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Squat
V squat machine reverse. What muscles does the reverse V squat train?
The reverse V squat is a great exercise for overall fitness and strength. It is a challenging exercise and can be done at a variety of depths.
V squat machine reverse
V squat machine reverse
And this article bernard-thevenet.com will help you answer the following questions about V squat machine reverse:
• reverse v squat machine benefits
• v-squat vs reverse v-squat
• reverse v squat vs hack squat
• reverse v squat glutes
• reverse v squat reddit
• hack squat on v squat machine
• reverse v squat muscles worked
• v squat rdl
What is the Reverse V Squat?
The reverse V squat is a variation of the traditional squat that helps to improve body composition and flexibility.
What is the Reverse V Squat?
The reverse V squat places the feet in a wider stance than in the traditional squat, which helps to increase the range of motion and challenge your muscles more.
What muscles does the reverse V squat train?
The reverse V squat is a great exercise for the quadriceps, hamstrings, and glutes.
What muscles does the reverse V squat train?
It targets the quadriceps by using the resistance of gravity to help you lift your body up off the ground, and it also works the hamstrings and glutes because they are required to maintain your balance while you are in a squat position.
Reverse v squat vs hack squat
Reverse v squat vs hack squat
The reverse V squat is a great exercise to improve your quadriceps strength and function. The hack squat is a great exercise to improve your hamstring strength and function.
Reverse v squat glutes
Reverse v squat glutes
If you’re looking to target your glutes, the reverse V squat is a great exercise to use. By squatting backwards, you engage your glutes more effectively and can really work them hard. Plus, it’s a great way to get your quadriceps and hamstrings involved as well.
Reverse v squat reddit
Reverse v squat reddit
The Reverse V Squat is a great exercise for building strength and power in the legs. It can be done on a regular squat machine, or you can use a reverse V squat machine to make the movement more challenging.
Hack squat on v squat machine
There’s no one-size-fits-all answer to this question, as the best way to hack squat on a V squat machine will vary depending on your own body composition and strength levels.
Hack squat on v squat machine
However, some tips on how to reverse hack squat on a V squat machine include using a higher weight stack and positioning your feet wider than shoulder width apart.
How to do the Reverse V Squat?
The reverse V squat is a great exercise for strengthening the quadriceps, hamstrings, and gluteus maximus.
How to do the Reverse V Squat?
To do the reverse V squat, start by standing with your feet hip-width apart. Place your hands on your hips and lower your body until you are sitting down in front of the machine with your thighs parallel to the floor. Drive through your heels to return to the starting position.
Reverse v squat machine benefits
The reverse V squat machine is a great tool for those looking to increase their quad strength and overall fitness.
Reverse v squat machine benefits
The machine simulates the movement of a squat by having the user stand with their feet shoulder-width apart and their back pressed against the back plate of the machine. They then lift their heels off of the ground and lower themselves down until their thighs are parallel to the ground.
Tips for Improving Your Reverse V Squat?
Tips for Improving Your Reverse V Squat?
If you’re looking to improve your reverse V squat, keep these tips in mind: -Start with a light weight and gradually increase the load as you become more comfortable. -Use a squat rack or bench to help support your body weight, and keep your back straight throughout the movement. -Keep your core engaged while performing the reverse V squat, and focus on using your glutes to help lift your body upward.
F.A.Q V squat machine reverse:
1. Why Do People v squat backwards?
Many people squat backwards because it feels better. The weight is more evenly distributed over the back, hamstrings, and glutes when squatting backwards. Additionally, the back muscles are used to create stability and balance in the spine when squatting backwards.
2. Is reverse V squat good?
Reverse V Squat is not a good exercise. It does not provide any real benefit to the body and can even be harmful.
3. What muscles does the reverse hack squat work?
The reverse hack squat machine is designed to work the muscles in your thighs, glutes, and hips. This machine is a great way to increase your strength and muscle mass while also improving your flexibility.
4. What do reverse squats work?
Reverse squats work the same muscles as regular squats, but with a few key differences. First, you keep your back straight and your core engaged throughout the movement. This helps to maintain balance and stability in the hips and spine. Second, you use your legs to drive yourself up instead of relying on your upper body. This engages more muscle groups and helps to increase strength and power.
Conclusion:
The reverse V squat is a great exercise for overall fitness and strength. It is a challenging exercise and can be done at a variety of depths. If you want to improve your fitness, try adding some extra resistance or changing up your technique.
