and cause a breakout. Take a clean cloth with you to wipe your face every time you sweat to avoid any dirt clogging your pores.
When removing makeup and excess grime from your face at the end of the day, it is advisable to do this in a two step process. First, use just click the following page to remove makeup and sunscreen products. Next, use a secondary cleanser designed to soothe and replenish the now clean skin. As with any facial skin regime, ensure that all hand strokes are in an upward motion from the neck up.
Spray-on sunscreen can help you properly care for your skin. Particularly, if you are susceptible to acne, spraying on an oil-free sunscreen helps to stop the spread of bacteria from your hands onto your face. This keeps your pores clear and your skin looking fresh. It also reduces the likelihood that you will experience a sunburn.
Keeping the skin on your hands healthy is just as important as keeping your facial skin healthy. Having rough hands can actually cause an infection or fungus to grow. When doing chores or manual labor, wear rubber gloves. At nighttime, gently rub lotion all over your hands, even rubbing into the skin surrounding your nails. Remove any excess lotion.
If you suffer from dry skin, you may want to stay away from bar soaps. Instead, use a body wash that contains moisturizing agents. When you take a bath, stay away from bubble baths, because the ingredient in the soap can damage your skin. Try using bath oil or a body wash that contains oatmeal, as these will soothe dry, itchy skin. Always use moisturizer after you dry off.
To help prevent sagging of the delicate skin under the eyes, always pat your face dry instead of rubbing with your towel. Because the skin under your eyes is thinner, vigorous rubbing more easily damages it. A gentle pat should also be used to apply eye cream after cleansing and patting dry.
Taking the herb Gotu Kola can do wonders for your skin! It helps to reduce cellulite and contains antioxidants that promote elasticity and tightening of the skin, making the skin incredibly soft and supple. It is also used in the treatment of varicose veins and spider veins. Despite it's name, Gotu Kola contains no caffeine.
When it comes to skincare, serums should be your new best friend. Serums contain much smaller molecules which work to penetrate your skin at a much deeper level. Many serums contain anti-aging properties and powerful anti-oxidants. When you use serums, it is like putting vitamins on your skin.
Eating properly is one of the best possible things you can do for your skin. If https://myvivaablog.wordpress.com eating plenty of fresh fruits and vegetables, that means you're getting the right amount of vitamins and minerals. That means your skin should remain looking its best.
If you want to look great, no matter your age, you will need to take really good care of your skin. This article was full of great information that should keep you looking young and beautiful as long as you want to. There is no reason you should have to look older than you are.
Weight Loss Can Be As Easy As Following Directions
Losing weight is an uphill battle for many. If you're struggling to shed some extra pounds, you're likely to be inundated with much information about how to do so, and may be unable to decide which method is the best option for you. This article aims to provide you with advice that is easy to understand and follow.
When losing weight it's important to not deny yourself. If you tell yourself you can't have something, you are going to end up wanting it even more. When that craving hits, only have a bite or two, and see if that causes your craving to pass. If losing weight becomes too complicated, you probably won't stick to it.
One of the quickest ways to lose weight is to swap out the sugary soft drinks for something else. Sugary, carbonated beverages are comprised of nothing but empty calories in the diet and have been a major contributor to obesity in recent years. Switching to noncarbonated drinks, homemade lemonade (where you control the sugar) or juices diluted 50/50 with water, will cut the calories and make your weight-loss journey that much easier.
A great way to lose weight is purchasing a few instructional fitness DVDs. When it comes to fitness DVDs, the variety is endless. You can go with dance fitness programs or you can even ones that focus on stretching or balance. You'll also be able to workout from the comfort of your own home.
Steaming foods that you would ordinarily bake or fry is a great way to decrease the fat content in your food. Steaming https://food.ndtv.com/health/10-ayurvedic-tips-to-gain-weight-1789182 will cook it without adding butter or any other unhealthy supplement. Choose fresh foods with lots of flavor,that way steaming or grilling can be a great way to cook your meals without adding fat.
Eating salads can be a helpful when trying to lose weight. A salad consisting of a ton of fresh vegetables and a few of your favorite fixings on top (bacon, cheese, dried cranberries, fresh fruit, cold cuts, chicken, or nuts) could be your favorite meal of the day. https://getpocket.com/@myvivaa with your favorite low fat or fat free dressing and you have a fabulous low-fat, nutrient dense meal.
Meditation is a great weight loss technique. Stress can cause you to crave bad food and sabotage yourself. When you meditate, you release pent up stress and anxiety that can affect your moods. The better your mood, the more positive you will feel about all of the small steps that it takes to reach your weight loss goal.
Say you're a condiment lover. You love to slather mayonnaise on your sandwiches. One of many small changes that can save you hundreds of calories over time is to simply use mustard instead of mayo on your next sandwich. Depending on how much mayo you used to use, you could save up to 100 calories from that simple swap.
The best way to accelerate weight loss is to include some sort of weight training regiment. One pound of muscle burns ten times the calories as one pound of fat, and that is just sitting idly. So next time you go to the gym don't just hit the treadmill, but hit some weights to, your waist line will thank you.
An easy way to lose weight is to lower your calorie intake. 3,500 calories equal one pound. Those people who tend to be a little overweight, are consuming more calories then they are burning. If https://twitter.com/vivaa2015 are eating 1,500 calories a day and burning 1,300 calories a day, you will have an extra 200 calories you are putting into your body every day and over about 18 days, you will have gained a pound.
There are many programs that offer support to people trying to lose weight. These programs can help by offering phone calls or meetings, that teach new skills to help you on your weight loss journey. They can also help you by forming a meal plan for you. Having this type of support will help ensure that you stick with the program and have weight loss success.
Be sure to pay attention to your portion sizes. Most foods have nutritional info that will tell you what a portion size is. Take up measuring your food into these portion sizes so that you can learn what they look like. If you know how much you should have, you can be sure to only eat that much.
Diets that use drugs to help you shed pounds may actually work, but they tend to do more harm to your body than good. Instead of losing fat, a lot of these drugs have you losing essential water and muscle, which can produce harmful effects on your organs.
Low-fat yogurt is one of the best snacks that you can have when you are on a diet. Not only is this selection delicious, but you will have a large variety of flavors to choose from, increasing your level of convenience. Choose check this site out as your snack if you are on a diet.
Pasta is one of the worst things that you can eat during the day for a diet, given its high fat and carb content. If you really love pasta, you can try eating whole wheat pasta, which is much better for you in your quest to lose weight and tastes great too.
If you are looking for a snack to notch on to reduce the cravings that you have as the day wears on, eat sunflower seeds. These seeds contain a lot of healthy oils, helping you if you have severely dry skin. Also, they will help to curb your cravings, reducing consumption of poor quality foods.
If you buy a daily lunch while you are at work you can burn some calories by walking a few blocks to go and get it instead of opting for delivery. Even if your job has a cafeteria inside the building, you should still go out to get the exercise.
The best way to lose weight and maintain it is to treat yourself from time to time. If you are really craving something "� if you deny having it "� it will make it harder for you to stay happy with your weight loss program. Instead, eat these treats in moderation, and as they are meant to be eaten - as treats!
As stated at the beginning of this article, few people even realize the basic premise of weight-loss, and thus they're failing miserably at their diets. It's getting to the point that many people feel diets are a failure before they even start them. Use what you've learned throughout this article to change your mindset and ultimately your life.
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International Staging System (ISS)
Description
A system used to describe the extent (stage) of multiple myeloma.
The 3 stages in the ISS are based on the amount of albumin (the main protein found in plasma that helps to maintain blood volume) and beta-2-microglobulin (a protein found on the surface of cells that plays a role in immune response) in the blood.
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COVID-19 (Coronavirus) Update: Testing and Information | Vaccine Updates | Visitor Guidelines
Endoscopy is the best technique for evaluating diseases of the digestive tract. Endoscopy, which means “looking inside,” allows a physician to see directly inside the GI tract.
An endoscope is a flexible fiber-optic tube which can be directed and moved around the digestive tract. At the end of the endoscope tube is a tiny camera connected to a video screen. The tube is placed in the body through the mouth or anus and advanced to the area being examined.
Endoscopy Techniques to Diagnose and Evaluate
Endoscopy, often enables both the diagnosis and treatment of disease in one procedure. Today, technological advances have made endoscopic treatments a preferred alternative to surgery for many procedures involving the digestive tract.
• Upper endoscopy is an examination of the inside of the upper digestive tract — the esophagus, stomach and duodenum (first part of the small intestine). The procedure is used to diagnose the reason for swallowing difficulties, nausea, vomiting, reflux, bleeding, indigestion, abdominal pain or chest pain.
• Lower endoscopy is an examination of the inside of the colon (lower digestive tract). A flexible endoscope is inserted through the anus and rectum and moved into the colon to obtain tissue samples, remove polyps, detect cancer and diagnose causes of bleeding or inflammation. A colonoscopy examines the entire colon.
Froedtert & the Medical College of Wisconsin use a variety of endoscopic techniques to diagnose and evaluate disorders of the digestive tract. These include:
Endoscopic Retrograde Cholangiopancreatography (ERCP)
Endoscopic retrograde cholangiopancreatography (ERCP), which combines video endoscopy and fluoroscopy. ERCP is commonly performed to diagnose conditions of bile ducts and pancreatic ducts, such as narrowing, stones, blockages, tumors and cysts. ERCP is also used to treat these conditions.
Capsule Endoscopy
Capsule endoscopy, used to detect disease of the small intestine. In this procedure, the patient swallows a tiny digital camera shaped like a capsule (“camera pill”).
• As it travels down the esophagus, the camera takes many pictures and sends them to a wireless receiver.
• A computer assembles the images into a digital movie.
The procedure requires no sedation and allows the diagnosis of many diseases. In the esophagus, the camera pill is used to look for conditions such as gastroesophageal reflux disease (GERD). In the small intestine, the capsule can help determine the cause of persistent abdominal pain, unexplained rectal bleeding or diarrhea, and detect polyps, cancer and other causes of bleeding and anemia, such as Crohn’s disease
Endoscopic Ultrasound (EUS)
Endoscopic ultrasound (EUS), combines ultrasound and endoscopy to view the lining and the walls of the upper and lower gastrointestinal tract. An EUS exam may be performed through the mouth or the anus. EUS allows accessing and imaging otherwise unseen areas and is primarily used to detect suspected cancers and benign lesions of the digestive tract and to evaluate the spread (stage) of cancer in order to determine treatment.
EUS is used to stage cancers of the esophagus, stomach, pancreas and rectum, as well as cancer that has spread to adjacent lymph nodes and blood vessels (combining the imaging and fine-needle aspiration capabilities of EUS).
In the digestive tract, EUS is used to evaluate:
Recognized as High Performing by U.S. News & World Report
Froedtert Hospital is nationally ranked in three adult specialties by U.S. News & World Report. Froedtert Hospital is also recognized as high performing in four adult specialties and 14 procedures and conditions, including gastroenterology and GI surgery. Learn more.
Virtual Visits Are Available
Safe and convenient virtual visits by video let you get the care you need via a mobile device, tablet or computer wherever you are. We'll assess your condition and develop a treatment plan right away. To schedule a virtual visit, call 414-805-3666.
Learn More
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5eff3d1f6f98e57329caed0ceb9053d3
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7,809,270,580,226,609,000
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Lung - Hypertrophy, Smooth Muscle
Image of hypertrophy, smooth muscle in the lung from a male F344/N rat in a chronic study
Lung, Bronchiole, Smooth muscle - Hypertrophy in a male F344/N rat from a chronic study. The smooth muscle around this bronchiole is markedly thickened; there is concurrent epithelial hyperplasia.
Figure 1 of 1
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comment:
Bronchial smooth muscle hypertrophy ( Figure 1image opens in a pop-up window ) is characterized by increased size of smooth muscle cells and thickening of the smooth muscle layer around airways. It is a feature of airway wall remodeling in disease states resembling chronic asthma. Increased airway smooth muscle mass usually consists of both smooth muscle cell hyperplasia and hypertrophy, and may contribute to bronchial narrowing and airway hyperresponsiveness. It is occasionally seen in control animals ( Figure 1image opens in a pop-up window ) in toxicity studies, but the significance of the lesion is unclear.
recommendation:
Lung, Smooth muscle - Hypertrophy should be diagnosed and assigned a severity grade. A site modifier (i.e., bronchus or bronchiole) should be included to indicate which type of airway is affected. If both types of airways are affected, the site modifier may be omitted and the affected airways described in the pathology narrative. Associated lesions, such as inflammation or fibrosis, should be diagnosed separately. In some cases, where the smooth muscle hypertrophy is a minor component of a more prominent inflammatory or reactive process, the smooth muscle hypertrophy may be described in the pathology narrative as a component of that process, in lieu of a diagnosis. If hyperplasia of the smooth muscle cells is present concurrently, it may be described in the pathology narrative.
references:
Brewster CE, Howarth PH, Djukanovic R, Wilson J, Holgate ST, Roche WR. 1990. Myofibroblasts and subepithelial fibrosis in bronchial asthma. Am J Respir Cell Mol Biol 3:507-511.
Abstract: http://www.ncbi.nlm.nih.gov/pubmed/2223105
Ebina M, Yaegashi H, Chiba R, Takahashi T, Motomiya M, Tanemura M. 1990. Hyperreactive site in the airway tree of asthmatic patients revealed by thickening of bronchial muscles. A morphometric study. Am Rev Respir Dis 141:1327-1332.
Abstract: http://www.ncbi.nlm.nih.gov/pubmed/2187387
Heard BE, Hossain S. 1973. Hyperplasia of bronchial smooth muscle in asthma. J Pathol 110:319-332.
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Skip to main content
Are you suffering from back breaking pain? If yes, it’s more than likely that you’ve ventured onto the web to find out what’s caused your back pain and how you can alleviate it. New research into these searches, conducted by OTTY Sleep, reveals our biggest back pain queries and where in the UK people suffer the most from a bad back.
The data comes just two months after it was announced, a number of patients are still waiting upwards of a year for help for chronic back pain. Understandably, the pandemic has put more pressure on NHS services than ever, so it’s important to understand how our back pain is being caused and how we can alleviate the pain.
Here, we explore the cities with the biggest back-breaking problems, how these issues may have been caused, and how you can help alleviate the pain and treat the problem.
Back-Breaking Belfast
The research compared Google searches across the 20 most populated cities in the UK. Each city was probed for how often they searched for back pain-related terms. In total, 116 search terms were analyzed for their search frequency, identifying our biggest back-breaking problems, our growing pains, and which city was most likely to feel the effect of spinal aches and back-busting agony.
Back pain is a frequently searched phrase on Google
The study found that people in Belfast were the most likely to suffer from back pain. For every 100,000 people in the Northern Irish capital, 742 people search for a back pain-related term every month.
This is 36 percent above the average city. Of the back pain search terms, people in Belfast were most likely to search for ‘back pain middle’, perhaps indicating where the main issue with their back pain lies.
Belfast was followed by Newcastle upon Tyne and Glasgow as the next most back pain suffering cities. They searched for back pain-related terms 27 percent and 20 percent more than the average city respectively. People in Newcastle sought out “exercises for lower back pain” while Glaswegians searched for ‘back stretches’ over any other back pain-related terms.
For other cities, back pain was less of a sore issue. People in London only searched for back pain 353 times for every 100 thousand people – 35 percent below average. Cardiff and Bradford also suffered less than average back pain; their back pain searches were 35 percent and 16 percent below the average UK city.
The Causes Of Back Pain
Searches for back pain-related terms increased in 14 of the top 20 most populated cities in the UK. So, what are the causes of back pain? And is there a reason why these city people are feeling more back pain?
Back-breaking pain can be non-specific. What does this mean?
We can’t always identify the root cause of back pain. Most back pain is categorized as “non-specific”, meaning that the cause isn’t obvious. However, most pain will originate from the joints, bones, or soft tissue around the spine. For the purpose of identifying the causes of back pain, we’ll stay away from broken bones and infections — the cause is fairly obvious in those cases.
Non-specific back-breaking pain can vary based on our position, will often feel worse when we’re moving, and can appear suddenly or gradually. The most common causes of this type of back pain include:
• Poor posture
• Lifting something awkwardly
• A minor injury, such as a sprain or strain
• Feelings of stress or fatigue
But why do some cities experience worse back pain than others? And what’s changed in the past year to cause this?
As stated, our health and lifestyle are linked to our back pain. Exercise and quality sleep are therefore integral for alleviating back pain. Interestingly, previous OTTY research has found that Belfast has more trouble sleeping than other major UK cities. It mirrors Belfast as the UK city with the most back pain. Could then our sleep quality be linked to our back pain?
In the past year, feelings of fatigue have also increased. Spurred on by the stress of the pandemic and the effects of COVID-19 and its long-term symptoms, muscle tiredness is becoming a concern for many who have suffered from the virus. The study shows that Leicester increased their searches for back pain-related terms by 37 percent in the past year, more than any other city. Therefore, the pandemic may have also contributed to a back pain epidemic in the UK. Don’t fear, most back pain is reversible and can be easily treated.
Putting Back Breaking Pain To Rest
As your back pain can be related to your health and lifestyle, it’s important to tackle these issues head-on to alleviate your spinal sores. In essence, fixing back pain lies in ensuring you are well-rested and that your back has the strength to do all the activities you want to do in the day.
Exercise
We know that you probably won’t feel like it when you’re in pain, but exercise is very important when treating back pain. You should aim to exercise at least three times a week.
This can be as simple as a brisk walk for thirty minutes. Over time, you’ll be building strength in your spine. Idleness allows the muscles around the spine and in the back to become weak. In turn, this means that your spine is less supported, and it becomes more difficult to hold your body in good posture, further leading to more pain.
Quality Rest
Poor sleep and fatigue can also contribute to back-breaking pain. It’s important that we get the rest we need; otherwise, our muscles do not have time to repair and strengthen. This begins with ensuring you’re getting around seven to nine hours of sleep per night.
An uncomfortable bed may also be contributing to your sleep and back pain issues. A hybrid mattress is recommended for supporting your body during sleep, spreading out pressure, and conforming to your body and sleeping position. This allows your muscles to fully rest and repair at night.
Photo by Sinitta Leunen on Unsplash
General Health
While sleep and exercise can go a long way to alleviate and treat your back pain, of course, our general health must improve to help with back pain.
Research has shown that current smokers have a higher occurrence of back pain than former or non-smokers. Meanwhile, our body weight can contribute to back pain. One pound of weight gain can cause four pounds of pressure on your spine.
If you’re looking to help with back-breaking pain, quitting smoking and losing weight should be a priority.
Conclusion
Whether you live in Belfast or London, back pain can be a huge issue for many people who suffer from this problem. Of course, not all back pain can be cured by exercise and quality sleep. Seeing your GP may be the best option for some people. However, getting yourself out for a walk, finding a new mattress, and living a healthier lifestyle is a good place to start.
Who Is The Author?
author
Beth Riley
Beth Riley is the Content Manager at OTTY Sleep.
Beth Riley
Beth Riley
Beth Riley is the Content Manager at OTTY Sleep
Longevity Live is a digital publisher AND DOES NOT OFFER PERSONAL HEALTH OR MEDICAL ADVICE. IF YOU’RE FACING A MEDICAL EMERGENCY, CALL YOUR LOCAL EMERGENCY SERVICES IMMEDIATELY, OR VISIT THE NEAREST EMERGENCY ROOM OR URGENT CARE CENTER. YOU SHOULD CONSULT YOUR HEALTHCARE PROVIDER BEFORE STARTING ANY NUTRITION, DIET, EXERCISE, FITNESS, MEDICAL, OR WELLNESS PROGRAM.
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rubrica
Lavoro
• Dario Consonni1
1. Clinica del lavoro, Milano
Dario Consonni -
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LAVORO Periodo 1 novembre 2012 – 15 gennaio 2013
Ricerca bibliografica periodo dal 1 novembre 2012 al 15 gennaio 2013
Per leggere le caratteristiche di questa ROUTINE di ricerca clicca qui
Stringa: ("occupational exposure"[MeSH Terms] OR "occupational diseases"[MeSH Terms]) OR "occupational health"[MeSH Terms]) OR "workplace"[MeSH Terms]) OR "accidents, occupational"[MeSH Terms]) OR "employment"[MeSH Terms]) OR occupation[Title/Abstract]) OR occupational[Title/Abstract]) OR worker[Title/Abstract]) OR workers[Title/Abstract]) AND ("italy"[MeSH Terms] OR "italy"[All Fields]) AND ("2012/11/01"[PDAT] : "2013/01/15"[PDAT])
1. Rosecrance J, Marras T, Murgia L, Tartaglia R, Baldasseroni A. Carpal tunnel syndrome among ewe dairy farmers in Sardinia, Italy. Am J Ind Med. 2013 Jan 8. doi: 10.1002/ajim.22153. [Epub ahead of print]
Department of Environmental and Radiological Health Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado. [email protected].
Abstract
BACKGROUND: The region of Sardinia, Italy is known internationally for the production of cheeses made from ewe's milk. Although the use of automated milking equipment is available in ewe dairy operations, traditional hand milking is still performed on many ewe farms. The purpose of this study was to evaluate the prevalence of carpal tunnel syndrome (CTS) among farmers that manually milk ewes. METHODS: Worker demographics, upper limb symptoms, and electrophysiologic studies were obtained on 76 ewe farmers recruited from a random sample of 109 in northern Sardinia. Characteristic hand symptoms and electrophysiologic studies were used in the case definition of CTS. RESULTS: Of the 76 farmers evaluated, 42 (55.3%) fit the case definition of CTS in at least one hand. Assuming that all non-respondents did not have CTS, the CTS prevalence ratio would have been 38.5% (42/109) among the randomized sample of ewe farmers. CONCLUSIONS: These findings suggest that CTS is a significant occupational health issue for ewe farmers that continue the traditional methods of manual milking. The recent trend in automated ewe milking machines may help reduce the prevalence of CTS among the next generation of Italian ewe farmers.
Breve commento a cura di Dario Consonni
Lo studio è stato effettuato su un campione casuale di addetti alla mungitura manuale delle pecore. Si è evidenziata una elevatissima (55% sul totale dei partecipanti, quindi almeno il 40% tenendo conto della quota dei non partecipanti) frequenza di casi di sindrome del tunnel carpale (diagnosi documentata con esami elettrofisiologici).
2. Ciarrocca M, Capozzella A, Tomei F, Tomei G, Caciari T. Exposure to cadmium in male urban and rural workers and effects on FSH, LH and testosterone. Chemosphere. 2013 Jan 2. pii: S0045-6535(12)01299-4. doi: 10.1016/j.chemosphere.2012.10.060. [Epub ahead of print]
Department of Occupational Medicine, "Sapienza" University of Rome, Viale Regina Elena 336, 00161 Rome, Italy.
Abstract
OBJECTIVE: This cross-sectional study was conducted to assess the relationship between exposure to cadmium and circulating reproductive hormone levels in urban and rural male workers. MATERIALS AND METHODS: Urinary cadmium, blood cadmium, luteinizing hormone (LH), follicle stimulating hormone (FSH) and testosterone were obtained from 86 non-smoking traffic policemen and 86 subjects working as roadmen in a rural area. All subjects were monitored to evaluate airborne exposure to cadmium. RESULTS: The mean value of exposure to cadmium was 1.3ngm(-3) in traffic policemen, while the mean value was less than 0.5ngm(-3) in roadmen. The mean concentrations of urinary cadmium (1.4 vs. 0.9μgg(-1) creatinine; p=0.001), blood cadmium (1.1 vs. 0.7μgl(-1); p=0.000), FSH (2.6 vs. 3.2μlUml(-1); p=0.02) and LH (2.6 vs. 3.1μlUml(-1); p=0.03) were significantly different between traffic policemen and roadmen. No differences were found in the mean values of testosterone between the two groups. Multiple linear regression models showed associations between (a) urinary cadmium, airborne cadmium, working life, job category and consumption of water from water supply (b) blood cadmium, airborne cadmium and job category (c) the values of FSH and age, working life, job category, urinary cadmium and blood cadmium (d) the values of LH and both the age and working life. CONCLUSION: The above results must be confirmed by further studies, but they indicate the influence of exposure to the cadmium present in urban air on the circulating FSH, even at low doses.
3. Filiberti R, Marroni P, Mencoboni M, Mortara V, Caruso P, Cioè A, Michelazzi L, Merlo DF, Bruzzone A, Bobbio B, Del Corso L, Galli R, Taveggia P, Dini G, Spigno F. Individual predictors of increased serum mesothelin in asbestos-exposed workers. Med Oncol. 2013 Mar;30(1):422. doi: 10.1007/s12032-012-0422-6. Epub 2013 Jan 1.
Epidemiology, Biostatistics and Clinical Trials, IRCCS AOU San Martino-IST - Istituto Nazionale per la Ricerca sul Cancro, Largo Rosanna Benzi, 10, 16132, Genoa, Italy, [email protected].
Abstract
The soluble mesothelin-related peptide (SMRP), a candidate marker for screening of subjects with asbestos exposure, is influenced by some individual and clinical factors. The aim of this study was to quantify the role of age, smoking, weight, presence of diseases and exposure to asbestos on serum SMRP levels in a large series of subjects exposed to asbestos, possible candidates for mesothelioma screening. One thousand seven hundred and four participants underwent clinical examination and were interviewed on medical anamnesis, occupation, smoking and weight. SMRP was measured by an ELISA assay. Overall, median SMRP was 0.4 (IQR 25-75: 0.3-0.7) nmol/l. It was higher in current smokers and in subjects with a cumulative asbestos exposure >50 ff/cc/years than in all the other subjects (p < 0.001 and p = 0.002, respectively). SMRP was positively correlated with age (ρ = 0.11, p < 0.001) and, inversely, with BMI (ρ = -0.15, p < 0.001). SMRP was lower in healthy subjects (n = 1,217: median 0.4 nmol/l) than in subjects with malignant tumors (n = 118: 0.5 nmol/l; p = 0.01), asbestos-related pleural lesions (plaques or thickenings, n = 152: 0.6 nmol/l; p < 0.001) and other benign diseases (n = 182: 0.5 nmol/l; p = 0.04). Multivariate analysis revealed significant predictors of increased SMRP: age >57 years, current smoking, a positive anamnesis for cancer and for asbestos-related pleural lesions, and BMI < 25. Some clinical and demographic variables are associated with serum SMRP levels. The degree of these associations is low, nevertheless they should be accounted for in the interpretation of SMPR as a candidate marker predictive of mesothelioma. The potential predictive value of serum SMRP in screening/surveillance programs must be validated in prospective studies.
4. Zanardi F, Salvarani R, Cooke RM, Pirastu R, Baccini M, Christiani D, Curti S, Risi A, Barbieri A, Barbieri G, Mattioli S, Violante FS. Carcinoma of the Pharynx and Tonsils in an Occupational Cohort of Asphalt Workers. Epidemiology. 2013 Jan;24(1):100-103.
From the aSection of Occupational Medicine, Department of Internal Medicine, Geriatrics and Nephrology, Alma Mater Studiorum-University of Bologna, Bologna, Italy; bOccupational Health Unit, Bologna Local Health Authority, San Giorgio di Piano, Bologna, Italy; cDepartment of Biology and Biotechnology "Charles Darwin," La Sapienza University of Rome, Rome, Italy;dDepartment of Statistic, University of Florence, Florence, Italy; eHarvard University, Environmental Health and Epidemiology Departments, Boston, MA; and fOccupational Medicine Service, Alma Mater Studiorum-University of Bologna, Bologna, Italy.
Abstract
BACKGROUND:: We investigated a possible association between pharyngeal/tonsillar carcinoma and mixed carcinogen exposures in an asphalt roll company in Italy that used asbestos until 1979, when a new factory was built using a different production process. METHODS:: We evaluated all workers involved in the entire production history of the company, divided into two subcohorts based on exposure status (workers in the original factory, 1964-1979, and those who worked only in the new factory, 1980-1997). We ascertained the vital status of the study population in February 2001. RESULTS:: Among the subset of workers in the earlier subcohort, there were five deaths from pharyngeal/tonsillar carcinoma for a standardized mortality ratio of 21 (95% confidence interval = 8.8-51). No cases were recorded among workers hired after 1979. CONCLUSION:: The increased standardized mortality ratio for this relatively rare cancer among workers exposed before 1979 may have been due to carcinogenic exposures at the plant.
5. Cocco P, Satta G, Dubois S, Pili C, Pilleri M, Zucca M, 't Mannetje AM, Becker N, Benavente Y, de Sanjosé S, Foretova L, Staines A, Maynadié M, Nieters A, Brennan P, Miligi L, Ennas MG, Boffetta P. Lymphoma risk and occupational exposure to pesticides: results of the Epilymph study. Occup Environ Med. 2013 Feb;70(2):91-8. doi: 10.1136/oemed-2012-100845. Epub 2012 Nov 1.
Department of Public Health, Occupational Health Section, University of Cagliari, Asse Didattico - Policlinico Universitario, SS 554, km 4,500, 09042 Monserrato (Cagliari), Italy; [email protected].
Abstract
OBJECTIVES: We investigated the role of occupational exposure to specific groups of agrochemicals in the aetiology of lymphoma overall, B cell lymphoma and its most prevalent subtypes. METHODS: In 1998-2003, 2348 incident lymphoma cases and 2462 controls were recruited to the EPILYMPH case-control study in six European countries. A detailed occupational history was collected in cases and controls. Job modules were applied for farm work including specific questions on type of crop, farm size, pests being treated, type and schedule of pesticide use. In each study centre, industrial hygienists and occupational experts assessed exposure to specific groups of pesticides and individual compounds with the aid of agronomists. We calculated the OR and its 95% CI associated with lymphoma and the most prevalent lymphoma subtypes with unconditional logistic regression, adjusting for age, gender, education and centre. RESULTS: Risk of lymphoma overall, and B cell lymphoma was not elevated, and risk of chronic lymphocytic leukaemia (CLL) was elevated amongst those ever exposed to inorganic (OR=1.6, 95% CI 1.0 to 2.5) and organic pesticides (OR=1.5, 95% CI 1.0 to 2.1). CLL risk was highest amongst those ever exposed to organophosphates (OR=2.7, 95% CI 1.2 to 6.0). Restricting the analysis to subjects most likely exposed, no association was observed between pesticide use and risk of B cell lymphoma. CONCLUSIONS: Our results provide limited support to the hypothesis of an increase in risk of specific lymphoma subtypes associated with exposure to pesticides.
6. Mirabelli D, Cacciatore AM, Ferrante D, Amendola P, Vermeulen R, Merletti F. Cohort study of workers employed in an Italian tire manufacturing plant, 1962-2004. Cancer Causes Control. 2012 Dec;23(12):2023-9. doi: 10.1007/s10552-012-0083-y. Epub 2012 Oct 20.
Unit of Cancer Epidemiology, University of Turin and CPO-Piemonte, via Santena 7, 10125, Turin, Italy. [email protected]
Abstract
PURPOSE: To investigate mortality and bladder cancer incidence among workers of a tire manufacturing plant where antioxidants severely contaminated by beta-naphthylamine were never used. METHODS: Mortality follow-up was performed of 9,501 workers first hired between 1962 when the plant started operations and 2000. Person-years of observation from 1962 to 2004, expected deaths, and standardized mortality ratios (SMR) were calculated. Follow-up for bladder cancer incidence from 1988 to 2003 was carried out, and standardized incidence ratios (SIR) were calculated. Multivariable (Poisson) analyses of bladder cancer incidence and mortality by duration of employment (DOE) and time since first employment (TSFE) were performed. RESULTS: Among men, SMRs were significantly reduced for all causes, all cancers, lung cancer, cardiovascular, and ischemic heart diseases. Bladder cancer mortality and leukemia mortality were close to expectation but increased with TSFE. Seventy-two incident cases of bladder cancer were observed (SIR = 1.15; 95 % confidence interval 0.90-1.44), and multivariable analysis suggested a possible increase in rate ratios with DOE. Among women, mortality was close to expectation, but the limited number of observed deaths prevented detailed analyses. CONCLUSIONS: No significant cancer excess was observed. A suggestion of increased risks of bladder cancer and leukemias after extended TSFE was present in men, deserving consideration as exposure to carcinogens possibly occurred early in plant operation. Furthermore, this cohort of workers is still relatively young and less than 10 % have died. There was, thus, limited power to detect small increases in risk at rare cancer sites. Further epidemiological surveillance of this cohort is planned.
7. Peluso M, Bollati V, Munnia A, Srivatanakul P, Jedpiyawongse A, Sangrajrang S, Piro S, Ceppi M, Bertazzi PA, Boffetta P, Baccarelli AA. DNA methylation differences in exposed workers and nearby residents of the Ma Ta Phut industrial estate, Rayong, Thailand. Int J Epidemiol. 2012 Dec;41(6):1753-1760. Epub 2012 Oct 13.
Cancer Risk Factor Branch, Cancer Prevention and Research Institute, Florence, Italy, Department of Occupational and Environmental Health, University of Milan and Istituto Di Ricovero e Cura a Carattere Scientifico Ca' Granda Maggiore Policlinico Hospital, Milan, Italy, Molecular Epidemiology Unit, Research Division, National Cancer Institute, Bangkok, Thailand, Molecular Epidemiology Unit, National Cancer Institute, Genoa, Italy, The Tisch Cancer Institute and Institute for Translational Epidemiology, Mount Sinai School of Medicine, New York, NY, USA, International Prevention Research Institute, Lyon, France and Laboratory of Environmental Epigenetics, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA.
Abstract
BACKGROUND: Adverse biological effects from airborne pollutants are a primary environmental concern in highly industrialized areas. Recent studies linked air pollution exposures with altered blood Deoxyribo-nucleic acid (DNA) methylation, but effects from industrial sources and underlying biological mechanisms are still largely unexplored. METHODS: The Ma Ta Phut industrial estate (MIE) in Rayong, Thailand hosts one of the largest steel, oil refinery and petrochemical complexes in south-eastern Asia. We measured a panel of blood DNA methylation markers previously associated with air pollution exposures, including repeated elements [long interspersed nuclear element-1 (LINE-1) and Alu] and genes [p53, hypermethylated-in-cancer-1 (HIC1), p16 and interleukin-6 (IL-6)], in 67 MIE workers, 65 Ma Ta Phut residents and 45 rural controls. To evaluate the role of DNA damage and oxidation, we correlated DNA methylation measures with bulky DNA and 3-(2-deoxy-β-D-erythro-pentafuranosyl)pyrimido[1,2-α]purin-10(3H)-one deoxyguanosine (M(1)dG) adducts. RESULTS: In covariate-adjusted models, MIE workers, compared with rural residents, showed lower LINE-1 (74.8% vs 78.0%; P < 0.001), p53 (8.0% vs 15.7%; P < 0.001) and IL-6 methylation (39.2% vs 45.0%; P = 0.027) and higher HIC1 methylation (22.2% vs 15.3%, P < 0.001). For all four markers, Ma Ta Phut residents exhibited methylation levels intermediate between MIE workers and rural controls (LINE-1, 75.7%, P < 0.001; p53, 9.0%, P < 0.001; IL-6, 39.8%, P = 0.041; HIC1, 17.8%, P = 0.05; all P-values vs rural controls). Bulky DNA adducts showed negative correlation with p53 methylation (P = 0.01). M(1)dG showed negative correlations with LINE-1 (P = 0.003) and IL-6 methylation (P = 0.05). CONCLUSIONS: Our findings indicate that industrial exposures may induce alterations of DNA methylation patterns detectable in blood leucocyte DNA. Correlation of DNA adducts with DNA hypomethylation suggests potential mediation by DNA damage.
8. Peluso M, Srivatanakul P, Jedpiyawongse A, Sangrajrang S, Munnia A, Piro S, Ceppi M, Boffetta P, Godschalk RW, van Schooten FJ. Aromatic DNA adducts and number of lung cancer risk alleles in Map-Ta-Phut Industrial Estate workers and nearby residents. Mutagenesis. 2013 Jan;28(1):57-63. doi: 10.1093/mutage/ges053. Epub 2012 Sep 17.
Cancer Risk Factor Branch, Cancer Prevention and Research Institute, Florence, Italy.
Abstract
The Map-Ta-Phut Industrial Estate (MIE) in Rayong, Thailand, is the location of one of the largest industrial complexes in southeastern Asia. The MIE complex produces a mixture of air pollutants, including polycyclic aromatic hydrocarbons, compounds capable to induce the generation of DNA adducts. DNA adducts are considered to be a biomarker of carcinogen exposure; however, its production can be modulated by genetic susceptibility. Thus, we analysed the influence of EPHX1 His139Arg (A>G, rs2234922) and NQO1 Pro187Ser (C>T, rs1800566) involved in the metabolism of polycyclic aromatic hydrocarbons; MnSOD(2) Val16Ala (C>T, rs1799725) a gene that acts against the free radical generation; APE1/Ref-1 Asp148Glu (T>G, rs3136820) a gene involved in the repair of DNA, and in the control of cell-cycle and apoptosis on leucocyte DNA adducts in 77 MIE workers, 69 Map-Ta-Phut residents, and 50 rural controls, Rayong, Thailand. We searched for associations with the 'sum of at-risk alleles' by combining the variant alleles of EPHX1, NQO1 and MnSOD(2) together with the wild-type allele of APE1, since they appeared to influence lung cancer risk. Although our findings revealed significant associations between DNA adducts and the EPHX1 His139Arg and NQO1 Pro187Ser polymorphisms, the combination of at-risk alleles was found to affect DNA damage much stronger. DNA adducts were significantly increased in the individuals bearing 4 and ≥5 at-risk alleles [mean ratio (MR) = 1.55, 95% CI 1.10-2.18, P = 0.012, and MR = 2.11, 95% CI 1.27-3.51, P = 0.004, respectively)]. After correction for residence/employment categorisation, a significant increment was present in the MIE workers with ≥5 alleles (MR = 2.88, 95% CI 1.46-5.71, P = 0.003). Our data indicate relationships between the generation of DNA adducts and the enzymatic activities of EPHX and NQO1. The combination of unfavourable genetic variants seems to determine the individuals' susceptibility, rather than a single polymorphism.
9. Abballe A, Barbieri PG, di Domenico A, Garattini S, Iacovella N, Ingelido AM, Marra V, Miniero R, Valentini S, De Felip E. Occupational exposure to PCDDs, PCDFs, and PCBs of metallurgical workers in some industrial plants of the Brescia area, northern Italy. Chemosphere. 2013 Jan;90(1):49-56. doi: 10.1016/j.chemosphere.2012.06.073. Epub 2012 Aug 14.
Dipartimento Ambiente e connessa Prevenzione Primaria, Istituto Superiore di Sanità, Roma, Italy.
Abstract
BACKGROUND: The study was carried out in order to respond to public concern on the occupational exposure of metallurgical workers to highly toxic PCDDs, PCDFs, and PCBs in the area of the city of Brescia, northern Italy. OBJECTIVES: The study investigated the effects on the haematic burden of occupational exposures to the aforesaid contaminants in different work environments, attempting to establish causal relationships and providing indications for occupational health preventive measures. METHODS: Chemical concentrations were measured in blood serum of "professionally exposed" (PE) and "not professionally exposed" (NPE) subjects. NPE subjects included industrial administrative employees, Brescia inhabitants, and remote rural people. RESULTS: The central tendency indexes of contaminant cumulative concentrations were higher in PE than in NPE samples (for the mean values: PCDDs+PCDFs, 22.9 vs. 19.5 pgWHO-TEQ(1997)/g lb; DL-PCBs, 26.0 vs. 23.6 pgWHO-TEQ(1997)/g lb; PCDDs+PCDFs+DL-PCBs (TEQ(TOT)), 48.9 vs. 43.1 pgWHO-TEQ(1997)/g lb; Σ(6)[NDL-PCBs], 427 vs. 401 ng g(-1)lb); however, no statistical differences were detected at P=0.05. A significant difference for PCDDs+PCDFs and TEQ(TOT) was observed as the NPE data were progressively reduced to those of the remote rural people. The existence of a differential occupational exposure due to different environments was detected by applying the factor analysis to congener-specific data (analytical profiles). CONCLUSIONS: Findings indicate that metallurgical workers may be exposed to PCDD, PCDF, and PCB more than the general population, in particular due to non-negligible contributions to exposure from workplace ambient air. Findings also suggest that an improvement of preventive measures may be required to avoid chemical overexposure in certain metallurgical workplaces. To identify exposure groups, the DL- and NDL-PCB analytical profiles seemed to be more sensitive to environmental exposure sources/pathways than those of PCDDs and PCDFs.
10. Rui F, Bovenzi M, Prodi A, Fortina AB, Romano I, Corradin MT, Filon FL. Concurrent sensitization to metals and occupation Contact Dermatitis. 2012 Dec;67(6):359-66. doi: 10.1111/j.1600-0536.2012.02100.x. Epub 2012 May 12.
Clinical Unit of Occupational Medicine, Department of Medical Sciences, University of Trieste, Trieste 34129, Italy. [email protected]
Abstract
BACKGROUND: Cosensitization to nickel, cobalt and chromium occurs in the general population and in some occupational groups. OBJECTIVES: To estimate the isolated and concurrent occurrence of nickel, cobalt and chromium contact sensitization and their association with individual and occupational risk factors. PATIENTS/METHODS: Twelve thousand four hundred and ninety-two patients were patch tested with the European baseline series between 1997 and 2004 in north-eastern Italy. The associations between patch test results and patient characteristics and occupations were investigated by means of multinomial logistic regression analysis. RESULTS: Of the patients, 34.7% (4334 patients) had one or more positive patch test reactions to metals. As compared with those with negative reactions to all three metals, nickel sensitization was significantly higher in females than in males, not only as monosensitization, but also as cosensitization with cobalt, with chromium, or with both metals. Building and related trades workers showed positive reactions to chromium + nickel [odds ratio (OR) 1.99; 95% confidence interval (CI) 1.05-3.76) and chromium + cobalt (OR 2.61; 95% CI 1.46-4.67]. Cleaning workers showed a high prevalence of nickel, chromium, nickel + chromium and nickel + cobalt + chromium cosensitization (ORs 1.29, 1.66, 2.11, and 1.79, respectively). An excess risk for cosensitization to all three metals was found in textile and leather workers (OR 2.19; 95% CI 1.10-4.33), and in bartenders (OR 2.10; 95% CI 1.03-4.26). CONCLUSIONS: Some occupational groups are more likely to develop nickel, cobalt and chromium cosensitization.
11. Ciarrocca M, Tomei G, Palermo P, Caciari T, Cetica C, Fiaschetti M, Gioffrè PA, Tasciotti Z, Tomei F, Sancini A. Environmental and biological monitoring of arsenic in outdoor workers exposed to urban air pollutants. Int J Hyg Environ Health. 2012 Nov;215(6):555-61. doi: 10.1016/j.ijheh.2011.11.014. Epub 2011 Dec 24.
Department of Occupational Medicine, Sapienza University of Rome, Viale Regina Elena 336, 00161 Rome, Italy.
Abstract
The aim of this study is to evaluate personal exposure to As in urban air in two groups of outdoor workers (traffic policemen and police drivers) of a big Italian city through: (a) environmental monitoring of As obtained by personal samples and (b) biological monitoring of total urinary As. The possible influence of smoking habit on urinary As was evaluated. We studied 122 male subjects, all Municipal Police employees: 84 traffic policemen and 38 police drivers exposed to urban pollutants. Personal exposure to As in air was significantly higher in traffic policemen than in police drivers (p=0.03). Mean age, length of service, alcohol drinking habit, number of cigarettes smoked/day and BMI were comparable between the groups of subjects studied. All subjects were working in the same urban area where they had lived for at least 5 yrs. Dietary habits and consumption of water from the water supply and/or mineral water were similar in traffic policemen and in police drivers. The values of total urinary As were significantly higher in traffic policemen (smokers and non smokers) than in police drivers (smokers and non smokers) (p=0.02). In the subgroup of non-smokers the values of total urinary As were significantly higher in traffic policemen than in police drivers (p=0.03). In traffic policemen and in police drivers total urinary As values were significantly correlated to the values of As in air (respectively r=0.9 and r=0.8, p<0.001). This is the first research in literature studying the exposure to As in outdoor workers occupationally exposed to urban pollutants, such as traffic policemen and police drivers. Personal exposure to As in the air, as well as the urinary excretion of As, is significantly higher in traffic policemen compared to drivers. These results can provide information about exposure to As in streets and in car for other categories of outdoor workers similarly exposed.
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Seasonal allergies
Seasonal allergies are most commonly caused by pollens from trees, grasses, or weeds. Mold spores are another common cause of allergy symptoms.
Symptoms of seasonal allergies include runny nose, sneezing, stuffy nose, cough, itchy or red eyes, sore throat or itching.
Over-the-Counter Treatment:
1. Nasal rinses: Multiple forms are available over-the-counter including neti pot and rinse bottles. These work by rinsing the pollen out of the nose, thereby reducing exposure.
2. Steroid nasal sprays: Flonase (fluticasone) and Nasacort are the most common forms. These work by reducing the swelling, congestion, and mucus production. These are best used daily, and may take a few weeks to see the full effect. May cause minor nasal irritation or nose bleeds.
3. Antihistamines: Numerous over-the-counter forms are available: allegra (foxofenadine), claritin (loratidine), zyrtec (cetirizine), etc. Reduce itching, sneezing, and runny nose. Most commonly cause fatigue.
4. Decongestants: Phenylephrine, sudafed, Afrin (oxymetazoline). Reduce stuffy nose symptoms. Do not take if you have high blood pressure as these medications can raise your blood pressure. Do not use for more than a few days in a row, particularly the nasal sprays, as they can worsen symptoms with long term use.
5. Some people benefit from a combination of the above treatments.
Prescription Treatment:
If the over-the-counter treatments are not sufficiently covering your symptoms contact your doctor about these other treatments.
1. Singulair: A daily pill which may reduce symptoms of runny nose and congestion.
Specialist Treatment:
If these treatments fail to adequately control allergy symptoms, the next step would be a referral to an allergist. At the allergist appointment you will likely undergo skin testing to see which pollens or molds may be causing your symptoms. This involves injecting small amounts of the allergen into your skin to check for color change or swelling. Once the allergen is identified, you may be able to be treated with weekly allergy shots or daily tablets which dissolve under the tongue. These shots and tablets contain small amounts of the allergen as well and allow your body to slowly build tolerance to them. These take several months to work, but are very effective at reducing allergy symptoms.
Allergy prevention:
1. Start your allergy medication a couple of weeks prior to the season which triggers your allergies.
2. Stay inside as much as possible, keeping windows closed, and keeping car windows closed.
3. Take a shower before bed to rinse pollens off of your body.
4. Use an air purifier in your bedroom at night.
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Category: DEFAULT
Back bones chart able
Changing Shape NE 63rd St, # Vancouver, Wa Ambesonne Human Anatomy Pencil Pen Holder, Vintage Chart of Body Front Back Skeleton and Muscle System Bone Mass Graphic, Printed Ceramic Pencil Pen Holder for Desk Office Accessory, Ruby Cream. Anatomy of the Spine Overview. The spine is made of 33 individual bones stacked one on top of the other. This spinal column provides the main support for your body, allowing you to stand upright, bend, and twist, while protecting the spinal cord from injury.
Back bones chart able
Anatomy of the Spine Overview. The spine is made of 33 individual bones stacked one on top of the other. This spinal column provides the main support for your body, allowing you to stand upright, bend, and twist, while protecting the spinal cord from injury. Aug 07, · Human Back Bone Chart, Find out more about Human Back Bone Chart. Skip to content. Human Anatomy Body. Human Anatomy for Muscle, Reproductive, and Skeleton. Home. Human Bone Name Picture 12 photos of the "Human Bone Name Picture" human body bones names picture, human bones name and picture, human bones pictures names, Bone, human body bones. "Chart of the Effects of Spinal Misalignments": Listing of the spine, its bones and areas along which which parts are affected and what symptoms correspond with each. Chiropractic Chart, love this shotsdaily.com people to understand that nerve supply effects EVERYthing in the body! Jun 15, · At the same time the bones grow larger by growing back into the growth plates. This process continues until the end of puberty, when the growth plate stops growing and the bones fuse permanently into a single bone. The vast difference in height and limb length between birth and adulthood are mainly the result of endochondral ossification in the. Lower back pain is a common ailment. This can arise for reasons ranging from improper posture to a compression fracture. Lower back issues can put pressure on the lumbar spine nerves and create. Spinal Anatomy The Regions of the Spine. The spine is an intricate set of bones, muscles, nerves and discs. thoracic spine and low back. Each Vertebral Bone. The strong fibers of the disc annulus, and the posterior facet joints, prevent excessive movement. The spine is able to bend and extend because there are many motion segments which. Ambesonne Human Anatomy Pencil Pen Holder, Vintage Chart of Body Front Back Skeleton and Muscle System Bone Mass Graphic, Printed Ceramic Pencil Pen Holder for Desk Office Accessory, Ruby Cream. Apr 02, · Using a Bone Density Chart to Estimate Total Bone Loss. To better understand the current health of your bones, you should multiply your T-score by 10 percent (as shown in the bone density results chart below). This will give you a rough estimate of how much bone density has already been lost. Bone Density Chart for Estimated Amount of Bone Loss. Changing Shape NE 63rd St, # Vancouver, Wa Date: /12/01 (Rev. /09/30) Disabled World - shotsdaily.com Synopsis: Information and pictures of the spine and spinal cord showing C1 to S5 vertebra and which vertebra effect various body functions. The human spinal cord consists of nerves that connect the brain to nerves in the body Author: Disabled World.Table 2 describes the bone markings, which are illustrated in (Figure ). There are Bone Markings (Table 2). Marking Spine, Sharp process, Ischial spine. Fractures, dislocations, and soft tissue injuries involving the thoracic spine are frequent, and often they are associated with serious clinical manifestations. Table . The spinal column (or vertebral column) extends from the skull to the pelvis and is made up of 33 individual bones termed vertebrae. A spine chart is a popular visualisation that shows, at a glance, how one it is common to display the data table for the spine chart beside it. Diagram of the human spine showing C1 to S5 vertebrae identification letters and of spinal injury may still be able to breathe on their own and speak normally. The spinal cord is the continuation of the brainstem, it lies protected within the vertebral column of the spine. A spinal nerve is any of the The vertebral column is also known as the spinal column or spine (Figure 1). These curves increase the vertebral column's strength, flexibility, and ability to . This diagram shows how the thoracic vertebra connects to the angle of the rib. TABLE OF CONTENTS. Page 3: The Spine. Page 4: Spine Surgery. Page 7: Before Surgery. Page 9: Pre-operative Medications. Page Day of Surgery. The vertebral column, also known as the backbone or spine, is part of the axial skeleton. . The cervical curve forms when the infant is able to hold up its head ( at three or four months) and to sit upright (at nine months). The lumbar curve forms. Columbia minx slip on omni-heat sleeping, exodus movement from the depths, survival craft 1.19 apk, texture packs for minecraft mac, amrabat nordin video er, qurani wazaif in urdu
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Quick Answer: Does Caffeine Cause Tension Headaches?
How do you relax the muscles in your head?
Take several deep breaths.
Breathe out slowly, relaxing areas that feel tight and cramped, while you picture a peaceful scene.
Drop your chin toward your chest, then gently and slowly move your head in a half circle from one side to the other.
Take another deep breath and let the air out slowly..
What does a dehydration headache feel like?
A dehydration headache can feel like a dull headache or an intense migraine. Pain from a dehydration headache can occur at the front, back, side, or all over the head. Unlike a sinus headache, a person experiencing a dehydration headache will likely not experience facial pain or pressure.
How long do headaches last after quitting caffeine?
Kuhar explained that caffeine blocks receptors in the brain that can dilate blood vessels causing headaches. “Withdrawal symptoms can start from 12 to 20 hours after your last cup of coffee and peak about two days later and can last about as long as a week,” Kuhar added.
What does caffeine headache feel like?
Symptoms. This type of headache is typically moderately to severely painful, located on both sides of the head, and tends to worsen with physical activity. The pain will usually peak after one or two days without caffeine and lasts two to nine days.
Why am I getting tension headaches everyday?
They may be due to tension in the muscles at the back of the head and neck, but it is now clear that this is not always the cause. Other causes reported by patients include stress, tiredness, hunger and eye strain. Many chronic tension headaches develop for no apparent reason.
What is a natural way to relieve tension headaches?
18 Remedies to Get Rid of Headaches NaturallyDrink Water. Inadequate hydration may lead you to develop a headache. … Take Some Magnesium. … Limit Alcohol. … Get Adequate Sleep. … Avoid Foods High in Histamine. … Use Essential Oils. … Try a B-Complex Vitamin. … Soothe Pain with a Cold Compress.More items…•
How do tension headaches feel?
Signs and symptoms of a tension headache include: Dull, aching head pain. Sensation of tightness or pressure across your forehead or on the sides and back of your head. Tenderness on your scalp, neck and shoulder muscles.
How do you stop tension headaches?
Can you prevent tension headaches?Try to reduce stress.Make sure you sleep, exercise, and eat on a regular schedule.Make sure you practice good posture. … Try not to strain your eyes when you use your computer.Get treatment for depression or anxiety if you have those health problems.Try using a headache diary.
What’s best for tension headaches?
Pain relievers. Simple OTC pain relievers are usually the first line of treatment for reducing headache pain. These include the drugs aspirin, ibuprofen (Advil, Motrin IB, others) and naproxen (Aleve). Prescription medications include naproxen (Naprosyn), indomethacin (Indocin) and ketorolac (Ketorolac Tromethamine).
How long can a tension headache last?
You may also feel the neck muscles tighten and a feeling of pressure behind the eyes. A tension headache normally is not severe enough to prevent you doing everyday activities. It usually lasts for 30 minutes to several hours, but can last for several days.
Does magnesium help with tension headaches?
Low levels of magnesium levels in the blood and brain have been found in a larger number of tension headache and migraine sufferers. Magnesium supplementation has been shown to help significantly reduce and eliminate the occurrence of tension headaches by stabilizing the magnesium deficiency.
What happens when you quit caffeine cold turkey?
Caffeine withdrawal can occur in anyone who regularly consumes caffeine and then abruptly discontinues its use. Common symptoms include headache, fatigue, low energy, irritability, anxiety, poor concentration, depressed mood and tremors, which can last anywhere from two to nine days.
What relieves a tension headache?
The following may also ease a tension headache:Apply a heating pad or ice pack to your head for 5 to 10 minutes several times a day.Take a hot bath or shower to relax tense muscles.Improve your posture.Take frequent computer breaks to prevent eye strain.
Does heat help tension headache?
Ease muscle tension Tense muscles can trigger tension-type headaches. Apply heat or ice to relieve tense neck and shoulder muscles. Use a heating pad set on low, a hot water bottle, a hot shower or bath, a warm compress, or a hot towel.
Can Sleep Help tension headaches?
Although more studies are needed, a small study has shown promise for sleep being a combatant against headache pain. Out of 32 participants with persistent tension-type headaches, 81 percent said going to sleep was their most effective strategy for getting rid of a headache.
Will a muscle relaxer help a tension headache?
Muscle relaxants: These medications work by relieving muscle tension and stiffness. Tizanidine (Zanaflex) is an example of a muscle relaxant used to treat tension headaches. Opioids: Also known as narcotics, opioids pack a powerful punch when it comes to treating your tension headache pain.
Does caffeine help with tension headaches?
Whether it’s a run-of-the-mill tension headache or a migraine, caffeine can help. That’s why it’s an ingredient in a lot of popular pain relievers. It can make them as much as 40% more effective. Sometimes you can stop the pain in its tracks just by having caffeine alone.
Can lack of caffeine cause tension headaches?
Caffeine narrows the blood vessels in your brain. Without it, your blood vessels widen. The resulting boost in blood flow could trigger a headache or result in other symptoms of withdrawal.
What triggers tension headaches?
Tension headaches occur when neck and scalp muscles become tense or contract. The muscle contractions can be a response to stress, depression, head injury, or anxiety. They may occur at any age, but are most common in adults and older teens. It is slightly more common in women and tends to run in families.
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15 259
Cited 0 times in
Blood Volume Change and Side Effects during Various Sodium Ramping in Hemodialysis
Other Title
다양한 고염투석액을 이용한 혈액투석시 혈액량의 변화 및 부작용 발생의 관찰
Authors
Ma, KA; Kim, HS; Kim, MS; Kim, SJ; Jeong, CG; Kim, HJ; Ko, KH; Kim, SD; Ji, SB; Shin, GT; Kim, DH
Citation
Taehan Sinjang Hakhoe chi, 18(3):436-444, 1999
Journal Title
Taehan Sinjang Hakhoe chi; The Korean journal of nephrology; 대한신장학회지
ISSN
1225-0015
Abstract
Chronic hemodialysis patients frequently experience hemodialysis(HD)-related side
effects caused by excessive ultrafiltration and abrupt change of osmolality. Sodium
ramping in HD is known to reduce ultrafiltration-related side effects, but it frequently induces symptoms related to sodium overload. We wanted to know the relationship between blood volume changes and the side effects related to ultra-filtration during hemodialysis and whether we can individualize various sodium ramping methods according to the effect of change in blood volume(BV) and side effects of sodium
ramping. We studied 9 hypotension-prone patients during HD. The duration of the study lasted (or 5 weeks, each week using different sodium ramping protocols: protocol 1; dialysate [Na+] of 140mEq/L, protocol 2; dialysate [Na+] same as the predialysis seam [Na+], protocol 3; dialysate [Na+] was 20mEq/L greater than that of the patient's serum for 1hr, 10mEq/L greater than patient's serum [Na+] for 2hr and den the same as patient's serum [Na+] for the last 1hr, protocol 4; at the beginning of
dialysis, dialysate sodium was ramped to 20mEq/L above the patient's seam sodium and
then on a straight linear fashion lowered to the predialysis serum [Na+] at the end of dialysis, protocol 5; sodium was constantly ramped to 10 mEq/L above serum [Na+]. We measured the △BV with Crit-Line IIR(In-Line Diagnostics, Corp., Riverdale, USA), the blood Pressure during each HD and interdialytic weight gain.
We documented subjective symptoms which occurred during the 5 treatment protocols
by patient's questionnaire after each HD.
The results were as follows.
1) The mean age of the patients(M : F=3 : 6) was 54.1 years and 6 patiens were diabetics.
2) There was no significant difference in the △BV among the 5 protocols in both
whole study population and individual. Neither was there a statistically signigicant difference in the △BV with respect to hypotension during HD.
3) There were no episodes of hypotension(P value <0.001) with protocols 3, 4, 5
compared to protocols 1 and 2.
4) Three patients during protocols 4 and 5 experienced more thirst after HD than
during protocol 1 and one Patient during protocol 4, 5 had more interdialytic weight gain than the protocol 1. As a whole, patients while on protocol 4 & 5 experienced more thirst than protocol 1 but patients during protocol 3 experienced the same degree of thirst as protocol 1.
In summary, sodium ramping reduced HD-related side effects but this benefit could
not be explained on the basis of blood volume change measured by the Crit-Line IIR.
protocol 3 may be more appropiate sodium ramping method in 4 of the 9 patients. These
data suggest that protocol 3 may be used before protocol 4, 5 when we apply sodium
ramping to the patients who frequently have hypotension during HD.
Keywords
Blood volume changeSodium rampingCrit-lineSide effects
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Nephrology
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Get Help Anytime, 24/7.
What Is Opioid Use Disorder?
What Is Opioid Use Disorder?
Opioid Use Disorder Explained
Understanding “What is Opioid Use Disorder (OUD)?” can be complicated. This is because there’s a lot of wrong information available about opioid use and the opioid crisis. Thus, it can be hard to understand exactly who suffers from OUD. To clarify these matters, we’ll provide an exact definition of OUD, and the signs that you or someone you know may have it. We’ll also suggest the best treatment options for dealing with OUD. Since anyone who has been prescribed opioid painkillers could easily get OUD, this information could help prevent this destructive disorder from gaining hold in your life.
What are Opioids?
The first area of misunderstanding comes from the drugs themselves. Before you can identify OUD, you need to know what an opioid is, and what drugs fall into the category of opioid. In a nutshell, an opioid is any drug that interacts with the opioid receptors in the brain. These drugs are called opioids because they are made from poppy plants, which are used to create opium. When viewed on a chemical level, opioids are shown to contain some of the same chemical properties of opium. This makes them very powerful pain relievers. It also causes them to create a strong sense of euphoria, or intense joy when used. It is this euphoric feeling that causes addiction and leads to OUD.
Below are a few of the most common opioid drugs. A full list of opioids – including brand names – is available from the National Institute on Drug Abuse.
• Heroin
• Morphine
• Codeine
• Fentanyl
• Hydrocodone
• Oxycodone
• Methadone
• Meperidine
• Hydromorphone
• Oxymorphone
What is Opioid Use Disorder?
Opioid Use Disorder occurs when a person cannot stop taking opioids. It often begins when someone is prescribed pain relievers from their doctor for short-term pain. Commonly, this occurs after surgery or injury. Here’s are some of the common symptoms of OUD:
• Taking opioid prescription drugs in greater amounts than prescribed.
• Using opioids for a longer period than prescribed.
• Needing increasing amounts of the opioid to feel the same effects.
• Spending large quantities of time getting, using and recovering from the effects of using opioids.
• “Doctor shopping” or seeking out new doctors to get more opioids.
• An inability to meet responsibilities because of opioid use.
• Seeking out heroin or other illegal drug sources when unable to get enough opioid prescription drugs.
• Using opioids in dangerous situations such as driving a car or operating other machinery.
• Experiencing withdrawal symptoms when the person stops using opioids.
Withdrawal from opioids can be especially dangerous. It can also be difficult to identify.
Withdrawal from Opioid Use
When going through opioid withdrawal a person will feel like they have a bad case of the flu. This is because their body has become dependent on the drug. They don’t feel normal without it. These are the most common signs of withdrawal:
• Depression.
• Anxiety.
• Physical pain.
• Restlessness and insomnia.
• Tearing of the eyes and running of the nose.
• Sweating.
• Yawning.
• Dilated pupils.
• Diarrhea and stomach cramps.
• Nausea and vomiting.
These symptoms usually last for a few days. However, some can last for weeks after stopping the drug. Most often, a person will continue to feel depression and anxiety as well as physical pain for longer periods than the other symptoms. This happens because of the mental addiction. Their brain is attempting to create reasons to use more opioids.
How Common is Opioid Use Disorder
In 2018, nearly a million people reported that they had used heroin in the past year. During that same year, more than 11 million people said they used narcotic pain relievers without a prescription. That is only in the United States. Global estimates show that in 2016, nearly 27 million people were living with OUD. This leads to more than 100,000 deaths from overdose each year, worldwide. Almost half of those deaths – 47,000 – occurred in the United States.
To put these numbers in perspective, governmental data shows about 70,000 people in the U.S. died from drug overdoses in 2019. Meaning, more than half of all drug overdoses in the United States can be tied to opioids.
Treatments for Opioid Use Disorder
One of the problems with Opioid Use Disorder is that it tends to be very difficult to treat. The cravings that come with OUD are overwhelming. This is due to the way opioids interact with the body. Because opioids create such an intense feeling of happiness, a person constantly feels depressed when they stop.
The unnatural “highs” create devastating lows. In addition, the body will create pain in order to try to get more of the drug. This makes every minute agony. This is worse if the person suffers from a chronic pain condition, where they have actual physical suffering. Quitting opioids makes these much worse. Therefore, it is necessary to have medical help in order to treat OUD. Because the person feels so terrible, and the cravings are so powerful, they frequently need medication to manage their symptoms. Here’s some of the treatments recommended for anyone with OUD:
• Medication Assisted Treatment (MAT).
• Cognitive Behavioral Therapy (CBT).
• Support groups and group therapy.
These should all be used together to treat the physical and mental problems that affect OUD sufferers. Here’s how they work:
MAT for Opioid Use Disorder
One of the first steps necessary to treat OUD involves the use of prescription medication. The goal is to gradually reduce the person’s physical dependence on the opioids. Doctors often use light doses of buprenorphine and methadone to manage the symptoms of withdrawal. A mixture of buprenorphine and naloxone is also common. The buprenorphine is a painkiller that assists by reducing the pain that comes from withdrawal. Methadone is an opioid, but can be given in mild doses to help combat cravings. Naloxone is often considered an “anti-drug” that helps block opioid receptors in the brain. This prevents opioids from having any effect.
Any MAT should only be undertaken with the care and supervision of a physician.
CBT and OUD
Research has shown CBT is able to assist with pain management, as well as helping people cope with difficult emotions. By learning to deal with pain mentally, and learning to feel good without drugs, those who battle OUD can deal with many of the symptoms that lead them back to opioid use.
Support Groups and Group Therapy
In addition to treating the body and mind, complete recovery from OUD requires social support. People with OUD often feel isolated and misunderstood. Because their addiction is so painful, and relapse is so common, having people who understand is extremely valuable during recovery.
Get Help with OUD Now
Hopefully you now know “What is opioid use disorder” and some of the ways to fight it. Success depends on help. If you or someone you know is fighting OUD, reach out. We are ready and able to aid. Our staff is trained to handle all the difficult parts of opioid addiction. They begin with medication-assisted treatment, then create a personalized treatment plan for anyone that eases the pain of addiction. We used evidence-based therapies to recover the body and mind so as to prevent relapse. We can provide all of the tools necessary to get you back to your life and free from the agony of opioids.
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Passionate People
Lifestyle Insights, resources and products information
for people with reduced mobility
wheelchair
Bariatric wheelchair: benefits, characteristics and some tips
bariatric-wheelchair
Does your wheelchair make you feel cramped and uncomfortable? Do you constantly feel that it is struggling to get you from A to B?
A bariatric wheelchair may be the solutions to some of this problems. This unique product is designed to empower larger users with all of the benefits provided by a conventional wheelchair. If there’s one thing as important as mobility, it is safety and comfort.
Why use a bariatric wheelchair?
Mobility is essential for anyone who wishes to maintain their independence. A Bariatric wheelchair lets users retain their autonomy and move around. Users are able to leave their home, go shopping, visit friends or neighbours without the risk of being uncomfortable or compromising their safety. Greater mobility leads to greater social interaction. This is vital for maintaining good mental health, and a high quality of life.
It’s not just increased mobility that comes with a Bariatric wheelchair. There is also the possibility of increased comfort and security for heavy users. Bariatric wheelchairs are designed specifically to accommodate the increased size of a user, and provide a comfortable experience for them. They do this through the way the chair is constructed to take account of both the size and weight of the user.
Designed for comfort and security
The seats and backs of these chairs have extra reinforcement, and are constructed of heavyweight vinyl or upholstery material. They are bigger than a typical wheelchair, allowing users greater comfort, and additional support for their sitting position, upper and lower back. The seat and the backrest can usually be tilted to take into account an individual’s centre of gravity, and to provide appropriate support where it is needed.
Tilting the back rest is also important for users who may suffer with pulmonary or cardiovascular issues, and need a particular position to help them breath better.
Built either from heavy duty PVC or reinforced metal tubing, a bariatric wheelchair is made to last and can often support users up to 700 or even 1000 pounds in weight. You can be sure that your chair is strong enough to take you everywhere you need to go without any risk of breaking the chair or endangering yourself. The whole design, including the leg and foot rests, has been put together with larger users in mind, so your comfort and safety is the top priority at every stage of the design. While lightweight chairs are usually made form lighter materials such as aluminium, heavy duty wheelchairs are usually crafted from steel, for improved resistance.
Is a bariatric wheelchair right for you?
If you are more than 100 pounds overweight with a BMI in excess of 30 then a bariatric wheelchair may be a good solution for your mobility needs. Typically the chairs’ users may have conditions including:
• cardiopulmonary disease
• cardiovascular disease
• osteoarthritis of the lower extremities
It is also possible that such a wheelchair could be used by people who have severe muscle weakness, resulting from neuromuscular or musculoskeletal issues. Examples of these conditions would be:
• Huntington’s disease
• Muscular dystrophy
• Multiple Sclerosis
• Spinal cord injuries
In some cases the people with higher weight and muscle weakness could create additional risks when in a conventional wheelchair. A bariatric wheelchair is built to overcome these issues and can be the best choice for heavier users who need both comfort and security alongside their mobility and independence.
Ebook- Mobility - CTA POST
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Antiretroviral treatment (ART) has transformed human immunodeficiency computer virus (HIV) from
Antiretroviral treatment (ART) has transformed human immunodeficiency computer virus (HIV) from a deadly disease to a chronic illness that potentially has small effect on life span. One explanation is certainly these markers neglect to really describe HIVs general immune system dysfunction adding to todays morbidity and mortality. The Compact disc4/Compact disc8 proportion more accurately represents this overall immune system dysfunction and could be considered a better biomarker for disease development, response to treatment, morbidity, and mortality for the suppressed. A greater knowledge of the Compact disc4/Compact disc8 proportion and the influence of its manipulation ought to be a focus on for potential HIV research. What’s the Compact disc4/Compact disc8 proportion? Compact disc4 helper/inducer cells and Compact disc8 cytotoxic/suppressor cells are 2 phenotypes of T lymphocytes, seen as a unique surface markers and functions that mostly Pimaricin supplier reside in lymph nodes but also circulate in the blood. The normal CD4/CD8 ratio in healthy hosts is usually poorly defined. Ratios between 1.5 and 2.5 are generally considered normal; however, a wide heterogeneity exists because sex, age, ethnicity, genetics, exposures, and infections may all impact the ratio [4C7]. Normal ratios can invert through isolated apoptotic or targeted cell death of circulating CD4 cells, growth of CD8 cells, or a combination of both Pimaricin supplier phenomena. A low or inverted CD4/CD8 ratio is an immune risk phenotype and is associated with altered immune function, immune senescence, and chronic inflammation in both HIV-infected and uninfected populations [8C11]. The prevalence of an inverted CD4/CD8 ratio increases with age. An inverted ratio is seen in 8% of 20- to 59-year-olds and in 16% of 60- to 94-year-olds [7]. Women across all age groups are less likely to have an inverted ratio than their male counterparts [7]. Age- and hormone-related atrophy of the thymus is usually theorized to explain the differences between populations. Hormonal influence around the ratio is usually supported by a correlation between low plasma estradiol levels, high circulating CD8, and low CD4/CD8 ratios in women with premature ovarian failure [12]. Mouse models further spotlight the importance of age and estrogen around the CD4/CD8 ratio because lower ratios are reported in mice following both natural menopause and ovariectomy [13]. Persistence of the thymus is usually associated with better ratio recovery in HIV treatment [14]. Are abnormal CD4/CD8 ratios connected with pathology Pimaricin supplier in the HIV detrimental people? In the HIV detrimental people, a minimal Compact disc4/Compact disc8 immune system risk phenotype shows immune Pimaricin supplier system senescence, is normally connected with wide-ranging pathology, and could also anticipate morbidity and mortality [7,15C22]. Irreversible disruption of self-immunologic tolerance to endogenous antigens is definitely a hallmark of autoimmune disease. With this establishing of immune dysfunction, an irregular CD4/CD8 percentage can emerge. Furthermore, Pimaricin supplier while an irregular percentage is not uniformly present in all autoimmune diseases, a decreased CD4/CD8 percentage is definitely consistently seen in systemic lupus erythematosus [15C17]. A low CD4/CD8 percentage reflects -cell damage and may forecast diabetes diagnoses in first-degree relatives of type 1 diabetic probands [18]. Inside a human population study of solid neoplasms, an inverted CD4/CD8 percentage is definitely associated with metastatic disease as compared with cancer individuals without metastasis [19]. Moreover, following acute myocardial infarction and cardiopulmonary resuscitation, a fixed low CD4/CD8 percentage is definitely a poor prognostic sign [20]. Despite these associations, it is important to acknowledge that the presence of a low CD4/CD8 percentage is not clearly the cause LY6E antibody or the effect of the above pathology. This acknowledgment is definitely additional highlighted by the current presence of a minimal proportion in conditions beyond your umbrella of traditional organic pathology, including a link between low pessimists and ratios [21]. Conflicting literature is available regarding the usage of an inverted Compact disc4/Compact disc8 proportion ( 1.0) being a predictor for mortality in older HIV-negative populations. Two longitudinal cohorts of older Swedish individuals showed an inverted proportion ( 1.0) was connected with frailty and mortality [7,10]. These research helped specify the immune system risk phenotype and elevated the chance of using the Compact disc4/Compact disc8 proportion being a biomarker to stratify risk in older populations. Afterwards cohort research in Spain and the uk discovered that while a minimal Compact disc4/Compact disc8 proportion was connected with time to loss of life in unadjusted analyses, no association between your morbidity and proportion was within multivariable analyses [22,23]. Moreover, a recently available cross-sectional research of frailty and potential cohort research of morbidity in citizens of Canadian assisted living facilities found that better percentages of central storage Compact disc8+ T cells had been even more predictive of elevated frailty than various other immune system phenotypes, including an inverted Compact disc4/Compact disc8 proportion [24]. Hence, the Compact disc4/Compact disc8 percentage may possibly not be.
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These Local Practices In CBD For Rest Are Thus Unusual That They Are Going To Create Your Jaw Drop!
There CBD for sleep is a group of folks who are going to find it complicated to sleep as their physical body is regularly humming with the signs that the brain is sending. This is referred to as sleep problems or even sleep condition. Because CBD is actually not habit forming and also it serves as a worry reliever, several sufferers of rest problems have actually tried utilizing CBD for rest.
Rest may be hard for lots of folks. Lack of sleeping has an effect on every component of your everyday life including your brainpowers. If you don’t acquire sufficient rest, your performance will certainly go through. Certainly not just can this trigger unsatisfactory functionality at the workplace or property, but an absence of premium sleep may likewise have unfavorable results on your state of mind.
If you are among those people that discover it challenging to sleep because of your insomnia or even rest ailment, you may desire to try CBD for rest. It is actually an all-natural type of different drug that lots of folks utilize to alleviate the signs and symptoms of sleep problems. It is much safer and a lot more effective than taking prescribed drug.
As mentioned over, CBD is actually not a drug and also has no habit forming premiums. It works as an all-natural medicine and it additionally functions as a sedative. You will definitely likewise discover that after taking CBD for rest, you really feel a little bit more alert. It can easily operate to unwind you.
Sleeping CBD for sleep can be very complicated for some individuals. A shortage of rest can create you to feel irritable as well as overreacts. If you have sleep problems, your invulnerable system is actually not as sturdy.
All-natural therapies for sleeping issues might aid you heal your sleeplessness and also give you much better sleeping. There are actually a lot of over the counter items that will certainly help to help you sleep a lot better.
You might CBD for sleep additionally would like to look at sleep problems organic supplements to aid you sleep much better. Nettle herbal tea works as a barbiturate as well as is actually valuable for mild rest concerns. Nettle tea can assist to eliminate your sleeplessness as well as aids you to obtain a good night’s sleeping.
There are actually other kinds of sleeping disorders natural supplements that can assist you acquire a good night’s sleep. L-Theanine is yet another cannabis that has actually been verified to be efficient. This is actually discovered in an amount of natural remedies to assist you rest a lot better. You will need to find one that is right for you.
Some folks have claimed that taking excessive coffee can easily support sleeplessness. Most individuals that possess rest issues drink coffee or even tea while they are actually trying to rest. High levels of caffeine induces you to feel distressed and also tired thus if you are not receiving sufficient sleeping, this can lead to irritation.
In add-on to high levels of caffeine, you need to additionally steer clear of booze as it can produce your rest troubles much worse. The effects of booze may be actually ravaging on the body system when you are attempting to rest.
Sleeping professionals state that you require to rest a lowest of 8 hrs each evening. You ought to try to get a lowest of 8 hrs of sleep each evening, but you might have the ability to acquire 9 or 10 hrs of sleeping. If you are actually looking for a choice to prescription sleeping pills, you may have the ability to treat your insomnia utilizing a plant based treatment.
It is achievable that CBD for sleeping can easily assist you if you are actually certainly not capable to sleep or even you are experiencing insomnia or even sleep issues. You can utilize this to aid you feel much more rested as well as you might locate that you manage to sleep additional conveniently. as a result.
Are you wondering if CBD for sleeping is actually definitely one thing you should be investigating? Or even maybe you are actually only interested to know even more regarding it. In either case, rest assured that you are actually not the exception in your interest, and also many people are asking themselves the exact same inquiry.
It’s been actually stated that when your mind is actually correctly rested and you get proper remainder, your body system is in the greatest condition possible to survive the day. If your body system is actually rested well, it is actually much easier to make it through the day, no matter what you perform. It is actually a fact.
Meanwhile, if there is actually a disorder in your physical function as well as your mind is not in the greatest of condition, it could be difficult to make it through the day. This is actually not an advantage, as well as there are opportunities that it makes it required to respond to obtain your body and mind back in the correct purchase.
Yet permit’s be sincere, there are actually those individuals that will definitely not consider placing CBD in their physical body to advertise leisure and also rest. Those individuals have an aspect, given that for a lot of us, CBD for sleeping is something that we carry out not need to do, neither does it carry out everything for our company in the method of advertising leisure or even the process of sleeping. I’m sure we’ve all been aware of it prior to – the substances that are meant to rest our bodies and minds.
What has taken place over the past years is actually that the adverse effects of CBD have been actually so effectively advertised that there are actually folks who don’t intend to take CBD at all. They see it as a powerful stimulant, and also they feel that it is going to ruin their day. There is actually no clinical documentation for this and there are still great deals of researches being carried out to find out the long-term has an effect on.
Given that CBD is certainly not habit forming and it takes action as an anxiety reducer, numerous patients of rest ailments have actually made an effort making use of CBD for sleep.
If you are actually one of those people that locate it challenging to sleep because of your sleep problems or rest ailment, you might want to make an effort CBD for sleeping. Organic therapies for sleeping concerns might aid you remedy your insomnia as well as additionally offer you much better sleeping. If you are certainly not capable to rest or even you are actually experiencing insomnia or sleep complications, it is feasible that CBD for sleeping can easily aid you. Those people possess an aspect, considering that for most of our team, CBD for rest is one thing that our team do certainly not need to carry out, neither does it carry out anything for our team in the means of advertising leisure or even the process of rest.
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Influenza*
Posted on: May 29, 2018 by John Cannell, MD
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Should I take vitamin D to reduce the risk of colds and flu (URI)?
Yes, you should because so many studies show that vitamin D helps reduce the risk of colds and flu. The best dose to use is unknown, but the Vitamin D Council recommends that adults take 5,000 to 10,000 IU per day, depending on body weight. Children should take at least 100 IU/kg/day. However, there is a wide variation in human response to any one vitamin D dose so, after taking vitamin D for a few months, it is important to have your vitamin D blood level checked to make sure it is > 40 ng/ml. The Vitamin D Council offers a convenient in-home vitamin D blood spot kit or your doctor can order the test.
The Vitamin D Council recommends vitamin D to help prevent colds and flu (URI or upper respiratory infections) based on the findings of two large meta-analyses (the strongest proof in medicine) published in respected medical journals. For example, Bergman et al analyzed 11 placebo controlled trials involving 5,660 subjects and found that those taking a daily dose of vitamin D had half the risk of developing a URI.[1] Many of the studies they analyzed used very low doses of vitamin D, meaning the overall effect may be greater with an adequate dose. For a detailed analysis of the study, see our blog.
In another meta-analysis, Martineau et al analyzed 25 randomized controlled trials (most reliable type of study) involving 11,320 subjects, and found that vitamin D reduced the risk of developing a URI.[2] Even those subjects with very low vitamin D levels experienced 1/3 the risk when supplementing with vitamin D compared to those who did not take any vitamin D. Like the study above, Matineau et al found daily dosing to be the most effective. For a detailed analysis of the BMJ study, see our blog.
Regarding children, a recent study of 400 infants found that influenza A infection was much more common among infants taking 400 IU/day compared to infants given 1,200 IU/day.[3] For a detailed analysis of this study, see our blog.
Should I take high doses of vitamin D for ten days if I get a URI?
There is simply no data on this question. If you decide to take vitamin D to treat a URI, 50,000 IU/day for ten days is certainly safe.
What is influenza?
Influenza, also known as the flu, is a contagious respiratory infection caused by the influenza virus that infects the nose, throat and lungs. In the United States, peak flu season is from late November through March, but flu season can last through May. Young children, the elderly and people with chronic diseases are more likely to have serious complications after getting the flu. Influenza infections can require hospitalization or even death in serious cases.[4] In 1918, the flu killed 50 million people worldwide and nothing, including modern anti-virals or flu shots, can prevent this from happening again. It is just a matter of time.
Since the common influenza virus changes every season, so does the vaccine but, even so, the vaccines are of marginable effectiveness. The severity and prevalence of the flu changes each season. The flu shot is based on a guess about which three strains are likely to be active in any one year, and the experts often guess incorrectly.
The three types of influenza that affect humans are A, B and C, however types A and B are typically responsible for seasonal influenza epidemics. Type C influenza viruses can cause a mild respiratory infection, but do not cause flu epidemics. There are also subtypes of type A influenza viruses based on two proteins found on the virus, abbreviated H and N. For example, H1N1 is usually very common, however the most common influenza virus during the 2016-2017 flu season was H3N2.
What are the symptoms of influenza?
A person infected with the influenza virus may experience some or all these symptoms:[5]
• Fever or chills
• Cough
• Sore throat
• Muscle, body and head aches
• Fatigue
• Vomiting and diarrhea, which is more common in children with influenza.
• Prostration or the need to lie down. (This clinical sign helps differentiate colds from flu. For example, in 1918 prostration after infection was so common among GIs in France that they called it the “knock-me-down fever.”)
A healthy person will normally recover from influenza in a few days to less than two weeks, although some may develop serious complications from influenza, such as pneumonia, bronchitis, or sinus and ear infections. Influenza can also make a chronic condition, such as asthma, worse. When influenza is fatal, the death is usually due to a bacterial infection, such as pneumonia, that is secondary to the influenza.[6]
What are the risk factors for influenza?
Annually, influenza affects about one-tenth the U.S. population.[7] During the 2016-2017 flu season, more than half of hospitalizations related to influenza were in adults over the age of 65.
On average, about 10% of the U.S. population will get the flu each year.[8] However, during the AH1N1 pandemic of 2009-10, the number of cases rose to 95,000 or 20%.[9]
• Between 30,000 to 100,000 adults are hospitalized each year in the U.S. because of flu complications.[10]
• In the 30-year period from 1976 to 2006, as low of 3,000 and as high of 49,000 people died each year from flu-related causes in the U.S., although some experts believe that most excess wintertime deaths are due to the flu.
People who are at higher risk for developing influenza include:[11]
• People over age 65
• Children, especially those under age two
• People with chronic diseases, such as asthma, diabetes, lung or heart disease
• People with weakened immune systems, such as those with cancer or HIV/AIDS
• People who are morbidly obese
• Pregnant women
• American Indians and Alaskan natives
It is important to note that many people with these risk factors are also vitamin D deficient.
How does influenza spread?
A person infected with the influenza virus can be contagious one day before symptoms develop and up to seven days after they become sick. Young children and people with compromised immune systems can infect others for a longer period of time.[12]
It is widely thought that the influenza virus can spread when an infected person coughs, sneezes or speaks, but this has never been proven. Droplets holding the influenza virus are thought to travel through the air and can be directly inhaled by another person through the mouth or nose. The droplets may also land on a surface where they can be picked up by someone else who is in turn infected when they touch their eyes, nose or mouth.[13]
However, all six attempts to prove that respiratory infections are transmitted person-to-person or sick-to-well have failed. Also, other characteristics of influenza continue to puzzle scientists, and a decision to not take vitamin D during flu season is a kind of Pascal’s Wager with influenza.
The peak influenza season is near the end of the year in the northern hemisphere, a time when it is coldest and the air is driest. This climate allows the influenza virus to live outside of the human body for an extended period.[14]
Once an individual has had influenza, their body creates antibodies to help protect against that specific virus in the future. However, because influenza viruses change from year to year, these antibodies will not fight off newer virus strains. Vaccines only help the human body make antibodies against the current influenza virus.[15]
What is the link between influenza and vitamin D?
Vitamin D is an important factor in immune system health. Some studies have shown a link between vitamin D status and the risk of developing influenza. People with low vitamin D levels may have an increased risk of developing influenza.[16]
Vitamin D receptors are found on the surface of a cell where they receive chemical signals. By attaching themselves to a receptor, these chemical signals direct a cell to do something, for example, to act in a certain way, or to divide or die.
There are vitamin D receptors found on cells in the immune system, and vitamin D can bind to these receptors.[17] Vitamin D works in the immune system by reducing levels of inflammatory proteins called cytokines, as well as increasing the amount of antimicrobial proteins, which are naturally occurring antibiotics that destroy invading germs and viruses. This combination of lowering inflammation and increasing antimicrobial defenses can help an individual’s immune system fight infections more effectively.[18],[19] These actions also reduce the risk of developing pneumonia, which is the primary complication of influenza that can result in death.[20]
There are two branches of the immune system: adaptive and innate. The adaptive immune system develops based on previous exposure to a virus. The innate immune system responds quickly to foreign invaders, and its effectiveness is determined by the levels of immune cells and proteins an individual has.[21] Low vitamin D levels result in some aspects of the innate immune system not functioning as well as they should.[22]
Influenza epidemics occur in the winter when vitamin D levels in the greater population are dramatically lower.[23] Considering the seasonal nature of influenza, vitamin D might be a factor affecting someone’s chances of getting the flu, a theory first proposed by Cannell in 2006.[24]
What does the research say in general about influenza and vitamin D?
Preventing influenza
Most studies about influenza have shown that people with lower levels of vitamin D are more likely to get the flu. One study looked at the levels of vitamin D in people with prostate cancer and their immune response to the influenza vaccine. The study found that people with higher levels of vitamin D had an improved response to the vaccine, meaning that they would be more protected against getting influenza.[25] However, another study evaluated vitamin D and influenza in people over age 50 , and found that vitamin D levels didn’t have a significant effect on their immune response to the influenza vaccine.[26]
A study comprised of healthy adults found that people with lower levels of vitamin D were twice as likely to develop influenza, compared to people with high levels of vitamin D.[27]
Treating and recovering from influenza
Some research has shown a relationship between vitamin D status and the duration of the influenza infection. Other studies have looked at influenza outcomes, such as pneumonia or death, in large influenza epidemics in the past.
A study that looked at deaths associated with the large 1918-1919 influenza pandemic found that the lowest influenza-related death rates in the United States were in the city with the highest amounts of UVB light, which helps the body make vitamin D. They also found that the highest number of influenza deaths were in the city with the lowest amounts of UVB radiation.[28]
People with enough vitamin D may recover from influenza faster than people with low levels of vitamin D. One study found that people with vitamin D levels above 38 ng/ml recovered from influenza in an average of two days; whereas people with vitamin D levels below 38 ng/ml took an average of nine days to recover from influenza.[29]
What does recent research say about vitamin D and influenza?
An experiment conducted in the United States gave elderly African-American women 800 IU of vitamin D per day for two years and then 2,000 IU per day for the third year. The control group was given a dummy pill. The researchers looked at how many times those women got influenza over the three-year period and found that:[30]
• The vitamin D group had fewer influenza symptoms compared to the dummy pill group.
• Only one person in the vitamin D group contracted influenza when taking 2,000 IU per day, compared to 30 cases of influenza or colds for those taking the dummy pill.
• The dummy pill group had influenza symptoms during the winter, while those who got the flu in the vitamin D group had symptoms that were independent of the season.
An experiment evaluated the effects of vitamin D supplementation on influenza risk in Japanese school children. The researchers gave children either 1,200 IU vitamin D per day for three months during the winter or a dummy pill. They found that:[31]
• More children in the dummy pill group got influenza A than children in the vitamin D group.
• There was a preventive effect of 1,200 IU vitamin D per day on children getting influenza A.
The researchers concluded that taking 1,200 IU of vitamin D can help protect children against seasonal influenza A. In this study, vitamin D had no effect on influenza B, possibly because vitamin D may respond in different ways to the inflammatory proteins in the viruses.
A study conducted in 2011 looked at vitamin D levels and respiratory infections, like influenza, in a large group of British adults. The researchers found that:[32]
• For each 4 ng/ml increase in vitamin D levels in the body, there was a 7% lower chance of developing influenza.
• There was a seasonal pattern of influenza, which was the same as the seasonal pattern of vitamin D levels.
• Influenza infections decreased when vitamin D levels increased. However, since this study was observational, the researchers couldn’t conclude for certain if higher vitamin D levels protected against the flu.
Key points from research
• People who get influenza are more likely to have low levels of vitamin D.
• Vitamin D can help reduce inflammation caused by the influenza virus and increase the number of antimicrobial proteins that fight against viruses.
• Influenza infections increase during the winter, when vitamin D levels are known to decrease in the population.
• At least a dozen studies have shown that taking vitamin D supplements can reduce the chances of getting influenza.
• Having elevated levels of vitamin D may help decrease the time it takes to recover from an influenza infection.
• More and more doctors are recommending taking vitamin D to protect against influenza.
What does this mean for me?
The Vitamin D Council recommends adults take 5,000 to 10,000 IU/day, depending on body weight. Children should take about 100 IU/kg/day. Since there is a wide variation in human response to any vitamin D dose, it is important to have your vitamin D blood levels checked, after you have taken vitamin D for a few months, to make sure it is > 40 ng/ml. The Vitamin D Council offers a convenient in-home vitamin D test kit or your doctor can order the test. If get influenza, you can safely take 50,000 IU/day for 10 days to help fight off the infection, but there are no clinical studies showing it helps.
Citation
John Cannell, MD. Health condition: Influenza. The Vitamin D Council Blog & Newsletter, May 29, 2018.
References
[1] Bergman P., Lindh, AU., Bjorkhem-Bergman, L. & Lindh, JD. Vitamin D and Respiratory Tract Infections: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. PLoS One, 2013.
[2] Martineau, AR. et al. Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data. BMJ¸2017.
[3] Zhou, J. et al. Preventive Effects of Vitamin D on Seasonal Influenza A in Infants: A Multicenter, Randomized, Open, Controlled Clinical Trial. Pediatr Infect Dis J, 2018.
[4] Grant, W.B. and E. Giovannucci, The possible roles of solar ultraviolet-B radiation and vitamin D in reducing case-fatality rates from the 1918-1919 influenza pandemic in the United States. Dermatoendocrinol, 2009. 1(4): p. 215-9.
[5] The Centers for Disease Control and Prevention. Seasonal Influenza: Flu Basics, 2015.
[6] Grant WB, Giovannucci E. The possible roles of solar ultraviolet-B radiation and vitamin D in reducing case-fatality rates from the 1918-1919 influenza pandemic in the United States. Dermatoendocrinol, 2009. 1(4): p. 215-9.
[7] Rees, J.R., Hendricks, K., Barry, E.L., et al., Vitamin D3 supplementation and upper respiratory tract infections in a randomized, controlled trial. Clin Infect Dis, 2013. 57(10): p. 1384-92.
[8] Molinari, N.A., Ortega-Sanchez, I.R., Messonnier, M.L., et al., The annual impact of seasonal influenza in the US: measuring disease burden and costs. Vaccine, 2007. 25(27): p. 5086-96.
[9] Shrestha, S.S., Swerdlow, D.L., Borse, R.H.,et al., Estimating the burden of 2009 pandemic influenza A (H1N1) in the United States (April 2009-April 2010). Clin Infect Dis, 2011. 52 Suppl 1: p. S75-82.
[10] Ortiz, J.R., Neuzil, K.M., Shay, D.K., et al., The burden of influenza-associated critical illness hospitalizations. Crit Care Med, 2014. 42(11): p. 2325-32.
[11] The Centers for Disease Control and Prevention. Seasonal Influenza: Flu Basics, 2015.
[12] The Centers for Disease Control and Prevention. Seasonal Influenza: Flu Basics, 2015.
[13] Mayo Clinic. Diseases and Conditions: Influenza (flu), 2015.
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[21] Cannell, J.J., Zasloff, M., Garland, C.F., et al., On the epidemiology of influenza. Virol J, 2008. 5: p. 29.
[22] Yusupov, E., Li-Ng, M., Pollack, S., et al., Vitamin d and serum cytokines in a randomized clinical trial. Int J Endocrinol, 2010. 2010.
[23] Hypponen, E. and C. Power, Hypovitaminosis D in British adults at age 45 y: nationwide cohort study of dietary and lifestyle predictors. Am J Clin Nutr, 2007. 85(3): p. 860-8.
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[25] Chadha, M.K., Fakih, M., Muindi, J., et al., Effect of 25-hydroxyvitamin D status on serological response to influenza vaccine in prostate cancer patients. Prostate, 2011. 71(4): p. 368-72.
[26] Sundaram, M.E., McClure, D.L., VanWormer, J.J., et al., Influenza vaccination is not associated with detection of noninfluenza respiratory viruses in seasonal studies of influenza vaccine effectiveness. Clin Infect Dis, 2013. 57(6): p. 789-93.
[27] Sabetta, J.R., DePetrillo, P., Cipriani, R.J., et al., Serum 25-hydroxyvitamin d and the incidence of acute viral respiratory tract infections in healthy adults. PLoS One, 2010. 5(6): p. e11088.
[28] Grant, W.B. and E. Giovannucci, The possible roles of solar ultraviolet-B radiation and vitamin D in reducing case-fatality rates from the 1918-1919 influenza pandemic in the United States. Dermatoendocrinol, 2009. 1(4): p. 215-9.
[29] Cannell, J.J., Vieth, R., Umhau, J.C., et al., Epidemic influenza and vitamin D. Epidemiol Infect, 200 Aloia, J.F. and M. Li-Ng, Re: epidemic influenza and vitamin D. Epidemiol Infect, 2007. 135(7): p. 1095-6; author reply 1097-8.. 134(6): p. 1129-40.
[30] Sundaram, M.E., McClure, D.L., VanWormer, J.J., et al., Influenza vaccination is not associated with detection of noninfluenza respiratory viruses in seasonal studies of influenza vaccine effectiveness. Clin Infect Dis, 2013. 57(6): p. 789-93.
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PLoS ONE
PUBLISHED: 01-01-2013
Hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) lead to significant cardiovascular morbidity and mortality worldwide. Mutations in the genes encoding the sarcomere, the force-generating unit in the cardiomyocyte, cause familial forms of both HCM and DCM. This study examines two HCM-causing (I79N, E163K) and two DCM-causing (R141W, R173W) mutations in the troponin T subunit of the troponin complex using human ?-cardiac myosin. Unlike earlier reports using various myosin constructs, we found that none of these mutations affect the maximal sliding velocities or maximal Ca(2+)-activated ADP release rates involving the thin filament human ?-cardiac myosin complex. Changes in Ca(2+) sensitivity using the human myosin isoform do, however, mimic changes seen previously with non-human myosin isoforms. Transient kinetic measurements show that these mutations alter the kinetics of Ca(2+) induced conformational changes in the regulatory thin filament proteins. These changes in calcium sensitivity are independent of active, cycling human ?-cardiac myosin.
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Cardiomyocytes from diseased hearts are subjected to complex remodeling processes involving changes in cell structure, excitation contraction coupling and membrane ion currents. Those changes are likely to be responsible for the increased arrhythmogenic risk and the contractile alterations leading to systolic and diastolic dysfunction in cardiac patients. However, most information on the alterations of myocyte function in cardiac diseases has come from animal models. Here we describe and validate a protocol to isolate viable myocytes from small surgical samples of ventricular myocardium from patients undergoing cardiac surgery operations. The protocol is described in detail. Electrophysiological and intracellular calcium measurements are reported to demonstrate the feasibility of a number of single cell measurements in human ventricular cardiomyocytes obtained with this method. The protocol reported here can be useful for future investigations of the cellular and molecular basis of functional alterations of the human heart in the presence of different cardiac diseases. Further, this method can be used to identify novel therapeutic targets at cellular level and to test the effectiveness of new compounds on human cardiomyocytes, with direct translational value.
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Authors: Diederik W.D. Kuster, David Barefield, Suresh Govindan, Sakthivel Sadayappan.
Institutions: Loyola University Chicago.
Biomarkers are becoming increasingly more important in clinical decision-making, as well as basic science. Diagnosing myocardial infarction (MI) is largely driven by detecting cardiac-specific proteins in patients' serum or plasma as an indicator of myocardial injury. Having recently shown that cardiac myosin binding protein-C (cMyBP-C) is detectable in the serum after MI, we have proposed it as a potential biomarker for MI. Biomarkers are typically detected by traditional sandwich enzyme-linked immunosorbent assays. However, this technique requires a large sample volume, has a small dynamic range, and can measure only one protein at a time. Here we show a multiplex immunoassay in which three cardiac proteins can be measured simultaneously with high sensitivity. Measuring cMyBP-C in uniplex or together with creatine kinase MB and cardiac troponin I showed comparable sensitivity. This technique uses the Meso Scale Discovery (MSD) method of multiplexing in a 96-well plate combined with electrochemiluminescence for detection. While only small sample volumes are required, high sensitivity and a large dynamic range are achieved. Using this technique, we measured cMyBP-C, creatine kinase MB, and cardiac troponin I levels in serum samples from 16 subjects with MI and compared the results with 16 control subjects. We were able to detect all three markers in these samples and found all three biomarkers to be increased after MI. This technique is, therefore, suitable for the sensitive detection of cardiac biomarkers in serum samples.
Molecular Biology, Issue 78, Cellular Biology, Biochemistry, Genetics, Biomedical Engineering, Medicine, Cardiology, Heart Diseases, Myocardial Ischemia, Myocardial Infarction, Cardiovascular Diseases, cardiovascular disease, immunoassay, cardiac myosin binding protein-C, cardiac troponin I, creatine kinase MB, electrochemiluminescence, multiplex biomarkers, ELISA, assay
50786
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Using Caenorhabditis elegans as a Model System to Study Protein Homeostasis in a Multicellular Organism
Authors: Ido Karady, Anna Frumkin, Shiran Dror, Netta Shemesh, Nadav Shai, Anat Ben-Zvi.
Institutions: Ben-Gurion University of the Negev.
The folding and assembly of proteins is essential for protein function, the long-term health of the cell, and longevity of the organism. Historically, the function and regulation of protein folding was studied in vitro, in isolated tissue culture cells and in unicellular organisms. Recent studies have uncovered links between protein homeostasis (proteostasis), metabolism, development, aging, and temperature-sensing. These findings have led to the development of new tools for monitoring protein folding in the model metazoan organism Caenorhabditis elegans. In our laboratory, we combine behavioral assays, imaging and biochemical approaches using temperature-sensitive or naturally occurring metastable proteins as sensors of the folding environment to monitor protein misfolding. Behavioral assays that are associated with the misfolding of a specific protein provide a simple and powerful readout for protein folding, allowing for the fast screening of genes and conditions that modulate folding. Likewise, such misfolding can be associated with protein mislocalization in the cell. Monitoring protein localization can, therefore, highlight changes in cellular folding capacity occurring in different tissues, at various stages of development and in the face of changing conditions. Finally, using biochemical tools ex vivo, we can directly monitor protein stability and conformation. Thus, by combining behavioral assays, imaging and biochemical techniques, we are able to monitor protein misfolding at the resolution of the organism, the cell, and the protein, respectively.
Biochemistry, Issue 82, aging, Caenorhabditis elegans, heat shock response, neurodegenerative diseases, protein folding homeostasis, proteostasis, stress, temperature-sensitive
50840
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The Xenopus Oocyte Cut-open Vaseline Gap Voltage-clamp Technique With Fluorometry
Authors: Michael W. Rudokas, Zoltan Varga, Angela R. Schubert, Alexandra B. Asaro, Jonathan R. Silva.
Institutions: Washington University in St. Louis.
The cut-open oocyte Vaseline gap (COVG) voltage clamp technique allows for analysis of electrophysiological and kinetic properties of heterologous ion channels in oocytes. Recordings from the cut-open setup are particularly useful for resolving low magnitude gating currents, rapid ionic current activation, and deactivation. The main benefits over the two-electrode voltage clamp (TEVC) technique include increased clamp speed, improved signal-to-noise ratio, and the ability to modulate the intracellular and extracellular milieu. Here, we employ the human cardiac sodium channel (hNaV1.5), expressed in Xenopus oocytes, to demonstrate the cut-open setup and protocol as well as modifications that are required to add voltage clamp fluorometry capability. The properties of fast activating ion channels, such as hNaV1.5, cannot be fully resolved near room temperature using TEVC, in which the entirety of the oocyte membrane is clamped, making voltage control difficult. However, in the cut-open technique, isolation of only a small portion of the cell membrane allows for the rapid clamping required to accurately record fast kinetics while preventing channel run-down associated with patch clamp techniques. In conjunction with the COVG technique, ion channel kinetics and electrophysiological properties can be further assayed by using voltage clamp fluorometry, where protein motion is tracked via cysteine conjugation of extracellularly applied fluorophores, insertion of genetically encoded fluorescent proteins, or the incorporation of unnatural amino acids into the region of interest1. This additional data yields kinetic information about voltage-dependent conformational rearrangements of the protein via changes in the microenvironment surrounding the fluorescent molecule.
Developmental Biology, Issue 85, Voltage clamp, Cut-open, Oocyte, Voltage Clamp Fluorometry, Sodium Channels, Ionic Currents, Xenopus laevis
51040
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Visualizing Neuroblast Cytokinesis During C. elegans Embryogenesis
Authors: Denise Wernike, Chloe van Oostende, Alisa Piekny.
Institutions: Concordia University.
This protocol describes the use of fluorescence microscopy to image dividing cells within developing Caenorhabditis elegans embryos. In particular, this protocol focuses on how to image dividing neuroblasts, which are found underneath the epidermal cells and may be important for epidermal morphogenesis. Tissue formation is crucial for metazoan development and relies on external cues from neighboring tissues. C. elegans is an excellent model organism to study tissue morphogenesis in vivo due to its transparency and simple organization, making its tissues easy to study via microscopy. Ventral enclosure is the process where the ventral surface of the embryo is covered by a single layer of epithelial cells. This event is thought to be facilitated by the underlying neuroblasts, which provide chemical guidance cues to mediate migration of the overlying epithelial cells. However, the neuroblasts are highly proliferative and also may act as a mechanical substrate for the ventral epidermal cells. Studies using this experimental protocol could uncover the importance of intercellular communication during tissue formation, and could be used to reveal the roles of genes involved in cell division within developing tissues.
Neuroscience, Issue 85, C. elegans, morphogenesis, cytokinesis, neuroblasts, anillin, microscopy, cell division
51188
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A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses
Authors: Daniel T. Claiborne, Jessica L. Prince, Eric Hunter.
Institutions: Emory University, Emory University.
The protective effect of many HLA class I alleles on HIV-1 pathogenesis and disease progression is, in part, attributed to their ability to target conserved portions of the HIV-1 genome that escape with difficulty. Sequence changes attributed to cellular immune pressure arise across the genome during infection, and if found within conserved regions of the genome such as Gag, can affect the ability of the virus to replicate in vitro. Transmission of HLA-linked polymorphisms in Gag to HLA-mismatched recipients has been associated with reduced set point viral loads. We hypothesized this may be due to a reduced replication capacity of the virus. Here we present a novel method for assessing the in vitro replication of HIV-1 as influenced by the gag gene isolated from acute time points from subtype C infected Zambians. This method uses restriction enzyme based cloning to insert the gag gene into a common subtype C HIV-1 proviral backbone, MJ4. This makes it more appropriate to the study of subtype C sequences than previous recombination based methods that have assessed the in vitro replication of chronically derived gag-pro sequences. Nevertheless, the protocol could be readily modified for studies of viruses from other subtypes. Moreover, this protocol details a robust and reproducible method for assessing the replication capacity of the Gag-MJ4 chimeric viruses on a CEM-based T cell line. This method was utilized for the study of Gag-MJ4 chimeric viruses derived from 149 subtype C acutely infected Zambians, and has allowed for the identification of residues in Gag that affect replication. More importantly, the implementation of this technique has facilitated a deeper understanding of how viral replication defines parameters of early HIV-1 pathogenesis such as set point viral load and longitudinal CD4+ T cell decline.
Infectious Diseases, Issue 90, HIV-1, Gag, viral replication, replication capacity, viral fitness, MJ4, CEM, GXR25
51506
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Analysis of Tubular Membrane Networks in Cardiac Myocytes from Atria and Ventricles
Authors: Eva Wagner, Sören Brandenburg, Tobias Kohl, Stephan E. Lehnart.
Institutions: Heart Research Center Goettingen, University Medical Center Goettingen, German Center for Cardiovascular Research (DZHK) partner site Goettingen, University of Maryland School of Medicine.
In cardiac myocytes a complex network of membrane tubules - the transverse-axial tubule system (TATS) - controls deep intracellular signaling functions. While the outer surface membrane and associated TATS membrane components appear to be continuous, there are substantial differences in lipid and protein content. In ventricular myocytes (VMs), certain TATS components are highly abundant contributing to rectilinear tubule networks and regular branching 3D architectures. It is thought that peripheral TATS components propagate action potentials from the cell surface to thousands of remote intracellular sarcoendoplasmic reticulum (SER) membrane contact domains, thereby activating intracellular Ca2+ release units (CRUs). In contrast to VMs, the organization and functional role of TATS membranes in atrial myocytes (AMs) is significantly different and much less understood. Taken together, quantitative structural characterization of TATS membrane networks in healthy and diseased myocytes is an essential prerequisite towards better understanding of functional plasticity and pathophysiological reorganization. Here, we present a strategic combination of protocols for direct quantitative analysis of TATS membrane networks in living VMs and AMs. For this, we accompany primary cell isolations of mouse VMs and/or AMs with critical quality control steps and direct membrane staining protocols for fluorescence imaging of TATS membranes. Using an optimized workflow for confocal or superresolution TATS image processing, binarized and skeletonized data are generated for quantitative analysis of the TATS network and its components. Unlike previously published indirect regional aggregate image analysis strategies, our protocols enable direct characterization of specific components and derive complex physiological properties of TATS membrane networks in living myocytes with high throughput and open access software tools. In summary, the combined protocol strategy can be readily applied for quantitative TATS network studies during physiological myocyte adaptation or disease changes, comparison of different cardiac or skeletal muscle cell types, phenotyping of transgenic models, and pharmacological or therapeutic interventions.
Bioengineering, Issue 92, cardiac myocyte, atria, ventricle, heart, primary cell isolation, fluorescence microscopy, membrane tubule, transverse-axial tubule system, image analysis, image processing, T-tubule, collagenase
51823
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In Vivo Modeling of the Morbid Human Genome using Danio rerio
Authors: Adrienne R. Niederriter, Erica E. Davis, Christelle Golzio, Edwin C. Oh, I-Chun Tsai, Nicholas Katsanis.
Institutions: Duke University Medical Center, Duke University, Duke University Medical Center.
Here, we present methods for the development of assays to query potentially clinically significant nonsynonymous changes using in vivo complementation in zebrafish. Zebrafish (Danio rerio) are a useful animal system due to their experimental tractability; embryos are transparent to enable facile viewing, undergo rapid development ex vivo, and can be genetically manipulated.1 These aspects have allowed for significant advances in the analysis of embryogenesis, molecular processes, and morphogenetic signaling. Taken together, the advantages of this vertebrate model make zebrafish highly amenable to modeling the developmental defects in pediatric disease, and in some cases, adult-onset disorders. Because the zebrafish genome is highly conserved with that of humans (~70% orthologous), it is possible to recapitulate human disease states in zebrafish. This is accomplished either through the injection of mutant human mRNA to induce dominant negative or gain of function alleles, or utilization of morpholino (MO) antisense oligonucleotides to suppress genes to mimic loss of function variants. Through complementation of MO-induced phenotypes with capped human mRNA, our approach enables the interpretation of the deleterious effect of mutations on human protein sequence based on the ability of mutant mRNA to rescue a measurable, physiologically relevant phenotype. Modeling of the human disease alleles occurs through microinjection of zebrafish embryos with MO and/or human mRNA at the 1-4 cell stage, and phenotyping up to seven days post fertilization (dpf). This general strategy can be extended to a wide range of disease phenotypes, as demonstrated in the following protocol. We present our established models for morphogenetic signaling, craniofacial, cardiac, vascular integrity, renal function, and skeletal muscle disorder phenotypes, as well as others.
Molecular Biology, Issue 78, Genetics, Biomedical Engineering, Medicine, Developmental Biology, Biochemistry, Anatomy, Physiology, Bioengineering, Genomics, Medical, zebrafish, in vivo, morpholino, human disease modeling, transcription, PCR, mRNA, DNA, Danio rerio, animal model
50338
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Isolation, Culture, and Functional Characterization of Adult Mouse Cardiomyoctyes
Authors: Evan Lee Graham, Cristina Balla, Hannabeth Franchino, Yonathan Melman, Federica del Monte, Saumya Das.
Institutions: Beth Israel Deaconess Medical Center, Harvard Medical School, Sapienza University.
The use of primary cardiomyocytes (CMs) in culture has provided a powerful complement to murine models of heart disease in advancing our understanding of heart disease. In particular, the ability to study ion homeostasis, ion channel function, cellular excitability and excitation-contraction coupling and their alterations in diseased conditions and by disease-causing mutations have led to significant insights into cardiac diseases. Furthermore, the lack of an adequate immortalized cell line to mimic adult CMs, and the limitations of neonatal CMs (which lack many of the structural and functional biomechanics characteristic of adult CMs) in culture have hampered our understanding of the complex interplay between signaling pathways, ion channels and contractile properties in the adult heart strengthening the importance of studying adult isolated cardiomyocytes. Here, we present methods for the isolation, culture, manipulation of gene expression by adenoviral-expressed proteins, and subsequent functional analysis of cardiomyocytes from the adult mouse. The use of these techniques will help to develop mechanistic insight into signaling pathways that regulate cellular excitability, Ca2+ dynamics and contractility and provide a much more physiologically relevant characterization of cardiovascular disease.
Cellular Biology, Issue 79, Medicine, Cardiology, Cellular Biology, Anatomy, Physiology, Mice, Ion Channels, Primary Cell Culture, Cardiac Electrophysiology, adult mouse cardiomyocytes, cell isolation, IonOptix, Cell Culture, adenoviral transfection, patch clamp, fluorescent nanosensor
50289
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Semi-automated Optical Heartbeat Analysis of Small Hearts
Authors: Karen Ocorr, Martin Fink, Anthony Cammarato, Sanford I. Bernstein, Rolf Bodmer.
Institutions: The Sanford Burnham Institute for Medical Research, The Sanford Burnham Institute for Medical Research, San Diego State University.
We have developed a method for analyzing high speed optical recordings from Drosophila, zebrafish and embryonic mouse hearts (Fink, et. al., 2009). Our Semi-automatic Optical Heartbeat Analysis (SOHA) uses a novel movement detection algorithm that is able to detect cardiac movements associated with individual contractile and relaxation events. The program provides a host of physiologically relevant readouts including systolic and diastolic intervals, heart rate, as well as qualitative and quantitative measures of heartbeat arrhythmicity. The program also calculates heart diameter measurements during both diastole and systole from which fractional shortening and fractional area changes are calculated. Output is provided as a digital file compatible with most spreadsheet programs. Measurements are made for every heartbeat in a record increasing the statistical power of the output. We demonstrate each of the steps where user input is required and show the application of our methodology to the analysis of heart function in all three genetically tractable heart models.
Physiology, Issue 31, Drosophila, zebrafish, mouse, heart, myosin, dilated, restricted, cardiomyopathy, KCNQ, movement detection
1435
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Pull-down of Calmodulin-binding Proteins
Authors: Kanwardeep S. Kaleka, Amber N. Petersen, Matthew A. Florence, Nashaat Z. Gerges.
Institutions: Medical College of Wisconsin .
Calcium (Ca2+) is an ion vital in regulating cellular function through a variety of mechanisms. Much of Ca2+ signaling is mediated through the calcium-binding protein known as calmodulin (CaM)1,2. CaM is involved at multiple levels in almost all cellular processes, including apoptosis, metabolism, smooth muscle contraction, synaptic plasticity, nerve growth, inflammation and the immune response. A number of proteins help regulate these pathways through their interaction with CaM. Many of these interactions depend on the conformation of CaM, which is distinctly different when bound to Ca2+ (Ca2+-CaM) as opposed to its Ca2+-free state (ApoCaM)3. While most target proteins bind Ca2+-CaM, certain proteins only bind to ApoCaM. Some bind CaM through their IQ-domain, including neuromodulin4, neurogranin (Ng)5, and certain myosins6. These proteins have been shown to play important roles in presynaptic function7, postsynaptic function8, and muscle contraction9, respectively. Their ability to bind and release CaM in the absence or presence of Ca2+ is pivotal in their function. In contrast, many proteins only bind Ca2+-CaM and require this binding for their activation. Examples include myosin light chain kinase10, Ca2+/CaM-dependent kinases (CaMKs)11 and phosphatases (e.g. calcineurin)12, and spectrin kinase13, which have a variety of direct and downstream effects14. The effects of these proteins on cellular function are often dependent on their ability to bind to CaM in a Ca2+-dependent manner. For example, we tested the relevance of Ng-CaM binding in synaptic function and how different mutations affect this binding. We generated a GFP-tagged Ng construct with specific mutations in the IQ-domain that would change the ability of Ng to bind CaM in a Ca2+-dependent manner. The study of these different mutations gave us great insight into important processes involved in synaptic function8,15. However, in such studies, it is essential to demonstrate that the mutated proteins have the expected altered binding to CaM. Here, we present a method for testing the ability of proteins to bind to CaM in the presence or absence of Ca2+, using CaMKII and Ng as examples. This method is a form of affinity chromatography referred to as a CaM pull-down assay. It uses CaM-Sepharose beads to test proteins that bind to CaM and the influence of Ca2+ on this binding. It is considerably more time efficient and requires less protein relative to column chromatography and other assays. Altogether, this provides a valuable tool to explore Ca2+/CaM signaling and proteins that interact with CaM.
Molecular BIology, Issue 59, Calmodulin, calcium, IQ-motif, affinity chromatography, pull-down, Ca2+/Calmodulin-dependent Kinase II, neurogranin
3502
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Ex Vivo Assessment of Contractility, Fatigability and Alternans in Isolated Skeletal Muscles
Authors: Ki Ho Park, Leticia Brotto, Oanh Lehoang, Marco Brotto, Jianjie Ma, Xiaoli Zhao.
Institutions: UMDNJ-Robert Wood Johnson Medical School, University of Missouri-Kansas City, Ohio State University .
Described here is a method to measure contractility of isolated skeletal muscles. Parameters such as muscle force, muscle power, contractile kinetics, fatigability, and recovery after fatigue can be obtained to assess specific aspects of the excitation-contraction coupling (ECC) process such as excitability, contractile machinery and Ca2+ handling ability. This method removes the nerve and blood supply and focuses on the isolated skeletal muscle itself. We routinely use this method to identify genetic components that alter the contractile property of skeletal muscle though modulating Ca2+ signaling pathways. Here, we describe a newly identified skeletal muscle phenotype, i.e., mechanic alternans, as an example of the various and rich information that can be obtained using the in vitro muscle contractility assay. Combination of this assay with single cell assays, genetic approaches and biochemistry assays can provide important insights into the mechanisms of ECC in skeletal muscle.
Physiology, Issue 69, extensor digitorum longus, soleus, in vitro contractility, calcium signaling, muscle-tendon complex, mechanic alternans
4198
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Isolation of Cardiomyocyte Nuclei from Post-mortem Tissue
Authors: Olaf Bergmann, Stefan Jovinge.
Institutions: University of Lund, University of Lund.
Identification of cardiomyocyte nuclei has been challenging in tissue sections as most strategies rely only on cytoplasmic marker proteins1. Rare events in cardiac myocytes such as proliferation and apoptosis require an accurate identification of cardiac myocyte nuclei to analyze cellular renewal in homeostasis and in pathological conditions2. Here, we provide a method to isolate cardiomyocyte nuclei from post mortem tissue by density sedimentation and immunolabeling with antibodies against pericentriolar material 1 (PCM-1) and subsequent flow cytometry sorting. This strategy allows a high throughput analysis and isolation with the advantage of working equally well on fresh tissue and frozen archival material. This makes it possible to study material already collected in biobanks. This technique is applicable and tested in a wide range of species and suitable for multiple downstream applications such as carbon-14 dating3, cell-cycle analysis4, visualization of thymidine analogues (e.g. BrdU and IdU)4, transcriptome and epigenetic analysis.
Medicine, Issue 65, Stem Cell Biology, Cardiology, Physiology, Tissue Engineering, cardiomyocyte, post mortem, nuclei isolation, flow cytometry, pericentriolar material 1, PCM-1
4205
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Measurement of Antibody Effects on Cellular Function of Isolated Cardiomyocytes
Authors: Lars G. Eckerle, Stephan B. Felix, Lars R. Herda.
Institutions: University Medicine Greifswald.
Dilated cardiomyopathy (DCM) is one of the main causes for heart failure in younger adults1. Although genetic disposition and exposition to toxic substances are known causes for this disease in about one third of the patients, the origin of DCM remains largely unclear. In a substantial number of these patients, autoantibodies against cardiac epitopes have been detected and are suspected to play a pivotal role in the onset and progression of the disease2,3. The importance of cardiac autoantibodies is underlined by a hemodynamic improvement observed in DCM patients after elimination of autoantibodies by immunoadsorption3-5. A variety of specific antigens have already been identified2,3 and antibodies against these targets may be detected by immunoassays. However, these assays cannot discriminate between stimulating (and therefore functionally effective) and blocking autoantibodies. There is increasing evidence that this distinction is crucial6,7. It can also be assumed that the targets for a number of cardiotropic antibodies are still unidentified and therefore cannot be detected by immunoassays. Therefore, we established a method for the detection of functionally active cardiotropic antibodies, independent of their respective antigen. The background for the method is the high homology usually observed for functional regions of cardiac proteins in between mammals8,9. This suggests that cardiac antibodies directed against human antigens will cross-react with non-human target cells, which allows testing of IgG from DCM patients on adult rat cardiomyocytes. Our method consists of 3 steps: first, IgG is isolated from patient plasma using sepharose coupled anti-IgG antibodies obtained from immunoadsorption columns (PlasmaSelect, Teterow, Germany). Second, adult cardiomyocytes are isolated by collagenase perfusion in a Langendorff perfusion apparatus using a protocol modified from previous works10,11. The obtained cardiomyocytes are attached to laminin-coated chambered coverglasses and stained with Fura-2, a calcium-selective fluorescent dye which can be easily brought into the cell to observe intracellular calcium (Ca2+) contents12. In the last step, the effect of patient IgG on the cell shortening and Ca2+ transients of field stimulated cardiomyocytes is monitored online using a commercial myocyte calcium and contractility monitoring system (IonOptix, Milton, MA, USA) connected to a standard inverse fluorescent microscope.
Immunology, Issue 73, Medicine, Cellular Biology, Molecular Biology, Biomedical Engineering, Physiology, Anatomy, Cardiology, cardiomyocytes, cell shortening, intracellular Ca2+, Fura-2, antibodies, dilated cardiomyopathy, DCM, IgG, cardiac proteins, Langendorff perfusion, electrode, immunoassay, assay, cell culture, animal model
4237
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Isolation and Culture of Neonatal Mouse Cardiomyocytes
Authors: Elisabeth Ehler, Thomas Moore-Morris, Stephan Lange.
Institutions: King’s College London, University of California San Diego .
Cultured neonatal cardiomyocytes have long been used to study myofibrillogenesis and myofibrillar functions. Cultured cardiomyocytes allow for easy investigation and manipulation of biochemical pathways, and their effect on the biomechanical properties of spontaneously beating cardiomyocytes. The following 2-day protocol describes the isolation and culture of neonatal mouse cardiomyocytes. We show how to easily dissect hearts from neonates, dissociate the cardiac tissue and enrich cardiomyocytes from the cardiac cell-population. We discuss the usage of different enzyme mixes for cell-dissociation, and their effects on cell-viability. The isolated cardiomyocytes can be subsequently used for a variety of morphological, electrophysiological, biochemical, cell-biological or biomechanical assays. We optimized the protocol for robustness and reproducibility, by using only commercially available solutions and enzyme mixes that show little lot-to-lot variability. We also address common problems associated with the isolation and culture of cardiomyocytes, and offer a variety of options for the optimization of isolation and culture conditions.
Cellular Biology, Issue 79, Biomedical Engineering, Bioengineering, Molecular Biology, Cell Culture Techniques, Primary Cell Culture, Cell Culture Techniques, Primary Cell Culture, Cell Culture Techniques, Primary Cell Culture, Cell Culture Techniques, Disease Models, Animal, Models, Cardiovascular, Cell Biology, neonatal mouse, cardiomyocytes, isolation, culture, primary cells, NMC, heart cells, animal model
50154
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Measuring Cation Transport by Na,K- and H,K-ATPase in Xenopus Oocytes by Atomic Absorption Spectrophotometry: An Alternative to Radioisotope Assays
Authors: Katharina L. Dürr, Neslihan N. Tavraz, Susan Spiller, Thomas Friedrich.
Institutions: Technical University of Berlin, Oregon Health & Science University.
Whereas cation transport by the electrogenic membrane transporter Na+,K+-ATPase can be measured by electrophysiology, the electroneutrally operating gastric H+,K+-ATPase is more difficult to investigate. Many transport assays utilize radioisotopes to achieve a sufficient signal-to-noise ratio, however, the necessary security measures impose severe restrictions regarding human exposure or assay design. Furthermore, ion transport across cell membranes is critically influenced by the membrane potential, which is not straightforwardly controlled in cell culture or in proteoliposome preparations. Here, we make use of the outstanding sensitivity of atomic absorption spectrophotometry (AAS) towards trace amounts of chemical elements to measure Rb+ or Li+ transport by Na+,K+- or gastric H+,K+-ATPase in single cells. Using Xenopus oocytes as expression system, we determine the amount of Rb+ (Li+) transported into the cells by measuring samples of single-oocyte homogenates in an AAS device equipped with a transversely heated graphite atomizer (THGA) furnace, which is loaded from an autosampler. Since the background of unspecific Rb+ uptake into control oocytes or during application of ATPase-specific inhibitors is very small, it is possible to implement complex kinetic assay schemes involving a large number of experimental conditions simultaneously, or to compare the transport capacity and kinetics of site-specifically mutated transporters with high precision. Furthermore, since cation uptake is determined on single cells, the flux experiments can be carried out in combination with two-electrode voltage-clamping (TEVC) to achieve accurate control of the membrane potential and current. This allowed e.g. to quantitatively determine the 3Na+/2K+ transport stoichiometry of the Na+,K+-ATPase and enabled for the first time to investigate the voltage dependence of cation transport by the electroneutrally operating gastric H+,K+-ATPase. In principle, the assay is not limited to K+-transporting membrane proteins, but it may work equally well to address the activity of heavy or transition metal transporters, or uptake of chemical elements by endocytotic processes.
Biochemistry, Issue 72, Chemistry, Biophysics, Bioengineering, Physiology, Molecular Biology, electrochemical processes, physical chemistry, spectrophotometry (application), spectroscopic chemical analysis (application), life sciences, temperature effects (biological, animal and plant), Life Sciences (General), Na+,K+-ATPase, H+,K+-ATPase, Cation Uptake, P-type ATPases, Atomic Absorption Spectrophotometry (AAS), Two-Electrode Voltage-Clamp, Xenopus Oocytes, Rb+ Flux, Transversely Heated Graphite Atomizer (THGA) Furnace, electrophysiology, animal model
50201
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High Efficiency Differentiation of Human Pluripotent Stem Cells to Cardiomyocytes and Characterization by Flow Cytometry
Authors: Subarna Bhattacharya, Paul W. Burridge, Erin M. Kropp, Sandra L. Chuppa, Wai-Meng Kwok, Joseph C. Wu, Kenneth R. Boheler, Rebekah L. Gundry.
Institutions: Medical College of Wisconsin, Stanford University School of Medicine, Medical College of Wisconsin, Hong Kong University, Johns Hopkins University School of Medicine, Medical College of Wisconsin.
There is an urgent need to develop approaches for repairing the damaged heart, discovering new therapeutic drugs that do not have toxic effects on the heart, and improving strategies to accurately model heart disease. The potential of exploiting human induced pluripotent stem cell (hiPSC) technology to generate cardiac muscle “in a dish” for these applications continues to generate high enthusiasm. In recent years, the ability to efficiently generate cardiomyogenic cells from human pluripotent stem cells (hPSCs) has greatly improved, offering us new opportunities to model very early stages of human cardiac development not otherwise accessible. In contrast to many previous methods, the cardiomyocyte differentiation protocol described here does not require cell aggregation or the addition of Activin A or BMP4 and robustly generates cultures of cells that are highly positive for cardiac troponin I and T (TNNI3, TNNT2), iroquois-class homeodomain protein IRX-4 (IRX4), myosin regulatory light chain 2, ventricular/cardiac muscle isoform (MLC2v) and myosin regulatory light chain 2, atrial isoform (MLC2a) by day 10 across all human embryonic stem cell (hESC) and hiPSC lines tested to date. Cells can be passaged and maintained for more than 90 days in culture. The strategy is technically simple to implement and cost-effective. Characterization of cardiomyocytes derived from pluripotent cells often includes the analysis of reference markers, both at the mRNA and protein level. For protein analysis, flow cytometry is a powerful analytical tool for assessing quality of cells in culture and determining subpopulation homogeneity. However, technical variation in sample preparation can significantly affect quality of flow cytometry data. Thus, standardization of staining protocols should facilitate comparisons among various differentiation strategies. Accordingly, optimized staining protocols for the analysis of IRX4, MLC2v, MLC2a, TNNI3, and TNNT2 by flow cytometry are described.
Cellular Biology, Issue 91, human induced pluripotent stem cell, flow cytometry, directed differentiation, cardiomyocyte, IRX4, TNNI3, TNNT2, MCL2v, MLC2a
52010
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Immunostaining of Dissected Zebrafish Embryonic Heart
Authors: Jingchun Yang, Xiaolei Xu.
Institutions: Mayo Clinic College of Medicine.
Zebrafish embryo becomes a popular in vivo vertebrate model for studying cardiac development and human heart diseases due to its advantageous embryology and genetics 1,2. About 100-200 embryos are readily available every week from a single pair of adult fish. The transparent embryos that develop ex utero make them ideal for assessing cardiac defects 3. The expression of any gene can be manipulated via morpholino technology or RNA injection 4. Moreover, forward genetic screens have already generated a list of mutants that affect different perspectives of cardiogenesis 5. Whole mount immunostaining is an important technique in this animal model to reveal the expression pattern of the targeted protein to a particular tissue 6. However, high resolution images that can reveal cellular or subcellular structures have been difficult, mainly due to the physical location of the heart and the poor penetration of the antibodies. Here, we present a method to address these bottlenecks by dissecting heart first and then conducting the staining process on the surface of a microscope slide. To prevent the loss of small heart samples and to facilitate solution handling, we restricted the heart samples within a circle on the surface of the microscope slides drawn by an immEdge pen. After the staining, the fluorescence signals can be directly observed by a compound microscope. Our new method significantly improves the penetration for antibodies, since a heart from an embryonic fish only consists of few cell layers. High quality images from intact hearts can be obtained within a much reduced procession time for zebrafish embryos aged from day 2 to day 6. Our method can be potentially extended to stain other organs dissected from either zebrafish or other small animals.
Developmental Biology, Issue 59, Zebrafish, Danio rerio, Embryonic Heart, Cardiology, Dissection, Immunostaining
3510
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A Strategy to Identify de Novo Mutations in Common Disorders such as Autism and Schizophrenia
Authors: Gauthier Julie, Fadi F. Hamdan, Guy A. Rouleau.
Institutions: Universite de Montreal, Universite de Montreal, Universite de Montreal.
There are several lines of evidence supporting the role of de novo mutations as a mechanism for common disorders, such as autism and schizophrenia. First, the de novo mutation rate in humans is relatively high, so new mutations are generated at a high frequency in the population. However, de novo mutations have not been reported in most common diseases. Mutations in genes leading to severe diseases where there is a strong negative selection against the phenotype, such as lethality in embryonic stages or reduced reproductive fitness, will not be transmitted to multiple family members, and therefore will not be detected by linkage gene mapping or association studies. The observation of very high concordance in monozygotic twins and very low concordance in dizygotic twins also strongly supports the hypothesis that a significant fraction of cases may result from new mutations. Such is the case for diseases such as autism and schizophrenia. Second, despite reduced reproductive fitness1 and extremely variable environmental factors, the incidence of some diseases is maintained worldwide at a relatively high and constant rate. This is the case for autism and schizophrenia, with an incidence of approximately 1% worldwide. Mutational load can be thought of as a balance between selection for or against a deleterious mutation and its production by de novo mutation. Lower rates of reproduction constitute a negative selection factor that should reduce the number of mutant alleles in the population, ultimately leading to decreased disease prevalence. These selective pressures tend to be of different intensity in different environments. Nonetheless, these severe mental disorders have been maintained at a constant relatively high prevalence in the worldwide population across a wide range of cultures and countries despite a strong negative selection against them2. This is not what one would predict in diseases with reduced reproductive fitness, unless there was a high new mutation rate. Finally, the effects of paternal age: there is a significantly increased risk of the disease with increasing paternal age, which could result from the age related increase in paternal de novo mutations. This is the case for autism and schizophrenia3. The male-to-female ratio of mutation rate is estimated at about 4–6:1, presumably due to a higher number of germ-cell divisions with age in males. Therefore, one would predict that de novo mutations would more frequently come from males, particularly older males4. A high rate of new mutations may in part explain why genetic studies have so far failed to identify many genes predisposing to complexes diseases genes, such as autism and schizophrenia, and why diseases have been identified for a mere 3% of genes in the human genome. Identification for de novo mutations as a cause of a disease requires a targeted molecular approach, which includes studying parents and affected subjects. The process for determining if the genetic basis of a disease may result in part from de novo mutations and the molecular approach to establish this link will be illustrated, using autism and schizophrenia as examples.
Medicine, Issue 52, de novo mutation, complex diseases, schizophrenia, autism, rare variations, DNA sequencing
2534
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What is Visualize?
JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.
How does it work?
We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.
Video X seems to be unrelated to Abstract Y...
In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.
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DBS Surgery Risks, Possible Side Effects
Neuroanimations.com
Strip recording of electrical interference
With any surgery there are the risks of bleeding and infection. Although rare, when significant bleeding occurs, it can be serious. Bleeding can behave like a stroke. Infection in the brain is meningitis.
Stimulation related issues include paresthesias (numbness and tingling sensations), dysarthria, nasal and hypophonic speech (low volume), muscle contractions, disequilibrium. Usually, these can be improved with programming over time.
Equipment malfunction include broken or fractured leads which can cause electric shocks or no stimulation requiring replacement surgery.
Difficulties at surgery such as suboptimal testing due to difficult microelectrical recordings, dementia, testing with sedation, may result in less than wanted results requiring repositioning (further surgery) of the brain electrodes. Electrode recording strip
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Skip to main content
Are T cells the only HIV-1 reservoir?
An Erratum to this article was published on 08 February 2017
Abstract
Current antiretroviral therapies have improved the duration and quality of life of people living with HIV-1. However, viral reservoirs impede complete eradication of the virus. Although there are many strategies to eliminate infectious virus, the most actively pursued are latency reversing agents in conjunction with immune modulation. This strategy, known as “shock and kill”, has been tested primarily against the most widely recognized HIV-1 latent reservoir found in resting memory CD4+ T cells. This is in part because of the dearth of conclusive evidence about the existence of non-T cell reservoirs. Studies of non-T cell reservoirs have been difficult to interpret because of technical and biological issues that have hampered a better understanding. This review considers the current knowledge of non-T cell reservoirs, the challenges encountered in a better understanding of these populations, and their implications for HIV-1 cure research.
Background
In the twenty years since combination antiretroviral therapy (ART) for HIV-1 was first announced, people living with HIV-1 (PLWH) have had marked improvements in mortality and quality of life. However, whereas ART is remarkably effective at preventing new cells from becoming infected, it does not eliminate long-lived cells that are already infected prior to ART initiation. Latent reservoirs have thwarted attempts to eliminate all replication competent forms of the virus from infected individuals [1,2,3,4,5,6].
There is reason for balanced optimism in the HIV-1 cure field. The ‘Berlin’ and ‘Boston’ patients who underwent bone marrow transplants from donors lacking one or both copies of full-length CCR5, a key HIV-1 entry co-receptor, had prolonged remissions without evidence of HIV-1; in the case of the ‘Berlin’ patient, there is still no evidence of HIV-1 since his transplant [7, 8]. The ‘Mississippi Baby’ and results of the VISCONTI study highlight the possibility of long drug-free remission periods if ART is initiated during primary infection [1, 2, 7, 9,10,11]. Central to each case of a potential cure or ART-free remission has been a reduction in the size of the HIV-1 reservoir. Therefore, it is critical for cure strategies to target all potential reservoirs.
Many cells are susceptible to HIV-1 in vitro, but not all potential reservoirs have been studied in vivo during ART with the same rigor. Resting memory CD4+ T cells are the most widely recognized and best-described HIV-1 reservoir in research that has been extensively reviewed elsewhere [12, 13]. For cells to constitute an HIV-1 reservoir, they have to harbor replication competent forms of the virus that persist for years despite long-term ART suppression of viremia [14]. Against the standard of the T cell reservoir, in this review we consider evidence suggesting the possible long-term persistence of non-T cell reservoirs in individuals on ART, and the current challenges involved in their identification.
Usual and unusual suspects
Viral latency is defined as a reversible nonproductive state of infection in individual cells [15]. Reservoirs are cells that harbor replicative forms of HIV-1 following long periods of ART-suppressed viremia [14, 16]. Resting memory CD4+ T cell reservoirs have been estimated to have a half-life of 44 months, meaning that their clearance during ART may take as long as 73 years [13, 17, 18]. Subsequently, distinct populations of CD4+ T cells have also been recognized to contribute to the pool of latently infected cells [19,20,21], although those are outside the scope of the present review. The half-life of resting memory CD4+ T cell reservoirs corresponds to the long-phase decay of residual plasma viremia in persons taking long-term ART [22]. The phases of plasma HIV-1 RNA decline on ART have been attributed to infection of different cell types that are infected by the virus, and much has been inferred about the identities of those cells without clear evidence (Fig. 1). Here, we enumerate several candidate cell types that could potentially serve as HIV-1 reservoirs (Table 1).
Fig. 1
figure 1
Phasic decline of viremia due to death of HIV-1 infected cells following ART. The multiphasic decay in plasma viremia following initiation of ART has been attributed to the varying half-life of infected cells. Death of productively infected activated CD4+ T cells with a half-life of 1–2 days contributes to the first phase of decline. The slower second phase during which viremia becomes undetectable is contributed to by cells with a half-life in the order of weeks. The cells contributing to the second phase have not been conclusively identified. This is followed by the third phase of decline, characterized by undetectable steady viremia due to infected resting memory CD4+ T cells with a half-life of 44 months
Table 1 Summary data on HIV-1 reservoirs and assays in various cell populations
Macrophages and myeloid cells
Found primarily in tissues, macrophages are mononuclear leukocytes that are key components of innate immunity. For decades, the origin of tissue resident macrophages (TRM) was explained by the concept of the mononuclear-phagocyte system: monocytes were thought to continually replenish TRM that died in tissues [34, 35]. Consistent with this early concept, the death of HIV-1 infected macrophages was thought to be responsible for the second phase of HIV-1 viral kinetic decline during ART. However, recent findings based on murine models suggest that the principal origin of TRM in steady state is from embryonic haematopoietic precursors, while monocytes only contribute in the setting of inflammation and injury [36]. Similarly, detection of TRM even in individuals with monocytopenia suggests monocyte-independent maintenance, a long half-life of embryonically derived macrophages, or likely a combination of both [37]. Studies in patients who received lung transplantation have also shown long-term persistence of donor alveolar macrophages [32]. In parallel, the rapid second phase decline of HIV-1 was found not to be attributable to macrophages [38]. Taken together, these findings have led to a marked revision in our understanding of the maintenance and longevity of TRM.
It is well established in animal models and in vitro that macrophages can be productively infected by lab strains of HIV-1 [39, 40], although there may be anatomical variation in their susceptibility to HIV-1 infection. For example, there are reports of HIV-1 and SIV in brain macrophages such as microglia [41, 42]. Vaginal macrophages have been shown to support HIV-1 replication better than intestinal macrophages, which may be explained by differential expression of entry co-receptors [43]. Comparative in situ fluorescence also suggests higher HIV-1 susceptibility of rectal macrophages compared to colonic macrophages [44]. Cai et al. have shown that SIV infection of lung macrophages leads to preferential destruction of interstitial macrophages, in comparison to alveolar macrophages that experience minimal cell death and low turnover [45].
Several reports in the pre-ART era demonstrated HIV-1 infection in TRM [46,47,48,49,50]. More recently alveolar macrophages from individuals on ART have been shown to harbor HIV-1 nucleic acids (both proviral DNA and RNA) [51]. Our lab has extended earlier studies of liver macrophages (Kupffer cells), the largest population of TRM in the body, to show that these cells can harbor virus from individuals on ART for as long as 11 years, although their functional significance is still unclear [25]. Other tissue macrophages that have also been implicated as harboring HIV-1 include those in the seminal vesicle, duodenum, urethra, adipose tissue, and liver [25, 46, 52,53,54,55].
The study of HIV-1 infection of macrophages is not without controversy. Recent in vivo data from an SIV macaque model has demonstrated the presence of both proviral DNA and T cell receptors (TCR) in myeloid cells: the authors concluded that the presence of viral DNA in macrophages was due to phagocytosis of infected dying cell rather than de novo infection of myeloid cells [56]. However, a subsequent report by Baxter et al. showed that primary monocyte-derived macrophages could selectively capture HIV-1 infected CD4+ T cells, leading to macrophage infection along with efficient HIV-1 cell-to-cell spread [57]. Indeed, others and we have confirmed the exclusion of T cells and TCRs in ex vivo studies of TRM reservoirs [25, 58]. Thus it is important to differentiate between phagocytosis and actual infection of macrophages following detection of nucleic acids in macrophages. In addition, it is clear from in vitro studies that HIV-1 replication dynamics differ in myeloid cells compared to CD4+ T cells: virions can be found dwelling for prolonged periods in long cytoplasmic channels in macrophages and are not immediately released, in contrast to the typical burst that has been described in CD4+ T cells [59].
Monocytes, closely related myeloid cells, were initially reported as being infected in vivo; however, it has now been shown that monocytes are not susceptible to HIV-1, and largely lack proviral HIV-1 DNA in both viremic and ART suppressed individuals [24, 60].
Dendritic cells
Dendritic cells (DCs) are a heterogeneous group of antigen-presenting cells that play vital roles in orchestrating immune responses [61]. DCs can be broadly divided into those of myeloid or lymphoid origin [62], and further categorized as plasmacytoid (pDCs), myeloid (mDCs), Langerhans cells (found in the epidermis), and interstitial [63].
Although DCs comprise a small proportion of cells in various anatomical sites [64], their role as immunologic sentries makes them among the first cells that encounter invading pathogens like HIV-1. Indeed, analyses of transmitted/founder viruses have shown that they have enhanced binding to mDCs compared to viruses isolated from chronic infection, a feature that may facilitate virus transport across the mucosa [65, 66].
pDCs and mDCs have been noted to have differential susceptibility to HIV-1 infection, although this has largely been ascertained in vitro [67,68,69]. In vivo, the presence of HIV-1 DNA in DCs has been noted to occur at lower frequency compared to CD4+ T cells [70, 71]. There have been several reports of productive HIV-1 infection of DCs in vitro for as long as 45 days [72,73,74,75], but limited data in vivo. Langerhans cells have been considered as a potential reservoir, but largely based on data in the pre-ART era [76, 77].
To fulfill their role as a reservoir, DCs have been posited to transfer infection to T cells, in particular to antigen specific CD4+ T cells, following their encounter with HIV-1, whether or not they themselves are infected [78,79,80]. This infection in trans is mediated by the formation of an infectious/virological synapse [33]. During trans infection, compartmentalized HIV-1 has been observed to emerge from DCs and fuse with the T cell membrane [81]. Envelope specific inhibitors maintain their potency against these compartmentalized virions [81]. These are tantalizing hypotheses that have been difficult to find evidence for in vivo.
Follicular dendritic cells
Follicular dendritic cells (FDCs) that are found in B cell follicles in secondary lymphoid organs are not typical DCs, although they are similarly named: FDCs develop from perivascular precursors of stromal cell origin and are not known to present antigens using MHC-restricted pathways [26, 64].
FDCs can potentially serve as viral reservoirs by maintaining a stable pool of HIV-1 on their surface without being infected [82, 83]. In vitro studies have revealed that HIV-1 virions adhere on the surface of FDCs through interactions with complement receptors mediated via a C3-dependent mechanism [84]. The binding of C3 fragments to the virus allows its adherence to complement receptors CR1 and CR2, present on FDCs [26]. In addition, the presence of non-neutralizing antibodies specific for HIV-1 in patients may enhance binding to FDCs via FcR-mediated binding [26].
HIV-1 has been known to persist on these cells even in the presence of neutralizing antibodies, with reports suggesting that FDCs can restore the infectivity of neutralized viruses [85, 86]. FDCs transfer antigens in the B cell follicles of all secondary lymphoid tissues, and in the process may transfer HIV-1 to T follicular helper cells that are also present in the B cell follicles [21].
In mice, FDCs have been shown to trap HIV-1 following a single exposure, and these virions remained infectious for at least 9 months [85]. A recent study reported visualization of HIV-1 in cycling endosomes in FDCs isolated from individuals on prolonged ART (median = 8 years) [87]. Mathematical models have suggested that FDCs are the major contributor to the low-level viremia detected during the third phase of viral decay, and have been estimated to have a half-life of 39 months [22].
Epithelial cells
There have been reports suggesting the possible infection and transmission of infection by epithelial cells even though they do not express CD4 and have undetectable or low expression of the co-receptors CCR5and CXCR4 [88, 89]. Renal epithelial cells have been reported to be susceptible to HIV-1 in vitro [90]. Cultures of renal tubule epithelial cells were productively infected by HIV-1 following co-culture with infected T cells [90]. Transmission of infection was observed to occur by formation of virological synapses [91]. HIV-1 mRNA and DNA have also been detected in renal tubular epithelial cells using in situ hybridization done on biopsies obtained from individuals with HIV-1 associated nephropathy [92]. Phylogenetic analyses of sequences obtained from renal epithelial cells were found to cluster together within the radiation of sequences obtained from peripheral blood mononuclear cells [93]. These cells could play a role in persistence of HIV-1 infection in individuals on ART based on indirect evidence [94, 95].
Mammary epithelial cells have been conjectured to harbor a separate compartment of HIV-1: phlyogenetic analyses of HIV-1 DNA from paired breast-milk and peripheral blood samples from HIV-1 infected women have shown the existence of genetically distinct compartments [96, 97]. Studies of breast-milk from HIV-1 infected women on treatment have shown negligible impact of ART on cell-associated or HIV-1 proviral DNA levels, in contrast with a rapid decline in cell-free HIV-1 RNA [98, 99].
Similar to DCs, oral keratinocytes have been shown to support transmission of virus to susceptible cells without supporting replication [100, 101]. However there is no evidence that these cells serve as HIV-1 reservoirs, and there are no published data on the half-life of epithelial cells in vivo in this context.
Kong et al. have reported detection of integrated HIV-1 DNA and release of infectious virus in liver epithelium following in vitro infection of hepatocyte cell lines and primary hepatocytes [102]. In addition, hepatic stellate cells have also been shown to release infectious virus following infection in vitro [103]. However, the translation of this research to studies of in vivo reservoirs has been more challenging, and data are lacking.
Miscellaneous
There have been isolated reports of other cells that can possibly be infected with HIV-1. Fibrocytes, defined as CD34+CD45+ collagen I+, have recently been reported to have characteristics of cells that can be persistently infected [104]. In vitro, infected fibrocytes resisted HIV-1 induced cell death and stably expressed low levels of HIV-1 mRNA for >60 days. However, there are no data on whether fibrocytes are HIV-1 infected in vivo [104].
Other cell types that could be explored as HIV-1 reservoirs in individuals on ART include astrocytes in the CNS and CD56+/CD3− NK cells [105,106,107]. Hematopoietic progenitor cells (HPCs) that were initially reported to harbor infectious virus are now not considered to fulfill the criteria to be a reservoir following development of enhanced techniques to purify HSCs from bone marrow [108, 109].
Challenges in studying non-T cell reservoirs
In ART-suppressed individuals the number of latently infected T cell varies from 1 to 10 infectious units per million (IUPM) [110]. Estimation of these numbers in ART-suppressed individuals requires isolation of millions of cells from large volume blood draws [111]. Similar studies on cells from HIV-1 infected people that have low or absent numbers in circulation, or that are principally found in tissues, have been technically challenging or unethical [25, 51].
Technical challenges
The gold standard for quantifying the amount of replication competent HIV-1 in a purified population of cells during ART has been the quantitative viral outgrowth assay (QVOA), which was initially developed to measure the amount of latent HIV-1 infection in resting memory CD4+ T cells [23, 112]. The potency of the QVOA is that it hinges on the recovery of infectious, replication competent HIV-1 that propagates exponentially, plausibly explaining the virological rebound seen in patients who discontinue ART. The QVOA is a highly consistent assay, but nonetheless poses a number of technical challenges, including that it is expensive, time-consuming, requires large amounts of starting materials, has a limited dynamic range, and underestimates the size of the latent reservoir [111,112,113]. Several groups have employed PCR-based approaches as alternative tools [23]. PCR-based assays sensitively detect viral nucleic acid over a large dynamic range, and can differentiate between total, integrated, and LTR HIV-1 DNA [114, 115]. Although easier, PCR-based approaches do not differentiate between replication competent and defective viruses, of which the latter constitute the majority of viral forms, and do not correlate well with the number of cells with replication competent virus [13]. PCR-based approaches typically yield infected cell frequencies that are 100–1000 times higher than what is resulted from the QVOA [23]. More recently, an approach called the TILDA (Tat/rev Induced Limiting Dilution Assay) that measures multiply spliced HIV-1 RNA was developed as an alternative [116]. This assay has a quick turnaround time and requires fewer than a million cells of starting material. However, the TILDA does not measure virus production and does not address whether measured RNAs derive from replication competent viruses [116, 117]. Moreover, the TILDA correlates poorly with the QVOA when performed on the same samples [116].
Therefore, as of now the most accurate measurement of the replication competent viral reservoir requires the QVOA, limiting the quantification of HIV-1 reservoirs in tissues that are poorly accessible. However, an overlooked challenge of using the QVOA is that it has been specifically “tuned” to CD4+ T cells, and may not be sensitive for detecting infection in cells that bear different HIV-1 replication dynamics than CD4+ T cells. Recent advances in adapting the QVOA to macrophages are steps in the right direction for quantifying these HIV-1 reservoirs [58].
Biologic solutions
To address the challenges posed in isolating a large number of these cells to study latency, the field has resorted to the use of alternate models that complement each other—in vitro, animal, and mathematical models [22, 58, 118, 119]. Although more feasible, these approaches have their drawbacks. In vitro models are used frequently because of their convenience, but do not fully mimic in vivo infections. [64, 120]. Similarly, heterogeneous cell phenotypes can be observed in in vitro models, such as in monocyte-derived macrophages (MDMs) subpopulations [121,122,123]. Fundamentally, HIV-1 susceptibility and longevity in vitro may be quite different than in the immunological context of natural infection. Hence, in vitro modeling can only be used to complement findings in vivo.
Non-human primates (NHP) and humanized mice models have been invaluable for understanding HIV-1 pathogenesis [24, 27, 58]. NHP are typically infected either with simian immunodeficiency virus (SIV) or SIV/HIV-1 chimeric viruses (SHIV) [27, 124]. However, SIV and HIV-1 have notable distinctions, sharing only approximately 53% sequence homology and differing in the organization of their overlapping ORFs [124]. For instance, sooty mangabey SIV (SIVsmm) and macaque SIV (SIVmac) lack the HIV-1 accessory gene vpu. Instead, they encode for vpx, which may be a critical difference: vpx degrades SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1 (SAMHD1), a key retroviral restriction factor in macrophages and DCs [125, 126]. Nevertheless, SIV infection of NHP remains a key experimental tool, especially for in vivo and ex vivo studies of tissues that are inaccessible in humans, such as the brain.
Recent advances in humanized mouse technology have facilitated their infection with HIV-1 [127,128,129]. A recent humanized model referred to as myeloid-only-mice (MoM), developed from NOD/SCID mice, has been very useful to study infection and persistence in non-T cells [24, 130]. These mice lack T cells, and are developed by adoptive transfer of human CD34+ stem cells, enabling reconstitution of the mouse with human monocytes, macrophages, B cells, and dendritic cells [24, 130]. However, a major hurdle impeding more widespread use of humanized mice is that each experiment requires the surgical engraftment of human tissue, since this aspect cannot be bred [124]. A promising and creative use of humanized mice is in the development of a murine viral outgrowth assay where HIV-1 latency is estimated by adoptive transfer of human cells into humanized mice [131].
Conclusion
Whereas promising improvements to antiretroviral therapy have improved the quality of life of PLWH, they have not bridged the gap toward an HIV-1 cure [132]. Although it has been debated whether resources for HIV-1 research should be focused on a cure when there are other challenges facing PLWH, we argue that latent reservoirs harbor the potential for high-level virologic rebound in each of the 37 million HIV-1 infected people worldwide, which bears both individual and public harm. Indeed, we further argue that without exploring the true extent of HIV-1 reservoirs with the same rigor as has been used to study peripheral resting memory CD4+ T cells, we risk developing incomplete cure strategies [18, 110]. The current “shock and kill” strategy hinges on the drugs known as latency reversing agents (LRAs) that induce viral production in latently-infected cells [13, 133,134,135]. Presently, however, latency reversal has been developed to be specific for CD4+ T cell biology, and does not account for the possibility of persistent reservoirs in cells other than T cells [136, 137], reflecting lacunae in our understanding of non-T cell reservoirs [28]. Therefore, a dedicated strategy to eliminate HIV-1 reservoirs requires a better understanding of the role of non-T cell reservoirs using in vivo and ex vivo experimentation.
Abbreviations
ART:
antiretroviral therapy
PLWH:
people living with HIV-1
TRM:
tissue resident macrophages
TCR:
T cell receptors
DCs:
dendritic cells
pDCs:
plasmacytoid dendritic cells
mDCs:
myeloid dendritic cells
FDCs:
follicular dendritic cells
HPCs:
hematopoietic progenitor cells
IUPM:
infectious units per million
QVOA:
quantitative viral outgrowth assay
TILDA:
Tat/rev Induced Limiting Dilution Assay
MDMs:
monocyte-derived macrophages
NHP:
non-human primates
SIV:
simian immunodeficiency virus
SHIV:
SIV/HIV-1 chimeric viruses
SIVsmm:
sooty mangabey SIV
SIVmac:
macaque SIV
SAMHD1:
SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1
MoM:
myeloid-only-mice
LRAs:
latency reversing agents
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Authors’ contributions
AJK prepared the figures and wrote the manuscript. SS assisted with writing of the manuscript. AB wrote and supervised preparation of the manuscript. All the authors read and approved the final manuscript.
Acknowledgements
We would like to thank David L. Thomas for helpful discussions and critical review of our manuscript.
Competing interests
The authors declare that they have no competing interests.
Funding
AB and SS was supported by NIH/NIAID Grants R56 AI118445, NIH/NIDA Grant R01 DA016078, and The Johns Hopkins Center for AIDS Research (JHU CFAR) P30AI094189-01A1.
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An erratum to this article is available at http://dx.doi.org/10.1186/s12977-017-0333-x.
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Kandathil, A.J., Sugawara, S. & Balagopal, A. Are T cells the only HIV-1 reservoir?. Retrovirology 13, 86 (2016). https://doi.org/10.1186/s12977-016-0323-4
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Updated on: February 5, 2018
Your OB Coding Questions Answered
By
Original story posted on: February 2, 2018
Erica Remer, MD responds to listeners questions from the Talk Ten Tuesday broadcast Jan. 30th.
Since I am out of town on an empty-nesting trip with my husband, I decided to answer the questions we couldn’t get to last week, in writing.
When Linda Holtzman and I were bandying about how the correct code for a condition which is neither complicating or complicated by a pregnancy would be the Z33.1 code, Pregnant state, incidental, we did not give the detail that the provider must explicitly state that the condition is not affecting the pregnancy (Official Guidelines, Section I, C. 15. a. 1). All conditions are presumed to be pregnancy-relevant unless the provider states they are not.
Many of you wrote in to point this out – thanks for the clarification. Providers will have to be trained to give the information that the “pregnant is incidental; ” it will not be intuitive or natural for them to do that for you. Linda’s example of a subcutaneous foreign body was a great example. As I mentioned before, almost ANYTHING else will fall into complicating or complicated by pregnancy!
Tammany asked: If a patient comes in with Right upper quadrant (RUQ) pain and + preg test and the diagnosis is pregnancy of unknown location, what diagnosis would you use with the pain?
The RUQ pain will be coded with R10.11. If the doctor’s documentation had just documented, “positive pregnancy test,” the code would be Z32.01, Encounter for pregnancy test, result positive. However, no provider would consider abdominal pain in pregnancy unrelated. In this case, the provider documented, “Pregnancy of unknown location” (which makes me think that he has recently been burned assuming a pregnancy was intrauterine when it was not).
My opinion is that unless and until a provider performs an ultrasound to disprove intrauterine status which would lead you to the O00- category, you just consider codes which refer to “in pregnancy, childbirth, or the puerperium” (“in pregnancy” isn’t specifying WHERE the pregnancy is). The bottom line is I think this is another opportunity to use O99.89, Other specified diseases and conditions complicating pregnancy, childbirth, and the puerperium.
Tammany also asked: What diagnosis code would you use for a nonstress test for a patient with a 2- vessel cord? Would it be O69.89?
O69.89, Labor and delivery complicated by other cord complications would be the appropriate code IF the patient was delivering. Prior to onset of labor, you wouldn’t use this code. The correlate to this code in the “maternal care for” variety is O36.89, Maternal care for other specified fetal problems. This would be the appropriate code.
Candi asked: Mom comes in for acute pancreatitis at 27 weeks. Does not deliver. Dr. lists that mom had a previous c/section. There was nothing directed towards the scar or any monitoring, treatment, etc. The code affects severity of illness (SOI) and payer is denying this citing does not meet reportable secondary diagnosis guidelines.
If having a previous cesarean delivery is relevant, such as trying to determine whether or not to try a VBAC (vaginal birth after Csxn) or to do a repeat section (either during an antepartum visit or at the time of delivery), it is obvious to use the O34.21- code set. If the provider is counseling the patient, or working up a potential uterine rupture due to the previous scar, the O34.21- codes would be applicable. The payor would not need more substantiation to consider it relevant (and worthy of increasing SOI).
The dilemma arose in this situation because “listing that there was a previous c/section” seems here to be more informational. If she were not pregnant, this clearly would be coded with: Z98.891, History of uterine scar from previous surgery.
However, since she is gravid, we must consider Coding Clinic, 2016 Q4, pp. 76-79 which states, “For a patient who is currently pregnant, a code from subcategory O34.2 should be used instead of Z98.891.”
So the choice becomes: code O34.21- (depending on type of previous Csxn) or don’t capture that information at all?
Philosophically, I do not believe in adapting coding to make payers happy. I believe in documenting to tell the truth, and coding to tell the story. The fact that we have to fight denials is unfortunate. This may be a case where you should proactively request clarification from the provider as to whether the fact that the patient had a previous cesarean section was clinically relevant or not. If the provider documents supporting evidence, it establishes legitimacy as a secondary diagnosis and should be captured.
By the way, before you all can complain: O99.613, Diseases of the digestive system complicating pregnancy, third trimester + K85.90, Acute pancreatitis without necrosis or infection, unspecified + Z3A.27, 27 weeks gestation. You guys are so tough on me!
Hope this clears up any confusion. See you in two weeks. I will be out next week, too, on an onsite visit. And a big thank you to Linda Holtzman of Clarity Coding who was our guest last Tuesday and edited this article to make sure I wasn’t making ANOTHER coding faux pas!
Disclaimer: Every reasonable effort was made to ensure the accuracy of this information at the time it was published. However, due to the nature of industry changes over time we cannot guarantee its validity after the year it was published.
Erica E. Remer, MD, CCDS
Erica Remer, MD, CCDS has a unique perspective as a practicing emergency physician for 25 years, with extensive coding, CDI, and ICD-10 expertise. She was a physician advisor of a large multi-hospital system for four years before transitioning to independent consulting in July 2016. Her passion is educating CDI specialists, coders, and healthcare providers with engaging, case-based presentations on documentation, CDI, and denials management topics. She has written numerous articles and serves as the co-host of Talk Ten Tuesdays, a weekly national podcast. Dr. Remer is a member of the ICD10monitor editorial board, a former member of the ACDIS Advisory Board, and the board of directors of the American College of Physician Advisors.
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Neuromusculer blocking drugs
neuromusculer blocking drugs Use of volatile anesthetics reduce the requirement for neuromuscular blocking drugs in a dose-related fashion (1 mac reduces ed95 by approx 1/3) back to top of page.
Pharmacology of neuromuscular blocking drugs and anticholinesterases dr dominic o’connor, consultant, royal perth hospital, australia dr carl gwinnutt, consultant, hope hospital, salford. Neuromuscular blocking agents the intent of the neuromuscular blocking agent policy is to ensure appropriate selection of patients for. Start studying neuromuscular blocking drugs learn vocabulary, terms, and more with flashcards, games, and other study tools. Compare neuromuscular blocking agents view important safety information, ratings, user reviews, popularity and more.
Looking for online definition of neuromuscular-blocking drugs in the medical dictionary neuromuscular-blocking drugs explanation free what is neuromuscular-blocking. Neuromuscular blockers differ from each other in case studies of neuromuscular blocking agents - case studies of neuromuscular blocking agents jay horrow. Neuromuscular blocking agents: use and controversy in the hospital setting neuromuscular blocking agents and neuromuscular dysfunction acquired in critical. Pharmacology of neuromuscular blocking drugs and anticholinesterases dr dominic o’connor, consultant, royal perth hospital, australia dr carl gwinnutt, consultant. Clinical should consider dosing this patient population based on ideal body weight as with other neuromuscular blocking drugs, raplon (rapacuronium. Neuromuscular blocking agents drug information from drugscom includes neuromuscular blocking agents side effects, interactions and indications.
Learn about the veterinary topic of neuromuscular blocking agents find specific details on this topic and related topics from the merck vet manual. Problem: neuromuscular blocking agents have been inadvertently administered to patients who were not receiving proper ventilator assistance because the respiratory muscles were paralyzed. Neuromuscular blocking drugs skeletal muscle relaxants spasmolytic agents spasticity-characteristics increased in tonic stretch.
Neuromuscular blocking drugs - depolarizing & nondepolarizing - duration: 3:19 usmlefasttrack 79,822 views 3:19 neuromuscular blocking agents. Neuromuscular blocking agents scope: unless otherwise stated, these items pertain to all neuromuscular blocking agents used in any inpatient and outpatient. Find out information about neuromuscular blocking drug 1 any synthetic, semisynthetic, or natural chemical substance used in the treatment, prevention. Neuromuscular-blocking drug's wiki: neuromuscular-blocking drugs block neuromuscular transmission at the neuromuscular junction,[2] causing paralysis of the affected.
Neuromusculer blocking drugs
Bridion is a modified gamma cyclodextrin it forms a complex with the neuromuscular blocking agents rocuronium and vecuronium.
• Neuromuscular blocking agents (nmbas or “paralytics”) are categorized as depolarizing (classically succinylcholine) and nondepolarizing they’re important drugs to know because we routinely.
• Definitions of neuromuscular blocking drug, synonyms, antonyms, derivatives of neuromuscular blocking drug, analogical dictionary of neuromuscular blocking drug (english.
• Neuromuscular blockers, nondepolarizing: dosing, uses, side effects, interactions, patient handouts, pricing and more from medscape reference.
• Nmj-blocking agents block nerve stimulation on muscle cells and cause paralysis of the muscles directly without total cns depression and its many systemic effects.
Mechanism of action suxamethonium: • block transmission by causing prolonged depolarization of endplate at neuromuscular junction • manifestation by initial. Neuromuscular-blocking drugs block neuromuscular transmission at the neuromuscular junction, causing paralysis of the affected skeletal musclesthis is accomplished either by acting. Depolarizing blocking agents edit a depolarizing neuromuscular blocking agent is a form of neuromuscular blocker that depolarizes the motor end plate an example is succinylcholine. Depolarizing blocking agents edit a neuromuscular depolarizing agent is a form of neuromuscular blocker which will depolarize the motor end plate. An anesthesiologist explains why your muscles sometimes need to be reversibly paralyzed during anesthesia neuromuscular blocking agents are used to achieve this goal. Neuromuscular blocking agents neuromuscular blocking agents may be used in pigs to provide muscle relaxation for thoracic, abdominal, and orthopaedic surgery, and. Neuromuscular blocking agents (nmbas) for rapid sequence intubation in adults outside of the operating room.
Neuromusculer blocking drugs
Rated 3/5 based on 24 review
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Co-administration of GnRH-agonist and hCG for final oocyte maturation (double trigger) in patients with low number of oocytes retrieved per number of preovulatory follicles-a preliminary report
Abstract
Background
Recently, the co-administration of GnRH agonist and hCG for final oocyte maturation- 40 and 34 hours prior to OPU, respectively (double trigger) was suggested as the treatment of genuine empty follicle syndrome. In the present study, we aim to evaluate whether the double trigger improves the number of oocytes retrieved in patients with low (<50%) number of oocytes retrieved per number of preovulatory follicles.
Methods
In this proof of concept cohort historical study, we compared the stimulation characteristics of 8 IVF cycles, which include the double trigger to the patients’ previous IVF attempt, triggered with hCG-only.
Results
Patients who received the double trigger (study group) had a significantly higher number of oocytes retrieved, number of 2PN, number of embryos transferred and significantly higher proportions of the number of oocytes retrieved to the number of follicles >10 mm and >14 mm in diameter on day of hCG administration, with a tendency toward a higher number of TQE, as compared to their previous cycles (hCG-only trigger). Three ongoing clinical pregnancies were recorded in the study group and none in the hCG-only trigger group.
Conclusions
Co-administration of GnRH-agonist and hCG for final oocyte maturation, 40 and 34 hours prior to OPU, respectively (double trigger), is suggested as a valuable new tool in the armamentarium for treating patients with low/poor oocytes yield despite an apparently normal follicular development and E2 levels and in the presence of optimal hCG levels on the day of OPU.
Background
Controlled ovarian hyperstimulation (COH) is considered a key factor in the success of in vitro fertilization-embryo transfer (IVF-ET) because it enables the recruitment of multiple healthy fertilizable oocytes [1]. Moreover, human chorionic gonadotropin (hCG) is usually used at the end of COH, as a surrogate LH surge, to induce final oocyte maturation and resumption of meiosis [2].
Lack of oocyte yield during ovum pick-up (OPU), following COH with an apparently normal follicular development and E2 levels and in the presence of optimal hCG levels on the day of OPU- the genuine empty follicle syndrome (EFS) [3], is a rare entity, with an estimated prevalence of 0–1.1% [4, 5]. On the other hand, a more frequently encountered situation is the normally responding patients with a low oocytes yield, i.e. a low ratio (<50%) between the number of oocytes retrieved to the number of follicles >14 mm in diameter on the day of hCG administration.
Despite many years of clinical experience [6], the underlying mechanism of the aforementioned conditions is still obscure and no precise prevention methods exist [5]. Several strategies were offered to patients with EFS [summarized in [5]], including another standard ART cycle; shifting from an GnRH-agonist to GnRH-antagonist COH protocol; re-administering hCG from a different batch and aspirating the second ovary; changing the hCG from a urinary to a recombinant preparation; using GnRH-agonist for final; prolonging the interval between ovulation triggering and OPU; and follicle flushing during oocyte retrieval [7].
Recently, a new treatment modality has been clinically implemented to EFS patient, with the co-administration of GnRH agonist and hCG for final oocyte maturation- 40 and 34 hours prior to OPU, respectively (double trigger) [5]. This method combines the advantage of both: (1) the prolongation of the time between ovulation triggering and OPU; and (2) the GnRH agonist trigger with the consequent simultaneous induction of an FSH surge.
Prompted by this new remedy, we offered the double trigger to all our patients, who underwent the GnRH-antagonist COH protocol, resulting with poor oocytes yield due to low (<50%) number of oocytes retrieved per number of follicles > 14 mm in diameter on day of hCG administration. In the present study, we aim to further evaluate whether the double trigger improves the number of oocytes retrieved and the ratio between the number of oocytes retrieved per number of follicles > 14 mm in diameter on day of hCG administration.
Methods
All consecutive patients with poor oocytes yield, despite normal response to COH, due to low (<50%) number of oocytes retrieved per number of follicles > 14 mm in diameter on day of hCG administration, who were treated in our IVF unit during one year period were evaluated. Of whom, only those who received in the subsequent IVF cycle, a double trigger (GnRH-agonist and hCG) for final follicular maturation were included. The study was approved by the Institutional Research Ethics Board of our center.
All patients underwent the multi-dose GnRH-antagonist COH protocol during both IVF cycles. In both cycles, ovulation induction was performed by the administration of recombinant FSH, started at the 2nd or 3rd day of menses, using the same starting dose in each patient. Once the leading follicle had reached a size of 13 mm, or/and E2 levels exceeded 1200 pmol/L, co-treatment with the GnRH antagonist 0.25 mg/day, was initiated and the recombinant FSH was substituted by human menopausal gonadotropins. Gonadotropins doses were further adjusted according to serum estradiol levels and vaginal ultrasound measurements of follicular diameter, obtained every two or three days. Final follicular maturation was triggered by, either:
1. (1)
In the first IVF cycles: recombinant hCG (Choriogonadotropin alfa, ovitrelle 250 mcg, Serono), 36 hours prior to OPU, or; (2) In subsequent cycles: the co-administration of GnRH-agonist (Triptorelin acetate, decapeptyl 0.2 mg, Ferring Pharmaceuticals, Israel) and recombinant hCG (250 mcg), 40 and 34 hours prior to oocyte retrieval, respectively.
Routine IVF or intracytoplasmic sperm injection (ICSI) was then performed, as appropriate. Transvaginal ET was performed 48 to 72 hours after OPU in both cycles. All patients received luteal support with progesterone.
Data on patient age and infertility-treatment-related variables were collected from the files. Ovarian stimulation characteristics, number of follicles >10 mm and >14 mm in diameter on day of hCG administration, number of oocytes retrieved, embryo quality and number of embryos transferred were assessed and compared between the study (double trigger) cycle and the previous (hCG-only trigger) control cycle.
Embryos classification was based on the individual embryo scoring parameters according to pre-established definitions [8]. While a top quality embryo (TQE) was defined as seven or more blastomeres on day 3, equally-sized blastomeres and <20% fragmentation, poor quality embryos consist of all the rest. Clinical pregnancy was defined as visualization of a gestational sac and fetal cardiac activity on transvaginal ultrasound.
Statistical analysis was performed with Student’s paired t-test and chi square, as appropriate. Results are presented as means ± standard deviations; p value < 0.05 was considered significant.
Results
Eight consecutive patients were evaluated. Mean age and body mass index during the study cycle were 38.0 ± 4.8 years and 27.7 + 5.4 kg/m2, respectively. The clinical characteristics of the IVF cycles in the two study cycles are shown in Table 1.
Table 1 Comparison between IVF cycles with hCG versus double trigger (GnRH-ag + hCG)
In the present study, while using the same COH protocols which differ only in the methods of triggering final follicular maturation, as expected, no differences were observed between the groups in the length of stimulation, the number of gonadotropin ampoules administered, peak estradiol and progesterone levels and numbers of follicles >10 mm and >14 mm in diameter on day of hCG administration. However, patients who received the double trigger (study group) had a significantly higher number of oocytes retrieved (7.0 ± 4.6 vs. 2.3 ± 2.5, p < 0.02), number of 2PN (6.0 ± 4.6 vs. 1.7 ± 1.2, p < 0.002), number of embryos transferred (2.2 ± 0.7 vs. 0.85 ± 0.9, p < 0.002) and significantly higher proportions of the number of oocytes retrieved to the number of follicles >10 mm (80.3% ±31.1% vs. 18.5% ± 16.6%, p < 0.001) and >14 mm in diameter (118.0% ± 71.2% vs. 23.7% ± 21.5%, p < 0.01) on day of hCG administration, with a tendency toward a higher number of TQE (3.7 ± 0.8 vs. 0.4 ± 0.5, p = 0.06) respectively, as compared to the hCG-only trigger cycles.
Five pregnancies were recorded in the study group and none in the hCG-only trigger group (Table 1). Of which, 3 are ongoing, one resulted in a blighted ovum and one was biochemical pregnancy.
Discussion
In the present preliminary cohort historical study, the co-administration of GnRH agonist and hCG for final oocyte maturation- 40 and 34 hours prior to OPU, respectively, to patients with poor oocytes yield due to low (<50%) number of oocytes retrieved per number of follicles > 14 mm in diameter on day of hCG administration, resulted in significantly higher numbers of oocytes’ retrieved and embryos transferred and a significantly higher proportion of the number of oocytes’ retrieved to number of preovulatory follicles. Of notice, the observed improved in oocyte yield was despite a non-significant decrease in the number of follicles of >14 mm and >10 mm on day of hCG administration.
Five biochemical (positive hCG) pregnancies were recorded in the study group (double trigger) and none in the hCG-only trigger group. Of which, 3 (37.5%) are ongoing and one resulted in a blighted ovum. However, it should be emphasized that the increased pregnancy rate in the study group (double trigger) is biased due to the study design which offered this protocol to patients who had failed a previous IVF attempt.
As part of a standard/conventional COH regimen, final oocyte maturation and resumption of meiosis are usually triggered by one bolus of hCG (5000–10,000 units), that is administered as close as possible to the time of ovulation (i.e. 36 hours before oocyte recovery) [2]. In 1990, Gonen et al. [9] have demonstrated that ovulation may be also triggered by GnRH agonist, causing the release of both endogenous LH and FSH, while in 2008, Shapiro et al. [10] have established the concept of ‘Dual trigger’, combining both hCG and GnRH-agonists, aiming to trigger ovulation with the questionable ability to prevent severe ovarian hyperstimulation syndrome [11, 12].
Recently, Beck-Fruchter et al. [5] have described a case of recurrent empty follicle syndrome, successfully treated by ovulation trigger with GnRH agonist 40 hours and hCG added 34 hours prior to OPU. They assumed that by prolonging the time between ovulation triggering and OPU and the GnRH agonist trigger with the consequent simultaneous induction of an FSH surge, the “double trigger” could overcome any existing impairments in granulosa cell function, oocyte meiotic maturation or cumulus expansion, resulting in successful aspiration of mature oocytes, pregnancy and delivery.
In the present preliminary report, we further extended the aforementioned indications to the “double trigger” and offered it to patients with poor oocytes yield due to low (<50%) number of oocytes retrieved per number of follicles > 14 mm in diameter on day of hCG administration, despite an apparently normal follicular development and E2 levels during COH. While number of follicles of >14 mm and >10 mm on day of hCG administration wwere non-significantly decrease, we could demonstrate a significant increase in oocytes yield, a trend toward a higher number of TQE, with a reasonable clinical pregnancy rate. These observations are in agreement with Lin et al. [13], who compared the IVF outcome of normal responders, undergoing triggering of final oocyte maturation with either hCG and GnRH-agonist, both administered 35-36 hours prior to OPU, or hCG-only. The double trigger group demonstrated statistically significantly higher implantation, clinical pregnancy and live-birth rates as compared with the hCG trigger group.
Conclusions
“Double trigger” is suggested as a valuable new tool in the armamentarium for treating patients with low/poor oocytes yield, despite an apparently normal follicular development and E2 levels and in the presence of optimal hCG levels on the day of OPU. Further large prospective studies are needed to elucidate the aforementioned recommendation in this and other situations, such as patients with high proportion of immature oocytes or poor responder patients, prior to its routine implementation.
Authors’ information
Drs. Haas and Zilberberg should be considered “similar in author order.”
Abbreviations
COH:
Controlled ovarian hyperstimulation
EFS:
Empty follicle syndrome
hCG:
Human chorionic gonadotropin
IVF-ET:
In vitro fertilization-embryo transfer
OPU:
Ovum pick-up
TQE:
Top quality embryo.
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Correspondence to Raoul Orvieto.
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Competing interests
The authors declare that they have no competing interests.
Authors’ contributions
JH- Participated in the clinical management and collected the data, performed the statistical evaluations, assisted in writing the paper and edited it in all its revisions. EZ- Collected the data, performed the statistical evaluations, assisted in writing the paper and edited it in all its revisions. SD- Participated in the clinical management and edited the paper in all its revisions. AK- Participated in the clinical management and edited the paper in all its revisions. RM- Participated in the clinical management and edited the paper in all its revisions. RO- The principal investigator, designed the study, participated in the clinical management, performed the statistical evaluations, assisted in writing the paper and edited it in all its revisions. All authors read and approved the final manuscript
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Haas, J., Zilberberg, E., Dar, S. et al. Co-administration of GnRH-agonist and hCG for final oocyte maturation (double trigger) in patients with low number of oocytes retrieved per number of preovulatory follicles-a preliminary report. J Ovarian Res 7, 77 (2014). https://doi.org/10.1186/1757-2215-7-77
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Keywords
• Oocytes retrieval
• GnRH-antagonist
• hCG
• GnRH-agonist
• Final oocyte maturation
• IVF outcome
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How Much Water Should You Drink and Why? Optimal Hydration for Health & Performance
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When thinking about optimal hydration, how much water should you drink and why? As you’ve heard 100 times, water is the most critical nutrient for human existence, yet still so undervalued in our daily lives. This post will give you essential research-based facts about hydration and simple tips for optimizing it.
How Much Water Should You Drink and Why? #hydration for #health & #performance | Beyond Sapiens
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Why optimal hydration?
Your body is primarily made of water, from 60 to 80%. Based on these numbers, you would have to agree that water consumption should be one of your very top priorities. But is it? Several studies highlighted that 80% of adults don’t drink enough water, so chances are, you might be one of them.
Hydration is key to maximizing your well-being and performance, as it plays a huge role in body temperature regulation, metabolism, and functioning of the cardiovascular and nervous systems. Even a mild state of dehydration can have significant implications on your welfare, from headaches and tiredness to decreased muscle strength and endurance, just to mention a few.
To sum it up, staying constantly hydrated is a must. A simple way for you to understand how well – or poorly – hydrated you are, is to check how many trips you take to the ladies or gentlemen’s room in a day. If you take that trip rarely, you might not be well hydrated. Not drinking enough, in fact, makes your body preserve water, and it’s linked to several health risk factors.
A good rule of thumb is to drink before you are thirsty, as that’s already a sign of dehydration. So how can you make sure you are well hydrated?
Water quality plays a significant role for optimal hydration
The overall hydration process of what goes in and what comes out is important, but what happens inside on a metabolic level is also vital. So, even though you drink enough, drinking too much can become an issue. Drinking too much plain water will enhance your metabolism, and clean your internal liquid balance, meaning that you may “overclean” your balance of essential electrolytes, a set of minerals.
Sodium, potassium, magnesium, and calcium, among others, are all electrolytes that we get from food and supplements. But why are they important? Electrolytes are essential for many life functions, including cells, our nervous system, and our muscles, so you should strive to get an optimal amount of them.
If you are dehydrated, your electrolyte levels will go above the right amount, while overhydration will lower them under the optimal level. This is where it gets tricky, as most of us can’t directly measure this in our daily lives, but there are some signs you can identify.
As electrolytes have a vital role for your nerves and muscles, the most common way to identify a lack of them is if you feel thirsty even if you drink a lot, have muscle cramps, or feel dizzy after not having drunk in a while or after an exercise.
Physical aspects for optimal hydration
Talking about exercise, hydration plays a key role in performance, injury prevention, and recovery. It’s pretty self-evident given that 80% of our muscles are made out of water, and when you sweat a lot, that number goes down.
There are many variables to consider, such as body size, exercise intensity, duration, environment, and clothing, but just to give you some numbers, track and field athletes lose from half to 3 liters of water per hour. So hydrating yourself is crucial when you do endurance exercise. T
hat you probably knew already, but how about anaerobic efforts such as strength training at the gym? According to Judelson et al., dehydration reduces strength by 2%, power by 3%, and high-intensity endurance by 10%.
How can you avoid all this? The NATA recommends the following: drink about half a liter of water 2 hours prior to exercise, a cup 15 minutes before exercise, and a cup every 15 minutes during exercise. Once you’re finished, you should rehydrate and refuel with drinks that contain sodium to help with water retention, and of course, the usual carbohydrates + proteins to maximize recovery.
Remember, these are just guidelines and are highly dependent on many factors, so you should use them as a starting point to find what works best for you.
Mental and cognitive implications of staying hydrated
Hydration affects you not only physically but also mentally. So let’s talk about its impact on your brain functions, cognition, and mood. Yes, you read right; a simple act like drinking water will affect your mental performance. A
s you have learned, the balance of electrolytes is essential for your cells, muscles, and overall nervous system, which all take part in transporting information from your senses to your brain and back. The speed and flow with which this information flows and moves highly depend on how well-hydrated you are.
So, due to this correlation, dehydration also highly influences your short-term memory, which plays a massive role in the working memory that you use daily to connect simple thoughts while performing several cognitive tasks such as writing, talking, and brainstorming.
But this is not all. Also, your mood and visual perception are negatively affected. On the positive side, drinking water can almost immediately improve your visual perception, short-term memory, and overall mood.
Optimal water intake on a daily basis
It’s time for the million-dollar question: how much water should you drink? 2 to 3 liters depending on your body composition. Use these numbers as a starting point, and remember there’s no one-size-fits-all approach. These are general guidelines, so the amount should vary depending on several factors, including size, activity level, and nutrition.
That’s not all, as there is another important question to answer to: how often should you drink? Chunking down 2 liters in a short window will not keep you well-hydrated. The key is drinking consistently. Start the day with a big glass of water to rehydrate after the night, to which you can add some lemon juice to help detox the body, and some electrolytes or Himalayan salt.
Then, the best thing you can do to ensure you drink enough is to have a big bottle always next to you. It’s that simple. I recommend you choose a bottle with a big opening, as that will help you drink more per sip, and opt for a glass or metal bottle to avoid plastic.
We hope this post gave you everything you need to ensure you stay well hydrated in your journey towards ultimate peak performance.
If you need help with optimizing your hydration, and you’re ready to go Beyond Sapiens, we recommend you read more about our Business & Individual Maximization Coaching programs!
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Gene Set: JINESH_BLEBBISHIELD_TRANSFORMED_STEM_CELL_SPHERES_UP
Standard name JINESH_BLEBBISHIELD_TRANSFORMED_STEM_CELL_SPHERES_UP
Systematic name M38971
Brief description Genes up-regulated in transformed spheres compared to blebbishields from RT4 cells
Full description or abstract Apoptosis is a process that kills cells. However, cancer stem cells find ways to escape death after commencement of apoptosis. One such mechanism is blebbishield emergency program, in which the apoptotic cancer stem cells first undergo apoptotic body formation but then reassemble apoptotic bodies with main body (nuclei containing) of the apoptotic cells to form spherical to elongated structures called blebbishields. Blebbishields in turn are capable of blebbishield-blebbishield fusion to form transformed stem cell spheres (transformation phase) and then give rise to individual cancer cells from spheres (exit phase). We identified blebbishield emergency program in RT4 bladder cancer cells (RT4P=P stands for parental) and did microarray analysis of live RT4P cells, blebbishields and transformed spheres. This data set is a comparison of blebbishields with transformed spheres and the gene list includes the genes that are upregulated in transformed spheres. A separate set is provided for downregulated gene list too. In addition we provide separate gene lists for upregulated and downregulated gene lists for blebbishields compared to RT4 live cells.
Collection C2: curated gene sets
CGP: chemical and genetic perturbations
Source publication Pubmed 28855211
Exact source Supplementary table-1 & Figure-2B Genes Upregulated in transformed stem cell spheres Log2Fold change >1.0
Related gene sets (show 5 additional gene sets from the source publication)
External links
Filtered by similarity
Organism Homo sapiens
Contributed by Goodwin G. Jinesh and Ashish M. Kamat (UT MD Anderson Cancer Center)
Source platform Human_ILLUMINA_Array
Dataset references (show 1 datasets)
Download gene set format: grp | text | gmt | gmx | xml
Compute overlaps (show collections to investigate for overlap with this gene set)
Compendia expression profiles GTEx compendium
Human tissue compendium (Novartis)
Global Cancer Map (Broad Institute)
NCI-60 cell lines (National Cancer Institute)
Advanced query Further investigate these 176 genes
Gene families Categorize these 176 genes by gene family
Show members (show 213 members mapped to 176 genes)
Version history
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Radiation Poisoning History
Radiation was discovered in the late 19th century. However, people were not initially aware of the damage radiation exposure and radioactive rays could cause.
The acute effects of radiation exposure were first seen in 1896 when Nikola Tesla purposefully subjected his fingers to X-rays and reported that this caused burns to develop, although at the time he attributed the burns to ozone.
The mutagenic effects of radiation were not realized until decades later. The genetic effects and increased cancer risk associated with radiation exposure were first recognized by Hermann Joseph Meller in 1927. Muller went on to receive the Nobel prize in 1946 for his research.
However, before these effects were understood, many radioactive substances had already been marketed by corporations and various physicians. Examples included radium enema treatments and radium-containing water tonics. It was Marie Curie who protested against these therapies and pointed out that the effects of radiation exposure were poorly understood. Radiation poisoning was the cause of the aplastic anemia that eventually killed Curie.
In 1932, a famous American socialite called Eben Byers died after ingesting large amounts of radiation over the course of several years. This death and many others among radiation enthusiasts sparked intrigue over the effects of consuming radiation-containing products and they were eventually removed from the market.
The gravity of the effects caused by radiation were not fully understood until the 1940s. Two scientists from the USA died in 1946 after working with fissile materials without using protective clothing or shielding. The Hiroshima bombing also caused wide-scale radiation poisoning and the actress Midori Naka, present during the bombing, was studied extensively for radiation poisoning. Her death in 1945 was the first to be officially documented as having been caused by radiation poisoning. At the time, this radiation poisoning was referred to as Atomic bomb disease.
Further Reading
Last Updated: Feb 27, 2019
Dr. Ananya Mandal
Written by
Dr. Ananya Mandal
Dr. Ananya Mandal is a doctor by profession, lecturer by vocation and a medical writer by passion. She specialized in Clinical Pharmacology after her bachelor's (MBBS). For her, health communication is not just writing complicated reviews for professionals but making medical knowledge understandable and available to the general public as well.
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The palatine tonsils | Anatomy of the palatine tonsils - Anatomy-Medicine.COM
» » The palatine tonsils
The palatine tonsils
The palatine tonsils are located at the back of the throat. One tonsil is located on the left side of the throat and the other is located on the right side. The tonsils play a role in protecting the body against respiratory and gastrointestinal infections.
Each tonsil consists of a network of crypts (pits) that store cells used to fight infection. The tonsils contain B cells, a type of white blood cell that fights infections. They also produce antibodies against polio, streptococcal pneumonia, influenza, and numerous other infections. Antibodies are proteins that help the body identify and attack harmful invaders.