And this article bernard-thevenet.com will help you answer the following questions about V squat machine reverse:
• reverse v squat machine benefits
• v-squat vs reverse v-squat
• reverse v squat vs hack squat
• reverse v squat glutes
• reverse v squat reddit
• hack squat on v squat machine
• reverse v squat muscles worked
• v squat rdl
Field John
If you are an avid believer in health and fitness and want to do something for your team, I can help. As the founder of Field Goals Fitness, I lead a collective of health and fitness professionals dedicated to helping Australians lead a more active and healthier lifestyle. With a warm, friendly, and supportive approach that gets results, I enjoy helping individuals & organisations achieve sustainable success with their health and fitness goals. Certifying as a Personal Trainer in 2009, was a turning point in my life. I had spent 14 years in the corporate world in Business Development roles and decided to take all that I had learnt in sales and marketing and start my own business.
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Smart Ideas: Revisited
Home Remedy for Bad Breath
It is important to ensure that you find a solution to your bad smell or bad breath in case you are suffering from something like that. It is usually very difficult to do your normal work if you realize that you have a bad breath. It is also important to learn that there are several remedies for a bad breath and one can get treatment from home. It is very important to understand the real cause of bad breath before making a decision on how to seek and administer treatment for it. Some of these causes can be avoided because any kind of bad breath in your mouth is an embarrassment because you cannot manage to talk freely. This makes it important that you ensure there is a fresh breath for one to be able to boost their confidence and ensure that they can interact freely without fear of bad breath and such related embarrassments.
The greatest cause of bad breath is the accumulation of food on your teeth. This makes it necessary that everyone adopts the process of ensuring that their teeth are clean and maintained that way at all times. It is important to learn that the act of not brushing one’s teeth is carelessness making it necessary that one ensures they have a fresh breath at all times by regularly cleaning their teeth. You need to take care of everyone around you by encouraging them to clean their teeth regularly and have a fresh odor. In this case you need to hire one professional to advise you on how to live a better and easy life with no fresh breath threats. You need to have a professional that will treat your cavity and ensure it does not interfere with holding bacteria that may dirty your breath.
You also need to know that if you have a cavity; it is possible for a bacteria or virus to settle on your cavity. In this regard, you are advised to ensure that you do not have big cavities that can cause you problems but just a fee well maintained to avoid accumulation of germs and bacteria. In other words you are advised to ensure that your cavity is regularly cleaned with professional advice from a dentist to ensure that the cavity is well taken care of and the bad breath is a thing of the past. You need to know that any unattended cavity is a time bomb waiting to explode on you. This makes it possible to have a professional that can help you treat your bad breath instantly.
What Do You Know About
What You Should Know About This Year
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What are Treatments for Prolapsed Disc? - Apollo Hospitals
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Undefined
Exercise Continuously!
You should continue with your normal daily activities, as much as you can. This may seem impossible at first if the pain in your back is severe. However, try to move around and return to your normal activities as soon as possible. As a rule, refrain from doing anything that may cause a lot of pain.
Before, patients used to be told to rest until the pain disappear. It is now discovered to be a wrong piece of advice. Being active can make you recover more quickly because your back pain is less likely to become chronic (persistent) if you keep moving rather than resting a lot. It is advisable you sleep in the most natural and convenient position on any comfortable surface. People have been wrongly advised in the past to sleep on a thick mattress.
Medication
If painkillers are necessary for your recovery, it is advisable to take them regularly. This is more appropriate than taking them when your back pain suddenly appears every now and then or when the pain is getting bad. If you take them everytime you will be relieved of your back pain most of the time and have the strength to continue your exercise and moving around.
Physical treatments
Some patients visit an osteopath, chiropractor or physiotherapist for physical treatments and manipulation. It is still under scrutiny whether physical treatments could be of help to all people suffering from a prolapsed disc. However, it is reasonable to agree that physical treatments can offer some short-term relief and quicken the recovery process in certain cases.
Surgery
If other treatments aren’t effective, surgery may be a viable option in certain cases. Generally, surgery is considered if the symptoms have not disappeared after about six weeks or more. This happens on a few occasions, because almost in 9 out of 10 cases the symptoms have gone and are not bad enough to require surgical treatment within six weeks. The primary purpose of surgery is to remove the prolapsed section of the disc. A specialist will normally advise you on the pros and cons of using surgery manage back pain, and also introduce you to the other available techniques.