The tonsils also contain several types of T cells, which are white blood cells that destroy cells infected with viruses and help the body build immunity to infectious organisms.
Tonsillitis occurs when bacterial or viral organisms cause inflammation of the tonsillar tissue. This results in fever, difficulty swallowing, sore throat, ear pain, loss of voice, and throat tenderness. Recurrent tonsillitis sometimes results in the need for a tonsillectomy. During this procedure, a surgeon removes the palatine tonsil tissue. This may lessen the frequency of new infections.
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Common Dental Problems and Toronto Dentist
Details
Date & time Mar 3
Event ends Mar 4 '22
Location
dentistry
Creator Behroz Hassan
Who's attending
Behroz Hassan
Description
There are so many health problems of That the teeth associated are really bothersome. Some common dental problems include the gum disorders, tooth infection, root canal, broken tooth, and plaque. You will observe that the dentists Davisville always occupied with their patients from creating them free from common difficulties. The teeth often start bleeding and individuals don't take them seriously, but bleeding can cause clots leading to a heart disease. You need to make an effort and care for your gums and if bleeding does not stop after a couple of days, better visit a dentist. Poor eating habits frequently result in bleeding in gums, and at times the pockets develop. Plaque is also quite common that occurs because of the poor eating habits, like taking a lot of caffeine or having tobacco. The Davisville dentist includes resources to remove plaque, making your teeth fresh new. There is also an option of scaling, bonding, and whitening to deal with the plaque.
Dental infection is so severe that It can lead to death. Often time, people have to handle the wisdom tooth that triggers a lot and get an illness. Occasionally a poor dentist removes the knowledge without treating illness and it becomes worse. You have to see the Davisville dentist to get a wisdom tooth since he or she will first deal with the infection, and then will remove the teeth. Some great antibiotics are essential to care for the tooth infection. Occasionally fever also happens because of disease and you will need a mix of drugs to cure both. Your dental structure may damage by not fixing the infection at the right time. Always work to reach some best Toronto dentistso called, which means you get an accurate and quick therapy. Wisdom is common just in young age, however, at times it can reappear in the old era.
Top Dentists in Toronto
Sometimes cracks also happen and you Have to fix the tooth. Cracks often happen Because of an injury or due to the incorrect Use of teeth, such as opening the jar lids or attempt to break something with your teeth. The sooner you approach the Toronto dentist, like Dr. Adibfar The fastest you will have a remedy at the ideal time. Get online to look for a Couple dentists also see the background of their patients. Attempt to understand the bad dentists And just employ the top dentists at Toronto because they can shield Your teeth out of acute diseases, keeping you healthy forever.
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Balance Body Chemistry with Nutrition - Paula Owens, MS
Educating and Empowering You to Heal, Thrive, and Live a Happy, Healthy Lifestyle
Paul Owens - Functional Health Expert
Sign Up for Free Health News & Wellness Videos
Balance Your Body Chemistry with Nutrition
Balance Body Chemistry with Nutrition and a Functional Blood Chemistry AnalysisWhen was the last time you had a thorough and functional analysis of your blood work? Reference ranges on your blood tests are so broad that they cannot be used to spot sub-clinical conditions. Did you know that lab normals are not necessarily healthy or optimal? I cannot tell you how often my clients have been told, “your blood work looks perfectly normal or your thyroid is fine.” How would you know?
When most physicians review a patient’s blood test results, their primary concern is any result that falls outside the laboratory reference range. The problem is that standard laboratory reference ranges are too broad and usually represent “average” populations rather than the optimal, ideal or healthy levels required to maintain good health. Most standard reference ranges are too broad to adequately detect health problems or prescribe appropriate therapy on an individual basis. This is especially true when these reference ranges are relied on to treat a patient with a serious medical disorder.
“A blood test is essentially a blueprint of your health and a glimpse of its future — and it never lies.” — Dr. James LaValle
One of my clients, a woman in her 40’s was deeply concerned about her hair loss and low energy. She had been to a number of doctors who claimed everything was perfectly normal. Needless to say she felt hopeless and frustrated. Upon her blood chemistry analysis, several nutrient deficiencies were detected including zinc, essential fatty acids, folate, vitamin B12, hydrochloric acid, vitamin D, protein and water! She was eating low fat diet and very little protein. In addition, she had an overgrowth of Candida and low thyroid function. In just 4-1/2 months of implementing dietary changes, removing inflammatory food, eradicating the infections, making changes in her environment, and nourishing her body with nutrients to support her biochemistry she is no longer experiencing hair loss, it’s growing back and it’s thicker! She’s sleeping more soundly throughout the night, has an abundance of energy throughout the day, is no longer experiencing bloating or cravings, and what she loves the most is the 18 pound weight loss!
Many universities and doctors have developed “optimal” ranges for lab values. The lifelong work of one of my mentors, Dr. Harry Eidenier, Jr., Ph.D., and others including Dr. Jonathan Wright, M.D., Dr. James LaValle and Abrishamian, Tipps, Cessna all support the fact that optimal lab ranges can be used to recognize conditions that puzzle the doctors.
Balance Your Body Chemistry with Nutrition
A functional blood chemistry analysis will . . .
• prevent and rule out future risk of disease
• identify any possible underlying health issues
• address sub-clinical issues years in advance
• bio-individualized identification of your personal nutrient deficiencies or excesses
• learn which supplements are ideal for you biochemistry
• create optimal health and homeostasis
Be smart. Take control and responsibility for your health and balance your body chemistry with nutrition via a functional blood chemistry analysis. Test to assess, don’t guess!
Nutrition is a science, but it is also an art. Using it to balance body chemistry in a human and the difference it can make in the performance of that person is like a master piano tuner and the difference it can make in the sound of his instrument once tuned. —Dr. Harry Eidenier, Jr., Ph.D., author and grandfather of Functional Blood Chemistry Analysis, Scientist, Researcher and Biochemist
Blood Test Results: Clinical Pearls to Balance Body Chemistry
* Fasting glucose is a simple test that reveals a great deal about your health. Glucose is the main sugar found in your blood. It’s formed by the digestion of carbohydrates and the conversion of glycogen in the liver.
Every glucose rise of 1 point above 84, increases the risk of developing type 2 diabetes by 6%. For example, a glucose level of 85, the risk percentage is 6%; at 86, 12%; 87, 18% and so on. Decreased glucose can be an indication to rule out hypoglycemia and adrenal dysfunction.
High blood sugar (95 and higher) can indicate that you are:
• consuming too many carbohydrates, and not metabolizing carbohydrates, grains and sugars well
• having trouble absorbing glucose into the cells
• thiamine deficiency and other B vitamin deficiencies, zinc deficiency, magnesium deficiency
• low thyroid function (hypothyroid)
• environmental toxins and chemicals including pesticides, plastics, glyphosate, phthalates and more,
• WiFi sensitivity, EMF exposure, blue light at night, disrupted circadian rhythm
• chronic stress
• any combination of the above factors
High blood sugar is inflammatory, which influences the immune system. High blood sugar affects kidney function, brain function, memory, hormonal health, mood, levels of anxiety, depression, aches and pains, and overall health.
* Higher levels of hemoglobin A1C (a measure of a person’s average blood glucose or sugar in the blood over a 2-3 month period) are linked to lower cognitive function, dementia, and a risk factor for diabetes. HbA1C is a primary biomarker for pre-diabetes and diabetes. An elevated HbA1C indicates overall diet and reveals that the individual is eating an excessive amount of processed carbohydrates, grains, fructose, sugars and alcohol.
* Increased uric acid has to do with systemic inflammation. Uric acid is the most abundant antioxidant in the blood. Its values increase as a result of inflammation, methylation dysfunction, gout, alcoholism, GI inflammation, non-alcoholic fatty liver disease, and lead toxicity. Sugar, fructose and beer will spike uric acid.
* A high HDL (>80) is not necessarily an indication that the person is super healthy. Those with an HDL (>80) are either inflamed, infected, or eat a bad diet. Inflammation causes your HDL to become dysfunctional, therefore a need to rule out mycotoxins, inflammation, infection, bad diet, nutritional deficiencies, etc. Identify the root cause!
* Fasting glucose >100, HbA1C >5.7 and elevated your triglycerides equate to an early warning sign that you’re not metabolizing sugars adequately, insulin resistance and pre-diabetes.
* The most common reason for a low alkaline phosphatase is a zinc deficiency.
* Androgen use (testosterone) can cause a decrease in T4 and an increase in T3 (opposite pattern seen with estrogen use).
* C-reactive protein (CRP) is the best vascular inflammation marker. An elevated CRP is the body’s cry for repair.
* Intestinal parasites and hypochlorhydria are major contributing factors to rule out when there is low hemoglobin, hematocrit and red blood count, collectively.
* Aside from sugar, dairy and processed carbs, parasites feed off heavy metals. Always rule out parasites when there are autoimmune disorders, asthma and cancer. Parasites almost always have a role in autoimmune disorders.
* When total cholesterol is normal with decreased triglycerides and increased HDL, the probability of an autoimmune phenomenon is increased and should be ruled out.
* There is a relative increased risk of dementia, heart disease and cognitive disorders in relation to homocysteine levels. Increased homocysteine (>8) is linked with 2x the risk of developing Alzheimer’s disease compared to those with lower levels. Elevated homocysteine can be the result of vitamin D, B12 and folate deficiencies, dairy intolerance, dysbiosis or increased bone loss. Low folate and elevated homocysteine levels are associated with an increased risk of dementia and Alzheimer’s disease.
* Those with non-alcoholic fatty liver disease often present with elevated AST, ALT, and GGT levels on their blood labs. This is not a liver problem; it’s a metabolic imbalance and an insulin-handling problem.
* When monocytes, eosinophils and basophils are elevated collectively this is an indication to rule out the possibility of parasites.
* If neutrophils are increased (>60) in conjunction with decreased lymphocytes (<24) and either a low (<5) or high (>8) WBC, the possibility of an underlying bacterial infection must be factored in and ruled out.
* Elevated creatinine levels often reveal prostate problems before an elevated PSA. Those with increased muscle mass can also have slightly higher creatinine levels.
* An increased BUN often points to hypochlorhydria or dehydration. A low BUN value is found with protein malnutrition and sometimes adrenal hypofunction.
Invest in YOU • Invest in your Health • Balance Your Body Chemistry!
For a deeper understanding of how to balance your body chemistry with nutrition, contact my office for your Blood Chemistry Analysis, a functional analysis designed to evaluate your metabolic status and indicate those food and supplemental food factors that are either excessive or insufficient in your diet. Annual blood work is one of the smartest things you can do for your health. Remember, just because lab values fall within so-called normal ranges, does not mean healthy or optimal.
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Op.Dr. Nurettin Türktekin
Age Factor in Infertility
Age Factor in Infertility
One of the most prominent factors causing infertility is age. Particularly with increasing age, the dynamics of how couples conceive and have children can change.
Some genetic syndromes, such as achondroplasia, neurofibromatosis, Marfan syndrome, and osteogenesis imperfecta, can increase the impact on infertility history. In addition, age is a factor that should not be overlooked in men. Especially after the age of 40, the quality and quantity of sperm in men can decrease, which can have a negative impact on a couple's chances of pregnancy.
The age of the woman is another important determinant of infertility. Especially older women can face certain difficulties if they are among the couples who want to have a baby. With today's medical advances, it is possible to conceive at the age of 40 and beyond. However, in the past, it was known to be a difficult situation, especially after the age of 35.
In vitro fertilization (IVF) treatments can be used by all couples who want to have a child but are unable to do so and who meet certain conditions. However, the age factor is a parameter that affects the success rate of these treatments. After 35 years of age, the number of eggs and ovarian reserve of women may decrease, which has an effect on the chance of pregnancy.
Factors Causing Infertility in Humans
Reproductive health is the cornerstone of a happy and healthy family. However, certain conditions and factors can prevent people from having the children they want. The items listed below are the most common of these:
• Age
• Genetic factors
• Hormonal problems
• Uterine and ovarian problems
• Infections
• Endometriosis
• Obesity
Advanced age has a significant impact on infertility. Especially in women, advancing age can negatively affect the quality and number of eggs. In men, sperm quality may also decrease with age. Today, approximately 20 out of every 100 couples have this problem.
Age and Pregnancy in Women
Among women, the age factor has a decisive influence on the pregnancy process. As people age, their reproductive capacity and chances of conception may naturally decrease. For this reason, it is very important for couples who want to have children to evaluate all factors, act at the right time and, if necessary, turn to alternative solutions.
A woman's ovarian reserve tends to decrease over time. The number of innate eggs decreases over time, which naturally affects the chances of conception. Especially after the age of 35, a more pronounced decline in ovarian reserve can be seen. Aging affects not only the number of eggs but also their quality. Older eggs may have an increased risk of genetic abnormalities, which can lead to miscarriage and hereditary problems.
On the other hand, advanced age can lead to irregular ovulation. Irregular ovulation can reduce the chances of conception or make pregnancy more difficult. The risk of complications in pregnancy also increases during this period. Especially after the age of 40, this possibility increases even more.
The Relationship Between Age and Infertility in Men
Although infertility is often associated with women as a reproductive health issue, this is a common misconception. Recent studies have shown that the age of the father-to-be also has a significant impact on reproductive ability. In men, age is an issue that needs to be taken into account in terms of the fertility capacity and health of couples.
A man's advancing age can negatively affect the quality and quantity of sperm. In older men, sperm count naturally decreases and morphological problems may occur. This can reduce fertilization capacity and the likelihood of conceiving a partner. On the other hand, old age in men can also increase the risk of genetic anomalies in the child. Older fathers-to-be are considered more at risk of passing these problems on to the next generation.
Age in men is also an important determinant for alternative fertility treatments. Especially in assisted reproductive techniques such as in vitro fertilization (IVF), the sperm quality and fertilization ability of older men are generally lower compared to younger couples. Today, many people prefer to become fathers at a more mature age. However, it is important to consider reproductive health when making this choice. Men who are considering becoming fathers at an older age should be more aware of this and take the necessary steps in consultation with health professionals.
Success in IVF Treatment in Advanced Age
IVF treatment is a promising option for couples with sexual health problems. It can be considered as a great chance, especially for people who want to have children at an advanced age. However, the probability of success varies depending on some factors. Women who plan IVF treatment at a late age may have the opportunity to freeze their eggs for future use. This method allows the eggs obtained at a younger age to be used during the treatment, thus increasing the chances of success.
When planning IVF treatment in a certain age group, it is very important that both women and men pay attention to their health status. A healthy body will increase the likelihood of success in treatment. Factors such as regular exercise, a healthy diet, and avoiding stress play a role in the preparation process. In addition, it is often recommended by experts to quit smoking and alcohol consumption.
IVF treatment can be an emotionally challenging process. Couples who plan this at an advanced age can manage this process in a healthier way by receiving psychological support. It is essential for partners who have this idea to consult a reproductive health specialist first. Doctors will comprehensively evaluate their health conditions and recommend the most appropriate treatment plan. Op. Dr. Nurettin Türktekin, who performs the best infertility treatment in Turkey, welcomes people who want to have children but face problems to his clinic. Please contact us for detailed information about the procedures.
WHAT IS OVARIAN CYST?
Ovarian cysts are fluid-filled sacs or vesicles seen inside the ovary. Normally, during each menstrual period, a cyst called a follicle, which carries the egg cell and can reach 3 cm in size, forms in the ovaries. Then this cyst cracks and the egg is released. In young girls with ovulation problems, normal or physiological follicle cysts that cannot rupture can grow every month and reach 5-10 cm, while small numbers of 0.5-1 cm in size, which we call polycystic ovaries, can be seen in series. Apart from these functional cysts, benign or malignant ovarian cysts can also be seen in all age groups.
Except for the most common functional ovarian cysts, cysts can be benign or malignant tumoral cysts. In addition, as a result of infection, abscess-shaped cysts may occur, which is usually accompanied by pain and high fever.
FAQ
Pregnancy at an older age can be challenging, so seeking psychological support can provide emotional support.
Because after the age of 35, the chances of pregnancy decrease due to a decline in egg reserve and quality.
The use of frozen eggs in IVF treatment at older ages and determining the most appropriate treatment approach for couples can increase success.
Copyright © 2024 Dr. Nurettin TÜRKTEKİN. All right reserved.
Design By
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TY - JOUR AU - Pejman Pourfakhr AU - Khaton Nouri AU - Hamid Reza Shariefnia AU - Reza Shariat Moharari AU - Mohammad Reza Khajavi PY - 2019/11/17 Y2 - 2021/10/21 TI - Dexmedetomidine Versus Ketamine Combined With Fentanyl for Sedation-Analgesia in Colonoscopy Procedures: A Randomized Prospective Study JF - Acta Medica Iranica JA - Acta Med Iran VL - 57 IS - 6 SE - Articles DO - 10.18502/acta.v57i6.1878 UR - https://acta.tums.ac.ir/index.php/acta/article/view/8054 AB - Colonoscopy is a painful, embarrassing and short-term procedure that needs temporary sedation and rapid recovery. The aim of this study was to compare the sedation and analgesia effect and hemodynamic changes due to bolus intravenous injection of dexmedetomidine and ketamine during elective colonoscopy. This clinical trial was conducted on 70 patients aged 20-70 years, candidates for elective colonoscopy, who randomly divided into two equal groups. For all patients 0.03 mg/kg midazolam 10 min before procedure was injected. Fentanyl 1 µ/kg was administrated in both groups 5 min before procedure, and one min before colonoscopy. K group received 0.5 mg/kg ketamine and D group received 1 µ/kg dexmedetomidine. Then, the normal saline infusion was used as maintenance. Fentanyl 25-50 µg was prescribed as the rescue dose if needed during the procedure. Hemodynamic changes, sedation level during procedure, patients and colonoscopists satisfaction were recorded in recovery. The mean heart rate and mean blood pressure was significantly less in the dexmedetomidine group than in the ketamine group. All of the patients in the ketamine group were deep to moderately sedated during colonoscopy, and the amount of fentanyl required in this group is much less than dexmedetomidine group (68.02±25.63 vs 91.45±38.62 µg P-0.003). In terms of satisfaction, only 42% of patients in the dexmedetomidine group were completely satisfied with colonoscopy, while 65% of Ketamine group had complete satisfaction with colonoscopy (P=0.001). The level of colonoscopist satisfaction during colonoscopy was similar in both group, and complete satisfaction was 43%. In patients undergoing colonoscopy, IV bolus injection of dexmedetomidine in comparison with ketamine provides less patients satisfactory and low level of sedation with supplemental multiple doses of fentanyl during the procedure. ER -
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1. Neuroscience
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Epigenetic regulation of lateralized fetal spinal gene expression underlies hemispheric asymmetries
1. Sebastian Ocklenburg Is a corresponding author
2. Judith Schmitz
3. Zahra Moinfar
4. Dirk Moser
5. Rena Klose
6. Stephanie Lor
7. Georg Kunz
8. Martin Tegenthoff
9. Pedro Faustmann
10. Clyde Francks
11. Jörg T Epplen
12. Robert Kumsta
13. Onur Güntürkün
1. Ruhr University Bochum, Germany
2. St. Johannes Hospital, Germany
3. University Hospital Bergmannsheil, Germany
4. Max Planck Institute for Psycholinguistics, Netherlands
5. Radboud University, Netherlands
6. Wallenberg Research Centre at Stellenbosch University, South Africa
Research Article
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Cite this article as: eLife 2017;6:e22784 doi: 10.7554/eLife.22784
Abstract
Lateralization is a fundamental principle of nervous system organization but its molecular determinants are mostly unknown. In humans, asymmetric gene expression in the fetal cortex has been suggested as the molecular basis of handedness. However, human fetuses already show considerable asymmetries in arm movements before the motor cortex is functionally linked to the spinal cord, making it more likely that spinal gene expression asymmetries form the molecular basis of handedness. We analyzed genome-wide mRNA expression and DNA methylation in cervical and anterior thoracal spinal cord segments of five human fetuses and show development-dependent gene expression asymmetries. These gene expression asymmetries were epigenetically regulated by miRNA expression asymmetries in the TGF-β signaling pathway and lateralized methylation of CpG islands. Our findings suggest that molecular mechanisms for epigenetic regulation within the spinal cord constitute the starting point for handedness, implying a fundamental shift in our understanding of the ontogenesis of hemispheric asymmetries in humans.
https://doi.org/10.7554/eLife.22784.001
Introduction
Compared to the almost infinite complexity of vertebrate cognition and behavior, the number of genes influencing central nervous system development is staggeringly small (Kadakkuzha and Puthanveettil, 2013). Thus, understanding the molecular mechanism underlying the epigenetics of vertebrate central nervous system architecture has become an issue central to neuroscience (Kundakovic and Champagne, 2015).
One fundamental principle of brain organization is lateralization, i.e. structural or functional difference between the left and the right hemisphere of the brain (Corballis, 2014). Lateralization is a conserved feature across the vertebrate lineage (Ströckens et al., 2013; Ocklenburg et al., 2013a; Bisazza et al., 1998; Rogers et al., 2012; Versace and Vallortigara, 2015) and recent studies strongly suggest it is also present in invertebrates (Frasnelli et al., 2012). This ubiquity of behavioral and brain lateralization strongly supports the idea that lateralized central nervous system organization provides an evolutionary advantage (Vallortigara and Rogers, 2005). Suggestions about why a lateralized brain would increase an organism’s fitness include avoidance of unnecessary duplication of neuronal activity in both hemispheres, faster neuronal processing due to not being constrained by slow callosal transfer of information between the hemispheres and better coordination of unilateral behaviors in swarms or other social groups of animals (Vallortigara and Rogers, 2005; Corballis, 2009). In humans, hemispheric asymmetries have been shown in almost all major cognitive systems (Ocklenburg et al., 2014a) including language (Friederici, 2011; Sepeta et al., 2016), memory (Giammattei and Arndt, 2012; Tat and Azuma, 2016; Habib et al., 2003), attention (Falasca et al., 2015; Duecker et al., 2013), emotional processing (Demaree et al., 2005), face perception (De Winter et al., 2015), working memory (Langel et al., 2014; Nagel et al., 2013) and executive functions (Ocklenburg et al., 2011a, 2012; Stock and Beste, 2014).
By far the most widely investigated manifestation of lateralization in humans is handedness (Corballis, 2014). Importantly, handedness is related to the lateralized organization of cognitive systems in the human brain (Ocklenburg et al., 2014b; Frässle et al., 2016). For example, left-hemispheric language dominance is found in 96% of right-handed subjects, but only in 73% of left-handed subjects (Knecht et al., 2000). The relevance of handedness has recently been highlighted by Willems et al. (Willems et al., 2014), who state that it is one of the most important factors influencing the individual brain organization and that explicit inclusion of left-handers in experimental studies has strongly improved our understanding of language, motor behavior and visual processing. Handedness might not only be a behavioral proxy for individual brain organization, but is also interesting from a clinical perspective: A variety of neuropsychiatric and developmental disorders like autism spectrum disorders (Colby and Parkison, 1977; Forrester et al., 2014; Preslar et al., 2014; Rysstad and Pedersen, 2016), depression (Denny, 2009; Elias et al., 2001; Logue et al., 2015), bipolar disorder (van Dyck et al., 2012; Nowakowska et al., 2008), anxiety disorders (Logue et al., 2015; Hicks and Pellegrini, 1978; Orme, 1970; Wright and Hardie, 2012; Hardie et al., 2016; Lyle et al., 2013), schizophrenia (Hirnstein and Hugdahl, 2014; Dragovic and Hammond, 2005; Sommer et al., 2001) or alcoholism (Denny, 2011; Mandal et al., 2000; Sperling et al., 2000) has been associated with left- and mixed-handedness. Thus, understanding the ontogenesis of handedness and hemispheric asymmetries in general could potentially yield important insights into pathogenesis of these disorders.
However, despite their importance for many aspects of brain organization, the ontogenetic background of brain asymmetries is still far from being understood. Initially, single gene theories have been suggested to explain the emergence of handedness as a function of one gene with two alleles (Annett, 1998; McManus, 1985). However, recent genome wide association studies failed to detect any genome-wide significant single nucleotide polymorphisms, refuting single gene theories (Armour et al., 2014; Eriksson et al., 2010). Candidate gene studies revealed a number of genes that display an association with handedness, among them leucine rich repeat transmembrane neuronal 1 (LRRTM1) (Francks et al., 2007), proprotein convertase subtilisin/kexin type 6 (PCSK6) (Scerri et al., 2011; Arning et al., 2013; Brandler et al., 2013) and the androgen receptor gene (AR) (Arning et al., 2015; Hampson and Sankar, 2012; Medland et al., 2005). However, these genes explain only a fraction of the variance in handedness data. Moreover, a number of studies has suggested that only about one quarter of the variance in handedness is attributed to genetic variation, whereas the remaining 75% of variance are explained by non-shared environmental factors (Medland et al., 2006, 2009; Vuoksimaa et al., 2009). These findings highlight the importance of integrating both genetic variation and epigenetic processes modulating gene expression when investigating the ontogenesis of hemispheric asymmetries (Geschwind and Miller, 2001).
Asymmetric gene expression in the fetal cortex has been suggested as the molecular basis of left-right differences in hand-use: Sun et al. (Sun et al., 2005) compared gene expression levels in the right and left perisylvian cortex of the human fetus. At 12 gestational weeks, the authors identified 27 consistently asymmetrically expressed genes, which are mostly responsible for gene expression regulation, signal transduction, and cortical development. One of the consistently asymmetrically expressed genes was LIM Domain Only 4 (LMO4). Further investigation revealed that unilateral variation of Lmo4 expression in embryonic mice suppresses neurogenesis in one hemisphere, leading to the asymmetric functional area formation, neuronal production and axonal projection as well as altered paw preference (Li et al., 2013). Analysis of gene expression in the adult human brain yielded less clear results, since two independent studies found no differences in gene expression between analogous regions across the cerebral hemispheres (Hawrylycz et al., 2012; Pletikos et al., 2014). In a recent study, Karlebach and Francks reanalyzed both datasets and showed that subtle lateralization at single gene level translates to stronger asymmetries at the level of functional gene ontology (GO) groups. The authors found lateralized gene sets to be associated with neuronal electrophysiology, synaptic transmission, nervous system development, and glutamate receptor activity (Karlebach and Francks, 2015).
However, recent research indicates that cortical tissue might not be the optimal choice to investigate the relation of gene expression asymmetries and behavioral asymmetries. Ontogenetically, handedness starts early in development since coordinated hand movements begin 8 weeks post conception (PC), i.e. 10 weeks gestational age, when 85% of fetuses exhibit more right arm than left arm movements (Hepper et al., 1998; de Vries et al., 1985). Investigation of thumb sucking in 274 fetuses revealed that at 13 weeks PC 90% prefer to suck their right thumb whereas only 10% suck their left thumb more often (Hepper et al., 1990, 1991). Interestingly, a follow up study of 75 infants revealed that thumb sucking preference is significantly positively correlated with subsequent handedness: The 60 children showing a right thumb preference were right-handed whereas out of the 15 children displaying a left thumb preference, five were right-handed and 10 were left-handed (Hepper et al., 2005). Importantly, the motor cortex is not yet functionally linked to the spinal cord at that stage of development as the outgrowth of corticospinal projections does not enter the anterior spinal cord before 15 weeks PC (ten Donkelaar et al., 2004). This implies that handedness is unlikely to be under brain control (Hepper et al., 1991) and asymmetrical hand movements have to arise from spinal activity patterns. Thus, it is likely that spinal rather than cortical gene expression asymmetries represent the molecular basis of handedness.
Asymmetrical gene expression patterns are likely to be influenced by epigenetic variation. The most important epigenetic mechanism is DNA methylation. Binding of methyl (-CH3) groups to CpG sites or islands causes a reduction or prevention of transcription and thus gene expression. DNA methylation is confirmed to be involved in the development of basic central nervous system functions like synaptic function, neuronal plasticity, learning and memory (Nikolova and Hariri, 2015; Day et al., 2015; Roth, 2012). Especially intrauterine stressors have been shown to influence DNA methylation (Turecki and Meaney, 2016; Vaiserman, 2015), which is particularly interesting in the context of handedness ontogenesis. Moreover, a recent study showed that methylation plays a role in the ontogenesis of handedness: methylation levels in a CpG block in the promoter region of LRRTM1 were associated with atypical handedness (Leach et al., 2014).
Post-transcriptionally, gene expression is further regulated by microRNAs (miRNAs) that are composed of small, 21–25 nucleotide, non-coding RNAs. In humans and other mammals, miRNAs primarily cause destabilization of target mRNAs instead of reduced translation (Guo et al., 2010). This has also been shown to be relevant for hemispheric asymmetries, as neuronal asymmetries in the nematode Caenorhabditis elegans are controlled for by different miRNAs (Alqadah et al., 2013; Cochella and Hobert, 2012; Johnston and Hobert, 2003; Hsieh et al., 2012).
Pronounced changes in spatiotemporal expression profiles are a key feature of human embryogenesis (Yi et al., 2010) and formation of functional asymmetries in vertebrates has been shown to strongly depend on critical periods in early development (Le Grand et al., 2003; Zappia and Rogers, 1983). To investigate the molecular determinants of human behavioral asymmetries we analyzed asymmetries in genome-wide mRNA expression, miRNA expression and DNA methylation patterns in human fetal spinal cord tissue. Importantly, we specifically wanted to investigate the spinal cord segments innervating arms and hands. While rostral cervical segments (C2–C5) innervate the head, neck and shoulder region, the subsequent segments directly innervate arms and hands with C6 innervating the thumb, C7 innervating the middle finger and C8 innervating the little finger. T1 innervates the medial site of the antecubital fossa (Maynard et al., 1997). Based on the findings on the start of left-right asymmetries in coordinated hand movements (Hepper et al., 1998; de Vries et al., 1985), we focused on fetal tissue samples obtained between 8 and 12 weeks PC.
We hypothesized that gene expression asymmetries between the left and right spinal cord start at 8 weeks PC, as this is the starting point of coordinated asymmetrical hand movements. Based on the findings about the role of non-genetic influence factors for handedness development, we also assumed a pronounced modulation of these mRNA expression asymmetries by asymmetric DNA methylation and asymmetric miRNA expression.
Results
Gene expression
Asymmetries in mRNA expression in spinal cord segments C2 to T2 were observed at all three developmental stages, with the largest differences evident at 8 weeks PC. At 8 weeks PC, 1690 transcripts (3.29%) showed left-right gene expression differences with log2(fold change) > 1.5. The fact that 39 transcripts showed stronger left-sided gene expression, while 1651 transcripts showed stronger right-sided gene expression highlights increased right-sided gene expression in the spinal cord at this developmental stage. The number of asymmetrically expressed genes with a log2(fold change) > 1.5 was reduced to only 24 genes (0.05%) at 10 weeks PC. Among these, 15 displayed leftward asymmetrical gene expression and nine showed rightward asymmetrical gene expression. Four genes (0.01%) showed a log2(fold change) of 1.5 or higher (see Figure 1 for top 25 asymmetrically expressed genes per developmental stage and Supplementary file 1G for individual samples) at 12 weeks PC, all indicating stronger gene expression in the right spinal cord. Among the candidate genes associated with the development of hemispheric asymmetries (see Figure 2A), forkhead box P2 (FOXP2) (Ocklenburg et al., 2013b) displayed a rightward asymmetry in the spinal cord at 10 weeks PC. BDNF antisense RNA (BDNF-AS) (Manns et al., 2008) was higher expressed in the left spinal cord at 8 weeks PC.
Gene expression asymmetries in human fetal spinal cord at 8, 10 and 12 weeks PC.
X-axis shows the extent of asymmetry measured in log2(fold change) between right and left spinal cord samples. Blue bars show leftward asymmetrically expressed genes, red bars show rightward asymmetrically expressed genes. For 8 weeks PC, the top 25 genes with highest rightward/leftward gene expression asymmetries are depicted. For 10 and 12 weeks PC, all genes with a log2(fold change) > 1.5 are shown. The source files of asymmetrically expressed genes per developmental stage with corresponding fold change values are available in Figure 1—source data 1.
https://doi.org/10.7554/eLife.22784.002
Functional genes and gene groups.
(A) Gene expression asymmetries for previously published candidate genes for handedness and functional lateralization. Asterisks indicate biologically relevant gene expression asymmetry with a log2(fold change) > 1.5. (B) Number of significant Gene Ontology (GO) groups for the three main categories ‘biological processes’, 'molecular function' and 'cellular component' for weeks 8, 10 and 12 PC. (C) Main GO groups for 8 and 10 weeks PC with p-value and number of involved genes for the left and right spinal cord. The source files of all enriched GO groups are available in Figure 2—source data 1.
https://doi.org/10.7554/eLife.22784.004
GO groups
Recently, it has been suggested that subtle expression asymmetries at the level of individual genes may translate to stronger asymmetries within the gene ontology (GO) groups (Karlebach and Francks, 2015). The number of significant GO groups (p<0.05) as displayed by enrichment analysis over asymmetrically expressed genes per hemisphere and developmental stage was the highest at 8 weeks PC (123 overall). For the 69 transcripts showing asymmetrical gene expression towards the left spinal cord, WebGestalt revealed three enriched GO groups: Platelet-derived growth factor binding (p<0.05), collagen (p<0.05), and fibrillary collagen (p<0.05). In contrast, for the 1651 transcripts showing asymmetrical gene expression towards the right spinal cord, GO analysis revealed 120 enriched GO groups displaying particular involvement in biological processes like cell cycle (p<0.001), cellular component organization or biogenesis (p<0.001), and metabolic processes (p<0.001). Enriched molecular functions include protein binding (p<0.001), transferase activity (p<0.001), and protein binding transcription factor activity (p<0.001). The number of significant GO groups was reduced at 10 weeks PC (41 overall): The 15 genes showing leftward asymmetric gene expression cluster in 4 GO categories representing cellular components: DNA-directed RNA polymerase II, holoenzyme (p<0.05), nuclear DNA-directed RNA polymerase complex (p<0.05), RNA polymerase complex (p<0.05), and DNA-directed RNA polymerase complex (p<0.05). GO categories enriched in the nine genes asymmetrically expressed towards the right spinal cord include system development (p<0.05), regulation of reproductive process (p<0.05), cell proliferation (p<0.05), and multicellular organismal process (p<0.05). At 12 weeks PC, no GO group reached statistical significance (see Figure 2B–C and related Figure 2—source data 1).
miRNA
At 8 weeks PC, 301 miRNA transcripts were expressed in both the left and the right spinal cord. Out of those, five (1.66%) showed a biologically relevant asymmetry towards the right spinal cord. At 10 weeks PC, six of 382 transcripts (1.57%) displayed a log2(fold change) > 1.5, thereof three leftwards and three rightwards. At 12 weeks PC, seven of 294 expressed transcripts (2.38%) were differentially expressed with six being more strongly expressed in the left spinal cord and one being more strongly expressed in the right spinal cord (see Figure 3A and related Figure 3—source data 1). For each developmental stage, target genes of asymmetrically expressed miRNA transcripts were compared to asymmetrically expressed genes. At 8 weeks PC, 65 of the 1690 asymmetrically expressed genes (3.85%) were likely to be targets of asymmetrically expressed miRNA transcripts. At 10 weeks PC, six of the 24 asymmetrically expressed genes (25%) were targets of differentially expressed miRNAs. At 12 weeks PC, one of the four asymmetrically expressed genes (25%) was a target of the asymmetrically expressed miRNAs of that developmental stage. For the miRNAs asymmetrically expressed towards the right spinal cord at 8 weeks PC, 12 KEGG pathways reached FDR-corrected significance. By far the largest effect was observed for the Transforming growth factor beta (TGF-β) signaling pathway (p<0.001), which all five miRNAs asymmetrically expressed towards the right spinal cord were involved in. Additionally, among the 10 genes involved in this pathway, two (SP1, SMAD3) were differentially expressed at 8 weeks PC. At 10 weeks PC, four pathways reached FDR-corrected significance (two left, two right). For 12 weeks PC, 16 pathways were detected in KEGG analyses (14 left, two right).
Epigenetic regulation of gene expression asymmetries in human fetal spinal cord.
(A) Asymmetrically expressed miRNA transcripts at 8, 10 and 12 weeks PC. The extent of expression asymmetries is measured in log2(fold change). Red bars show rightward asymmetrically expressed microRNA transcripts, blue bars show leftward asymmetrically expressed miRNA transcripts. (B) Number of CpG sites showing differential DNA methylation per chromosome, compared between the left and right spinal cord for 8 and 10 weeks PC. Depicted are only CpG sites with methylation asymmetries in both samples. Red bars represent the number of CpG sites that showed significantly higher DNA methylation on the right side, blue bars show the number of CpG sites that showed significantly more DNA methylation on the left side. (C) Percentage of differential DNA methylation in leftward (blue) and rightward (red) asymmetrically methylated CpG sites as a function of p-value. (D) Percentage of gene expression asymmetries on each chromosome at 8 weeks PC that can be explained by regulation via asymmetrically expressed miRNAs or asymmetric DNA methylation of CpG sites within and 1500 nucleotides upstream of the expressed genes. The source files of asymmetrically expressed miRNAs, asymmetrically expressed targets of miRNAs, enriched KEGG pathways and differentially methylated CpG sites are available in Figure 3—source data 1, Figure 3—source data 2, Figure 3—source data 3, and Figure 3—source data 4 respectively.
https://doi.org/10.7554/eLife.22784.006
DNA methylation
At 8 weeks PC, 31,278 CpG sites showed higher DNA methylation (FDR-corrected p-value below 0.01 and the % methylation difference between left and right above 25%) in the left spinal cord over both samples, whereas only 8615 CpG sites were more extensively methylated in the right spinal cord of both samples. At 10 weeks PC, 10,892 CpG sites showed side-specific asymmetrical DNA methylation towards the left side and 11,081 towards the right side of both samples (see Figure 3B–C and related Figure 3—source data 4). At 12 weeks PC, for which only one sample was available, 281,119 CpG sites showed higher DNA methylation in the left and 352,118 in the right spinal cord. Comparing the methylation data to gene expression data revealed that at 8 weeks PC, 451 of 1690 asymmetrically expressed genes were asymmetrically methylated towards the opposite direction, thus, 27% of the variance in asymmetrical gene expression could be explained by differential methylation alone. Moreover, 1% of variance (18 genes) could be explained by the asymmetrical miRNA expression as well as differential methylation and 3% of variance (47 genes) could be explained by miRNA alone, which leaves 69% of variance unexplained (Figure 3D). At 10 weeks PC, 25% of variance in asymmetrical gene expression (six genes) could be explained by miRNA alone, followed by methylation (8%, two genes). 67% of variance remained unexplained. At 12 weeks PC, 25% of variance (one gene) was explained by miRNA and 25% (one gene) by methylation. 50% of variance remained unexplained at 12 weeks PC.
Discussion
Hemispheric asymmetries in brain and behavior are a major organizational principle in the vertebrate central nervous system, but their ontogenesis is not well understood (Ocklenburg et al., 2014b). While it is general consensus that both genetic and epigenetic factors play a role (Ocklenburg et al., 2013c), it is unclear, which molecular processes underlie the epigenetic modulation of gene expression asymmetries, a potential origin of behavioral asymmetries (Sun et al., 2005; Karlebach and Francks, 2015). To elucidate this question we analyzed asymmetries in genome-wide mRNA expression, miRNA expression and DNA methylation patterns in human fetal tissue samples. Importantly, we focused on spinal cord, not brain, tissue. Eight weeks after conception, human fetuses exhibit pronounced lateralized motor behavior of the arms. As cortical control of this behavior is unlikely (Hepper et al., 1998; de Vries et al., 1985; Hepper et al., 2005; ten Donkelaar et al., 2004), it has been suggested that it is under spinal control (Hepper, 2013).
In line with our hypothesis, our findings suggest that gene expression asymmetries in the spinal cord segments innervating the hands and arms might be critical for the ontogenesis of functional asymmetries. For the first time we show that the left and right cervical and anterior thoracal segments of the fetal spinal cord do show biologically relevant gene expression differences. Importantly, these gene expression asymmetries are highly developmental stage-specific. At eight weeks after conception, gene expression asymmetries between the two halves of the spinal cord were most pronounced, with 3.29% of all transcripts showing biologically relevant left-right gene expression differences, largely higher towards the right side and involved in numerous GO categories contributing to neurodevelopment. At 10 weeks PC, this number decreased substantially to 0.05% and further so at 12 weeks PC (0.01%). While the findings for 10 and 12 weeks PC are largely comparable to what has been reported for gene expression asymmetries in the fetal cerebral cortex (Sun et al., 2005; Karlebach and Francks, 2015), the data for eight weeks PC indicate a substantial increase over previous reports of gene expression asymmetries in CNS tissue that goes along with the first onset of coordinated hand movements.
In line with the suggestion that non-shared environmental influences account for more than 75% of the variance in functional hemispheric asymmetries in humans (Medland et al., 2009), we could show that a large part of these gene expression asymmetries is regulated by epigenetic processes.
On the one hand, we could show that DNA methylation of CpG islands shows substantial asymmetries that are related to RNA expression asymmetries. In week 8 tissue samples, there was a strong left-lateralization of CpG island methylation, indicating a stronger repression of gene transcription in the left spinal cord. This is well in line with our finding of increased overall right-sided gene expression at that time point. Direct comparison of the location of asymmetrically methylated CpG islands and asymmetrically expressed genes indicated that 27% of the variance in asymmetrical gene expression at week 8 could be explained by differential methylation. In week 10 tissue samples, methylation asymmetries are massively decreased as compared to week eight, also in line with the gene expression data. Week 12 is difficult to interpret as here only one sample was analyzed, greatly increasing the number of asymmetrically methylated CpG sites.
On the other hand, we could also show that the asymmetries in gene expression are modulated by miRNA expression asymmetries. Particularly interesting was our finding that for the miRNAs asymmetrically expressed towards the right spinal cord at week eight, KEGG pathway analysis revealed a substantial effect of the TGF-β signaling pathway. This is an intriguing finding, as both nodal growth differentiation factor (Nodal) and left-right determination factor (Lefty), two of the key proteins for establishing bodily left–right asymmetry during development are part of the TGF-β superfamily (Mittwoch, 2008; Shiratori and Hamada, 2014). Importantly, TGF-β signaling has directly been linked to handedness, as proprotein convertase subtilisin/kexin type 6 (PCSK6), one of the major candidate genes for handedness, encodes for a protease that cleaves NODAL (Scerri et al., 2011).
Our data collection was limited to weeks 8 to 12 PC and for future studies, it could potentially be interesting to include tissue samples from even earlier stages to get a more detailed picture of the developmental trajectory. Also, independent replication in larger samples is needed in order to make more in-depth functional conclusions. As limb preferences have been reported in many non-human primates, but the strong 90 to 10 distribution of right- and left-handedness in humans seems to be rather unique, comparative analysis of primate tissue samples might yield unique insights into the evolution of the molecular basis of hemispheric asymmetries.
One potential issue with the interpretation of our data is to what extent the observed gene expression asymmetries are linked to visceral situs and not necessarily nervous system asymmetries. A particular interesting experiment in this regard would be to investigate spinal cord gene expression asymmetries in the inversus viscerum (iv) line of mouse mutants (Okada et al., 1999). These mutants show randomized visceral laterality and by comparing spinal cord gene expression asymmetries between animals with normal and atypical visceral asymmetries a potential impact of visceral asymmetries on spinal cord gene expression could easily be identified.
Taken together, these results are a strong indicator of epigenetic influences on human spinal cord gene expression asymmetries, a potential precursor of handedness. In birds, it has been shown that a behavioral preference for turning the head to the right, caused by epigenetic modulation during a critical period just before hatch, induces not only motor, but also visual and cognitive asymmetries (Casey and Martino, 2000; Manns and Güntürkün, 2009; Rogers, 1982; Skiba et al., 2002). Based on our data, a similar model is conceivable in humans. As week eight after conception represents the onset of coordinated hand movements and behavioral asymmetries of the hands occur first at this time point (Hepper et al., 1998; de Vries et al., 1985), we assume that a certain time frame before 10 weeks PC represents the critical period for handedness formation. During this period, asymmetrical DNA methylation and posttranscriptional regulation by asymmetrically expressed miRNAs lead to a spike in RNA expression asymmetries in the spinal segments innervating the arms and hands. These expression asymmetries of genes relevant for CNS development could lead to a differential development of neuronal circuits influencing the right arm and hand, causing the described behavioral asymmetries. For example, it has been shown that spinal cord segments innervating the right arm contain motoneurons with larger somata than left arm segments. In contrast, there are no size differences in left and right segments innervating the upper trunk (Melsbach et al., 1996). Furthermore, at eight weeks PC, the spinal cord and motor cortex are functionally not connected (ten Donkelaar et al., 2004), also supporting that behavioral asymmetries in arm use at that stage are controlled for by the spinal cord. At a later developmental stage when the spinal cord and motor cortex are functionally connected, the established behavioral asymmetry then could lead to asymmetries in use-dependent neuronal plasticity processes (Cirillo et al., 2010) in the motor cortex, ultimately leading to the cortical correlates of handedness (Ocklenburg et al., 2013c). This process could start at around 14 weeks PC, as asymmetric fetal hand use at that stage strongly correlates with later handedness at school age (Hepper et al., 1990, 2005). Unlike models assuming that handedness is primarily controlled by allelic variations in one or more candidate genes (Annett, 1998), our suggestion is in line with the finding that more than 75% of the variance in handedness data is explained for by non-shared environmental influences (Medland et al., 2009). Moreover, our data do not contradict neither linkage studies in extended left-handed pedigrees nor genome-wide association studies which were unable to identify allelic variants that explain more than a fraction of the variance in handedness data (Armour et al., 2014; Eriksson et al., 2010; Somers et al., 2015). Whereas our findings suggest that a large part of these influencing factors act prenatally, there remain several important peri- and postnatal environmental factors like social modulation to shape actual handedness (Schaafsma et al., 2009).
In summary, we could show pronounced, time sensitive gene expression asymmetries in human fetal spinal tissue that overlap with the onset of behavioral asymmetries. Thus, our data suggest a spinal, not a cortical, beginning of hemispheric asymmetries. The observed gene expression asymmetries were modulated by asymmetric CpG island methylation and asymmetries in miRNA expression, suggesting that these processes form the molecular basis of asymmetry epigenetics. In conclusion, our data strongly suggest a multifactorial model for the ontogenesis of hemispheric asymmetries, including both multiple genetic and epigenetic factors.
Materials and methods
Sample collection
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The human spinal cord was collected from fetal tissue discarded following induced pregnancy termination in a regional gynecology clinic. None of the physicians or other medical personnel involved in conducting the pregnancy terminations was involved in this scientific study. The study was approved by the Ethics Committee of the Medical Faculty of the Ruhr University Bochum (registration number 5056–14). All fetal tissue donors signed written informed consent at least 24 hr before the pregnancy termination was conducted. Following informed consent, the handedness of fetal tissue donors was determined using the Edinburgh Handedness Inventory (EHI) (Oldfield, 1971).
Tissue preparation
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Tissue samples were dissected from the spinal cord of six fetuses after pregnancy terminations at 8, 10, and 12 weeks post conception (PC), i.e. 10, 12 and 14 weeks gestational age. Due to ethical considerations when working with aborted human fetal tissue, the sample size was limited to six fetuses for which we got allowance by the Ethics Committee. This number was based on effects in previous studies with fetal cortical tissue (Sun et al., 2005). Fetal pathologies were ruled out as far as possible by excluding pregnancy terminations due to medical indications as well as karyotype aberrations. The samples were also excluded in case of heavily destructed tissue. Following pregnancy termination, fetal and surrounding tissue was immediately rinsed with sterile 1x phosphate buffered saline (PBS) in order to hold ion concentrations constant while blood was removed. In case the spine was detectable, it was fixed with sterile cannulas with a diameter of 0.6 mm (B Braun, Melsungen, Germany) and opened longitudinally with ball-ended dissecting scissors. In order to differentiate left and right, the right spinal cord was marked with small injections of 1% cresyl violet. Tissue samples were stored in 1 ml Allprotect Tissue Reagent (Qiagen, Hilden, Germany). Spinal cord tissue preparation was conducted as quickly as possible to ensure that RNA was not degraded (7:50–16:40 min, see Supplementary file 1A). Subsequently, 50–100 mg of chorionic villi were removed and stored in 10 ml of RPMI 1640 Medium (Life Technologies GmbH, Carlsbad, California) for subsequent karyogram analysis. All tissue samples were transported to Ruhr University Bochum, Germany. Spinal cord samples were stored at 4°C to preserve the gene expression profile. 24 hr later, the upper third of the spinal cord was separated on a Teflon freezing plate in order to include spinal cord segments C2 to T2. The left and right spinal cord were dissected by separating the tissue longitudinally along the midline and restored in the Allprotect Tissue Reagent at −80°C.
Karyotyping
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Karyograms were assembled at the Department of Human Genetics (Ruhr University Bochum) to ensure that karyotypes were normal without major chromosomal aberrations. Cell cultures were incubated with 1 µg colcemid (Gibco, Karlsruhe, Germany) for 80 min and were then harvested from flask applying trypsin-EDTA (0.05/0.02 w/v) (Biochrome, Berlin, Germany) for 2–4 min. After transferring to tube and centrifugation (170 g for 10 min) cells were incubated in 0.56% KCl hypotonic solution for 20 min and subsequently fixed and washed using a 3:1 methanol–glacial acetic acid fixative. After spreading on slides and air drying samples were stained in 0.025% quinacrine hydrochloride (Sigma, Steinheim, Germany) for 20 min. Q bands were visualized on a Zeiss Axioskop 2 fluorescent microscope and 100 metaphases per sample were analyzed in Ikaros software (Metasystems, Altlussheim, Germany).
Assessment of RNA and DNA
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Total RNA including miRNA and DNA was extracted using the AllPrep DNA/RNA/miRNA Universal Kit (Qiagen, Hilden, Germany) according to the manufacturer’s instructions. Concentration and purity of RNA and DNA were determined photometrically (NanoDrop ND-1000 Spectrophotometer, Thermo Scientific, Waltham, Massachusetts). RNA quality was controlled using the Agilent RNA 6000 Pico Kit and Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, California) according to the manufacturer’s recommendations. Extracted RNA and DNA were stored at −80°C until gene expression analysis was performed. For RNA and DNA quality measurements see Supplementary files 1B–C.
Gene expression analysis and bioinformatics
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‘INVIEW Transcriptome Discover’ provided by GATC Biotech AG (Konstanz, Germany) was used to analyze the extracted mRNA. Sample VI did not pass entry quality control and was not further processed. For the remaining samples, rRNA was depleted from total RNA for purification and subsequent fragmentation of mRNA into RNA-Seq reads. A strand-specific cDNA-library was generated for subsequent Illumina paired-end sequencing with 60 million reads. The RNA-Seq reads were aligned to the reference genome (Homo sapiens, hg19) using Bowtie (RRID:SCR_005476). Read statistics are reported in Supplementary files 1D–E. Potential exon-exon splice junctions were discovered (TopHat, RRID:SCR_013035). The software Cufflinks (RRID:SCR_013307) (Trapnell et al., 2010) then recognized and quantified transcripts, which were merged to full length transcripts and annotated. Cuffdiff (RRID:SCR_001647) tracked the mapped reads and determined the relative gene expression value (fragment per kilo base of transcript per million fragments mapped [FPKM]) for each transcript in each sample.
Overall, gene expression was investigated in 51,408 transcripts in left and right spinal cord of five samples. Asymmetric gene expression was determined for annotated genes, which were identified using the RefSeq database (http://www.ncbi.nlm.nih.gov/refseq/; RRID:SCR_003496). Differential gene expression is usually reported as a fold change in FPKM. In case of very small FPKM values the fold change is likely to be high although the difference in gene expression is small (Warden et al., 2013), so a gene was considered as abundant if FPKM was at least 1. The number of protein coding genes with an FPKM-threshold of 1 on both sides was slightly lower in sample II (9102, 17.7%) than in the other samples (I: 10,618, 20.7%, III: 10,970, 21.3%, IV: 10,854, 21.1%, V: 10,989, 21.4%). Due to the small sample size, differential gene expression for 8 and 10 weeks PC was determined by fold change of means using a threshold of log2(fold change) > 1.5. This value is commonly acknowledged to indicate a gene expression difference with possible functional relevance (Hawrylycz et al., 2012). At 12 weeks PC, only one sample was included and genes with a log2(fold change) > 1.5 of FPKM values were considered as asymmetrically expressed.
After the initial analysis on the single gene level, we targeted candidate genes that had previously been associated with the development of hemispheric asymmetries: LRRTM1 (Francks et al., 2007), PCSK6 (Scerri et al., 2011Arning et al., 2013Brandler et al., 2013), meiosis specific nuclear structural 1 (MNS1) (Brandler et al., 2013), polycystin 2, transient receptor potential cation channel (PKD2) (Brandler et al., 2013), AR (Arning et al., 2015; Hampson and Sankar, 2012; Medland et al., 2005), SET domain bifurcated 2 (SETDB2) (Ocklenburg et al., 2016), and catechol-O-methyltransferase (COMT) (Savitz et al., 2007) have been reported as specific candidate genes for handedness, whereas glutamate ionotropic receptor NMDA type subunit 2B (GRIN2B) (Ocklenburg et al., 2011b), FOXP2 (Ocklenburg et al., 2013bPinel et al., 2012), KIAA031945 (Pinel et al., 2012), and cholecystokinin A receptor (CCKAR) (Ocklenburg et al., 2013d) have been associated with language lateralization. Other genes associated with left-right differentiation are left-right determination factor 1 (LEFTY1) (Mittwoch, 2008) and nodal growth differentiation factor (NODAL) (Mittwoch, 2008), BDNF (Manns et al., 2008), LIM homeobox 1 (LHX1) (Tsang et al., 1999), and bone morphogenetic protein 7 (BMP7) (Abu-Khalil et al., 2004). Among these, AR and NODAL were not expressed above the detection level at any developmental stage.
In order to identify functional groups of asymmetrically expressed genes, we used WebGestalt (RRID:SCR_006786) (Wang et al., 2013; Zhang et al., 2005) to carry out an enrichment analysis over all genes with a log2(fold change) > 1.5 per hemisphere and developmental stage with respect to GO groups (biological process, molecular function, cellular component).
miRNA expression analysis and bioinformatics
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The amount of RNA for miRNA sequencing was only sufficient in sample II, IV, and V (see Supplementary file 1B). The service 'Regulome sequencing' of GATC Biotech AG provided the analysis of miRNA and included the generation of a small- / miRNA-library for subsequent Illumina single-read sequencing with 5 million reads as well as identification of common miRNAs with corresponding expression values (read counts). Originally, all samples yielded between 618 and 858 expressed miRNAs (sample II: 638 left, 858 right; sample IV: 838 left, 799 right; sample V: 618 left, 658 right). miRNAs with less than 10 read counts on both sides of the spinal cord were removed from analysis to prevent unrealistically high fold changes (Hu et al., 2011), which left 300 miRNA transcripts for sample II, 381 transcripts for sample IV, and 293 transcripts for sample V. In contrast to pure read counts, RPKM (reads per kilo base of exon model per million mapped reads) values correct for sequencing depth and gene length, so RPKM was calculated (RPKM = [109 × reads mapped to the transcript)/(total number of reads in the library × transcript length] [Kazemian et al., 2015]). Differential miRNA expression was defined as a minimum log2(fold change) of 1.5. Using Mirpath v3.0 (Vlachos et al., 2015), we identified genes that were likely (probability of interaction > 0.8) to be targeted by the asymmetrically expressed miRNA transcripts, which were then compared to the differentially expressed genes. Variance in asymmetrical gene expression was considered to be explained by miRNA if asymmetrically expressed genes were targets of asymmetrically expressed miRNAs. Additionally, we performed KEGG (RRID:SCR_012773) analyses (Vlachos et al., 2015) to identify biological pathways regulated by asymmetrically expressed miRNA transcripts.
Methylation analysis and bioinformatics
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DNA was bisulfite treated and adapter and primer sequences as well as bases with a phred quality score lower than Q15 were removed. After transformation into a C-to-T and G-to-A version, BISMARK (RRID:SCR_005604) (Krueger and Andrews, 2011) and Bowtie2 (Langmead et al., 2009) were applied on the sequence reads in order to align them to the in silico converted reference (Homo sapiens, hg19), which was refined using Bis-SNP (RRID:SCR_005439) (Liu et al., 2012) adopted GATK (RRID:SCR_001876) (McKenna et al., 2010; DePristo et al., 2011) modules. Bis-SNP then simultaneously determined the genotypes and methylation rates at each CpG site using Bayesian inference. DNA read statistics and methylation levels are reported in Supplementary file 1F. The annotation was performed using the UCSC genome browser (http://genome.ucsc.edu/.) for detected CpG sites and using the RefSeq database (http://www.ncbi.nlm.nih.gov/refseq/) for genes. Comparative methylation analysis (left vs. right) was performed by using Fishers exact test using the R-package methylKit (RRID:SCR_005177) (Akalin et al., 2012). P-values were adjusted for false discovery rate (FDR) using the SLIM method (Wang et al., 2011). CpG sites were considered as differentially methylated if FDR-corrected p-value was below 0.01 and % methylation difference between left and right was above 25%. For week 10 and 12, average % methylation difference was calculated for every CpG site that was asymmetrically methylated in both samples, whereas for week 14, only one sample was available. CpG sites were compared to asymmetrical gene expression data by matching chromosome positions. For each asymmetrically expressed gene, the number of hyper-methylated CpG sites in the left and in the right spinal cord within this gene and 1500 nucleotides upstream was determined. A laterality quotient (LQ) was calculated [(right−left)/(right+left)*100] for each gene. Variance in asymmetrical gene expression was considered to be explained by differential methylation if methylation of CpG sites within one gene was strongly asymmetric (i.e. LQ > 25/LQ < −25) towards the opposite direction of gene expression.
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Decision letter
1. Heidi Johansen-Berg
Reviewing Editor; University of Oxford, United Kingdom
In the interests of transparency, eLife includes the editorial decision letter and accompanying author responses. A lightly edited version of the letter sent to the authors after peer review is shown, indicating the most substantive concerns; minor comments are not usually included.
Thank you for submitting your article "Epigenetic regulation of lateralized fetal spinal gene expression underlies hemispheric asymmetries" for consideration by eLife. Your article has been reviewed by three peer reviewers, and the evaluation has been overseen by a Reviewing Editor and Marianne Bronner as the Senior Editor. The following individuals involved in review of your submission have agreed to reveal their identity: Peter Hepper (Reviewer #2); Chris McManus (Reviewer #3).
The reviewers have discussed the reviews with one another and the Reviewing Editor has drafted this decision to help you prepare a revised submission.
Summary:
This paper studies asymmetry of gene expression in human fetal spinal cord. This is important as it allows for the demonstration that asymmetries are present before the spinal cord is connected to the cortex. The reviewers agreed that this was an exciting, important and novel paper.
Essential revisions:
1) There were originally six fetuses, the small number not being the fault of the researchers. Later there are only five and it took a while to find out what happened to the sixth one. The number of fetuses should also be stated in the Abstract, lest readers are potentially misled.
2) Figure 1 in particular has 2 fetuses at 8 and 10 weeks and only 1 at week 12. I wonder, given the very small Ns, and the novelty of the questions and the analyses whether perhaps it would make sense at 8 and 10 weeks to show the results separately for each of the two fetuses, as that would give readers some sense of the reliability of the results. Ditto perhaps for Figures 2 and 3. It was nice though, in the supplementary file to see information for each fetus (but it was only in a footnote to Supplementary file 1B that I found the fate of the sixth fetus).
3) I was not at all clear in the second paragraph of the subsection “Gene expression analysis and bioinformatics” how the bootstrapped t-tests were carried out. If there are two cases, with scores A and B, then the bootstrap can only come up with AA, AB or BB, with AB being the actual case. Is there any point in that? Or is the analysis somehow being done across all genes? More detail please. Sometimes, of course, it is also not really necessary to do statistics, and this might be one of those occasions.
https://doi.org/10.7554/eLife.22784.012
Author response
Essential revisions:
1) There were originally six fetuses, the small number not being the fault of the researchers. Later there are only five and it took a while to find out what happened to the sixth one. The number of fetuses should also be stated in the Abstract, lest readers are potentially misled.
In accordance with the reviewers’ suggestions, we now added the number of fetuses to the Abstract. The failure of quality control for one sample that was not further processed is mentioned in the Methods section (Gene expression analysis and bioinformatics).
2) Figure 1 in particular has 2 fetuses at 8 and 10 weeks and only 1 at week 12. I wonder, given the very small Ns, and the novelty of the questions and the analyses whether perhaps it would make sense at 8 and 10 weeks to show the results separately for each of the two fetuses, as that would give readers some sense of the reliability of the results. Ditto perhaps for Figures 2 and 3. It was nice though, in the supplementary file to see information for each fetus (but it was only in a footnote to Supplementary file 1B that I found the fate of the sixth fetus).
We would prefer to retain the pooled expression analysis across both samples for the different timepoints for several reasons:
First, this approach has been used by previous studies on expression asymmetries (e.g. Sun et al., 2005; Karlebach & Francks, 2015) and essentially is standard in the field.
Especially given the low n, some control for sparse findings is essential. In the pooled analysis, only genes that showed reliable expression (FPKM > 1) in both the left and the right spinal cord of both fetuses were included in the analysis. By only analyzing genes that were reliably expressed in all four samples, we excluded sparse findings. Making the analysis on single fetus level potentially would lead to much more “noisy” data, which we would like to avoid.
Last, we doubt that doubling the number of figures in this manuscript that already has a large number of figures would enhance the manuscript’s readability.
We however see the adding more information on the single fetuses would benefit the manuscript and added a new Supplementary file 1G showing the top 25 hits for each fetus separately.
We explicitly state in the Methods that the sixth fetus was not further analyzed due to quality control issues of the sample. The sentence reads: “Sample VI did not pass entry quality control and was not further processed.”
3) I was not at all clear in the second paragraph of the subsection “Gene expression analysis and bioinformatics” how the bootstrapped t-tests were carried out. If there are two cases, with scores A and B, then the bootstrap can only come up with AA, AB or BB, with AB being the actual case. Is there any point in that? Or is the analysis somehow being done across all genes? More detail please. Sometimes, of course, it is also not really necessary to do statistics, and this might be one of those occasions.
Bootstrapped t-tests were carried out as described by the reviewers (AA, AB or BB). We fully agree with the reviewer that making meaningful statistics with sample sizes this small is difficult and that instead relying on the biologically relevant fold changes might be a better representation of the data. Thus, in accordance with the reviewer’s suggestion, we now deleted these tests from the manuscript and completely rely on the fold changes for our results.
https://doi.org/10.7554/eLife.22784.013
Article and author information
Author details
1. Sebastian Ocklenburg
Institute of Cognitive Neuroscience, Department Biopsychology, Ruhr University Bochum, Bochum, Germany
Contribution
SO, Conceptualization, Formal analysis, Supervision, Writing—original draft, Project administration, Writing—review and editing
Contributed equally with
Judith Schmitz
For correspondence
[email protected]
Competing interests
The authors declare that no competing interests exist.
ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-5882-3200
2. Judith Schmitz
Institute of Cognitive Neuroscience, Department Biopsychology, Ruhr University Bochum, Bochum, Germany
Contribution
JS, Data curation, Software, Formal analysis, Visualization, Writing—original draft, Writing—review and editing
Contributed equally with
Sebastian Ocklenburg
Competing interests
The authors declare that no competing interests exist.
3. Zahra Moinfar
Department of Neuroanatomy and Molecular Brain Research, Ruhr University Bochum, Bochum, Germany
Contribution
ZM, Data curation, Investigation, Writing—review and editing
Competing interests
The authors declare that no competing interests exist.
4. Dirk Moser
Department of Genetic Psychology, Ruhr University Bochum, Bochum, Germany
Contribution
DM, Data curation, Investigation, Methodology, Writing—review and editing
Competing interests
The authors declare that no competing interests exist.
5. Rena Klose
Institute of Cognitive Neuroscience, Department Biopsychology, Ruhr University Bochum, Bochum, Germany
Contribution
RKl, Formal analysis, Writing—review and editing
Competing interests
The authors declare that no competing interests exist.
6. Stephanie Lor
Institute of Cognitive Neuroscience, Department Biopsychology, Ruhr University Bochum, Bochum, Germany
Contribution
SL, Formal analysis, Writing—review and editing
Competing interests
The authors declare that no competing interests exist.
7. Georg Kunz
Department of Obstetrics and Gynecology, St. Johannes Hospital, Dortmund, Germany
Contribution
GK, Methodology, Project administration, Writing—review and editing
Competing interests
The authors declare that no competing interests exist.
8. Martin Tegenthoff
Department of Neurology, University Hospital Bergmannsheil, Bochum, Germany
Contribution
MT, Methodology, Project administration, Writing—review and editing
Competing interests
The authors declare that no competing interests exist.
9. Pedro Faustmann
Department of Neuroanatomy and Molecular Brain Research, Ruhr University Bochum, Bochum, Germany
Contribution
PF, Data curation, Investigation, Writing—review and editing
Competing interests
The authors declare that no competing interests exist.
10. Clyde Francks
1. Language and Genetics Department, Max Planck Institute for Psycholinguistics, Nijmegen, Netherlands
2. Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, Netherlands
Contribution
CF, Formal analysis, Validation, Methodology, Writing—review and editing
Competing interests
The authors declare that no competing interests exist.
11. Jörg T Epplen
Department of Human Genetics, Ruhr University Bochum, Bochum, Germany
Contribution
JTE, Data curation, Validation, Investigation, Writing—review and editing
Competing interests
The authors declare that no competing interests exist.
12. Robert Kumsta
Department of Genetic Psychology, Ruhr University Bochum, Bochum, Germany
Contribution
RKu, Conceptualization, Formal analysis, Investigation, Methodology, Writing—review and editing
Competing interests
The authors declare that no competing interests exist.
13. Onur Güntürkün
1. Institute of Cognitive Neuroscience, Department Biopsychology, Ruhr University Bochum, Bochum, Germany
2. Stellenbosch Institute for Advanced Study (STIAS), Wallenberg Research Centre at Stellenbosch University, Stellenbosch, South Africa
Contribution
OG, Conceptualization, Resources, Formal analysis, Supervision, Funding acquisition, Project administration, Writing—review and editing
Competing interests
The authors declare that no competing interests exist.
Funding
Deutsche Forschungsgemeinschaft (Gu227/16-1)
• Onur Güntürkün
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Acknowledgements
We thank the medical personnel at the gynecological clinic for their support and help.
Ethics
Human subjects: The study was approved by the Ethics Committee of the Medical Faculty of the Ruhr University Bochum (registration number 5056-14). All fetal tissue donors signed written informed consent.
Reviewing Editor
1. Heidi Johansen-Berg, University of Oxford, United Kingdom
Publication history
1. Received: October 29, 2016
2. Accepted: January 31, 2017
3. Accepted Manuscript published: February 1, 2017 (version 1)
4. Version of Record published: February 7, 2017 (version 2)
Copyright
© 2017, Ocklenburg et al.
This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
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ADHD
ADHD should not stop me from reaching my dreams
INTRODUCTION
Attention Deficit and Hyperactivity Disorder (ADHD) is a complex neurobehavioural problem that affects 2 – 16 % of school-going children.1,2 It is considered the most common psychiatric disorder in children and is known to persist into adulthood in 60 – 70 % of cases.Males are more likely to be affected than females.3 The essential feature of ADHD is a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with daily functioning or development.3
adhd-girl-keyhole
What causes ADHD?
ADHD is inherited in most cases, which is why it tends to run in families.4 There is also evidence to suggest that environmental insults that occur around pregnancy, such as alcohol use, smoking during pregnancy and low birth weight, may increase the risk of ADHD.4
How is ADHD diagnosed?
An accurate diagnosis of ADHD is essential and should only be made by a specialist psychiatrist, paediatrician or other healthcare professional with training and expertise in the diagnosis of ADHD.2,4
The diagnosis of ADHD is based on the Diagnostic and Statistical Manual of Mental Disorders – 5th edition (DSM-5™) criteria:
adhd-symptoms
adhd-impairment
adhd-setting
adhd-history
Symptoms of inattention (at least 6 needed): 3
1. Makes careless mistakes
2. Difficulty sustaining attention
3. Doesn’t listen
4. Instructions not followed through
5. Cannot organise
6. Avoids sustained mental effort (e.g. schoolwork or homework)
7. Loses important items
8. Distracted
9. Forgetful
Symptoms of hyperactivity and impulsivity (at least 6 needed): 3
1. Fidgets or squirms
2. Cannot stay seated
3. Runs/climbs excessively
4. Cannot work/play quietly
5. On the go
6. Talks excessively
7. Blurts out answers
8. Cannot wait turn
9. Interrupts others
adhd-64369516_custom
adhd-challenges
Symptoms change as the child grows from childhood into adulthood.3 The main symptom in preschool is hyperactivity, whereas inattention becomes more prominent in school-aged children.3 During adolescence and adulthood, motor symptoms become less obvious but difficulties with restlessness, inattention, poor planning and impulsivity persist.3
adhd-challenges2
How is ADHD treated?
The aim of treatment is to alleviate symptoms and optimise cognitive, social and emotional functioning, allowing the affected individual to reach his/her full potential.2,4 In children with mild to moderate ADHD, first-line treatment is a behavioural programme with or without medication.4 In moderate to severe ADHD, first-line treatment is medication plus a behavioural programme.4 In adults, however, behavioural treatment is less effective and medication is the cornerstone of management.2
adhd-adult-keyhole
The underlying problem in ADHD has been identified as an imbalance of two brain chemicals, i.e. dopamine and noradrenaline.1 Medicines that improve ADHD act on these chemicals and are effective in 75 – 90 % of cases.1
adhd-hormones
Stimulants are by far the best studied and the most effective medication for ADHD across all age groups.2 In addition to relieving the core symptoms of ADHD, stimulants improve associated features, such as academic performance and social functioning.2 Methylphenidate is the stimulant of choice.2,4 Long-lasting, extended-release formulations are preferred because they give more even efficacy and result in less troublesome side effects.4 They also avoid the need for medication at school, which can be potentially embarrassing for the child.4 In addition, a survey has shown that children with ADHD find the afternoon/evening period at least as difficult as the school day, which highlights the importance of a treatment that lasts the full day.7
adhd-girl-thinking
What are the typical side effects of stimulants?
Typical side effects (headache, reduced appetite, palpitations, nervousness, initial insomnia and dry mouth) are usually mild and transient.2 Although there will always be concerns about the addictive potential of stimulants, studies have shown they actually reduce the risk of substance use disorder by 50 %.6
Children continue to grow while taking stimulants and any stunting in growth is reversible if the stimulant is discontinued during adolescence.6 Doctors will routinely monitor growth and, if affected, may reduce the dosage of the stimulant and institute a ‘drug holiday’ so that catch-up growth can occur.4
adhd-growing-kids
The non-stimulant atomoxetine, is an appropriate alternative for people who experience intolerable side effects or have a contra-indication to stimulants.2,4
Diet and supplements
Children and adults with ADHD should eat a well balanced, nutritious diet and exercise regularly.8 Supplementation with substances thought to be deficient (e.g. fatty acids) and elimination of substances thought to be harmful (e.g. artificial colourants and preservatives) is not routinely recommended.8 Should a relationship between specific foods and behaviour become apparent, a professional should be consulted before embarking on an elimination diet.8
Tips for parents:
• Don’t waste your time on self-blame: ADHD is inherited in the majority of cases and is not caused by poor parenting 9
• Learn about ADHD: look for accurate information and stick to reputable websites from non-profit organisations, governments or universities 9
• Make sure your child has a comprehensive assessment: this should include medical, educational and psychological evaluations 9
• Join a support group: check out the Attention Deficit and Hyperactivity Support Group of Southern Africa at: http://www.adhasa.co.za 9
Tips at home:
• Provide clear expectations: children with ADHD need to know exactly what is expected of them. Set limits and follow through with consequences 9
• Enforce discipline: consistently reward appropriate behaviour and respond to misbehaviour with alternatives such as time-outs or loss of privileges9
• Notice your child’s success: improve your child’s self-esteem by telling him/her exactly what he/she did well rather than focusing on what went wrong9
• Identify your child’s strengths: your child may be good at things like art, athletics or computers – encourage your child to build on these strengths 9
Remember that children with ADHD are: 10
adhd-behaviour
Like Medinformer
1. Greydanus DE, Sloane MA, Rappley MD. Psychopharmacology of ADHD in adolescents. Adolesc Med. 2002;13(3):599-624.
2. Schoeman R, Liebenberg R. The South African Society of Psychiatrists/
Psychiatry Management Group management guidelines for adult attention deficit/hyperactivity disorder. S Afr J Psychiat. 2017;23(0):a1060.
3. American Psychiatric Association, 2013, Diagnostic and statistical manual of mental disorders, 5th ed., Arlington, VA: American Psychiatric Publishing, p. 59-63.
4. Fisher AJ, Hawkridge S. Attention deficit hyperactivity disorder in children and adolescents. S Afr J Psychiat. 2013;19(3):136-140.
5. Biederman J. Attention-Deficit/Hyperactivity Disorder: A Selective Overview. Biol Psychiatry. 2005;57:1215-1220.
6. Biederman J, Faraone SV. Attention-defi cit hyperactivity disorder. Lancet. 2005;366:237-248.
7. Coghill D, Soutullo C, d’Aubuisson C, Preuss U, Lindback T, Silverberg M, et al. Impact of attention-deficit/hyperactivity disorder on the patient and family: results from a European survey. Child Adolesc Psych Ment Health. 2008;2(1):31. doi:10.1186/1753-2000-2-31.
8. National Clinical Practice Guideline Number 72. National Collaborating Centre for Mental Health commissioned by the National Institute for Health & Clinical Excellence. British Psychological Society and Royal College of Psychiatrists, 2009.
9. Understanding ADHD. For parents & caregivers. National Resource Centre on ADHD, a program of Children and Adults with Attention Deficit/Hyperactivity Disorder (CHADD®), 2017. [cited 2017 Nov 20]; Available from: http://www.help4adhd.org/Understanding-ADHD/For-Parents-Caregivers.aspx.
10. Tips for managing ADHD in the classroom. The Children’s Attention Project (CAP). Murdoch Children’s Research Institute. [cited 2017 Nov 20]; Available from: http://www.education.vic.gov.au/Documents/school/principals/participation/tipsmanagingadhdinclass.pdf.
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Frozen donor egg treatment
Why do you need to have so much drug prep for frozen donor egg? Can't the egg be implanted in timing with your own natural cycle, if you are ovulating normally, through use of scans and LH surge?
Our Expert's Answer
This information was published 6 years, 5 months ago and was correct at the time of publication. It may not reflect our current practices or regulations.
Please note that all the answers we give are on a generic basis only, as we cannot provide more in-depth answers without access to your medical history. If you need a more detailed response, tailored to you, we would recommend a consultation with one of our Fertility Specialists for more comprehensive medical advice.
Drug prep for frozen donor eggs is generally required for patients who require additional hormonal support, usually for older ladies undergoing treatment with frozen donor eggs.
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Accessibility View Close toolbar
• Conjunctivitis
Conjunctivitis, also known as pink eye, is a common eye problem that can afflict children and adults alike. It is highly contagious and spreads quickly in environments like classrooms or offices filled with multiple people in close proximity to one another. The good news is that conjunctivitis is easily
Read more
• Allergies
Caused by the same irritants as hay fever, runny nose, coughing, and sneezing, eye allergies commonly affect those who suffer from other allergy symptoms. Not only do eye allergies cause discomfort, but they can also interfere with daily activities. Eye Allergy Causes Medically referred to as allergic
Read more
• Acanthamoeba Keratitis
Acanthamoeba keratitis is a relatively rare type of eye infection, but it can become quite serious. If left untreated, Acanthamoeba eventually leads to vision loss, requiring a corneal transplant to restore sight. Understanding how to prevent this infection is key. What Is Acanthamoeba Keratitis? Acanthamoeba
Read more
• Stye
A stye, sometimes spelled as "sty," is a red, painful bump near the edge of the eyelid. It may look like a pimple or abscess, and it can form on the inside or outside of the eyelid. A stye is actually a localized infection that usually disappears by itself after a few days, although in rare cases, a
Read more
• Chalazion
A chalazion is the medical term for a slowly developing lump on the eyelid that occurs due to an oil gland blockage. At first, the eyelid may appear to be red, tender and swollen. After several days, the chalazion will form on the eyelid, appearing as a slow growing lump. While it is initially painless
Read more
• Blepharitis
Stinging, irritated eyes, and blurred vision may indicate nothing more than a case of blepharitis -- an unpleasant but, in most cases, relatively harmless condition. Blepharitis is a chronic eyelid inflammation caused by a variety of irritants and/or the inability to maintain proper eye lubrication.
Read more
• Bell's Palsy
If you suffer from Bell's palsy, a paralysis of one side of the face caused by nerve inflammation, you may lose control over your eyelids. This eyelid paralysis can create problems for the sensitive cornea that protects the eye's lens and helps focus light waves into clear images. Fortunately, an experienced
Read more
• Uveitis
Uveitis refers to the inflammation of the eye's middle layer, which consists of the iris, ciliary body, and choroid. Several fungal, viral, or bacterial infections lead to uveitis, as do certain autoimmune (systemic) and inflammatory conditions. In most cases of uveitis, however, the exact cause is unknown. Types
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• Computer Vision Syndrome
Almost everyone uses computers in the modern world, whether for recreation, employment, education or any combination of the three. Unfortunately, our increased use of computers in almost every aspect of our lives -- even using a smartphone to make a telephone call -- requires our eyes to read a computer
Read more
• Strabismus
Commonly called crossed eyes, strabismus is a condition in which eyes do not work together, failing to maintain proper alignment. While one eye focuses on an object, the other does not. The failure of the eyes to work together causes double vision, and if untreated can lead to an extreme reduction of
Read more
• Sjogren's Syndrome
Pronounced SHOW-grins, Sjogren's syndrome is a disorder of the immune system, or an autoimmune disease, which causes the body's immune system to attack and harm the body's glands. Your glands are responsible for the production of saliva, tears, and other lubrication necessary for the proper function
Read more
• Optic Neuritis
Also known as demyelinating optic neuritis, optic neuritis refers to the inflammation of the optic nerve due to the loss of or damage to a protective covering called myelin, which surrounds the optic nerve. The myelin is essential to the function of the optic nerve. A more general term, optic neuropathy,
Read more
• Nystagmus
Nystagmus is a vision condition characterized by repetitive, uncontrolled eye movements. These involuntary eye movements may be side-to-side, up and down, or in a circular pattern, which hinders the eyes’ ability to focus on a steady object. Individuals with nystagmus may hold their heads in unusual
Read more
• Macular Hole
The condition known as a macular hole refers to a tiny break in the macula that results in blurry or distorted vision. To fully understand the condition, one must understand eye anatomy. The macula is a spot located in the center of the retina (the back portion of the eye). Located where light comes
Read more
• Eye Occlusions
An eye occlusion is a blockage in one of the arteries or veins supplying blood to the retina and/or optic nerve. These blockages can cause severe and sudden vision loss. Contact your eye care professional immediately if you experience sudden vision loss, and follow up right away with your family doctor.
Read more
• Astigmatism
Many correctable vision problems are caused by abnormal eye anatomy. Very few people have perfectly shaped eyes that facilitate ideal vision. Rather, most people have some degree of abnormal curvature or other anatomical irregularities that cause slight visual changes. Astigmatism is one common form
Read more
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Know the Human Motion System
Humans have the ability to move and do activities, such as walking, running, jumping and other activities. The ability of human motion is influenced by the motion system, which is the result of harmonious cooperation between the organs of the motion system, for example the skeleton (bones), joints, and muscles.
Skeletal (bone) function is a passive locomotor, which can be moved if assisted by muscles.
The function of the muscles is as a means of active motion, which can move other organs so as to produce a motion.
Joint function as a link between the bones of one bone to another.
Chapter List
Frame (Bone)
Bone-forming elements are calcium elements in the form of salts which are preserved by callogens. In the study of the shape of the bones and body skeletons that are arranged can experience abnormalities caused by disorders carried from birth, disease, nutritional factors, and others.
Function of the body’s framework
The framework has important functions for the body, for example as follows:
1. Body builder
2. Body shaper
3. The place where muscles are attached
4. Protector of important body parts
5. Passive movers
6. Place of formation of red blood cells
The human framework can be divided into 3 parts
Skull section (Head)
The head is composed of several flat bones that function as a place for making red blood cells and white blood cells.
The arrangement of the skull consists of the following components:
• Forehead bone
• 1 Bone filter
• 2 Tornbone
• 2 Nose Bone
• 2 cheekbones
• 2 Ceiling bones
• 2 Bone Wedge
• 2 Bare bones
• 2 Tearbone
• 2 Upper jawbone
• 1 Bone of the tongue
• 1 skull bone
• 2 Upper bone
Body Parts
The Agency Section is divided into 5 groups
1. There are 33 segments of the spine
2. The 12 pair ribs consist of:
3. 7 pairs of true rusu bones
4. 3 pairs of fake ribs
5. 2 pairs of floating ribs
6. Chest bone, consisting of:
7. Upstream bone
8. Body bone and
9. Sword bones
10. The shoulder band consists of:
11. 2 collarbone (left and right)
12. 2 shoulder blades (left and right)
13. The hip ring consists of:
14. 2 sitting bones (left and right)
15. 2 intestinal bones (left and right)
16. 2 pubic bones (left and right)
Parts of the limbs
The limbs can be divided into 2 parts, namely:
1) Upper limb (left and right hand)
• 2 pelvic bones
• 2 upper arm bones
• 2 cubits
• 16 wrist bones
• 10 palm bones
• 28 segments of the finger joint
2) Lower limbs (right and left legs), including:
• 2 femur
• 2 bones of the kneecap
• 2 dry beds
• 2 calf bones
• 14 ankle bones
• 10 palm bones
• 28 segment of the toe bone
Bone type and function
According to the types of bones found in the human body can be divided into 2 groups:
A) Cartilage
This cartilage is composed of several cartilage cells, the space between cartilage cells contains a lot of adhesives and lime, which are flexible. Cartilage is widely owned by young children and in adults, namely at the ends of the ribs, larynx, trachea, bronchi, nose, ears, anatar vertebrae. The process of changing cartilage to hard bone is called ossification.
B) Hard bones
The formation of hard bones is caused by bone-forming cells, or what is called osteoblasts, the segment between hard bone cells is lime, with little adhesive, which is hard. Lime is formed by calcium carbonate (CaCO3) and calcium phosphate (Ca (PO4) 2) carried by the blood. There are havers in the hard bones in which there are many blood vessels that regulate the life of bone cells. The hard bones function in the framework. For example the thigh bone, arm bone, calf bone, and collarbone.
Bone forms
Based on the shape of the bone is divided into 3 forms, including the following:
1 # Pipe Bones
Pipe bone has a pipe-like shape that is round, long and the center resembles a pipe. Inside it contains yellow marrow. Examples of pipe bones are the thigh bone, middle bone, and upper arm bone.
2 # Flat bones
This flat or flat bone shape functions as a place for the formation of red blood cells and white blood cells. Examples of flat bones are the breastbone, ribs, and shoulder blades.
3 # Short bones
The shape of the short bone is short and sticky, the inside of the bone contains red marrow. Examples such as vertebrae, ankle bones and wrist bones.
Several types of abnormalities in the bone (Order)
There are several factors that cause disturbances or abnormalities in the bones, such as abnormalities since birth, food or drink factors, infectious disease factors and incorrect posture habits.
Some abnormalities in the skeleton or body bones, as follows:
1. Scoliosis, is an abnormality in the spine that is curved to the side. This can occur in people who suffer from heart disease that endures the pain by tilting the body sideways, resulting in his backbone tilting.
2. Rickets, is an abnormality in the bones caused by lack of a source of vitamin D, which causes leg bones shaped like the letter X or O.
3. Lordosis, is an abnormality in the backbone that experiences bending towards the back, this is due to a bad habit of sleeping with a waist prop.
4. Kyphosis, which is an abnormality in the spine that is bent forward, this can occur due to the habit of sitting or working in a bent position.
5. Polio, is a bone carcinoma caused by infection with a virus, so that the bones are chopped and abnormal.
Joints
In the human body there are more than 200 bones connected together. The relationship between bones is called joints or articulation. Joints have a very important role in the human motion system. Based on the nature of the motion of the joints can be grouped into three parts, namely as follows:
A) Dead Joints
Dead joints are joints that do not have joint gaps so movement cannot occur. Examples of dead joints are joints between the skull bones.
B) Motion Joints
Joints are joints that occur in one bone with another bone that is not connected to the network, causing free movement. In the motion joints can be grouped into four types, namely:
1. Hinge joints, are joints that can be moved in one direction. For example, joints between the femur and calf bones, joints between the bones of the arm with cubits.
2. Rotating Joints, are joints that can be rotated. For example, joints between the cervical vertebrae with atlas, joints between cubits and picking bones.
3. Saddle joints, are joints that can be moved both For example, joints in the thumb, joints between the wrist bones with the bones of the palm.
4. Bullet Joints, are joints that can be moved in all directions. For example, the joints between the shoulder bracelets with the bones of the upper arm, the joints between the hip and thigh bones.
C) Stiff joints
Rigid joints are joints consisting of the ends of cartilage, so stiff motion can still occur, for example joints between stiff joints.
Muscle
Muscles in humans work by contracting so the muscles will shorten, the middle part bulging and hardening. Shortened muscles can cause bones to be attached by these muscles to be pulled and lifted. With the contraction of one muscle can cause the bones to move only in one particular direction, to be able to return to its original place, there must be a muscle that reacts. Therefore, it requires at least two kinds of muscles with different performance.
Muscles can be divided into 3 groups, namely as follows:
A) Based on how it works
1 # Antagonistic Muscle
This muscle that causes antagonistic motion occurs or more often called the opposite muscle motion. Examples of antagonistic muscle movements are the work of the biceps and triceps on the upper and lower arms.
The biceps is a muscle that has two tendons (ends) attached to the bone and is located in the upper arm bone in front. While the triceps muscle is a muscle that has three tendons (ends) attached to the bone and is located in the upper arm of the back.
To lift the forearm, the biceps contract and the triceps react. And to lower the forearm, the triceps muscle contracts and the biceps react.
2 # Synergistic muscles
This muscle causes synergistic movements, which are concurrent movements in one direction. So, both of these muscles contract and relax simultaneously. Examples of synergistic muscle movements are hand movements, face down.
This movement occurs because of the cooperation between the pronator teres muscle with the quadratus protator muscle. Another example is rib motion due to the cooperation of muscles between the ribs when humans breathe.
B) According to the form and how it works
1) Plain muscle
The characteristics of smooth muscle are as follows:
1. Has one cell nucleus.
2. Spindle-shaped, with both ends tapered and bulging in the middle.
3. Located in the intestinal muscles, circulatory tract muscles, urinary tract muscles, etc.
4. Do not have transverse lines (plain).
5. Working out of awareness, which means not under the brain’s command
2) Striated Muscle
The characteristics of striated muscles are as follows:
1. Cylindrical and elongated.
2. Has many cell nuclei.
3. Found in the thigh muscles, calf muscles, and chest muscles.
4. Visible cross lines are arranged like dark and alternating bright areas
5. Working under consciousness, Muscles work on the brain’s command.
3) Heart muscle
The characteristics of the heart muscle are as follows:
1. The work of the heart muscle cannot be controlled by our will, but it works according to the motion of the heart.
2. This heart muscle is only found in the heart. The structure is the same as the striated muscle, alternating dark light and intermittent branching of cells.
Heart muscle according to its shape like a striated muscle and from how it works like smooth muscle, therefore called special muscle.
Muscle abnormalities
Abnormalities in human muscles can be caused due to the amount of motion and work of muscles. This happens because of interference from outside factors and internal factors. External factors are caused by illness and illness. And while factors from within due to inbornity or the occurrence of muscle errors that have never been trained.
The following kinds of abnormalities in the muscles, among others:
1. Tetanus, is a disorder in the muscles that experience continuous tension caused by bacterial toxins.
2. Stiff neckor stiff , is a muscle disorder that occurs due to motion or pounding that causes inflamed trapesius muscles.
3. Atrophy, is a muscle disorder that causes the muscles to become smaller caused by the polio virus or because the muscles do not function for motion due to paralysis.
4. Sprains, are muscle disorders caused by synergistic movements of one muscle working in opposite directions.
5. Cramps, is a muscle disorder that occurs due to continuous muscle activity so that the muscles become spasms.
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HealthyWorld101.com
How to calculate the calories a person burns while sleeping
The body continues to burn calories during sleep to sustain life and essential bodily functions. A person can use a specific formula to estimate how many calories they burn at night.
Even when resting and sleeping, the body requires a constant source of energy to maintain a wide range of metabolic processes.
Many different factors influence metabolism, which can make it difficult to calculate accurately how many calories a person burns during sleep. However, by estimating a person’s basal metabolic rate (BMR), it is possible to come up with an approximate figure.
In this article, we discuss what BMR is, how to calculate it, and how to use the result to estimate the number of calories that a person burns while sleeping. We also provide some sleep hygiene tips.
What is BMR?
Woman sleeping and burning calories
A person should calculate their BMR first, to determine how many calories they burn during sleep.
It is essential for the body to use energy continuously for maintenance and to function correctly. Although the body burns some of its calories through physical activity, basal metabolism accounts for around 80% of all energy expenditure.
Basal metabolism refers to all of the processes that keep the body alive, functioning, and healthy. These include:
• breathing
• blood circulation
• cellular growth and repair
• brain and nerve function
• temperature control
These metabolic processes require a constant supply of energy, so the body is always burning calories, even when a person is resting or sleeping.
BMR is the number of calories that the body burns every 24 hours due to basal metabolism. Essentially, it is how many calories a person would use in a day if they just rested and did no physical activity.
Many different factors affect BMR, including age, body size, sex, and genetics. For this reason, everyone’s BMR is different.
Calculating BMR
To determine how many calories the body burns during sleep, it is first necessary to calculate the BMR. This calculation is not straightforward because many factors influence BMR.
Accurately measuring BMR requires using special equipment to determine how much oxygen a person is breathing in and out over a specified period.
However, it is possible to estimate BMR using the Harris-Benedict equation, which takes into account a person’s sex, height, weight, and age.
For females, the formula is:
BMR = 665.1 + (4.34 x weight in pounds) + (4.7 x height in inches) – (4.68 x age in years)
For males, the formula is:
BMR = 66.47 + (6.24 x weight in pounds) + (12.71 x height in inches) – (6.78 x age in years)
These formulae will give the number of calories that the body will burn over a whole day due to its BMR alone.
For example, a 40-year-old male who weighs 195 pounds (lb) and is 5 feet (ft) 9 inches (in) tall would have an approximate BMR of 1,889 calories per day:
BMR = 66.47 + (6.24 x 195) + (12.71 x 69) – (6.78 x 40)
BMR = 66.47 + 1,216.8 + 877.0 – 271.2
BMR = 1,889.07 calories per day
A 50-year-old female who weighs 160 lb and is 5 ft 4 in tall would have an approximate BMR of 1,426 calories per day:
BMR = 665.1 + (4.34 x 160) + (4.7 x 64) – (4.68 x 50)
BMR = 665.1 + 694.4 + 300.8 – 234
BMR = 1,426.3 calories per day
Calculating calories burned while sleeping
The body continues to burn calories throughout the night to support its metabolic processes. However, because the body is physically inactive, the metabolic rate is around 15% lower when a person is asleep than when they are awake.
To estimate how many calories the body burns during sleep, a person needs to calculate their hourly BMR and multiply that by the number of hours that they sleep before reducing the figure by 15%.
They can do this using the following formula:
Calories burned while sleeping = (BMR / 24) x number of hours asleep x 0.85
The 40-year-old male who weighs 195 lb and is 5 ft 9 in will burn approximately 535 calories during an 8-hour sleep:
Calories burned asleep = (1889.07 / 24) x 8 x 0.85
Calories burned asleep = 78.71 x 8 x 0.85
Calories burned asleep = 629.68 x 0.85
Calories burned asleep = 535.23 calories
The 50-year-old female who weighs 160 lb and is 5 ft 4 in will burn approximately 404 calories during an 8-hour sleep.
Calories burned asleep = (1426.3 / 24) x 8 x 0.85
Calories burned asleep = 59.43 x 8 x 0.85
Calories burned asleep = 475.43 x 0.85
Calories burned asleep = 404.12 calories
It is important to remember that these calculations provide only a rough estimate of BMR and calories burned while sleeping.
Factors that affect BMR
mage of scales and measuring tape
Height and weight can influence BMR.
A range of factors can influence a person’s BMR. These include:
• age
• gender
• ethnicity and race
• height and weight
• hormone levels
• muscle-to-fat ratio
• physical activity levels
• diet
• amount and quality of sleep
• pregnancy and lactation
• general health
• health conditions that affect the metabolism, such as hypothyroidism and hyperthyroidism
Sleep hygiene tips
Getting enough sleep is vital to a person’s physical and mental health. Both the amount of sleep and its quality are important. Not getting enough quality sleep can affect a person’s energy levels, mood, concentration, and work performance.
According to the National Institute of Neurological Disorders and Stroke, research shows that inadequate sleep can also increase a person’s risk of several health conditions, including:
The American Academy of Sleep Medicine and the Sleep Research Society recommend that people between the ages of 18 and 60 years get at least 7 hours of sleep every night.
Some tips that can help improve a person’s quality of sleep include:
• avoiding caffeine or other stimulants in the hours before bedtime
• going to sleep and waking up at the same time each day
• getting regular exercise
• ensuring that the bedroom environment is dark, comfortable, and cool
• waking up to natural light
• doing something relaxing before bed, such as reading a book or taking a warm bath
Summary
Even when resting or asleep, the body is constantly burning calories to sustain a range of vital bodily functions, which we refer to collectively as the basal metabolism. Basal metabolism incorporates all of the processes that keep the body alive, functioning, and healthy, such as breathing, blood circulation, and brain function.
BMR is the number of calories that the body burns each day due to basal metabolism. BMR depends on a variety of factors, such as age, body size, and genetics. As a result, everyone’s BMR will be different.
A person can estimate their daily BMR using a formula that takes into account their sex, age, weight, and height. Using this BMR value, it is possible to estimate how many calories the individual burns while sleeping.
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Citrom és Rák: Védőek?
Tartalomjegyzék:
Videó: Citrom és Rák: Védőek?
Videó: Citrom és Rák: Védőek?
Videó: Bruno x Spacc - Rémálom ( OFFICIAL VISUALIZER ) [ PARANOIA ALBUM ] 2023, Lehet
Citrom és Rák: Védőek?
Citrom és Rák: Védőek?
Anonim
adding more lemons to a whole food, plant-based diet may reduce your risk of cancer.
lemons are popular in many cuisines, but they also have a long history of medicinal uses. you may wonder about the benefits of lemon for cancer prevention or as part of your diet during cancer treatment. here's what the research says.
read more: benefits and side effects of lemon juice
what makes lemons so healthy?
lemons contribute little in terms of calories, carbs or fiber. they contain just a trace of most vitamins and minerals. instead, their superpower comes from phytonutrients - health-promoting plant compounds.
one key nutrient is vitamin c. the pulp of one lemon provides 34 milligrams of it, according to the usda. (that's about a third to half of your daily value, per mayo clinic.) this vitamin plays many roles in your body. the office of dietary supplements explains that one of its most important functions is as a powerful antioxidant. antioxidants prevent oxidative damage to your cells and dna from free radicals, harmful molecules generated both inside your body and in the environment.
according to a january 2020 review study in the journal plants , lemons are a source of many other important antioxidants, found in nearly every part of the fruit - pulp, juice, seeds and peel. they include:
• flavonoids naringin, hesperidin and quercetin, among others.
• phenolic acids like ferulic acid and synaptic acid.
• limonoids.
lab tests on these compounds show that they have anti-inflammatory and anti-cancer properties, according to the review.
benefits of lemon for cancer
as for a link between lemons and fighting cancer, research has focused on how isolated compounds in lemons affect cancer cells in the lab. according to the plants study, the active compounds inhibit the growth of some cancer cells and tumors and can induce apoptosis, or cell death, in others.
naringin and hesperidin are two of the most abundant and well-researched antioxidant compounds in lemons and other citrus fruits. according to a study published in november 2016 in nutrients , they have anti-cancer benefits for prostate, breast, stomach, liver, cervix, pancreas and colon cancer cells.
it's important to note that these findings are from controlled studies on cancer cells in a lab. there is no direct evidence that eating lemons or drinking lemon juice can kill cancer cells or inhibit their growth in people. instead, human studies look at diet patterns in large groups of people to see if there might be a link between certain foods and cancer risk. it turns out that citrus fruit-eaters do, in fact, have a lower risk of several different types of cancer.
for example, an analysis of 17 small studies, published in the may 2018 issue of the journal pharmacological research , looked at the risk of oral cancer in people who ate citrus fruits. compared to people who ate very little citrus fruits, those who ate the most had a 50 percent reduced risk of oral and pharyngeal cancers. still, population studies don't show a cause and effect, only an association, so it's not clear if one type of citrus played a role or if other lifestyle factors contributed to the lower cancer risk.
lemons and anti-cancer diets
the national cancer institute cautions that no one food can prevent or cure cancer. but the combination of a healthy diet and lifestyle may reduce your risk. a whole food, plant-based diet is what most cancer specialists recommend.
kim dalzell, phd, rd, founder of cancer nutrition advisor and an oncology nutrition specialist in colorado springs, colorado, believes in the power of plants, and especially citrus fruits, for those with cancer or anyone who wants to reduce their risk. "citrus fruits are full of bioflavonoids, which help repair dna, support immunity and reduce inflammation, " says dalzell. "those functions positively impact several cancer control pathways."
the best way to include lemons in an anti-cancer diet isn't to eat them whole or drink lemon juice all day. indeed, the american dental association lists citrus as one of the top foods that can damage teeth and irritate your mouth.
instead, add various parts of the fruit to other healthy foods. use lemon juice on fish, add a bit of the pulp to your smoothie, and make good use of the peel by zesting it. says dalzell, "use a pinch of lemon zest to brighten up sauces, vinaigrettes and baked goods because the peel contains more vitamin c per ounce than the fruit itself."
read more: the best foods to eat if you have cancer
A téma által népszerű
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A lesson on the glycemic index
How – and if – having a working knowledge of the glycemic index can help you cut the pounds.
A classification of carbohydrate foods and their influence on your blood sugar levels, the glycemic index permeates the world of quick-fix diets.
From the Zone Diet to Sugar Busters to Nutrisystem, the glycemic index reigns supreme. Originally, diets revolving around the glycemic index were first created as a way to help control diabetes, but were later found to benefit anyone who needed to lose weight.
Glycemic index diets (often called low GI diets) aren’t like your traditional carb-counting or low-fat diets. On a glycemic index diet, you don’t count carbs and you don’t count calories, but you watch what type of carbs you eat. This is where the index comes in. The glycemic index tells you what kind of carbs to eat and drink in order to balance your blood sugar level. Advocates of a glycemic index diet claim such a diet will help you lose weight and reduce your risk for certain disease.
Are the claims true?
Glycemic index diets are based on the idea that high blood sugar levels are directly related to health problems such as obesity, heart disease, and diabetes. Therefore, eating a diet that balances your blood sugar is thought to reduce your risk for such health conditions.
When you eat or drink carbs (sugars, starches, fiber), your body converts them to sugar. This sugar enters your blood, where it then reaches cells and provides your body with energy or gets stored in your muscles and liver to be used later. The hormones insulin and glucagon then help regulate the amount of sugar in your blood. Certain foods disrupt the balance of your blood sugar by causing a spike or drop. Over time, this fluctuation of blood sugar can lead to insulin resistance, which can lead to the health conditions listed above.
If you desire to eat foods that are good for your blood sugar level, the glycemic index is what you need. It ranks carbohydrate-containing foods and drinks from zero to 100. Foods with high numbers are digested quickly and cause your blood sugar to spike. Foods with a low score are digested slowly and keep your blood sugar at a nice, even level. Since these foods are digested slower, they keep you feeling fuller for longer and help with weight management.
Here are where some of your favourite foods fall on the scale.
Fifty-five or less: Low. Foods include raw apples, peas, raw carrots, peanuts, skim milk, lentils and kidney beans.
Fifty-six – 69: Medium. Foods include bananas, raisins, sweet corn, pineapple, and certain ice creams.
Seventy and above: High. Foods include brown rice, instant white rice, skinless baked potato, white bread, and watermelon.
Many wonder what it is about the glycemic index diet that makes for weight loss success. Is it eating foods that regulate blood sugar? Is it because it’s not an extreme diet, so it’s easier to maintain long term? Or is it because you eat more protein and fiber, which reduces your portion sizes? Depending on where you ask your questions, the answers vary.
But the real answer to weight loss is always the same – reduced calorie intake and additional calorie burning. That means eating less and working out more. Any diet that helps you lose weight will reduce your risk factors for certain health conditions.
A quick look at the glycemic index will show that healthy foods are low on the scale, but some unhealthy foods also score low. Surprisingly, ice cream and potato chips are lower on the index than baked potatoes. But don’t let this number fool you. When dealing with the glycemic index, you can’t just go by the numbers. You’ve got to use a dash of common sense as well.
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第二产程
2016-09-14 17:20 阅读： 编辑：sunyoung 来源：
标签： 第二产程 分娩
分享到：
内容简介：第二产程是指胎儿娩出期，指从子宫口开全到胎儿娩出。初产妇约需1～2小时，经产妇较快，但也有长达1小时者。一般情况下，第二产程不得超过2个小时。
第二产程（胎儿娩出期）指从子宫口开全到胎儿娩出。初产妇约需1～2小时，经产妇较快，但也有长达1小时者。第二产程不得超过2个小时。为达到经阴道自然分娩，胎头在下降过程中必须不断适应产道径线的变化，为达到这一目的，儿头位置按以下顺序产生一系列的变化：俯曲、内旋转（胎头旋转90°，枕骨朝前）、仰伸、复位及外旋转。这些过程主要发生在第一产程末和第二产程。
第二产程
一、临床表现
宫口开全后，胎膜多已破裂。此时胎头应下降至盆底并压迫直肠，故使产妇有排便感和不自主的向下用力屏气的动作。此时，宫缩更加频繁，约1—2分钟一次，每次持续时间可达1分钟。当胎头降至骨盆出口时，会阴逐渐膨隆变薄，肛门被压开并逐渐在阴道口可见胎头。开始时，宫缩时胎头露出于阴道口外，间歇期又缩回，称为胎头拨露。随着产程继续进展，胎头露出的部分逐渐增多，在宫缩间歇时也不缩回，称着冠。
此时，胎头的双顶径已达阴道口，会阴极度扩张变薄，应注意保护会阴。当胎儿枕骨到达耻骨弓下方后，宫缩时胎头仰伸，依次将额、鼻、口和颏部相继娩出。胎头娩出后发生转回和外旋转，此时胎肩到达阴道口处，随之前肩和后肩以及胎体也相继娩出，后羊水跟着涌出。胎儿娩出后产妇顿觉轻快。
二、主要流程
第二产程时医生在阴道检查以明确胎位，指导产妇在每次宫缩时配合用力屏气,使胎头逐渐下降,经过盆腔,逐渐扩张阴道口。宫缩时,接生者用左手掌覆于胎头上控制胎头的进展速度。右手手指弯曲保护会阴部,协助胎儿娩出，接生者对胎头娩出速度的控制是分娩安全的关键。
第二产程
当胎头娩出后,胎体旋转,双肩处于出口前后径位置,轻压胎头,前肩自耻骨弓下娩出。胎头略抬高,后肩从会阴处娩出,最后胎体相继娩出。助产士清理新生儿的呼吸道，吸尽口、鼻、咽的黏液和羊水,刺激新生儿的脚心，就能听见宝宝的响亮的第一声啼哭了，然后进行脐带处理,最后将新生儿放置于温暖的婴儿床或母亲怀中，就能够看到宝宝的样子了。
三、产程的观察和处理
1、观察产程和胎心：第二产程时宫缩更加频和强，所以要特别注意观察胎心的变化。尤其要注意胎心与宫缩的关系，如出现胎心变慢而且在宫缩后不恢复或恢复慢，应尽快结束分娩。
2、指导产妇用力：宫口开全后，指导产妇正确的屏气用力，以增加腹压并使产程加快。产妇的两脚蹬在产床或腿架上，两手握住产床上的扶手，当宫缩时，产妇先吸一大口气，然后屏气使腹肌和膈肌收缩，两手向上拉扶手，而身体向下用力如排便样，宫缩后产妇呼气并使全身放松。宫缩再次出现时，重复上述动作。当胎头着冠后。宫缩时不应再令产妇用力，以免胎头娩出过快而使会阴裂伤。此时应指导产妇在宫缩时张口哈气，在宫缩间歇屏气用力，使胎头和胎肩缓慢娩出。
四、接生
第二产程
1、产妇的体位：目前国内产妇分娩时采用的体位有两种，即仰卧位分娩和坐位分娩。
2、接生和保护会阴：仰卧位分娩时，接生者站在产妇的一侧（右手保护会阴者站在产妇的右侧，左手保护会阴者站在左侧）。当胎头拨露时即开始保护会阴。保护会阴的原则是，按照分娩机制协助胎儿娩出，并控制胎头和胎肩娩出的速度，不使因娩出过快而造成会阴裂伤。
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Home > Adrenal Fatigue
Stress and Adrenal Fatigue
adrenal fatigue
We will start this basic discussion with the hormone cortisol. Cortisol, produced from cholesterol in the adrenal glands, is a member of the family of steroid hormones and is widely known as the "stress hormone". When your body experiences a stressor, your adrenal glands secrete cortisol into your bloodstream. A rise in your cortisol level acts to give you a quick burst of energy, to heighten your memory functions, to increase your immunity, and to lower your sensitivity to pain. This is an effective system, as long as this rise in cortisol level is "turned off" relatively quickly and you don't need to use this "flight or fight" response too often.
Unfortunately, in today's hectic world, our cortisol levels can frequently be elevated with the job of dealing with day-to-day stress. For some of us, our cortisol gets "stuck on high", and for many of us, our adrenal glands can become exhausted from overproduction.
If it isn't tough enough on the body that its stress-handling glands are overworked, cortisol happens to play an essential role in many vital bodily functions -- regenerative processes, protein synthesis, inflammatory mediation, blood sugar regulation, mood, cognition, memory, and more. Fortunately or unfortunately, the body prioritizes its cortisol use for handling day-to-day challenges, tensions, and pressures -- almost always at the expense of other core bodily functions. This means that for many of us, cortisol is shunted away from its critical role in regenerating the colonic mucosa, rebuilding bones, keeping blood sugar stable, regulating the sleep cycle, and other processes vital to long-term health.
clouds and sea
In other words, if your cortisol levels remain too high over extended periods, you cannot fully heal, so if you are not already struggling with your health, you are likely to be soon. For a short time, high cortisol is functional. However, sustained high cortisol essentially tears your body down, weakening muscle and bone, slowing down normal cell regeneration, co-opting biochemicals needed to make other vital hormones, impairing digestion, metabolism, and cognitive function, interfering with healthy endocrine function, and weakening your immune system.
Because of the importance of keeping the hormone cortisol in a persistent optimal range, it is crucial to good health to monitor your cortisol levels seasonally and, if needed, to support the adrenal glands via lifestyle changes, herbs, and/or supplements.
I recommend the quality products below for adrenal support. Please also read my #1 Health Tip, which speaks fundamentally to long-term adrenal health!
By Kristina Amelong, CCT, CNC
I-ACT-Certified Colon Hydrotherapist
Certified Nutritional Consultant
ADRENAL STRESS INDEX (ASI)
The most effective and inexpensive way to monitor your cortisol levels seasonally is via a multi-sample saliva test. Called Adrenal Stress Index (ASI), this type of saliva test is offered by our lab partner Diagnos-Techs, Inc..
The Adrenal Stress Index (ASI) consists of 4 saliva samples which are submitted for the following 10 tests:
4 x Cortisol
Helps evaluate stress response
2 x Insulin
Helps investigate blood sugar control
DHEA
Helps determine stress adaptation
Secretory IgA
Helps evaluate toll on immunity, including gut permeability
17-OH Progesterone
Helps determine adrenal reserve
Gluten Antibodies
Helps identify grain intolerance
LEARN MORE
Herbal Tonic to Boost Immune System and Regulate Cortisol OHN REAL Herbal Tonic - 240 ml
The herbs in this Optimal Health Network tonic -- rehmannia, echinacea, ashwaganda and licorice root -- work together to boost the immune system, regulate cortisol levels, and overall contribute to optimal health.
$85.00
Ortho Adren-All 120 count Ortho Adren-All - 120 capsules
Ortho Adren-All is an effective supplement for reducing stress and fatigue. It restores balance and well-being for the adrenal glands.
Resale Prohibited: Learn More
$53.20
Ortho Adren-All 60 count Ortho Adren-All - 60 capsules
Ortho Adren-All is an effective supplement for reducing stress and fatigue. It restores balance and well-being for the adrenal glands.
Resale Prohibited: Learn More
$30.40
AdreneVive Stress Resilience Ortho AdreneVive - 60 capsules
AdreneVive improves stress resilience, supports healthy energy levels, strengthens the body’s stress response, improves mental and physical performance, and supports healthy cortisol levels.
Resale Prohibited: Learn More
$50.80
Ortho DHEA - 5 mg Ortho DHEA 5 mg - 100 tablets
Ortho DHEA promotes healthy hormonal balance and supports mood regulation.
Resale Prohibited: Learn More
$13.50
Ortho Thyrotain Ortho Thyrotain - 120 capsules
Thyrotain helps maintain a healthy thyroid function, promotes the synthesis of thyroid hormones, supports a healthy metabolism, and helps improve stress responses.
Resale Prohibited: Learn More
$39.40
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• Research article
• Open Access
A random set scoring model for prioritization of disease candidate genes using protein complexes and data-mining of GeneRIF, OMIM and PubMed records
BMC Bioinformatics201415:315
https://doi.org/10.1186/1471-2105-15-315
• Received: 7 January 2013
• Accepted: 17 September 2014
• Published:
Abstract
Background
Prioritizing genetic variants is a challenge because disease susceptibility loci are often located in genes of unknown function or the relationship with the corresponding phenotype is unclear. A global data-mining exercise on the biomedical literature can establish the phenotypic profile of genes with respect to their connection to disease phenotypes. The importance of protein-protein interaction networks in the genetic heterogeneity of common diseases or complex traits is becoming increasingly recognized. Thus, the development of a network-based approach combined with phenotypic profiling would be useful for disease gene prioritization.
Results
We developed a random-set scoring model and implemented it to quantify phenotype relevance in a network-based disease gene-prioritization approach. We validated our approach based on different gene phenotypic profiles, which were generated from PubMed abstracts, OMIM, and GeneRIF records. We also investigated the validity of several vocabulary filters and different likelihood thresholds for predicted protein-protein interactions in terms of their effect on the network-based gene-prioritization approach, which relies on text-mining of the phenotype data. Our method demonstrated good precision and sensitivity compared with those of two alternative complex-based prioritization approaches. We then conducted a global ranking of all human genes according to their relevance to a range of human diseases. The resulting accurate ranking of known causal genes supported the reliability of our approach. Moreover, these data suggest many promising novel candidate genes for human disorders that have a complex mode of inheritance.
Conclusion
We have implemented and validated a network-based approach to prioritize genes for human diseases based on their phenotypic profile. We have devised a powerful and transparent tool to identify and rank candidate genes. Our global gene prioritization provides a unique resource for the biological interpretation of data from genome-wide association studies, and will help in the understanding of how the associated genetic variants influence disease or quantitative phenotypes.
Keywords
• Semantic Similarity
• Causal Gene
• Unify Medical Language System
• Global Ranking
• Phenotypic Profile
Background
Genome-wide association studies (GWAS) have been successful in the discovery of many novel genetic variants associated with human diseases. However, identifying the causative variant(s) is still a daunting task, as the mechanisms through which the variants influence disease or quantitative phenotypes are often unclear, particularly when the associated genes are of unknown function or have no clear connection to disease biology. Network-based approaches to prioritize candidate genes associated with human diseases have been proposed in a number of studies [16]. They build on the idea that mutations in the same gene or mutations in different members of a gene complex, which here are defined as a set of genes sharing (the deleted) functional identity, may lead to similar disease phenotypes. The functional identity of a gene complex can be co-expression patterns, or functional association of proteins in physical complexes or in pathways. This means that, once a gene complex with members involved in one disease has been identified, the other members of the complex become candidates for having a biological relationship with the same disease.
Thus, a method of disease gene prioritization is to search for genes or gene complexes that have a phenotypic profile similar to the phenotypic profile of the target disease. The disease phenotype can be described as the disease characteristics such as pathogenesis and clinical features. Biomedical records in the life sciences (e.g., OMIM, GeneRIF, PubMed) provide reviewed facts under a wide variety of biological conditions. A global examination of biological textual data will thus establish the phenotypic profile of genes with respect to their connection to disease biology. The phenotypic profile of a gene, referred to as the gene-associated phenotype, can be obtained by large-scale text-mining of biomedical records using information extraction and retrieval techniques, and filtering the biomedical terms with specific vocabularies such as that from the Unified Medical Language System (UMLS) [7].
A potential bottleneck in phenotypic profiling using text-mining of biomedical records is that currently the candidate genes can be of unknown function or have no clear connection to known disease biology. However, network-based inference may partially alleviate this problem, because the phenotypic profile of a candidate gene will be based on all phenotypes linked to the genes in a protein complex that consists of physical interactions or functional associations, rather than just to the gene itself.
This poses the need for a method that can summarize the relevance signals between the disease and candidate complex as a whole. Because the information to be integrated in this approach (i.e., protein complexes, biomedical text records, and associations between genes and textual records) is frequently updated and the choice is optional (e.g., the use of PubMed abstracts instead of OMIM records), it also requires a method that easily adapts to these factors. A promising method is based on a random-set scoring model used for gene-set enrichment analysis of genome-wide expression data [8]. It can be used to compute a score per gene or per complex representing an overall enrichment signal for the association of the candidate gene with the disease. It is computationally fast [9] and it can be calibrated in a number of ways (e.g., few gene-associated phenotypes that are highly similar to the disease phenotype or many gene-associated phenotypes moderately similar to the disease phenotype), providing a flexible and powerful way to quantify the relevance of the candidate gene to the disease.
The network-based phenotypic profile of a candidate gene depends on several factors. These include the source or the type of the biomedical records and the type of vocabularies [9, 10], such as Medical Subject Headings (MeSH) [11] and International Classification of Diseases (ICD), as well as the stringency of protein associations to define the protein complexes. These factors may affect disease gene prioritization regardless of the quantification method used. Examining the influences of these factors will provide a thorough evaluation of the prioritization performance of the random-set scoring model.
The objectives of this study were 1) to implement and validate a random-set scoring model to quantify the disease relevance of genes in a network-based disease gene-prioritization approach; 2) to investigate the influence on the model of protein association validity and the type of gene-associated phenotypic profile; and 3) to apply this model to identify and rank human genes on a genome-wide scale according to their phenotypic relevance to a wide range of human diseases.
Results
We implemented and validated a random-set scoring model for a network-based gene prioritization approach. This approach uses biomedical records (e.g., OMIM, PubMed, and GeneRIF) as phenotypic profile for candidate genes to infer their association with diseases. The candidate gene is prioritized as a gene complex based on the physical and functional protein-protein interaction (PPI) network from STRING [1218]. We validated our approach using the known disease and gene relationships in the OMIM database. Several of the key factors in the prioritization approach were investigated including the influence of the PPI confidence score threshold, distinct sources of gene-associated phenotypes and different vocabularies. We also compared the prioritization ability of the random-set scoring model with two alternative network-based prioritization approaches. Finally, the approach was used for a global ranking of all human genes according to their relevance for a range of human diseases in OMIM.
Influence of protein-protein interaction (PPI) confidence scores
We investigated the influence of protein complexes defined with different confidence thresholds on the performance of our network-based prioritization approach. The prioritization was examined with various confidence scores (500–990) of protein complexes, corresponding to different levels (median to high) of PPI quality (0.75–0.99) in STRING. The result (Figure 1) showed that, at the maximum Matthews correlation coefficient (MCC) (see Additional file 1), the precision of the method increased from 0.18 to 0.59, positively correlated with the PPI confidence scores. The sensitivity (recall) of the method was consistent, ranging between 0.31 and 0.34, using various protein complexes; only when the confidence threshold was relaxed to 500 or restricted to 990 did the sensitivity increase to 0.38 and decrease to 0.26, respectively. We then compared the number of highly ranked causal genes for different PPI confidence thresholds (Figure 2). The proportion of causal genes that could be ranked in the top one (top five) was between 0.28 (0.58) and 0.48 (0.77). Increasing the PPI confidence threshold led to a larger percentage of causal genes being highly ranked. However, with higher PPI confidence scores the proportion of causal genes that could be prioritized decreased from 0.89 to 0.45, primarily because of the availability of PPIs dependent on the confidence thresholds (see Additional file 1).
Figure 1
Figure 1
Performance of the approach using different protein-protein interaction (PPI) confidence score thresholds. The influence of different PPI thresholds on the precision (red) and recall (black) is shown. The precision (y-axis) and recall (y-axis) were determined for each PPI threshold (x-axis) at the maximal Matthews correlation coefficient (MCC).
Figure 2
Figure 2
Influence of protein-protein interaction (PPI) thresholds on the prioritization of causal genes in the test sets. The proportion (y-axis) of prioritized test-sets where causal genes were ranked within the top five (black) or top one (red) is shown according to different PPI confidence score thresholds (x-axis).
Influence of gene-associated phenotype sources and phenotype vocabulary filters
The biomedical records from three different databases (OMIM, PubMed, and GeneRIF) together with four vocabulary filters (MeSH, ICD ninth revision, clinical modification (ICD9CM), Gene Ontology (GO), and Semantic Type (STY) defined 12 sets of phenotypic profiles (see Additional file 1). Our overall evaluation showed that the random-set scoring model was an accurate and reliable predictor for disease gene prioritization. The area under the receiver operating characteristic (ROC) curve (AUC) was between 0.70 and 0.90 (Figure 3 and Table 1) for all the phenotypic profiles. Prioritization performance went in decreasing order for OMIM, PubMed, and GeneRIF. For the vocabulary filters, STY and MeSH were superior to ICD9CM and GO in revealing disease gene associations. The best performance, with an AUC of 0.85–0.90 (Table 1), was based on using OMIM records or PubMed abstracts with STY or MeSH.
Figure 3
Figure 3
Receiver operating characteristic (ROC) curves of prioritizations using different phenotype sources and vocabulary filters. Each ROC curve represents the prioritization performance when combining a specific gene-associated phenotype with a vocabulary filter. The phenotype sources were OMIM (brown), PubMed (green), and GeneRIF (purple). The vocabulary filters were STY, MeSH, ICD9CM, and GO (colored from dark to light accordingly).
Table 1
Comparison of AUC (area under the curve), precision, and recall using different sources for the gene-associated phenotypes and phenotype vocabulary filters
OMIM
PubMed
GeneRIF
AUC
Precision
Recall
AUC
Precision
Recall
AUC
Precision
Recall
STY
0.90
0.52
0.48
0.87
0.40
0.43
0.82
0.40
0.32
MeSH
0.89
0.48
0.49
0.85
0.36
0.38
0.83
0.36
0.37
ICD9CM
0.81
0.31
0.38
0.75
0.31
0.28
0.71
0.35
0.19
GO
0.82
0.38
0.30
0.73
0.32
0.18
0.71
0.23
0.19
AUC, area under the curve.
The gene prioritizations were consistent across different phenotypic profiles. For example, our model ranked 50% (OMIM), 40% (PubMed), and 40% (GeneRIF) of the prioritized causal genes as the top candidates (Additional file 1: Table S10) according to the different phenotypic profiles (MeSH terms). Impressively, at least 57% of these cases were accurately predicted by all types of biomedical records. When taking only the causal genes that were ranked in the top five, the proportion was even higher (75%). When examining the prioritization results from any two phenotypic profiles, the common set of top-ranked causal genes accounted for a minimum of 39–82% between biomedical records, and 28–91% between vocabulary filters (Additional file 1: Tables S8 and S9). When applying protein complexes defined by different stringencies, the prioritization was generally more robust between two similar confidence scores than between two that were substantially different from each other (e.g., between 500 and 990) (Additional file 1: Figure S4).
Comparison with other methods
We compared the prioritization ability of our random-set scoring model with that of two other network-based prioritization approaches that rely on gene-associated phenotypic profiles: a Bayesian prediction model proposed by Lage et al. [4] and a regression prediction model, CIPHER-DN, proposed by Wu et al. [6]. We estimated the recall and precision specifically for these comparisons using our matching test-sets. One group consisted of 84% (1177/1404) of the test cases from Lage et al. and the other consisted of 83% (1193/1444) of the test cases from Wu et al. The protein networks used in these approaches were restricted to protein interaction data that did not include the co-occurrence of genes in the biomedical literature. Our approach is based on protein complexes retrieved from the STRING database, which integrates both physical interactions and predicted protein associations based on multiple information sources, including text-mining of PubMed records for the co-occurrence of two genes. To assess the influence of gene co-occurrence in the literature, we recalculated the PPI confidence scores independent of the text-mining evidence (see Additional file 1). Table 2 shows the prioritization performance of the three different approaches. Our model demonstrated higher recall (0.43 versus 0.21) and higher precision (0.56 versus 0.45) than the Bayesian prediction approach. When adding the predicted interactions based on text-mining of the biomedical literature, the superiority of our method became more obvious. Our approach worked almost equally as well as the regression prediction approach (recall: 0.57 vs. 0.55; precision: 0.52 vs. 0.55) when the evidence from text-mining was included. When the protein complexes were defined excluding the text-mining evidence, we observed a decrease in recall whereas precision remained largely unaffected.
Table 2
Comparison with other network-based approaches
Testing sets
Evaluation metrics
Random-set scoring model
Bayesian/regression method
*PPI evidence incl. co-mention
PPI evidence excl. co-mention
Bayesian
Recall
0.55
0.43
0.21
Precision
0.58
0.56
0.45
Regression
Recall
0.57
0.43
0.30 − 0.55
Precision
0.52
0.47
0.73 − 0.55
*PPI, protein-protein interaction.
Global ranking of human genes according to their disease relevance
We performed a genome-wide phenotypic screen (Additional file 1 in project website) on 19,032 human genes to predict their relevance to a range of disorders represented in the OMIM database (3053 phenotype descriptions). For many of these disorders, the molecular basis is known and does not represent a unique locus. We pinpointed the responsible causal gene for the corresponding disorder as the top candidate in 8% of known heterogeneous relationships. We observed that 66% of causal loci were ranked in the top 1% across the whole genome for causality with the associated disorder. Our genome-wide predictions provide a global ranking list, thus suggesting novel yet-to-be-validated candidate genes for a large number of human disorders.
We identified 680 (3.6%) genes that were ranked at least once as the top candidate gene for another range of (1921) OMIM phenotypes for which no susceptible loci have been identified. The gene most frequently (78 times) top-ranked (for 4% of the phenotypes) was catechol-O-methyltransferase (COMT).
To evaluate the ability of our gene-prioritization model to identify known disease genes as well as to identify unknown susceptibility factors, we selected two neurodegenerative disorders: amyotrophic lateral sclerosis (ALS; OMIM id: 105400) and Parkinson disease (PD; OMIM id: 168600). For both disorders, several causal genes have been identified although additional genetic risk factors remain to be found [19, 20]. The positions of recognized disease genes according to the prioritization model for each disease were identified. Thus, ten ALS-associated genes SOD1 (position 9), FUS (position 34), ANG (position 19), TARDBP (position 1), ALS2 (position 4), VAPB (position 29), OPTN (position 190), VCP (position 46), MAPT (position 32), C9ORF72 (position 126) were prioritized among the top 1%, while an additional four genes (SETX (position 816), FIG 4 (position 1024), DAO (position 1441), SPG11 (position 1085) were among the top 7.5%. One gene SIGMAR1 position 2809) occurred among the top 15%, while only one of the known ALS-associated genes, UBQLN2 (position 16068), failed to be highly prioritized by our approach. For PD, the six top-ranked genes, ATP13A2 (position 1), LRRK2 (position 2), PINK1 (position 3), PARK2 also known as PRKN (position 4), PARK7also known as DJ1 (position 5), and SNCA (position 6) are all recognized disease genes, whereas additional genes linked to PD, UCHL1 and HTRA2, were ranked in positions 10 and 138, respectively [21]. Among the highly prioritized genes in which mutations have not yet been identified, we observed a number of highly interesting genes, including CCS (position 2), RNF19A (position 5), DERL1 (position 6), and XRN2 (position 10) for ALS, and KLK6 (position 7), SLC6A3 (position 8), and TPPP (position 9) for PD. The possible pathogenic roles of these genes are dealt with in the Discussion.
Discussion
We have implemented and validated a network-based disease gene-prioritization approach using a random-set scoring method. This approach prioritizes candidate disease genes using protein complexes and text-mining of the biomedical literature. We examined the influence of the key parameters of the approach, including the quality of the PPI information and the use of different sources of gene-associated phenotypes and vocabulary filters. Our implementation has a great transparency as it relies on publicly available data including PPI from the STRING database and biomedical publications from the National Center for Biotechnology Information (NCBI) databases. We used our approach to conduct a global ranking of all human genes for phenotypic association with a broad range of human diseases. These results provide a unique resource for the biological interpretation of results from GWAS, and will help understand how the associated genetic variants influence disease or quantitative phenotypes. Overall, we have shown that our network-based approach provides a powerful and flexible tool to identify and rank candidate disease genes.
Assessment of our network-based gene-prioritization approach
Comparison of the random-set scoring method with the Bayesian prioritization model [4] and the regression prioritization model [6] sheds light on the overall performance of network-based gene-prioritization approaches. The PPI data used in our study was from STRING, which is a public and comprehensive database that integrates various molecular interactions from other repositories including MINT (Molecular INTeraction database) [22], HPRD (Human Protein Reference Database) [23], and BIND (Biomolecular Interaction Network Database) [24]. By applying the original STRING data, we ensured the transparency and reliability of our approach. The STRING data includes both physical interactions and functional or predicted interactions derived from, for example, text-mining of the biomedical literature. The usefulness of text-mining of the biomedical literature in STRING is to enable searching for the co-occurrence of two biological entities (e.g., genes or proteins) in a textual context, and thereby establish an association between them. In contrast, the text-mining of the biomedical literature used in this study for gene prioritization was to convert a text record into a list of disease-relevant biomedical terms that phenotypically characterize the linked gene. These are two different applications of text-mining techniques for biomedical text data. Our result indicates that the use of text-mining in identifying the co-occurrence of two genes in biomedical text could provide new knowledge on PPIs, which could improve disease gene identification.
Our scoring method is very similar to gene set enrichment analysis (GSEA) commonly used in expression analyses where gene-level scores (i.e. differential expression levels) are used for detecting the enrichment signal. In our procedure the gene-level scores are correlations measuring the similarity between text (an individual document or a set of documents) linked to the gene and text linked to the disease. A summary statistic is subsequently computed by averaging the correlations of the genes to the disease phenotype in the complex. The averaging is superior when the gene being tested contains many gene-associated phenotypes that weakly correlates with the target disease phenotype. This characteristic is in line with the hypothesis that complex diseases or traits are influenced by multiple genes and other environmental factors. Furthermore quite a number of studies comparing various GSEA approaches and gene set summary statistics show that the mean/sum statistics used in our procedure yield overall very good results [25]. We believe that contrary to other highly parametric Bayesian approaches, that our random-set scoring method is a simple, but robust approach for disease gene prioritization.
Influence of gene-associated phenotypes
Our approach has the option of choosing different types of biomedical records for gene-associated phenotypes, including those from OMIM, PubMed, and GeneRIF. We showed that the source influenced the performance of the model. The use of OMIM records resulted in the highest recall and precision when tested on the human diseases present in the OMIM database. This was not surprising because, using OMIM, the phenotype for the genes and the disease comprised the same type of data; OMIM is the primary source of phenotypic descriptions for human diseases in similar network-based prediction approaches [4, 6]. However, these other studies did not examine the effect of using other types of biomedical literature. OMIM records are curated text that reviews the relevant references, of which the majority is indexed publications in the PubMed database. PubMed comprises nearly half a million gene-phenotype associations that involve more than 28,000 human genes. This suggests that PubMed articles and abstracts provide global phenotypic information for gene prioritization on a genome-wide scale. Our results also support the importance and validity of PubMed as the best source of gene-associated phenotypes apart from OMIM. A great advantage of PubMed (and GeneRIF) is that it is not restricted to human studies, but also includes other organisms; the phenotypic and genetic discoveries based on experimental models (in, for example, the mouse) can provide great insight into human diseases. PubMed may capture the phenotype-genotype relationships more comprehensively than OMIM does. This has important implications for disease gene prioritization in livestock species [26], for which only a limited number of phenotypic descriptions have accumulated in disease databases (e.g., OMIA), although many more gene-associated phenotypes may exist in literature databases such as PubMed or GeneRIF. The performance evaluation using the set of known causal genes from OMIM could be potentially overestimated even if the associations between a test gene and diseases (including test disease) were excluded from validation study. This is because the PubMed abstracts may contain the information that a test gene is involved in a test disease (e.g. the association between the gene and disease could be mentioned in abstracts linked to proteins that interact with the protein encoded by the test gene). In addition the prioritization could perform modest in discovering novel disease genes, because these genes may have limited information in terms of phenotypes and PPI. Some study suggested using an older version of phenotypic source (e.g., PubMed) and newly discovered causal genes, which would give less biased estimation of the method [27] Alternatively, one can probably adjust the semantic similarity between phenotypes according to the publication years to control the bias.
Influence of the PPI interaction score
Protein complexes defined by high confidence PPI scores increased the precision of our network-based disease gene-prioritization approach. Thus, our results support the fact that the genes likely leading to similar disorders are strongly connected. Meanwhile, the recall was maintained for most PPI confidence score thresholds (600–950). However, further increasing the confidence threshold reduced the number of genes for which a candidate complex could be identified. The influence of protein confidence score thresholds was stronger on non-causal genes than on known causal genes in test. This is likely because known disease genes are usually better characterized and more frequently studied, and therefore have more known protein-protein interactions. Particularly, those disease genes which are also essential genes show a strong trend to encode hub proteins [28]. Despite the high stringency, we could have included more PPIs, particularly those non-physical functional associations predicted in STRING. In practice, this may help detect less-studied disease genes. It is important to note that our method is not limited to genes with known PPIs, although our validation was entirely dependent on the interaction partners of the causal genes. As long as the gene itself has one or more gene-associated phenotypes, we could quantify the association with any disease phenotype. This is a clear advantage compared with some existing network-based disease gene-prioritization approaches. In particular, as more information about gene function and PPI data become available, we expect that network-based approaches will become ever more accurate and sensitive in their ranking of candidate genes.
Global ranking of genes for human diseases in OMIM
We used our approach to generate a global ranking of all human genes according to their relevance to a large set of human diseases. These results provide a unique resource for the biological interpretation of results from GWAS and will help understand how the associated genetic variants might influence disease or quantitative phenotypes. In addition, the global ranking profile (Additional file 1 in project website) may help to identify a set of genes encoding for the proteins in the protein complex that have co-susceptibility/resistibility to a common set of disorders, and similarly, disease clusters that share relevant/irrelevant genes.
For a more detailed assessment of the ability of the gene-prioritization model to identify disease genes accurately, as well as to identify unknown susceptibility factors, we selected two complex disorders for closer scrutiny: ALS and PD. ALS is a neurodegenerative disease, usually of adult onset, caused by the loss of motor neurons in the brain and spinal cord. ALS is clinically characterized by progressive muscular paralysis, leading to respiratory failure and death usually within five years of diagnosis. A subgroup of ALS patients develops frontotemporal dementia. ALS is predominantly a sporadic disease, while 10% of cases are familial. To date, 13 genes and two chromosomal loci have been linked to ALS, two genes with ALS-frontotemporal dementia, and one gene with ALS-Parkinsonism-dementia complex [19]. Ideally, a prioritization model should rank all known causal genes in the top positions, which is essentially what we observed. Inspection of the prioritized genes showed that ten genes associated with ALS occurred among the top 1%, four genes were among the top 7.5%, one was in the top 15%, and only one gene was poorly prioritized. Importantly, the model also prioritized several genes that have not yet been annotated as being associated with ALS. One such gene was CCS, which encodes a copper chaperone for Cu, Zn-superoxide dismutase 1 (SOD1). CCS is essential for SOD1 activity because it delivers the copper cofactor to the enzyme and promotes oxidation of an intra-subunit disulfide bond, which is important for the structural stability of SOD1. SOD1 mutations are responsible for up to 20% of the hereditary forms of ALS, and a hallmark of both familial and sporadic cases of ALS is aggregates of misfolded SOD1 protein [29]. Ccs-null mice have markedly reduced Sod1 activity and, like Sod1-knockout mice, exhibit reduced fertility and an increased sensitivity to paraquat [30]. Furthermore, Ccs-deficient mice showed an increased loss of motor neurons after facial nerve axotomy, similar to Sod1 mutants [31]. Intriguingly, loss of Ccs did not affect the time of onset or progression of motor neuron disease in Sod1 mutants, whereas in contrast, over-expression of Ccs in a Sod1-mutant background strongly accelerated neurological disease. This occurred without the formation of insoluble Sod1 aggregates, but generated a markedly mitochondrial pathology, suggesting that Ccs may modulate disease progression by affecting the subcellular distribution of Sod1 between the cytosol and mitochondria [32, 33].
Another putative disease gene that might be linked to ALS is XRN2, which was ranked at position 10. The Xrn2 protein possesses 5′–3′ exoribonuclease activity and is involved in the termination of transcription. Behind the elongating RNA II polymerase, the nascent transcript forms RNA-DNA hybrid structures (R-loops), in particular in the G-rich pause sequences downstream of the poly(A) signal. The R-loops are subsequently resolved by the RNA/DNA helicase activity of senataxin, which is encoded by the ALS-related disease gene SETX[34]. This is a critical step because it allows the Xrn2 exoribonuclease to degrade the transcript from the free 5′ end generated by cleavage of the RNA at the poly(A) site, leading to transcriptional termination and the release of free RNA polymerase II [35]. The neurodegenerative mechanisms associated with mutations in SETX, and possibly also XRN2, are presently not understood. It is noteworthy, however, that Xrn2 has been shown to interact with TDP43, which is also involved in various aspects of RNA transcription and processing [36]. Mutations in the gene encoding TDP43, TARDBP, have been found in both familial and sporadic ALS [37]. Together, these observations support the notion that aberrant RNA processing plays a role in ALS pathogenesis [38].
Failure to fold newly synthesized proteins in the endoplasmic reticulum (ER) can result in the accumulation of misfolded proteins in the lumen, which activates ER stress signaling to protect the cell from the adverse effects of protein accumulation or aggregation [39]. For example, protein mutations may prevent their correct folding, which leads to retrotranslocation of the terminally misfolded proteins into the cytosol, where they are subjected to ubiquitin-dependent degradation in the proteasome, a process known as ER-associated degradation (ERAD). However, prolonged activation of ER stress may induce cell death by apoptosis, and the ER stress response has been shown to be involved in the pathogenesis of a number of different diseases, including SOD1-related ALS [40]. Interestingly, two of the genes that were prioritized by our pipeline, DERL1 and RNF19A, are implicated in the ERAD response to SOD1 mutations. Thus, DERL1 or derlin 1 (position 6) is most likely a component in the channel responsible for the retrotranslocation of proteins across the ER membrane, and derlin 1 has been demonstrated to interact specifically with mutated SOD1, apparently leading to the inhibition of ERAD and the induction of apoptotic death in motor neurons [41]. Likewise, the RNF19A gene product dorfin (position 5) is also implicated in protein degradation by virtue of its ubiquitin-ligase activity. Dorfin selectively ubiquitinates and degrades mutated Sod1 in a dorfin-mediated ubiquitin-proteasome pathway, thereby protecting neuronal cells against the toxic effects of mutated Sod1 [42]. Furthermore, overexpression of dorfin in a mouse model of ALS reduced the number of Sod1 aggregates in the spinal cord, reduced motor neuron degeneration, and increased the life-span of the mutant mice [43]. Finally, dorfin colocalizes with valosin-containing protein (VCP) in Lewy body-like inclusions composed of ubiquitinylated protein aggregates in both ALS and PD. The two proteins interact and the ATPase activity of VCP contributes to the ubiquitin ligase activity of dorfin [44]. Notably, mutations in VCP are associated with ALS [45]. Taken together, the tight association of derlin 1 and dorfin with the ER stress response and degradation of mutant Sod1 makes them strong candidates for ALS susceptibility.
PD is characterized by slow movements, rigidity, impaired balance, and tremor at rest, and the pathological hallmarks include degeneration of dopaminergic neurons in the substantia nigra and accumulation of protein inclusions or Lewy bodies within nerve cells of the substantia nigra and several other brain regions [21]. In addition to correctly identifying known disease-linked genes, our computational approach prioritized three unrecognized genes among the top ten candidates. Among these was KLK6, also called neurosin, which encodes a serine protease primarily expressed in nervous tissue. Interestingly, neurosin is able to degrade alpha-synuclein, which is a major constituent of Lewy bodies in the brains of PD patients as well as one of the known disease genes. Thus, fragmentation of alpha-synuclein by neurosin inhibits the polymerization and aggregation of alpha-synuclein, suggesting that neurosin may play a role in pathogenesis [46]. Our model further suggested an involvement for SLC6A3, a dopamine transporter, an obvious candidate risk factor considering that PD is associated with the loss of dopaminergic neurons. Indeed, loss-of-function mutations in SLC6A3 have recently been linked to a complex movement disorder involving infantile Parkinsonism and dystonia [47, 48]. Finally, the TPPP gene, encoding the tubulin polymerization-promoting protein or p25alpha, was top-ranked on the candidate gene list for PD. The TPPP gene is specifically expressed in the brain; its exact biological function is unknown but it seems to modulate the organization and dynamics of the microtubular network by interacting with tubulin [49]. Interestingly, p25alpha is primarily expressed in oligodendrocytes; however, abnormal expression has been observed in affected nerve cells in PD and Lewy body dementia. Furthermore, p25alpha promotes the aggregation of alpha-synuclein and co-localizes with alpha-synuclein in neuronal Lewy body inclusions. This indicates that dysregulated expression of TPPP may contribute to an increased risk of PD [50].
Conclusions
We have implemented and validated a network-based approach to prioritize genes for human diseases based on their phenotypic profile. We have devised a powerful and transparent tool to identify and rank candidate genes. Our global gene prioritization provides a unique resource for the biological interpretation of data from genome-wide association studies, and will help in the understanding of how the associated genetic variants influence disease or quantitative phenotypes.
Methods
Network-based gene-prioritization approach
The prioritization approach works as follows. For each candidate gene, a candidate complex is determined from PPI data in STRING. Each gene in the complex is then linked to its biomedical text records in the OMIM, PubMed, or GeneRIF databases. Text-mining is used to convert the biomedical text into a vocabulary list based on the UMLS. For each gene, the result is a vector of weighted counts of occurrence of each of the UMLS terms present in the biomedical text record. This vector defines a standardized gene-associated phenotype. Vectors for standardized disease phenotypes are determined in a similar way. In both cases, the terms used can be limited to specific vocabularies by applying different vocabulary control filters (e.g., MeSH, GO). A disease relevance score for each candidate gene is computed from the pair-wise semantic similarities between the disease phenotype and each of the gene-associated phenotypes in the complex. A random-set scoring model is used to calculate the disease relevance score. The random-set scoring model gives a z-score per gene complex that represents an overall enrichment signal for the association of the candidate gene with the disease. The z-score is used to determine whether the gene is associated with the disease, and is used to rank/compare genes for their disease relevance.
Website
More information regarding this network-based approach can be found on the project website at https://djfextranet.agrsci.dk/sites/txtphenome/public/Pages/front.aspx. This site contains the R-package txtPhenome and data packages containing processed data from OMIM, GeneRIF, and PubMed, and genome-wide ranking of genes for relevance to OMIM disorders (Additional file 1). txtPhenome contains functions for dealing with the data in the data packages.
Disease and gene-associated phenotypes
Disease and gene-associated phenotypes were obtained from text-mining of the biomedical text data (OMIM, GeneRIF, PubMed records). The phenotypic profile of the disease, referred to as the disease phenotype, was obtained from OMIM records, which include a textual description of the disease characteristics such as pathogenesis and clinical features. The biomedical text records linked to human Entrez gene identifiers were from three repositories: 1) the text field of OMIM records; 2) the titles and abstracts of PubMed articles; and 3) the text field of GeneRIF records. The links between the specific Entrez gene identifiers and the biomedical text records were obtained from the NCBI (ftp://ftp.ncbi.nih.gov/gene/DATA/). Additional file 1: Table S11 shows an overview of the biomedical records and the links to the genes in different repositories.
Text-mining of biomedical records
The text field of the biomedical records from OMIM, PubMed, or GeneRIF was processed through the text-mining program MMTx (version V2.4.C) [51]. Each document was mapped into to a set of UMLS (release version: 2009AA) concepts/terms. UMLS is a metathesaurus comprising various vocabularies (58 sources in version 2009AA) including MeSH, ICD9CM, and GO. In addition, the UMLS defines 135 semantic types, which provide a consistent categorization of all concepts represented in the UMLS metathesaurus. The set of UMLS concepts obtained from each document was filtered in one of two ways: (1) by a specific vocabulary; or (2) by a group of semantic types. In (1), three UMLS vocabularies (MeSH, ICD9CM, and GO) were applied independently to the concept vector for each document. In (2), the concepts that belonged to a group of semantic types (see Additional file 1) were retained in the phenotypic vectors. The removed concepts were those that belong to semantic types (e.g., “governmental or regulatory activity”) that were clearly not relevant to biological phenotype. The concept volumes of different vocabulary filters are given in Additional file 1: Table S13. The frequencies of concepts within the document and the occurrences of concepts across documents were calculated. Finally the term frequency-inverse document frequency [52] was used to weight all the terms in each document.
The semantic similarity used in this study was the correlation between two documents. One was the disease-associated phenotype (an OMIM record) and the other was the gene-associated phenotype (an OMIM record, a PubMed abstract, or a GeneRIF record). The semantic similarity was computed as the cosine coefficient between the weighted term occurrences in a disease-associated phenotype and a gene-associated phenotype according to the Vector Space Model [53, 54]. The biomedical records from the three gene-associated phenotype sources and the four vocabulary filters defined 12 sets of phenotypic profiles. The number of associations between human genes and biomedical records was highest for the PubMed database with ~473,000 PubMed abstracts linked to more than 28,000 genes (Additional file 1: Table S11). The vocabulary volume within each of the vocabulary filters varied from tens of thousands (for GO or ICD9CM) to hundreds of thousands (for MeSH), to nearly one and a half million (for STY) (Additional file 1: Table S13). Because of the length of the records and vocabulary volumes, the concept size derived from the phenotypes varied considerably (Additional file 1: Table S12).
Candidate complexes
The candidate complex for each gene was determined from PPI data obtained from the STRING database (version 8.1). STRING is a database and web resource dedicated to PPIs, which contains both physical and functional interactions [12, 15]. The Ensembl protein encoded by the candidate gene was used to retrieve first-order protein interaction partners in the network that associate directly with that protein. Each pair of protein associations from STRING was annotated with an interaction confidence score ranging from 150 (low credibility) to 999 (high credibility). Additional file 1 shows the counts of PPI pairs ordered by their credibility scores. We examined the random-set scoring model with candidate complexes defined by different confidence score thresholds (500–990), corresponding to various levels of association likelihoods (0.75–0.99).
Disease relevance score of a candidate gene complex
To prioritize the disease candidate genes, a disease relevance score that quantifies the association strength between a candidate gene complex and the disease was proposed. This score was based on a random-set scoring model [8], which was originally applied to study gene set enrichment analysis. Analog to the expression profile, in the context of this study, the semantic similarities (the cosine coefficient) between the documents are regarded as the phenotype profile. The random-set scoring model measures the enrichment signal of the set of semantic similarities between the disease phenotype (narrative description) and the set of gene-associated phenotypes (narrative descriptions) linked to the candidate gene complex. The semantic similarity between the disease phenotype and a gene-associated phenotype is defined as S e . The overall association between a disease and a candidate gene complex is represented by a set of semantic similarities that contains m elements, where m is the number of biomedical records linked to the genes in the candidate complex. The unstandardized enrichment signal is defined as the mean of the semantic similarities in set C[8] X ¯ = 1 m e C S e , where C is the set of m biomedical records that linked to a specific gene candidate complex, and is a random set of m documents drawn from the entire cohort of E documents. Under the random-set scoring model [8], and thus conditional on element-level scores {S e } of semantic similarities between disease phenotype and all documents:
μ ^ = e = 1 E S e E
(1)
and
σ ^ 2 = 1 m E m E 1 e = 1 E S e 2 E e = 1 E S e E 2
(2)
A standardized enrichment score [9] is then calculated as Z = X ¯ μ ^ / σ ^ , representing the disease relevance score. Under the null hypothesis that says “no association between the gene-associated phenotypes and the disease phenotype”, the disease relevance scores have a normal distribution with zero mean and unit variance [8]. A large positive disease relevance score (z-score) favors the positive enrichment hypothesis: that the candidate gene (or candidate complex) is strongly associated with the disease.
Validation of the approach
We validated our network-based gene-prioritization approach using the known disease and gene relationships in the OMIM database. We used 3395 test cases, each corresponding to a known relationship between a disease phenotype and a disease-“causing” gene in the OMIM database. The test cases were identified from the morbid map downloaded from the NCBI (ftp://ftp.ncbi.nih.gov/gene/DATA/). Each relationship between an OMIM descriptive entry and a human Entrez gene labeled with “phenotype” was referred to as a test case in which the OMIM record represented the disease phenotype and the linked Entrez gene was the true “causal” gene. The 3395 test cases represented 2525 known human disorders and 2135 unique human genes. The intention was to mimic a situation in which we have identified a genomic region where one or several genetic variants are known to be associated with a specific disease phenotype. The challenge was to identify which of the genes located in that genomic region was the most likely candidate gene harboring a causal mutation. For each test case, a set of candidate genes, referred to as the test set, was identified by choosing 50 genes upstream and 50 genes downstream of the true “causal” gene. If the true “causal” gene was located close to the telomere then the test set would include more genes in the opposite direction to ensure a set of 100 candidate genes for each test case.
Although the genomic regions were relatively large compared with the resolution power of GWAS, they allowed us to compare the performance of our approach directly with that of two alternative complex-based prioritization approaches: the Bayesian prioritization model [4] and the regression prioritization model [6]. Both of these approaches have been previously validated on the OMIM data. To ensure fair comparisons, we applied the same vocabulary filters (either STY or MeSH) and used the same test sets as in the original studies. We estimated the recall and precision of our approach using two groups of test sets. One group consisted of 1177 test cases used for the Bayesian approach and the other group consisted of 1193 test cases used for the regression approach. The protein complexes were defined with credibility scores above 900. The protein complexes used in the alternative approaches were restricted to PPI data that did not include the co-occurrence of genes in the biomedical literature. Our approach was based on protein complexes retrieved from the STRING database, which integrates both physical interactions and predictive protein associations based on different information sources, including text-mining of PubMed records for the co-occurrence of two genes. To assess the influence of the text-mining evidence on the prioritizations, we recalculated the confidence scores leaving out this specific channel of PPI data (see Additional file 1).
We investigated the influence of the PPI confidence score threshold using GeneRIF as the gene-associated phenotype and STY as the vocabulary control. We assessed the influence of different sources of gene-associated phenotypes and phenotype vocabulary filters using a minimal PPI confidence score of 900.
We measured the performance of our approach in two ways: 1) for each test set, we ranked the candidate genes according to the standardized z-score. We determined the rank of the true causal gene and counted the number of times that the true “causal” gene ranked at the top or was among the five highest-ranking genes across all test sets; 2) we selected z-scores derived from the null hypothesis distribution (see Additional file 1) at cumulative quantiles (from 0.1% to 100%) as discriminators (cut-offs) to classify whether a gene from a test-set was associated with the disease phenotype. True positives (tp) and false negatives (fn) were identified when the z-score of a true causal gene from a test-set was above or below the discriminator, respectively. True negatives (tn) and false positives (fp) were identified when the z-score of a candidate gene was below or above the discriminator, respectively. The prioritization performance of the approach was examined by recall: tp tp + fn ; precision: tp tp + fp ; MCC: MCC = tp × tn fp × fn tp + fp tp + fn tn + fp tn + fn ; the ROC curve (sensitivity vs. 1–specificity) [55] and the AUC.
Application of our approach
We used our approach to conduct a global ranking of all human genes for their relevance to human diseases represented in the OMIM database. The complete set of human genes was retrieved using an R package (org.Hs.eg.db) that is based on the Entrez gene database. The protein complexes for human genes were collected from the STRING database, and the threshold for PPIs was restricted to 0.95 or higher, which corresponds to a confidence score of 900. The phenotypic profile of each gene complex was generated from PubMed articles (titles and abstracts). The remaining phenotypic concepts were specifically limited to MeSH terms. According to the approach described above, we ranked all the human genes and scored them for their relevance to a large number of disease phenotypes from the OMIM database, which comprised either a descriptive entry, usually of a phenotype, and did not represent a unique locus (3053 OMIM identifiers marked by “#”), or a description of a phenotype for which the Mendelian basis, although suspected, has not been clearly established or the separateness of this phenotype from that in another entry is unclear (1921 OMIM identifiers without a label).
Declarations
Acknowledgments
We thank Rui Jiang and Xuebing Wu, from the MOE Key Laboratory of Bioinformatics and Bioinformatics Division, Tsinghua University, for providing the data for comparison. We also acknowledge Olof E. L. Karlberg and Páll I. Ólason, from the Center for Biological Sequence Analysis, Technical University of Denmark, for their assistance with the data processing. This work was in part supported by a Cutting Edge Genomics for Sustainable Animal Breeding (SABRE) research project that was co-financed by the European Commission within the Sixth Framework Program, contract no. FOOD-CT-2006-016250. Additional financial support was kindly granted by Quantomics, a collaborative project under the Seventh Framework Program. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Authors’ Affiliations
(1)
Department of Molecular Biology and Genetics, Aarhus University, DK-8830 Tjele, Denmark
(2)
Center for Biological Sequence Analysis, Department of Systems Biology, Technical University of Denmark, DK-2800 Lyngby, Denmark
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Especially as we age, it’s common to have an ailment or two. Everyday health issues arise, such as aches from arthritis and other common joint pains. You also want to take care of your cardiovascular health as you get older. Sometimes, natural remedies can be helpful in between doctor visits. If you’re a health enthusiast looking for a few more tricks to improve your wellbeing, read these tips for reducing pain and improving cardiovascular health.
Acupuncture and Salt Therapy
Acupuncture and salt therapy are both used to treat the symptoms of asthma. In acupuncture therapy, needles are placed in the skin and, for some people, it might help them breathe easier. In salt therapy, there are both wet and dry treatments. In a dry treatment, the participant is placed in a room where salt is ground into breathable-sized particles that are then released into the air. Wet treatments can involve gargling, drinking, bathing and using salt water for nasal irrigation. The basic concept is that the salt particles absorb negative particles that are affecting breathing.
Muscle Testing for Allergies
As you get older, you’ll find that many of the same foods and substances you enjoyed when you were younger are no longer healthy for you. Even worse, you may become allergic to some of them. It can be hard to figure out what your body has become allergic to, but new technologies and procedures have emerged to make this process easier. One alternative method for testing for allergies is muscle testing. By tapping into the subconscious of your body’s biomagnetic energy field, you can deduce which toxins or chemicals your body has formed a resistance against. This will allow you to enjoy your lifestyle without worrying about which substances will set off an allergic reaction.
Green Tea
There is some support that drinking green tea can lower LDL cholesterol and helps reduce heart disease and strokes. The number of cups of tea that you should drink per day should be fewer than five, however, because it can also raise the likelihood of kidney stones. It’s the catechins in the green tea that are responsible for the lowering of LDL cholesterol, so be sure that you are drinking real green tea rather than a drink that has green tea but is mostly made of other ingredients and flavorings. Many people have had success in taking green tea supplement capsules instead of drinking the tea itself. Many people are always on the lookout for natural alternatives to traditional Western medicine, but be aware that research into these methods is still ongoing.
CBD Oil
Derived from the hemp plant, CBD oil has many natural health benefits, namely alleviating pain. Although it is derived from the same plant as marijuana, CBD oil does not have any mind-altering properties. CBD and marijuana are both from cannabis plants, but the marijuana plant has high levels of THC, the drug that is psychoactive. CBD does not have these elevated levels of THC, so it is not psychoactive. CBD can be taken as a pill or mouth spray, or it can be applied to the affected area as a gel. It is also sometimes used to help manage arthritis pain because it can function as an anti-inflammatory. As an anti-inflammatory it can also assist with asthma, CBD oil can help suppress the response of T-helper cells, which can result in helping reduce the cytokines often responsible from inflammation, and help patients breathe. It is also known for helping alleviate the pain associated with asthma attacks.
As with all treatments, some will work better for others, and some won’t work as well as people would like. What’s important is to have an open mind and to scale everything slowly. In our modern age, we all want immediate results, which rarely occur in the field of medicine. It’s important to try something, and if it doesn’t feel like it works, that’s okay! Try something new, and keep going. As you continue to make your journey towards wellness, keep an eye out for new trends and advancements to help you along the way.
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Menopause And How To Rebalance The Hormones
Menopause And How To Rebalance The Hormones
Menopause is biological process that is bound to happen naturally in women. Most women are afraid of reaching menopause because they associate menopause with end of fertility and can have negative sexual impacts. Although menopause marks the end of fertility, if it occurs naturally, the woman can still remain healthy, sexual and vital.
In most cases, menopause occurs after twelve months of the last menstrual period in women and it marks the end of child bearing age. There is no specific age that marks the normal beginning of menopause but in most cases it is perceived to begin at late 40s.
Also, there are positive side effects of menopause in women, one of them being a natural way of family planning. Since the woman is still sexually active after menopause, she no longer needs to worry about pregnancy. Some of the negative of menopause effects include emotional imbalance that may often disrupt your sleep.
Withdrawal Symptoms Of Menopause
In most cases, most people associate withdrawal as a happening that only takes place in individuals who are rehabbing from heavy alcohol or drug abuse. Basically, in women menopause is a different kind of withdrawal.
Menopause can be perceived as oestrogen withdrawal. Once the level of oestrogen production in the body dramatically drops, the female body starts undergoing through menopause. Although the production of oestrogen dramatically drops, the oestrogen factory does not completely close rather there is still minimal production of oestrogen in the woman’s body.
Due to this fact, there is creation of hormonal imbalance in the woman’s body, therefore, the withdrawal symptoms.
Although every woman goes through oestrogen withdrawal, it can be more intense in some women. The oestrogen withdrawal is associated with some serious mental and physical side effects, such as:
1. Oestrogen is linked with regulating body temperature; therefore, oestrogen withdrawal is associated with hot flashes.
2. Oestrogen also helps the body’s intake of serotonin. Serotonin helps the body in regulating moods; therefore, oestrogen withdrawal is associated with regular mood swings.
3. There are also other many side effects associated with menopause that include pain during sex, weight gain, memory loss, dryness, itching and headaches.
All these negative side effects of menopause puts a woman in a situation where is regularly under intense stress and anxiety.
What Happens To Hormones During Menopause?
During the perimenopause period (period slightly before the menopause), most of the menopausal symptoms appear. Depending on the woman, perimenopause can last for one to ten years. During this period, most of the hormonal changes occur and cause most of the symptoms of menopause to appear.
Menopause period leads to ovaries producing fewer eggs resulting to production of fewer hormones. Oestrogen and progesterone are the two hormones that are essentially responsible for reproduction and menstrual cycle.
The production of these hormones is limited during the transition from reproductive to non-reproductive cycles in the woman’s life. In most cases, the production of these hormones eventually stops and this marks the end of menstrual cycles in women marking the beginning of postmenopause.
Hormonal change is significantly associated with causing menopausal symptoms hence the withdrawal. Basically, during perimenopause, the levels of progesterone, oestrogen and testosterone produced by female’s body eventually drops. During the transition period, hormones fluctuate vastly. Hormonal imbalance and fluctuation leads to a rough transition period.
How To Rebalance The Hormones?
There are several lifestyle changes that you can implement during perimenopause and the body can naturally adjust to the change in hormone levels. Some of the lifestyle changes that the woman is required to observe include:
• eating a healthy, well-balanced diet;
• staying hydrated;
• exercising daily for at least thirty minutes;
• practising breathing exercises;
• avoiding excessive amounts of caffeine and alcohol;
• taking time to distress;
• sleeping seven to eight hours per night;
• increasing your vitamin B, D, C and E intake.
Like all other withdrawals, ensure that you have a close friend or a specialist to talk to and share your problems.
Symptoms of Menopause
Conclusion
Menopause is one of the various transitions that a woman’s body undergoes through her lifespan. Menopause is perceived as a woman’s body going through withdrawal because like any other withdrawal, menopause is associated with symptoms and side effects.
There are various methods to help curb the negative side effects of the symptoms associated with oestrogen withdrawal that ranges from natural ways to the use of medication. In severe cases, women are advised to seek for appropriate menopause advice and, where necessary, treatment.
This is a guest post written by Margaux Diaz (@Gaux_Beauty), an inspirational writer who’s main motive is to give information to readers through her health and fitness articles. If you enjoyed this article about menopause and its withdrawal symptoms, feel free to share it with your friends and family!
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Generated with MOOJ Proforms Version 1.5
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Abstract
Background An accumulating body of research demonstrates that risk of suicide varies between occupational groups. Identification of the occupations at risk, and the factors that contribute to the increased risk of suicide in these groups is essential for the development of effective suicide prevention strategies. There is preliminary evidence to suggest that veterinary surgeons are a group at risk.
Aims To conduct a systematic review of studies of rates and methods of suicide in the veterinary profession.
Methods A systematic search of the international research literature was performed in May 2008. The data from the 19 studies of the prevalence of suicide in the veterinary profession were extracted by two independent reviewers and analysed.
Results Between 0 and 43% of veterinary surgeon deaths were due to suicide. In all but one of the 15 studies presenting risk of suicide in veterinary surgeons with a comparison population, an elevated risk was found. The better quality studies with the lowest risk of bias indicated that in the UK, the rate of suicide in the veterinary profession was at least three times the general population rate. Studies of the methods of suicide veterinary surgeons use suggest that self-poisoning and firearms are particularly common.
Conclusions There appears to be an elevated risk of suicide for veterinary surgeons in several countries. Access to means of suicide influences the methods used and may contribute to increased risk.
Introduction
Internationally around a million people die by suicide each year, making it a leading cause of death in both developing countries and the Western world [1]. Suicide has important emotional, social and economic consequences and understanding the risk factors associated with suicidal behaviour is essential if effective preventive measures are to be developed. A substantial body of research shows that members of certain occupational groups are at greater risk of suicide than others.
Observational studies from across the world have established elevated rates of suicide in doctors [2–4], nurses [2], dentists [4,5] and farmers [6–9]. In these studies, national mortality databases have been used to study suicide rates as well as methods of suicide. Both doctors and farmers are significantly more likely to use methods of suicide obtained through work than those in the general population [10,11]. Easy access to a relatively lethal means of suicide is one factor that may explain why these occupations are at particularly elevated risk.
Increasing attention has been paid to suicide in the veterinary profession, since veterinary surgeons may also have easy access to lethal drugs. Early indications of an increased risk of suicide in the veterinary profession came from observational studies conducted in the USA [12–15]. However, elevated rates of suicide have also been found in observational studies of veterinary surgeons in England and Wales [16–18], Scotland [8], Norway [3] and Australia [19]. Preliminary research suggests that veterinary surgeons may be exposed to high levels of occupational stress [20] related to client relations and time and work management [21], long working hours [22] and delivering bad news [23].
We have conducted the first systematic review of the research literature on risk of suicide in the veterinary profession. The aim of the study was to gain a reliable and accurate indication of the extent to which the prevalence of suicide is elevated in the veterinary profession by aggregating data from the international research literature. In order to gain a better understanding of the contribution that access to a means of suicide has on suicide rates within the profession, studies that present data on the methods of suicide were also collated and summarized.
Methods
The search strategy used to identify studies of the prevalence and methods of suicide was carried out as part of a wider systematic review of the research literature on suicidal behaviour and wellbeing of the veterinary profession. Studies not reporting suicide prevalence data, or which report data on the wellbeing of veterinary students, will be reported elsewhere. The systematic review procedure is illustrated in Figure 1.
Figure 1.
Flow chart of systematic review process.
Figure 1.
Flow chart of systematic review process.
An electronic search of the databases MEDLINE (1950-present), EMBASE (1980-present), AMED (1982-present), BNI (1985-present), CINAHL (1982-present), PsycINFO (1806-present), SCOPUS, Web of Science (1945-present) and IBSS (1951-present) was conducted in May 2008. The terms ‘wellbeing’, ‘emotion*’, ‘anxiet*’, ‘psycholog*’, ‘mortalit*’, ‘mental illness’, ‘mental health’, ‘stress*’, ‘depress*’, ‘self harm’, ‘suicid*’ were combined with ‘veterinar*’ and ‘vets’ in a free-text search. In addition, the subject headings associated with suicide- and veterinary-related terms were searched in order to identify any references not coded with the appropriate terms by the managers of the electronic reference databases. No restrictions were made about the language of the publication.
References retrieved in this search were randomly distributed to reviewers 1–4 (K.H., S.S., R.M., L.S.) who independently screened reference abstracts (according to the study inclusion criteria; see Table 1). In addition, the abstract for each reference was screened by reviewer 5 (B.P.). On occasions when reviewers disagreed, the decisions of a sixth independent reviewer (L.H.) were used to determine whether the reference was identified for review at the full-text level or not. In total, 970 references were forwarded for full-text screening. Each of these reports was then randomly assigned to reviewers 1–3 and reviewer 5 for screening. Full-text screening required reviewers to categorize each paper as described in Table 1.
Table 1.
Abstract screening criteria and full-text screening categories
Abstract screening criteria
Paper includes information on suicide, mental illness, stress and other related issues and
Paper reports the above issues in relation to veterinary surgeons or students of veterinary medicine
Full-text screening categories
The paper presents empirical data in relation to suicidal behaviour or wellbeing in veterinarians and/or veterinary medical students
The paper presents theoretical accounts of suicidal behaviour or wellbeing in veterinarians and/or veterinary medical students e.g. models of suicide
The paper presents non-theoretical accounts of suicidal behaviour or wellbeing in veterinarians and/or veterinary medical students e.g. personal account of suicidal thoughts
The paper is irrelevant to the study protocol.
Abstract screening criteria
Paper includes information on suicide, mental illness, stress and other related issues and
Paper reports the above issues in relation to veterinary surgeons or students of veterinary medicine
Full-text screening categories
The paper presents empirical data in relation to suicidal behaviour or wellbeing in veterinarians and/or veterinary medical students
The paper presents theoretical accounts of suicidal behaviour or wellbeing in veterinarians and/or veterinary medical students e.g. models of suicide
The paper presents non-theoretical accounts of suicidal behaviour or wellbeing in veterinarians and/or veterinary medical students e.g. personal account of suicidal thoughts
The paper is irrelevant to the study protocol.
When there was disagreement about the category to which a reference should be assigned, the respective reviewers discussed their views until a consensus decision could be reached. Papers that were not available in English were translated and categorized according to the above criteria in a collaborative effort between a native speaker of the respective language and reviewer 5. Additional search methods included hand-searching the references of studies that fell into Category 1, asking international experts in the field to review the final list of studies in Category 1 and searching a weekly updated electronic database of injury prevention research literature. Any references identified by these additional methods were randomly allocated to reviewers 1–3 and reviewer 5 for full-text screening.
A standardized form containing 106 items was developed by the authors specifically for the purpose of extracting data from papers on the prevalence and methods of suicide in the veterinary profession. In addition, a form was developed to assess the overall quality and risk of bias associated with each paper. The quality rating scale contained 12 items, which were rated by two independent reviewers on a binomial scale and summed to give an overall indication of quality (Table 2).
Table 2.
Quality rating scale
Item number Description of quality rating item Score
Definition of suicide
Clear definition of suicide used e.g. International Classification of Diseases codes identified
Unclear definition of suicide e.g. ‘cases where death was due to suicide’
Source of numerator data
National or official source of mortality data e.g. Office for National Statistics
Regional or unofficial source of mortality data e.g. obituaries
Source of denominator data
National or official source of population data
Regional or unofficial source of population data
Study duration
>5 years
≤5 years
Study period
Clear definition of study period e.g. 1966–2000
Study period unclear e.g. ‘10 year period’
Veterinary population data
No. suicides/no. all deaths reported or rate of suicide reported
No. suicides/no. all deaths not reported or rate of suicide not reported
Comparison population data
No. suicides/no. all deaths reported or rate of suicide reported
No. suicides/no. all deaths not reported or rate of suicide not reported
Number and type of comparisons made
Statistical comparisons made with general population and a specific occupational group
None or one comparison made
Appropriateness of comparison group (gender)
Comparisons made by gender or comparison group statistics adjusted for gender
Comparisons not made by gender or comparison group not adjusted for gender
10 Appropriateness of comparison group (age)
Comparisons made by age or comparison group statistics adjusted for age
Comparisons not made by age or comparison group not adjusted for age
11 Significance of comparison statistics
P-values or confidence intervals reported
P-values or confidence intervals not reported
12 Study limitations
Authors identify possible sources of bias
Authors do not identify possible sources of bias
Item number Description of quality rating item Score
Definition of suicide
Clear definition of suicide used e.g. International Classification of Diseases codes identified
Unclear definition of suicide e.g. ‘cases where death was due to suicide’
Source of numerator data
National or official source of mortality data e.g. Office for National Statistics
Regional or unofficial source of mortality data e.g. obituaries
Source of denominator data
National or official source of population data
Regional or unofficial source of population data
Study duration
>5 years
≤5 years
Study period
Clear definition of study period e.g. 1966–2000
Study period unclear e.g. ‘10 year period’
Veterinary population data
No. suicides/no. all deaths reported or rate of suicide reported
No. suicides/no. all deaths not reported or rate of suicide not reported
Comparison population data
No. suicides/no. all deaths reported or rate of suicide reported
No. suicides/no. all deaths not reported or rate of suicide not reported
Number and type of comparisons made
Statistical comparisons made with general population and a specific occupational group
None or one comparison made
Appropriateness of comparison group (gender)
Comparisons made by gender or comparison group statistics adjusted for gender
Comparisons not made by gender or comparison group not adjusted for gender
10 Appropriateness of comparison group (age)
Comparisons made by age or comparison group statistics adjusted for age
Comparisons not made by age or comparison group not adjusted for age
11 Significance of comparison statistics
P-values or confidence intervals reported
P-values or confidence intervals not reported
12 Study limitations
Authors identify possible sources of bias
Authors do not identify possible sources of bias
Scores between 0–4 were taken to represent relatively low quality, 5–8 moderate quality and 9–12 relatively high quality. Five items from the quality rating scale were related to risk of bias: (i) the definition of suicide, (ii) the source of numerator data, (iii) the source of denominator data, (iv) the appropriateness of the comparison population in terms of gender and (v) the appropriateness of the comparison population in terms of age. The scores on these items were summed to give an indication of the likelihood that data on the prevalence of suicide were biased. Score of 4 or 5 indicated a relatively low risk of bias.
Each report of prevalence of suicide and methods of suicide was randomly allocated to reviewers 1–3 and reviewer 5 for independent data extraction. Any resulting disagreements were discussed between the reviewers until a joint decision could be reached. Data were entered into an Excel spreadsheet, which was used for descriptive analyses.
Results
The initial electronic search strategy identified 12 948 references, once duplicates had been removed. Disagreement between reviewers existed in relation to 837 (7%) of the references at the abstract screening level (kappa = 0.504; moderate agreement [24]). There was disagreement about whether 42 (5%) of the studies at the full-text level presented data that met review criteria 1 (presenting data) or not (kappa = 0.717; substantial agreement [24]).
Nineteen studies presented primary empirical data on the prevalence of suicide in the veterinary profession (Table 3). Data are presented in the format in which they appear in the paper they are extracted from. Where comparative statistics were not reported in the paper but there were sufficient data available to calculate these, the present authors have performed the relevant statistical tests.
Data on the absolute rate of suicide in the veterinary profession were provided in the majority of papers. The proportion of all deaths that were from suicide (proportional mortality; PM) varied from 0/3195 (0%) in a study of veterinarians in Denmark [2] to 6/14 (43%) in a study of female veterinary suicides in California [30]. The lowest absolute rate of suicide (per 100 000) was 41.8 (95% CI: 19.9–87.7) for veterinarians in Victoria, Australia [19] and the highest rate was in veterinarians in Western Australia, 52.6 (95% CI: 19.7–140.1) [19]. Eleven studies compared veterinary suicide PM with a comparison population (proportional mortality ratio; PMR). All of these indicated that the proportion of veterinary deaths that were suicides was elevated compared with the proportion in the general population. Seven of these studies reported that the elevated rate was significant at the P < 0.05 level [13,14,16,26,28,30,31].
In two studies, the relative risk (RR) of suicide in the veterinary profession was presented [25,27]. These showed an elevated risk of suicide compared with the general population. Two studies reported standardized mortality ratios (SMR) [19,29]. Neither found the risk of suicide in the veterinary profession to be significantly greater than that of the general population.
The included studies varied greatly in their relative quality and risk of bias. The findings of the four studies that scored 9–12 on the 12 point quality scale and 4 or 5 on the 5 point risk of bias scale are discussed in more detail below as more robust conclusions about the extent to which the rate of suicide is truly elevated in the veterinary profession can be drawn from them [2,8,16,25].
A case–control study of suicide in the national population of Denmark between 1991 and 1997 identified 3195 cases of suicide and 63 900 controls (alive when the case died) [2]. While 49 of the controls were veterinary surgeons, none of the cases of suicide were and therefore it was not possible to calculate the RR of suicide in the veterinary profession.
In a second case–control study, the number of cases of suicide in veterinary surgeons in England and Wales between 1990 and 1992 was compared with the number of suicides by controls (not employed in 1 of 10 highest professional groups at risk of suicide) [25]. The RR of suicide was significantly elevated in female veterinarians aged 16–64 years (RR = 7.62, 95% CI: 1.04–55.94, P < 0.05), male veterinarians aged 16–44 years (RR = 4.61, 95% CI: 1.49–14.25, P < 0.01) and male veterinarians aged 45–64 years (RR = 5.62, 95% CI: 1.6–19.74, P < 0.01).
A third study investigated suicides in veterinary surgeons in England and Wales between 1979 and 2000 [16]. Male and female veterinary surgeons were at significantly increased risk of suicide (PMR = 361, 95% CI: 252–503 and PMR = 414, 95% CI: 166–853, respectively). Male veterinarians were significantly more likely to die by suicide than dentists or doctors. When deaths with an open verdict were also included, the risk of suicide for male and female veterinary surgeons was even greater (PMR = 374, 95% CI: 244–548, P < 0.0005 and PMR = 1240, 95% CI: 446–2710, P < 0.05, respectively).
The final study compared the relative numbers of deaths due to suicide in male Scottish veterinary surgeons with other males in Scotland [8]. An elevated risk of suicide for veterinary surgeons was reported in those aged 16–45 years (PMR = 293, 95% CI: 80–749) and 46–64 years (PMR = 301, 95% CI: 36–1088). This was not statistically significant, probably due to relatively few cases of suicide.
Data on the methods of suicide in the veterinary profession were provided in 8 of 19 studies (Table 4). The two most common methods of suicide used by veterinary populations were poisoning and firearms. Three studies showed that firearms were the most common method of suicide; two of these were from the USA [13,14,18]. In five studies, self-poisoning was the most common method of suicide [19,26,30–32], although the percentage of self-poisoning cases ranged from 23 [31] to 100% [19,26].
Table 3.
Observational studies of the prevalence of suicide in the veterinary profession
Study and country of research Quality rating (risk of bias) Time period Veterinary study population
Comparison population Comparative statistics
Data source (verdict) Description [studies with overlapping population] Prevalence of suicide
Charlton [25] England and Wales 10 (5) 1990–92 National/official (suicide and open) Male veterinarians aged 16–44 [16,26 Married males in general population aged 16–44, not in 10 highest occupational groupsb RR = 4.61 (1.49–14.25), P < 0.01
Male veterinarians aged 45–64 [16,26 Married males in general population aged 45–64, not in 10 highest occupational groupsb RR = 5.62 (1.6–19.74), P < 0.01
Female veterinarians aged 16–64 [16,262 suicides 3 deaths from natural causes Married females in general population aged 16–64, not in 10 highest occupational groupsb RR = 7.62 (1.04–55.94), P < 0.05
Stark et al. [8] Scotland 10 (5) 1981–99 National/official (suicide and open) Male veterinarians aged 16–45 Males in general population PMR = 293 (80–749), ‘not significant’
Male veterinarians aged 46–64 PMR = 301 (36–1088), ‘not significant’
Mellanby [16] England and Wales 10 (4) 1979–90 except 1981 National/official (suicide) Female veterinarians aged 20–74 PM = 7/30 (23%) General population PMR = 414 (166–853) Higher than medical practitioners (X2 = 8.3, P < 0.005)
1991–2000 National/official (suicide and open) Female veterinarians aged 20–74 [25PM = 6/36 (17%) General population PMR = 1240 (446–2710) Higher than medical practitioners (X2 = 4.5, P < 0.05)
1979–90 except 1981 National/official (suicide) Male veterinarians aged 20–74 [17PM = 35/383 (9%) General population PMR = 361 (252–503) Higher than medical practitioners (X2 = 32.1, P < 0.0001) and dentists (X2=13.7, P < 0.001)
Agerbo et al. [2] Denmark 9 (5) 1991–97 National/official (suicide) Veterinarians aged 25–60 0 suicides Suicides controls (N = 3195) in general population (matched for gender and year of birth)
Lange [27] USA 9 (3) 1965–89 Regional/official (suicide) Veterinarians on active duty in commissioned corps PM = 1/3 (33%) General population adjusted for age, race, ethnicity (PM = 24/118, 20%) RR = 4, ‘significant’
Milham and Ossiander [28] USA 9 (3) 1950–99 Regional/official (suicide) Male Washington state veterinarians aged >19 19 suicides Male Washington state residents aged ≥20 (18 736 suicides) PMR = 197 (P = 0.00156)
1974–99 Female Washington state veterinarians aged >19 3 suicides Female Washington state residents aged ≥20 (2128 suicides) PMR = 180 (P = 0.23326)
Kelly and Bunting [26] England and Wales 8 (4) 1982–87 National/official (suicide and open) Male veterinarians aged 20–64 [16,2517 suicides General population (adjusted for age and gender) PMR = 349 (203–559), ‘significant’
1991–96 Male veterinarians aged 20–64 [16,259 suicides General population (adjusted for age and gender) PMR = 324 (148–615), ‘significant’
1991–96 Female veterinarians aged 20–59 [16,254 suicides General population (adjusted for age and gender) PMR = 500 (136–1279), ‘significant’
Kinlen [18] Great Britain 8 (4) 1949–75 National/unofficial (suicide) Male veterinarians PM = 27/699 (2%) Males in social class 1 aged <75 PMR = 206a
Blair and Hayes [13] USA 8 (3) 1966–77 National/unofficial (suicide) White male veterinarians [14PM = 65/1551 (4%) White males matched for age and time period PMR = 216 (X2 = 42.91, P < 0.005)
Blair and Hayes [14] USA 8 (3) 1947–77 National/unofficial (suicide) White male veterinarians [13PM = 137/5016 (3%) White males matched for age and time period PMR = 170 (X2 = 41.31, P < 0.005)
Hem et al. [3] Norway 8 (3) 1960–2000 National/official (suicide) Male veterinarians age >20 13 suicides, 43.7 per 100 000 deaths (25.4–75.2) Males in the general population >20 (15 705 suicides) RR = 1.87a
Medical practitioners RR = 1.02a
Charlton et al. [17] England and Wales 7 (4) 1979–90 National/official (suicide and open) Male veterinarians aged 16–64 [1635 suicides Males in the general population aged 16–64 PMR = 364
Fasal [29] USA 7 (3) 1950–62 Regional/unofficial (suicide) White male veterinarians in California [30PM = 4/148 (3%) White males in general population of California in 1960 (adjusted for age) SMR = 79, ‘not significant’
Miller and Beaumont [30] USA 7 (2) 1960–92 Regional/unofficial (suicide) Californian veterinarians PM = 42/450 (9%) General population PMR = 263 (199–347), P < 0.05
Californian male veterinarians PM = 36/436 (8%) General male population PMR = 248 (183–335), P < 0.05
Californian female veterinarians PM = 6/14 (43%) General female population PMR =5 (302–1148), P < 0.05
Jones-Fairnie et al. [19] Australia 6 (2) 1990–2002 Regional/official (suicide and open) Veterinarians in Victoria 61 deaths, 41.8 per 100 000 deaths (19.9–87.7) Adults in Victoria (matched for age) SMR = 3.8
Veterinarians in Western Australia 26 deaths, 52.6 per 100 000 deaths (19.7–140.1) Adults in Western Australia (matched for age) SMR = 4
Veterinarians in Western Australia and Victoria PM = 11/89 (12%), 45.2 per 100 000, deaths (25–81.6)
Schnurrenberger et al. [12] USA 6 (1) 1950–73 Regional/unofficial (suicide) White male Illinois state veterinarians PM = 13/481 (3%) Illinois white male veterinarians in 1950 PMR = 168.3 (72.0–394.4)a
Californian veterinarians [28PMR = 129.3 (55–304.8)a
Illinois white male veterinarians in 1960 PMR = 193.0 (78.1–479.2)a
Illinois white male veterinarians in 1970 PMR = 223.7 (86.4–581.5)a
Botts et al. [15] USA 4 (0) 1949–64 Regional/unofficial (suicide) Male veterinarians in Missouri PM = 2/127 (2%)
Mammerickx [31] Belgium 4 (0) Not stated Not stated (suicide) Veterinarians in Belgium PM = 13/367 (4%) Non-veterinarians in general population (PM = 918/57 814, 2%) PMR = 223 (130.6–377.2)a
Veterinarians in Belgium who died at age <70 PM = 13/206 (6%) Non-veterinarians in general population who died at age <70 (PM = 918/23 567, 4%) PMR = 162 (95.3–270.6)a
Jeyaretnam et al. [32] Australia 2 (0) 10 year period not stated Regional/unofficial (suicide) Veterinarians in Western Australia PM = 4/20 (20%)
Study and country of research Quality rating (risk of bias) Time period Veterinary study population
Comparison population Comparative statistics
Data source (verdict) Description [studies with overlapping population] Prevalence of suicide
Charlton [25] England and Wales 10 (5) 1990–92 National/official (suicide and open) Male veterinarians aged 16–44 [16,26 Married males in general population aged 16–44, not in 10 highest occupational groupsb RR = 4.61 (1.49–14.25), P < 0.01
Male veterinarians aged 45–64 [16,26 Married males in general population aged 45–64, not in 10 highest occupational groupsb RR = 5.62 (1.6–19.74), P < 0.01
Female veterinarians aged 16–64 [16,262 suicides 3 deaths from natural causes Married females in general population aged 16–64, not in 10 highest occupational groupsb RR = 7.62 (1.04–55.94), P < 0.05
Stark et al. [8] Scotland 10 (5) 1981–99 National/official (suicide and open) Male veterinarians aged 16–45 Males in general population PMR = 293 (80–749), ‘not significant’
Male veterinarians aged 46–64 PMR = 301 (36–1088), ‘not significant’
Mellanby [16] England and Wales 10 (4) 1979–90 except 1981 National/official (suicide) Female veterinarians aged 20–74 PM = 7/30 (23%) General population PMR = 414 (166–853) Higher than medical practitioners (X2 = 8.3, P < 0.005)
1991–2000 National/official (suicide and open) Female veterinarians aged 20–74 [25PM = 6/36 (17%) General population PMR = 1240 (446–2710) Higher than medical practitioners (X2 = 4.5, P < 0.05)
1979–90 except 1981 National/official (suicide) Male veterinarians aged 20–74 [17PM = 35/383 (9%) General population PMR = 361 (252–503) Higher than medical practitioners (X2 = 32.1, P < 0.0001) and dentists (X2=13.7, P < 0.001)
Agerbo et al. [2] Denmark 9 (5) 1991–97 National/official (suicide) Veterinarians aged 25–60 0 suicides Suicides controls (N = 3195) in general population (matched for gender and year of birth)
Lange [27] USA 9 (3) 1965–89 Regional/official (suicide) Veterinarians on active duty in commissioned corps PM = 1/3 (33%) General population adjusted for age, race, ethnicity (PM = 24/118, 20%) RR = 4, ‘significant’
Milham and Ossiander [28] USA 9 (3) 1950–99 Regional/official (suicide) Male Washington state veterinarians aged >19 19 suicides Male Washington state residents aged ≥20 (18 736 suicides) PMR = 197 (P = 0.00156)
1974–99 Female Washington state veterinarians aged >19 3 suicides Female Washington state residents aged ≥20 (2128 suicides) PMR = 180 (P = 0.23326)
Kelly and Bunting [26] England and Wales 8 (4) 1982–87 National/official (suicide and open) Male veterinarians aged 20–64 [16,2517 suicides General population (adjusted for age and gender) PMR = 349 (203–559), ‘significant’
1991–96 Male veterinarians aged 20–64 [16,259 suicides General population (adjusted for age and gender) PMR = 324 (148–615), ‘significant’
1991–96 Female veterinarians aged 20–59 [16,254 suicides General population (adjusted for age and gender) PMR = 500 (136–1279), ‘significant’
Kinlen [18] Great Britain 8 (4) 1949–75 National/unofficial (suicide) Male veterinarians PM = 27/699 (2%) Males in social class 1 aged <75 PMR = 206a
Blair and Hayes [13] USA 8 (3) 1966–77 National/unofficial (suicide) White male veterinarians [14PM = 65/1551 (4%) White males matched for age and time period PMR = 216 (X2 = 42.91, P < 0.005)
Blair and Hayes [14] USA 8 (3) 1947–77 National/unofficial (suicide) White male veterinarians [13PM = 137/5016 (3%) White males matched for age and time period PMR = 170 (X2 = 41.31, P < 0.005)
Hem et al. [3] Norway 8 (3) 1960–2000 National/official (suicide) Male veterinarians age >20 13 suicides, 43.7 per 100 000 deaths (25.4–75.2) Males in the general population >20 (15 705 suicides) RR = 1.87a
Medical practitioners RR = 1.02a
Charlton et al. [17] England and Wales 7 (4) 1979–90 National/official (suicide and open) Male veterinarians aged 16–64 [1635 suicides Males in the general population aged 16–64 PMR = 364
Fasal [29] USA 7 (3) 1950–62 Regional/unofficial (suicide) White male veterinarians in California [30PM = 4/148 (3%) White males in general population of California in 1960 (adjusted for age) SMR = 79, ‘not significant’
Miller and Beaumont [30] USA 7 (2) 1960–92 Regional/unofficial (suicide) Californian veterinarians PM = 42/450 (9%) General population PMR = 263 (199–347), P < 0.05
Californian male veterinarians PM = 36/436 (8%) General male population PMR = 248 (183–335), P < 0.05
Californian female veterinarians PM = 6/14 (43%) General female population PMR =5 (302–1148), P < 0.05
Jones-Fairnie et al. [19] Australia 6 (2) 1990–2002 Regional/official (suicide and open) Veterinarians in Victoria 61 deaths, 41.8 per 100 000 deaths (19.9–87.7) Adults in Victoria (matched for age) SMR = 3.8
Veterinarians in Western Australia 26 deaths, 52.6 per 100 000 deaths (19.7–140.1) Adults in Western Australia (matched for age) SMR = 4
Veterinarians in Western Australia and Victoria PM = 11/89 (12%), 45.2 per 100 000, deaths (25–81.6)
Schnurrenberger et al. [12] USA 6 (1) 1950–73 Regional/unofficial (suicide) White male Illinois state veterinarians PM = 13/481 (3%) Illinois white male veterinarians in 1950 PMR = 168.3 (72.0–394.4)a
Californian veterinarians [28PMR = 129.3 (55–304.8)a
Illinois white male veterinarians in 1960 PMR = 193.0 (78.1–479.2)a
Illinois white male veterinarians in 1970 PMR = 223.7 (86.4–581.5)a
Botts et al. [15] USA 4 (0) 1949–64 Regional/unofficial (suicide) Male veterinarians in Missouri PM = 2/127 (2%)
Mammerickx [31] Belgium 4 (0) Not stated Not stated (suicide) Veterinarians in Belgium PM = 13/367 (4%) Non-veterinarians in general population (PM = 918/57 814, 2%) PMR = 223 (130.6–377.2)a
Veterinarians in Belgium who died at age <70 PM = 13/206 (6%) Non-veterinarians in general population who died at age <70 (PM = 918/23 567, 4%) PMR = 162 (95.3–270.6)a
Jeyaretnam et al. [32] Australia 2 (0) 10 year period not stated Regional/unofficial (suicide) Veterinarians in Western Australia PM = 4/20 (20%)
a
Comparative statistics were calculated by the authors of the review based on available data.
b
Age range of comparison population appears incorrect in original report; we have included what we believe to be likely correct age range.
Table 4.
Methods of suicide in the veterinary profession
Study and country of research Time period Veterinary study population Number of suicides Method of suicide (% of all suicide cases)
Modal method of suicide Suicide cases accounted for (%)
Poisoning (% barbiturates) Firearms Hanging Drowning Other
Blair and Hayes [13] USA 1966–77 White males in clinical practice 54 54 (37) 33 Poisoning 87
White males not in clinical practice 11 27 (0) 64 Firearms 91
Blair and Hayes [14] USA 1947–77 Practitioners 137 36 (28) 37 Firearms 73
Non-practitioners 13 (0) 69 Firearms 82
Jeyaretnam et al. [32] Australia 10 year period Resident in Western Australia 50 (100) Poisoning 50
Jones-Fairnie et al. [19] Australia 1990–02 Western Australians and Victorians 11 82 (not stated) Poisoning 100
Male Western Australian and Victorians 78 (not stated) 11 11 Poisoning 100
Female Western Australian and Victorians 100 (not stated) Poisoning 100
Kelly and Bunting [26] England and Wales 1982–96 Males aged 20–64 38 79 (not stated) 16 Poisoning 100
Females aged 20–59 100 (not stated) Poisoning 100
Kinlen [18] Great Britain 1949–75 Males 27 19 Firearms 19
Mammerickx [31] Belgium Not stated Aged <70 13 23 (not stated) 15 15a Poisoning 61
Miller and Beaumont [30] USA 1960–92 Males 36 47 (not stated) 3% Poisoning 100
Females 67 (not stated) 17 17 Poisoning 100
Study and country of research Time period Veterinary study population Number of suicides Method of suicide (% of all suicide cases)
Modal method of suicide Suicide cases accounted for (%)
Poisoning (% barbiturates) Firearms Hanging Drowning Other
Blair and Hayes [13] USA 1966–77 White males in clinical practice 54 54 (37) 33 Poisoning 87
White males not in clinical practice 11 27 (0) 64 Firearms 91
Blair and Hayes [14] USA 1947–77 Practitioners 137 36 (28) 37 Firearms 73
Non-practitioners 13 (0) 69 Firearms 82
Jeyaretnam et al. [32] Australia 10 year period Resident in Western Australia 50 (100) Poisoning 50
Jones-Fairnie et al. [19] Australia 1990–02 Western Australians and Victorians 11 82 (not stated) Poisoning 100
Male Western Australian and Victorians 78 (not stated) 11 11 Poisoning 100
Female Western Australian and Victorians 100 (not stated) Poisoning 100
Kelly and Bunting [26] England and Wales 1982–96 Males aged 20–64 38 79 (not stated) 16 Poisoning 100
Females aged 20–59 100 (not stated) Poisoning 100
Kinlen [18] Great Britain 1949–75 Males 27 19 Firearms 19
Mammerickx [31] Belgium Not stated Aged <70 13 23 (not stated) 15 15a Poisoning 61
Miller and Beaumont [30] USA 1960–92 Males 36 47 (not stated) 3% Poisoning 100
Females 67 (not stated) 17 17 Poisoning 100
a
One train, one car and five unknown.
One study compared methods of suicide between 54 practising and 11 non-practising male veterinarians in the USA between 1966 and 1977 [13]. For practising veterinarians, self-poisoning was a more common method of suicide than firearms, whereas in non-practising veterinarians, the most common method of suicide was firearms. In a replication of this study with a longer study period (1947–77), firearms were still more commonly used by non-practitioners than poisoning but there was little difference between the two methods in practising veterinarians. Information on the type of drugs with which veterinarians poisoned themselves was limited to three of the studies. Barbiturates were commonly used, particularly by practising veterinarians [13,14].
Discussion
Following a systematic review of the international research literature, 19 studies were identified as presenting data on the prevalence of suicide in the veterinary profession. Between 0 and 43% of all deaths were suicides and the rate of suicide per 100 000 members of the profession ranged from 41.8 to 52.6. In the majority of studies, the suicide rate in the veterinary profession was elevated compared with the general population. The quality and risk of bias of these studies varied greatly. In two of the four studies of highest quality, there was no significant difference between the rate of suicide in the veterinary profession and general population [2,8]. In contrast, in a high-quality study conducted in England and Wales, the risk of suicide in the veterinary profession was at least three times that of the general population [16]. The comparison group in the final high-quality study were members of the general population who were employed in occupations with a lower rate of suicide, therefore the increased risk of four to seven times that of the general population was artificially elevated [25]. In the majority of studies that reported methods of suicide, poisoning and firearms were the most common.
One issue associated with validity of the studies in this review is the basis upon which cases of suicide are identified. In England and Wales, a verdict of suicide requires strong evidence that the individual intended to die by suicide. If a coroner is not satisfied beyond reasonable doubt that an act was self-inflicted and intended to cause death, they may give an open verdict. Therefore, researchers in the field frequently include open verdicts when identifying suicide cases [33] and studies that identify suicide cases using verdicts of suicide alone are likely to underestimate the prevalence of suicide. In 13/19 studies in the review, open verdicts were not included as suicides and therefore, the level of suicide was probably underestimated. Different criteria for suicide are used in some countries; this also makes it difficult to directly compare studies of suicide prevalence. Furthermore, some studies used an age range with a lower limit than the age at which veterinary surgeons qualify [8,17,25]. This is because of lack of population data in more narrow age groups.
A final limitation of the studies included in the review is the statistical methods used to assess suicide risk. The most reliable and accurate method of performing relative statistics involves comparing the rate of suicide in the target occupational population to the rate in an appropriate comparison population (RR). Just two studies reviewed presented data in the form of a RR [25,27]. In 11 of the studies, a PMR was calculated. This is an alternative statistical method, used when population denominator data are unavailable. PMR is a relatively crude measure of suicide prevalence; it assumes the relative risk of other causes of death is the same in the two populations. Given that the socio-economic status (SES) of the veterinary profession is likely to be particularly high and hence the risk of deaths from some natural causes reduced, this assumption is unlikely to be valid. However, where the use of a PMR is unavoidable, additional comparisons with occupational groups matched for SES (such as doctors or teachers) are advantageous.
Our use of a quality rating scale to assess the risk of bias and overall quality of the survey studies enabled more valid generalizations to be made. Unfortunately, it was beyond the scope of the review to test the validity and reliability of this measure. Tests of the inter-reviewer reliability and external validity of the tool would help further development, such that it could be used as a reliable means of assessing the quality of studies in similar reviews.
Based on the findings of this review, several other suggestions can be made about the direction of future research on suicide and issues of wellbeing in the veterinary profession. Updates of suicide prevalence studies from the USA, Denmark, Norway, Belgium and Scotland, as well as other countries would be welcome. At the time the search strategy was conducted (May 2008), just one observational study of suicide in the veterinary profession had been published that reviewed rates of suicide beyond the year 2000 [19]. The existence of more accessible and comprehensive mortality databases should facilitate continued evaluation of the extent to which veterinary surgeons are at risk of suicide. Given that suicide patterns vary across the world and in different cultures, further investigation of cross-cultural differences in suicide rates in the veterinary profession are also warranted. The majority of observational studies in this review were conducted in Western Europe, USA and Australasia. While many studies found suicide risk to be elevated in the veterinary profession, the study of Danish veterinary surgeons found no cases of suicide [2].
Gathering detailed information on methods of suicide in the veterinary profession should also be a focus of future observational studies, as it is important to understand more about how access to a means of suicide may contribute to risk of suicide. In addition, few studies made comparisons with other occupational groups and such studies may provide information on the particular risk factors for suicide to which veterinarians are exposed.
The observational studies in the present review show that the rate of suicide in the veterinary profession is generally higher than in comparison populations, and by at least three times in the UK. Therefore, the veterinary profession is an occupation for which effective suicide prevention strategies should be developed. Preliminary evidence suggests that one factor contributing to the elevated risk in this occupational group may be easy access to a means of suicide. However, more observational studies are needed to confirm that veterinary surgeons use methods of suicide obtained through work. Investigations on the influence that other work-related factors might have on suicide risk in the veterinary profession are also required.
Key points
• This systematic review demonstrates veterinary surgeons in the UK are at least three times as likely to die from suicide as members of the general population and that risk is also elevated in some other countries.
• The research provides evidence that more in-depth investigation of suicidal behaviour in the veterinary profession is essential and identifies the particular methodological limitations of research conducted to date.
• The study is likely to stimulate further research into the factors associated with veterinary suicide in addition to encouraging the profession to develop strategies to prevent its members from taking their lives.
Funding
Hill's Pet Nutrition, the Royal College of Veterinary Surgeons Trust Fund and the Veterinary Benevolent Fund (VBF). K.H. is funded by Oxfordshire and Buckinghamshire Mental Health NHS Foundation Trust and the National Institute for Health Research, for which he is a senior investigator. S.S. is funded by a NIHR Programme Grant (‘A multi-centre programme of clinical and public health research in support of the National Suicide Prevention Strategy for England’).
Conflicts of interest
None declared.
The authors acknowledge the help of Lesley Sutton and Louise Harriss in the abstract and full-text screening stages of the review. International experts in the field Helen Fairnie, Keren Skegg, Austin Kirwan, Lin Fritschi and Rosie Allister identified any references omitted from the search prior to full-text screening (Figure 1). We are also extremely grateful to Karen Smith who provided advice on the statistical methods used in the review.
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A.Vogel Blog
A.Vogel Blog – Natural and Healthy
Inspiration for a healthy life!
How to eliminate bloating during perimenopause
by Sonia Chartier, on 21 December 2015, Digestion, Menopause, Women's Health
bloating
Whatever you call it—farting, flatulence or gas—bloating is the accumulation of gas in the small intestine. This digestive disorder is particularly common during PMS and perimenopause.
So what’s the link? And more importantly, how can you get rid of it?
Bloating distends the abdomen, sometimes to the point that you look eight months pregnant. Generally, gas builds up throughout the day and causes major discomfort. You leave home in the morning with properly fitting pants and by mid-afternoon they’re about to pop at the waist. While bloating can affect all menopausal women, those who experienced it during PMS are more likely to experience it during menopause.
What’s to blame?
Bloating is caused by a number of factors including a diet high in carbohydrates and starchy foods, endurance sports and stress. But why is bloating so common during perimenopause and what causes it?
Blame it all on your hormones! First of all, estrogens play a role in bile production. When estrogen levels drop, so does the amount of bile produced, which changes the way your body digests fats and, in turn, makes it produce more gas. What’s more, since bile acts as an intestinal lubricant, having less of it in the bowel can cause constipation.
Then there’s the fact that estrogens—yup, those darned estrogens again—influence water retention. During PMS, when estrogen levels are at their highest, the body tends to retain more water, which can add to that bloated feeling. During perimenopause, when estrogen variations become sporadic, water retention follows suit.
Bloating typically lasts anywhere from a few hours to several days. If it doesn’t go away within two weeks, go see your doctor to find out why. That’s because bloating can be a sign of a more serious underlying disorder such as Crohn’s disease or poor nutrition. It’s also worth noting that hormone therapy can cause bloating.
How can you stop it?
To prevent or stop bloating, you need to watch what you eat. As menopause approaches, many women adopt a healthier diet, which often includes eating more legumes. It’s well known that legumes and cheese cause gas. Despite the best of intentions, sudden changes in diet can wreak havoc on the bowel, so it’s best to go easy.
Here are a few tips:
• Eat small meals regularly to effectively ease digestion and avoid bloating.
• Avoid coffee, alcohol and soft drinks.
• Cut down on salt.
• Avoid onions, which can cause gas.
• Say good-bye to sweet snacks.
• Walk to promote peristalsis and avoid constipation.
• Take up a sport: exercise reduces stress, a major contributor to digestive problems.
• Drink a lot of water.
N.B. For some people, lactose can be another cause of bloating.
Natural products to the rescue!
To regulate hormones in women suffering from PMS or experiencing perimenopause, there’s nothing like Vitex. Given that many symptoms, including bloating, are caused by hormonal imbalances, this is the treatment of choice. It straightens things out, but it does so gently: allow two or three months for Vitex take full effect.
While you’re waiting for Vitex to reach its full effectiveness, you can treat the symptoms to get immediate relief. Boldocynara stimulates the production of bile and can help make up for deficiencies caused by fluctuations in estrogen levels. It’s particularly effective in promoting fat digestion. Spices can also prove useful due to their bitter components. Digestive Health is a product containing spices that halt the production of gas and, in so doing, relieve bloating.
When bloating is caused by a diet too high in sugar and starches, promoting healthy intestinal flora is key to feeling better. That’s where whey comes in: it fosters an ideal pH for the proliferation of good intestinal bacteria.
These simple solutions should enable you to keep your pants from popping open all day long.
Read more:
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Different allergy types = different reactions
Allergies manifest as a range of symptoms: they can be unnoticeable, make you miserable, or pose a life-threatening danger. One...
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This site is part of the Natural News Network © 2019 All Rights Reserved. Privacy | Terms All content posted on this site is commentary or opinion and is protected under Free Speech. Truth Publishing International, LTD. is not responsible for content written by contributing authors. The information on this site is provided for educational and entertainment purposes only. It is not intended as a substitute for professional advice of any kind. Truth Publishing assumes no responsibility for the use or misuse of this material. Your use of this website indicates your agreement to these terms and those published here. All trademarks, registered trademarks and servicemarks mentioned on this site are the property of their respective owners.
Regular visits with your doctor are also key to controlling your blood pressure. If your blood pressure is well-controlled, check with your doctor about how often you need to check it. Your doctor may suggest checking it daily or less often. If you're making any changes in your medications or other treatments, your doctor may recommend you check your blood pressure starting two weeks after treatment changes and a week before your next appointment.
Diabetics often have lower recommendations for blood pressure, the maximum normal value being seen as 130/80-85. However, it’s questionable whether it’s a good idea to medicate your blood pressure levels down to those values. Diabetics can probably stick to approximately the same upper limit as people with heart disease: 140/90 (according to new studies and expert comments, as well as the latest recommendations from the American Diabetes Association, ADA).
Sleep apnea, diabetes, and stress, each of which may be controlled (though this can be difficult), can also put a strain on the cardiovascular system and intensify blood pressure and related problems. Factors that put you in a high-risk category but that are difficult (or impossible) to control include family history, gender, and chronic kidney disease.
If you have not been active for quite some time or if you are beginning a new activity or exercise program, take it gradually. Consult your healthcare professional if you have cardiovascular disease or any other preexisting condition. It's best to start slowly with something you enjoy, like taking walks or riding a bicycle. Scientific evidence strongly shows that physical activity is safe for almost everyone. Moreover, the health benefits of physical activity far outweigh the risks.
While making these changes may not mean you can immediately go off your blood pressure medications or never have to take them, they will improve your overall health and reduce your risk for developing other diseases, including diabetes and possibly even cancer. Making healthy lifestyle changes can reduce your risk of stroke, heart attack or kidney damage, and reduce the likelihood that your dose of blood pressure medication will need to be increased in the future.
Stress and hypertension (high blood pressure) are tightly connected but still this fact is still not examined well and given the attention it deserves. Dr. Kennedy, who examined the connection between these two, has come up with revolutionary technique which helps you decrease your blood pressure in 15 min. This easy technique is remarkable because it may release you from stress and help your body relax. You may learn it by watching the video bellow.
3. Quit soda. One 12-ounce can of soda contains about 40 grams of fructose, one of the leading high blood pressure risk factors in North America. Consuming 74 or more grams of fructose per day increases your risk of high blood pressure by 77 percent. For people accustomed to drinking a can or two of soda daily, cutting the pop can have a dramatic effect on blood pressure, even eliminating the problem altogether.
Salt is everywhere, and high blood pressure (the result of too much salt in our diets) is an American epidemic. New CDC guidelines (and decades-old Pritikin guidelines) advise that most of us should eat no more than 1,500 mg of sodium a day. We average 3,500 to 5,000 mg daily. Why are we so blasé about the massive doses of salt we’re consuming? How can we change?.
Hypertension, or high blood pressure, refers to the pressure of blood against your artery walls. Over time, high blood pressure can cause blood vessel damage that leads to heart disease, kidney disease, stroke, and other problems. Hypertension is sometimes called the silent killer because it produces no symptoms and can go unnoticed — and untreated — for years.
“We have many people with hypertension who come to Pritikin,” says Pritikin’s Associate Medical Director Danine Fruge, MD, “and within three days, many have blood pressures that have dropped so low that we need to reduce their medications or take them off their pills altogether. Yes, just three days. That’s how quickly and powerfully our bodies respond to healthy food, exercise, and other lifestyle changes.”
Omega 3 and omega 6 are very important fats for your body. Omega 6 usually is found in corn, soy canola oil, sunflower oil and omega 3 usually is found in fish. Unfortunately the average Americans import more omega 6 than omega 3 and this leads to high blood pressure. In order to avoid this try to regulate the 6:3 ratio and take care of what you are consuming.
Americans eat far too much dietary sodium, up to three times the recommended total amount, which is 1,500 milligrams (mg) daily for individuals with high blood pressure, says Dr. Fisher. It doesn't take much sodium to reach that 1,500-mg daily cap — just 3/4 of a teaspoon of salt. There's half of that amount of sodium in one Egg McMuffin breakfast sandwich. Weed out high-sodium foods by reading labels carefully. "It is very difficult to lower dietary sodium without reading labels, unless you prepare all of your own food," says Dr. Fisher. Beware in particular of what the American Heart Association has dubbed the "salty six," common foods where high amounts of sodium may be lurking:
Blood pressure is written as two numbers, such as 112/78 mm Hg. The top, systolic, number is the pressure when the heart beats. The bottom, diastolic, number is the pressure when the heart rests between beats. Normal blood pressure is below 120/80 mm Hg. If you’re an adult and your systolic pressure is 120 to 139, or your diastolic pressure is 80 to 89 (or both), you have pre-hypertension. High blood pressure is a pressure of 140 systolic or higher and/or 90 diastolic or higher that stays high over time.
High blood pressure, a potentially dangerous health condition also known as hypertension, is quite common in the modern day. One of the most significant issues faced with high blood pressure is the fact that many people do not express obvious symptoms during the earlier stages of this condition. This is why many people refer to hypertension as a silent killer. Realizing what causes blood pressure to become elevated, identifying the symptoms and becoming educated about particular techniques that can help to reduce blood pressure levels quickly is essential to avoid the dangerous complications of this condition. In one study, over 70% of all participants had elevated blood pressure levels, causing a need formore adequate education on making the worldwide population more aware of the condition.
Oatmeal is one of a few semi-processed foods that lower blood pressure. That’s because getting the right amounts of dietary fiber and whole grains is vital to maintaining normal blood pressure, and oatmeal is a tasty source of both. Classic studies have proven that eating oatmeal can lower systolic and diastolic blood pressure. Plus, the fiber can help you maintain a healthy body weight and prevent obesity, a risk factor for high blood pressure. These are the 10 silent signs you could have low blood pressure.
Swearing off cigarettes is probably the single best thing you can do for your heart. It’s good for your health in general, too. Not only does smoke hurt you over the long term, but your blood pressure goes up every time you have a cigarette. Lower your blood pressure and prolong your life by quitting. If you need help getting started, talk to your doctor.
Banana is the best natural home remedy for high blood pressure that really works and lower the blood pressure fast. The potassium in the bananas has the ability to lower the blood pressure quickly. Also, then it counters the negative effects of sodium in the body. Sodium has ill effects on your blood pressure. Eating bananas will fight its bad effects. Eat 1-2 bananas daily to lower your high blood pressure. It also helps you to control your cholesterol, with its low sodium levels. Along with bananas, you can also eat spinach, orange juice, dried apricots, raisins, baked sweet potatoes, currants, winter squash, cantaloupe and zucchini.
It is must to keep your body well hydrated and it is highly recommended if you are suffering from high Blood pressure. Drink about 8-10 glasses of water each day. You can also drink warm coconut or coconut water, along with normal water for best results. Coconut water is delicious and develops nutritional values as well. They help in controlling and lowering the hypertension levels. It is an easy and simple method to improve blood pressure level by just consuming coconut water regularly. Try to use coconut oil than your regular oil for cooking.
Exercise can also lead to lower blood pressure. Although performing moderate to vigorous exercise leads to higher blood pressure during activity, it is lowered afterwards. A wealth of studies indicate that getting 150 minutes per week of exercise—whether walking, cycling, gardening, dancing, or weights—can lead to significant drops in blood pressure over time. Try to exercise every day, but even three or four times per week can bring on big improvements.
In a hot tub, as the water comes through the pipes, it has a degree of force. This force is caused by the action of the pump, which puts energy into the circulating system and forces the water through the pipes. When the pump is off, there still may be water in the pipes, but there is no force. The degree of force in the system when the pump is on can be gauged in several ways, such as by putting your hand in front of a “jet.” Another way would be to have a device to measure the amount of force that the water exerts against the walls of the pipes as it circulates. Such a device might yield a numerical measurement of the force, or pressure, of the water within the pipes.
In addition to these methods being effective, other lifestyle changes and diet adjustments may also be useful in lower blood pressure. One study explains that losing weight can have a significant positive impact on patients that have been diagnosed with hypertension. Even small reductions in bodyweight amongst those individuals who are both obese and hypertensive can yield life-saving benefits. Dietary changes can also help. In particular, the patient should aim to lower their daily intake of sodium, which causes an elevation in blood pressure. The patient should also focus on obtaining more calcium, potassium and other minerals that are useful in balancing blood pressure levels. Fiber, fruits and a lot of vegetables should also be an essential part of the patient’s daily diet.
Low- and no-fat dairy foods are good sources of calcium and protein, which can help maintain a healthy blood pressure. Try to get three servings of dairy every day. Choose skim or 1% milk and low- or no-fat cheeses and yogurt. Frozen low-fat yogurt is OK, too. One serving equals 1 cup of yogurt or milk, or 1 1/2 ounces of cheese -- about the size of three dice.
Listening to your favorite song not only will improve your feeling of well-being but also lower your blood pressure. A study published in the journal Netherland Heart Journal found musicians had lower blood pressure than non-musicians because their somatosensory nerve activity benefited their autonomic nervous system. If you’re not a musician, listening to music alone, especially classical, will do just as good.
Reduce sodium in your diet. One easy way to reduce your sodium intake is to limit or avoid processed foods, such lunch meats, hot dogs, bacon, frozen dinners, canned vegetables with added salt, and that sort of thing. Most packaged convenience foods, like macaroni and cheese, soups, side dishes, pizzas, and other multi-ingredient foods have a lot of added sodium. Start reading labels and pay attention to the sodium content. You should aim for 1500mg or less every day.
Common painkillers (so-called non-steroidal anti-inflammatory drugs, NSAID), can increase your blood pressure by inhibiting the production of salt in your kidneys. This includes over-the-counter pills such as Ipren, Ibumetin, Ibuprofen, Diklofenak and Naproxen as well as the prescription drug Celebra. Painkillers with the active substance paracetamol are better for your blood pressure.
If you have hypertension, ask your doctor if OSA could be behind it. (In addition to loud snoring, common symptoms include excessive daytime tiredness and early morning headaches.) Getting your sleep apnea under control could be helpful for improving your blood pressure, says Robert Greenfield, MD, Medical Director of Non-Invasive Cardiology & Cardiac Rehabilitation at MemorialCare Heart & Vascular Institute at Orange Coast Medical Center in Fountain Valley, CA.
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Your circulatory system is very much like the hot tub’s. Your blood is like the water. Your heart is like the pump, and your blood vessels are like the pipes. Your heart pumps your blood through the circulatory system in order to feed oxygen and nutrients to cells throughout your body, and to remove waste products. By circulating through the system, your blood is filtered and re-utilized, again and again.
Arteries are naturally flexible and smooth, which allows blood to easily move throughout the body. High blood pressure creates extra force against the artery walls, which damages the lining of the arteries. As they become narrower and harder, this restricts blood flow, and when blood flow is lowered, the heart has to work harder to pump it through the body, which only makes the problem worse.
Banana is the best natural home remedy for high blood pressure that really works and lower the blood pressure fast. The potassium in the bananas has the ability to lower the blood pressure quickly. Also, then it counters the negative effects of sodium in the body. Sodium has ill effects on your blood pressure. Eating bananas will fight its bad effects. Eat 1-2 bananas daily to lower your high blood pressure. It also helps you to control your cholesterol, with its low sodium levels. Along with bananas, you can also eat spinach, orange juice, dried apricots, raisins, baked sweet potatoes, currants, winter squash, cantaloupe and zucchini.
Omega-3 fats are typically found in flaxseed oil, walnut oil and fish, with fish being by far the best source. Unfortunately, most fresh fish today contains dangerously high levels of mercury. Your best bet is to find a safe source of fish, or if this proves too difficult, supplement with a high quality krill oil, which has been found to be 48 times more potent than fish oil.
Don’t get too excited. Turns out that dark chocolate (at least 50% to 70% cocoa) can give you a boost of a plant compound called flavanol. As with garlic, this antioxidant can raise your nitric oxide levels and widen blood vessels. That can make your blood pressure drop a notch. It goes without saying that a little bit of chocolate is all you need.
A comprehensive exercise regimen, such as my Peak Fitness program, is very important in producing long-term benefits in people with high blood pressure. Nearly every program should incorporate anaerobic sprint or burst-type exercises one to three times a week, as these have been shown to be even more effective than aerobic exercises at reducing your risk of dying from a heart attack.
Developed thousands of years ago in India, Ayurveda is the sister philosophy of yoga, the medication form of it. The therapies and treatments work after the identification of an individual’s Dosha- Vata, Pitta, and Kapha. Dosha imbalance is the foremost reason for any health issues and hypertension is the result of the imbalance of the two doshas- Vata and Pitta.
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Also focus on eating nitrate and nitrite-rich vegetables (not to be confused with the other types of nitrates and nitrites that are found in processed meats) . Nitrates and nitrates from vegetables help to relax and dilate blood vessels throughout your body and increase blood flow. Although it’s a short-term effect, eating more nitrate-rich vegetables like beets, cabbage, leafy greens, and vegetable juices, can reduce blood pressure for a few hours. Recent studies have also shown that those who drank beetroot juice showed an immediate effect on lowering blood pressure. By eating plant-based foods consistently, you’ll see their regular benefits.
Cayenne pepper is also good for treating hypertension and including reducing blood pressure. It makes the blood flow. You can add cayenne pepper to your vegetable, salad or fruit salad. You can also add a small pinch of cayenne pepper powder into your smoothies and soups. Use only a small amount of cayenne pepper as it is very spicy. Try this method to lower blood pressure at home.
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Blood pressure is a measurement of the force that blood applies to your arterial walls as it pumps from your heart throughout your body. It also represents how hard your heart is working to push the blood. When blood pressure is higher, it means the heart must work harder to push blood through your system. In turn, the risk of heart disease or heart attack increases.
I totally agree with you that we should not rely on medication for high blood pressure. End of the day, high blood pressure is a symptom that our body requires immediate attention. The kidneys work extremely hard to send out the “signal” to us and what we did is to pop a high blood pressure pill to suppress the signal. With this medication, our body has to work even harder to send us another signal. No wonder over the long run people who are suffering from high blood pressure needs an additional pill for deteriorating kidneys. Our body is fully capable of healing itself without us realizing it. I strongly encourage high blood pressure sufferers to listen to this and say goodbye to high blood pressure once and for all:
If you already have high blood pressure, home monitoring can let you know if your fitness routine is helping to lower your blood pressure, and may make it so you don't need to visit your doctor to have your blood pressure checked as often. Home blood pressure monitoring isn't a substitute for visits to your doctor, and home blood pressure monitors may have some limitations.
The sweet serves up flavanols that help lower blood pressure by relaxing blood vessels and boosting blood flow. On average, regular dark chocolate consumption could help lower your systolic blood pressure (the top number) by 5 points and your diastolic blood pressure (the bottom number) by almost 3 points, suggests an Australian analysis. How dark are we talking? Experts haven't been able to determine an ideal percentage of cocoa, says Vivian Mo, MD, Clinical Associate Professor of Medicine at the Keck School of Medicine of the University of Southern California. But the higher you go, the more benefits you'll get.
Vegetables give you fiber, vitamins, and minerals. They don't have a lot of calories or fat -- a good recipe for controlling blood pressure. Have four to five servings of vegetables a day. That’s 1/2 cup of cooked or raw vegetables, 1 cup of raw leafy vegetables, or 1/2 cup of vegetable juice for each serving. Iffy about veggies? Start by adding a salad at lunch and dinner.
Fruits offer lots of fiber and vitamins that are good for your heart. Many also have potassium and magnesium, which lower blood pressure. Have four to five servings of fruit every day. One serving is a medium apple or orange, or 1/2 cup of frozen, fresh, or canned fruit. One-half cup of fruit juice or 1/4 cup of dried fruit also counts as a serving. Try adding bananas or berries to your breakfast cereal or have fruit for dessert.
Is there anything garlic can’t do? The vegetable is praised in natural medicine and is linked to lowering cholesterol and high blood pressure, too, according to Healthline. This natural antibiotic has the active ingredient allicin to thank for its health benefits. Plus, more research shows eating garlic alters how blood vessels dilate, resulting in blood pressure changes as well.
8. Take less stress: If you want to stay healthy, take less stress. Every individual faces some kind of difficulty in their life. What matters is the attitude you have towards these difficulties. If you constantly take stress or tension, you are likely to have blood pressure problems. Being chronically stressed puts your body in constant fight-or-flight mode. This could lead to faster heart rate and constricted blood vessels. Listen to good music, do yoga, meditate. These are some effective ways to control your stress and also keep your blood pressure under control.
The right tunes can help bring your blood pressure down, according to Italian research. Researchers asked 29 adults who were already taking BP medication to listen to soothing classical, Celtic, or Indian music for 30 minutes daily while breathing slowly. When they followed up with the subjects six months later, their blood pressure had dropped by an average of 4 mmHg.
6. Getting (a little) sunshine. Researchers at the University of Edinburgh confirmed previous studies that found that subjects exposed to UV light experienced a significant drop in blood pressure, apparently because the sun’s rays convert nitrate stored in your skin to nitric oxide, a compound that helps blood vessels retain their elasticity. Of course, you should never spend more than 10 minutes a day in the sun without sunscreen, because of the risk of skin cancer.
In Sweden, blood pressure is often wrongly measured at clinics with the subjects lying down. The differences tend to be small, however: when seated, the systolic blood pressure registers a little lower, and the diastolic a little higher. Trying this on myself, I noted readings of 116/73 averaged over several seated measurements and an average of 119/72 lying down.
8. Take less stress: If you want to stay healthy, take less stress. Every individual faces some kind of difficulty in their life. What matters is the attitude you have towards these difficulties. If you constantly take stress or tension, you are likely to have blood pressure problems. Being chronically stressed puts your body in constant fight-or-flight mode. This could lead to faster heart rate and constricted blood vessels. Listen to good music, do yoga, meditate. These are some effective ways to control your stress and also keep your blood pressure under control.
7. Cut down on sodium intake: Processed and packaged food needs to go out of your kitchen, if you want healthy levels of blood pressure. This is because processed food is loaded with added preservatives to increase their shelf life. Also, prepare your food with lesser salt as high intake of salt is linked to risks of high blood pressure and stroke.
It does not even have to be animal contact. Human contact is great too, so if you are suffering from high blood pressure then a cuddle with your spouse could be just what you need. Being able to laugh with our partner or friends is a great way to reduce stress, so spending regular time socialising is a good tool when it comes to keeping a normal blood pressure level.
If you have hypertension, ask your doctor if OSA could be behind it. (In addition to loud snoring, common symptoms include excessive daytime tiredness and early morning headaches.) Getting your sleep apnea under control could be helpful for improving your blood pressure, says Robert Greenfield, MD, Medical Director of Non-Invasive Cardiology & Cardiac Rehabilitation at MemorialCare Heart & Vascular Institute at Orange Coast Medical Center in Fountain Valley, CA.
If you injure yourself right at the start, you are less likely to keep going. Focus on doing something that gets your heart rate up to a moderate level. If you're physically active regularly for longer periods or at greater intensity, you're likely to benefit more. But don't overdo it. Too much exercise can give you sore muscles and increase the risk of injury.
As long as the measurement is conducted correctly, with certified blood pressure meter, you’ll be getting results just as accurate as you would at a medical clinic. In fact, in Sweden, an investigation has shown that medical practices sometimes wrongly take blood pressure measurements with the patient lying down – so you might even be getting more accurate results at home!
“Beware of the American Heart Association’s (AHA) 'Salty Six' — six popular foods that can add high levels of sodium to your diet,” says Rachel Johnson, PhD, a professor of nutrition at the University of Vermont in Burlington and the former chair of the AHA’s nutrition committee. The Salty Six include breads and rolls, cold cuts and cured meats, sandwiches, pizza, soup, and chicken.
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allHealth
Sleeping Pills – An Effective Alternative
Overcoming insomnia is a journey – and, as you may have discovered, it can also be a matter of trial and response. Undertaken systematically overcoming insomnia and getting a good night’s sleep is an ultimately rewarding process. But, if you’ve already made basic changes to your diet and sleep routine, and you’ve tried specific techniques for reducing stress and improving the quality of your sleep, you may be tempted to turn to artificial sleep aids like sleeping pills.
While sleeping pills may promise a miracle cure for insomnia, the inherent risks of taking sleeping pills to combat insomnia are myriad. Regardless of whether you opt for short-term sleeping pills or a longer course, barbiturates, benzodiazepines and non-benzodiazepines alike all carry similar risks – namely the potential for over-use or, in the worst cases, the possibility of addiction.
Because sleeping pills serve to depress your body’s nervous system in order to create an artificial “sleep”, they do not facilitate the essential healing and restorative cycles and functions normally undertaken by your body during sleep. That’s why taking sleeping pills can often leave you feeling drowsy or inadequately rested in the morning.
Instead of turning to sleeping pills to overcome insomnia, try using one of the numerous natural and time-tested remedies that are widely available. Often referred to as a “natural sleeping pill”, melatonin offers one viable sleep-enhancing option.
Melatonin is the hormone naturally produced by your body to induce sleep, and many people have successfully restored their own productive sleep patterns by using melatonin to help stimulate the body’s own urge to sleep. Melatonin can be an effective natural alternative to sleeping pills, but should nonetheless be used with caution as it is not yet regulated by any government body.
Herbal remedies are another excellent alternative to sleeping pills and also to melatonin. Consumed in the form of herbal teas and supplements, or even as aromatherapy, herbs like valerian root and chamomile have been lauded as effective sleep-enhancers for centuries. Unlike melatonin or sleeping pills, chamomile does not have to be consumed over a period of time before it becomes effective. Chamomile tea can be used on an as-needed basis and many people have used its sleep-enhancing qualities to successfully combat bouts of insomnia.
Slightly stronger than chamomile and usually taken in pill form, valerian root is another well-known herbal sedative recognized for its ability to overcome insomnia and promote quality sleep. Valerian’s sleep-inducing properties are so effective that it is actually medically recognized as the herbal equivalent of Valium™. Indeed, it is said that the name Valium™ was derived from Valerian, although Valium™ itself is not otherwise connected with valerian in any way.
As with all adjustments to your sleep cycle or sleep routine, you should choose one natural sleep remedy and use it consistently for two weeks before making any other changes – this gives your body time to incorporate and respond to the sleep enhancing benefits of the remedy you have chosen.
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• Research article
• Open Access
Analysis of 16S rRNA gene sequences and circulating cell-free DNA from plasma of chronic fatigue syndrome and non-fatigued subjects
• 1Email author,
• 2,
• 2,
• 1 and
• 1
BMC Microbiology20022:39
https://doi.org/10.1186/1471-2180-2-39
Received: 25 October 2002
Accepted: 23 December 2002
Published: 23 December 2002
Abstract
Background
The association of an infectious agent with chronic fatigue syndrome (CFS) has been difficult and is further complicated by the lack of a known lesion or diseased tissue. Cell-free plasma DNA could serve as a sentinel of infection and disease occurring throughout the body. This type of systemic sample coupled with broad-range amplification of bacterial sequences was used to determine whether a bacterial pathogen was associated with CFS. Plasma DNA from 34 CFS and 55 non-fatigued subjects was assessed to determine plasma DNA concentration and the presence of bacterial 16S ribosomal DNA (rDNA) sequences.
Results
DNA was isolated from 81 (91%) of 89 plasma samples. The 55 non-fatigued subjects had higher plasma DNA concentrations than those with CFS (average 151 versus 91 ng) and more CFS subjects (6/34, 18%) had no detectable plasma DNA than non-fatigued subjects (2/55, 4%), but these differences were not significant. Bacterial sequences were detected in 23 (26%) of 89. Only 4 (14%) CFS subjects had 16S rDNA sequences amplified from plasma compared with 17 (32%) of the non-fatigued (P = 0.03). All but 1 of the 23 16S rDNA amplicon-positive subjects had five or more unique sequences present.
Conclusions
CFS subjects had slightly lower concentrations or no detectable plasma DNA than non-fatigued subjects. There was a diverse array of 16S rDNA sequences in plasma DNA from both CFS and non-fatigued subjects. There were no unique, previously uncharacterized or predominant 16S rDNA sequences in either CFS or non-fatigued subjects.
Keywords
• chronic fatigue syndrome
• CFS
• novel infectious agents
• 16S rDNA
Background
Chronic fatigue syndrome (CFS) is a complex illness defined by unexplained disabling fatigue and a combination of non-specific accompanying symptoms [1]. There are no consistent anatomic lesions or clinical chemistry abnormalities. While no known infectious agents or immunologic perturbations have been consistently associated with CFS [27], the illness has many features suggestive of an infectious disease. Fatigue, muscle and joint pain, sore throat, and swollen glands are all common symptoms shared by infection and CFS. In addition, many people with CFS describe the onset of their illness as sudden or "flu-like", anecdotally suggesting a possible infectious etiology [8]. However, identification of an infectious agent specifically associated with CFS has eluded conventional laboratory analysis. Extensive seroepidemiologic surveys to detect antibody responses to numerous known viral, bacterial, and rickettsial agents have failed to show a difference between CFS cases and normal controls [9, 10].
Searching for known or novel infectious agents in persons with CFS is complicated by the lack of a known lesion or diseased tissue to sample. Recently, circulating cell-free DNA from plasma and serum [11] has been shown to contain sequences of tumor [12], viral [13], and bacterial origin [14]. This plasma DNA therefore serves as a sentinel of occult disease occurring in diverse sites throughout the body. We used this plasma DNA to search for previously uncharacterized as well as known bacterial pathogens. To do so, we used broad range PCR of the bacterial 16S ribosomal RNA gene (rRNA) [15]. This broad range amplification scheme has been successful in detecting and characterizing bacterial pathogens from several disease states and in several types of clinical specimens [16].
We determined the level of circulating plasma DNA in CFS subjects as one possible indicator of increased cellular turnover or chronic inflammation. We also amplified and sequenced the 16S rRNA gene to search for known and or previously uncharacterized bacterial agents in cell-free circulating DNA to determine if a bacterial pathogen was associated with CFS.
Results
Evaluation of methods
We first determined whether the bacterial 16S rDNA sequence could be amplified if present in cell-free plasma DNA. To do this, we spiked 100 ng of plasma DNA with 14 ng to 1.4 × 10-9 ng of purified Escherichia coli template DNA. As shown in Figure 1, as little as 1.4 × 10-3 ng of E. coli DNA could be detected after amplification of the 16S rRNA gene by using the 515F and RD1 primers. This amount is the equivalent of 1.9 × 102 E. coli genomes per 100 ng cell-free plasma DNA. All amplified products were sequenced and confirmed to be the same E. coli strain (data not shown).
Figure 1
Figure 1
Titration of E. coli template DNA for 16S rDNA PCR assay, using 515F and RD1 primers. Lanes: L, 100-bp DNA ladder; 1, 14 ng; 2, 1.4 ng; 3, 0.14 ng; 4, 1.4 × 10-2 ng; 5, 1.4 × 10-3 ng; 6, 1.4 × 10-4 ng; 7, 1.4 × 10-5 ng; 8, 1.4 × 10-6 ng; 9, 1.4 × 10-7 ng; 10, 1.4 × 10-8 ng; 11, 1.4 × 10-9 ng; 12, Negative control (sterile distilled water); 13, Positive control (purified E. coli DNA).
Characterization of plasma DNA
The amount of cell-free DNA ranged from 0 to 1320 ng per ml of plasma (average 128 ng DNA), with 91% (81/89) having detectable levels. CFS subjects tended to have less plasma DNA than non-fatigued subjects (average 91 versus 151 ng), but this difference was not significant. Six (18%) of 34 plasma samples from CFS subjects had no detectable cell-free DNA, whereas only 2 (4%) of 55 non-fatigued subjects had no detectable cell-free DNA in their plasma (P = 0.08). No differences in plasma DNA concentration were noted between subjects when grouped by sex, age, CFS onset type, or duration of illness.
All 89 samples, whether plasma DNA was isolated or not, were evaluated for the presence of bacterial 16S rDNA sequences. Overall, 23 (26%) subjects had 16S rDNA sequences amplified and characterized. The average number of distinct 16S rDNA sequences in the 23 subjects was 9 (range 3–14). The CFS subjects had on average 11 distinct 16S rDNA sequences and the non-fatigued subjects had an average of 9 distinct 16S rDNA sequences. The plasma DNA of 4 (14%) of 28 CFS subjects had 16S rDNA sequences compared with 17 (32%) of 53 of non-fatigued subjects (P = 0.03). No differences were noted in detection of bacterial 16S rDNA sequences between subjects when grouped by sex, age, CFS onset type, or duration of illness. There was no correlation between the amount of plasma DNA and the ability to amplify 16S rDNA sequences (Figure 2) since these sequences were detected in samples from CFS and non-fatigued subjects with plasma DNA concentrations that ranged from 24 to 294 ng/ml.
Figure 2
Figure 2
Graphical representation of the number of 16S rDNA sequences in each subject (primary y axis and represented as bars) in relation to the subjects' plasma DNA concentration (secondary y axis and represented as points on the line). All 34 CFS subjects are represented on the left side of the graph and all 55 non-fatigued subjects are shown on the right side. Each group was sorted from lowest to highest plasma DNA concentration to illustrate the lack of correlation between DNA concentration and 16S rDNA sequences.
All 16S rDNA-amplified products were sequenced to identify the prokaryotic origin. Each of the sequences was either identical or highly similar (97% or higher) to prokaryotic sequences in GenBank (data not shown). To determine whether a particular bacterial sequence was found in CFS cases versus non-fatigued controls, a cluster analysis was performed. There were no 16S rDNA sequences that were unique or predominant in either the CFS or the non-fatigued group, as indicated by the random distribution and lack of clustering of CFS or non-fatigued subjects (Figure 3). There was also no indication that bacteria known to cause prolonged fatiguing illness (e.g., Coxiella sp. or Borellia sp.) were more prevalent in CFS subjects.
Figure 3
Figure 3
Cluster analysis of the 23 subjects positive for 16S rDNA sequences from the 300 bp cloned insert to determine whether a particular bacterial sequence was found in CFS cases versus non-fatigued controls. The subjects' classification as non-fatigued (NF) or CFS is shown at the top of the columns. The identification of the 16S rDNA sequence is shown at the right. The colored block indicates the presence and number of clones of that particular bacterial sequence; white is negative, blue is one clone, green is two clones, red is three clones, and black is four clones.
Discussion
Since CFS has no known anatomic lesion, we decided to examine the levels of cell-free plasma DNA as a systemic indicator of disease. Plasma DNA was isolated from most of the CFS and non-fatigued subjects. We detected a higher concentration of plasma DNA in the non-fatigued subjects than in the CFS subjects and there were fewer non-fatigued subjects who were plasma DNA negative than CFS subjects, however, these differences were not significant. The physiologic significance and the source of cell-free DNA in the plasma are not fully appreciated, but we suspect that it may result from cellular degradation. To date, plasma DNA has been used as a relatively noninvasive sample to detect ongoing pathogenic events, such minimal residual disease or cancer [10]. Our data show no significant difference in the level of plasma cell-free DNA in CFS versus non-fatigued subjects, indicating that there may be no unusual cell turnover in this population of CFS subjects. It is also possible that cell-free plasma DNA concentration is not a sensitive indicator for increased cellular turnover or chronic inflammation.
Despite an exhaustive search for known pathogens by conventional laboratory methods, no single pathogen has been consistently identified as a causal agent of CFS. Almost every known viral and bacterial agent that can cause fatiguing illness has been tested for in CFS subjects, and there has been no difference in the prevalence of these agents between CFS and healthy subjects [9, 17]. One explanation is that the pathogen associated with CFS is novel or previously uncharacterized. To search for prokaryotic agents that might be specifically associated with CFS, we used consensus PCR primers to the conserved 16S rRNA subunit to detect and characterize these sequences. Of the 89 subjects, 4 CFS subjects and 17 non-fatigued subjects had 16S rDNA sequences amplified. This difference in the presence or absence of the 16S rDNA amplified product between CFS and non-fatigued was not related to differences in plasma DNA concentration. There were no unique or previously uncharacterized prokaryotic sequences identified in either the CFS or non-fatigued group. Rather, a diverse array of known prokaryotic sequences was found circulating in the plasma.
While it is unlikely that the 16S rDNA sequences characterized here are due to experimental or environmental contamination, we cannot exclude the possibility that the vacutainer tubes used for blood collection were a source of bacterial DNA detected. However, the vacutainer tubes were not likely a significant source since all plasma samples, whether DNA was present or not, were subjected to amplification for the 16S ribosomal subunit. All of the plasma DNA-negative samples were negative for the 16S rDNA-amplified product. In addition, water controls taken through the entire extraction process were consistently negative. Finally, only 23 of the 89 plasma samples were positive for 16S rDNA sequences. If our results are a reflection of the occurrence of 16S rDNA sequences in healthy subjects, it is plausible to hypothesize that the presence, rather than absence, of these sequences reflects the normal physiologic state and symbiotic relationship between humans and microbes. This is not the first illustration of the apparent symbiotic relationship that exists between humans and bacteria. The assessment of blood from healthy subjects by amplification of the 16S rRNA gene revealed numerous bacterial sequences that were not found in reagent controls [18]. Weber et al [19] have identified a number of microbial and viral transcripts from human cDNA libraries by computational subtraction method. Not surprisingly, the human body has been referred to as "microbial observatory" [20]. Further analysis of the microbial flora that exists at various sites within the body in both healthy and diseased persons should further our understanding of the interrelationships between microbes and their human hosts.
The experimental design used for this study has some limitations for addressing our hypothesis that a novel pathogen is associated with CFS. The plasma DNA sample may not be the ideal sample for detecting prokaryotic sequences. Granulocyte cell subsets may be more appropriate since this peripheral blood cell fraction contains neutrophils and other scavenger cells important for viral and bacterial clearance. These peripheral blood samples may not all have been collected and processed optimally for preservation of DNA in plasma but all samples from all subjects were processed similarly. Finally, the CFS subjects were years past the onset of illness and may have cleared the agent that provided the trigger for illness.
Conclusions
DNA isolated from the plasma can be used to investigate the association of pathogens with occult disease. Those CFS subjects with plasma DNA had slightly lower concentrations than the non-fatigued subjects and there were more CFS subjects with no detectable DNA in plasma. There was a diverse array of 16S rDNA sequences in plasma DNA from both CFS and non-fatigued subjects. Future assessment of 16S rDNA sequences in peripheral blood will focus on the granulocyte cell subset.
Subjects and methods
Case and control subjects
As part of a longitudinal population-based study of CFS in Wichita, Kansas [21], peripheral blood specimens were collected during clinical evaluation of fatigued subjects identified as having potential CFS ("CFS-like") and a random selection of non-fatigued subjects. Among persons clinically evaluated at baseline, samples from 34 subjects who met the 1994 CFS case definition [1] and 55 non-fatigued subjects with sufficient plasma stored were selected for analysis.
Blood was collected in sodium citrate vacutainer tubes and shipped by overnight courier to the Centers for Disease Control and Prevention (CDC) Serum Bank Facility in Lawrenceville, Georgia. The uncoagulated blood was diluted 1:2 with physiologic saline and separated on Ficoll to collect plasma and mononuclear cells. The diluted plasma was stored in 1-ml aliquots at -70°C until needed.
Plasma DNA isolation
A 1-ml aliquot of plasma was concentrated to approximately 250 μl in a Centricon Centrifugal Filter Device YM-100 (Millipore Corporation, Bedford MA) and DNA was extracted by using the QIAmp DNA Mini Kit (Qiagen Inc., Valencia, CA), according to manufacturers' instructions. A DyNA Quant 200 Fluorometer (Amersham Biosciences, Inc., Piscataway, NJ) was used to determine DNA concentration.
Polymerase chain reaction (PCR)
A 50-μl amplification reaction consisted of 5 μl of 10 × PCR buffer (100 mM Tris HCl, pH 8.3; 500 mM KCl), 2 mM of MgCl2, 0.2 mM of dATP, dCTP, dGTP, dTTP, 2.5 U of Taq polymerase, 10 pmol each of forward and reverse primers, and 5 μl of the template plasma DNA. Water samples that were taken through the plasma DNA concentration and extraction process were included as samples to identify background bacterial sequences present in reagents and supplies. Two sets of 16S rDNA primers 515F/RD1 and 515F/806R [16, 17] were used in separate amplifications. These primers yield amplification products of ~1045 and ~300 bp, respectively. The 515F/806R primers were included to amplify smaller templates and low copy number targets. The PCR was performed in a PE 9700 thermocycler with an initial incubation at 94°C for 4-min, followed by 35 cycles of 94°C for 30 sec, 55°C for 30 sec, and 72°C for 90 sec. A final step consisted of a 5-min extension at 72°C. The amplified products were resolved in 1.5% Nusieve agarose gel and photographed under UV light by using a GelDoc 2000 imaging system (Bio-Rad Laboratories).
16S rDNA sequence determination
The 1045- and 300-bp amplified products were purified by gel exclusion chromatography to remove unincorporated nucleotides and enzymes, and then either sequenced directly or after cloning into a vector. The direct sequencing was done with Cy5-labeled, nested sequencing primers 806R, and 515F in an ALFexpress sequencer (Amersham Pharmacia). All products amplified with the 515F/806R primer set were cloned into a PGEM-T easy vector (Promega Corp., Madison, WI) or into a TOPO TA cloning vector for sequencing (Invitrogen Corp., Carlsbad, CA) by following the manufacturer's protocol. Ninety six clones from each reaction amplified with the 515F/806R primers were selected for further investigation. Each clone was grown overnight in 2.0 ml of LB broth and a plasmid miniprep was prepared. Unique clones were determined by PCR-RFLP of the amplified inserts. The inserts in the plasmid were amplified in a 30 μl PCR reaction using T3 and T7 vector based primers followed by double digestion of the products with Msp I and HinP I. The clones containing unique inserts were identified on the basis of unique restriction pattern and were selected for sequencing. Typically, ten to twenty unique restriction patterns were identified resulting in the sequencing of at least 10 clones from each sample. The plasmid inserts were sequenced in both directions using vector-based sequencing primers T3, T7, or SP6 in an ABI 377 sequencer (Perkin Elmer Corp., Norwalk CT).
Data analysis
We used the chi square to identify differences in plasma DNA concentrations between the CFS and non-fatigued subjects. Subjects were stratified on the basis of sex, age (<45 years vs >45 years), CFS onset type (sudden vs gradual), and duration of illness (<5 years vs > 5 years) and compared by using a non-parametric Wilcoxon two-sample test. Cluster analysis was accomplished using BioNumerics (Applied Maths, Antwerp Belgium). For sequence analysis, contiguous sequences were generated using the DNASTAR program for each clone from sense and antisense strand sequences. The GenBank database was searched by using the BLAST tool to identify bacterial sequence similarities. A sequence similarity of 97% or greater was considered as an acceptable identification.
Author's contributions
SDV contributed to the conception and design of this study, the analysis of the results and drafted the manuscript. SKS contributed to the design of the experimental approach, implemented the experimental approach, analyzed the bacterial sequences, assisted in interpretation of the results and assisted in drafting the manuscript. JC conducted all amplification, cloning and sequence reactions and assisted in sequence analysis. ERU and WCR contributed to the conception and design of this study, interpretation of results and assisted in drafting the manuscript.
All authors read and approved the final manuscript.
Declarations
Acknowledgments
This research was supported in part by extramural research funding from the Viral Exanthems and Herpesvirus Branch in the Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention to SKS at the Marshfield Medical Research Foundation. Informed consent was obtained from all subjects, and human experimentation guidelines of the US Department of Health and Human Services were followed in the conduct of this research. The authors thank the Sedgwick County Department of Public Health, the Centers for Disease Control and Prevention CFS Research Group, the CFIDS Association of America, and the National Chronic Fatigue Syndrome and Fibromyalgia Association for their collaboration and Kurt Reed for helpful discussions.
Authors’ Affiliations
(1)
Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, USA
(2)
Clinical Research Center, Marshfield Medical Research Foundation, Marshfield, USA
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Health
On a Plant-based Diet Why are people Gaining Weight?
On a Plant-based Diet Why are people Gaining Weight?
Like any eating example, a plant-based eating routine necessitates that people focus on calories.
EATING PLATEFULS of plant-based nourishments may appear to be a simple method to shed pounds and get over into their thin pants. All things considered, plants are for the most part water and are stacked with nutrients, minerals, and phytochemicals. Yet, don’t be tricked: Plant-based weight control plans accompany a similar essential rule of any eating example. “If you’re not burning off more calories than you’re consuming, you’ll gain weight,” says Kristin Gustashaw, a progressed clinical dietitian with Rush Medical Center.
What Is a Plant-based Diet?
A plant-put together diet centers with respect to vegetables, entire grains, vegetables, organic products, nuts, seeds, and unsaturated oils. The eating design incorporates unobtrusive measures of fish and other fish, poultry, dairy items, (for example, eggs or cheddar) and little, intermittent measures of lean red meat.
Numerous weight control plans have a plant-based eating style. They are recognized by different qualities. For instance:
A veggie lover diet disposes of meat and once in a while other creature items. It has various varieties. For instance, a pescatarian diet permits fish; a lacto-ovo veggie lover diet permits dairy items; a vegetarian diet kills all nourishments that originate from creatures, including spread, eggs, and mayonnaise.
A Mediterranean eating regimen inclines toward fish as the protein of decision and joins little day by day measures of olive oil. Limited quantities of red wine are additionally suggested. This is a well-examined eating style related with life span and a diminished hazard for creating coronary illness and diabetes.
The Flexitarian Diet is a vegan eating design that leaves space for the periodic burger. The eating regimen likewise utilizes calorie limits for every dinner.
The Nordic Diet incorporates bunches of fish and entire, natural nourishments that are privately sourced. It centers around canola oil as opposed to olive oil.
Proof proposes that these eating regimens are related with weight reduction. In any case, that doesn’t mean they’ll work for people. “Any intervention that doesn’t focus on reducing calories won’t lead to weight loss. Just eating fruits and vegetables and increasing healthy fat intake hasn’t consistently shown that it leads to weight loss over time,” says Colleen Tewksbury, an enrolled dietitian and bariatric program supervisor at Penn Medicine.
Calorie Concerns
Plant-based nourishments are not made equivalent. Some have more calories, sugars and fats than others. For instance, one medium cucumber contains 12 calories, 2 grams of sugars and a minute measure of fat. One medium avocado, in any case, contains 322 calories, 17 grams of starches and 29 grams of fat. “Avocados, olive oil, whole grain, lentils – they are all high in calories,” Tewksbury notes.
The fat alone could be a tipoff to higher calories: one gram of fat contains 9 calories, which is more than double the measure of calories in 1 gram of sugar.
Different ways that calories sneak into plant-based weight control plans include:
• Bit size. Plant-based nourishments are anything but difficult to indulge in light of the fact that they’re scrumptious, and people accept that they’re beneficial for people. “You think you can eat as much as you want. But it’s not true. For example, a whole cup of nuts could exceed 700 calories,” Gustashaw says. Moreover, a serving of cooked quinoa (a large portion of a cup) has around 100 calories. That would make a decent establishment for cooked vegetables. Be that as it may, a plateful of quinoa could have 300 or 400 calories.
• Garnishes. Now and again it’s the nourishment besting that slopes up calorie admission. A bowl of low-calorie vegetables like kale and other serving of mixed greens can go from a couple dozen calories to two or three hundred on the off chance that people douse it in unhealthy Caesar dressing and include bread garnishes. Or then again in the event that people top dark espresso with cream, chocolate sauce and other sugary syrups, people could fire up the carbohydrate content to 500 calories or more – as much in general supper.
• Low quality nourishment. A lot of items are free of creature based nourishments yet at the same time exceptionally high in sugar, fat and calories. Models incorporate chips, treats, doughnuts, French fries and sans dairy frozen yogurt.
• Meat substitutes. “A plant-based meat product like textured vegetarian soy or pea protein can be heavily processed with a lot of extra sugar, fat, binders and additional carb-based items,” Tewksbury says.
• Beverages. Calories include immediately when people’re swallowing them down in smoothies, juice, sports drinks, enhanced coconut water, pop, seasoned nut milks (like soy or almond) and mixed beverages. “Some drinks and beverages can have a thousand calories depending on the size,” Gustashaw says.
Start Counting Calories
So as to make sense of why people are putting on weight on a plant-based eating routine, people will need to make sense of two things.
One is the thing that their everyday calorie objective ought to be so as to get in shape relentlessly without giving up supplements or vitality. To discover, converse with their primary care physician or a dietitian or utilize an online calorie mini-computer.
The other is to begin checking what number of calories people are devouring every day. Measure their nourishment with scales, look into data on the web or utilize the Nutrition Facts mark on a nourishment bundle.
At that point record the amount people are devouring. “Keep a food journal,” Tewksbury exhorts. “Tracking what you’re having and being able to see what might be leading to weight gain is really important. A food journal is one of the strongest predictors that someone will be able to maintain or lose weight.”
Notwithstanding calories, people might need to take note of what number of grams of starches, fat, sugar or sodium is in their nourishment. This data can assist people with making changes toward a more advantageous eating routine.
Different Tips For Success
Tallying calories is a significant method to comprehend why people are putting on weight on a plant-based eating regimen. However, there are different advances people can take.
Eat entire grains and stay away from refined grains. Entire grains contain fiber, which assists prevent with blooding sugar from spiking and encourages people feel full more. “Aim for 25 to 30 grams per day,” Gustashaw recommends.
Get enough protein. Protein takes more time to process than starches, which assists fight with offing hunger. To assess the measure of protein people need (in grams) every day, Gustashaw suggests separating your weight by two. “For example, if you weigh 150 pounds, aim to eat about 75 grams of protein each day,” they say.
Go for not so much organic product but rather more vegetables. “It’s a good idea to eat fruits and vegetables, but if you’re trying to lose weight, load up on non-starchy vegetables and just a smattering of fruit, which is higher in calories,” Gustashaw says.
Maintain a strategic distance from larger than usual parts. Tewksbury suggests utilizing the USDA’s their Plate approach: Fill half of their plate with for the most part vegetables and a few natural products, a fourth of their plate with entire grains and a fourth of their plate with protein.
• Be aware of fake sugars. Fake sugars have no calories and can be helpful instruments (with some restraint) to make nourishments progressively attractive. Be that as it may, researchers are exploring potential symptoms identified with weight control. “Some research indicates artificial sweeteners trick our bodies into thinking we’re still hungry,” Gustashaw notes, “and some research even suggests artificial sweeteners change our gut bacteria to make it harder to lose weight.”
• Find different garnishes. “If you really like sweet and salty toppings on salad, find a lower-calorie dressing or just add cranberries and a few nuts,” Tewksbury says. For espresso, include cinnamon and skim milk rather than whipped cream and syrup.
Furthermore, recall that getting in shape isn’t just about their eating regimen. Physical movement decides what number of calories people consume in a day. Furthermore, there are different components that assume a job. “You have to consider access to foods, genetics, gut hormones, social psychology, peer pressure, weight status, lifestyle activity and even self-esteem,” Tewksbury explains. “Your diet is just one piece of a very large puzzle.”
Topics #are people #Calorie Concerns #EATING PLATEFULS #Flexitarian Diet #Nordic Diet #Plant-Based Diet #Start Counting Calories #What Is Plant-Based Diet?
Mendel Gordon
Mendel Gordon is a writer of fantasy and science fiction books and news articles. In high school, Mendel was the editor of the school newspaper and joined the writing club. He starts his writing career from this club. Firstly, he writes short stories, somewhat little things about ongoing things like news. Now he writes news articles and published it on infusenews.com.
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5eff3d1f6f98e57329caed0ceb9053d3
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1,451,051,530,869,785,000
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Mental Health
Stress Relief: Implementing Self-Care Techniques for Lasting Resilience
If you like it then share it
Introduction:
In today’s fast-paced world, stress has become an unwelcome guest in our lives. However, by implementing a few self-care strategies, you can build resilience and better manage the pressures you face.
1. Identify Stressors:
One of the first steps towards stress management is identifying the sources of your stress. This might be work, relationships, finances, or other factors. Once you understand what’s causing your stress, you can start addressing it effectively.
2. Establish Healthy Boundaries:
Learning to say ‘no’ can be one of the most powerful self-care techniques. Establish healthy boundaries in your personal and professional life to avoid over-committing yourself.
3. Regular Exercise:
Exercise is a proven stress reliever. Regular physical activity releases endorphins, the body’s natural mood lifters, and can also improve your sleep quality, another essential element in stress management.
4. Mindful Meditation:
Mindful meditation helps you stay in the present moment, reducing the impact of stressors. Regular practice can help lower stress levels and improve your overall sense of well-being.
5. Balanced Nutrition:
Eating a balanced diet can help your body better cope with stress. Opt for whole foods, lean proteins, fruits, and vegetables, and stay hydrated. Avoid excessive caffeine and alcohol, which can exacerbate stress.
6. Quality Sleep:
Sleep is crucial for stress management. Aim for 7-9 hours of quality sleep per night. Develop a sleep routine that includes winding down activities, such as reading or listening to soft music.
7. Reach Out:
Never hesitate to reach out to friends, family, or a professional if you’re feeling overwhelmed. Sometimes, talking about your stressors can help you gain a fresh perspective and develop coping strategies.
Conclusion:
Remember, self-care is not selfish; it’s essential for maintaining your mental, emotional, and physical health. As you navigate life’s stressors, these self-care strategies can help you foster resilience and find a sense of calm.
(Please note the content of this blog post is for informational purposes only. It is not a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your healthcare provider with any questions you may have regarding a medical condition or treatment.)
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Quecksilberdampf aus Zahnquecksilber hoch toxisch
Mercury vapours are continuously released from the fillings every time we chew – in fact, chewing gum doubles the mercury levels in the blood and trebles them in the urine.
The World Health Organization has found that the average individual could absorb as much as 120 micrograms of mercury per day from their amalgam fillings, which is considered a toxic dose. (WHO 1990)
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Psychiatry InvestigPsychiatry InvestigPIPsychiatry Investigation1738-36841976-3026Korean Neuropsychiatric Association23482680359043010.4306/pi.2013.10.1.47Original ArticleAn fMRI Study Investigating Adolescent Brain Activation by Rewards and FeedbackChoiWon-Hee1SonJung-Woo1KimYeoung-Rang2OhJong-Hyun1LeeSang-Ick1ShinChul-Jin1KimSie-Kyeong1JuGawon1LeeSeungbok3JoSeongwoo3HaTae Hyon4Department of Psychiatry, Chungbuk National University Hospital, Cheongju, Republic of Korea.Department of Psychiatry, Cheongju Medical Health Hospital, Cheongju, Republic of Korea.Department of Psychology, Chungbuk National University, Cheongju, Republic of Korea.Department of Psychiatry, Bundang Seoul National University Hospital, Seongnam, Republic of Korea. Correspondence: Jung-Woo Son, MD, PhD. Department of Psychiatry, Chungbuk National University Hospital, 776 1Sunhwan-ro, Heungdeok-gu, Cheongju 361-711, Republic of Korea. Tel: +82-43-269-6182, Fax: +82-43-267-7951, mammosss@hanmail.net3201308220131014755043201206620121682012Copyright © 2013 Korean Neuropsychiatric Association2013This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.Objective
This study aimed to investigate the adolescent brain activation patterns in response to performance feedback (PF), social reward (SR) and monetary reward (MR) and their association with psychological factors.
Methods
Functional magnetic resonance imaging (fMRI) was performed while middle school boys (n=15) performed tests pertained to PF, SR and MR. The brain activation pattern in each condition was investigated, and the extent of brain activation in each of the three conditions was compared at once.
Results
The caudate and the dorsal prefrontal area were activated in all three conditions. Furthermore, the cuneus showed significantly greater activation in the PF condition than the SR or MR condition. And the self - related areas, such as the right precentral gyrus and paracenral lobule, were more activated in the SR condition than the PF or MR condition. The left middle frontal gyrus was more activated in the MR condition than the PF or SR condition.
Conclusion
Not only various reward stimuli but also feedback stimulus might commonly activate dorsal prefrontal and subcortical area in adolescents. Moreover, several different brain activation patterns were also observed in each condition. The results of this study could be applied to planning of learning and teaching strategy for adolescents in various ways.
AdolescentPerformance feedbackSocial rewardMonetary rewardfMRI
INTRODUCTION
Of the many characteristics of adolescence, 'reward seeking behavior' is gaining much attention.1 Reward seeking helps adolescents achieve independence by increasing their desire for achievement, but can also cause an obsession with risky behaviors, instability or deviations to satisfy immediate pleasure. Drug abuse and eating disorders, which appear during adolescence, are also closely related to reward-seeking behaviors.2
Recent studies have used brain imaging to investigate reward-seeking behaviors in adolescents. Galvan et al.3 conducted a functional magnetic resonance imaging (fMRI) study investigating the brain activation by reward stimulus in groups of normal children, adolescents and adults. This study found that adolescents show significantly lower activation of the orbitofrontal cortex, which is associated with stimulus control and the regulation of emotions, than adults, while the activation of nucleus accumbens, which is associated with reward seeking, was very close to the level of activation in adults. In contrast, a study by Bjork et al.4 reported that the anticipation for gaining rewards caused greater activation of the right ventral striatum and amygdala in adolescents than in young adults. Van Leijenhorst et al.5 have reported that the activation of the anterior insula was much higher in adolescents than in adults when performing a task that cannot accurately predict the extent of the reward.
The above studies all used monetary rewards. Monetary reward have also been used frequently in brain imaging studies investigating the brain activation by reward stimulus in adults.6,7 However, monetary reward is just one of the many stimuli that trigger human behavior. Di Chiara and Vanentina8 have claimed that all stimuli that function as a positive reinforcement in motivating individuals could be rewards. Meanwhile, 'feedback' is considered to be something that is similar to a reward and can act as positive or negative reinforcement. Even in real life, adolescents consider other people's evaluation of their own lives important, and they also modify their current study plans through feedback on their test results. Some brain imaging studies have also used reinforcements other than monetary reward, such as social reward and performance feedback.
Social reward is comprised of social status (e.g., reputation) and social assessment (e.g., praise) and provides important motivation for an individual's decision-making and goal-oriented activities. Izuma et al.9 used monetary and social rewards (e.g., a good reputation) in an fMRI study on adults, showing that both stimuli activated the striatum. Zink et al.10 have also reported a similar result. A study that compared the differences between men and women with regards to monetary and social rewards during 'anticipation' found that the activation of the mesolimbic brain region of men was far more noticeable for monetary rewards than for social rewards, whereas women showed activation of the mesolimbic brain region in both reward conditions.11
Performance feedback refers to providing objective facts (e.g., "correct/incorrect") about the final outcome of task performance, and using this feedback can help in modifying a strategy or decision making. Tricomi et al.12 have reported that the bilateral caudate nucleus was clearly activated when performance feedback was provided during task performance. Moreover, a study by Nieuwenhuis et al.13 reported that the rostral anterior cingulate cortex, posterior cingulate cortex, right superior frontal gyrus and striatum were activated when positive feedback (rather than negative feedback) was given. A different report found that when evaluative feedback (clever/stupid), which is considered a social reward, was compared with performance feedback (correct/incorrect), the cortical midline structure was activated in response to the social reward, but no region was activated for the performance feedback.14
As mentioned above, various studies investigating reinforcements other than monetary rewards are being conducted in adults. However, our search results revealed that there are few reports that have studied the brain activation patterns for social reward and performance feedback in adolescents. In particular, no single study has investigated the brain responses to monetary rewards, social rewards and performance feedback together in adolescents.
Alternatively, reward-seeking behaviors during adolescence may also be linked to the psychological characteristics of this period in life. Depressive feelings may be one of these characteristics. Pizzagalli et al.15 claimed that depressed individuals lose their ability to integrate the reinforced experiences with the passage of time when performing a task with the likelihood of a reward, and an fMRI study by Forbes et al.16 also reported that children with major depressive disorder have a relatively reduced neurological response in the caudate nucleus and the orbitofrontal cortex in response to the social reward stimulus of a smiling picture compared to normal children. In addition, Narcissism is also one of the important factors in adolescents. It is divided into 'overt narcissism' and 'covert narcissism', in which the former appears as actively demanding praise from others and flaunting magnificence, while the latter is related to identifying other people's reactions and avoiding situations in which one might be criticized or condemned and thereby protecting oneself.17 Considering all of these facts, we believe it would be very meaningful to investigate the correlation between the adolescent brain activation patterns related to rewards or feedback and depressive feelings and narcissistic tendencies.
Therefore, we used fMRI to examine the adolescent brain responses when asked to perform tasks associated with performance feedback, social reward and monetary reward. Moreover, we wanted to identify what kinds of relationship exists between depressive feeling or covert narcissism and the brain regions associated with rewards.
METHODSParticipants
The subjects were recruited through advertisements in hospitals and schools targeting male middle school students in Cheongju city. The inclusion criteria were as follows: 1) between 13 and 15 years of age; 2) right-handedness; 3) IQ above 80, as determined by the abbreviated IQ test; 4) no history of head trauma, convulsive disorder, or other major neurological disorders; 5) not suffering from serious medical or surgical illness and 6) not affected with psychiatric disorders, as determined by interviews using the Kiddie-Schedule for Affective Disorders and Schizophrenia-Present and Lifetime Version-Korean Version (K-SADS-PL-K).18 Ultimately, 15 subjects were analyzed.
This study obtained approval from the Bioethics Committee at the Chungbuk National University Hospital, and written consent forms were obtained after the study objectives and methods were fully explained to the study participants.
Behavioral testing
The short-form of the Wechsler Intelligence Scale for Children-Revised (WISC-R) was used to assess the intelligence of the study group. This assessment method included 4 subtests from the WISC-R, including arithmetic, vocabulary, sequence arrangement and block design.19
The assessment of depressive feeling was evaluated using the standardized Korean translation20 of Kovacs Children's Depression Inventory (CDI).21 The Covert Narcissism Scale (CNS) developed by Gang and Chung22 was used to determine covert narcissism. This scale, which was designed from the study by Akhtar and Thomson,23 has a total of 45 questions to be answered with the 5 point likert scale. A higher score indicates a higher tendency for covert narcissism. The CNS is divided into the following sub-factors: 1) insecurity about goals, 2) a desire for recognition/grandiose self-fantasy, 3) exploitation/egocentricity, 4) over-sensitivity/weakness and 5) timidity/lack of self-confidence. The total CNS score and each score for the 5 sub-factors were used in this study.
fMRI implementation plan and data analysesExperimental stimulus
This study was designed with block condition. The right-left discrimination test, which was created by adopting the task used in the study by Ghandi et al.24 was presented to the participants. Galvan1 has claimed that large differences in the task completion rates of the subjects of a brain imaging study related to rewards make it difficult to distinguish whether the brain activation results were indeed related to the rewards or whether those differences were due to success or failure in the task. Therefore, we selected a very simple task to maintain task success rate. The subjects were asked to click on the mouse button (left or right) corresponding to the location (left or right) of an abstract design that was momentarily shown on the monitor screen. E-prime software version 2.0 was used for the stimulation.
Each block corresponded to the situation with performance feedback (PF), social reward (SR), monetary reward (MR), or no reward (NR). NR block was included as a control condition. A total of 8 blocks were implemented, including the 2 blocks that corresponded to each condition. 10 trials were conducted for each block, in which an abstract design appeared on the left or right side of the screen. The abstract design was set to randomly appear 5 times on the left side and 5 times on the right side, for a total of 10 trials. In addition, 8 blocks were set to appear randomly. As a safeguard for the subjects becoming bored if continuously presented with the same stimulus, the research team itself created the abstract designs and selected a total of 5 designs to be presented twice in each block. Each design was presented once on the left side and once on the right. Thus, the condition for all of the designs seen in each block was set to be identical.
The organization of each trial was as follows: right-left discrimination stimulus (200 ms) - blank screen (1,000 ms) - word related to rewards (1,300 ms) - screen where a small cross appears (500 ms). The subjects were to determine left or right with a click of the mouse button at the moment when the blank screen appeared after the right-left discrimination stimulus, and the reward-related word was presented to the subject based on the result. 30 seconds were allotted for each block, and the rest period between the blocks was 15 seconds. The total amount of time for the fMRI screening was 6 minutes and 15 seconds, including the 15 seconds of the dummy period.
For each of the 4 conditions (NR, PF, SR and MR), the reward-related words were presented as follows. This method is similar to the technique used in the study by Pan et al.:14
1) For NR, the Korean word meaning 'next' ('그다음') was continuously presented after performing the task, regardless of the correct answer.
2) For PF, the Korean word meaning 'correct' ('정답임') or 'right' ('맞았음') appeared when the task was performed correctly, while the Korean word for 'next' ('그다음') was presented when the task was performed incorrectly. If all 10 trials within one block were performed correctly, then 'correct' and 'right' would each be presented to the subject 5 times.
3) For SR, the Korean word meaning 'great' ('대단해') or 'good' ('잘했어') appeared when the task was performed correctly, while the Korean word for 'next' ('그다음') was presented when the task was performed incorrectly. If all 10 trials within one block were performed correctly, then 'great' and 'good' would each be presented to the subject 5 times.
4) For MR, the Korean word that corresponds to Korean currency [300 won ('300원') or 400 won ('400원')] appeared when the task was performed correctly, while the Korean word for 'next' ('그다음') was presented when the task was performed incorrectly. If all 10 trials within one block were performed correctly, then '300 won' or '400 won' would each be presented to the subject 5 times. 300 won is equivalent to approximately 0.267 US dollars and 400 won is equivalent to approximately 0.357 US dollars. The subjects received the amount that corresponds to the total of the correct answers as prize money. If all of the performances were correct, 14,000 won (approximately 12.50 US dollars) could be received. We used '300 won' and '400 won' to restrain the calculation of the prize money during task performance as much as possible. Therefore, we selected combinations in which mental arithmetic was not relatively easy.
All of the reward-related words were 3-syllable Korean words. The reward stimulus presented for the MR condition ('300 won', '400 won') had to include 3 numbers and 1 syllable. However, when these words are actually read in Korean, they are read as 3 syllables instead of 4 syllables.
All of the subjects heard the description of this experiment prior to fMRI screening and performed practice task. The description of this experiment also included the statement that the prize money would actually be given based on the results from the MR condition. After the description of the experiment, a practice task consisting of 4 blocks was completed. The prize money awarded from the results of the MR was not paid for the practice task.
fMRI scanning and analyses
The magnetic resonance images were taken using a 3.0 Tesla whole-body ISOL Technology FORTE scanner (ISOL Technology, Korea) at Daejeon KAIST. After the first fMRI scan was completed, the T1 anatomical scan was obtained. To prevent possible head-movement artifacts, the subject's head was firmly fixed with a strap across the subject's forehead that was secured by calipers built into the head coil. The stimuli were shown to the subject through an LCD projector on the RF coil inside the gantry. The blood-oxygen-level-dependent (BOLD) technique using the echo planar imaging (EPI) sequence was applied during fMRI scanning. The thickness of each image slice was 5 mm, and no gap was allowed between the slices. The other MR parameters were: TR=3,000 ms, TE=35 ms, flip angle=80°, field of view=220×220 mm and matrix=64×64. 30 slices were obtained through the axial section image. The total duration of fMRI scanning was 6 min and 15 sec, so the number of EPI volumes per each condition was 60. Furthermore, the MRI parameters in the T1 anatomical scan were: TR=2,800 ms, TE=16 ms, flip angle=80°, field of view=192×220 mm and matrix=192×256.
The imaging data were analyzed using SPM2 (Wellcome Department of Cognitive Neurology, London, UK) software, and a general linear model was applied. For motion correction and co-registration and to identify the anatomical location of the functional image, the brain imaging data obtained were analyzed using normalization and smoothing processes that matched a standard brain template to the image data from the experiment. The size of the smoothing kernel was 7 mm.
In this study, the whole brain analysis was first conducted to investigate the regions of brain activation. Clusters that passed the voxel-level uncorrected threshold of p<0.001 and an extent threshold of 5 contiguous voxels in size were considered activation regions. After conducting an individual level analysis, one-sample t-test was conducted for the group analysis. In other words, the relative activation of each region was examined for the remaining 3 conditions (PF, SR, MR) using NR as the control condition (PF vs. NR, SR vs. NR, MR vs. NR). Then, within-subject ANOVA for the brain activation results from the PF, SR and MR conditions was conducted to investigate which regions showed significant differences in activation during the 3 conditions.
Moreover, the regions that were significantly activated in the PF vs. NR, SR vs. NR and MR vs. NR were selected as the regions of interest (ROI). The effective values (5 mm radius) were extracted from the normalizing image using the MarsBaR (http://marsbar.sourceforge.net) toolbox. We extracted the beta values for each condition from the individual ROIs and then calculated the value of each condition. We ran a correlation analysis to examine the relationship between the CDI or CNS scores and the extent of brain activation in each ROI.
Other statistical analyses
The response accuracy and the average reaction time for NR, PF, SR and MR were tested with repeated measures of ANOVA. The correlation between the subjects' CDI or CNS scale scores and ROI activation was analyzed using Spearman's correlation analysis with Bonferroni correction. SPSS 12.0K for Windows was used for the statistical analyses. Because the number of the ROI was different in each condition, the significance levels according to Bonferroni correction were as follows; 1) in PF vs. NR, p<0.005, 2) in SR vs. NR, p<0.004, 3) in MR vs. NR, p<0.005.
RESULTSAge, IQ, and psychological characteristics of the subjects
The age distribution of all 15 participants was as follows; 1) age of 13, n=6, 2) age of 14, n=7, 3) age of 15, n=2. The average age of the subjects was 13.80±0.86 years, and their average IQ was 108.93±14.01. All of the subjects were right-handed, and none of the subjects were smokers or currently taking any medications. In addition, there was no case that exceeded the clear clinical diagnostic threshold of K-SADS-PL-K.
The CDI score for the subjects was 8.93±4.38 points, with 17 points being the highest CDI score among the subjects. None of the subjects scored more than 21 points, which is the cutoff point for suspecting clinical depression in Korean students.
The total score for the CNS was 109.73±26.20 points, with factor 1=20.87±6.92, factor 2=26.87±6.40, factor 3=18.87±5.43, factor 4=23.00±6.50 and factor 5=20.13±6.85.
Comparison of response accuracy and reaction time among each of 4 conditions
The accuracy for the right-left discrimination test was found to be as follows: NR 99.00%, PF 99.67%, SR 100% and MR 99.67%. No statistically significant differences were found between the accuracy for each condition (F=0.189, df=3, p=0.903). And, the subjects' reaction times were 179.67±67.95 msec for the NR condition, 175.60±57.49 msec for the PF condition, 175.00±63.97 msec for the SR condition and 163.33±51.19 msec for the MR condition. No statistically significant differences in reaction time were identified by the ANOVA test (F=1.876, df=3, p=0.148).
Results of fMRI data analysesRegions that were activated significantly more in each reward condition compared to the NR condition (<xref ref-type="table" rid="T1-pi-10-47">Table 1</xref>, <xref ref-type="fig" rid="F1-pi-10-47">Figure 1</xref>)
The left superior frontal gyrus (BA 9), the right caudate body and the right ventral anterior nucleus of the thalamus were activated significantly more in the PF condition than the NR condition. The right middle frontal gyrus (BA 46), the right postcentral gyrus (BA 3), the right culmen of the cerebellum and the right caudate head showed significantly more activation in the SR condition than the NR condition. The left pulvinar of the thalamus, the right middle frontal gyrus (BA 10) and the right caudate head showed significantly more activation in the MR condition than the NR condition.
ANOVA results for brain activation in the 3 conditions
When the extent of brain activation in each of the three conditions (PF, SR and MR) was compared, the region that showed significant difference included the right cuneus (BA 30) only. In case that the cluster criteria were lowered to p<0.002 and extent threshold k=5, the regions that showed significant differences included the right precentral gyrus (BA 6), the left paracentral lobule (BA 31) and the left middle frontal gyrus (BA 46). The right cuneus showed greater activation in PF condition than in the other two conditions, whereas the activation of the right precentral gyrus and the left paracentral lobule in SR condition were significantly higher than in the other two conditions. Finally, the activation of the left middle frontal gyrus in MR condition was significantly higher than in the other two conditions (Figure 2).
Correlation between the brain activity of significant regions in reward conditions and the CDI and CNS scores
The regions that were activated significantly higher in each reward condition than in the NR condition were considered as ROI to examine for a correlation with CDI and CNS scores. There was no significant correlation between the degree of activation of the ROIs in each condition and each score.
DISCUSSION
The right caudate area was activated in all of the conditions. The caudate nucleus is a subdivision of the dorsal striatum where dopaminergic nerve terminals are closely distributed. The caudate nucleus has been reported frequently as being activated in association with monetary rewards,11,25 and a broad range of areas in the striatum, including the caudate nucleus and the putamen, have been reported to be activated in response to stimuli providing social rewards.9,10 Several studies have also reported the activation of the caudate nucleus in response to performance feedback.12,13 With reference to the reward response of adolescents, Van Leijenhorst et al.5 proved that the striatum showed a reward-related peak in middle adolescence (14- to 15-year-old) in anticipation of uncertain outcome. Galvan et al.3 also showed similar results. The result of our study suggest that the various rewards might activate caudate area in adolescents, especially, regardless of the type of reward.
The left superior frontal gyrus (BA 9) in PF-NR condition, the right middle frontal gyrus (BA 46) in SR-NR condition and the right middle frontal gyrus (BA 10) in MR-NR condition correspond to the dorsomedial or the dorsolateral prefrontal cortex (DLPFC). Although the BA 9 activation region in the PF-NR condition is close to the dorsomedial area, no particular difference in the function of the medial and lateral areas has been reported for the BA 9 region. Is the activation of the DLPFC area also common in the brain response to feedback and rewards? Wallis and Kennerley26 suggested that reward signals in lateral prefrontal cortex are consistent with a role in using reward to guide other cognitive processes, such as the allocation of attentional resources. They also insisted that lateral prefrontal neurons encode the association between the stimulus and response rather than information about the outcome (that is, reward itself). The studies about the DLPFC in related with reward task in adolescents were not yet reported. However, considering that the prefrontal region of brain undergo a startling transformation in adolescent period (for example, synapse pruning) and 'reward seeking behavior' is gaining much attention to adolescents, the noticeable activation of dorsal prefrontal area for various reward tasks might easily occur in adolescents. A follow-up study to investigate this assumption seems necessary.
The thalamic area was activated in both the PF-NR and the MR-NR conditions. The thalamus is a structure that is located in the center of the brain near the caudate nucleus, accepting external stimuli and governing arousal27 rather than logical thinking. Our result suggest that the adolescents in our study might be little aroused by the social reward such as 'great' or 'good'.
The right postcentral gyrus was activated in the SR-NR condition only. Several studies in the field of social neuroscience report that this area is related to self-related processing28 or feelings about oneself.29 Such a response to the SR was also found in a previous study on adults.14 The studies about direct interaction between the SR and brain response in adolescents are not yet reported, but Steinberg30 reported the brain response on performing a driving game in adolescents. When they performed the game with peer-present condition, the medial frontal cortex, left superior temporal sulcus, and left medial temporal structure were activated. These areas are related with self-related processing or theory of mind. This report would be one of the evidence that the brains of adolescents react very sensitively to other people's assessments about them, which are similar with SR. The fact that only the right brain area was activated in the SR-NR condition may support this belief. The right brain is known to be more closely related to the self-referential function than the left brain.
Meanwhile, there were some differences in the regions that were activated for each condition when all reward conditions were compared at once.
In case of the cluster criteria of p<0.001 and extent threshold k=5, the PF condition activated the right cuneus significantly more than the other conditions. The cuneus is mainly responsible for basic visual processing, but a study found that the degree of response inhibition and the volume of the cuneus showed a positive correlation in bipolar disorder patients31 and the cuneus has even been reported as one of the regions that is also activated by feedback-related tasks.32
In case that the cluster criteria were adjusted to p<0.002 and extent threshold k=5, another regions that showed somewhat different activation among 3 reward conditions were found. First, the SR condition activated the right precentral gyrus and the right paracentral lobule slightly more than the other conditions. Similar with the postcentral gyrus, the right precentral gyrus is a region associated with self-related processing, and the right paracentral lobule is also part of the cortical midline structure, which is the major self-related area. The cortical midline structure was reported to be a region related to reward outcome rather than reward anticipation.33 Second, the MR condition activated the left middle frontal gyrus slightly more than the other conditions. This region corresponds to the dorsolateral prefrontal area. Considering that the the right middle frontal gyrus in the MR vs. NR condition also showed significant activation in within-subject analysis, the activation of bilateral dorsal prefrontal area for maintaining attentional resources would be very important for performing monetary-related task in adolescents.
Finally, the correlation between the extent of activation in each condition and the psychological characteristics was not significant. If the general threshold (that is, p<0.05) without Bonferroni correction was adopted, there was a considerable result between the degree of right caudate activation and CDI score in the MR conditions (r=0.555, p=0.332). However, according to Fobes et al.,34 the MR-mediated activation of the reward-related brain region was lower in depressed adolescents than in normal adolescents. The fact that the CDI scores in our study were all below the clinical cutoff point, which is different from the study of Fobes et al., can suggest one important idea. That is, the increase of the depressive feeling in normal adolescents make their brain respond more sensitively to monetary rewards. But, once the depressive feeling develops into major depressive disorder, then the brain responses related to monetary reward might decrease. A follow-up study to investigate this assumption seems necessary.
The limitations of this study are as follows.
First, the total duration of fMRI scanning was slightly short. If we chose the paradigm that included longer task, the statistical power of our results would be higher. Second, the sample size was small, which limits the comparison of various psychological test scales and the extent of brain activation. Third, because this study was conducted with block-based design, we were unable to observe more detailed brain activation for reward anticipation or reward outcome. Fourth, the fact that the subjects of this study were early adolescents must be taken into consideration.
Despite the above limitations, this study is meaningful in that it examined various responses to rewards and feedback in adolescents. Not only various reward stimuli but also feedback stimulus might commonly activate the caudate nucleus and the dorsal prefrontal area in adolescents. The results of this study can be applied to planning of adolescent learning and teaching at home or school in various ways. Furthermore, these results are also expected to be one of the basic reference of brain studies investigating reward responses for adolescents with psychopathology. We look forward to more sophisticated reward-related brain research on adolescents in the future.
Acknowledgments
The authors gratefully acknowledge the assistance of all persons and volunteers whose participation was essential in the successful completion of the study.
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Significantly activated brain regions associated with each reward vs. no reward condition (uncorrected, p<0.001, extent threshold κ=5). A: lt. superior frontal gyrus. B: rt. caudate body. C: rt. Thalamus (VAN). D: rt. middle frontal gyrus. E: rt. postcentral gyrus. F: rt. caudate head. G: rt. middle frontal gyrus. H: rt. caudate head. I: lt. thalamus. PF: performance feedback, SR: social reward, MR: monetary reward, NR: no reward, VAN: ventral anterior nucleus.
Contrast estimate among PF, SR, and MR conditions (A: uncorrected, p<0.001, extent threshold κ=5). B-D: uncorrected, p<0.002, extent threshold k=5). A: rt. cuneus (BA 30). B: rt. precentral gyrus (BA 6). C: lt. paracentral lobule (BA 31). D: lt. middle frontal gyrus (BA 46). Coordinates follow atlas by Talairach and Tournoux (1988). PF: performance feedback, SR: social reward, MR: monetary reward, BA: Brodmann area.
Significantly activated brain regions associated with each reward vs. no reward condition (uncorrected, p<0.001, extent threshold κ=5)
The statistical analyses were done by one sample t-test. Coordinates follow atlas by Talairach and Tournoux (1988). PF: performance feedback, SR: social reward, MR: monetary reward, NR: no reward, VAN: ventral anterior nucleus, BA: Brodmann area, N/A: not applicable
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Skip to main content
Substance abuse disorders (SUDs) and mental health issues are so closely related medical experts aren’t always sure if one leads to other. However, it is clear that having certain mental health disorders makes a person more likely to abuse alcohol and drugs to an effort to self-medicate. There’s also research that shows using drugs and alcohol can bring on symptoms of a mental health disorder.
Clearly, using drugs and alcohol isn’t the best means of treatment for a mental health issue. But the more we understand the connection between substance abuse and mental health problems the better we can treat them both at addiction treatment centers.
Ways That Drug and Alcohol Use Impact Mental Health
Using alcohol and drugs may be a quick fix for some mental health symptoms, but years of research has shown it’s much more harmful than helpful. Substance and alcohol abuse changes the way the brain works. That alone has a widespread impact on mental health, but there are even more direct ways that drug and alcohol use impact mental health.
Increases Stress – Ironically, some people use alcohol and drugs as a way to escape stress only to ultimately create more stress in their life. When the affects of the drugs or alcohol wear off the person still has to deal with the stress from before, but now the shame of using alcohol or drugs as well as choices that were made while high add to the problem. Using alcohol or drugs can also be a costly habit that leads to financial stress.
Triggers Depression and Anxiety – There’s research that strongly suggests substance use disorders trigger depression and anxiety. Since an SUD can increase stress it makes total sense that anxiety can be made worse by alcohol and drug abuse. However, it can also intensify feelings of depression as well.
Memory Loss – Our memory is vital to our existence and how we experience life, which impacts mental health. Some studies have found that memory impairment from drug and alcohol abuse is either long-term lasting for years, or it can be permanent in some situations.
Mood Changes – Addiction can cause noticeable mood swings that go from high to low very quickly. So it isn’t surprising to find that mood disorders and substance abuse have a high comorbidity rate. There is actually something called substance-induced mood disorder as well. This is a mood disturbance that is directly related to drug and/or alcohol use.
Drug-Induced Psychosis – Psychosis refers to a condition in which a person processes the world around them, but it isn’t based in reality. During an episode of psychosis a person’s perception is disturbed preventing them from experiencing things as they actually are. Using drugs and alcohol can bring on psychosis and worsen symptoms if the condition already exists.
What It Means to Have a Dual Diagnosis
Dual diagnosis means that you are diagnosed with addition or an SUD as well as a mental health disorder. It’s also referred to as comorbility, which means having co-occuring mental health disorders. This is something that we see often at our Dallas addiction centers.
Having co-occuring mental disorders is actually much more common than most people realize. The latest National Survey on Drug Use and Health (NSDUH) found that 45% of those who have a substance use disorder receive a dual diagnosis. But that could be a conservative estimate. A study from 1990 discovered that 64.4% of those who experience addiction to drugs will experience a psychiatric disorder as well in their lifetime. Since addiction is a chronic disease, that means co-occuring mental health disorders will happen at some point for the majority of people with an SUD.
Treating dual diagnosis at an addiction recovery center is different than only addressing addiction. You can’t simply treat one and then the other, acting as if they are two separate conditions. Effective dual diagnosis treatment involves creating a plan to address both disorders simultaneously, because ultimately the two issues are intertwined.
Do you suffer from co-occurring mental health disorders? A free assessment from the trained professionals at Lighthouse Recovery addiction treatment center is the first step to understanding all of the underlying issues connected to substance abuse. If you receive a dual diagnosis know that our Dallas addiction center can provide an effective treatment plan. Lasting recovery and relief is possible when you work with addiction experts that understand how to treat comorbidity.
Learn more about our services or contact us below to discover how Lighthouse can help you on your road to recovery today. Thank you for your trust.
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Can Berberine Improve Prostate Health?
The market is packed with supplements promising to ease various health issues. But, one specific product has managed to gain a lot of attention – berberine.
Berberine has been used as a natural treatment alternative in traditional Chinese medicine for a very long time.
Studies indicate that berberine could treat inflammation and unstable blood sugar alongside obesity, diabetes, and other health issues.
The question is, can it benefit prostate health? We decided to take a closer look at this dietary supplement and all the berberine benefits.
What Is Berberine?
Berberine is a compound in many plants, such as tree turmeric, goldenseal, Oregon grape, and barberry. This alkaloid is extracted from these plants, which are a key component in traditional Chinese medicine. Its primary use is to lessen insulin resistance in type 2 diabetes
Berberine is a chemical that has a yellow color and bitter taste. According to experts, it may improve heartbeat and blood sugar. This could help individuals with specific heart problems.
It may also eradicate bacteria, keep the swelling in check, and manage the way the body uses the sugar in the blood.
Consumers often choose a berberine supplement for diabetes with either type 1 or 2 diabetes, as well as individuals with high blood pressure, cholesterol, fatty liver disease. If you decide to use berberine extract, it is best to consult with a doctor first.
Berberine Uses and Possible Effectiveness
Berberine hydrochloride has many uses. It works in a number of ways for the human body and can induce changes in the body’s cells. That’s why it can treat:
• Metabolic conditions (obesity, heart problems, diabetes that affects blood sugar)
• Bacterial infection (it inhibits the growth of Staphylococcus aureus. This bacteria is known for causing meningitis, pneumonia, and sepsis)
• Inflammation (making it an essential component in diabetes and heart disease management)
• Cholesterol management (since berberine could be as effective as some cholesterol drugs)
• High blood pressure control (berberine supplementation can delay the onset of high blood pressure and decrease its severity)
Taking berberine can slightly decrease blood sugar levels, making it a viable option for diabetes management. When combined with other agents, berberine showed a consistent improvement in lipid and glycemic parameters.
Insulin sensitivity was also improved as the HOMA-IR value decreased by almost 50%. The HOMA-IR value is the Homeostatic Model Assessment of Insulin Resistance.
It lets you and your doctor know the level of insulin the pancreas requires to control glucose. It is measured from the fasting insulin and blood glucose levels.
The chemical improves insulin similarly to metformin. It stimulates glucose intake to enhance insulin signal transduction.
Berberine and Prostate Health – What to Expect?
The odds of developing prostate cancer increase with age, creating a physical and emotional burden for patients.
People with increased blood sugar concentration tend to have a higher risk for prostate enlargement. Those with high blood glucose had three times the risk of developing enlargement of the prostate.
Diabetics are twice as likely to develop prostate inflammation compared to healthy men. That’s because the insulin receptor can affect prostate gland growth.
Conventional treatment, like chemotherapy, radiotherapy, and anti-hormonal therapy, is often not enough to treat advanced prostate cancer. These limitations have inspired scientists to use new and improved methods that can benefit cancer cells.
Besides maintaining healthy blood sugar levels, cholesterol, and insulin levels, the berberine alkaloid may support prostate health.
What Studies Say
There is more to berberine than meets the eye. According to a 2017 report, berberine HCL may treat prostate cancer by regulating multiple factors in the human body. That includes:
• Linoleic acid metabolism
• Arginine and proline metabolism
• Purine metabolism
• Spermine biosynthesis and retinoate biosynthesis
• Retinol metabolism
Based on another study, berberine improves benign prostatic hyperplasia. This is another typical disease of the prostate in older patients. It is recognized by urinary tract symptoms and increased prostate size. Berberine treatment alleviated all detrimental effects.
Not just weight loss, but PSA suppression (prostate-specific antigen) as well. These results suggest that berberine may have a beneficial effect on benign prostatic hyperplasia. This means it could be used as a therapeutic agent with fewer adverse events compared to conventional treatment.
Further research shows that berberine treatment resulted in an obvious drop in oxidative stress in rats with diabetes. Oxidative stress is linked to numerous pathological conditions, such as infection and inflammation.
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Additional Health Benefits of Berberine
Reduced risk of heart disease
High blood sugar and cholesterol can have a heavy impact on the heart. Berberine can help alleviate some of these problems. It might lessen the odds of heart disease by keeping the cholesterol level, glucose metabolism, and lipid metabolism in check.
One trial indicates that berberine improved the symptoms and lessened mortality risk in patients with heart failure.
Fat loss
Healthy weight loss can protect the body from type 2 diabetes, specific types of carcinoma, stroke, and osteoarthritis. Berberine could aid with shrinking some of that extra belly fat.
Based on a small berberine weight loss report, 37 women and men with metabolic syndrome consumed 300mg of berberine three times a day for three months. By the end of the trial, their BMIs went down.
The participants lost 2 inches around the waist on average. It may not be a drastic change, but it is more than enough to give the body a boost in the right direction.
Canker Sores
Smearing berberine gel on the affected area can ease pain, oozing, size, and redness of canker sores. Gum disease can also impact glucose levels.
Diabetes links with an increased risk for thrush. Therefore, anyone with diabetes has an elevated risk for dry mouth. This could lead to mouth ulcers, cavities, dental infections, and soreness.
Fatty liver
This supplement can drastically boost liver function. It can also increase blood lipids in individuals with NAFLD (non-alcoholic fatty liver disease).
Moreover, it also provides a beneficial advantage in decreasing glucose in NAFLD patients. Further research is necessary, but it seems that liver enzymes can benefit from berberine.
Although NAFLD won’t usually cause harm in its earlier stages, it can eventually lead to liver damage. And can progress over time.
Having high amounts of fat in the liver can increase the likelihood of liver problems and other health issues, like kidney disease, elevated blood pressure, and diabetes.
Conclusion
When using berberine for blood glucose, cholesterol, or prostate, it is best to consult with a doctor first. Ideally, you should focus on stabilizing the high cholesterol. As well as blood sugar and blood pressure with proper medication, a healthy diet, and physical activity.
Berberine may create some potential benefits on blood sugar and blood pressure. However, it is not a magic pill. Individuals who have something to gain from a product such as this struggle with high cholesterol and blood sugar.
Some data strongly supports its use in diabetes and heart health. With that in mind, berberine could also prove useful for the prostate.
Not only can it manage blood sugar, but it can also lessen the odds of prostate health problems.
Next Up
prostate health supplement
Learn 9 Best Prostate Supplements.
Sources
1. Yin J, Xing H, Ye J. Efficacy of berberine in patients with type 2 diabetes mellitus. Metabolism. 2008. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2410097/
2. Liu CH, Tang WC, Sia P, et al. Berberine inhibits the metastatic ability of prostate cancer cells by suppressing epithelial-to-mesenchymal transition (EMT)-associated genes with predictive and prognostic relevance. Int J Med Sci. 2015. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4278877
3. Youn DH, Park J, Kim HL, et al. Berberine Improves Benign Prostatic Hyperplasia via Suppression of 5 Alpha Reductase and Extracellular Signal-Regulated Kinase in Vivo and in Vitro [published correction appears in Front Pharmacol. 2019. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6054997/
4. Moghaddam HK, Baluchnejadmojarad T, Roghani M, Khaksari M, Norouzi P, Ahooie M, Mahboobi F. Berberine ameliorate oxidative stress and astrogliosis in the hippocampus of STZ-induced diabetic rats. Mol Neurobiol. 2014. https://pubmed.ncbi.nlm.nih.gov/24113841
5. Zeng XH, Zeng XJ, Li YY. Efficacy and safety of berberine for congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol. 2003. https://pubmed.ncbi.nlm.nih.gov/12860219/
6. Wei X, Wang C, Hao S, Song H, Yang L. The Therapeutic Effect of Berberine in the Treatment of Nonalcoholic Fatty Liver Disease: A Meta-Analysis. Evid Based Complement Alternat Med. 2016. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4947506/
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How Can Cold Weather Affect Your Heart?
A cardiologist shares tips for protecting your heart health in chilly temperatures.
Image of a person experiencing a cardiovascular event in cold weather.
As temperatures drop and some areas get a blanket of ice and snow, protecting yourself from slips, falls, and chilly weather is key — and so is protecting your heart.
“People tend to think about frostbite or hypothermia, but the number of cardiac events like heart attacks is higher during the winter months, as cold weather can put more stress on the cardiovascular system,” says Dr. Jeremy Berman, a cardiologist at NewYork-Presbyterian Brooklyn Methodist Hospital.
“Even walking through heavy snow can put tremendous strain on the body if someone isn’t used to it.” he says. “Whether or not you have a preexisting condition, it’s important to listen to your body and seek appropriate attention if something doesn’t feel right.”
Dr. Berman, who is also assistant professor of clinical medicine at Weill Cornell Medicine, spoke with Health Matters about how cold weather can affect your heart, symptoms to look out for, and how to protect your heart this winter.
What can happen to your heart when it’s cold outdoors?
Dr. Berman: Imagine walking out of the house and being immediately hit by the cold. Your body will naturally react to preserve your core temperature. Vasoconstriction — the narrowing of the arteries in the arms, the legs, and the periphery of your body — will happen to keep blood flowing to your major organs and protect them, and this can raise your blood pressure.
Dr. Jeremy Paul Berman
Dr. Jeremy Berman
Your heart must pump against those narrowed arteries, and that puts more wear and tear and strain on it. You also have a surge in stress hormones, which has an impact. As the body temperature decreases, even by just a couple of degrees, you have an increased risk for blood clotting. All those factors together can contribute to a heart attack or stroke.
Why are heart attacks more common in the winter?
Research shows that more people die from heart attacks during the winter holidays than at any other time of the year. There are several factors that can contribute: the cold weather, stress, and dietary indiscretion around the holidays.
More darkness in the wintertime can also have an impact, with increased cardiovascular risk associated with disturbances in circadian rhythms.
For people who aren’t used to strenuous activity, shoveling snow can be a critical factor leading to a cardiac event — along with reduced blood flow from the cold, the strain of lifting and tossing snow can increase a person’s risk.
What are common symptoms?
Common symptoms of a heart attack or major cardiovascular event can include:
• Sudden, severe chest discomfort or pain
• Discomfort or pain in other areas of the upper body, including the arms, back, neck, jaw, or stomach
• Shortness of breath
• Nausea
• Lightheadedness
Call 911 and seek immediate medical attention. Do not try to drive yourself or take public transportation to a hospital.
Not everyone who goes out in the cold is going to have a cardiac episode, but everyone should be aware and take any new symptoms seriously.
Whether or not you have a preexisting heart condition, listen to your body. And for those with heart conditions, winter is a good time of year to make sure you are up to date on your appointments and care plan.
How can you protect your heart during cold weather?
People may not always want to go outside when it’s cold, but there are ample opportunities to get moving and safely exercise indoors. You can do stretches or yoga, or even visit a larger indoor space such as a mall to get your steps in.
When outdoors, ease yourself into activity. Take small steps, and make sure you’re not in the cold for hours on end. Dress appropriately and wear layers, keeping the head and neck warm to protect your core temperature.
And make sure you speak with your doctor ahead of time about your blood pressure and cholesterol, especially if you have risk factors for cardiovascular disease. Don’t let snow shoveling be your stress test.
We see the transmission of common colds and viruses during the winter months, so getting your flu shot and handwashing are also important.
All of this can help protect your heart in cold weather but should also be top of mind year-round.
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Image caption appears here
SODA LOADING
SODA-LOADING
Photo credit: RUN 4 FFWPU / Pexels
Soda loading with LACTAT BUFFER increases the lactate tolerance in high-intensity sports
Muscle hyperacidity and the consequent accumulation of lactate as well as a short-term drop in blood pH are performance-limiting factors when it comes to high-intensity training and competition. The athlete becomes «acidic» and therefore limited in his performance. In this situation, sodium citrate and sodium bicarbonate offer great benefits. SPONSER sells both ingredients in its beverage powder LACTAT BUFFER.
Soda loading: function and benefit
Supplementation with LACTAT BUFFER or sodium bicarbonate and/or citrate is also called «soda loading». If sodium citrate and sodium bicarbonate are used in high-intensity sports that last from approx. 1 to 10 minutes, significant performance improvements can be expected. The greater the anaerobic-lactacid load, and thus the more pronounced the induced metabolic acidosis, the more effective an increased buffering capacity may improve performance.
Which sports benefit?
In practice, this means that athletes such as middle distance runners, rowers, swimmers, alpine ski athletes etc. benefit significantly from this specific kind of supplementation. More than, for example, endurance athletes such as long-distance runners, triathletes or cyclists. This is because anaerobic sports train significantly higher lactate tolerance than endurance sports. Another group of athletes that potentially benefits from a soda loading is the one working with repetitive interval loads. This applies to many team sports, ball sports and martial arts.
Soda loading is also interesting for strength athletes, as the isolated training of fewer muscles produces very high local lactate values, which must be removed as quickly as possible. If the muscle remains «sour» for too long, the next set cannot be completed quickly enough and with sufficient strain. Since soda loading also means an increased sodium intake, supplementation in weight training should not be carried out permanently but reserved for intensive phases. The same applies to sports where one or even several competitions take place every week.
Increased lactate tolerance, improved acid buffer capacity
Due to the mode of action of an increased bicarbonate buffer in the blood, the individual lactate value of the athlete is not necessarily increased, but primarily the lactate tolerance. This means that the athlete with his individual lactate value can endure a load for a longer time or achieve a higher performance. The athlete does not necessarily interpret the perceived load as lower if the maximum achievable performance in competition is aimed at. In contrast however, a given, defined performance should be perceived as less stressful. In all cases a much faster recovery is to be expected, because the acid removal is accelerated by the increased buffer capacity. This means faster disappearance of the «stiff» muscle feeling after exercise as well as faster recovery.
Studies prove effectiveness
As early as 1993, a first meta-analysis examined 29 studies on athletes with soda loading. Overall, the performance until exhaustion was massively increased with an average of 27%. Due to the diversity of the study designs, however, also with a large variation of +7% to +47% (average thus +27%). In the meantime, many other studies have been carried out and soda loading is considered one of the supplementation measures with the scientifically most broadly supported, performance-enhancing effect.
Dosage and intake
In the past, soda loading was practiced about 3 hours before the competition, which was an enormous dose when taking 0.3-0.5 g sodium bicarbonate and/or citrate per kg body weight. This led to gastrointestinal problems very often. According to the latest study findings, supplementation is now carried out over several days. Thus, the tolerance problems of a high single dosage can be avoided.
Ideally, LACTAT BUFFER should be consumed 3-5 days before the competition, spread over the day as recommended, with the last dose being taken 3 hours before the start at the latest. Interestingly, the performance-enhancing effect of this multi-day intake strategy seems to last up to 2 days after discontinuation of supplementation. This is accordingly important for sports events lasting several days.
Combined increase of intra- and extracellular buffer capacity
Many studies about supplementation to increase intra- and extracellular buffer capacity haven been published so far; with many different intake profiles and forms of workouts. As expected, and as explained above, the greatest benefit is achieved with highly intensive loads of 1 to 10 minutes duration. Such forms of performance produce the highest acidosis in the musculature and consequently in the blood. In order to achieve maximum benefit in the anaerobic-lactacid performance range, the increase in extracellular buffer capacity through soda loading can be combined with an increase in intracellular buffer capacity through beta-alanine. The combination of these two measures can lead to an additional increase in performance, at least if chronic soda loading is carried out (approx. 3-4 days before the competition). Since the intake of BETA-ALANINE also requires a chronic intake for about 8 weeks in order to increase the body's own carnosine stores, such an intake strategy does not give rise to any tolerance problems compared to acute intake on the day of the competition.
Related articles
on » performance optimisation
on » race preparation
on » science
Author: Remo Jutzeler
Head R&D SPONSER SPORT FOOD
Ing. Applied Food Sciences UAS
MAS Nutrition & Health ETHZ
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RT Journal Article SR Electronic T1 Beyond the Ligand: Extracellular and Transcellular G Protein–Coupled Receptor Complexes in Physiology and Pharmacology JF Pharmacological Reviews JO Pharmacol Rev FD American Society for Pharmacology and Experimental Therapeutics SP 503 OP 519 DO 10.1124/pr.119.018044 VO 71 IS 4 A1 Dunn, Henry A. A1 Orlandi, Cesare A1 Martemyanov, Kirill A. A2 Barker, Eric L. YR 2019 UL http://pharmrev.aspetjournals.org/content/71/4/503.abstract AB G protein–coupled receptors (GPCRs) remain one of the most successful targets of U.S. Food and Drug Administration–approved drugs. GPCR research has predominantly focused on the characterization of the intracellular interactome’s contribution to GPCR function and pharmacology. However, emerging evidence uncovers a new dimension in the biology of GPCRs involving their extracellular and transcellular interactions that critically impact GPCR function and pharmacology. The seminal examples include a variety of adhesion GPCRs, such as ADGRLs/latrophilins, ADGRBs/brain angiogenesis inhibitors, ADGRG1/GPR56, ADGRG6/GPR126, ADGRE5/CD97, and ADGRC3/CELSR3. However, recent advances have indicated that class C GPCRs that contain large extracellular domains, including group III metabotropic glutamate receptors (mGluR4, mGluR6, mGluR7, mGluR8), γ-aminobutyric acid receptors, and orphans GPR158 and GPR179, can also participate in this form of transcellular regulation. In this review, we will focus on a variety of identified extracellular and transcellular GPCR-interacting partners, including teneurins, neurexins, integrins, fibronectin leucine-rich transmembranes, contactin-6, neuroligin, laminins, collagens, major prion protein, amyloid precursor protein, complement C1q-likes, stabilin-2, pikachurin, dystroglycan, complement decay-accelerating factor CD55, cluster of differentiation CD36 and CD90, extracellular leucine-rich repeat and fibronectin type III domain containing 1, and leucine-rich repeat, immunoglobulin-like domain and transmembrane domains. We provide an account on the diversity of extracellular and transcellular GPCR complexes and their contribution to key cellular and physiologic processes, including cell migration, axon guidance, cellular and synaptic adhesion, and synaptogenesis. Furthermore, we discuss models and mechanisms by which extracellular GPCR assemblies may regulate communication at cellular junctions.SIGNIFICANCE STATEMENT G protein–coupled receptors (GPCRs) continue to be the prominent focus of pharmacological intervention for a variety of human pathologies. Although the majority of GPCR research has focused on the intracellular interactome, recent advancements have identified an extracellular dimension of GPCR modulation that alters accepted pharmacological principles of GPCRs. Herein, we describe known endogenous allosteric modulators acting on GPCRs both in cis and in trans.
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Kidney Failure Treatment
By stage 5, also called kidney failure, your kidneys can no longer function on their own and you will require treatment with kidney replacement therapy -. Treated with therapies, such as erythropoietic agents for anemia, or vitamin D and medicines that lower cholesterol and blood pressure; Followed over time for. A treatment plan will be comprehensive and may include: A person may also need treatment for the complications of kidney disease. For example, to treat anemia. Medication. Medication can help treat the symptoms of chronic kidney failure. Kidney failure is linked to high blood pressure, so a doctor may prescribe. Kidney failure, also known as renal failure, is a term used to describe a situation in which the kidneys are no longer able to function effectively. Your doctor.
Blockages, such as tumors or kidney stones, may need to be removed. Because treating the causes of acute renal failure takes time, your body will be unable to. Preventing chronic kidney disease (CKD) and its complications is possible by managing risk factors and treating the disease to slow its progression and. Treatment options for kidney failure include dialysis, transplant or non-dialysis comprehensive conservative care. On this page. What is kidney failure? How is kidney disease treated in a child? · A hospital stay · IV (intravenous) fluids in large amounts to replace fluid loss · Medicines called diuretics to. There are many treatment options for kidney failure, including transplant, peritoneal dialysis, hemodialysis, and hospice or conservative care. Treatment for Kidney Disease Treatment for kidney disease can include lifestyle changes and medication. For advanced kidney disease, dialysis or a transplant. Peritoneal dialysis is a treatment for kidney failure that you can do at home. This type of dialysis uses the lining of your belly to filter wastes and extra. Dialysis does not always help people live longer. For some, the best way to treat kidney failure may be to let nature take its course. We call this comfort. Treatment may include: Hospitalization. Administration of intravenous (IV) fluids in large volumes (to replace depleted blood volume). Diuretic therapy or. Chronic Kidney Failure Treatment · Control blood pressure. Help with growth; Prevent bone density loss; Treat anemia · Specific diet restrictions · Intravenous. What is the treatment for acute and chronic renal failure? · Medications (to help with growth, prevent bone density loss, and/or to treat anemia) · Diuretic.
AKI requires immediate treatment and may be reversible if diagnosed and treated quickly—unlike chronic kidney disease (CKD), which is kidney damage that. Find out about the main treatments for chronic kidney disease (CKD), including lifestyle changes, medication, dialysis and kidney transplants. There's no cure for CKD, but treatment can help relieve the symptoms and stop it getting worse. Your treatment will depend on how severe your condition is. The. Can a Person Recover From Kidney Failure? · Acute kidney failure (AKF) usually responds well to treatment, and kidney function often returns to almost normal. Treatment. ESRD may need to be treated with dialysis or kidney transplant. You may need to stay on a special diet or take medicines to help your body work. Dialysis. Dialysis is a treatment that cleans your blood and removes excess fluid from your body when your kidneys are no longer healthy enough to do these. Kidney failure treated with dialysis or kidney transplant is called end-stage renal disease (ESRD). Learn more about ESRD. Not all patients with kidney disease. Explore Potential Treatment Options for Kidney Failure. A kidney transplant is the best possible treatment option for patients with kidney failure. Kidneys are severely damaged with GFR between 15 and 29 mL/min/ m2. This is the last stage before complete kidney failure. Symptoms such as fatigue.
Treatment usually occurs in two phases, first flushing the kidneys and removing the accumulated toxins from the blood, and then providing treatments to manage. Symptoms of chronic kidney disease · hypertension (high blood pressure) · night-time urination (weeing) · changes in how your urine looks (such as frothy or. The aim of treatment is to remove the cause of acute renal failure if possible and to keep the amount of salts and minerals at the correct levels in your body. You may be considering the possibility of eventually having some form of kidney replacement therapy (also known as renal replacement therapy) which will do some. Dialysis is the standard treatment to sustain the lives of people with kidney failure. However, if you feel you would be better off without dialysis, we can and.
Treatment. Treating the myeloma should reverse kidney impairment, sometimes even in a patient whose kidneys fail or a patient who requires dialysis. However. Transplantation: live and deceased donor kidneys; Dialysis: hemodialysis or peritoneal dialysis. Transplantation. The best current treatment for kidney failure.
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Healing the NSAID Nation: Finding Safer Alternatives for Chronic Inflammation
SpicesComplications from the overuse of non-steroidal anti-inflammatory drugs (NSAIDs) cause more than 20,000 deaths in the US each year. Many herbs and spices contain antiinflammatory compounds. Extracts of herbs like turmeric, ginger, and black pepper are proving to be effective and safe alternatives to NSAIDs for a variety of chronic inflammatory conditions. (Image courtesy Paul Cowan/Dreamstime)What if there were an outbreak of a largely preventable syndrome that caused more than 20,000 deaths and 100,000 hospitalizations every year; a scourge that indiscriminately struck people of any age, from teens to elders, often without warning symptoms?
As a doctor, you would expect to hear about it. Moreover, you'd expect that health care professionals would be doing everything possible to contain it.
But what if you learned that your medical colleagues were unwittingly facilitating spread of this disorder, that perhaps you yourself had unknowingly exposed patients to the pathogen, or turned a blind eye as they put themselves at risk?
There is such a disease. It's called overuse of non-steroidal anti-inflammatory drugs (NSAIDs). In light of statistics, it should be considered a public health crisis.
"Every year, 6 times as many people die of NSAID-related GI bleeds than died on September 11, yet this gets very little media attention," says Sunil Pai, MD, director of Sanjevani Integrative Medicine , a holistic healthcare center in Albuquerque. "Since the mid-80s, more than 300,000 Americans have died of NSAID complications, and 1.7 million were hospitalized."
Dr. Pai, who is working on a book called, Inflammation Nation, has made it his mission to raise awareness about this issue, and to provide patients with healthier, less-dangerous approaches for managing the chronic inflammation.
Illusion of Safety
Indomethacin, Naproxen, Ibuprofen and Celecoxib represent, "the most widely used class of drugs in the world," Dr. Pai told Holistic Primary Care. "Americans fill 70 million NSAID prescriptions yearly, and consume roughly 30 billion doses of over-the-counter NSAIDs. Between 20-30% of US adults take them daily."
Those numbers may sound like exaggerations, but consider that big box retailers sell NSAIDs to the public in thousand-dose quantities. Though they're marketed predominantly for joint pain, in reality, people take them for every imaginable pain or ache, even for emotional stress.
"We have moved these meds to the OTC side, so now there's no guidance or accountability Sunilpaiwhatsoever on how they are marketed or how they're taken," said Dr. Pai. "Most people—doctors and consumers alike—assume that if something is sold OTC it must be safe...or it wouldn't be over the counter. Yet every day, in community hospitals, people are dying of fatal GI bleeds caused by NSAIDs."
"Black Box" Warnings Aptly Named
GI ulcers and perforations are the most common, dramatic, and arguably most tragic of NSAID side effects, because they can occur in anyone, often without warning. "An 18-year-old girl taking Ibuprofen for menstrual cramps can develop a bleed just as easily—and as suddenly—as a 75-year-old taking it for arthritis.
But GI side effects are only part of the picture. Constant NSAID use also increases cardiovascular risk, particularly for thrombotic events. Risk rises with duration of use, and can be problematic in people with existing CVD. NSAIDs are contraindicated after bypass surgery, though many people do not know this.
Likewise, many men are unaware that long-term ibuprofen use can cause erectile dysfunction. The irony, says Dr. Pai, is that doctors treat ED with prescriptions that can cost as much as $10-15 per pill. In some cases, the root of the problem is overuse of drugs that are dirt-cheap.
There are now "Black Box" warnings on Ibuprofen and Naproxen products. "They call it a "Black Box" warning for a reason," Dr. Pai joked. "Use these products and that's where you can quickly end up---in a black box!" The government only requires Black Box warnings when potentially life-threatening adverse effects become common.
If one decides to take a drug with a Black Box warning, one is legally accepting the risks described in the Black Box. If something goes wrong, there's no legal recourse. "As soon as you tear the package or open the bottle, you've essentially signed and accepted the terms and conditions."
Cheap Drugs, Costly Complications
Our nation's over-reliance on NSAIDs carries a heavy price. Several studies published since the early 1990s indicate that side effects from NSAIDS---properly prescribed—cause roughly 100,000 hospitalizations and 20,000 deaths each year, on average (Singh G. Am J Medicine. 1998; Wolfe M, et al. N Engl J Med. 1999; 340(24): 1888-1889; Frech EJ, et al. Therapeutics Clin Risk Man. 2009; 65-73; Fries JF, et al. J Rheumatol. 1991 (Suppl 28): 18; 6-10).
Dr. Pai pointed out that these are conservative estimates, and do not include complications from non-prescription NSAIDs, or misuse of prescribed drugs.
NSAID complications have cost the country upwards of $38 billion since the mid 1980s, when NSAID use began to soar. "We're giving a lot of people very "cheap" drugs, that in the long term cause all sorts of expensive problems."
Making Matters Worse
In truth, NSAIDs are not even good medicine for many of the conditions for which they're taken. Constant use actually worsens some of the problems that people hope to ameliorate by taking these drugs.
Arthritis is a prime example. NSAIDs provide short-term symptom relief, but chronic use accelerates radiographic progression of osteoarthritis, decreases joint space width, down-regulates chondrocyte proliferation, and inhibits synthesis of proteoglycans, collagen and cellular matrix components.
In other words, NSAIDS make arthritis worse, not better. This phenomenon was well described in a 2010 review by Ross Hauser, who analyzed 135 papers published since 1967 (Hauser R. J Prolother. 2010; 2 (1): 305-22).
Dr. Pai added that some people take NSAIDS to treat hangovers, a very bad idea because alcohol itself can induce GI mucosal damage. Adding an NSAID to "cure" the effects of over-indulgence will only compound the damage.
Willful Ignorance
Some of the research highlighting NSAID complications was done by orthopedists in the 1960s, but it was categorically ignored. Likewise, international arthritis and rheumatoid disease organizations have issued position statements against indiscriminate NSAID use, but these too have gone largely unheeded.
"Doctors really aren't telling people the straight story. We need to explain the realities to our patients," said Dr. Pai, though he admitted this is a tall order. The din of advertising often drowns out the warnings.
Through the 1980s, most ads for branded NSAIDs, portrayed people in their 60s and 70s--elders playing golf or having fun with their grandkids. Gradually the people in the commercials got younger. Today, ads target college students, with the message of "All day long, all day strong!"
"They're now marketing this stuff to kids! We have to ask ourselves why do young people have chronic inflammation?" said Dr. Pai. "What is causing all these 'itises?'"
NSAID and Done
Inflammation is not new; it's as old as humanity itself. What is new is dying from GI bleeds or other adverse effects from drugs taken to relieve inflammation. Several years ago, that insight led Dr. Pai on a journey to find better ways of managing inflammation.
Diet should be the first place to look when working with NSAID-popping patients. Many Americans are eating in a way that's guaranteed to promote inflammation: lots of red meats, dairy products and refined carbohydrates with very few fruits and vegetables. That means massive amounts of pro-inflammatory omega-6 fatty acids, and little anti-inflammatory omega-3.
High omega-6 levels drive over-production of arachidonic acid, the precursor to inflammatory prostaglandins and leukotrienes. In many Americans, the dietary omega-6 to omega-3 ratio is as high as 30:1. A healthy ratio is 2:1.
The first step in helping patients off the NSAID-go-round is to get them to eat more produce and less animal proteins, and to up their intake of omega-3s, preferably from high-quality fish oil (from wild-caught fish, validated for purity, free of fillers, not enterically coated). He recommends a daily dose of 750-1500 mg EPA, and 500-800 mg DHA.
Better Therapeutic Options
A desire to find safer alternatives led Dr. Pai to Ayurveda, India's traditional healing sciences. "In the Ayurvedic system, inflammation is considered to be a reflection of imbalances in Pitta, the fiery element. So I started looking at what traditional Indian doctors were using to treat Pitta conditions. Consistently, it was four things: Curcumin (also known as turmeric), Boswellia (aka Frankincense), Ginger and Black Pepper.
There is strong biochemical and clinical evidence to support use of all four of these herbs in the care of people with inflammatory conditions.
Curcumin (Curcuma longa): A tangy, golden spice used widely throughout Asia, Curcumin is one of the most well-researched botanicals, with over 5,000 published papers. Compounds within the rhizome modulate 97 distinct inflammatory mechanisms and pathways, including: NF-kappa-B, COX-2, 5-LOX, IL-12, TNF-alpha, IFN-gamma, matrix metalloproteinase, and several types of protein kinases.
TurmericflowerFlower of Curcuma longa. Rhizomes of this plant, the source of turmeric, are rich in anti-inflammatory compounds (Image courtesy Dreamstime)Curcumin has show anti-oxidant, anti-inflammatory, and anti-microbial properties. "These effects are mediated through regulation of various transcription factors, growth factors, cytokines, protein kinases and other enzymes," Dr. Pai said. Clinically, this translates into benefit for people with arthritis, ulcerative colitis, diabetes & diabetic retinopathy, cardiovascular risk, neurological conditions, and psoriasis.
In combination with Glycyrrhiza (licorice) and Boswellia (frankincense), a standardized extract called Curcumin C3 complex (Sabinsa) was effective in controlling asthma as well as in reducing leukotrienes and other inflammatory markers in asthma patients (Houssen ME, Clin Biochem. 2010 Apr 26).
The C3 complex, which delivers consistent levels of curcuminoids in the most bioavailable form, has been the subject of 25 clinical trials, alone and in combination with other botanicals. In addition to the expected benefits in arthritis and other inflammatory conditions, it is also proving beneficial in treatment of colon and pancreatic cancer, cervical neoplasia, and Barrett's metaplasia (Bar-Sela G, Curr Med Chem. 2010;17(3):190-7).
Recently, investigators at Baylor Medical center compared a standardized Curcumin extract (500 mg twice daily) against Diclofenac (50 mg twice daily) in 45 people with Class I or II rheumatoid arthritis. Patients were randomized to Diclofenac alone, Curcumin alone (BCM-95 Bio-Curcumin) or both, for 8 weeks.
All groups showed significant reductions in pain, swelling and tenderness. Curcumin alone gave the biggest reductions, though the difference was not statistically significant. The data were published in Phytotherapy Research.
There were no dropouts in the Curcumin group and no serious side effects, while14% of Diclofenac patients withdrew due to adverse effects. "Since RA can strike at a much younger age than other types of arthritis, we need healthy ways to treat these people," said Dr. Ajay Goel, one of the authors.
Dr. Pai noted that most clinical trials showing positive anti-inflammatory effects have used 1-3 grams of curcumin in divided doses. So far, there have been no serious GI, renal or hepatic side effects associated with Curcumin in any of the published studies, even at higher dose levels.
Boswellia (Boswellia Serrata): This is also a well-studied herb, with over 230 studies many of which were published in the last 5 years. It has well-documented anti-inflammatory, anti-arthritic, and anti-diabetic, analgesic and lipid-regulatory effects. Boswellic acids found in the resin of this tree have unique activities in inhibiting 5-LOX and human leukocyte elastase (HLE). Boswellic acids can also inhibit NF-kappa-B, TNF-alpha, and a host of inflammatory cytokines.
A study published last year compared Aflapin, a standardized Boswellia extract, against placeboBoswelliatreeBoswellia serrata tree, the source of Boswellia (aka Frankincense), another natural anti-inflammatory in treatment of 60 people with recalcitrant osteoarthritis of the knee. The Boswellia extract, at a dose of 100 mg per day, gave significant improvements on pain and physical function scores, the benefit becoming apparent within 5 days (Vishal AA, et al. Int J Med Sci. 2011;8(7):615-22).
Raychaudhuri and colleagues did a 90-day, head-to-head comparison of two Boswellia products—Aflapin and 5-Loxin—in 60 people with knee osteoarthritis. At doses of 100 mg per day, both products reduced pain and improved function, but Aflapin produced bigger changes in both parameters (Sengupta K, et al. Int J Med Sci. 2010:1;7(6):366-77)
Ginger (Zingiber officinale): A popular culinary seasoning in many parts of the world, ginger has also been used in Indian and Chinese medicine for over 4,000 years. In addition to inhibiting COX-2, 5-LOX, and NF-kappa-B, it also affects glucose and lipid metabolic pathways. Clinically, it attenuates hyperglycemia, and modulates lipid profiles, making it a helpful herb for people with diabetes and metabolic syndrome, said Dr. Pai.
Ginger also has anti-emetic effects, and studies have shown it to be effective in reducing chemotherapy-associated nausea (Hickock JT, et al. Planta Med. 2008; 74(13): 1560-9) and in post-operative nausea (Nanthakomon T, et al. Biochem Biophys Res Commun. 2007; 362(1): 218-23).
Black Pepper (Piperine): Though it has inflammation-mediating properties of it's own (it reduces COX-2), extracts of black pepper are used in traditional Ayurvedic formulations primarily to improve the absorption of Curcumin, Boswellia and other inflammation-regulating herbs. Dr. Pai said these formulations usually include 5 mg of black pepper per 250-300 mg curcumin.
In an effort to provide his patients with safer alternatives to NSAIDs, Dr. Pai began formulating a botanical combination based on traditional formulas but utilizing Sabinsa's standardized ingredients, Curcumin C3 Complex, Boswellin PS, BioPerine, and Ginger, which he believes to be the most well-researched and validated extracts on the market.
After several years of experimentation, he recently introduced the product to the broader clinical community as Bosmeric SR. "What took a long time—3 years to be exact—was the development of a sustained release formulation that would down-regulate inflammation for long periods. We ended up having to formulate a bi-layered tablet. It wouldn't work to encapsulate all these ingredients together. The enzymes from one herb can degrade active compounds in another."
Bosmeric-SR was tested in a not yet published preliminary study of 30 patients, aged 40-65, with knee osteoarthritis. They took the Bosmeric formula, 2 tablets twice daily, for 56 days. WOMAC scores began to decrease after the 3rd day, with pain scores dropping from a baseline mean of 11 to 8 at the conclusion. Stiffness scores decreased from 5 to 3, and disability scores dropped from 48 to 31. Distance walked in 6 minutes increased from a mean 270 meters at baseline to 360 meters at the close.
Underscoring the anti-inflammatory effect was a marked reduction of high-senstivity C-reactive protein (CRP) from 1.5 at baseline to 0.8.
Though some patients begin to experience pain relief within a few hours of taking Bosmeric-SR, Dr. Pai stressed that it is not a magic bullet. It is, however, a very safe option for down-regulating inflammation over time.
"We've used this combo formula in over 3,500 patients, and so far we've only seen 4 IgE reactions to the ginger, and 1 IgE reaction to the black pepper.
He emphasized that people could get some of the benefits of a formula like Bosmeric-SR by ramping up their dietary intake of curry. But unless one is planning to eat huge amounts of turmeric and ginger with nearly every meal, it would be difficult to quell a chronic inflammatory condition. "We take things another step, beyond what you could obtain with diet alone. But we're not hiding behind the "proprietary blend" appellation. We really want people and their physicians to know what they're taking."
END
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However, based on the results for the activity monitor, it is unl
However, based on the results for the activity monitor, it is unlikely that a larger C646 chemical structure sample
size would have resulted in a positive intervention effect for walking activity. A strength of this study was the location of the program in the children’s homes, in paediatric physiotherapy practices or special schools for children with disabilities. While different characters, motivational skills and training facilities might have influenced the effects of training, this variety increases the generalisability of our results to other paediatric practices. In conclusion, a physical activity stimulation program combining counselling through motivational interviewing, home-based physiotherapy and fitness training was not effective for increasing children’s physical activity, or improving mobility capacity, fitness, fatigue, and attitude towards sports. Further research should be performed to determine the separate contribution of each component of the program for improving physical activity. What is already known
on this topic: Children with cerebral palsy have lower levels of physical activity and fitness compared to their typically developing peers. Physical activity patterns may persist http://www.selleckchem.com/products/Temsirolimus.html into adolescence and adulthood. Exercise programs can improve the fitness of children with cerebral palsy. Studies of interventions to promote physical activity in this population have shown favourable, but non-significant, trends. What this study adds: A physical SB-3CT activity stimulation program consisting of fitness training, counselling and home-based therapy was not effective in children with cerebral palsy. Although the program improved the children’s attitude to sports, the effect was small. Footnotes: a StepWatch™ Activity Monitor 3.0, Orthocare Innovations, Seattle, USA. b MicroFet dynamometer, Biometrics, Almere, The Netherlands. c Corival V2 Lode B.V., Groningen, The Netherlands. d Cosmed, Rome, Italy. eAddenda: Tables 6 and
7 can be found online at doi:10.1016/j.jphys.2013.12.007 The following are the supplementary data to this article: Table 6. Ethics: The Medical Ethical Board of the VU University Medical Center, Amsterdam, approved this study. Parents and children aged 12 years and over gave written informed consent before data collection began. Competing interests: Nil. Grant providers were not involved in the design of the study, data collection, data analysis, manuscript preparation and publication decisions. Source(s) of support: This project is part of the Dutch national LEARN 2 MOVE research program and is supported financially by ZonMw (grant number 89000002), Johanna Kinderfonds, Stichting Rotterdams Kinderrevalidatie Fonds Adriaanstichting, Revalidatiefonds, Phelps Stichting, Revalidatie Nederland, and the Nederlandse Vereniging van Revalidatieartsen.
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The Ultimate Guide to IV Therapy: Boost Your Energy and Health
The Ultimate Guide to IV Therapy Boost Your Energy and Health
Maintaining good health and high energy levels is more important in today’s fast-paced world. Modern life can often leave us feeling drained, both physically and mentally. Thankfully, there’s a rejuvenating solution that’s been gaining popularity in recent years – IV therapy. This comprehensive guide will explore the wonders of IV therapy, its benefits, the different types available, and how it can significantly boost your energy and overall health.
Understanding IV Therapy
IV therapy, short for Intravenous Therapy, is a medical technique that involves delivering fluids, vitamins, minerals, and other essential nutrients directly into the bloodstream through a needle and catheter. This method ensures that the nutrients are absorbed rapidly and completely by the body, making it an efficient way to replenish what your body might be lacking.
The Science Behind IV Therapy
To truly appreciate the benefits of IV therapy, it’s important to understand the science behind it. When nutrients are administered intravenously, they bypass the digestive system, where a significant portion of these nutrients can be lost. This direct delivery method ensures that your body absorbs nearly 100% of the nutrients, leading to immediate and noticeable results.
Benefits of IV Therapy
Enhanced Hydration
IV therapy provides rapid rehydration, which is particularly useful after intense physical activities, hangovers, or during illness. Staying well-hydrated is essential for maintaining energy levels and overall health.
Increased Energy
By delivering a combination of B vitamins, minerals, and amino acids directly into your bloodstream, IV therapy can provide an instant energy boost. This is perfect for those times when you need a quick pick-me-up.
Immune System Support
IV therapy can be customized with immune-boosting nutrients such as vitamin C, zinc, and glutathione. This helps fortify your immune system, making you more resilient to illnesses.
Stress Reduction
Stress can take a toll on your body. IV therapy can include nutrients like magnesium and B vitamins, which promote relaxation and reduce stress, leaving you feeling rejuvenated.
Detoxification
IV therapy can aid in detoxifying your body by flushing out toxins and harmful substances. This can lead to improved organ function and an overall feeling of well-being.
Types of IV Therapy
There are several types of IV therapy, each tailored to address specific health concerns:
Hydration Therapy
This type of IV therapy is excellent for rehydrating the body and can be beneficial for athletes, individuals recovering from illness, or those looking for a quick energy boost.
Vitamin C IV Therapy
Vitamin C is known for its immune-boosting properties. This therapy is ideal for bolstering your immune system and helping your body fend off illnesses.
Hangover Relief
For those who’ve had a bit too much to drink, hangover relief IV therapy can alleviate the symptoms of a hangover and have you feeling better in no time.
Skin Rejuvenation
IV therapy with skin-enhancing nutrients can help you achieve a healthier and more youthful complexion. It’s a favorite among those looking to enhance their beauty.
Performance Enhancement
Athletes and fitness enthusiasts can benefit from IV therapy designed to boost performance and aid in recovery.
The IV Therapy Process
When you decide to undergo IV therapy, you can expect the following process:
Consultation
You’ll discuss your health goals and concerns with a qualified healthcare provider who will recommend the appropriate IV therapy for you.
IV Insertion
A small needle will be inserted into your vein, and the IV therapy will begin. You may experience a mild, temporary sensation.
Relax and Rejuvenate
Sit back and relax while the nutrients are delivered directly into your bloodstream. The process typically takes 30-60 minutes.
Enjoy the Benefits
Experience the effects of IV therapy almost immediately. Many people report feeling more energized and refreshed right after the treatment.
Who Can Benefit from IV Therapy?
IV therapy is suitable for a wide range of individuals, including:
• Athletes and fitness enthusiasts
• Individuals with busy lifestyles
• Those recovering from illness
• People seeking to boost their immune system
• Anyone looking to improve their overall health and well-being
Conclusion
IV therapy is a powerful and efficient way to boost your energy and improve your health. By directly delivering essential nutrients to your body, this method provides quick and noticeable results. Whether you’re in need of an energy boost, immune support, or simply looking to enhance your well-being, IV therapy offers a solution that’s tailored to your specific needs. So, consider exploring the world of IV therapy and embark on a journey to a healthier, more energetic you.
Dr Ebraham Jatta
DR. EBRAHAM JATTA, NMD
Dr. Ebraham Jatta, NMD, is a dedicated licensed physician, certified by the Naturopathic Physician Medical Board of Arizona. With a wealth of clinical expertise in Holistic and Primary Care… Read More
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Gestational Diabetes and Labour Induction – Is It Always Needed?
During pregnancy, certain hormones wreak havoc and do not allow your body to use insulin to keep your blood sugar levels under control. Insulin is what helps in converting sugar to energy, and sometimes, pregnancy does not allow that to happen which leads to high blood-sugar levels. This, unfortunately, leads to gestational diabetes. Gestational Diabetes among pregnant women means that labor has to be induced around 39-40 weeks of gestation failing which it could have adverse impacts on the unborn baby and the mother. Find out more information about the same and how to induce labor as one of the methods to ensure no neonatal complications.
Is Induction of Labour Necessary When You have Gestational Diabetes?
Some women have symptoms of GD whereas others don’t. Some can also fix it just by managing diet and some exercise whereas others need shots of insulin. A lot of health care providers recommend around 3940 weeks for inducing childbirth. The WHO says not before 41 weeks, albeit backed up by weak evidence. Guidelines for GD according to the American Congress of Obstetricians and Gynecologists recommends induced labor not before 39 weeks of gestation with controlled GD.
Each case is treated individually based on the patient’s medical analysis and requirement. For many women, if the diabetes labor through the course of the pregnancy, they can most likely have labor deliveries. However, inducing labor becomes important when diabetes is not controlled to maintain the health and safety of both the baby and the mother.
Why is Labour Induction Important in Case of Gestational Diabetes?
What used to be once a relatively rare condition is now becoming more and more common. Having GD can negatively impact the health of both, mother and unborn child but it does not affect the way you give birth. You can still give birth vaginally and can also have an uncomplicated delivery. Here are some reasons why inducing labor is a good option.
1. Stillbirth
One of the main reasons for inducing childbirth in women who have GD is to prevent stillbirth. The chances of stillbirth increase significantly after the 40-week benchmark for women with GD. Therefore, sometimes, labor is induced to make sure the mother and the child are safe.
2. Larger than a Normal Baby
Women with GD usually have babies that are slightly larger. The extra sugar crosses paths with the placenta and makes your baby fatter due to the storage of insulin. Inducing labor would be important because babies can weigh up to 4.5kgs sometimes.
3. Other Complications
Macrosomia or large baby can lead to other complications as well including damage to the tailbone, blood loss, tearing, etc. Inducing childbirth can help avoid these complications.
4. Preeclampsia
A situation, which combines high blood-pressure and the presence of protein in the urine during pregnancy. This can lead to complications such as preterm labor, abruptions or even seizures that can prove to be fatal for mother and child. A study showed that induction of labor for women with mild preeclampsia between 3437 weeks helped reduce the risk of the outcome by a little bit.
5. Mother-Baby Health
During childbirth, the most critical part is to keep the mother and baby as safe as possible. GD occurs in a lot of women nowadays, and scientists say that the number might go up. Monitor your blood sugar levels continuously and if induction is required, make sure you are well read and informed about it.
How Will You be Induced?
There are multiple ways to induce labor, but if you have to go through it, you should understand it completely and all the benefits and risks involved as well. Each way of inducing childbirth has its pros and cons. You should make sure to talk to your doctor in depth and understand which method is best suited for you after a thorough medical analysis. Here are some ways in which you can be induced.
• A common question is “will I be induced if I have Gestational Diabetes?” The answer is yes because that is a safer option for you and your baby. Gestational diabetes can lead to a lot of complications, so it is better to induce labour than try natural methods.
• Artificial Rupture of Membrane of ARM where an amnihook is inserted to pierce the water bag surrounding your baby labor help the baby crown. Many women opt for this option.
• Oxytocin is another method to induce labor wherein synthetic oxytocin is inserted via an IV drip. This will engage your hormones and trigger your system into labour. Some childbirths are induced at 38 weeks due to gestational diabetes which is earlier than what the WHO recommends.
• A low-risk option is a Foley Balloon catheter, which is placed in the vagina and inflated in the hope that the baby’s head will help encourage dilation. Since there are no drugs involved, this is a low-risk way to induce labour.
• Prostaglandin gel is used to encourage contractions. The doctor will insert the gel to soften and dilate the cervix. Although it is a synthetic hormone, it is useful for inducing labor.
Although natural childbirth is the best way to go, sometimes circumstances are unpredictable. In those situations, one should not worry and find a solution instead. If your condition can be managed, you should ideally have a normal birth. However, GD can be controlled as well so don’t worry, follow your doctor’s advice and you will have a safe delivery for you and your baby. GD can be tried and prevented by following a healthy diet and lifestyle. Regular check-ups can also be helpful in keeping your blood sugar levels in a safe range. Make an informed decision after consulting your doctor and all the best!
Also Read:
Is Vomiting While Labour Beneficial
Induce Labour Using Acupuncture
Timing Contractions While Labour
Previous articleThese Are the 8 Best Low Maintenance Pets
Next articleApple Cider Vinegar to Boost Fertility
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• Lauren Svensen FNP-C
Tips to Stay Well in the Heat
Dehydration
When the body does not have enough fluid it becomes dehydrated. In the summer, sweating causes dehydration. Some signs of dehydration are feeling very thirsty and having muscle cramps. You may also feel dizzy when you go from a sitting position to a standing position when you are dehydrated. This dizziness occurs because when your body does not have enough fluid, it causes your blood pressure to drop. Severe signs of dehydration are confusion and chest pain which occur due to low blood pressure caused by not having enough fluid. The more dehydrated you get, the lower your blood pressure will go.
Dehydration Treatment
If you have mild dehydration you can fix your dehydration by drinking water. If your symptoms do not improve with drinking water or if you have severe symptoms you should seek immediate medical attention by calling 911.
Severe cases may require IV fluid replacement. Dehydration can be deadly!
Prevent Dehydration
You can prevent dehydration by drinking water throughout the day. Most people do not need sports drinks to stay hydrated and one downside of sports drinks is the high sugar content. Avoid alcoholic beverages when having fun in the sun as these will lead to dehydration.
Hyperthermia
Hyperthermia occurs when your body gets overheated. Symptoms of hyperthermia are similar to dehydration and include dizziness, nausea, headache, fatigue, and muscle cramping. Some severe symptoms of hyperthermia are having a body temperature of 103 degrees Fahrenheit or higher, red, hot dry skin, having a very fast pulse, confusion, and unconsciousness.
Hyperthermia treatment
If you have symptoms of hyperthermia, get in the air conditioning, stop any exercise and remove any extra clothing if possible. If your symptoms don’t improve or if you have severe symptoms call 911; hyperthermia can be deadly.
What Will the Hospital Do?
The hospital has many different methods to cool you down safely and quickly. Some of them include submerging you in an ice bath, cooling blankets, and pouring cold water over you. Another method is applying ice packs to your armpits, neck, and groin, which are areas that have large blood vessels. When the ice packs are on top of large blood vessels the blood traveling through your body gets colder.
At this point, you are probably thinking that buying out all the ice at the grocery store will be way cheaper than that pesky hospital bill, so pay attention. If you lose consciousness due to being over-heated you may not be able to breathe without help and the ER staff can help manage your airway and keep you breathing. The hospital staff will be constantly checking your body temperature, to make sure your body temperature is getting cooler but not too cold. Too much ice bath can cause hypothermia, low body temperature which is also dangerous.
*This article is intended for general information purposes only and is not medical advice. Please seek counseling from your primary care provider for personalized medical advice.
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Supplementary MaterialsFigure S1: Cell morphology of AGS, MKN74 or NCI-N87 cells, not infected (NI) or upon 24 h infections with either and restriction sites downstream to luciferase gene
Supplementary MaterialsFigure S1: Cell morphology of AGS, MKN74 or NCI-N87 cells, not infected (NI) or upon 24 h infections with either and restriction sites downstream to luciferase gene. from the miRNA promoter in accordance with that of SV40 promoter reporter (n?=?2); lower -panel, Tubulin and ZEB1 immunoblots. (B) SV40 promoter (pGL3-p) or promoter (pGL3prom200b) actions in MKN-74 cells Rabbit Polyclonal to TFE3 upon 24 h infections with wt at MOI 100; pubs represent indicate SD of luciferase actions of every reporter vector (n?=?3; **P 0.01) (C) Schematic representation of putative transcription aspect binding sites within the promoter series, teaching the E-boxes (vibrant) as well as the Compound 401 overlapping NF-B binding site (underlined). The nucleotides which have been mutated in Fig. 4C are indicated by arrows.(DOCX) pone.0060315.s005.docx (148K) GUID:?7388F85B-B9D3-4089-B715-E3D433B75658 Figure S6: NF-B immunofluorescence in AGS cells transfected with pEGFP (still left panels) or pEGFP-IB (correct panels) in basal conditions or upon infection. Cells had been seeded in 8-well Labteck? chambers and transfected using the appearance vectors at 100 ng/well. 48 hrs Compound 401 post-transfection, cells had been contaminated with Compound 401 outrageous type Compound 401 at MOI 100. Six hrs afterwards, cell were set and tagged stepwise using a goat anti-NF-B antibody and using a AlexaFluor564-tagged anti-goat IgG supplementary antibody, seeing that described in Strategies and Materials. Images were obtained on the Zeiss microscope built with epifluorescence.(DOCX) pone.0060315.s006.docx (397K) GUID:?67EA3F7B-EC78-4960-AA4D-14DFB2770306 Desk S1: Set of oligonucleotide primers. (DOCX) pone.0060315.s007.docx (97K) GUID:?ACF24956-4B60-4222-AFD3-890D9E9DD8AC Desk S2: Expression from the miR-200 family in gastric epithelial cell lines. (A) Degrees of miR-200 in basal circumstances: beliefs represent indicate SD of RT-qPCR data for every miRNA in accordance with snoR25 (n?=?4). (B) Variants of miR-200a, -429 and -141, 24 h post-infection with (Horsepower WT) or the isogenic CagA-deficient stress, both at MOI 100. Data signify indicate SD of RT-qPCR data for every miRNA in accordance with snoR25 and in comparison to non contaminated cells (NI); n?=?4; *: p-value 0.05, ***: p-value 0.001.(DOCX) pone.0060315.s008.docx (79K) GUID:?B9B9EC66-BB73-4B97-B3EB-0B42B454DFA1 Materials and Strategies S1: (DOCX) Compound 401 pone.0060315.s009.docx (119K) GUID:?FDB9E824-1B9A-4091-8AA0-A7FA54225710 Abstract Chronic infection provokes an inflammation from the gastric mucosa, at risky for cancers and ulcer advancement. Probably the most virulent strains harbor the pathogenicity isle (stress or isogenic mutants. Morphological adjustments, epithelial and mesenchymal gene appearance and EMT-related microRNAs had been examined. up-regulates mesenchymal markers, including ZEB1. This transcription aspect is prominently mixed up in mesenchymal changeover of contaminated cells and its own up-regulation depends upon activates NF-B, which transactivates ZEB1, promoting mesenchymal transition subsequently. The unforeseen N-FB-dependent boost of miR-200 amounts most likely thwarts the irreversible lack of epithelial identification in that important situation. Launch The bacterium pathogenicity isle (the T4SS into gastric epithelial cells, and eventually cause cell innate immunity by activating the nuclear aspect B (NF-B), a get good at transcription element in inflammatory replies following microbial infections [3]. NF-B activation is certainly mediated by CagA connections with TRAF6 and TAK1 and PG identification by NOD1, and results in NF-B-dependent transcription of multiple focus on genes, like the pro-inflammatory interleukin (IL)-1, IL-6, IL-8 and tumor necrosis aspect [4]C[6]. Besides, CagA binds to amounts of various other web host protein involved with cell indication and junctions transductions, activating ERK-MAPK, ?-catenin and c-Met signaling pathway and impairing epithelial cell polarity [7]C[12]. In a few gastric epithelial cell lines such as for example AGS, a cell lifestyle model utilized to recapitulate early occasions of infections broadly, strains induce a quality morphological change termed the hummingbird phenotype, an elongated cell form alongside lack of cell-cell connections extremely. The relevance for the hummingbird phenotype in gastric carcinogenesis continues to be supplied by the observation that strains isolated from gastric carcinoma tissue, in bulk genes [17]C[19]. ZEB1/2 are reciprocally from the miR-200 family in a poor feedback loop, each regulating the appearance of the various other totally, thus controlling both reversibility and balance from the epithelial versus mesenchymal phenotypes [16]; [20]. MiR-200 are microRNA (miRNA), little noncoding RNA substances that post-transcriptionaly regulate gene appearance in a number of biological procedure [21]..
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Actigraphy in brain-injured patients – A valid measurement for assessing circadian rhythms?
Abstract
Background
Actigraphy has received increasing attention in classifying rest-activity cycles. However, in patients with disorders of consciousness (DOC), actigraphy data may be considerably confounded by passive movements, such as nursing activities and therapies. Consequently, this study verified whether circadian rhythmicity is (still) visible in actigraphy data from patients with DOC after correcting for passive movements.
Methods
Wrist actigraphy was recorded over 7–8 consecutive days in patients with DOC (diagnosed with unresponsive wakefulness syndrome [UWS; n = 19] and [exit] minimally conscious state [MCS/EMCS; n = 11]). The presence and actions of clinical and research staff as well as visitors were indicated using a tablet in the patient’s room. Following removal and interpolation of passive movements, non-parametric rank-based tests were computed to identify differences between circadian parameters of uncorrected and corrected actigraphy data.
Results
Uncorrected actigraphy data overestimated the interdaily stability and intradaily variability of patients’ activity and underestimated the deviation from a circadian 24-h rhythm. Only 5/30 (17%) patients deviated more than 1 h from 24 h in the uncorrected data, whereas this was the case for 17/30 (57%) patients in the corrected data. When contrasting diagnoses based on the corrected dataset, stronger circadian rhythms and higher activity levels were observed in MCS/EMCS as compared to UWS patients. Day-to-night differences in activity were evident for both patient groups.
Conclusion
Our findings indicate that uncorrected actigraphy data overestimates the circadian rhythmicity of patients’ activity, as nursing activities, therapies, and visits by relatives follow a circadian pattern itself. Therefore, we suggest correcting actigraphy data from patients with reduced mobility.
Peer Review reports
Background
In the last decades, the measurement of physical activity, so-called actigraphy, has received increasing attention for the classification of vigilance states in healthy individuals (see reference [1] for a review). Recently, actigraphy was also used for the investigation of day-night patterns as well as circadian rhythms (i.e., rhythms with a period length of approximately 24 h) in patients following severe brain injury [2,3,4,5]. As those patients often need full-time care, actigraphy measures may be highly influenced by passive movements in this patient population. Therefore, we sought to systematically control for passive movements in this study.
Severe brain injury can cause coma and, upon recovery, longer lasting changes in consciousness, which can be summarized as “disorders of consciousness (DOC)”. In a simplified approach, consciousness is thought to require both adequate levels of wakefulness and awareness [6]. More precisely, wakefulness refers to some degree of arousal at the brain level (e.g., eye-opening, limb movements) and awareness denotes the ability to have a conscious experience of any kind. While brain-dead or comatose patients are characterized by absent arousal and awareness, patients with an unresponsive wakefulness syndrome (UWS; formerly often referred to as vegetative state) show some return of arousal (i.e., alternating phases of sleep [closed eyes] and wakefulness [opened eyes]), however, without signs of awareness. In a minimally conscious state (MCS), cognitively mediated behavior indicating awareness occurs inconsistently, but is reproducible or long enough to be differentiated from reflexive behavior (e.g., response to command, verbalizations, visual pursuit) [7]. If patients are able to functionally use objects and communicate, their state is denoted exit MCS (EMCS) [8]. Thus, while UWS patients are assumed to be unconscious, MCS and EMCS patients show signs of consciousness. However, distinguishing between UWS and MCS is still a challenging task. Until now, behavioral methods like the “Coma Recovery Scale – Revised” (CRS-R) [9] and the “Glasgow Coma Scale” (GCS) [10] remain the best available tools for clinical diagnoses. Unfortunately, the rate of misdiagnoses is still high (~ 40%) [11] if behavioral scales are not performed by well-trained professionals. Therefore, the quest for ways to improve the validity of such assessments remains an important issue. As consolidated periods of wakefulness and sleep resulting from well-entrained circadian rhythms seem crucial for adequate arousal levels and thus (conscious) wakefulness, circadian rhythms have been the focus of recent research in patients with DOC. Research from our group [5, 12] suggests that a better integrity of patients’ circadian melatonin(-sulfate) and temperature rhythms is indeed related to a richer behavioral repertoire (as measured with the CRS-R). Knowing a patient’s circadian rhythm in turn has been suggested to help find the optimal time for behavioral assessments and therapies as cognitive functions also vary with the time of day [12,13,14]. However, besides temperature and melatonin rhythms, variability within a day can also be observed in other parameters in patients with DOC as for example in blood pressure, heart rate, and body movements [3, 15, 16].
Body movements can be monitored through actigraphy, which is frequently used in the clinical setting for evaluating rest-activity cycles (e.g., in insomnia, circadian rhythm disorders, or clinical monitoring in the rehabilitation process of patients with traumatic brain injury (TBI) [17, 18]) with the major advantage of being a cost-efficient and easy to use tool suitable for long-term investigations. More precisely, an actigraph, worn on the wrist or ankle, allows the continuous recording of data across days, weeks, and even months in a natural setting without restricting mobility and daily life routine of the participants.
Previous studies investigating rest-activity cycles in patients with DOC using actigraphy found that the sleep-wake cycle deteriorates with decreasing consciousness level [2]. When taking etiology into account, only patients with TBI show significant day-night differences (i.e., stronger motor activity during daytime [7 am–11 pm] than during nighttime [11 pm–7 am]) but not patients with anoxic-ischemic brain injuries (AI) [4]. Furthermore, circadian sleep-wake cycles (that is, not only day-to-night variations but the investigation of fluctuations in wrist actigraphy-derived physical activity over several days using cosinor rhythmometry analyses) are more impaired in UWS patients and patients with non-traumatic brain injuries (NTBI) as compared to MCS patients and patients with TBI. Therefore, Cruse et al. suggest that actigraphy should be considered as an alternative for assessing sleep-wake cycles in patients with DOC and appeal to also determine the prognostic utility of wrist actigraphy for UWS and MCS patients in future studies [3].
However, the use of actigraphy in patients with DOC may be severely limited by several factors. First, patients with DOC often suffer from severe motor impairments, spasticity, and the use of muscle relaxants, which have previously shown to, descriptively, decrease for example the concordance between polysomnography- and actigraphy-derived parameters [18]. Second, as most of them spend much time in bed and often need full-time care in hospitals or nursing homes, actigraphy data is likely to be confounded by passive movements due to nursing activities, therapies, or movements initiated by visitors. The latter issue becomes particularly crucial when actigraphy data are used to make inferences about patients’ circadian rhythms. This is because the rhythmicity might reflect daily patterns of for example nursing activities or therapies rather than a circadian rhythm of the patient. Unfortunately, correcting for passive movements is challenging and the previously published findings may thus be biased towards overestimating rhythmicity. In the current paper, we therefore sought to systematically control for passive movements and to assess the magnitude of the introduced bias by comparing corrected and uncorrected actigraphy-derived measures. Eventually, we aimed at revealing whether circadian rhythmicity can be identified in MCS and/or UWS patients using actigraphy data even if artificial biases are carefully controlled for.
Methods
Patients
From a total of 30 patients, one patient (P26) had to be excluded because hardly any activity was left after cleaning the data from passive movements (cf. Additional file 1: Tables S1, S2 and Figure S2). Thus, 29 patients (13 women) aged 19–78 (mdn = 55 years) from long-term care facilities in Austria were included in the study sample with 18 patients who were diagnosed with UWS (7 women), 7 were in a MCS (4 women), and 4 in an EMCS (2 women). Note that the data has been used in two previous publications, where we studied circadian rhythms in patients with DOC but without focusing on actigraphy data [5, 12]. Informed consent was obtained from the patients’ legal representatives, and the study had been approved by the local ethics committees. Please note that MCS and EMCS patients were combined to a single group in the analyses as we sought to analyze differences between unconscious UWS and (minimally) conscious (E)MCS patients. For more details on the study sample, please see Table 1.
Table 1 Demographic information
Experimental design
The study protocol comprised seven to eight full days (hereinafter “study week”) during which actigraphy was assessed continuously (for further measures recorded, see reference [5]). Patients’ behavioral repertoire or level of consciousness was assessed with the CRS-R in the morning of day 6 and in the afternoon of day 7 during the study week. Besides this, multiple additional CRS-R assessments (i.e., 10 additional assessments) were obtained in 16 patients (8 women; P2, P4, P6, P8, P10, P12, P14, P16, P18, P24–P30) on two consecutive days following the study week (note that multiple CRS-R assessments are not available for all patients as they were added to the study protocol later). Illuminance was kept < 500 lx at the eye level during the day (7 am–9 pm) and < 10 lx during the night (9 pm–7 am), which was ensured by continuous measurements with light sensors (wGT3X-BT Monitor, ActiGraph LLC., Pensacola, USA) and spot checks with a luxmeter (Dr. Meter, Digital Illuminance/Light Meter LX1330B). For further information on light levels, please refer to Additional file 1.
Behavioral assessment and data analysis
Coma Recovery Scale—Revised
The patients’ neurophysiological state was assessed behaviorally with the CRS-R [9]. It is composed out of six subscales reflecting auditory, visual, motor, oromotor, communication, and arousal functions that altogether make up 23 items. Whereas the lowest item on each subscale represents reflexive behavior, the highest item indicates cognitively mediated behavior. Patients are tested in a hierarchical manner, meaning that the examiner starts with the highest item of each subscale and moves down the scale until the patient’s response meets the criteria for one item. The scores of all subscales sum up to a maximum score of 23. The assessment was done twice in all patients by two trained experts, with 10 additional assessments being available for 16 patients. For the following analyses, we used those CRS-R assessments where the patients showed the highest behavioral reactivity (e.g., as characterized by the best diagnosis or highest sum score) as this is thought to best represent the true state of the patient. The highest CRS-R score and diagnosis across the whole study period of each patient are shown in Table 1. For further information on multiple CRS-R assessments, please refer to Additional file 1.
Actigraphy
We recorded actigraphy with a sampling rate of 30 Hz using GT3X+ devices (ActiGraph LLC., Pensacola, FL 32502). The actigraph was placed on the wrist of the arm with the greatest mobility and least spasticity. If both arms were equally mobile, it was placed on the wrist of the dominant hand. If the legs were more mobile, it was placed on the ankle of the most mobile leg. Actigraphs recorded continuously during the whole “study week” and were only taken off if the patients were showered or bathed. To monitor passive movements and remove artifacts resulting from them, we recorded all events deemed relevant in the patient room using an application (https://github.com/wolli2710/HospitalTracker) that enabled clinical and research staff as well as visitors to indicate the type of activity that was performed by simply tapping the screen of a tablet in the patient room. Specifically, we had start and end buttons for visits, nursing activities, actigraphy (i.e., to mark if the actigraph was taken off for showering or bathing), therapy, mobilizations in the wheelchair, and mobilizations outside the building (e.g., if they went for a walk with the patient). Furthermore, we had “single press buttons” (i.e., no start and stop option; only needed to be pressed once at the time of occurrence) for the administration of medication and nutrition as well as for lights on and out and eyes open and closed (cf. Additional file 1: Figure S1 to get an impression of the graphical user interface of the tablet). Upon tapping the screen, a time stamp was generated, which allowed us to correct the actigraphy data post hoc.
Cleaning and analysis of actigraphy data was done in R version 3.4.2 [19]. After integrating actigraphy and tablet data into one single dataset, the actigraphy data was down-sampled to 1/60 Hz (i.e., one value per minute). The actigraphy values of the time spans during which (i) clinical staff or visitors were with the patient, (ii) the patient was put into a wheelchair or back into bed, (iii) the CRS-R assessments took place, and (iv) the times when the actigraphs had been taken off for body care were removed. As the calculation of interdaily stability (IS; see below) requires a dataset without missing data, the first half of the removed values was replaced by the median activity during the 10 min preceding the event and the second half was replaced by the median activity during the 10 min following the end of the event. Importantly, to account for the issue that clinical staff or visitors indicated their presence too late, we additionally removed and imputed 5 min before and after each nursing activity as well as 10 min before and after each visit or usage of the wheelchair. This automatic artifact correction was followed by a visual screening and manual correction of residual artifacts. Thus, the resulting dataset can be assumed to be free from passive movements representing only the “true” internal motor activity of the patient (cf. Fig. 1 for an illustration of our correction procedure). For the analyses of the uncorrected actigraphy data, we down-sampled the data to 1/60 Hz. Thus, we arrived at a corrected as well as at an uncorrected dataset for each patient, which we used for the calculation of the following parameters using R.
Fig. 1
figure1
Graphical representation of the manual and automatic artifact correction of a 24-h actigraphy recording.a Uncorrected actigraphy data with the time of day being depicted on the x-axis and the amplitude of the motor activity on the y-axis. b Corrected actigraphy data after automatic (according to the tablet data) and manual artifact correction (marked with a red arrow). c External events recorded by the tablet in the patient room with longer vertical lines representing the start and shorter vertical lines the stop of the respective event
Interdaily stability and intradaily variability
Interdaily stability (IS) and intradaily variability (IV) are non-parametric measures [20], whose calculation is implemented in the R package “nparACT” [21]. In more detail, IS reflects how well a patient’s activity rhythm is entrained to a 24-h zeitgeber (i.e., the light-dark cycle) as indexed by values ranging between 0 for Gaussian noise and 1 for perfect IS. In contrast, IV quantifies the fragmentation of a rest-activity pattern. IV converges to 0 for a perfect sine wave and approaches 2 for Gaussian noise. It may even be higher than 2 if a definite ultradian component with a period length of 2 h is present in the rest-activity cycle. For individual patients’ results, please refer to Additional file 1: Tables S1 and S2.
Lomb-Scargle periodograms
To detect rhythmicity in our data, we computed Lomb-Scargle periodograms [22, 23]. For each patient, we calculated two parameters using the “lomb” package available for R [24]: (1) normalized power and (2) peak period. The normalized power describes the fit of a sine wave to the data. It is maximal where the sum of squares of the fitted sine wave to the data is minimal. For calculation of the period length of each patient’s activity rhythm, we looked for significant peaks in the normalized power of the periodogram and extracted the period length of the significant peak, which was closest to 24 h (i.e., as circadian rhythms should be entrained to a 24-h cycle in a natural setting which is close to the intrinsic period of the human circadian pacemaker that is on average 24.18 h [25]). We set the oversampling factor to 100 and the significance level to α = 0.001. The individual patients’ results are displayed in Additional file 1: Tables S1 and S2. For further information on the analyses, please refer to the supplementary material of Blume et al. [5]
Mean activity
Mean activity was calculated separately for daytime (7 am–9 pm) and nighttime (9 pm–7 am) and simply reflects the mean of the measured activity during the study week (arbitrary units). It takes the intensity and number of movements into account. For individual patients’ results, please refer to Additional file 1: Tables S1 and S2.
Statistical analyses
Statistical analyses were done in R. We investigated differences in actigraphy (IS, IV, normalized power, deviation of the peak period from a 24-h rhythm, mean activity) between corrected and uncorrected data as well as day-night differences in mean activity using Wilcoxon signed-rank test. Differences between diagnoses (i.e., UWS vs. MCS/EMCS) and etiology (i.e., TBI vs. NTBI) were investigated using Mann-Whitney U test. To check if the differences in actigraphy data between UWS and MCS/EMCS patients are also visible on a subscale level, we also investigated the correlation between patients’ CRS-R scores (sum score as well as subscale scores) and actigraphy data using Kendall’s tau. The significance level was α = .05 (two-sided) with p values .05 < p ≤ .1 being denoted trends. Regarding effect sizes, r\( \left(\left|\frac{Z}{\sqrt{N}}\right|\right) \) was calculated for the results of Wilcoxon signed-rank test and Mann-Whitney U test. According to Cohen [26], the following conventions are applied when interpreting r: small effect: r = .1; medium effect: r = .3; and large effect: r = .5.
Results
Circadian rhythms
Comparisons between corrected and uncorrected actigraphy data revealed that interdaily stability (IS) (Z(N = 29) = − 2.96, p = .003, r = .55; cf. Fig. 2a) and IV (Z(N = 29) = − 4.22, p < .001, r = .78; cf. Fig. 2b) were higher in the uncorrected data than in the corrected data. The period length was closer to 24 h in the uncorrected data (Z(N = 29) = − 3.29, p = .001, r = .61; median deviation from 24 h: uncorrected data = 0.41 h, corrected data = 1.11 h; cf. Fig. 3a). The strength of the circadian rhythm (i.e., normalized power) did not differ between datasets (Z(N = 29) = −.86, p = .39, r = .16; cf. Additional file 1: Figure S3).
Fig. 2
figure2
Interdaily stability (a) and intradaily variability (b) in uncorrected vs. corrected data. a Interdaily stability (IS). The IS was overestimated and significantly higher in the uncorrected data (IS approaches 0 for Gaussian noise and converges to 1 for perfect IS). UWS and MCS/EMCS patients did not differ in both corrected and uncorrected data (cf. Additional file 1: Figures S4 A-B). b Intradaily variability (IV). The IV was also overestimated and significantly higher in the uncorrected data (IV converges to 0 for a perfect sine wave [i.e., no IV] and approaches 2 for Gaussian noise. Values > 2 indicate an ultradian component with a period length of 2 h). UWS and MCS/EMCS patients only differed in the uncorrected data (cf. Additional file 1: Figures S4 C-D). Horizontal lines represent the medians, boxes the interquartile range (IQR; distance between the 1st [Q1] and 3rd quartile [Q3]), and whiskers extend at most to Q1−1.5*IQR (lower whisker) and Q3+1.5*IQR (upper whisker). Asterisks indicate significance: ***p ≤ .001, **p ≤ .01. Abbreviations: MCS minimally conscious state, EMCS exit MCS, UWS unresponsive wakefulness syndrome
Fig. 3
figure3
Circadian rhythmicity contrasted between datasets (a) and circadian rhythm strength contrasted between diagnoses (b).a Deviation of the patients’ peak period from 24 h. The patients’ activity rhythms were significantly better aligned with a 24-h rhythm in the uncorrected data (=less deviation from 24 h). UWS and MCS/EMCS patients did not differ in both uncorrected and corrected data (cf. Additional file 1: Figures S4 E-F). b Normalized power of the patients’ peaks closest to 24 h. UWS and MCS/EMCS patients differed in the uncorrected and corrected data. Pooling both patient groups, the normalized power did not differ between datasets (cf. Additional file 1: Figure S3). For better illustration, the data was log-transformed (right-hand y-axes); statistics were performed on the untransformed data (left-hand y-axes). Horizontal lines represent the medians, boxes the interquartile range (IQR; distance between the 1st [Q1] and 3rd quartile [Q3]), and whiskers extend at most to Q1−1.5*IQR (lower whisker) and Q3+1.5*IQR (upper whisker). Asterisks indicate significance: ***p ≤ .001, *p ≤ .05, +p ≤ .1. Abbreviations: MCS minimally conscious state, EMCS exit MCS, UWS unresponsive wakefulness syndrome
Contrasts between diagnoses showed that intradaily variability (IV) was higher in UWS patients than in MCS/EMCS patients in the uncorrected data (Z(n1 = 11, n2 = 18) = − 2.20, p = .028, r = .41; cf. Additional file 1: Figure S4 C). This was not the case in the corrected data (Z(n1 = 11, n2 = 18) = − 1.42, p = .157, r = .26; cf. Additional file 1: Figure S4 D). Furthermore, while MCS/EMCS patients showed a stronger circadian rhythm – as indicated by a higher normalized power – than UWS patients in the uncorrected data (Z(n1 = 11, n2 = 18) = 2.16, p = .031, r = .40), this difference was only visible by trend in the corrected data (Z(n1 = 11, n2 = 18) = 1.84, p = .065, r = .34; cf. Fig. 3b). Moreover, we found no significant differences between etiologies (TBI vs. NTBI) on any of the circadian rhythm indices in the corrected dataset (cf. Additional file 1: Figures S5 A-D).
Day vs. night
Patients’ activity levels were higher during day than night in both uncorrected (Z(N = 29) = − 4.13, p < .001, r = .77) and corrected data (Z(N = 29) = − 3.31, p < .001, r = .61) with effect sizes being larger in the uncorrected data (cf. Additional file 1: Figure S6). Furthermore, day-night differences were more pronounced in MCS/EMCS patients than in UWS patients in both datasets (uncorrected data: MCS/EMCS: Z(n = 11) = − 2.89, p = .004, r = .87; UWS: Z(n = 18) = − 2.92, p = .004, r = .69; corrected data: MCS/EMCS: Z(n = 11) = − 2.45, p = .014, r = .74; UWS: Z(n = 18) = − 2.22, p = .026, r = .52; cf. Fig. 4).
Fig. 4
figure4
Patients’ mean activity during day vs. night in uncorrected and corrected data separately for diagnoses. The mean activity was significantly higher during the day (7 am–9 pm) than during the night (9 pm–7 am) in both uncorrected and corrected data in UWS and MCS/EMCS patients with stronger day-night effects in MCS/EMCS patients and uncorrected data. For better illustration, the data was log-transformed (right-hand y-axes); statistics were performed on the untransformed data (left-hand y-axes). Horizontal lines represent the medians, boxes the interquartile range (IQR; distance between the 1st [Q1] and 3rd quartile [Q3]), and whiskers extend at most to Q1−1.5*IQR (lower whisker) and Q3+1.5*IQR (upper whisker). Asterisks indicate significance: **p ≤ .01, *p ≤ .05. Abbreviations: MCS minimally conscious state, EMCS exit MCS, UWS unresponsive wakefulness syndrome
When comparing activity levels during day and night between diagnoses, we found that MCS/EMCS patients show higher mean activity than UWS patients during day and night in both uncorrected (day: Z(n1 = 11, n2 = 18) = 2.16, p = .031, r = .40; night: Z(n1 = 11, n2 = 18) = 2.20, p = .028, r = .41) and corrected data (day: Z(n1 = 11, n2 = 18) = − 2.69, p = .007, r = .50; night: Z(n1 = 11, n2 = 18) = 3.06, p = .002, r = .57) with larger effect sizes for comparisons between diagnoses in the corrected dataset (cf. Additional file 1: Figures S7 A-D). When looking at etiology, we found no significant differences between patients with TBI and NTBI in the activity levels during day and night in the corrected dataset (cf. Additional file 1: Figure S8).
Discussion
Our results indicate that actigraphy data from clinical populations suffering from severe motor impairments such as patients with DOC is strongly influenced by passive movements, i.e., movements not initiated by the patients. Not correcting for these passive movements leads to an overestimation of the patients’ circadian rhythmicity rendering the validity of the uncorrected data highly questionable.
Analyses revealed that using uncorrected data resulted in an overestimation of how well patients’ circadian rhythms were entrained to a 24-h zeitgeber (as indicated by interdaily stability [IS] and the deviation from the peak closest to 24 h in the periodogram analyses) and in more pronounced day-night differences. Specifically, 25/30 patients (83%) showed a circadian rhythm (i.e., less than 1 h deviation from 24 h) in the uncorrected data (cf. Additional file 1: Table S1). This is well in line with the results from Cruse et al. [3] who found a circadian rhythm in 46/55 patients (84%). However, after correcting the actigraphy data for passive movements, we found a circadian rhythm in only 13/30 patients (43%) (cf. Additional file 1: Table S2). This is most probably because nursing activities, therapies, and visiting times that cause such passive movements follow a regular (daily) schedule and are more prominent during the day than during the night. Thus, previous studies investigating circadian rhythmicity of activity levels in patients with DOC might be subject to this bias. Furthermore, we found higher variability within the 24-h day (as indicated by higher intradaily variability [IV]) in the uncorrected data, thus suggesting a stronger fragmentation of the patients’ activity. In other words, IV increases when periods of low “real” patient activity are followed by strong activity initiated by moving the patient passively. Thus, while passive movements occur in a regular pattern over several days (i.e., resulting in more IS), the variability of the measured activity within a day is increased due to passive movements.
When looking at day-night variations of activity levels separately for patient groups, patterns between diagnoses stayed the same in the corrected and uncorrected dataset with MCS/EMCS patients showing stronger day-night effects than UWS patients (cf. Fig. 4) as well as higher mean activity during day and night (cf. Additional file 1: Figures S7 A-D). Consequently, one might argue that the correction of actigraphy data is dispensable. However, as soon as the amount of passive movements differs between UWS and MCS/EMCS patients, we will get distorted results when contrasting actigraphy data between diagnoses. Even in our sample, where all of the patients were expected to receive equivalent levels of care, therapies, and visits, the results from contrasting UWS and MCS/EMCS patients in the uncorrected data differed from the corrected data when looking at IV (cf. Additional file 1: Figures S4 C-D). Specifically, while UWS patients showed a significantly higher IV as compared to MCS/EMCS patients in the uncorrected dataset, no difference could be detected after correcting for passive movements.
Given the overestimation of circadian rhythms in the uncorrected dataset and the differing results of the two datasets when comparing diagnoses, we suggest using the corrected dataset when comparing actigraphy data of UWS and MCS/EMCS patients. Our analyses between diagnoses based on the corrected dataset revealed that the activity during both day and night was higher in MCS/EMCS patients than in UWS patients (cf. Additional file 1: Figures S7 B+D) and generally in patients with higher CRS-R scores (cf. Additional file 1: Figure S9). Also, MCS/EMCS patients had more pronounced circadian rhythms (i.e., normalized power; cf. Fig. 3b). This indicates more preserved circadian rhythms in MCS/EMCS patients and is well in line with previous studies that investigated circadian rhythms in patients with DOC. Specifically, these studies showed that a higher integrity of circadian temperature and melatonin rhythms predicts a richer behavioral repertoire, which is directly related to results of CRS-R assessments [5, 12]. Also on a brain level, day-night changes of EEG signal complexity are more pronounced in MCS than in UWS patients (with significantly higher signal complexity during day than during night [27]), and periods of “daytime wakefulness” and “nighttime sleep” are better distinguishable in MCS than in UWS patients [28].
Besides this, the general usefulness of actigraphy data in severely brain-injured individuals especially for diagnostic and prognostic purposes seems questionable as the validity of motor data is severely limited by several factors such as motor impairments, spasticity, and the usage of muscle relaxants in these patients. In a previous study of our lab, we did not find any relation between the IS of the patients’ physical activity levels and the CRS-R scores [5]. In the current study, IS correlated positively only with the motor subscale score, but not with the other subscale scores. Moreover, the effect was gone when contrasting UWS and MCS patients. We also did not find any significant correlations of the CRS-R scores with IV and the patient’s period length (i.e., deviation from the peak closest to 24 h). Therefore, we should be careful when drawing associations between circadian variations of physical activity in patients with DOC and consciousness levels (cf. Additional file 1: Figure S9). Instead, other measures such as hormones (i.e., melatonin(-sulfate)) seem to better describe circadian rhythms in patients with DOC, i.e., while we found a circadian rhythm in the corrected actigraphy data in only 13/30 patients (43%) in the current study (cf. Additional file 1: Table S2), 19/21 patients (90%) showed a circadian melatoninsulfate rhythm in our previous study [5].
Conclusions
To summarize, our study shows that actigraphy from patients with DOC does not exclusively reflect the patients’ activity as it is strongly influenced by passive movements, which leads to an overestimation of the circadian rhythmicity of the activity initiated by the patients themselves. Consequently, actigraphy data needs to be corrected to allow for meaningful conclusions about circadian rhythms in patients with DOC. Considering this correction, we found that MCS/EMCS patients show higher mean activity during the day and night as well as stronger circadian rhythms than UWS patients. However, the general usefulness of actigraphy in patients with DOC should be considered carefully, especially with regard to frequent motor impairments, spasticity, and the usage of muscle relaxants in these patients. Thus, while actigraphy is a tool that received increasing attention in measuring arousal because of its efficiency regarding costs and time, it must be treated with caution in clinical populations with severe motor impairments such as patients with DOC.
Availability of data and materials
The data that support the findings of this study are available from the corresponding author upon reasonable request.
Abbreviations
AI:
Anoxic-ischemic brain injury
CRS-R:
Coma Recovery Scale – Revised
DOC:
Disorders of consciousness
EMCS:
Exit minimally conscious state
GCS:
Glasgow Coma Scale
IQR:
Interquartile range
IS:
Interdaily stability
IV:
Intradaily variability
MCS:
Minimally conscious state
NTBI:
Non-traumatic brain injury
TBI:
Traumatic brain injury
UWS:
Unresponsive wakefulness syndrome
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Acknowledgements
We thank Sarah Haberl and Julius Köppen as well as the staff at the Albert-Schweitzer-Klinik Graz and the Gunther-Ladurner Pflegezentrum Salzburg for their constant support and help with the data collection.
Funding
MA is and CB was supported by a grant from the Austrian Science Fund (FWF; Y-777) and the Doctoral College “Imaging the Mind” (FWF; W1233-G17). CB was additionally supported by the Konrad-Adenauer-Stiftung e.V. and is supported by an FWF-funded Erwin-Schroedinger Fellowship (J-4243), a grant from the Freiwillige Akademische Gesellschaft Basel, a grant from the Psychiatric Hospital of the University of Basel, and a grant from the Novartis Foundation for biological-medical research.
Author information
Affiliations
Authors
Contributions
Study design: MaS and CB; data acquisition: MA, CB, MR, GP, MoS, and ABK; data analysis and interpretation: MA, CB, MaS, and MR; drafting the manuscript: MA, CB, and MaS; critical revision of the manuscript: MA, CB, MR, GP, MoS, ABK, ET, and MaS. The authors read and approved the final manuscript.
Corresponding author
Correspondence to Christine Blume.
Ethics declarations
Ethics approval and consent to participate
The study had been approved by the ethics commission of the medical university of Graz (21-506 ex 09/10) and the ethics commission of Salzburg (415-E/2034). Informed consent was obtained from the patients’ legal representatives.
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Not applicable.
Competing interests
The authors declare that they have no competing interests.
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Supplementary information
Additional file 1: Additional information on light levels, multiple CRS-R assessments [29] and monitoring of passive movements. Figure S1. Graphical user interface of the tablet in the patient room. Table S1. Circadian rhythm indices from the uncorrected actigraphy data. Table S2. Circadian rhythm indices from the corrected actigraphy data. Figure S2. Periodogram of the uncorrected (A) and corrected (B) actigraphy data from patient 26. Figure S3. Normalized power of the patients’ peaks closest to 24 h in uncorrected vs. corrected data. Figure S4. Interdaily stability (A + B), intradaily variability (C + D) and circadian rhythmicity (E + F) in MCS/EMCS vs. UWS patients separately for uncorrected and corrected data. Figure S5. Interdaily stability (A), intradaily variability (B), circadian rhythmicity (C) and circadian rhythm strength (D) in TBI vs. NTBI patients in the corrected data. Figure S6. Patients’ mean activity during day (7 am – 9 pm) vs. night (9 pm – 7 am) separately for uncorrected and corrected data. Figure S7. Mean activity levels during day (7 am – 9 pm) and night (9 pm – 7 am) in MCS/EMCS vs. UWS patients separately for uncorrected and corrected data. Figure S8. Mean activity levels during day (7 am – 9 pm) and night (9 pm – 7 am) in TBI vs. NTBI patients in the corrected data. Figure S9. Correlation Matrix.
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Angerer, M., Schabus, M., Raml, M. et al. Actigraphy in brain-injured patients – A valid measurement for assessing circadian rhythms?. BMC Med 18, 106 (2020). https://doi.org/10.1186/s12916-020-01569-y
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Keywords
• actigraphy
• circadian rhythms
• brain injury
• disorders of consciousness
• neuropsychological assessment
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Review
Epstein-Barr Virus (EBV)-associated Gastric Carcinoma
1
Division of Stem Cell Biology, Institute for Genetic Medicine, Hokkaido University, N15 W7, Kita-ku, Sapporo 060-0815, Japan
2
Graduate School of Pharmaceutical Sciences, Hokkaido University, N12 W6, Kita-ku, Sapporo 060-0812, Japan
3
Department of Gastroenterology and Hepatology, Yamaguchi University Graduate School of Medicine, Minami-Kogushi 1-1-1, Ube, Yamaguchi 755-8505, Japan
4
Research Center for Infection-Associated Cancer, Institute for Genetic Medicine, Hokkaido University, N15 W7, Kita-ku, Sapporo 060-0815, Japan
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Viruses 2012, 4(12), 3420-3439; https://doi.org/10.3390/v4123420
Submission received: 22 October 2012 / Revised: 22 November 2012 / Accepted: 26 November 2012 / Published: 29 November 2012
(This article belongs to the Special Issue Recent Progress in EBV Research)
Abstract
:
The ubiquitous Epstein-Barr virus (EBV) is associated with several human tumors, which include lymphoid and epithelial malignancies. It is known that EBV persistently infects the memory B cell pool of healthy individuals by activating growth and survival signaling pathways that can contribute to B cell lymphomagenesis. Although the monoclonal proliferation of EBV-infected cells can be observed in epithelial tumors, such as nasopharyngeal carcinoma and EBV-associated gastric carcinoma, the precise role of EBV in the carcinogenic progress is not fully understood. This review features characteristics and current understanding of EBV-associated gastric carcinoma. EBV-associated gastric carcinoma comprises almost 10% of all gastric carcinoma cases and expresses restricted EBV latent genes (Latency I). Firstly, definition, epidemiology, and clinical features are discussed. Then, the route of infection and carcinogenic role of viral genes are presented. Of particular interest, the association with frequent genomic CpG methylation and role of miRNA for carcinogenesis are topically discussed. Finally, the possibility of therapies targeting EBV-associated gastric carcinoma is proposed.
1. Introduction
Epstein-Barr virus (EBV) is a ubiquitous human herpes virus with oncogenic activity. The EBV genome can be detected in malignancies of both lymphoid and epithelial cell origin, such as Burkitt’s lymphoma (BL) and nasopharyngeal carcinoma (NPC) [1,2]. In 1990, EBV genomes were detected in gastric carcinomas using polymerase chain reaction [3] and in situ hybridization (ISH) for EBV-encoded small ribonucleic acid 1 (EBER1). These findings indicated that EBV-associated gastric carcinomas (EBVaGC) comprise about 10% of all gastric carcinomas worldwide [4,5,6]. Since EBVaGC are monoclonal proliferations of a single cell persistently infected with EBV, EBV infection may be involved in the early stages of gastric carcinogenesis [7,8,9].
EBV spreads by the oral route [10]. After primary infection, EBV establishes the lifelong virus carrier state, called latent infection, which expresses a limited set of viral genes required for viral episome maintenance, thereby conferring a survival advantage to the infected cell. BL, approximately half of the NPC, and EBVaGC belong to latency I, in which EBV nuclear antigen 1 (EBNA1), EBER1 and 2, and BamHI-A rightward transcripts (BART) are expressed. Latency II neoplasm includes the remaining NPC and Hodgkin’s lymphoma (HL) and is characterized by the expression of latent membrane protein 1 (LMP1) in addition to latency I transcripts. Latency III neoplasms, typified by lymphomas observed in immunosuppressed patients, additionally expresses EBNA2, 3A, 3B, 3C, and LP. Three promoters (Cp, Wp, and Qp) are utilized for EBNA transcription. The Cp- or Wp-initiated large transcript is differentially spliced into six EBNA mRNAs as observed in latency III cells, whereas Qp mediates selective expression of EBNA1 in Latency I or II cells [7]. The expression of latent genes is under a strict epigenetic regulation through DNA methylation. Cp and Wp are hypermethylated in latency I [11].
EBVaGC is a latency I neoplasm and expresses EBNA1, EBER, BART, and sometimes (40%) latent membrane protein 2A (LMP2A) [9]. Since EBVaGC does not express EBNA2 and LMP1, which are important for B cell immortalization and transformation [2,7], preexisting abnormalities may exist in gastric epithelial cells [12]. Not only viral gene, but also the host cell DNA methylation has been frequently observed in EBVaGC [13,14,15]. Promoter hypermethylation of tumor-related genes is known to cause down-regulation of their gene expression [16]. Target gene silencing by viral micro RNAs (miRNAs) [17] has also been observed in EBV infected cells. Both mechanisms may influence the tumor progression of EBVaGC.
2. Definition, Epidemiology, and Clinical Features
2.1. Definition
Almost 10% of the gastric carcinomas throughout the world are monoclonal proliferations of EBV-carrying tumor cells [4]. A characteristic feature of EBVaGC is lymphoepithelioma-like carcinoma, which presents a diffuse-type histology with lymphoid infiltration. EBVaGC is defined by the presence of EBV in neoplastic cells. EBER1-in situ hybridization (ISH) is used to identify EBVaGC, because EBER1 is highly abundant (10 million copies per cell) in each infected cell. Typically, tumor cells, of which nuclei are positive for EBER1-ISH, are surrounded by lymphoid stroma (Figure 1). EBVaGC has distinct clinicopathological features, which predominantly arises in men and presents a generally diffuse histological type [18].
Figure 1. Lymphoepithelioma-like subtype of Epstein-Barr virus-associated gastric carcinomas (EBVaGC). A. Hematoxylin-Eosin Staining. B.EBV-encoded small ribonucleic acid-in situ hybridization (EBER1-ISH) demonstrates positive nuclei in the carcinoma cells, which are surrounded by infiltrating lymphocytes.
Figure 1. Lymphoepithelioma-like subtype of Epstein-Barr virus-associated gastric carcinomas (EBVaGC). A. Hematoxylin-Eosin Staining. B.EBV-encoded small ribonucleic acid-in situ hybridization (EBER1-ISH) demonstrates positive nuclei in the carcinoma cells, which are surrounded by infiltrating lymphocytes.
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2.2. Epidemiology
Most studies did not show evident age dependence of EBVaGC frequency. Almost all studies have shown male predominance of EBVaGC, suggesting that risk from lifestyle or occupational factors may exist among males [19]. An interview study in Japan showed that salty food intake and wood dust and/or iron filings exposure, which may induce mechanical injury to the gastric epithelia, are related to a higher EBVaGC risk [20].
In contrast to BL and NPC, which are endemic in Equatorial Africa and Southeast Asia, respectively, EBVaGC is a non-endemic disease distributed throughout the world [6]. However, there are some regional differences in the incidence of EBVaGC. The incidence of EBVaGC in all cases of gastric cancer is distributed from highest (16-18%) in the USA and Germany to the lowest (4.3%) in China [6,21,22]. A Japanese study investigated incidence of EBV-positive cases in all gastric cancers in several areas. The study indicated that EBVaGC prevalence was inversely related to the GC incidence [23]. Prognosis of EBVaGC is relatively favorable.
2.3. Clinical Features
The most useful modality for the diagnosis of gastric carcinoma is endoscopy. By endoscopy, EBVaGC appears as superficial depressed (or ulcerated) lesions in the upper part of the stomach (Figure 2). Tumor locates predominantly in the non-antrum part of the stomach [19]. Because gastric cancer related to Helicobacter pylori (Hp), a causative agent of chronic gastritis, intestinal metaplasia, and cancer, locates predominantly in the antrum, these pathogens have been thought to cause gastric cancer by independent mechanisms [19]. Gastritis related to Hp frequently starts in the antrum. However, Yanai et al. reported that EBVaGC are frequently located near the mucosal atrophic border, where mild to moderate chronic atrophic gastritis (CAG) is common [24]. They also showed frequent detection of both EBV and Hp at the mucosa with moderate CAG, where inflammatory cell infiltration is abundant, and not at the mucosa with marked CAG, where inflammatory cell infiltration is scarce [25].
Figure 2. Endoscopic image of an early EBVaGC in the upper gastric body. The tumor shows protruded shape probably because of the abundant lymphocyte infiltration.
Figure 2. Endoscopic image of an early EBVaGC in the upper gastric body. The tumor shows protruded shape probably because of the abundant lymphocyte infiltration.
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3. Route of Epithelial Infection
EBV infects human B lymphocytes and epithelial cells via different entry mechanisms. In case of B cells, the major outer envelope glycoprotein, gp350/220, is responsible for attachment of the virus with high affinity to CD21 or the human complement receptor type 2 (CR2) on B cell surface [26,27,28,29]. EBV is subsequently internalized into the cells via endocytic pathway. Fusion with viral envelope and endosomal membrane of B cells is triggered by the interaction of a second envelope glycoprotein, gp42, with HLA class II [30], and is thereafter mediated by the core fusion complex, gH/gL/gp42 [31,32].
In contrast, the mechanism by which EBV infects human epithelial cells remains unclear. Human epithelial cells are CD21-negative or express CD21 at low level in some epithelial cells in culture and highly resistant to cell-free EBV infection [33,34]. At least three models have been proposed as mechanisms for the EBV attachment to epithelial cells independent of CD21. First, it has been demonstrated that EBV virions coated with immunoglobulin A (IgA) specific to gp350/220 can bind efficiently to the polymeric IgA receptor [35]. Polymeric IgA is commonly present in human saliva and binds to the secretory component (SC) protein, which is a transmembrane protein expressing on the basolateral surfaces of polarized epithelial cells. A complex of EBV/IgA/SC is internalized into epithelial cells via endocytic pathway. This may be relevant to infection through the basolateral surface of an epithelial cell, which presumably resembles the physiological environment that the virus encounters in vivo [36]. Second, a complex of gH and gL was proposed to serve as epithelial ligands in the absence of CD21. EBV derived from B cells binds with high affinity to CD21-negative epithelial cells, but recombinant viruses lacking gH/gL lose this ability [31,32], suggesting that there is an epithelial cell-specific receptor for gH/gL that serves in attachment of EBV. It has been also shown that the direct interaction between gH/gL and the integrins αVß6 and αVß8 can provide the trigger for fusion of EBV and plasma membrane of epithelial cells [37]. Finally, an interaction between an EBV-encoded membrane protein, BMRF2, and integrins on polarized epithelial cells has been proposed as a model for EBV attachment to the cell surface [38]. The tripeptide Arg-Gly-Asp (RGD) motif in the BMRF2 molecule is presented as a ligand for ß1, α5, α3, and αV integrins [39,40]. However, BMRF2 is not required for cell-to-cell fusion [41,42] and apparently very few BMRF2 molecules exist in the virion [43]. It remains unclear whether the interaction of BMRF2 with integrins is primarily responsible for attachment and/or post-attachment events.
Interestingly, EBV virions released from B cells are deficient in gp42 which renders them more efficient to infect epithelial cells, but less efficient to infect B cells [44,45]. In contrast, EBV released from infected epithelial cells possesses gp42 and efficiently infects B cells [44]. This change in cell type tropism for EBV infection suggests that EBV shuttles between epithelial cells and B cells in the host during infection cycle. This observation supports a model that pharyngeal epithelial cells are in lytic EBV infection and shed infectious EBV particles for transmission.
The fusion of EBV envelope with the plasma membrane of epithelial cells requires a trigger gH/gL complex [36,45,46,47,48,49]. The fusion of EBV with an epithelial cell is likely triggered by a direct interaction between gH/gL and unknown epithelial cell surface molecules, which might be the identical proteins that can serve as attachment receptors in the absence of CD21 [50].
Figure 3. Cell-to-cell contact-mediated EBV transmission to epithelial cells. In cell-free infection, EBV preferentially infects B cells using CD21 receptor. EBV also infects CD21-negative epithelial cells as part of its normal life cycle, however much less efficiently. EBV transfer mediated by cell-to-cell contact with B cells increases the infection efficiency 1,000 to 10,000-fold compared with cell-free virus infection.
Figure 3. Cell-to-cell contact-mediated EBV transmission to epithelial cells. In cell-free infection, EBV preferentially infects B cells using CD21 receptor. EBV also infects CD21-negative epithelial cells as part of its normal life cycle, however much less efficiently. EBV transfer mediated by cell-to-cell contact with B cells increases the infection efficiency 1,000 to 10,000-fold compared with cell-free virus infection.
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Several lines of evidence indicate that EBV infection into epithelial cells is mainly mediated by cell-to-cell contact [34,51,52,53,54,55]. The rate of EBV infection in epithelial cells is 103-fold higher by co-culturing with EBV-positive B cells than by cell-free infection [34,51,55]. Moreover, most EBV virions are retained on cell surfaces after binding to primary B cells and transferred to epithelial cells, resulting in the 103 to 104-fold increase of infection compared with cell-free virus infection [53,54]. All these studies support a model that EBV-infected B cells migrating into the epithelial stroma or intraepithelial space contribute to the efficient EBV transmission into epithelium via cell-to-cell contact (Figure 3). The detailed molecular mechanisms of cell-to-cell EBV transmission remain unclear. Shannon-Lowe et al. showed that EBV virions loaded on the surface of primary B cells facilitate the formation of a virological synapse (VS)-like intercellular conjugation between B cells and co-cultured epithelial cells [53,54]. The VS is a tight adhesive junction across which virus can be efficiently transferred from virus-infected cells to non-infected target cells without cell-cell fusion [56]. An important role of an EBV glycoprotein, BMRF2 in the cell-to-cell spread of EBV in polarized oral epithelial cells has been proposed [39,40]. The mucosa of oropharyngeal and nasopharyngeal regions are known to be heavily filtrated by lymphocytes, suggesting that cell-free virus in the saliva could first bind to the surface of B cells and then efficiently transfer to pharyngeal epithelial cells through a cellular conjugate between B cells and epithelial cells.
The detailed molecular mechanism by which EBV infects epithelial cells still remains unclear. Some key factors involved in viral attachment, membrane fusion, and cell-to-cell contact-mediated viral transmission, have been identified [48,49]. However, no cellular receptors for EBV infection have yet been identified on epithelial cells. Also very little insights have been provided for a conceptual understanding of viral entry mechanism into epithelial cells. Further investigations are still required.
4. Viral Genes and Carcinogenesis
4.1. Models of EBV infection of gastric epithelial cells
EBV infects both B lymphocytes and epithelial cells, since the virus is discovered in BL cells, HL cells, NPC cells, and EBVaGC cells. Experimental EBV infection to B cells is very efficient, since EBV uses high affinity receptor, CD21 for its entry [16]. However, epithelial cells are CD21-negative and infection of epithelial cells could not be achieved for a long time, exceptionally when CD21 expression was overcome by gene transfer [33,57].
We have clearly proved direct infection of human gastric epithelial cells by EBV [50]. The infection was achieved by using a recombinant EBV with a selectable marker gene [58,59], but without any operations, such as introduction of the CD21 gene. In our study, epithelial cells were negative for CD21 and the infection was not blocked by anti-CD21 monoclonal antibody [50]. We have next showed that efficient transfer of EBV to epithelial cells by mixed culture with recombinant EBV producing B cells [34]. Other than experimentally EBV-infected cells, SNU-719 cell [60] and KT cell [61] are few cells retaining the same clonal EBV genome and EBV gene expression pattern of latency I as the original tumor biopsy. EBV-harboring epithelial cells are difficult to propagate in vitro and in animal models.
4.2. Growth promoting effects of EBV
The KT cell is a good in vivo model of EBVaGC and expresses high IL-1ß compared with EBV-negative gastric tumor cells [62]. Primary cell cultures from healthy gastric mucosal biopsies were infected with recombinant EBV [63]. The established cells expressed Qp-driven EBNA 1, EBER, BART, and LMP2A, similar to EBVaGC. The EBV-positive clones showed rapid proliferation and p53 overexpression, and exhibited anchorage independence in colony formation assay.
Growth promotion by EBV infection was also observed in EBV-infected NU-GC-3 cells through secretion of insulin-like growth factor (IGF)-1 as an autocrine growth factor [64]. It has been shown that EBERs play an oncogenic role by inhibition of apoptosis [65,66] and IGF-1 induction [67]. The oncogenic role of other genes, such as BARF1 [68] and LMP2A [69] has been reported. A recent report showed that EBV infection affected miRNA expression [70]. While no consensus exits as to the exact mechanism by which EBV promotes EBVaGC, the establishment of EBVaGC cell lines and the development of an in vitro model represent significant progress towards this goal.
5. Virus and Host Interactions at Molecular Level
5.1. DNA Hypermethylation in EBV and Host Genomes
A number of CpG islands in the promoter region of an tumor suppressor gene have been methylated in cancer cells than in normal cells [71]. Expression of many genes, such as p16 and RUNX3, is suppressed in stomach cancer owing to promoter methylation [72,73]. Promoter hypermethylation is especially frequent in EBVaGC [74,75,76]. Methylation of promoter region in APC, p16, MINT1, MLH1, TP73, and HOXA10 [14,77,78] has been specifically observed in EBVaGC (Table 1). A large-scale analysis revealed that CXXC4, TIMP2, and PLXND1 are specifically methylated in EBVaGC [79]. Down regulation of CXXC4, a suppressor of the Wnt pathway, promotes tumor cell proliferation and invasiveness [80]. Down regulation of TIMP2, a suppressor of metalloproteinase, inhibits tumor cell metastasis [81]. Methylation of similar genes has been reported in cancers associated with hepatitis B or C infection [82,83], suggesting that a common mechanism may underlie the formation of infection-associated cancers.
Table 1. DNA hypermethylation in EBVaGC.
Table 1. DNA hypermethylation in EBVaGC.
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However, the precise molecular mechanism of host DNA methylation during the early stage of EBV infection of the gastric epithelium is not fully understood. It is reported that LMP2A induces the phosphorylation of STAT3, which activates DNA methyltransferase 1 (DNMT1) transcription and causes PTEN expression loss through CpG island methylation of the PTEN promoter [69]. Although LMP2A is expressed in substantial cases of EBVaGC [84], EBVaGC patients are usually negative for LMP2A antibody [85]. Constitutive overexpression of DNMT1 has been observed in EBV-infected gastric epithelial cells that do not express LMP2A significantly [69]. Further investigations using EBV mutants of LMP2A [86] may uncover its precise molecular mechanism.
5.2. miRNA and Carcinogenesis
miRNAs are endogenous 18 - 25 nt RNAs and play important gene-regulatory roles in eukaryotic cells via posttranscriptional repression of gene expression. miRNA targets 3′-untranslated region (UTR) elements of mRNA and mediates mRNA decay through degradation of polyA (RNA silencing: RNAi) [87]. Different expression patterns of miRNA from normal tissues were expected in cancer. Several miRNAs and non-coding RNAs have been found to have links with some types of cancer and are referred as “oncomirs”. This is because miRNAs have a role as oncogenes when they target tumor suppressor genes. On the other hand, miRNAs are tumor suppressors when they target oncogenes [88].
A clonal EBV infection has been found in EBV-associated epithelial tumors, such as NPC and EBVaGC [9,89]. EBV encodes a large number of miRNAs [90]. Up to 25 pre-miRNAs are encoded in the BHRF1 and BART regions of the genome, which result in four mature BHRF1 miRNAs and 40 BART miRNAs [91]. A prototypic EBV strain B95-8 is known to have 11 kbp deletion in BART region. However, B95-8 virus can be produced in large amount and possesses prominent B cell transformation ability. Moreover, a recombinant virus lacking entire region of BART region was still able to infect and transform B cells [92]. These findings indicate that BART transcripts are not required for B cell transformation and neglected the importance of BART for a long period. Cai et al. identified 13 BART miRNAs in the region of B95-8 deletion [91].
Table 2. EBV-derived miRNAs and their target genes.
Table 2. EBV-derived miRNAs and their target genes.
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EBV-encoded BART miRNAs target the 3'-UTRs of viral genes, such as LMP1, BALF5, and LMP2A genes, and negatively regulate expression of these viral genes [93,94,95]. On the other hand, EBV miRNAs repress cellular proteins, which include p53 up-regulated modulator of apoptosis (PUMA), DICER1, and BIM [96,97,98] (Table 2). Preservability of the 3'-UTR domain of the target gene between species is a common feature of mammalian miRNA. However, since EBV preferentially infects humans, some EBV miRNAs characteristically target only human gene and not genes for other mammals. EBV miRNAs have another characteristic feature, some of which binding motifs are found only on EBV genome and not preserved on other viral genomes [97,99]. In order to identify EBV miRNA targets, a transcriptome-wide identification of miRNA binding sites has been performed between EBV-negative and EBV-positive cell lines [99,100,101].
Biological significance of viral miRNA in EBV-infected cells was searched using EBV recombinants. In these recombinants, mutations were systematically introduced in EBV’s precursor miRNA transcripts to prevent their subsequent processing into mature viral miRNAs. Phenotypic analyses of miRNA mutants revealed that the viral miRNAs contribute to EBV-associated cellular transformation rather than regulation of viral lytic replication [102].
There are two complicated stories in EBV-infected cells. One is that expression of viral latent genes induces cellular miRNAs. Viral LMP1 induces human miR-146a and miR-155 expression [103,104,105]. And excessive miR-155 expression is known to form B lymphoma [106]. Two, infection of EBV conversely suppresses entire host cell miRNA expression [70,107]. Since down-regulation of the cellular microRNA family miR-200 causes epithelial-mesenchymal transition (EMT), this phenomenon must be an important step in the process of malignant transformation of both EBVaGC and nasopharyngeal carcinoma cells. The precise mechanism for dysregulation of host miRNA by EBV infection needs to be clarified. It is known that low expression level of miRNA processing enzymes, DICER1 and DROSHA, is well correlated with tumor progression in many cancers [108]. We have shown that the expression level of human DICER1 is also lower in EBV-infected cells than in non-infected cells [97,101]. These findings suggest that progression of EBV-associated tumor is possibly regulated by EBV through regulation of viral and host miRNA expression. However, most of the studies presented in this section are performed using BL cells. Further study using EBV positive gastric epithelial cells is required.
6. Diagnosis and Treatment of EBV-associated GC
6.1. Procedure
EBER1-ISH is a most sensitive method to identify EBV infection. Application of EBER1-ISH to gastric mucosal biopsy samples from patients who have undergone upper gastrointestinal endoscopy is very useful to make diagnosis of EBVaGC before treatment. Patients with EBVaGC had elevated serum antibodies against EBV early antigen and EBV capsid antigen. However, EBNA1 antibody titers did not show significant difference between patients and healthy counterparts [9].
Yanai et al. examined 124 gastric carcinomas from 117 patients using EBER1-ISH. Among them, twelve tumors (9.7%) were identified as EBV associated [109]. An interesting feature of EBVaGC is its predominance in the non-antrum part of the stomach (Figure 4A). EBVaGC appears as a superficial depressed- or ulcerated-lesion in the upper part of the stomach. Histology of EBVaGC is mainly diffuse-type carcinoma rich in lymphocyte infiltration (gastric carcinoma with lymphoid stroma). Endoscopic ultrasonography revealed a hypoechoic mass in the third layer, reflecting submucosal nodules [110].
Figure 4. EBVaGC by site in the stomach. A. Distribution of EBVaGC. EBV prevalence was more frequent in the cardia and middle stomach than in the antrum, where over half of EBV-negative gastric cancers were located. B. EBV involvement in remnant cancer by site. Note that frequency of EBV infection in the non remnant cardiac cancer was 10.5% [22].
Figure 4. EBVaGC by site in the stomach. A. Distribution of EBVaGC. EBV prevalence was more frequent in the cardia and middle stomach than in the antrum, where over half of EBV-negative gastric cancers were located. B. EBV involvement in remnant cancer by site. Note that frequency of EBV infection in the non remnant cardiac cancer was 10.5% [22].
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Gastric remnant cancer (gastric stump cancer) after distal gastric resection for benign disease, such as refractory gastric or duodenal ulcer disease or recurrent ulcer with gastric outlet obstruction, remains a substantial clinical concern, because the incidence of remnant cancer is still increasing (Figure 4B) [111]. A high prevalence of EBV involvement (25 to 41.2%) in gastric remnant carcinoma has been reported. High cell proliferation activity in the epithelium has been reported. The reflux of bile and pancreatic juice is considered to cause regenerative atypia and cell proliferation in epithelial cells [112]. Atrophic change of remnant gastritis in Billroth-II anastomoses was associated with EBV-positive gastric remnant carcinoma with high incidence [113].
6.2. Prognosis
To date there is no specific therapeutic method for EBVaGC. Since the frequency of undifferentiated type of cancer is high in EBVaGC, most of the tumor is surgically resected. CpG island methylation of the promoters of various tumor-related genes plays important roles in the development and progression of gastric cancer [16]. Statistical analysis showed that promoter hypermethylation is more frequently observed in EBVaGC than in EBV-uninfected gastric carcinoma [69,74,75,76]. Medical treatment with a demethylation agent, which induces lytic EBV infection in latently EBV infected cells, may lead to a lysis of cancer cells. This approach could be applied to the medical treatment of EBVaGC, since methylation of the tumor suppressor gene is also a key abnormality in EBVaGC [12,114,115].
Most of the previous reports did not observe any prognostic difference between EBV-positive and -negative gastric cancer [21]. However, early EBVaGC has the low frequency of lymph node metastasis even in submucosal type. Partial medical treatment, such as endoscopic treatment, can be adapted to such a case. The authors have experienced a case of early EBVaGC with submucosal invasion, in which palliative endoscopic treatment was performed. Recurrence was not observed in this case for more than four years [116]. A clinicopathological study in the Netherlands mentioned that EBVaGC accompanied lymph node metastasis in significantly lower frequency than EBV-negative stomach cancer. In the study, EBVaGC cases showed a better prognosis than negative cases [117].
7. Conclusion
Considerable studies suggest that EBV contributes to cell proliferation and survival, and may directly contribute to the development of EBVaGC through these effects. EBV affects multiple host proteins and pathways that normally promote apoptosis and regulate cell proliferation. However, the underlining molecular mechanisms of these effects are complex and certainly affecting each other.
In another aspect, inflammation of the stomach will recruit EBV-infected B-lymphocytes in the vicinity of gastric epithelia and may increase the frequency of EBV infection of epithelia. Differences in individual inflammatory response by either genetic and/or environmental effect, such as a predisposing loss of ARID1A in epithelial cells before EBV infection [118] or single nucleotide polymorphisms of promoter region of interleukin-10 and/or tumor necrosis factor-α [119], possibly affect the oncogenic pathway to EBVaGC.
Acknowledgments
This study was supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Science and Technology of Japan (no. 23590534 to H.Y.) and by a Grant for Joint Research Program of the Institute for Genetic Medicine, Hokkaido University (to H.Y.). The authors are indebted to Prof. Kenzo Takada and Dr. Hideo Yanai for their continual support. The authors would like to show sincere gratitude to Ms. Eri Kawanishi for critical reading of the manuscript.
Conflict of Interests
The authors declare no financial or commercial conflict of interest.
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Share and Cite
MDPI and ACS Style
Iizasa, H.; Nanbo, A.; Nishikawa, J.; Jinushi, M.; Yoshiyama, H. Epstein-Barr Virus (EBV)-associated Gastric Carcinoma. Viruses 2012, 4, 3420-3439. https://doi.org/10.3390/v4123420
AMA Style
Iizasa H, Nanbo A, Nishikawa J, Jinushi M, Yoshiyama H. Epstein-Barr Virus (EBV)-associated Gastric Carcinoma. Viruses. 2012; 4(12):3420-3439. https://doi.org/10.3390/v4123420
Chicago/Turabian Style
Iizasa, Hisashi, Asuka Nanbo, Jun Nishikawa, Masahisa Jinushi, and Hironori Yoshiyama. 2012. "Epstein-Barr Virus (EBV)-associated Gastric Carcinoma" Viruses 4, no. 12: 3420-3439. https://doi.org/10.3390/v4123420
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Exercise as it relates to Disease/Effect of physical activity and weight gain in obese pregnant women
This Wikibooks page is a critique of the research article "Exercise Training and Weight Gain in Obese Pregnant Women: A Randomised Controlled Trial (ETIP Trial)" by Garnæs, Mørkved, Salvesen and Moholdt (Jul. 2016).[1]
This page was created as an assignment for the unit Health, Disease and Exercise at the University of Canberra (Sep. 2020).
What is the background to this research?Edit
Gaining weight during pregnancy is normal, yet the amount of weight gained is important for the long-term health of both the mother and the baby.[2] Recent studies suggest that approximately one-third (32%) gained the recommended amount of weight during pregnancy; whereas, the majority of women were outside the recommended guidelines (48% too much and 21% too little).[3] The ideal amount of weight is based on the mother's body mass index (BMI) before falling pregnant. For example, overweight/obese women should gain less throughout pregnancy than someone who is underweight/normal. Consequently, women that are already an unhealthy weight and further gain too much while being pregnant, increase the risk of numerous health complications such as; preeclampsia, gestational diabetes mellitus (GDM) and caesarean birth.[4]
The present study being critiqued, aims to determine if regular physical activity in overweight/obese pregnant women could reduce gestational weight gain (GWG) and hence prevent other negative health complications. The study also compared the effects of exercise across 30 different measures including but not limited to; blood pressure, blood measurements, skinfold thickness and body composition. Since maternal obesity is related to GWG and GDM, there is a significant demand to evaluate whether prescribing exercise training programs to overweight/obese pregnant women could considerably decrease the risk of detrimental health complications for future pregnancies.
Where is the research from?Edit
The authors of this study are Kirsti Krohn Garnæs (researcher), Siv Mørkved (professor), Øyvind Salvesen (associate professor) and Trine Moholdt (researcher) from the University of Science and Technology in Norway (NTNU). The content of the study is likely to be of high-quality as all participating scientists have extensive knowledge on the effects of exercise on the human body as well as specialising in female research, particularly on the reproductive system. The Norwegian Fund for Post-Graduate Training in Physiotherapy as well as The Liaison Committee between the Central Norway Regional Health Authority partnered with the NTNU were the main organisations for funding and supporting this study. With this being said, it was specifically noted that there was no conflict of interest/bias as the sponsors had zero input in the way the study was designed, how the data was collected and analysed, the decision to publish the article nor the preparation of the manuscript.
What kind of research was this?Edit
This study was conducted as a randomised controlled trial (RCT), meaning participants were randomly assigned to one of two possible groups.[5] One being the experimental group receiving the intervention being tested and the other the control group receiving conventional treatment. The expected difference between the experimental and control group for this research design is the outcome variable being studied, in this case the effect of physical activity.
What did the research involve?Edit
Methods used for this research were taken from the previous study protocol Exercise Training in Pregnancy for Obese Women (ETIP): Study Protocol for a Randomised Controlled Trial; however, the following changes were made to predominately increase recruitment into the trial; body composition measurement, extension for baseline testing and inclusion as well as lowering BMI criteria.
This was a single centre study consisting of 91 pregnant women with a BMI of ≥ 28 kg/m2. Participants were then randomly assigned to either the exercise group or control group.
Exercise groupEdit
• Weekly 3 x 60 minute supervised hospital sessions (35 minutes of moderate intensity cardio followed by 25 minutes of strength training)
• Weekly 1 x 50 minute at home program (35 minutes of endurance training followed by 15 minutes of strength training)
• Standard maternity care
Control groupEdit
• Standard maternity care
All physiological assessments were conducted at pregnancy 12–18 weeks, then again at 34–37 weeks and lastly on delivery day.
The main limitation of this trial was the reduced statistical power. The study aimed to recruit a total of 150 participants as opposed to the 91 they received which could have been a result of the recruitment criteria, time frame as well as the population demographic. In addition, it was noted that only 50% of the participants in the exercise group performed the exercise training program making it extremely difficult to interpret data and detect any possible effects in the intervention. This should be considered when analysing the results.
What were the basic results?Edit
Overall, the research concluded that women in the intervention group gained 10.5 kg on average (towards the end of pregnancy); whereas, the control group only gained 9.2 kg on average. Upon examining the populations average BMI, the amount of weight gained throughout pregnancy could be considered 'healthy' when comparing with other normative data.[6] It was also evident towards the end of the last trimester, fewer women in the exercise group had GDM and their diastolic/systolic blood pressure was lower compared to those in the control group. All other measures tested showed no apparent differences between the two groups.
Unfortunately, the study found no changes in GWG between women assigned to an exercise program to those just receiving standard maternity care. Therefore, the effectiveness of prescribing exercise training programs to overweight/obese pregnant women to prevent GWG and GDM is still unclear and further studies are required.
What conclusions can we take from this research?Edit
According to this study, implementing exercise to specifically reduce GWG and GDM in overweight/obese pregnant women has little to no effect. This implies that both endurance and strength training followed by standard maternity care is just as effective as maternity care alone. The methodology and recruitment process for the study question the validity of the findings as the trail consisted of fewer participants than initially expected with only 50% complying to the described protocol. With these inconsistencies, it is unclear whether exercise alone would produce similar results if participants correctly adhered to the intervention program proposed. Likewise, exercise weight loss programs have been proven to be effective, especially when adopting a balanced diet.[7]
In future, studies should aim to incorporate different forms of exercise followed by appropriate nutrition to help encourage overall health and weight loss in overweight/obese pregnant women. Other factors including demographics, predisposition for health conditions, previous pregnancies and how these factors could influence the effect of GWG or the likelihood of developing GDM in already unhealthy women. Not only physical measures should be considered, but physiological parameters such as the link between depression and weight gain should further be explored.[8]
Practical adviseEdit
Exercise programs are an effective way for losing weight; however, results are subjective and rely on self-motivation. Unfortunately, it seems that overweight/obese pregnant women lack the ability and desire to change their lifestyle as illustrated by the compliance rate of this study. Before becoming pregnant, it is recommended that women consult their general practitioner (GP) for a pre-pregnancy check-up.[9] From there, any potential risks for the mother and baby are discussed as well as any medical concerns that need to be addressed such as weight loss. Even though weight is a sensitive topic for some, it is advised that women fall within a healthy BMI before conceiving.[10] Not only does this protect the mother's health and prevent complications during birth, but also the baby's well-being.
Further information/resourcesEdit
ReferencesEdit
1. Garnæs, K., Mørkved, S., Salvesen, Ø. and Moholdt, T., 2016. Exercise Training and Weight Gain in Obese Pregnant Women: A Randomised Controlled Trial (ETIP Trial). [online] plos.org. Available at: <https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1002079> [Accessed 17 September 2020].
2. Medibank page editors, 2018. Healthy Weight Gain During Pregnancy Calculator. [online] medibank.com. Available at: <https://www.medibank.com.au/livebetter/families/pregnancy/healthy-weight-gain-during-pregnancy-calculator/> [Accessed 17 September 2020].
3. CDC page editors, 2019. Weight Gain During Pregnancy. [online] cdc.org. Available at: <https://www.cdc.gov/reproductivehealth/maternalinfanthealth/pregnancy-weight-gain.htm> [Accessed 17 September 2020].
4. ACOG page editors, 2016. Obesity and Pregnancy. [online] acog.org. Available at: <https://www.acog.org/patient-resources/faqs/pregnancy/obesity-and-pregnancy> [Accessed 17 September 2020].
5. Kendall, J., 2003. Designing a Research Project: Randomised Controlled Trials and Their Principles. [online] emj.com. Available at: <https://emj.bmj.com/content/20/2/164> [Accessed 17 September 2020].
6. Raising children page editors, 2018. Healthy Pregnancy for Women Who Are Overweight. [online] raisingchildren.net. Available at: <https://raisingchildren.net.au/pregnancy/health-wellbeing/healthy-lifestyle/healthy-pregnancy-overweight> [Accessed 17 September 2020].
7. Mottola, M., Giroux, I., Gratton, R., Hammond, J., Hanley, A., Harris, S., McManus, R., Davenport M and Sopper, M., 2010. Nutrition and Exercise Prevent Excess Weight Gain in Overweight Pregnant Women. [online] ncbi.nlm.nih.gov. Available at: <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886034/> [Accessed 17 September 2020].
8. Source from the University of Warwick, 2015. Depression, Weight Gain in Pregnancy Linked to Sitting Down. [online] sciencedaily.com. Available at: <https://www.sciencedaily.com/releases/2015/11/151103213714.htm#:~:text=University%20of%20Warwick.-,The%20study%20found%20those%20suffering%20from%20symptoms%20of%20depression%20during,gain%20and%20contracting%20gestational%20diabetes.> [Accessed 17 September 2020].
9. Gaither, K., 2018. Your Pre-Pregnancy Checkup. [online] webmd.com. Available at: <https://www.webmd.com/baby/considering-pregnancy-see-your-doctor-first> [Accessed 17 September 2020].
10. RCOG committee editors, 2011. Why Your Weight Matters During Pregnancy and After Birth. [online] rcog.org. Available at: <https://www.rcog.org.uk/globalassets/documents/patients/patient-information-leaflets/pregnancy/pi-why-your-weight-matters-during-pregnancy-and-after-birth.pdf> [Accessed 17 September 2020].
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Projects
Name
Tumoral microenvironment: Immunohistochemistry M1 and M2 macrophage and its relationship with prognostic and predictive factors.
University
Universidad Nacional de Tucuman
Domain
Pathology
Departement
Service of Pathology.
Head
Sonia Marcela Ortiz Mayor
Tutor
Sonia Marcela Ortiz Mayor
Languages
Spanish, English
Duration
4 weeks
Availability
Cities/Months Jan Feb Mar Apr May Jun Jul Augt Sep Oct Nov Dec
No No No Yes Yes Yes No Yes Yes Yes Yes No
Type of Research Project
- Basic science
What is the background of the project?
Studies linked to the process of carcinogenesis and tumor progression have focused for years on the neoplastic cell with genotypic and phenotypic characteristics. Lately, after the extraordinary progress in this field it arises in addition to understanding tumor biology called cancer microenvironment. This consists of a variety of cells can be malignant or not. Among non-malignant cells are stromal cells, cells and an inflammatory infiltrate neovascularization where macrophages represent a prominent population. This present in the microenvironment of inflammatory infiltrate neoplastic tissues, there is a simple inflammation. Evidence suggests that these cells act as mediators stimulating growth factors that favor the proliferation of cancer cells. That is why their presence in the tumor microenvironment represent based on this premise a factor of poor prognosis. Evaluate the distribution pattern of the two subtypes of macrophages in front of tumor infiltration of colorectal cancer and its relationship with prognostic and predictive factors. Immunohistochemical study. The same will be done with four markers CD68, CD163, iNOS, VEGFA
What is the aim of the project?
Evaluate the distribution pattern of the two subtypes of macrophages in front of tumor infiltration of colorectal cancer and its relationship with prognostic and predictive factors.
What techniques and methods are used?
Immunohistochemical study. The same will be done with four markers CD68, CD163, iNOS, VEGFA
What is the role of the student?
- The student will mainly observe
- The student will observe the practical experiments but will be highly involved in the analysis of the results
- The tasks will be done under supervision
What are the tasks expected to be accomplished by the student?
The student perform a rotation through the various stages of processing biopsy material. Selection of samples for study, histological processing, immunohistochemistry, microscopic observation. Optionally it is offered to participate in the activities of teaching service.
Will there be any theoretical teaching provided (preliminary readings, lectures, courses, seminars etc)
not
What is expected from the student at the end of the research exchange? What will be the general outcome of the student?
- The student will prepare a poster
- The student will prepare a presentation
What skills are required of the student? Is there any special knowledge or a certain level of studies needed?
The student must have passed pathology
Are there any legal limitations in the student’s involvement
No
Hours
6
Type of students accepted
This project accepts:
- Medical students
- Graduated students (less than 6 months)
Articles
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Previous section Previous topic Next topic Next section Topic quiz References
Section 2 - Applied Pharmacokinetics
Bayesian analysis
Introduction
Practical application
To illustrate the practical application of Bayesian methods, suppose our patient is a 73 y/o F, 65 in, 62 kg, SCr=1. Around the 5th dose of a gentamicin 80mg Q 8 hour regimen, the trough level is reported as 4.5 and the peak as 5.4. You are then called in to consult by the patient's worried physician.
If we plug those levels into the traditional Sawchuk and Zaske equations, we get a Vd of 1.13 L/kg and half-life of 22.8 hours, giving an ideal dose of 340mg every 61 hours. Obviously this is not the proper dosage recommendation.
If we select the Bayesian algorithm for this set of levels, we get a Vd of 0.36 L/kg and half-life of 7.5 hours, giving an ideal dose of 112mg every 20 hours. Okay, that's a more reasonable dose than before, but let's dig a little deeper into this scenario.
An experienced pharmacokineticist would realize at first glance that these levels are just not right, they don't jive with what one would expect from this patient. Because any number of things could have gone wrong, your first step is to find out what when wrong from the nursing and lab staffs. You find out that the over-worked nurse hung the dose late. The hurried phlebotomist drew the trough "on time", but didn't notice that the infusion was already in progress.
Now that we know the "trough" is not a trough at all, what is the next step? If we throw out the trough level that we know is wrong, and use only the peak, we get a Vd of 0.32 L/kg and half-life of 5 hours, giving an ideal dose of 103mg every 14 hours. This is obviously the most reasonable of the three alternatives.
The lesson to take from this example is to never use bad data. Even a sophisticated Bayesian algorithm can not completely overcome bad data. The software engineer's cliche, "garbage in = garbage out", still applies. We must look at all "unusual" serum level data in a critical light.
Precautions
In general, the Bayesian approach to the determination of individual drug-dosage requirements performs better than other approaches. However, it should be emphasized that the population model must be appropriate for the patient. It is wrong to use a drug model derived from a dissimilar patient population. For example, you should never use a model based on data from otherwise healthy adults in a frail elderly patient.
Likewise, outlying patients in a population (ie, those patients whose pharmacokinetic parameters lie outside of the 95th percentile of the population) may be put at risk.
And, as shown in the example above, bad data will corrupt the analysis. As is always the case, the computerized algorithms outlined below can only assist in the decision-making process and should never become a substitute for rational clinical judgement.
Pharmacokinetic formulas
1. The Bayesian approach estimates pharmacokinetic parameters (e.g., CL, Kel and Vd) that will be most consistent with serum levels predicted by both the population model and the actual measured serum levels. To achieve that end, the least squares method based on the Bayesian algorithm estimates the parameters which minimize the following function:
Bayesian formula
2. For one compartment drugs, the following equation is used to estimate serum levels:
CPss = (MD / tinf x Vd x kel ) x (1 - e-kel x tinf /1 - e-kel x tau ) x e-kel x t
where
• MD = maintenance dose
• tinf = infusion time
• Vd = Volume of distribution
• kel = elimination rate constant
• tau = dosing interval
• t = time at which to predict serum concentration
3. For two compartment drugs, the following equation is used to estimate serum levels:
CPss = [k0 (k12-kd) (1 - ekd x tinf) ekd x t)] / [Vc x kd (kd-kel) (1 - ekd x tau)] +
[k0 (kel-k21) (1 - ekel x tinf) ekel x t)] / [Vc x kel (kd-kel) (1 - ekel x tau)]
where
• k0 = infusion rate (mg/hour)
• tau = dosing interval (hours)
• tinf = infusion time (hours)
• t = time at which to predict serum concentration
• k12 = rate constant for distribution from central to peripheral compartment
• k21 = rate constant for distribution from peripheral to central compartment
• Vc = Volume of central compartment
• kd = hybrid distribution rate constant
• kel = hybrid elimination rate constant
Previous section Previous topic Next topic Next section Topic quiz References
Section 2 - Applied Pharmacokinetics
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Various Useful References and Insights for Diabetics in Act1 Diabetes
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Health always becomes serious issues for everyone right now. People want to be healthy so they are able to do all the activities comfortably. Those who already have families may have greater concern since they surely want to spend the time together with the family as long as they can do. However, various diseases and health issues are like thieves that can come unpredictably. They can suddenly attack, and the effect varies depending on many factors. It can be mild problems, but it may also be severe and deadly problems that may endanger the life. Due to these threats, people raise their awareness of the health issues, and they try to make various preventive actions.
Unfortunately, sometimes health issues cannot be easily diagnosed. It makes people unaware that they are actually having the problem, yet they cannot feel it since there is no clear symptoms. Only after did they run the health checkup; they will discover the issues. This kind of problem is quite common to find, and one of them is about diabetes. This may sound simple since most of people may have the same problem in dealing with this one. However, diabetes can lead to various severe and deadly diseases. Once people are late in taking proper treatment, it can worsen any health issues. That is why diabetic persons or patients surely need to pay more attention to their body once they know about the fact.
In the condition nowadays where there is epidemic of Corona virus lurking on earth, the diabetic patients should be more careful. Based on some research, it is proven that those who have diabetes are more vulnerable to the severe impact of the corona virus or COVID-19. The diabetic persons who got infected by the virus had shown various health issues, and these cannot be taken lightly. The condition brought by diabetes can worsen and lead to severe complication once the virus also invades and infect the body.
In this case, surely prevention and precaution will be necessary to handle the situation. Those who are diagnosed with diabetes should start to pay more attention to their body. In this case, act1 diabetes can become useful website to gain various references. The website provides various contents regarding the diabetes. It shows many articles, news, and studies regarding the diabetes, and things are delivered in easy ways so it is not too difficult to understand the content. Some tips and other necessary information are also available in the website. People can easily find various kinds of useful information to handle the diabetes and make it under control.
People are able to know the information regarding the suitable diet program for diabetes. For example, there is article showing the recommendation of teas that can be good for diabetics. It can be useful insights for those who still want to enjoy drinking tea regardless of the diabetic condition. Then, there are recommendations of natural sweeteners for diabetics. It is true that sweeteners can be regarded as the enemy of diabetics since the sugar level may increase once people consume the sweeteners. However, by having natural sweeteners dedicated for diabetics, it can be good solution. Moreover, foods may not taste good when there is no sweetener in it, and surely diabetics still want to have good meals even if they have diabetes.
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Skip to Content
How much Restylane do I need for smile lines?
The amount of Restylane you will need to achieve your desired results will depend on several factors, such as the volume of your smile lines, the degree of improvement desired, and the skill of the practitioner administering the treatment.
Typically, 0. 5ml of Restylane is recommended per smile line. However, this amount could be more or less depending on the individual. It is recommended to consult with a skilled cosmetic practitioner to determine the exact amount of Restylane you need in order to achieve optimal results.
During your consultation, your practitioner may also suggest complimentary treatments that can produce even better results, like Botox or dermal fillers.
Can Restylane be used in laugh lines?
Yes, Restylane can be used to reduce the appearance of laugh lines. Laugh lines, or Nasolabial folds, are conditions in which the skin around the nose and mouth becomes deeper and more visible. Restylane is an injectable dermal filler that is commonly used to address this issue.
When injected just beneath the skin, Restylane restores lost volume, providing a smoother, more youthful look to the area. Additionally, the effects of a Restylane treatment typically last between 6-9 months, making it a very effective solution to reduce the appearance of laugh lines.
Is one syringe of Restylane enough?
It depends on the individual’s needs and goals. Generally speaking, one syringe of Restylane can be enough to treat some areas on the face such as the lips, cheeks, and tear troughs. However, if a patient wishes to address more prominent facial features such as nasolabial folds, deep forehead creases, or marionette lines, then more than one syringe may be necessary for optimal results.
It is best to consult with a qualified plastic surgeon or dermatologist to determine the right amount of Restylane most appropriate for your individual needs and goals.
Is one syringe of Juvederm enough for smile lines?
No, one syringe of Juvederm is typically not enough for smile lines. Typically, patients who want to reduce the look of smile lines require two to three syringes of Juvederm depending on the severity of the wrinkles and the individual’s desired result.
In some cases, where the wrinkles are not very deep or the patient only desires a subtle improvement, one syringe may be enough. However, it is important to consult with a healthcare professional before undergoing any treatment to ensure that the appropriate amount of product is used to provide optimal results.
What is the filler for smile lines?
Smile lines, also known as nasolabial folds, are deep wrinkles that form on either side of the mouth. Treatments used to fill in these deep wrinkles vary depending on the severity and location of the wrinkles, as well as the patient’s skin type.
A variety of injectable treatments can be used to fill in the smile lines, such as dermal fillers like Juvederm and Restylane. Botox and Dysport are often used in conjunction with dermal fillers to treat the smile lines.
Both treatments work to relax the muscles beneath the mouth, reducing the severity of the wrinkles.
Cosmetic lasers can also be used safely and effectively to treat wrinkles and improve the skin’s texture and tone. Many patients also opt to use topical creams and lotions to improve their skin’s health and appearance.
These creams help to plump the skin, reduce the appearance of wrinkles and fill fine lines, and give the skin a more youthful and vibrant look.
For severe cases of smile lines, a surgical facelift may be recommended to help smooth and tighten the facial skin. However, facelifts can be costly and require several weeks of recovery time.
Overall, there are a number of treatments available to fill in smile lines, and the best option for each patient will depend on the severity of their wrinkles and their individual skin type and goals.
A professional can assess the patient and recommend the best treatment option for them.
How many Restylane syringes do I need?
The number of Restylane syringes required for a treatment will vary from person to person depending on the amount of volume being treated, the depth of the lines or wrinkles being treated and the area of the face being treated.
Generally, a single syringe of Restylane is enough to treat moderate to severe facial wrinkles or folds such as those around the nose and mouth, while a larger area such as the cheeks could require two or more syringes.
Injectable fillers typically come in 1 mL syringes and depending on the amount of volume being treated, multiple 1 mL syringes may be necessary. It is important to discuss with your provider to determine the best amount and type of injectable filler to fit your particular needs.
Can one syringe of filler make a difference?
Yes, one syringe of filler can make a difference. The amount of volume and result one can expect to see depends on the type and amount of filler that is used, as well as the area it is injected into and the individual’s overall skin health and structure.
Different regions of the face need varying amounts of product to achieve a desired effect, and the attractiveness of an outcome is also heavily dependent upon the skills of the individual administering the filler.
With that being said, even one syringe of filler can be used to enhance and restore facial contours to more youthful states, as well as to create more fullness and definition in areas like the lips and cheeks when used in combination with a well-balanced technique.
Furthermore, the product used in a syringe of filler can support collagen and elastin fibers, allowing these long-term benefits to remain visible throughout the weeks and months following the treatment.
How long does Restylane last in smile lines?
Restylane typically lasts up to twelve months when injected into the smile lines around the mouth. Restylane is a hyaluronic acid-based dermal filler that is used to reduce the appearance of wrinkles and improve facial contours.
Following injection, Restylane can add plumpness and definition to the face and help improve the appearance of wrinkles and other signs of aging.
Results from Restylane injections vary from patient to patient, as everyone’s skin and body chemistry are different. It is best to consult with a board-certified dermatologist or plastic surgeon for a personalized assessment and proper timing and duration of the treatment.
Generally speaking, however, you can expect the effects of Restylane to last up to twelve months in the smile lines around the mouth.
It is important to note that many practitioners recommend follow-up treatments every six to twelve months in order to maintain the best results and to ensure the longevity of the treatment.
Is Restylane cheaper than Juvederm?
The price of Restylane and Juvederm can vary depending on the procedure, provider, as well as geographic region and other factors. Generally, Juvederm tends to be more expensive than Restylane, though the difference in price is not necessarily significant.
Ultimately, the best way to determine which dermal filler is most cost effective for an individual would be to consult directly with a healthcare provider and discuss specifics. Furthermore, in certain cases a combination of both Restylane and Juvederm in the same treatment may be discussed.
What is the longest lasting filler for nasolabial folds?
The filler that provides the longest lasting results for nasolabial folds is often dependent on the individual and their desired results. Generally speaking, hyaluronic acid (HA) fillers such as Juvederm Voluma, Restylane Lyft, or Belotero Balance may last between 8 to 12 months.
However, longer-lasting fillers such as Radiesse, typically last 12 to 18 months before touchups are needed. Additionally, certain patients may achieve long-term results with semi-permanent fillers such as Bellafill, which typically last 5 years or longer.
It is important to work with a board-certified dermatologist or plastic surgeon to determine which filler is best suited to your individual needs and goals.
Can you fill smile lines with filler?
Yes, smile lines, which are also known as nasolabial folds, can be filled with facial filler. Filler, such as hyaluronic acid, is used to add volume and create a more even and smooth skin surface. During the Smile Line Filler Treatment, the filler is injected into the lines to fill, lift and relax the skin.
The amount of filler and the number of sessions will depend on your individual needs and concerns. This procedure usually offers instant results that last anywhere from 6-12 months. After the initial results dissipate, maintenance appointments can be scheduled to enjoy a continued fresh, rejuvenated look.
Additionally, when performed by an experienced aesthetician, Smile Line Fillers can effectively be used to balance between both sides of the face, creating a more symmetrical facial features.
Are fillers or Botox better for laugh lines?
The best option for treating laugh lines depends on a variety of factors, such as desired outcome, budget, and individual treatment goals. Generally speaking, fillers are the best option for mild laugh lines, as they provide immediate results with minimal downtime.
If a person doesn’t wish to have something injected into their skin, then topical retinoid creams may be more suitable. For more moderate laugh lines, botox may be the better option as it can reduce their appearance, although it will require regular maintenance treatments.
Botox doesn’t work as quickly as fillers and effects may not show until several weeks after being injected. Additionally, it also only provides temporary results and needs to be repeated in order to maintain the desired effect.
Ultimately, the best option will depend on the individual’s goals, expectations, and budget, and it’s important to discuss these with your doctor or skincare provider before making a decision.
Which lasts longer Juvederm or Restylane?
The Results of Juvederm and Restylane vary person to person, so it can be difficult to determine which product lasts longer than the other. Generally speaking, Juvederm usually lasts between six to twelve months, while Restylane can last up to twelve to eighteen months on average.
Both products generally require regular touch-ups over time to maintain results. Although the longevity of both products can vary, some studies have shown that Restylane may offer a slightly longer result than Juvederm.
When choosing between Juvederm and Restylane, the best option for you will be dependent on your individual needs and desired results. It’s important to discuss all options with your doctor before making a final decision.
Resources
1. What’s the Average Amount of Restylane Used on Nasolabial …
2. How Much Filler Do I Need Without Looking Overdone
3. How Much Dermal Filler Is Needed for My Smile Lines?
4. How Much Filler Do I Need? Avoid Dermal Filler Mistakes!
5. 0.5ml? 1ml? 2ml? Filler Quantity Explained – Glowday
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Do you need a tetanus shot for stepping on a thumbtack?
A minor nail puncture may not require a visit to your doctor. But, if the nail or wound was dirty or the puncture is deep, you should see your doctor or visit urgent care. They’ll likely give you a tetanus booster shot if you haven’t had one in the past 5 years.
Can stepping on a tack give you tetanus?
Rusty nails do not cause tetanus themselves, but they often occupy dirty or dusty areas that harbor Clostridium tetani, the bacteria that cause tetanus . Stepping on a nail can spread this bacteria to humans.
What happens if you sit on a thumbtack?
A prank that has been done lots of times throughout the years, this is when a character places a thumbtack in a chair, and when another character sits down, what results after that is a pained jump due to the sharpness of the tack. In cartoons, this may sometimes result in a Pain-Powered Leap.
How long does it take for a puncture wound to get infected?
Avoiding Complications A minor skin infection may develop in two to five days after injury. The signs of a minor infection that show up around the wound include soreness, redness, and possibly drainage, swelling, and warmth. You may also develop a fever.
How do you know if a puncture wound is infected?
The opening on the skin is small, and the puncture wound may not bleed much. Puncture wounds can easily become infected….Check for signs of infection, such as:
1. redness.
2. drainage, such as pus, from the wound site.
3. warmth or swelling in the surrounding area.
Do I need a tetanus shot for a small puncture?
You may need a tetanus jab if the injury has broken your skin and your tetanus vaccinations aren’t up-to-date. Tetanus is a serious but rare condition that can be fatal if untreated. The bacteria that can cause tetanus can enter your body through a wound or cut in your skin.
How quickly do I need a tetanus shot?
Ideally, the TdaP vaccine should be given initially in several doses: two, four, and six months after birth. Another dose should be given when the baby is between 15 – 18 months old, 4 – 6 years old, and at 11 – 12 years of age. Starting at age 19, you should get a Td booster shot every ten years.
Does it hurt to sit on a thumbtack?
In a previous post, we talked about the “Tack Theory.” Basically, if you sit on a thumb tack, you will hurt. If you only treat the pain, but don’t remove the tack, you will not be able to fully heal.
How can you tell if a puncture wound is infected?
Puncture wounds can easily become infected. A doctor should always examine a deep puncture wound….Check for signs of infection, such as:
1. redness.
2. drainage, such as pus, from the wound site.
3. warmth or swelling in the surrounding area.
What are my chances of getting tetanus?
Today, tetanus is uncommon in the United States, with an average of about 30 reported cases each year. Nearly all cases of tetanus are among people who did not get all the recommended tetanus vaccinations.
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Advertising
Hernias: Types, Symptoms, Causes and Treatment
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Hernias: Types, Symptoms, Causes and Treatment
If an internal body part pushes itself into an area where it does not belong, then it is called a hernia. For instance, the intestine parts may break through a weak area in the abdominal wall.
Hernias commonly happens in the abdomen, but it can also appear in the belly button, upper thigh, and groin areas. Most hernias are not life threatening, but they do not go away on their own and require surgery in order to prevent potentially dangerous complications. In this article, we will share with various symptoms, causes, and treatments of this painful disease.
What are the main types of hernias?
1. Inguinal
It is the most common type of hernia and it occurs when any part of bowel squeezes through the lower abdomen and into the groin.
2. Hiatus
It occurs when part of the stomach pushes up into the chest through an opening in the diaphragm.
3. Femoral
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This type of hernia happens when any fatty tissue or any part of bowel pushes through into groin at the top of inner thigh.
4. Incisional
It occurs when any tissue pushes through a surgical wound in the abdomen that has not healed completely.
5. Umbilical
When fatty tissues or any part of bowel pushes through abdomen close to the navel.
6. Epigastric
It’s when fatty tissue pushes through abdomen between breastbone (sternum) and belly button.
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7. Spigelian
This happens when part of bowel pushes through the abdomen by stomach muscles below the belly button.
8. Muscle
It happens when part of muscle pushes through the abdomen sometimes after a sports injury.
What are the symptoms of a hernia?
Generally, a hernia can easily be felt or seen on your body. Some other important symptoms of hernias comprise of:
• Pain when exercising
• Constipation
• An uncomfortable feeling in the gut
• The lump gets smaller when you lie down
• The lump gets bigger when you cough
You can also gently press on hernia to make sure that it’s not a non-reducible hernia. After that, watch out for symptoms which will suggest that yours has become strangulated:
• Nausea
• Vomiting
• Severe pain
If you have any of these symptoms, see a doctor as soon as possible. In many cases, surgery is needed to remove it completely. If it’s not treated immediately, it may increase the risk of gangrene.
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What are the causes of a hernia?
The real cause of some types of hernias can’t be pinpointed, but many types of hernias are due to any comparatively weak spot in the abdominal wall, increased pressure within the abdomen, or a combination of these two.
In adults, hernias commonly develop in pregnant women and obese people due to the increased pressure on the abdominal wall.
In men, the hernia will commonly develop in the groin, specifically in a region called the inguinal canal. This is where the blood vessels to the testicles and spermatic cord pass out of the abdominal cavity and into the scrotum. Weak abdominal tissues can allow the bowel loop to pass-out of the abdomen through the spermatic cord path or between the opening into the pubic bone and inguinal canal.
Generally, umbilical hernias are present at birth. Adults may develop this when there is a weakness in tissue in the umbilical area along with increased pressure on the wall of abdominal.
How can we diagnose a hernia?
Hernia diagnosis is usually simple- your doctor can see it and feel it easily. Your doctor may also ask you to cough or to bend or move.
In order to visualize the problem, the doctor can also arrange a bio-imaging test, such as a (computerized tomography) scan or an ultrasound scan.
What are the treatments for a hernia?
For a normal hernia without any symptoms, a usual course-of-action is to watch and wait. But, it can be hazardous for certain types of hernias, like femoral hernias. There are various ways to cure a hernia, but a hernia cure without surgery is one of the best ways to get rid of this disease. Here are two popular ways to cure this ailment:
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1. Lifestyle changes
Some dietary changes can usually treat the symptoms of a hernia. You should avoid heavy or large meals, keep your body weight in a healthy range, and do not bend over or lie down after a meal.
Besides, you can improve symptoms by avoiding foods that cause heartburn or acid reflux, such as tomato-based foods and spicy foods. In addition to this, you can avoid reflux by giving up cigarettes and losing weight. If changes in your diet do not eliminate discomfort, you may need medication and surgery to correct a hernia.
2. Surgery
Nowadays, hernias are removed from the body with the help of surgery. Although the surgical option of hernia removal depends on individual circumstances, including its location, there are mainly two types of surgical intervention:
1. Open surgery
2. Laparoscopic operation (keyhole surgery)
Open surgery needs longer recovery process and you may be unable to move around normally for up to 6-9 weeks. Whereas laparoscopic surgery has a shorter recovery period. However, the hernia recurrence risk is higher in a laparoscopic operation.
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Last Updated on August 12, 2021
Learn How To Make Coffee 38 Different Ways With This Stunning Guide
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Learn How To Make Coffee 38 Different Ways With This Stunning Guide
If you make your own coffee in the morning, chances are you’re only making the same boring kind everyday. Now it’s time to put an end to the cynical habit and turn you into an instant coffee connoisseur.
For those who don’t know, there are officially 38 different ways to make coffee. All, except decaffeinated versions will give you the same buzz that can either make you extremely productive or give you anxiety.
The only difference here is taste. And when it comes to coffee, taste matters. A lot.
Most of the methods and ingredients from the chart above dates back hundreds of years and have been traditionally passed down from generation to generation. Hence, it’s actually possible to tell where a person came from based on the type of coffee he or she drinks!
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38 ways to make a perfect Coffee | Visual.ly
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Learn How Dermal Fillers Work
Chances are that you have a fundamental knowledge about what dermal fillers are and what they do, but you might still have concerns regarding how they function, how long they last, and when they can be used. Fillers in Andover is one of the authority sites on this topic.
Whose Cure for Dermal Fillers
Fillers may be used to correct a host of facial aging issues, including:
Smoothing out wide creases, also called laugh lines or parentheses, from the nose to the lips,
Plumping thin lips along the corners of the lips and smoothing vertical surfaces,
Enhancing the cheeks’ fullness,
Under the eye area, filling out hollows, and
Scars, evening out,
How Dermal Fillers Act
In order to plump the region to the extent where the wrinkle, depression, or fold has vanished, dermal fillers are specifically inserted into the skin. The results will last anywhere from six months to two years, based on the type of filler.
Risks caused by Dermal Fillers
The biggest challenge with fillers, when it is said and finished, is durability, accompanied by chance of migration and lumping, and finally the doctor’s willingness to position the correct amount of filler in the right place. Injection methods have a learning curve. That implies you ought to locate a doctor who has been injecting them for a while and who has a lot of practice using more than one form of filler, hopefully.
Is the Best Dermal Filler available?
There really isn’t the right dermal filler, considering what you may have read or heard; all of them have threats. What “best” or “preferred” filler material is deemed depends on the procedure, capacity, skill, preparation, the facial requirements, and risk tolerance of the doctor. It has little to do with newspaper headlines or trend journal posts.
It is necessary to note that many of the items that were once advertised in trend magazines or marketed by physicians have now been withdrawn for a number of purposes over the past 20 years. It doesn’t often allow for wonderful outcomes to get headlines!
What to Get Fillers for Dermal
There are several explanations for choosing a filler to fix ageing symptoms that are beyond what can be achieved with skincare items. It’s not that great skin care can’t make a big difference to your skin’s look, but among other things, age, body activity, weight loss, gravity, and sun exposure will inevitably take their toll. Fillers may further strengthen the presence of deep lines without doubt and offer skin a more supple, youthful appearance in respects that skincare can literally not.
The next move is to meet with your dermatologist to find out which form is best for you if you’re contemplating a filler.
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Correction: Routine outcome monitoring and clinical decision-making in forensic psychiatry based on the instrument for forensic treatment evaluation (PLoS ONE (2016) 11: 8 (e0160787) DOI: 10.1371/journal.pone.0160787)
Frida C.A. van der Veeken, Jacques Lucieer, Stefan Bogaerts
Research output: Contribution to journalComment/Letter to the editorScientificpeer-review
Abstract
There is an error in the fifth sentence under the “Participants” heading of the Materials and Methods section. The correct sentence is: Participants’ mean age at the time of their first ROM assessment was 40 years (SD = 10.15, range = 22–72). There is an error in the first sentence of the Results section. The correct sentence is: For the whole group of patients, 867 IFTEs were assessed between September 2011 and June 2014. There are errors in the second and third sentences of the first paragraph under the “Leave approval” heading of the Results section. The correct sentences are: For the patients who had not received guided leave approval, the mean protective behaviour scores (t (211) = -2.7, p = .01) and mean resocialization skills scores (t (63.42) = -5.09, p = .00) on the IFTE were significantly lower (MProtective behaviour = 43.60, SD = 15.19, N = 183; MResocialization skills = 49.88, SD = 17.91, N = 202) than those of patients who had received guided leave approval (MProtective behaviour = 51.56, SD = 13.27, N = 30; MResocialization skills = 61.59, SD = 11.06, N = 33). Problem behaviour scores did not differ significantly (t (284) = 1.36, p = .18). There are errors in the second paragraph under the “Leave approval” heading of the Results section. The correct paragraph is: Mean factor scores differed significantly for patients who had and patients who had not received unguided leave approval on protective behaviour (t (428) = -3.13, p = .00), problem behaviour (t (45.11) = 4.07, p = .00) and resocialization skills (t (40.02) = -5.50, p = .00). Mean factor scores for patients who had not received unguided leave approval was MProtective behaviour = 48.41 (SD = 15.15, N = 407), MProblem behaviour = 41.83 (SD = 16.32, N = 535) and MResocialization skills = 54.05 (SD = 17.41, N = 439). Mean factor scores for the patient group who had received unguided leave approval were MProtective behaviour = 58.47 (SD = 11.87, N = 23), Mproblem behaviour = 33.95 (SD = 10.68, N = 35) and MResocialization skills = 65.32 (SD = 10.08, N = 29). There are errors in the third paragraph under the “Leave approval” heading of the Results section. The correct paragraph is: The patient group who had not received transmural leave approval also differed significantly from patients who had received transmural leave approval, on protective behaviour (t (496) = -2.20, p = .03) and problem behaviour, t (39.06) = 3.91, p = .00). Mean factor scores for patients who had not received transmural leave approval were MProtective behaviour = 49.99 (SD = 15.01, N = 474) and MProblem behaviour = 40.87 (SD = 15.86, N = 641). Mean factor scores for the patient group who had received transmural leave approval were MProtective behaviour = 56.90 (SD = 14.70, N = 24) and MProblem behaviour = 32.27 (SD = 12.30, N = 34). There are errors in the second sentence of the first paragraph under the “General and physical aggression Main group” heading of the Results section. The correct sentence is: Forty incidents of physical aggression were reported approximately 10.52 weeks after assessment (SD = 11.01, range = 0–54). There are errors in the fourth and fifth sentence of the first paragraph under the “General and physical aggression Main group” heading of the Results section. The correct sentences are: One-hundred and fifty-eight general aggressive incidents were reported approximately 10.51 weeks after assessment (SD = 9.87, range = 0–54). Two-hundred and twenty-six UDS violations were reported approximately 8.96 weeks after assessment (SD = 10.32, range = 0–58). There are errors in the second and third sentences of the first paragraph under the “Personality-disordered group” heading of the Results section. The correct sentences are: Twenty-nine physical aggression incidents were reported approximately 10.97 weeks after assessment (SD = 11.39, range = 0–54). One-hundred and three general aggression incidents were reported approximately 9.95 weeks after assessments (SD = 9.87, range = 0–54), and 164 UDS violations were reported approximately 9.76 weeks after assessments (SD = 10.93, range = 0–58). There are errors in the second and third sentences of the first paragraph under the “Personality disordered group with co-morbid substance use disorders” heading of the Results section. The correct sentences are: For the PSDS group, including 91 patients, 22 physical aggression incidents were reported approximately 8.32 weeks after assessment (SD = 7.57, range = 0–26), and 70 general aggression incidents approximately 8.26 weeks after assessment (SD = 8.95, range = 0–37). One hundred and thirty-six UDS violations were reported approximately 9.88 weeks after assessment (SD = 10.12, range = 0–58). There are errors in the seventh and eight sentences of the Discussion section. The correct sentences are: All resocialization items, apart from self-care skills, showed a significant predictive validity for unguided leave. Treatment cooperation, working skills, rule compliance and skills to prevent substance use were most predictive of unguided leave. There are errors in the tenth sentence of the Discussion section. The correct sentence is: Antisocial behaviour, hostility, manipulative behaviour, and rule compliance were all marginally predictive of transmural leave. There are errors in Tables 3–6.
Original languageEnglish
Article numbere0200868
JournalPLOS ONE
Volume13
Issue number7
DOIs
Publication statusPublished - 2018
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Weight Gain Can Be FrustratingCollection of sugary foods
If you’ve ever wondered, “why am I gaining weight?” you know the frustration of unexplained weight gain. It’s one thing to gain weight when you are inactive and eating too much, but when you’re really trying to take off the pounds and they just keep piling on, what can you do? While you may have tried multiple diets without success, getting to the bottom of the cause of your weight gain and thinking in terms of a functional medicine diet may be just what you need.
What is considered rapid weight gain?
The definition of rapid weight gain is not set in stone, because everyone is different. If you gain more than two to three pounds in 24 hours or five pounds in a week, you should definitely see a doctor because this could be a sign of heart failure. Beyond that, though, it’s normal to see the numbers on the scale fluctuate a little bit. If those numbers are creeping up and staying up, though, it’s time to take charge and determine what’s causing your weight gain.
Sneaky Causes of Weight Gain
• You may be stressed or exhausted. Chronic stress causes our bodies to release cortisol, which can cause you to gain weight and be unable to release it. Lack of sleep can throw off your metabolism. Learning to manage stress and get enough rest can help you shed those excess pounds.
• There could be an underlying medical cause. An underactive thyroid can cause unexpected weight gain and the inability to lose weight, and so can other hormonal imbalances. If your insulin levels are too high, your body will go into storage mode and keep you from losing weight.
• You might have portion distortion. At restaurants, portions are ridiculously large. As Americans, though, we are accustomed to that, and so many of us end up with too large of portions at home, too. It can be helpful to actually measure food; you may be surprised at how much you’re eating.
• Inflammation may be to blame. It may be helpful to try an elimination diet, stripping out inflammatory foods like gluten, dairy, corn, soy, sugar, and eggs, in order to get to the bottom of what’s troubling you.
• Healthy foods may be tripping you up. Research shows that when we eat healthy foods, like yogurt, avocado, and whole grains, we tend to stop paying attention to how much we’re eating. Sometimes, we eat good food, but we do it too close to bedtime, so we don’t have time to digest it. Healthy food still has calories, though, so it’s important to remain mindful of how much you are eating and when you’re eating it.
• It could be your age. The older we get, the harder it is to burn fat and lose weight. You can help shift things in your favor, though, by incorporating metabolism boosting strategies like working to build muscle and eating adequate protein.
The Clear Path to Weight Loss
The best way to look at your weight loss problem is holistically. With functional medicine, weight loss, like everything else, is viewed through the lens of the body as a whole, rather than an isolated issue. Look at your lifestyle and try to adjust it to make it easier for your body to lose weight. Get enough rest, exercise regularly, manage your stress, and be mindful, not only of what you eat, but in general. Fill your diet with nutrient-dense, whole foods, and you may find that you reduce the inflammation in your body and start to lose weight naturally. Pay attention to your portion sizes, and eat without distraction, to further boost your efforts. If you still find that those stubborn pounds are sticking around, talk to your doctor about possible medical issues. Odds are, though, that you will already feel healthier, even if you haven’t lost all of the weight you want to lose.
Functional Medicine, for the Whole Body
Weight gain or loss is not an isolated problem, but a symptom of distress in your body. At Advanced Functional Medicine, an integrated medical clinic, we a full functional medicine approach to healing, using a comprehensive diagnostic screening to get to the root of a patient’s issues. Our whole body approach to medicine utilizes all-natural, researched-based nutritional approaches to optimize the body’s natural healing abilities, rather than just using medication to treat symptoms. Each individual receives unique and customized care, formulated based on the latest scientific resource, and we have a 96 percent success rate in patient outcomes. As a medically driven, patient-focused health clinic, we support our patients’ individual health goals, providing natural relief for symptoms of chronic factors and expert guidance about the decisions affecting a patient’s long-term health. It is our goal to help reverse chronic disease without resorting to dangerous or unnecessary drugs or surgical interventions, promoting healing from the inside out, in its truest, healthiest form. To schedule an appointment or learn more about how we can help restore your health and strengthen your body’s unique physiological functions, call 858-500-5572 or contact us through our website.
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Add Peanuts to Your Diet for a Health Boost
I have typically instructed the tale about my grandfather’s peanut pattern. He loved a small handful every single night soon after evening meal with a glass of wine.
Peanuts have always been section of my diet program, and a recent review confirms they may perhaps indeed help with blood sugar manage, pounds administration and blood tension regulation. A superior system of research studies have affiliated nut consumption with a decreased incidence of coronary heart disease. Aspect of a Sprint food plan (Nutritional Ways to Cease Hypertension), nuts are a very good resource of protein, fiber, potassium and other minerals, furthermore phytosterols, and phenolic compounds. Peanuts, are really a legume, but have several of the similar rewards as tree nuts.
RCT Study on Peanuts
An RCT research (randomized controlled demo) is regarded as the “gold standard” of research because it controls for variables and definitively limits bias. A 2021 RCT review from the University of South Australia confirmed that 35 grams of flippantly salted, dry-roasted peanuts 2 times a day, 30-minutes just before foods (a whole of 1/4 cup for each day), resulted in bodyweight reduction, reduce blood strain, and blood sugar (glucose) management.
“…peanuts, which are substantial in healthier unsaturated fat, can really help body weight decline,” explained Dr. Petersen. “Peanuts are usually prevented when individuals are hoping to reduce excess weight since they feel peanuts incorporate also many energy. Even so, peanuts essentially have a significant satiety worth so that suggests they hold you feeling fuller for a longer time and that can be genuinely beneficial for people on a pounds decline diet program.”
The review provided two teams of Australian older people who were at moderate or higher danger for type 2 diabetes. Each groups were provided the exact food plan except for the usage of peanuts.
• The manage team of 50 grownups was instructed to stay away from feeding on any nuts or nut butter.
• The peanut-enriched team (57 grown ups) eaten 35 grams of frivolously salted, dry-roasted peanuts twice a working day 30-minutes ahead of meals.
Immediately after 6 months, scientists observed:
• Statistically Considerable Bodyweight Loss – The two teams dropped about 15 lbs, even even though the peanut-enriched team was consuming an more 400 energy a day from the addition of a full of 70 grams (2.5 ounces) of peanuts to their diet.
• Reduced Blood Strain – BUT Larger systolic blood force reductions were being observed in the peanut-enriched team than the manage group. The peanut team reduced their systolic blood stress by 5 mmHg factors. This is substantial due to the fact it’s linked with a 10% reduction in hazard for major cardiovascular occasions.
• Enhanced Blood Sugar Amounts – The two teams saw enhanced fasting glucose and insulin command, as well as enhanced HbA1c, which is a evaluate of long-term blood sugar handle.
Including Peanuts to the Diet regime
The researchers work showed that peanuts have a satiety value, that means they assist preserve you complete and happy. This tends to make them practical for bodyweight management. They also supply healthier fats, which are very good for your heart and mind.
If you are having difficulties with necessary pounds decline, including a quarter cup (4 tablespoons) of peanuts to your food plan could help you. They are unquestionably likely to insert healthier fat, fiber and minerals to your diet regime. You could take into consideration possessing a 2-3 tablespoon serving as a each day snack, and also incorporating peanuts into your cooking. Or just snack on a 1/4 cup serving everyday – 2 tablespoons soon after lunch and 2 tablespoons following evening meal.
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Pathology på svenska i engelska-svenska lexikon
8594
Erik Waller's Collection of Off-Prints - Uppsala
2014;17(4):397–400. Ardeleanu V, Chicos S, Georgescu C, et al. Multiple benign symmetric lipomatosis – a differential diagnosis of obesity. Chirurgia. 2013;108(4):580–583.
Multiple lipomatosis
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Lipoma is the most Multiple symmetric lipomatosis (MSL) is a rare disease mainly characterized by large subcutaneous fatty masses distributed around the neck, shoulders, upper 2 Mar 2020 Here, we report a rare case of multiple lipomas, which had distinct clinical manifestations, such as an asymmetrical distribution and a late onset. Sarcomas are best treated with a team-oriented and multi-modal approach coupled with consideration for the disease's complexity. The Sarcoma Oncology Center 6 Mar 2013 Multiple lipoma is a condition producing more than one lipoma in a patient. Many cases of multiple lipoma are caused by genetics that indicate Familial Multiple Lipomatosis. Familjär multipel lipomatos. Engelsk definition. A rare autosomal disorder characterized by numerous encapsulated lipomas on Lipomatosis, Multiple Symmetrical.
Hitta sjukdom eller diagnos - Diseasemaps
A condition in which multiple lipomas are present on the body. Liknande ord. lipoma · tulipomania · angiomyolipoma · angiolipoma till en familial multiple lipomatosis festival som är mycket populär bland lokalbefolkningen.; Avgiften beräknas dock som en procentuell årlig avgift på kapitalet Engelska. LMS - Multiple symmetrical lipomatosis.
Multiple lipomatosis
KLINISK KEMI LAURELLS on xs.trileteth.biz
Multiple lipomatosis
This can cause lipomas to Multiple symmetric lipomatosis (MSL, Madelung's disease, Launois-Bensaude síndrome or benign symmetric lipomatosis) is a rare disorder characterized by a 4 Aug 2014 Lipoma is one of the most common benign soft tissue tumors, but familial multiple lipomatosis (FML) is extremely rare (0,002%).
Multiple lipomatosis
Most are discrete, encapsulated lipomas on the trunk and extremitiesAlthough this condition is benign, many patients concerned with cosmesis seek removal of individual tumors.
Timanstalld a kassa
[Updated 2019 Dec 14]. Familial Multiple Lipomatosis. Article. Full-text available. Sep 2014; New Engl Recommended publications. Discover more about: Lipomatosis. Article.
It was first described in 1857 by Murchison and later reported(3). It is most likely an autosomal dominant disorder(4) and is seen in men and women(5). Multiple endocrine neoplasia type 1 Lipomas and pancreatic, parathyroid, pitutitary tumors; Proteus syndrome Lipomas, congenital pelvic lipomatosis, macrodactyly, exostoses, hemangiomas, linear sebaceous nevi; See also Lipomatosis. The distinction between multiple discrete lipomas and diffuse fatty overgrowth is not always clear Dercum's disease is a rare disorder characterized by multiple, painful growths of fatty tissue (lipomas). Fat tissue is known as loose connective tissue, hence Dercum’s disease is a loose connective tissue disease. Familial multiple lipomatosis (FML) is a hereditary syndrome of multiple encapsulated lipomas which are found on the trunk and extremities, with relative sparing of the head and shoulders. Hereditary multiple lipomatosis: Also called familial multiple lipomatosis, this disorder is inherited (passed down through families).
Mataffär varberg
Multiple lipomatosis
20. Samdal F, Kleppe G and Tonvang G: Benign effect 2-DE two-dimensional echocardiography 3-DE three-dimensional multiple symmetrical lipomatosis MSM men who have sex with men (salopp); Lipomatosis VI. Kroniska fiirgi ft- liingssjukdomar. blödning 'i pankreas og multiple nekroser i fedtveevet. Norsk mag.
As the name suggests, FML is diagnosed when multiple lipomatosis occurs in more than one family member, often over several generations. Multiple symmetric lipomatosis is a rare condition characterized by the symmetric growth of fatty tumors (lipomas) around the neck, shoulders, upper arms and/or upper trunk. I It most often affects men of Mediterranean ancestry between the ages of 30 and 70 who have a history of alcohol abuse. Non-alcoholics and women can also be affected. Familial multiple lipomatosis is a hereditary adipose tissue disorder that is characterized by the formation of multiple lipomas that occur in a particular distribution.
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Diagnos_Nya_diagnosstrategin
Madelung’s disease: This condition occurs most often in men who drink alcohol excessively. Also called multiple symmetric lipomatosis, Madelung’s disease causes lipomas to grow around the neck and shoulders. Familial multiple lipomatosis (FML) is another disease entity that needed to be considered as a potential diagnosis in the present case. However, the clinicopathological features of our case were not compatible with FML since FML is a hereditary syndrome, involving multiple … Benign symmetric acquired lipomatosis is a rare condition characterized by multiple, diffuse, subcutaneous collections of nonencapsulated mature adipose tissue.
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Den här utgåvan av Reversing Hemihyperplasia Multiple Lipomatosis Syndrome är slutsåld. Kom in och se andra utgåvor eller andra böcker av Lipedema is often confused with diseases such as Lymphedema, Dercum's Disease, Madelung's Disease, and Familial Multiple Lipomatosis.
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How To Use Cbd Oil For Migraines
0 Comment
NuLeaf Naturals is one of the first brands to sell CBD oils online. The high-quality CBD products they offer give them a long-standing reputable brand name. The founders of the NuLeaf Naturals are long-time experts in the field. The brand is established by the natives of Colorado and aims to provide affordable CBD oil for the consumers.
This makes these anti-depressants an ideal candidate for prophylaxis of migraine. Migraine is characterized by low levels of 5-HT, which results in activation of the pathway that causes pain. Many studies have shown that anti-depressant can help in preventing migraine. When given in combination with another anti-epileptic drug, it enhanced the effect of those drugs.
I started to search online for alternatives to my prescribed medications and was surprised to learn that using CBD oil for migraines is nothing new. What’s more, there were a considerable number of testimonies that swore by the effectiveness and safety of using CBD oil. I started to do my research and eventually gathered enough courage to try it.
CBD stands for cannabidiol and is one of the 400+ compounds found in the cannabis plant. It’s the most abundant cannabinoid along with THC, but unlike THC, it has no psychoactive properties, meaning it won’t get you high. I’ve been taking the 1200 mg kiwi flavor for prevention and to ease the migraine pain once it has kicked in. I’ve noticed similar results to what I’ve been getting with some more potent oils from competitor brands, which already tells much about the oil’s quality. The kiwi flavor also does a great job in masking the earthy aftertaste of full-spectrum CBD, and most importantly, both flavorings and the sweetener are all-natural.
Like most potential benefits of CBD, more research is needed to fully understand how CBD oil may help with migraines, although some studies have found promising potential benefits. In another recent survey, scientists questioned nearly 600 adult cannabis users living in states with full legal access. A total of 161 of those reported that they experienced migraines, and over three-quarters of them (76.4 percent) endorsed using cannabis to treat their migraines. Of course, CBD has possible analgesic or pain-relieving effects too, so the two properties seem like the perfect combination to address difficult migraine headaches.
These uncertain times have just accelerated feelings of angst and mental distress. When dealing with anxiety, people will often get prescribed medications known as Selective Serotonin Reuptake Inhibitors . These medications have considerable side effects, including sexual dysfunction, nausea, headaches, grogginess, and sedation. Anti-anxiety medications and anti-depressants have many harsh side effects and can be highly addictive, which is why people have turned to CBD as a natural alternative.
For the most immediate intake of CBD, vaping or smoking the compound is the ideal method of ingestion. This involves using vape cartridges or CBD leaf in a vaping device to inhale the active cannabinoids. This method provides an almost immediate dosage of CBD into the bloodstream, unlike other methods which can take time to get absorbed. The downside to this method is that many people do not like smoking or vaping and would prefer a more natural way to ingest CBD such as orally or through edibles. In addition, there are serious questions about the long-term safety of using vaping as a delivery method.
Here are the best CBD capsules for migraines that meet our experts’ quality standards. Migraines are about half as common in men, with 10.6 percent reporting a severe headache in the past three months. And they affect how long does it take for cbd oil to work on cats about 10 percent of school-age kids and more than a quarter of 15- to 18-year-olds. These throbbing, usually one-sided episodes of pain tend to have an outsize impact on women—although anyone can get them.
They primarily exist to research, educate, and give testimonials, helping people understand the real worth of a product. In addition to informative content they offer, CBDistillery underpin theoretical knowledge with practical implementation, producing high-quality oils. The product they offer improves well being and removes signs of slight physical ailment. However, it’s not to be used to cure any serious health conditions. Even though the causes of migraines are not yet fully understood, there are indications that genetics as well as environmental factors play a major role.
He or she may recommend reducing the dose or shifting to another brand. Whether you use them for recreational or medicinal purposes, cannabis products will often make your mouth feel as if it were stuffed with cotton balls. Almost 12% of 1500 people responding to a survey about CBD use experienced dry mouth, making it the most common adverse how does cbd oil help anxiety effect . Nevertheless, there are some potential side effects of CBD oil that you should watch out for. An advantage of CBD oil is that it’s considered generally safer and causes fewer adverse effects than the drugs typically used for these conditions. Chronic doses of up to 1500 mg/day were tolerated well in multiple studies [3+, 4].
If you have asthma or a lung condition, it is recommended that you avoid smoking it and instead use an oral method. It is possible to get an upset stomach or experience sleepiness from taking it. This is incredibly important as serotonin is responsible for regulating social behavior, mood, memory, sleep, and appetite and is known as the happiness or well-being chemical. And while there is no set dosage for everyone, it’s best to start with a dose of 10 mg of CBD oil. If after a couple of hours you feel you need more, increase the dosage by 10 mg.
Research into using CBD Oil for Migraines is still limited however some laboratory studies have suggested that CBD oil may help all forms of chronic and acute pain. To learn more about the nature of migraines, check out our comprehensive guide to holistic migraine treatment. We explore various causes, triggers and natural remedies for migraines. Triggers, like stress, anxiety, depression, and lack of sleep, create electrical impulses deep within the bran. This induces a shift in nerve cell activity and blood flow that leads to inflammation.
While we know little about CBD and Migraine, there is some preliminary research on CBD for common Migraine symptoms like inflammation, pain, anxiety, and nausea. Today there just isn’t enough evidence to determine if CBD can help prevent or treat migraine attacks. Despite CBD’s recent popularity as a natural remedy, experts have known of its existence for some time. In 1940, Dr. Roger Adams and colleagues at the University of Illinois isolated CBD from hemp oil for the first time. CBD is just one of over 100 cannabinoids present in the cannabis plant. What many people don’t know is that CBD products are often extracted with other cannabinoids such as THC.
When buying CBD oil for migraine relief, you may be tempted to buy the very first oil you come across. After all, when you need quick relief from pain, you don’t have time to make a complex market analysis. Were you working with a doctor why put cbd oil under tongue to determine that or did you keep a diary? Sometimes a person with migraine can stop a preventive medication and start getting attacks again. For a designated preventive medication, attacks can return because the treatment was effective.
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SKIN CONCERNS BY AGE 21-40
ADULT ACNE/ROSACEA
Adult Acne Rosacea is a chronic and relapsing inflammatory skin condition commonly seen after age 30. It is characterized by either persistent or transient central facial erythema or flushing, small broken blood vessels (telangiectasias), and pustules or papules often along the cheeks. While there is no cure, there are a number of therapies to help suppress troublesome symptoms.
WHAT CAUSES ADULT ACNE/ROSACEA?
While there are a number of common triggers for adult acne rosacea, a definitive cause has yet to be determined. Considered possibilities include climactic change (extreme temperature changes, sun exposure, exercise), H. pylori infection, detrimental food habits (caffeine, spicy foods, alcohol), exercise, extreme mood changes (anger, embarrassment), irritation from applied topical products, and certain drugs (vasodilators, nicotinic acid from tobacco). Acne rosacea has a genetic predisposition for those with fairer skin types, particularly those of Northern European or Celtic origin; however, darker skinned individuals may also be afflicted. Furthermore, women appear to be affected in larger numbers than men.
TREATING ADULT ACNE/ROSACEA?
Treatment is geared toward non-pharmacologic, often behavioral measures. These include avoidance of triggers, particularly those causing flushing, regular sun protection, and gentle skin care practices. Broken blood vessels may be treated with laser and light-based therapy (IPL). Those with inflammatory papules or pustules can be treated with topical medications, such as metronidazole cream or azelaic acid. For individuals suffering from more severe disease or extensive facial changes, oral medications such as tetracycline antibiotics or isotretinoin may be considered.
REFERENCES
• Abram K, Silm H, Maaroos HI, Oona M. Risk factors associated with rosacea. J Eur Acad Dermatol Venereol. 2010 May;24(5):565-71. doi: 10.1111/j.1468-3083.2009.03472.x. Epub 2009 Oct 23. PubMed PMID: 19874433.
• Crawford GH, Pelle MT, James WD. Rosacea: I. Etiology, pathogenesis, and subtype classification. J Am Acad Dermatol. 2004 Sep;51(3):327-41; quiz 342-4. doi: 10.1016/j.jaad.2004.03.030. Review. PubMed PMID: 15337973.
• Elewski BE, Draelos Z, Dréno B, Jansen T, Layton A, Picardo M. Rosacea – global diversity and optimized outcome: proposed international consensus from the Rosacea International Expert Group. J Eur Acad Dermatol Venereol. 2011 Feb;25(2):188-200. doi: 10.1111/j.1468-3083.2010.03751.x. Epub 2010 Jun 25. PubMed PMID: 20586834.
EARLY AGING
Early aging is a complex of skin changes including sunspots, wrinkles, sagging skin, dry or itchy skin, skin thinning, and hair loss.
WHAT CAUSES EARLY AGING?
As aging is not a homogenous process, there exists a multitude of factors contributing to early age changes. These include environmental exposures, socioeconomic stressors, lifestyle choices, and one’s own genetics. Those causes most commonly implicated in early aging of the skin include sun and UV light exposure, stress, drug use (particularly methamphetamine abuse and tobacco smoking), and air pollution.
TREATING EARLY AGING
Good lifestyle habits, including managing stress and sleeping regularly, weighs heavily in prevention of early aging. Additionally, abstaining from drugs and alcohol, eating a well-balanced diet with healthy fats and reduced simple carbohydrates and sugars, and drinking enough water is essential. This will fuel your body with the necessary components to build and maintain healthy skin as your cell activity slows down in this phase of life. Supplements, such as iron and vitamin D, can aid in this endeavor.
UV-protective strategies, including photoprotective clothing and mineral-based sunscreens (zinc, titanium dioxide) with SPF ≥ 30 and avoiding tanning beds is critical.
There are numerous medical treatments for early aging, depending upon the main cause. Topical medications, including retinoic acid derivatives, azelaic acid, and niacinamide, are treatment mainstays in reversing aging signs, such as fine lines and dark spots. Chemical peels and laser treatments, as well as various injectables (fillers and neurotoxins) also have a marked impact on improving overall appearance of aged skin.
REFERENCES
• Bayerl C. [Skin aging and evidence-based topical strategies]. Hautarzt. 2016 Feb;67(2):140-7. doi: 10.1007/s00105-015-3737-3. PubMed PMID: 26683808.
• Yonei Y, Ichihashi M, Takabe W. Age-related diseases of the skin and anti-aging medicine. Nihon Rinsho. 2016 Sep;74(9):1541-1547. Review. PubMed PMID: 30557490.
MELASMA
Melasma is a common, asymptomatic condition of hyperpigmentation due to overactive pigment-producing skin cells (melanocytes) afflicting mostly women in their reproductive years. It is a chronic, recurring disorder affecting heavily sun-exposed areas, particularly the face.
Melasma lesions typically present as light brown-grey brown, irregularly-shaped macules and patches (small and big flat spots) symmetrically, usually along the nose bridge, upper lip, cheeks, forehead, and chin.
WHAT CAUSES MELASMA?
The pathogenesis of melasma is multifaceted; main triggers or predilections for its development include one’s UV light exposure, genetics, hormonal changes (pregnancy, oral contraceptives, hormonal treatments), and skin phototype. Additional factors contributing to the appearance of melasma include the use of photosensitizing drugs and zinc deficiency.
TREATING MELASMA
Treating melasma is challenging with frequent relapses commonplace. As causative factors are multifold, so, too, then must be the treatment plan. Caring for melasma starts with photoprotective strategies, such as sunscreen, sun avoidance, and sun-protective clothing. Topical therapy is then incorporated with the use of skin lighteners, such as hydroquinone, azelaic acid, niacinamide, kojic acid, and retinoids. Oral medications, such as Polypodium leucomotos and glutathione, are second-line agents. For those with extensive or refractory lesions, chemical peels and lasers may be considered.
REFERENCES
• Bak H, Lee HJ, Chang SE, Choi JH, Kim MN, Kim BJ. Increased expression of nerve growth factor receptor and neural endopeptidase in the lesional skin of melasma. Dermatol Surg. 2009 Aug;35(8):1244-50. doi: 10.1111/j.1524-4725.2009.01219.x. Epub 2009 May 12. PubMed PMID: 19438666.
• Grimes PE. Melasma. Etiologic and therapeutic considerations. Arch Dermatol. 1995 Dec;131(12):1453-7. doi: 10.1001/archderm.131.12.1453. Review. PubMed PMID: 7492140.
• Passeron T. Melasma pathogenesis and influencing factors – an overview of the latest research. J Eur Acad Dermatol Venereol. 2013 Jan;27 Suppl 1:5-6. doi: 10.1111/jdv.12049. Review. PubMed PMID: 23205539.
• Rajaratnam R, Halpern J, Salim A, Emmett C. Interventions for melasma. Cochrane Database Syst Rev. 2010 Jul 7;(7):CD003583. doi: 10.1002/14651858.CD003583.pub2. Review. PubMed PMID: 20614435.
PSORIASIS
Psoriasis is a common, immune-mediated, inflammatory skin disease with a strong polygenic component and multiple clinical subtypes. The most common of these subtypes is plaque psoriasis, which presents as sharply defined, erythematous (reddened), itchy plaques. The scalp, elbows, knees, and buttocks are most often affected. Additional subtypes less commonly seen are:
Guttate psoriasis: multiple smaller, erythematous plaques with a “rained-on” appearance along the torso and extremities
Pustular psoriasis: numerous tiny pustules develop superficially on the skin, often with accompanying erythema and/or fever. There are several pustular variants: von Zumbusch, annular pattern, exanthematic, localized patterns, and pustulosis of the hands and feet.
Erythrodermic psoriasis: extensive erythema, peeling, and scaling throughout the entire body. While uncommon, this condition makes patients more susceptible to complications due to their compromised skin barrier. They are often unable to properly regulate their body temperature or protect against infection or fluid loss.
WHAT CAUSES PSORIASIS?
Psoriasis has a strong polygenic component, meaning multiple genetic factors influence the development of the disease. These genetic predilections, when combined with environmental triggers, such as infections, medications, injury, and stress, result in the exacerbation of psoriatic lesions.
TREATING PSORIASIS
While there exists no cure for psoriasis, the goal of treatment is to maintain control of the disease and prevent widespread lesions. Limited disease can be treated with topical therapies, such as corticosteroids, vitamin D analogs, calcineurin inhibitors, and retinoids. More extensive disease may necessitate the use of phototherapy or systemic medications such as methotrexate, cyclosporine, oral retinoids, or biologic immune modifiers. These medications, while having the ability to clear lesions within several weeks, require informed consideration and prior lab work, due to their immunosuppressive effects.
REFERENCES
• Bolognia, J., Jorizzo, J. L., & Schaffer, J. V. (2012). Dermatology. Philadelphia: Elsevier Saunders.
• Menter A, Griffiths CE. Current and future management of psoriasis. Lancet. 2007 Jul 21;370(9583):272-284. doi: 10.1016/S0140-6736(07)61129-5. Review. PubMed PMID: 17658398.
• Michalek IM, Loring B, John SM. A systematic review of worldwide epidemiology of psoriasis. J Eur Acad Dermatol Venereol. 2017 Feb;31(2):205-212. doi: 10.1111/jdv.13854. Epub 2016 Aug 30. Review. PubMed PMID: 27573025.
COLLAGEN LOSS
The most abundant protein in our skin is collagen, which provides a kind of scaffolding for our skin. Natural aging results in a breakdown of collagen and elastic fibers of the skin. This loss, combined with decreasing hyaluronic acid content, results in the formation of wrinkles, sagging skin, and an overall deflated appearance.
WHAT CAUSES COLLAGEN LOSS?
Collagen production naturally begins to slow after age 35, with loss directly attributable to hormonal changes accompanying the aging process. This process accelerates after menopause. However, the causes of premature collagen loss are multifactorial. They include sun and UV light exposure, tobacco smoking, air pollution, and an inflammatory diet.
TREATMENTS FOR COLLAGEN LOSS
Unfortunately, even though collagen loss can have a dramatic impact on the psycho-social health of individuals, these treatments are not typically considered medically necessary by insurance. As such, collagen loss therapy is considered cosmetic and incurs an out-of-pocket cost.
Hormone replacement therapy, such as estrogen and DHEA supplementation, can help reduce the rate of collagen loss. Injectable therapies, such as hyaluronic acid fillers (i.e., Juvederm and Restylane products), can be used to increase fullness in lips and cheeks, and for facial contouring to decrease the appearance of wrinkles and sagging skin. Fractionated lasers (Fraxel) and microneedling stimulate neocollagenesis (new collagen growth) through micro-injuries that promote the release of growth factors necessary to induce collagen production. There are a plethora of treatments to choose from, all of which should be discussed with a dermatology provider in order to choose the best treatment plan to meet your skincare goals.
REFERENCES
• Castelo-Branco C, Duran M, González-Merlo J. Skin collagen changes related to age and hormone replacement therapy. Maturitas. 1992 Oct;15(2):113-9. doi: 10.1016/0378-5122(92)90245-y. PubMed PMID: 1345134.
• Fabbrocini, G., Mazzella, C., & D’Andrea, M. (2020). Microneedling for Neocollagenesis of the Face. In Minimally Invasive Aesthetic Procedures (pp. 625-630). Springer, Cham.
• Moragas A, Castells C, Sans M. Mathematical morphologic analysis of aging-related epidermal changes. Anal Quant Cytol Histol. 1993 Apr;15(2):75-82. PubMed PMID: 8318130.
• Varani, J., Dame, M. K., Rittie, L., Fligiel, S. E., Kang, S., Fisher, G. J., & Voorhees, J. J. (2006). Decreased collagen production in chronologically aged skin: roles of age-dependent alteration in fibroblast function and defective mechanical stimulation. The American journal of pathology, 168(6), 1861–1868. https://doi.org/10.2353/ajpath.2006.051302
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Navigating the Brain: Innovations in Neuro Endovascular Surgery
Introduction
Navigating the intricate pathways of the brain requires precision, skill, and cutting-edge technology. Say’s Dr. Ameer Hassan, neuro endovascular surgery has emerged as a groundbreaking approach to treating a wide range of cerebrovascular conditions, offering minimally invasive solutions with reduced risks and faster recovery times. In this article, we will explore the innovations in neuro endovascular surgery, highlighting its transformative impact on the treatment of complex neurological disorders.
Understanding Neuro Endovascular Surgery
Neuro endovascular surgery, also known as interventional neuroradiology or endovascular neurosurgery, involves the use of catheters, guidewires, and microcatheters to access and treat conditions affecting the blood vessels of the brain and spine. This minimally invasive approach allows neurosurgeons to deliver treatments directly to the site of the pathology, reducing the need for open surgery and minimizing trauma to surrounding tissues.
Innovations Driving Advancements
1. Advanced Imaging Techniques: Innovations in imaging technology, such as digital subtraction angiography (DSA), magnetic resonance imaging (MRI), and computed tomography (CT) angiography, provide detailed images of the brain’s blood vessels, enabling neurosurgeons to precisely visualize and navigate the intricate anatomy.
2. Endovascular Devices and Tools: The development of specialized catheters, guidewires, microcatheters, and embolic agents has revolutionized neuro endovascular surgery, allowing neurosurgeons to perform a wide range of procedures with greater precision and efficacy.
3. Minimally Invasive Techniques: Neuro endovascular surgery offers minimally invasive alternatives to traditional open surgery for treating aneurysms, arteriovenous malformations (AVMs), stroke, and other cerebrovascular conditions. These techniques reduce the risk of complications, shorten hospital stays, and accelerate recovery times for patients.
Applications in Clinical Practice
Neuro endovascular surgery is used to treat a variety of cerebrovascular conditions, including:
1. Aneurysm Repair: Endovascular coiling and flow diversion techniques are used to treat both ruptured and unruptured cerebral aneurysms, reducing the risk of bleeding and preventing future complications.
2. AVM Embolization: Endovascular embolization is performed to block abnormal blood vessels in arteriovenous malformations, reducing the risk of bleeding and improving neurological outcomes.
3. Ischemic Stroke Intervention: Endovascular thrombectomy is used to remove blood clots from blocked arteries in the brain, restoring blood flow and minimizing brain damage in patients with acute ischemic stroke.
Challenges and Future Directions
While neuro endovascular surgery offers significant benefits, it also presents challenges such as radiation exposure, contrast-induced nephropathy, and the risk of procedural complications. Ongoing research and development efforts are focused on addressing these challenges and further advancing the field of neuro endovascular surgery through innovations in imaging technology, device design, and procedural techniques.
Conclusion Innovations in neuro endovascular surgery have transformed the landscape of neurosurgical care, offering minimally invasive solutions for treating complex cerebrovascular conditions. By leveraging advanced imaging techniques, endovascular devices, and minimally invasive techniques, neurosurgeons can navigate the intricate pathways of the brain with unprecedented precision and efficacy. As technology continues to evolve and research progresses, the future of neuro endovascular surgery holds great promise for improving patient outcomes and advancing the field of neurosurgical intervention
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Friday, September 22, 2023
How To Control Lyme Disease
Must read
Stage : Early Localized Disease
Thermacell Tick Control Tubes: Kill Ticks, Prevent Lyme Disease
Symptoms of Lyme disease usually start 1 to 2 weeks after the tick bite. One of the earliest signs of the disease is a bulls-eye rash.
The rash occurs at the site of the tick bite, usually, but not always, as a central red spot surrounded by a clear spot with an area of redness at the edge. It may be warm to the touch, but it isnt painful and doesnt itch. This rash will gradually fade in most people.
The formal name for this rash is erythema migrans. Erythema migrans is said to be characteristic of Lyme disease. However, many people dont have this symptom.
Some people have a rash thats solid red, while people with dark complexions may have a rash that resembles a bruise.
The rash can occur with or without systemic viral or flu-like symptoms.
Other symptoms commonly seen in this stage of Lyme disease include:
What If A Tick Bites My Dog
The more ticks in your region, the likelier it is that your furry pal will bring them home.
Your dog is much more likely to be bitten by a tick than you are. And where Lyme disease is common, up to 25% of dogs have had it at some point.
About 10% of dogs with Lyme disease will get sick. 7-21 days after a tick bite, your dog might seem like theyâre walking on eggshells. They also might have a fever and enlarged lymph nodes. Plus, they might seem tired. Dogs also get antibiotics for Lyme.
What if my dog brings ticks into my home?
Use a tick control product on your pet to prevent Lyme disease. Also, have your dog vaccinated against Lyme.
Check your dogâs whole body each day for bumps. If you notice a swollen area, see if thereâs a tick there. If you find a tick, wear gloves while you use tweezers to separate it from your dog. Then, put it in soapy water or alcohol, or flush it down the toilet.
Use alcohol to clean the spot on your dog where the tick was attached. Keep an eye on that spot, and also on your dog to make sure theyâre behaving normally. If you notice any changes, check with your vet.
Show Sources
John Aucott, MD, assistant professor of medicine, Johns Hopkins University School of Medicine director, Johns Hopkins Lyme Disease Clinical Research Center.
CDC.
Morbidity and Mortality Weekly Report: âVital Signs: Trends in Reported Vectorborne Disease Cases — United States and Territories, 2004-2016.â
American College of Rheumatology.
Tick Talk On Ixodes Scapularis
Ixodes scapularis require high humidity, so they tend to be associated with habitats that are heavily shaded and covered with leaf litter. Tick habitats also include areas where hosts are frequently observed such as brush piles, stone wall bases, wood piles, wooded areas, edges of fields, and areas with low dense woody vegetation. White-tailed deer and white-footed mice are the primary hosts in the northeast of the United States. The large habitat of these hosts allows for a wide distribution.
Ixodes scapularis require two years to complete their life cycle from egg to larvae to nymph to adult. Adults are typically active from October-May but can be found year-round if the temperature exceeds freezing. Adults prefer larger hosts such as deer and humans. Once females fully engorge on their blood meal, they drop off the host into the leaf litter where they lay an egg mass in late spring, early summer. Larvae emerge from the egg mass in late summer and can attach to any size mammalian host and many bird species. After a blood meal the larvae will molt and re-emerge the following spring as a nymph. Nymphs are most active May-August. The poppy seed sized nymphs are known to be the most responsible in human disease transmission due to their extremely small size, often going unnoticed when attached. The nymphal ticks that have fed, as larvae, on infected hosts during the prior summer are now able to transmit the pathogens to people and their pets
Also Check: Natural Protocol For Lyme Disease
How Is Lyme Disease Diagnosed
Diagnosing Lyme disease can be difficult as symptoms vary from person to person. Symptoms can also be similar to other illnesses.
A diagnosis of Lyme disease is based on:
Laboratory testing may be recommended for patients with signs, symptoms and history of exposure to tick bite to support a clinical diagnosis.
Seek your health care provider right away if you develop symptoms of Lyme disease after being bitten by a tick or if you visited a known at risk area for Lyme disease. The earlier a diagnosis is made, the greater the chance of a successful treatment.
What Are The Symptoms Of Lyme Disease
This bookmark describes tips for preventing Lyme disease ...
Early symptoms of Lyme disease start between 3 to 30 days after an infected tick bites you. The symptoms can include:
• A red rash called erythema migrans . Most people with Lyme disease get this rash. It gets bigger over several days and may feel warm. It is usually not painful or itchy. As it starts to get better, parts of it may fade. Sometimes this makes the rash look like a “bull’s-eye.”
• Fever
• Muscle and joint aches
• Swollen lymph nodes
If the infection is not treated, it can spread to your joints, heart, and nervous system. The symptoms may include:
• Severe headaches and neck stiffness
• Additional EM rashes on other areas of your body
• Facial palsy, which is a weakness in your facial muscles. It can cause drooping on one or both sides of your face.
• Arthritis with severe joint pain and swelling, especially in your knees and other large joints
• Pain that comes and goes in your tendons, muscles, joints, and bones
• Heart palpitations, which are feelings that your heart is skipping a beat, fluttering, pounding, or beating too hard or too fast
• Shooting pains, numbness, or tingling in the hands or feet
Also Check: Lyme Disease And Behavior Problems
Keeping Cells Free Of Debris
You depend on your immune system to keep the spaces between cells free of debris so that they get good flow. Specialized immune cells, called macrophages, constantly patrol your tissues searching for debris they are the garbage collectors of the immune system. Macrophages engulf debris from dead cells and then break it down with strong acid and potent free radicals.
This process is happening in the body all the timeyou couldnt survive without it. As long as the collection of debris doesnt exceed the capacity of the immune system to clean it up, you never know its happening. Its deemed inflammation only when accumulation of debris from cell turnover is greater than the immune system can process.
Tissues congested with debris stresses cells. When cells suffer, you feel it as symptoms. The type of symptoms depend on the types and location of cells that are suffering. Symptoms associated with inflammation can be transient and localized when cell injury is finite, such as with an acute injury, or chronic and systemic when cell injury is ongoing, such as with chronic Lyme disease or really any chronic illness.
Lets take a look at inflammation in more detail, particularly chronic inflammation as it impacts people with Lyme disease, along with the best ways to quash it.
How Is It Treated
The main treatment for Lyme disease is antibiotics. These medicines usually cure Lyme disease within 3 weeks of starting treatment.
It’s important to get treatment for Lyme disease as soon as you can. If it goes untreated, Lyme disease can lead to problems with your skin, joints, nervous system, and heart. These can occur weeks, months, or even years after your tick bite. The problems often get better with antibiotics, but in rare cases they can last the rest of your life.
Don’t Miss: Lab Work For Lyme Disease
Overview Of Lyme Disease Pain Control
Most people with Lyme have pain. In this article I review the causes of Lyme pain and the steps a person can take to control and eliminate pain. I provide a strategy for controlling Lyme disease pain which uses:
• Sleep,
• Anti-cytokine herbs and supplements to lower inflammation,
• Supplements that support repair of mitochondria cell energy factories,
• Low dose naltrexone ,
• Medical marijuana and/or CBD oil,
• Magnesium to relax muscles,
Should You Use Antibiotics
How to prevent Lyme Disease
Different antibiotics may be used to treat children and adults. The decision to take medicines for Lyme disease may be based on one or more of these factors:
• You have symptoms of Lyme disease, especially the red, circular rash, and a history of exposure to ticks in geographic regions where Lyme disease is known to occur.
• Blood tests show that you have antibodies to the Lyme disease bacteria in your blood, spinal fluid, or joint fluid.
• You are pregnant or breastfeeding and are bitten by a tick.
Recommended Reading: Lyme Disease And Muscle Pain
What Causes Chronic Lyme Disease
The CDC says 10% to 20% of people treated for Lyme disease develop ongoing symptoms. These can include fatigue, joint and muscle pain, and thinking problems. The symptoms can last more than 6 months.
No one knows what causes chronic Lyme disease. One theory is the infection damages tissues or alters the immune system.
Some pain experts think the immune systemâs reaction to the Lyme infection causes changes that increase pain sensations and contribute to fatigue and poor sleep.
More research is underway.
No matter the cause, the symptoms are real. But most patients get better over time.
Show Sources
Neurologic Pain In Lyme Disease
Lyme disease can also cause neurologic pain. Nerve pain has qualities of sharp, stabbing, shooting, piercing, or electrical type pain. These qualities of pain occur when Lyme germs directly injure nerves. Or it occurs as a result of inflammation of those nerves from cytokines.
There is a second type of nerve pain known to occur in people with fibromyalgia and MS, that likely occurs in people with Lyme disease. This is due to infection in the brain activating a brain immune cell called microglia. When infections activate Toll-like receptors on microglia, this leads to neurologic pain felt throughout the body. Some think this is the cause of the muscle pain seen in people with fibromyalgia. It is also likely a major cause of the myalgia seen in Lyme disease.
Lyme Disease Pain Strategy
For nerve pain due to microglia activation in the brain, one strategy is to block the Toll-like receptors to stop the microglia from turning on. LDN helps with this.
Another strategy is to decrease the inflammation of nerves. LDN, anti-cytokine herbs, and medical marijuana/cbd oil may help with this.
The last nerve strategy is to decrease the nerve signals that transmit nerve pain. Sleep helps with this, medical marijuana/cbd, prescriptions anti-seizure prescriptions and anti-depression prescriptions can help this too.
Recommended Reading: Natural Remedies To Cure Lyme Disease
When Should You Call Your Doctor
• A tick is attached to your body and you are unable to remove the entire tick.
• You have a circular red rash that expands over the course of several days, especially if you know you were recently exposed to ticks. You may also have flu-like symptoms, such as fatigue, headache, stiff neck, fever, chills, or body aches.
• You feel very tired or have joint pain , irregular heartbeats, severe headache, or neck pain.
• You are pregnant or nursing and you think you may have been exposed to ticks.
Transmission Dynamics Of Tbds
Tick Prevention Guide
Pathogens can be acquired by ticks while feeding on infected hosts. In suitable tick vectors, TBPs have the ability to persist throughout the molting process to the next instar, a phenomenon called transstadial transmission. The efficiency of vertical transmission, from female tick to her offspring, varies from non-detectable for B. burgdorferi and B. microti , to ~40% for B. venatorum to close to 100% for R. helvetica . Ixodes ricinus is capable to transmit more than twenty different pathogenic parasites, bacteria and viruses via their blood meal to vertebrate hosts . Pathogen transmission by ticks requires many often unexplored tick-pathogen interactions, from the migration of these pathogens from the gut to their secretion in tick saliva .
Transmission dynamics can also be affected by weather and climatic conditions. The seasonal synchrony of larval and nymphal stages is an important driver of non-systemic transmission of TBEV via co-feeding of infected nymphs with uninfected larvae. This synchrony in tick activity and feeding, in turn, is affected by temperature patterns, in particular autumn cooling and spring warming . Climate change might therefore not only affect the distribution of ticks themselves, but also the distribution and nymphal infection rate of TBEV, and maybe also of other TBPs .
Read Also: Snow Plowing East Lyme Ct
Genetic Engineering For Reservoir And Vector Incompetence
The advent of CRISPR/Cas technologies have made targeted engineering of mice feasible. By incorporating the CRISPR/Cas machinery into an engineered cassette called a gene-drive and inserting it into the chromosome, animals can pass along the engineered trait in a dominant, non-Mendelian pattern as the inserted gene will create a copy of itself onto the other chromosome. Investigators have proposed using this tool to create B. burgdorferi resistant mice carrying a gene to express an anti-OspA antibody . Proof of principle studies are being carried out in mice without the use of the gene drive, but ultimately, use of gene drive technology could prove to be a low-cost mechanism for changing reservoir competence of an entire population of mice. However, the path to using this technology will be difficult due to concerns about the ability to control unforeseen events caused by a self-replicating, engineered mutation.
A similar genetic engineering strategy could be undertaken with a focus on ticks. Engineering ticks to be of a single sex to reduce tick populations or elimination of specific proteins required for vector competence could be an effective strategy for controlling tick transmitted diseases. Similar strategies have been proposed for mosquitos in the control of dengue virus . However, Ixodes tick biology with its 2-year cycle, may make tick gene drive approaches very challenging.
What Are The Stages Of Lyme Infection
There are three stages:
• Early localized Lyme: Flu-like symptoms like fever, chills, headache, swollen lymph nodes, sore throat, and a rash that looks like a bull’s-eye or is round and red and at least 2 inches long
• Early disseminated Lyme: Flu-like symptoms like pain, weakness, or numbness in your arms and legs, changes in your vision, heart palpitations and chest pain, a rash , and a type of facial paralysis known as Bellâs palsy
• Late disseminated Lyme: This can happen weeks, months, or years after the tick bite. Symptoms might include arthritis, severe fatigue and headaches, dizziness, trouble sleeping, and confusion.
About 10% of people treated for Lyme infection donât shake the disease. They may go on to have three core symptoms: joint or muscle pain, fatigue, and short-term memory loss or confusion. This is called post-treatment Lyme disease syndrome. It can be hard to diagnose because it has the same symptoms as other diseases. Plus, there isn’t a blood test to confirm it.
Experts arenât sure why Lyme symptoms donât always go away. One theory is that your body keeps fighting the infection even after the bacteria are gone, like an autoimmune disorder.
Recommended Reading: What Is Lyme Disease And What Are The Symptoms
Stage : Early Disseminated Lyme Disease
Early disseminated Lyme disease occurs several weeks to months after the tick bite.
Youll have a general feeling of being unwell, and a rash may appear in areas other than the tick bite.
This stage of the disease is primarily characterized by evidence of systemic infection, which means infection has spread throughout the body, including to other organs.
Symptoms can include:
• disturbances in heart rhythm, which can be caused by Lyme carditis
• neurologic conditions, such as numbness, tingling, facial and cranial nerve palsies, and meningitis
The symptoms of stages 1 and 2 can overlap.
What’s The Best Way To Prevent A Tick Bite
Are you risking Lyme disease? Hereâs how to remove ticks
Ticks can’t fly or jump. But they live in shrubs and bushes and can grab onto you when you pass by. To avoid getting bitten:
• Wear pants and socks in areas with lots of trees and when you touch fallen leaves.
• Wear a tick repellent on your skin and clothing that has DEET, lemon oil, or eucalyptus.
• For even more protection, use the chemical permethrin on clothing and camping gear.
• Shower within 2 hours after coming inside. Look for ticks on your skin, and wash ticks out of your hair.
• Put your clothing and any exposed gear into a hot dryer to kill whatever pests might be on them.
How do you know if you’ve been bitten?
Since ticks are so small, you’ve got to have pretty good eyes to see them.
If you have a small, red bump on your skin that looks like a mosquito bite, it could be a tick bite. If it goes away in a few days, itâs not a problem. Remember, a tick bite doesnât necessarily mean you have Lyme disease.
If you notice a rash in the shape of a bull’s-eye, you might have a tick bite. Talk to your doctor about treatment.
If you have an allergic reaction to ticks, you’ll notice a bite right away.
You May Like: Can Lyme Disease Cause Liver Damage
Clinical Presentation Of Other Tbds
In Europe, human babesiosis is caused by B. microti, B. divergens and B. venatorum . All Babesia species infect erythrocytes and cause haemolysis, leading to the clinical manifestations of fever, anaemia, jaundice, haemoglobinuria and potentially also renal insufficiency. Over 40 human babesiosis cases have been reported in Europe, mostly in asplenic patients. Other risk factors are immunosuppression, depletion of mature B-cells and old age . Judging from the discrepancy between case reports and seroprevalence, an asymptomatic and/or self-limiting course is common . Although serious infection appears to be uncommon, when acquired, the disease has a mortality rate of 42% in B. divergens and 5% in B. microti . Babesia divergens is the causal agent of bovine babesiosis in Europe. The clinical picture is similar to that seen in humans, with a bimodal seasonal occurrence of the disease that is associated with I. ricinus activity. In cattle, an inverse age resistance phenomenon is present in which calves up to the age of 912 months are susceptible for infection, but resistant to disease .
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What Is Cancer And What Causes Cancer
What Is Cancer?
Simply put, cancer is a growth in the body that’s outside of the body’s control and which operates on its own agenda. It’s unique among other tissues in that it doesn’t recognize itself as part of the body. Every normal tissue acts cooperatively with the rest of the body, but not cancer. It will grow, invade and metastasize, as it takes everything that it needs from the body to do that. And all at the body’s expense.
A number of things contribute to the development of cancer. The most well identified causes of cancer, in the scientific literature, are genetic instability and DNA damage. The cause of DNA damage has been traced most reliably to environmental toxins and radiation, but a diet void of nutrients and high in refined carbohydrates and poor quality fats, such as hydrogenated fats, also damages DNA. Trans-fatty acids, for example, have been known to alter DNA. So it’s not necessarily just about industrial toxins, but also denatured food. There’s a lot more cancer today than there was 50 years ago, as the quality of food deteriorates.
For Cancer To Occur, There Must Be Break Down
Research has shown that for cancer to occur in the body multiple normal functions must break down. Therefore multiple-agent treatments may be the only successful way to treat cancer. We used well-tolerated natural substances to assess their usefulness in combination anti-neoplastic (cancer-killing) therapy. The following has been the goal of our clinic in treating cancer patients: It is not enough to repair genetic damage or to stop angiogenesis (the formation of new blood vesicles) and neglect to reverse all other cancer-causing problems. It is also not enough to attack metastases and leave the primary tumor in a comfortable environment. In order to defeat cancer, it must be attacked at every level and with every method necessary to reverse cancer’s multiple-layered assault on the body, even if that means that some of the various treatments have redundant effects. And this all must be accomplished while maintaining the maximum possible wellbeing of the patient, and without sickening or weakening the patient.
The Seven Events That Must Occur For Cancer To Form
At least seven events must happen in the body before cancer can occur, so when formulating a treatment protocol for my patients, we take into account and address all of the ways in which cancer has attacked their bodies in order to reverse those events and thereby, their diseases.
As John Boik has described, cancer becomes possible, and has its only opportunity to arise in the body, when seven different events, such as genetic damage, angiogenesis, immune system evasion, etc. all occur,1 as listed below. Then, once established, cancer is adaptable enough to be able to thrive and grow with the continuation of just one or a few of those deviant events.
Boik describes the seven pro-cancer events as follows:
1. Genetic instability or vulnerability to mutation, necessarily the first of the variety of events that lead to a tumor;
2. Abnormal gene expression, in this case that produce proteins that facilitate cancer, or at least do not prevent it;
3. Abnormal and autonomous cell signal transduction, which allows cancer cells to grow through self-stimulation rather than depending on growth factors from other cells;
4. Abnormal cell-to-cell communication, which sets a tumor apart from its neighbouring cells metabolically, leaving the tumor in a position to ignore homeostatic mechanisms and, unlike cells throughout the rest of the body, to act in the best interests of the tumor rather than in the best interests of the organism.
5. Angiogenesis, the creation of blood vessels and resultant hoarding by the tumor of disproportionately large amounts of blood-borne molecules;
6. Invasion and metastasis, which not only results from the aggressive nature of the tumor, but also the low integrity and too friable nature of the surrounding normal tissue and basement membranes;
7. Evasion of the immune system, which involves both camouflage functions and immune-disabling functions of cancer cells.
Once Cancer Is Established In The Body
Once established in the body, cancer seems to have the ability to thrive and reproduce despite most of the efforts against it by oncologists, and without necessarily requiring all seven of the above pro-cancer events to still be in place. Therefore, without certain knowledge of the precise mechanisms governing any one patient’s cancer, any therapy that targets fewer than those seven major disturbances leaves the body of the cancer patient potentially vulnerable to the disastrous result of allowing continued growth of existing tumors. Shortchanging the patient of a diverse range of available, effective, well-tolerated, well-targeted, compatible, complementary and feasible treatment options also would allow too many of the conditions to persist that gave rise to tumors previously and may do so again, leaving the fertile ground and pro-neoplastic conditions that produced the cancer in the first place. For this reason, successful cancer therapy should be multi-purposed and with multiple agents, many more than are now used with each patient by oncologists.
We have used natural therapies for cancer treatment, because they are well adapted for multi-agent use. Unrefined plant materials have tens of thousands or more phytochemical components, originally useful for protecting a plant from extreme or adverse conditions in its environment, and ultimately employed as described below by naturopathic physicians in adaptation to the needs of the human patient. Because of thorough medical training as licensed naturopathic physicians, having more classroom hours and more than twice the number of courses in medical school as Medical Doctors2, as well as extensive training in the use of natural agents, we are well suited to choose appropriate combinations of natural therapies for the individual cancer patient. We also take advantage of the greater compatibility among natural substances than among numerous pharmaceuticals. It seems obvious that a meal may contain many different foods without the need for conscious consideration of potential interactions among nutrients and plant molecules. In the same way, we have combined many different nutrients and plant materials in each cancer patient’s treatment protocol, with regard for the specific cancer burden in the body, the origin of the cancer, the nature of that particular patient’s cancer and any co-morbid conditions.
The Treatment
More importantly than knowing what cancer is, is how to treat it. The treatments we do at Nature Works Best cancer clinic are multi-faceted. There’s a popular delusion among oncologists and practitioners of natural medicine that cancer can be fought with one well-chosen substance. Nothing could be further from the truth, in fact this viewpoint is disastrous for most patients, for the following reasons. Many agents are needed to fight cancer, primarily because it arises after several normal mechanisms in the body have broken down. Cancer preys on the body in numerous ways simultaneously, and no single agent, whether chemotherapeutic or natural, has yet been found to have enough anti-neoplastic (cancer-killing) effects to reverse all of those abnormalities in all patients and be “the cure” for cancer.
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Progressive Supranuclear Palsy (Steele-Richardson-Olszewski Syndrome)
What is Progressive Supranuclear Palsy?
Progressive supranuclear palsy (known as PSP) is a rare disorder that occurs as a result of damage to the brain cells. It causes problems with balance, coordination and speech and also affects vision and the ability to swallow properly. PSP is a progressive condition, which means that it gets worse over the course of time.
In most cases, PSP affects people aged over 60 years of age. It is thought to affect around 4,000 people in the UK, but the number may actually be higher as some cases are misdiagnosed.
What causes PSP?
PSP results from damage to the brain cells, which occurs when a form of protein called tau collects in the brain. It is normal to find tau in the brain, but it is normally broken down before it can reach excessive levels. In people with PSP, the protein is not broken down and this leads to a build-up, which results in collections in parts of the brain.
Although there is a belief that genetics may be involved, there is no evidence to suggest that faulty genes are inherited or passed down through generations and if you have a close relative with PSP, this doesn’t increase your risk of developing the condition.
What are the symptoms and signs?
PSP can cause a range of symptoms and it affects people in different ways. The nature and severity of symptoms may be heavily dependent on the location of the tau collections and the amount of tau in the brain. Examples of symptoms include:
• lack of balance and an increased risk of falling
• stiffness in the muscles
• involuntary eye movements
• slurred speech
• a loss of interest and enthusiasm
• dysphagia (problems with swallowing)
• difficulties related to memories
• sensitivity to light
• blurred vision
• double vision
• disturbed sleep patterns
As PSP is progressive, symptoms get worse with time. However, the rate at which the condition accelerates varies from one individual to another. When symptoms reach an advanced stage, it is common for people to need round the clock care. Swallowing is a particular worry, as there is a risk of choking and a feeding tube may be recommended. As balance and coordination deteriorate, there is also a high risk of falls and injuries, such as fractures, head injuries, bruising and dislocations.
How is PSP diagnosed?
PSP can be difficult to diagnose because the early symptoms are similar to other health conditions, most notably Parkinson’s disease.
Several types of test may be carried out to rule out other potential causes of symptoms, including strokes and Parkinson’s disease. Tests include CT and MRI scans and a PET scan (positive emission tomography). This test is used to identify radiation produced by substances injected into the body before the test begins. A DaT test can also be used to produce detailed images of the brain.
Sometimes it’s difficult to differentiate between PSP and Parkinson’s disease. In this case, a short course of medication may be prescribed to see if symptoms respond to treatment. The medication is known as levodopa. In cases of Parkinson’s disease, there is usually a significant improvement. However, in cases of PSP, improvement is minimal.
In some cases, patients may also be referred to a specialist neurologist for neuropsychological tests. These tests assess the ability to remember, concentrate and process information.
Treatment for PSP
There is no cure for PSP and sadly, there is no way of slowing the progress of the condition. However, there are treatments that can help to make people feel more comfortable and tackle some of the symptoms. Every individual with PSP is cared for by a multi-disciplinary team that includes a range of health professionals such as neurologists, physiotherapists, occupational therapist, speech therapists, social workers, ophthalmologists and specialist nurses.
There are no medicines proven to improve symptoms of PSP, however in the early stages, medication used to treat Parkinson’s disease may be beneficial. Sometimes, PSP can increase the risk of depression and anti-depressants may be prescribed in this case.
Physiotherapy can help to reduce stiffness, increase mobility and strengthen the muscles. Exercise is important, but it’s essential to do the right kinds of exercise and avoid overexertion. Breathing exercises can also help to reduce the risk of aspiration pneumonia, an infection that occurs when food debris falls into the lungs.
Speech and language therapy can help to improve speech and communication and also improve swallowing. As the ability to swallow becomes impaired, it may also be beneficial to follow an eating plan drawn up by a nutritionist.
PSP can affect eye sight and vision and regular eye tests are recommended. Botox can also be used to prevent involuntary movement of the muscles around the eyes. Some people prefer to wear dark glasses, as they become more sensitive to light.
As PSP is a progressive condition, palliative care is often provided in the advanced stages. This may be provided at a nursing home, hospice or hospital. It can often be beneficial for individuals and their families to plan in advance for when times get tougher and more assistance is required. The individual may have preferences in terms of where they want to be cared for and what kinds of care they hope to receive. Planning can also help to alleviate stress associated with making difficult decisions further down the line.
Living with PSP
Being diagnosed with PSP can be very distressing for the individual and their family. As the disease is progressive, you know that symptoms are going to get worse and gradually, you will need more help, support and assistance from the people around you, as well as health professionals. It can take time to come to terms with a diagnosis, but there are people who can help. Your care team can arrange counselling and the PSP Association also provides support for people affected by the condition.
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top of page
CBD or THC - What will benefit a cancer patient?
Cannabidiol (CBD) and tetrahydrocannabinol (THC) are both naturally occurring compounds found in plants in the cannabis genus. CBD was first isolated in 1940 whilst THC was isolated in 1964 by the preeminent cannabis scientist Raphael Mechoulam. At the most fundamental level, THC and CBD are different because of their different physiological effects. CBD is non-psychotropic and therefore does not illicit a “high” whereas THC is psychotropic and is the only known cannabis-derived compound to illicit a “high”.
Cannabinoids are defined as chemical compounds that interact with the cannabinoid receptors, which in humans include CB1, predominantly expressed on neurons in the brain and central nervous system, and CB2 expressed in non-neuronal tissues such as immune cells. Cancer cells can express these receptors as well, and studies are mixed as to whether it can indicate a better or worse prognosis compared to cells that do not have the receptors. But the effects of cannabinoids on cancer are not limited to interaction with these receptors as several studies have documented effects that are not prevented by blocking these receptors. THC is the cannabinoid classically associated with the psychoactive and appetite-stimulating effects, although it is not exclusively so. Cannabidiol is another cannabinoid that also has been studied for anti-cancer effects and is often referred to as CBD.
In one study conducted in 2008 and published in the International Journal of Cancer, cannabinoids were applied to normal pancreatic cells and cancerous pancreatic cells. The results indicated that activation of the CB2 receptor may induce apoptosis of pancreatic cancer cells without affecting the normal cells.
Can cannabis alone cure cancer? The short answer is no. The long answer is more complex. Let’s get deep into it.
One should understand what cancer cells are, how they are different from normal healthy cells. Cancer cells are rogue cells, they fail to obey the cellular regulation that keeps them under control. In cancer cells due to certain changes in DNA leads to change in cellular physiology, they keep proliferating without any checks and balances.
Studies have demonstrated cannabinoids can slow the cancer progression for several cancer types including lung, glioma, thyroid, lymphoma, skin, pancreas, uterus, breasts, prostate and colorectal carcinoma both in vitro and in vivo. Certain preclinical studies have suggested that Δ9-THC and other phytocannabinoids may have anti-cancer effects in vitro and in vivo by exerting antiproliferative qualities on cancer cells.
The First research in the 1970s
The first study to show evidence of the anti-cancer effect in cannabis came out in 1975. That study, which oncologist Dr. Donald Abrams mentions in a 2019 article, “Should Oncologists Recommend Cannabis?”, showed that THC and CBD could inhibit the growth of certain lung cancer cells in test tube experiments. Abrams is a renowned integrative oncologist, clinician, medical cannabis pioneer, and medical professor at the University of California, San Francisco. Subsequent studies found that cannabinoids selectively killed glioblastoma (brain cancer) cells in mice while leaving normal cells untouched.
Listen to Joy Smith in the video below. She was diagnosed in July 2016 with ovarian cancer. In August 2017 she was given six weeks to live after it was discovered that cancer has spread to her stomach and bowel. But now she's in remission and claims cannabis oil cured her terminal disease.
Joy Smith after her miraculous recovery
In India also, patients have been treated with cannabis THC extract. The video released by the Great Legalisation Movement, India for their series called "The Gaanja Situation" shows a 75 years old patient called Cliff. He can be seen speaking about the treatment in this video.
CBD VS THC
Although THC oil does have cancer-curing effects it isn’t to the same degree as CBD since THC is psychedelic and CBD isn’t. THC has a similar effect as CBD on cancer cell proliferation but is associated with the undesirable psychotropic effect. It works differently from the CBD, but the downstream target protein involved in the cell proliferation controls are like CBD. Furthermore, few studies have demonstrated that when both THC and CBD are given together, they work better to cure cancer when compared to individual treatment.
THC causes the psychoactive effect of cannabis, whereas CBD is non-psychoactive. This means that it does not produce sensations of intoxication. CBD is even considered to be anti-psychotic in its effects, mediating and neutralizing the psychoactivity of THC. For this reason, recreational strains of cannabis generally contain higher levels of THC, while medicinal cannabis might focus on either CBD or THC, depending on the condition being treated together.
As a treatment for cancer
There’s solid evidence supporting the idea that cannabinoids can reduce tumor growth in animal models of cancer. CBD may also enhance uptake or increase the potency of certain drugs used to treat cancer.
Here are some promising studies:
· A 2019 review ofin vitro and in vivo studies focusing on pancreatic cancer found that cannabinoids can help slow tumor growth, reduce tumor invasion, and induce tumor cell death. The study authors wrote that research into the effectiveness of different formulations, dosing, and precise mode of action is lacking and urgently needed.
· A 2019 studyindicated that CBD could provoke cell death and make glioblastoma cells more sensitive to radiation, but with no effect on healthy cells.
· A large, long-term study of men within the California Men’s Health Study cohort found that using cannabis may be inversely associated with bladder cancer risk. However, a cause and effect relationship hasn’t been established.
· A 2014 study in experimental models of colon cancer in vivo suggests that CBD may inhibit the spread of colorectal cancer cells.
· A review of 35 in vitro and in vivo studies found that cannabinoids are promising compounds in the treatment of gliomas.
· Other research demonstrated the efficacy of CBD in pre-clinical models of metastatic breast cancer. The study found that CBD significantly reduced breast cancer cell proliferation and invasion.
When it comes to cancer prevention, CBD research has a long way to go. Scientists will have to conduct long-term studies of people using specific CBD products, controlling for frequency of use, dosing, and other variables.
Watch this video below where Dr. Erik Johnson explains how cannabis (THC) tetrahydrocannabinol kills cancer cells. It doesn't work as well on slow-dividing cells, but works quite well on the softer, smaller and more rapidly growing cancers (glial, pancreatic).
Unanswered questions
There are still many unanswered questions about the potential for using cannabinoids to treat cancer. It’s not clear:
· which type of cannabinoid – either natural or synthetic – might be most effective
· what kind of doses might be needed
· which types of cancer might respond best to cannabinoids
· how to avoid the psychoactive effects of THC
· how best to get cannabinoids, which don’t dissolve easily in water, into cancer cells
· whether cannabinoids will help to boost or counteract the effects of chemotherapy
These questions must be answered for cannabinoids to be used as safe and effective treatments for cancer patients. It’s the same situation for the many hundreds of other potential cancer drugs being developed and tested in university, charity and industry labs all over the world.
Before cannabinoids could be used in clinical trials, there is a need to explore more knowledge on several issues such as anti-tumorigenic and anti-metastatic mechanisms as well as which type of cancer patient populations would be more responsive for cannabinoid-based therapies.
Cancer treatments such as chemotherapy and radiation can produce an array of side effects, such as nausea and loss of appetite, which can lead to weight loss. CBD is also thought to have anti-inflammatory and anti-anxiety properties. So far, only one CBD product has received Food and Drug Administration (FDA) approval.That product is Epidiolex, and its only use is in the treatment of two rare forms of epilepsy. No CBD products have been FDA-approved to treat cancer or symptoms of cancer or to ease the side effects of cancer treatment.
On the other hand, two marijuana-based drugs have been approved to treat nausea and vomiting caused by chemotherapy. Dronabinol (Marinol) comes in capsule form and contains THC. Nabilone (Cesamet) is an oral synthetic cannabinoid that acts similar to THC. Another cannabinoid drug, nabiximols, is available in Canada and parts of Europe. It’s a mouth spray containing both THC and CBD and has shown promise in treating cancer pain. It’s not approved in the United States, but it is the subject of ongoing research.
CBD and THC are cannabidiols which have different medical properties. Both substances are considered relatively safe for humans and can be a helpful solution for the effective treatment of versatile health problems. They can have different side effects, accumulate in the body and can be detected using a simple drug test. Scientists are also looking into how CBD could aid cancer treatment, but more research is needed before any conclusions can be made.
Conclusion
We at Himalayan Hemp are working to bring back ancient ayurvedic treatments by using hemp and treating disease and conditions like multiple sclerosis, spinal cord injury, spinal cord disease, cancer, AIDS side effects, arthritis, epilepsy, inflammatory bowel disease, end of life care, insomnia, etc and conducting holistic research to treat more diseases.
If you have a question you'd like us to address or comments about this blog, please mail your suggestions to [email protected]. Have a look around our website and join us if you wish to.
Note:People should always talk to a doctor before using CBD or any other compound during cancer treatment to ensure that it will not react with any of the medications that they are taking.
Source:
https://www.healthline.com/health/cancer/cbd-for-cancer
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For a study, researchers sought to look at the prevalence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antibodies in pregnant women, their partners, and their babies, as well as the relationship between such antibodies and obstetric and neonatal outcomes. From April 4 to July 3, 2020, all pregnant women and their partners, as well as their babies, were asked to participate in the study at a single university hospital in Denmark. A pharyngeal swab and a blood sample were obtained from participating women and partners upon admission, and a blood sample was drawn from the umbilical cord soon after birth. The polymerase chain reaction was used to detect SARS-CoV-2 RNA in swabs, and blood samples were tested for SARS-CoV-2 antibodies. There was a complete medical history as well as obstetric and neonatal information accessible.
The study included 1,313 pregnant women (72.5% of all women hospitalized for delivery at the hospital throughout the study period), 1,188 partners, and 1,206 babies. The adjusted serologic frequency in women was 2.6%, and 3.5% in partners. SARS-CoV-2 immunoglobulin G (IgG) antibodies were found in 17 infants, but no immunoglobulin M antibodies were found. There was no link found between SARS-CoV-2 antibodies and obstetric or neonatal complications (e.g., preterm birth, preeclampsia, cesarean delivery, Apgar score, low birth weight, umbilical arterial pH, need for continuous positive airway pressure, or neonatal admission), but the statistical power to detect such differences was low. Full serologic data from 1,051 couples revealed a 39% absolute probability of maternal infection if the spouse had antibodies.
There was no link identified between SARS-CoV-2 infection and obstetric or neonatal problems. SARS-CoV-2 IgG antibodies were found in 67% of babies born to moms who had antibodies. The study had a disadvantage in that it lacked the statistical power to identify modest but potentially significant differences between patients with and without signs of illness.
Reference:journals.lww.com/greenjournal/Fulltext/2021/01000/Severe_Acute_Respiratory_Syndrome_Coronavirus_2.7.aspx
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Water Aerobics – Get Fit in Water
Water aerobics has a bit of a reputation for being something that the elderly do but in fact, it’s a great way for people of all ages to stay fit and healthy.
Physical Health is the key to sound mental and emotional health. As it’s said, ‘a healthy body breeds a healthy mind’. Going to a gym is not the only fitness activity! There is a plethora of activities to choose from- walking, jogging, yoga, running, sports, dance classes and various others. One such fun physical activity that has gained popularity in the recent times is water aerobics. Aerobics has been a popular form of exercise; especially for women for a very long time now, Water Aerobics is just a more intense, fun and beneficial form of aerobics.
There is a plethora of activities to choose from- walking, jogging, yoga, running, sports, dance classes and various others. One such fun physical activity that has gained popularity in the recent times is water aerobics. Aerobics has been a popular form of exercise; especially for women for a very long time now, Water Aerobics is just a more intense, fun and beneficial form of aerobics.
Water Aerobics
The benefits of Water Aerobics:
• Help improve physical and mental health.
• It helps release stress and tension.
• Reduces stress on joints and muscles; it strengthens the body and has great effects on weight management.
• It helps control blood pressure levels and works against anxiety issues or panic attacks.
• It maximizes resistance of the body, thus working on the core muscles. An overall body workout, with minimum stress!
• It benefits the spine, causing no unnecessary stress, resulting in better balance and improved body movements.
• It relieves the wear and tear of joints.
• It can help rehab a knee, hip or shoulder.
• Has also proven to get cardiovascular and strength training.
• See more
Most fitness activities target a specific area of the body or act upon stamina. Water Aerobics is probably the only fitness activity that works on all physical aspects, all at once! From muscle building, core strengthening, relieve joints, build stamina… every part of the body, inside and out, gets worked upon simultaneously. Water Aerobics is excellent for pregnant women and can really help soothe the physical discomforts that are a natural part of pregnancy. Even senior and elderly women can benefit from water aerobics and its low-intensity workout regime.
Each hour of water aerobics burns around 400 to 500 calories, on an average. This varies from individual to individual and as you continue regularly it becomes better! It includes a combination of fast and slow movements that work on the whole body and the changing pace helps increase the metabolism rate over time. The older we grow, our metabolism rate drops and becomes slower and slower. Water aerobics normalizes, and over time increases the metabolism rate. Being a group activity it also promises a lot of fun and entertainment.
Get more lifestyle tips on our news section.
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lungsEven though lungs are not hugely to blame for bad breath, there are the rare occasions that this has not been the case. If you have lung breath it will not go away by just simply brushing your teeth.
Lung breath is the result of two things: infection and disease or it could be from something that you have eaten or drank, that has entered into your bloodstream, and once having reached the lungs, will then release these bad smelling odours. Let’s firstly tackle the disease angle.
Any lung disease or disorder will lead to bad breath. Lung cancer usually causes a distinct breath odour, so much so that breath is now being used as an early indicator. Other lung disorders known to cause bad breath are cystic fibrosis and asthma. They both have an acidic smell associated with them.
It is not only lung diseases however, that can affect ones breath. As we breathe out we are basically removing carbon dioxide that is carried to our lungs by our blood. One example is diabetes. Diabetes has been known to give breath a sweet and fruity smell. The smell alone could be a clue in having it diagnosed. Kidney and liver disorders also send unwanted smells into the blood stream and will be released via the lungs.
Now that we know about lung diseases that can cause bad breath, let’s look at the ones that are not caused through diseases. These are the kinds that come from smoking, drinking and certain foods we eat. These kinds can cause your breath to smell three times worse and could originate from the mouth, the stomach and the lungs. But this article is only about the lungs.
Let’s start with smoking. The reason that smoking causes bad breath is because of the chemicals found in cigarettes like tar and nicotine. These chemicals build up in your mouth and stick to the teeth, gums, tongue and on the sides of the cheeks. Tar and nicotine cause bacteria to build up in your mouth and if you do not brush your teeth often after having a cigarette it can cause bad breath because the bad breath bacteria will thrive on these chemicals. Dry mouth because of smoking is another cause for bad breath. Smoking dries out the mouth because it stops the continuous flow of saliva. Our saliva is essential as it washes out all the bacteria which could cause bad breath. To keep the saliva flow going in your mouth try Therabreaths mandarin mint lozenges or our sugar free gum.
Next we move on to alcohol. The body treats alcohol as a toxin and will try to convert it to a less harmful chemical. Metabolism will convert 90% of the alcohol to acetic acid, and the rest will be released through the respiratory system and through sweat. Because alcohol enters the blood stream it will go to the lungs, and from there give you alcohol breath which you breathe out (this is how the breathalyzer works).
Now let’s look at food and how some can cause bad breath. Certain foods and drinks can cause bad breath by feeding the bacteria that give off the sulphur compound we experience as bad breath. We did an in depth article on all the different kinds of foods and drinks to avoid. The article is named Foods to avoid for better teeth and breath. In this article we listed as well as gave a detailed description of how they cause bad breath and stain the teeth.
Bad breath can be solved by keeping a good oral hygiene going through brushing your teeth at least twice a day with Therabreath toothpaste, by flossing and using Therabreath alcohol free mouth rinse.
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Mellplasztika után duzzanat
Kts s varratszeds utni napon rheti vz a fleket. A doh nyz nkn l gyakran diagnosztiz lnak k l nb z st dium term ketlens get, a f rfiakn l ugyanakkor erekt v diszfunkci t tal lnak m r 35-40 ves korukban.
Arr l nem besz lve, hogy a h zas let k zben folyton hajtogatni kell, ami engem nagyon zavar. A dilemma: mindig bevg a pnt oldalt. Fahey ltal alrt dokumentummal s az alr szemlyvel kapcsolatban.
A biolgiai tesztek eredmnye azt mutatta, hogy a PIP implanttumokban hasznlt szilikon sem sejtkrost (cytotoxikus), sem pedig genetikai llomnyt krost (genotoxikus azaz rkkelt) hatssal NEM rendelkezik. Termszetesen az is befolysolja az eredmny tartssgt, hogy az els mttre milyen letkorban kerl sor. A sznyogok elleni harcomrl, e szemtelen vrszvk elzsrl mr rtam, sajnos azonban nincsenek egyedl, tbb pimasz vendg, kellemetlen krtev is rkezhet hozznk Mellplasztika után duzzanat. Term szetesen ezt pontosan az elzetes vizsg lat sor n tudjuk meg llap tani, ahol kezel si javaslatot adunk, megbesz lj k az elny ket s h tr Mellplasztika után duzzanat s seg t nk, hogy n szem lyre szabottan a lehet legjobb megold st v laszthassa.
Az Mellplasztika után duzzanat ll f l miatt gyakori a szorong s, Mellplasztika után duzzanat. A fl formja s mrete az egsz arc karaktert meghatrozza. Ez egy norml mret implanttumnak felel meg. Arc plasztikai mttek sorn az arc vonsait lgyabb, A plasztikai sebszet ma mr egyszer megoldsokat knl a vltoztatsra vgyk szmra. Nagyon tsks szemeknl esetleg szksges lehet a zsrfelesleg (tskk) rszleges eltvoltsra, de gyakran inkbb a zsr-tcsoportostst vlasztjuk, azaz pl.
Terveim kztt szerepel a lzerkezelsek bevezetse (kros hegek kezelse, tetovls eltvolts, s brfeljts. Mellplasztika után duzzanat ker l r egy implant tum fej s arra a fogp tl s, korona.
Az MRI a rgebben beltetett szilikon implanttumok legjobb vizsgl mdszere. A pnzgyi tancsads termszetesen kltsgmentes pcienseink szmra s az adminisztratv gyek intzsben is segtsget nyjtunk, hogy minl hamarabb sor kerljn a rgta vgyott plasztikai beavatkozsra. Mellnagyobbts rak Budapest s Mellnagyobbts rak 2016. J megoldsnak tnhet, hiszen elvileg nem juttatsz a szervezetbe semmilyen kros anyagot, hanem csak kenegetsz. Az implant tum az egyik legmodernebb fog szati fogp tl si megold s.
A t l nagy mellek is okozhatnak panaszt: h tf j st, brgyullad st, gomb s folyamatot, vagy egyszeren csak eszt tikai h tr nyt. Biztos lehetsz abban, hogy nincsenek rejtett vagy tovbbi kiadsok, hiszen a szmodra kialaktott egyedi r fedezi a szksges gygyszereket s a beavatkozs utni kontrollvizsglatokat is.
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5eff3d1f6f98e57329caed0ceb9053d3
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-6,460,061,387,955,283,000
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Open main menu
The corpus spongiosum is the mass of spongy tissue surrounding the male urethra within the penis.[1] Also called the corpus cavernous urethrae in older texts.
Corpus spongiosum penis
Grant 1962 197.png
Lower Parts of the Genital and Urinary Tracts in the Male
Grant 1962 198.png
Dissection of the Penis
Details
Identifiers
LatinCorpus spongiosum penis
(plural: Corpora spongiosa penium),
(corpus cavernosum urethrae)
TAA09.4.01.015
FMA19617
Anatomical terminology
Contents
AnatomyEdit
Behind, it is expanded to form the urethral bulb, and lies in apposition with the inferior fascia of the urogenital diaphragm, from which it receives a fibrous investment.
The urethra enters the bulb nearer to the superior than to the inferior surface. On the latter there is a median sulcus (groove), from which a thin fibrous septum (wall) projects into the substance of the bulb and divides it imperfectly into two lateral lobes or hemispheres.
The portion of the corpus spongiosum in front of the bulb lies in a groove on the under surface of the conjoined corpora cavernosa penis. It is cylindrical in form and tapers slightly from behind forward. Its anterior end is expanded in the form of an obtuse cone, flattened from above downward. This expansion, termed the glans penis, is moulded on the rounded ends of the corpus cavernosum penis, extending farther on their upper than on their lower surfaces.
At the summit of the glans is the slit-like vertical opening known as the external urethral orifice, or the urinary meatus.
The circumference of the base of the glans forms a rounded projecting border, the corona of glans penis, overhanging a deep retroglandular sulcus, behind which is the neck of the penis.
FunctionEdit
The function of the corpus spongiosum in erection is to prevent the urethra from pinching closed, thereby maintaining the urethra as a viable channel for ejaculation. To do this, the corpus spongiosum remains pliable during erection while the corpora cavernosa penis becomes engorged with blood.
Additional imagesEdit
See alsoEdit
ReferencesEdit
1. ^ Heide Schatten; Gheorghe M. Constantinescu (21 March 2008). Comparative Reproductive Biology. John Wiley & Sons. ISBN 978-0-470-39025-2.
This article incorporates text in the public domain from page 1248 of the 20th edition of Gray's Anatomy (1918)
External linksEdit
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Sodium thiosulfate prevents doxorubicin-induced DNA damage and apoptosis in cardiomyocytes in mice
Yukie Mizuta, Kentaro Tokuda, Jie Guo, Shuo Zhang, Sayoko Narahara, Takahito Kawano, Masaharu Murata, Ken Yamaura, Sumio Hoka, Makoto Hashizume, Tomohiko Akahoshi
Research output: Contribution to journalArticlepeer-review
13 Citations (Scopus)
Abstract
AIM: Doxorubicin (DOX) induces dose-dependent cardiotoxicity due to reactive oxygen species (ROS)-mediated oxidative stress and subsequent apoptosis of cardiomyocytes. We aimed to assess whether sodium thiosulfate (STS), which has antioxidant and antiapoptotic properties, exerts cardioprotective effects on DOX-induced cardiomyopathy.
MAIN METHODS: Male C57BL/6N mice were divided into four groups, control, DOX, STS, and DOX + STS, and administered DOX (20 or 30 mg/kg) or normal saline intraperitoneally, followed by an injection of STS (2 g/kg) or normal saline 4 h later.
KEY FINDINGS: The DOX group showed a poorer 6-day survival and decreased cardiac function than the DOX + STS group. The DOX group showed a marked increase in the plasma creatine kinase isoenzyme myocardial band (CK-MB) and lactate dehydrogenase (LDH) levels 10 h after DOX injection, while the DOX + STS group showed suppression of DOX-induced elevation of CK-MB and LDH levels. The DOX group showed increased 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels in the heart, whereas the DOX + STS group showed increased catalase and superoxide dismutase (SOD) activities and decreased 8-OHdG levels in the heart compared with DOX group, suggesting that STS reduces DOX-induced DNA damage by improving antioxidant enzymes activities in cardiomyocytes. Additionally, the DOX + STS group showed attenuation of cleaved caspase-3 and DNA fragmentation in cardiomyocytes compared with the DOX group, suggesting that STS suppresses DOX-induced apoptosis in cardiomyocytes.
SIGNIFICANCE: STS exerts cardioprotective effects against DOX-induced cardiac dysfunction partly by improving antioxidant defense and suppressing apoptosis, indicating the therapeutic potential of STS against DOX-induced cardiomyopathy.
Original languageEnglish
Pages (from-to)118074
JournalLife Sciences
Volume257
Early online dateJul 13 2020
DOIs
Publication statusE-pub ahead of print - Jul 13 2020
Fingerprint
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Cite this
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10-Dec-2023
HomeENGLISHUnderstanding the Ketogenic Diet and Its Advantages
Understanding the Ketogenic Diet and Its Advantages
The Ketogenic diet is a popular high-fat, low-carb, and moderate-protein diet with potential health benefits such as weight loss and improved blood sugar control.
The Ketogenic diet, or simply Keto, is a high-fat, low-carbohydrate, and moderate-protein diet that has gained popularity recently for its potential health benefits. The Keto diet involves drastically reducing your carbohydrate intake and increasing your fat intake. By doing so, your body enters a state of ketosis, which burns fat for energy instead of carbohydrates.
How the Ketogenic Diet Works
The primary aim of the Ketogenic diet is to reduce the amount of glucose in your body, which is the primary source of energy for the body. When you consume high amounts of carbohydrates, your body breaks them down into glucose for energy. However, when you restrict your carbohydrate intake, your body burns fat for energy. This metabolic state is called ketosis.
When your body is in a state of ketosis, it produces molecules called ketones, an alternative fuel source for the body. Ketones are produced when the liver breaks down fat; the body can use them as fuel instead of glucose. Burning fat for energy can lead to weight loss and increased energy levels.
Advantages of the Ketogenic Diet
One of the primary benefits of the Ketogenic diet is weight loss. When you restrict your carbohydrate intake and enter ketosis, your body burns fat for energy instead of glucose. This can lead to rapid weight loss, particularly in the first few weeks of the diet.
In addition to weight loss, the Ketogenic diet has also been shown to have other health benefits, such as improved blood sugar control, reduced inflammation, and increased cognitive function. The diet may also help to reduce the risk of certain diseases, such as heart disease, diabetes, and cancer.
Risks and Precautions to Consider
While the Ketogenic diet has many potential benefits, it is essential to note that it may not suit everyone. The diet can be challenging to follow, particularly in the initial stages when your body is adjusting to the changes in diet. Some people may also experience side effects like headaches, fatigue, and nausea.
Additionally, the Ketogenic diet may not be appropriate for people with certain medical conditions, such as liver or pancreatic disease, as well as pregnant or breastfeeding women. It is always important to consult a healthcare professional before starting any new diet or exercise program.
Conclusion
The Ketogenic diet is a popular high-fat, low-carb, and moderate-protein diet with potential health benefits such as weight loss and improved blood sugar control. It works by putting the body into ketosis, burning fat for energy instead of glucose. However, it’s important to consult a healthcare professional before starting the diet, especially if you have any medical conditions.
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Diet Plan With Glomerulonephritis
A freshly made kale salad.
Image Credit: ehaurylik/iStock/Getty Images
Glomerulonephritis is a type of kidney disease characterized by inflammation of the filtering mechanisms in your kidneys, called the glomeruli. When the glomeruli are inflamed, they cannot remove waste products and fluid from the blood efficiently. To control the amount of waste in your blood, you need to follow the proper diet plan developed by consulting with your doctor.
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Protein
The digestion of protein results in the formation of a waste product called urea. Normally, urea travels through the bloodstream to your kidneys where it is expelled from the body through your urine. If you have glomerulonephritis, your kidneys cannot remove urea from the blood properly. Urea in the blood puts strain on the kidneys, worsening your condition. Consuming too much protein can also cause urea to accumulate in your blood. Because protein performs a variety of functions in your body, including muscle growth and tissue repair, it is important that you do not restrict your protein intake too much. Work closely with a dietitian to determine exactly how much protein you need and do your best to meet your daily goals.
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Sodium
Sodium helps regulate the amount of fluid in your body. If your blood contains too much sodium, it triggers your kidneys to retain water, which increases your blood volume and can increase your blood pressure. High blood pressure puts excess strain on your kidneys, worsening your kidney disease. If you have glomerulonephritis, your dietitian may recommend a sodium restriction. When reducing your sodium intake, avoid adding salt to foods, as well as canned foods, processed foods, salted snacks and processed meats, like bacon and ham. You can use fresh herbs and sodium-free spices in place of salt, but do not use salt substitutes, which replace sodium with potassium.
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Potassium
When kidneys fail, they cannot properly filter excess amounts of potassium from the blood. If potassium levels get too high, it can disrupt proper muscle and nerve function, causing irregular heart beat and even heart attack. To prevent potassium from building up too high in your blood, your dietitian may recommend that you reduce your intake of potassium-rich foods, such as bananas, sweet potatoes, oranges, spinach, tomatoes, nuts, legumes and dairy products.
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Fluids
In the later stages of glomerulonephritis, you may be placed on a fluid restriction. When your kidneys are damaged, they cannot remove excess fluid from your body. As a result, fluid can build up in your body tissues, causing edema, which is a generalized swelling from too much fluid. The amount of fluid you are allowed to consume depends on your level of kidney function.
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Weight Calculator
Grams:
Kilograms:
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Calculate Ideal Body Weight
Calculate Ideal Body Weight
Weight Calculator
The percentage of body fat can be determined correctly using the weight calculator, which is a useful tool for people who want to enhance their physical fitness, health and beauty. Body Composition Analyzers, weight scales, and bioelectric impedance analyzers are the three most commonly used forms of weight calculators. Choosing the best type of weight calculator for you is crucial because it is all useful for various tasks.
Calorie Calculator
ideal weight calculator
Each type of weight calculator is covered in this post, along with some examples to help you understand the differences.
The optimal weight of a person can be calculated using a weight calculator. He achieves this by knowing the ideal weight of a person while calculating the current weight of a person.
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Cerebral Atrophy
Cerebral atrophy is a common feature of many of the diseases that affect the brain. Atrophy of any tissue means loss of cells. In brain tissue, atrophy describes a loss of neurons and the connections between them. Atrophy can be generalized, which means that all of the brain has shrunk; or it can be focal, affecting only a limited area of the brain and resulting in a decrease of the functions that area of the brain controls. If the cerebral hemispheres (the two lobes of the brain that form the cerebrum) are affected, conscious thought and voluntary processes may be impaired.Associated Diseases/Disorders: The pattern and rate of progression of cerebral atrophy depends on the disease involved. Diseases that cause cerebral atrophy include:stroke and traumatic brain injuryAlzheimer’s disease, Pick’s disease, and fronto-temporal dementiacerebral palsy, in which lesions (damaged areas) may impair motor coordinationHuntington’s disease, and other hereditary diseases that are associated with genetic mutationsleukodystrophies, such as Krabbe disease, which destroy the myelin sheath that protects axonsmitochondrial encephalomyopathies, such as Kearns-Sayre syndrome, which interfere with the basic functions of neuronsmultiple sclerosis, which causes inflammation, myelin damage, and lesions in cerebral tissueinfectious diseases, such as encephalitis, neurosyphilis, and AIDS, in which an infectious agent or the inflammatory reaction to it destroys neurons and their axonsSymptoms of cerebral atrophy: Many diseases that cause cerebral atrophy are associated with dementia, seizures, and a group of language disorders called the aphasias. Dementia is characterized by a progressive impairment of memory and intellectual function that is severe enough to interfere with social and work skills. Memory, orientation, abstraction, ability to learn, visual-spatial perception, and higher executive functions such as planning, organizing, and sequencing may also be impaired.Seizures can take different forms, appearing as disorientation, repetitive movements, loss of consciousness, or convulsions.Aphasias are a group of disorders characterized by disturbances in speaking and understanding language. Receptive aphasia causes impaired comprehension. Expressive aphasia is reflected in odd choices of words, the use of partial phrases, disjointed clauses, and incomplete sentences.
Research
The NINDS funds research looking at many of the diseases and disorders that cause cerebral atrophy. Understanding the biological mechanisms that cause neurons to die in the brain will help researchers find ways to prevent, treat, and even cure the diseases that lead to cerebral atrophy.
Organizations
Content Provided By
NINDS Disorders is an index of neurological conditions provided by the National Institute of Neurological Disorders and Stroke. This valuable tool offers detailed descriptions, facts on treatment and prognosis, and patient organization contact information for over 500 identified neurological disorders.
Neurological Disorders and Stroke »
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Artwork by
End Stage Dementia: Symptoms, Care, and Support in the Final Days
Medically reviewed by
Written by Sulagna Chakraborty
Imagine a parent who once knew your favorite movie suddenly not recognizing you or a spouse’s familiar laugh replaced by silence. This is the harsh reality of end-stage dementia, a disease affecting millions globally.
As dementia progresses, individuals may experience intensified cognitive decline, struggling with communication, recognition, and daily tasks. They may become increasingly dependent on assistance for even the most basic needs. Physical changes, like difficulty swallowing and incontinence, also become more common.
Navigating this stage requires a shift in focus from managing cognitive decline to prioritizing comfort and quality of life. This includes pain management, maintaining proper nutrition and hydration, and ensuring a safe and familiar environment.
However, caring for someone with end-stage dementia extends far beyond physical needs. Emotional support is crucial, both for the individual and their loved ones. Providing comfort, engaging in simple activities, and simply being present can offer solace and connection.
Remember, facing this stage is never easy. Seeking professional guidance from healthcare providers, joining support groups, and accessing community resources can equip you with the tools and support you need to navigate this journey with compassion and strength.
Recognizing End Stage Dementia
In the journey of dementia, recognizing the end stages is crucial. Tools include cognitive assessments, behavioral observations, and medical consultations. Embracing support from healthcare professionals, caregivers, and support groups becomes vital. Prioritize comfort, maintain open communication, and ensure legal and financial affairs are in order. Seeking solace in shared experiences can ease the emotional burden. In this challenging phase, fostering a supportive environment remains paramount for both individuals and their caregivers.
Key Symptoms and Signs
symptoms become more pronounced In the later stages of dementia. Look for profound memory loss, disorientation, and difficulty recognizing loved ones. Daily activities like eating and dressing become challenging. Behavioral changes may include aggression or withdrawal. Communication skills decline, often leading to incoherent speech. Loss of mobility and inability to control movements are common. Weight loss and frailty are evident as the body weakens. It's crucial to consult healthcare professionals for a comprehensive evaluation. Early identification ensures proper care and support. If you notice these signs, seek guidance promptly to navigate this challenging journey with understanding and compassion.
Challenges in End-Stage Dementia
Some challenges associated with end-stage dementia include:
1. Communication Difficulties: Communication breakdown poses a significant challenge as individuals with end-stage dementia struggle to express needs or comprehend information. Caregivers must employ patience and alternative methods, such as non-verbal cues, to ensure effective interaction and understanding.
2. Physical Health Decline: The deterioration of physical health is prominent, with weakened mobility, increased vulnerability to infections, and the risk of complications like pressure ulcers. Tailored care plans are crucial to address these challenges and maintain the individual's overall well-being.
3. Behavioral and Psychological Symptoms: Agitation, aggression, and anxiety can intensify, requiring nuanced strategies for behavioral management. Comprehensive approaches, including environmental modifications and therapeutic interventions, are essential to enhance the individual's quality of life and ease caregiver burden.
4. Feeding and Nutrition Issues: End-stage dementia often brings about a decline in appetite and swallowing difficulties, necessitating careful monitoring and creative solutions for nutritional support. Specialized diets, adaptive utensils, and the expertise of healthcare professionals become crucial in addressing these challenges.
5. Pain Management: Identifying and managing pain in individuals with limited verbal communication skills becomes complex. Close observation of behavioral cues, collaboration with healthcare providers, and the use of tailored pain assessment tools are vital to ensuring effective pain management for improved comfort.
6. End-of-Life Care Decisions: As the disease progresses, decisions regarding end-of-life care become pivotal. Clear communication among healthcare providers, caregivers, and family members is essential to align care with the individual's wishes and ensure a dignified and comfortable transition.
7. Emotional and Psychological Impact on Caregivers: Caregivers bear a heavy emotional burden, witnessing the decline of their loved ones. Emotional support, counseling, and respite care are essential to helping caregivers navigate the stress, grief, and emotional toll associated with caring for someone in the end stages of dementia.
8. Healthcare System Navigation: Navigating the complex healthcare system, coordinating various specialists, and accessing appropriate resources can be overwhelming for caregivers. Education and support services are crucial to empower caregivers to make informed decisions and access the necessary care and assistance.
9. Legal and Financial Issues: End-stage dementia often requires legal arrangements for decision-making, such as power of attorney and advance directives. It is crucial to engage in financial planning and comprehend available resources to effectively manage the legal and financial ramifications of long-term care.
10. Cultural and Ethical Considerations: Cultural perspectives on caregiving and end-of-life decisions demand sensitivity and cultural competence from healthcare providers. Addressing ethical dilemmas surrounding treatment choices and respecting cultural beliefs are integral components of providing holistic care in the context of end-stage dementia.
Progression of stages in end-stage Stage Dementia
Dementia typically advances through three stages: early, middle, and late. Early stages involve mild cognitive decline, often unnoticed. The middle stage witnesses increased memory loss and functional impairment. The late stage, leading to end-stage dementia, involves severe cognitive decline, loss of communication, and total dependency. The entire progression can span several years, with the rate varying based on the individual and the underlying cause, averaging around 8 to 10 years from diagnosis to end-stage in many cases.
Care Strategies for End-Stage Dementia
Adaptation of care strategies in end-stage dementia enhances the individual's quality of life by addressing specific needs. Tailored approaches, such as personalized communication methods and modified environments, mitigate distress and promote comfort. This customization optimizes care, offering dignity and support in the face of cognitive decline and fostering a more compassionate and effective caregiving experience.
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Managing Physical Needs
Managing physical needs in end-stage dementia involves a holistic approach. Addressing nutrition is vital, as is utilizing modified diets or supplements for those with swallowing difficulties. Hygiene care, including gentle assistance with bathing and toileting, maintains dignity. Monitoring mobility helps prevent complications like pressure sores. Pain management, through careful observation and communication interpretation, ensures comfort. Regular repositioning, skin checks, and managing incontinence contribute to overall well-being. Tailoring physical activities, even in minimal forms, supports muscle function. Collaborating with healthcare professionals for ongoing assessment and adapting interventions as needed ensures a comprehensive strategy for meeting the evolving physical needs of individuals with end-stage dementia.
Emotional and Psychological Support
Emotional and psychological support in end-stage dementia is crucial for both individuals and caregivers. Validation and empathy alleviate distress, fostering a sense of security. Activities, like music or art, offer pathways for self-expression and can prove to be therapeutic. Consistent routines provide reassurance. Collaborating with mental health professionals aids in managing behavioral changes. Encouraging reminiscence and preserving personal identity enhance a positive emotional environment. Caregiver support groups offer outlets for shared experiences.
Communication Tips and Techniques
1. Silence Appreciation: Embrace moments of silence, allowing individuals to process information at their own pace and reducing communication pressure.
2. Mirror Neuron Activation: Use mirroring techniques by subtly imitating facial expressions and gestures, promoting a sense of connection and understanding through non-verbal cues.
3. Redirection Through Positive Affirmations: Gently redirect conversations using positive affirmations, guiding individuals away from distressing topics toward more soothing and uplifting subjects.
4. Time-Frame Customization: Adjust the time frame for communication, recognizing that individuals with end-stage dementia may comprehend and respond more effectively during specific periods of the day.
5. Sensory Anchoring: Incorporate sensory stimuli, like holding a familiar object, to anchor and enhance communication, providing a tangible connection that aids in conveying emotions and needs.
Navigating the Last Days of Life with Dementia
In navigating the last days of life for end-stage dementia, advanced directives are crucial. These legal documents enable individuals to make informed decisions about their medical care when they can no longer communicate their preferences. Discussing and documenting preferences in advance empowers both individuals and their families, ensuring that medical interventions align with personal wishes, enhancing the quality of care, and honoring the individual's autonomy during this challenging phase.
Preparing for the Final Stage
In the final stage of dementia, managing basic needs like food and physical comfort is paramount. Tailoring nutrition to address swallowing difficulties, offering modified diets, or using supplements ensures adequate nourishment. Hygiene care, including gentle assistance with bathing and toileting, maintains dignity. Regular repositioning helps prevent discomfort and complications like pressure sores. Collaboration with healthcare professionals facilitates pain management, ensuring the individual's physical well-being. These measures, combined with open communication, create a compassionate and supportive environment, fostering the dignity and comfort of both the individual with dementia and their caregivers during this challenging phase.
Comfort Care and Pain Management
Pain management includes:
1. Regular assessments for pain signals like facial grimacing, vocalizations, and changes in movement
2. Medications tailored to individual needs and pain types, including opioid and non-opioid options
3. Non-pharmacological interventions such as light massaging music therapy and positioning techniques
Comfort care includes:
1. Providing a calm and familiar environment
2. Offering comforting touch, presence, and reassurance
3. Attending to basic needs like hydration, hygiene, nutrition, and sleep
Palliative Care and Comfort Measures
Palliative care measures for end-stage dementia encompass a comprehensive approach. Pain management is prioritized through tailored medications. Emotional and spiritual support involves counseling for both patients and their families. Nutrition plans are adapted to address swallowing difficulties, ensuring proper nourishment. Hygiene care is provided with sensitivity, preserving dignity. Sensory therapies, such as music and aromatherapy, offer comfort and connection. Regular communication with healthcare professionals ensures continuous adaptation of care strategies.
Supporting Families and Caregivers
Supporting families and caregivers of individuals with end-stage dementia involves open communication, empathy, and education. Provide emotional support through counseling and support groups. Educate them on the progression of dementia and managing expectations. Offer practical guidance on your daily care routines and coping strategies. prioritize self-care, emphasizing the importance of physical and emotional well-being. Facilitate discussions on end-of-life decisions, preparing them for the transition and ensuring alignment with the individual's wishes. Empowering caregivers with knowledge and emotional support eases the burden, fostering a more compassionate and informed approach to the challenges of end-stage dementia.
Embrace Compassion and Dignity in End-of-life Dementia Care with Cadabams
At Cadabams, we recognize the challenges of navigating end-stage dementia. Our compassionate support for caregivers and families includes counseling, support groups, and educational resources to enhance understanding. We prioritize dignity and comfort for individuals with end-stage dementia through personalized care plans, integrating sensory therapies, and addressing specific needs. Our services extend to pain management, nutritional support, and creating a calming environment. To improve quality of life, we use a multidisciplinary strategy that includes palliative care professionals. Cadabams is committed to providing comprehensive assistance, ensuring both caregivers and individuals with end-stage dementia experience the support and care needed during this challenging phase.
If you are searching for a solution to your problem, Cadabam’s Rehabilitation Centre can help you with its team of specialized experts. We have been helping thousands of people live healthier and happier lives for 30+ years. We leverage evidence-based approaches and holistic treatment methods to help individuals effectively manage their End Stage Dementia. Get in touch with us today. You can call us at +91 96111 94949.
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FAQs
1. How do you know when dementia is near the end?
Dementia symptoms include substantial memory loss, restricted speech, and loss of movement in the later stages. Individuals may have difficulty doing fundamental duties such as eating and dressing. Frailty, restricted response, and a deterioration in general health are frequent indicators of the end stage.
2. What is very important in the late stages of dementia?
Maintaining comfort and dignity is crucial in late-stage dementia. Addressing pain, promoting sensory engagement, and creating a calm, familiar environment enhance the individual's well-being. Emotional support for both the person with dementia and caregivers becomes paramount during this challenging phase.
3. What are the signs that dementia is getting worse?
Deterioration in cognitive abilities, increased forgetfulness, and challenges in daily tasks signal worsening dementia. Behavioral changes such as aggression or agitation may intensify. Progressive difficulty in communication and an escalation of physical limitations are clear indicators of the disease's advancement.
4. What is the most fatal form of dementia?
The most fatal form of dementia is Creutzfeldt-Jakob disease (CJD). It's an uncommon, degenerative, and fast-growing brain condition caused by prions, which are aberrant proteins. CJD leads to severe neurological symptoms and cognitive decline and often results in a rapid decline in health, typically leading to death within a year of onset.
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Women In Their Prime, LLC, does not warrant that this service will be uninterrupted or free of errors. Although we make every effort to provide factual and relevant information, delays, omissions, and inaccuracies may be present in images, text, opinions, statements, market information, and other data produced by Prime Women or third party contributors. We do not make any warranties, express or implied, of goods that are available or advertised or sold through this service. Prime Women is an affiliate ad supported site. If you follow a link from our site and purchase something, we may be paid a commission. Prime Women promotes those products and services with which we are personally familiar, and oftentimes, use ourselves.
People fast for so many reasons; some fast because they're trying to lose weight while others fast to improve medical conditions such as diabetes and high blood pressure. The science behind intermittent fasting has slowly been piling up, too, with research showing that participants of intermittent fasting experience a reduction in weight and inflammation and improvement in insulin sensitivities.
Jeremiah, I don’t think the author is suggesting that TRF in the later hours of the day is bad, but rather that it is DIFFICULT. The key finding in this study is that the 07:00-15:00 eaters had a reduced appetite (in other words, didn’t find it very hard to follow this regimen), whereas other approaches have been found to be kind of difficult for some.
I’m 63 years old and I have been following a daily 19 hour protocol called Fast 5, fast5.org for two years. I eat lunch at 3pm and dinner at 7pm close my eating window at 8pm. I’ve lost 43 lbs and kept it off, feel great and I am no longer pre diabetic. I eat what I want and don’t track anything. I belong to a Facebook Intermittent fasting group called Fast Club and would to have you check it out. Fasting is free and it works!
Yes — you read that correctly — 24 hours of intermittent fasting without any resistance training and these subjects were able to preserve more muscle mass than the subjects that ate fewer calories every day without fasting at all. This finding contradicts our common sense, but when we dig deeper into autophagy we can find the mechanism behind this result.
The thing is that if you want to slim down and get rid of excess pounds, then the fasted state is really the best way to do it. If you keep taking food into your body, insulin levels will remain high, and you will keep burning glucose for fuel instead of burning fat. Of course, to remain in the fasted state, you need to not be in the fed state, and that can be a problem. Starving yourself all of the time isn’t enjoyable, and it’s not healthy. To be blunt about it, your body needs nutrients, it just doesn’t need them all day, every day.
Before you start your IF plan, it's important to talk with a professional to make sure it's right for you. Women should be especially cautious as there are some mixed opinions on whether or not certain fasting protocols are healthy for female hormone balance. In addition, if you have adrenal fatigue or gut health issues you'll want to proceed with caution. If you have a history of disordered eating, you'll probably want to avoid fasting altogether..
Well, most notably, it’s a great way to get lean without going on a crazy diet or cutting your calories down to nothing. In fact, most of the time you'll try to keep your calories the same when you start intermittent fasting. (Most people eat bigger meals during a shorter time frame.) Additionally, intermittent fasting is a good way to keep muscle mass on while getting lean.
Even though this plan is advanced, it's very simple. Don't eat anything every other day. This is the most intense form of fasting but can produce amazing results. Every other day, eat healthy fats, clean meat sources, vegetables, and some fruit, and then on your fasting days, you can consume water, herbal tea, and moderate amounts of black coffee or tea.
If you want to lose weight, you need to be burning more calories than you consume. A good diet will help reduce your calorie intake. Working out will increase your calorie burn. But while each of these is a step in the right direction, why not approach the problem from both ends? Intermittent fasting empowers you cut down on the influx of calories while also training your body to become better and more efficient at using the calories stored in fat cells. The end result is a quicker path to a healthier you. You could even call it the “fast” track to weight loss success.
Of course, most people use IF with another weight-loss plan. For instance, you might decide to eat 1,200 calories a day to lose weight. You may find it much easier to spread out 1,200 calories within two meals and two snacks than in three meals and three snacks. If you’ve struggled with weight loss because your diet either didn’t work or was simply too hard to stick to, you might try intermittent fasting for quicker results.
If you have an addictive relationship with food and you struggle with portion control, track your calorie intake in your meals to make sure you’re not overeating. If you skip breakfast, you might be so hungry from this that you OVEREAT for lunch and this can lead to weight gain. Again, the important thing here is that with intermittent fasting you’re eating fewer calories than normal because you’re skipping a meal every day.
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Cardiovascular Disease - Naturopath Wellness Clinic - Natural Medicine
Brisbane & Sunshine Coast Naturopath and Psychology Clinic
Opening Hours : Mon to Fri - 9am to 5pm (later on req) Sat 8am-1pm
Contact : (07) 5458 4800
Cardiovascular Disease
Cadiovascular Disease Naturopath Sunshine Coast ClinicHave you ever questioned why the number of people suffering with cardiovascular disease is rising?
There are a magnitude of potential causes, and everyones causes are generally different.
Cardiovascular disease (CVD) is a collective term for diseases of the heart and blood vessels, mainly including coronary heart disease, stroke and heart failure/cardiomyopathy. There are many factors that may contribute to the development of cardiovascular disease, including:
• Smoking and binge drinking
• Lack of exercise
• A diet rich in refined carbohydrates/sugars and unhealthy fats
• High blood pressure (hypertension)
• Poor liver excretion of fats
• Diabetes and gall bladder disease
• Family history (genetics)
Two of the main disease processes involved in the development and progression of CVD are atherosclerosis and dyslipidaemia.
Atherosclerosis
Atherosclerosis is the hardening and/or narrowing of the arteries due to a build up of plaque (made up of cholesterol, fat, calcium and other substances) inside the arteries. Because arteries carry blood to the heart (and other areas of the body), the build up of plaque in the arteries reduces the flow of blood, which can eventually result in stroke or heart attack. Depending on which arteries are affected, various diseases can develop as a result of atherosclerosis. For example, Coronary Heart Disease is due to plaque build up on the coronary arteries, which reduces blood flow to the heart muscle.
Dyslipidaemia
Dyslipidamia is an imbalance of lipids (fat and cholesterol) in the blood, which in most patients presents as hyperlipidaemia (meaning high levels of fat in the blood). Elevated LDL-Cholesterol and triglycerides have been associated with CVD. HDL-Cholesterol, on the other hand, has been found to be protective against CVD. Statins (simvastatin, atorvastatin, rosuvastatin, etc.) are the most commonly prescribed treatment for high cholesterol. Whilst statins can be effective, they can actually deplete the body of important nutrients and cofactors that are involved in body processes, such as energy production and muscle function. Therefore, if you are using a statin to stabilise your cholesterol levels, you may also need additional nutrient support.
Our Practitioners may help in the prevention and management of Cardiovascular Disease, through focusing on:
1. Reducing triggers of stress and stress management strategies – stress increases the activity of the sympathetic nervous system, which can affect the cardiovascular system (leading to increased blood lipids, altered blood pressure, and atherosclerosis).
1. Assist in the achievement and management of a healthy weight – there is a strong association between excess body fat and increased blood pressure, therefore, weight loss may be an important factor in the management of CVD. Exercise, particularly yoga, has been shown to be beneficial in patients with high blood pressure and heart disease.
1. Dietary changes – just as poor food choices can increase the risk of CVD, healthy food choices can help to prevent or manage CVD. Dietary interventions may focus on an increased consumption of vegetables and fruits, assessing intake of various minerals (including sodium, magnesium, potassium and calcium), reducing refined carbohydrates and sugars, and increasing certain foods that promote healthy blood lipid levels, such as essential fatty acids from fish (EPA and DHA). A Nutritionist is often incorporated into Naturopathic plans.
1. Reducing homocysteine levels – elevated homocysteine levels are considered a risk factor for cardiovascular disease. Homocysteine is an amino acid that is made in a process called ‘methylation’. Therefore, reduced methylation function can lead to a build up of homocysteine. Dietary changes and specific nutrients can help to reduce homocysteine levels. Genetic mutations such as MTHFR gene may affect this.
There are many other factors that may also be addressed, including supporting the production of bile acids in the liver (bile acids help to manage cholesterol levels), increasing antioxidant status, and reducing CRP levels (CRP is an inflammatory protein that is associated with CVD).
Nutritional, herbal and/or lifestyle therapies alone may be effective in the management of cardiovascular disease, however, can also be beneficial when used alongside other medications prescribed.
We are more than comfortable to work alongside your doctor in cardiovascular management.
Want to know how we can help you?
We recommend booking a FREE Naturopathic Assessment Consultation with one of our Naturopaths either in one of our Sunshine Coast Naturopath Clinics or in our Brisbane Naturopath ClinicBook this highly educational free consultation online or click the phone number to speak with our team (07) 5458 4800 .
Free Consult with Naturopath Buderim & Caloundra Brisbane Naturopath
Click the above banner to easily book online
We would love to see you in our Brisbane Naturopath Clinic or our Sunshine Coast Naturopath Clinics in both Buderim and Caloundra. Alternatively, no matter where you are, we can offer naturopathy services by phone or skype consultations and provide nutritional supplementation and pathology testing advice.
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Health Library
Cancer: Home Treatment for Mouth Sores
Topic Overview
A painful sore or ulcer inside your mouth may make it hard to eat and drink. Be sure to let your doctor know you are having mouth sores. You may need to have your medicines adjusted. And try some of the following home treatment measures to help ease pain and speed healing.
What to eat and drink
• Drink a lot of water.
• Suck on ice chips, or try chilled foods, such as frozen ice pops, ice cream, or frozen yogurt.
• Try warm liquids, such as tea or soup.
• Eat soft, bland foods that are easy to swallow, such as ice cream, custard, applesauce, cottage cheese, macaroni and cheese, soft-cooked eggs, yogurt, or cream soups.
• Cut foods into small pieces, or grind, mash, blend, or puree foods.
• Stay away from:
• Spicy and salty foods, coffee, chocolate, citrus fruits, and tomatoes.
• Nuts, seeds, or potato chips or crackers that can scrape your mouth.
• Fizzy drinks, alcoholic drinks, and all tobacco products.
• Anything that is sweet or too hot or too cold if it makes your mouth hurt.
How to keep your mouth clean
• Rinse your mouth several times a day. You can use 1 cup of warm water mixed with 1/4 teaspoon baking soda and 1/8 teaspoon salt, followed by rinsing your mouth with plain water.
• Use an extra-soft toothbrush and a mild toothpaste.
• You can soften your toothbrush in hot water before using it. If using a toothbrush is too painful, try using soft foam mouth swabs.
• Stay away from whitening toothpastes because they can irritate a sore mouth.
• Gently floss your teeth and use a mouthwash that doesn't have alcohol in it.
• If your mouth is dry, try sugarless gum or candy. Or talk to your doctor about using a saliva substitute to keep your mouth moist.
How to reduce pain
• Use a straw for drinking liquids.
• Make a thin paste of baking soda and water and apply it to the sore. Or you can use a cotton swab to dab your sores with a liquid antacid, such as Maalox or Mylanta.
Try using a nonprescription medicine such as Anbesol or Orabase to coat your mouth sores before eating. If your child is under 2 years of age, ask your doctor if you can give your child numbing medicines.
To help ease pain, use a nonprescription medicine, such as Amosan, Anbesol, Gly-Oxide, Orabase, or Zilactin. Check with a doctor for correct dosage before using any of these on a baby or child.
If painful mouth sores are keeping you from being able to eat, talk to your doctor. He or she may prescribe medicines that can help with mouth pain.
Credits
Current as of: December 19, 2018
Author: Healthwise Staff
Medical Review: Anne C. Poinier MD - Internal Medicine
Adam Husney MD - Family Medicine
Kathleen Romito MD - Family Medicine
Douglas A. Stewart MD - Medical Oncology
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What is paracetamol Biogesic used for?
What is paracetamol Biogesic used for?
A trusted brand of paracetamol, Paracetamol (Biogesic) is a medication that is typically used to relieve mild to moderate pain such as headache, backache, menstrual cramps, muscular strain, minor arthritis pain, toothache, and reduce fevers caused by illnesses such as the common cold and flu.
Can I take paracetamol and phenylephrine together?
No interactions were found between Paracetamol and phenylephrine. This does not necessarily mean no interactions exist. Always consult your healthcare provider.
Can antihistamine be taken with paracetamol?
Yes, you can take cetirizine together with paracetamol or ibuprofen. Can I take 2 types of antihistamine in 1 day? Sometimes doctors recommend that people with a severe, itchy skin rash take 2 different antihistamines together for a few days.
What is the use of paracetamol phenylephrine hydrochloride chlorpheniramine maleate?
Paracetamol (PAR), phenylephrine hydrochloride (PHE) and chlorpheniramine maleate (CPM) are commonly used in clinical practice as antipyretic and analgesic drugs to ameliorate pain and fever in cold and flu conditions.
Can I take Biogesic every 4 hours?
The recommended dose of Biogesic® 500mg for minor aches and pains such as headache is 1 to 2 tablets every 4 to 6 hours, as needed. Do not take more than 8 tablets (or 4 grams of paracetamol) in any 24-hour period.
How do you take paracetamol with phenylephrine?
Adults, the elderly and children 12 years and over: 2 tablets every 4 hours, as required. Do not take more than 8 tablets (4 doses) in any 24 hour period. Do not give to children under 12 years. Do not take more medicine than the label tells you to.
Can phenylephrine make you sleepy?
Decongestants. Since the main symptom of a cold is congestion in your nose and/or chest, cold medicines usually contain a decongestant ingredient. Examples include phenylephrine and pseudoephedrine. These typically do not cause drowsiness and can make some people feel hyper or more alert.
Can I take vitamin C with antihistamine?
No interactions were found between Allergy Relief Tablets and Vitamin C. This does not necessarily mean no interactions exist. Always consult your healthcare provider.
How does chlorpheniramine work as an antihistamine?
Chlorpheniramine is an antihistamine that reduces the effects of natural chemical histamine in the body. Histamine can produce symptoms of sneezing, itching, watery eyes, and runny nose.
When to give chlorpheniramine to a child?
Chlorpheniramine is used to treat runny nose, sneezing, itching, and watery eyes caused by allergies, the common cold, or the flu. Chlorpheniramine may also be used for purposes not listed in this medication guide. Always ask a doctor before giving a cough or cold medicine to a child.
Are there any side effects of taking chlorpheniramine?
Chlorpheniramine may pass into breast milk and may harm a nursing baby. Antihistamines may also slow breast milk production. Do not use this medicine without your doctor’s advice if you are breast-feeding a baby.
Which is better for fever acetaminophen or chlorpheniramine?
Chlorpheniramine blocks muscle responses in histamine and acts as an antagonism of the constrictor effects of histamine on respiratory smooth muscle. Acetaminophen blocks pain impulse generation peripherally and may inhibit the generation of prostaglandin in the CNS. Reduces fever by inhibiting the hypothalamic heat-regulating center.
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