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T-type calcium channels antagonists
keyword
https://www.readbyqxmd.com/read/27759880/ph%C3%AE-1%C3%AE-acts-as-a-trpa1-antagonist-with-antinociceptive-effects-in-mice
#1
Raquel Tonello, Camilla Fusi, Serena Materazzi, Ilaria M Marone, Francesco De Logu, Silvia Benemei, Muryel C Gonçalves, Elisabetta Coppi, Celio J Castro-Junior, Marcus Vinicius Gomez, Pierangelo Geppetti, Juliano Ferreira, Romina Nassini
BACKGROUND AND PURPOSE: Peptides from venomous animals have long been important tools for understanding pain mechanisms and for the discovery of pain treatments. Here, we hypothesized that Phα1β, a peptide purified from the armed spider Phoneutria nigriventer venom, produces analgesia by blocking the transient receptor potential ankyrin 1 (TRPA1) channel. EXPERIMENTAL APPROACH: Cultured rat dorsal root ganglion (DRG) neurons, human IMR90 fibroblasts or HEK293 cells expressing the human TRPA1 (hTRPA1-HEK293), TRPV1 (hTRPV1-HEK293) or TRPV4 (hTRPV4-HEK293), were used for calcium imaging and electrophysiology...
October 19, 2016: British Journal of Pharmacology
https://www.readbyqxmd.com/read/27596273/lack-of-antiparkinsonian-effects-of-systemic-injections-of-the-specific-t-type-calcium-channel-blocker-ml218-in-mptp-treated-monkeys
#2
Adriana Galvan, Annaelle Devergnas, Damien Pittard, Gunasingh Masilamoni, Jocelyn Vuong, John Scott Daniels, Craig W Lindsley, Ryan Morrison, Thomas Wichmann
Dopaminergic medications ameliorate many of the motor impairments of Parkinson's disease (PD). However, parkinsonism is often only partially reversed by these drugs, and they can have significant side effects. Therefore, a need remains for novel treatments of parkinsonism. Studies in rodents and preliminary clinical evidence have shown that T-type calcium channel (TTCC) antagonists have antiparkinsonian effects. However, most of the available studies utilized nonselective agents. We now evaluated whether systemic injections of the specific TTCC blocker ML218 have antiparkinsonian effects in MPTP-treated parkinsonian Rhesus monkeys...
September 6, 2016: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/27439609/anti-nociceptive-and-desensitizing-effects-of-olvanil-on-capsaicin-induced-thermal-hyperalgesia-in-the-rat
#3
Mohammad Alsalem, Paul Millns, Ahmad Altarifi, Khalid El-Salem, Victoria Chapman, David A Kendall
BACKGROUND: Olvanil (NE 19550) is a non-pungent synthetic analogue of capsaicin, the natural pungent ingredient of capsicum which activates the transient receptor potential vanilloid type-1 (TRPV1) channel and was developed as a potential analgesic compound. Olvanil has potent anti-hyperalgesic effects in several experimental models of chronic pain. Here we report the inhibitory effects of olvanil on nociceptive processing using cultured dorsal root ganglion (DRG) neurons and compare the effects of capsaicin and olvanil on thermal nociceptive processing in vivo; potential contributions of the cannabinoid CB1 receptor to olvanil's anti-hyperalgesic effects were also investigated...
2016: BMC Pharmacology & Toxicology
https://www.readbyqxmd.com/read/27365170/the-t-type-calcium-channel-antagonist-z944-disrupts-prepulse-inhibition-in-both-epileptic-and-non-epileptic-rats
#4
Wendie N Marks, Quentin Greba, Stuart M Cain, Terrance P Snutch, John G Howland
The role of T-type calcium channels in brain diseases such as absence epilepsy and neuropathic pain has been studied extensively. However, less is known regarding the involvement of T-type channels in cognition and behavior. Prepulse inhibition (PPI) is a measure of sensorimotor gating which is a basic process whereby the brain filters incoming stimuli to enable appropriate responding in sensory rich environments. The regulation of PPI involves a network of limbic, cortical, striatal, pallidal and pontine brain areas, many of which show high levels of T-type calcium channel expression...
September 22, 2016: Neuroscience
https://www.readbyqxmd.com/read/27353765/growth-differentiation-factor-15-promotes-glutamate-release-in-medial-prefrontal-cortex-of-mice-through-upregulation-of-t-type-calcium-channels
#5
Dong-Dong Liu, Jun-Mei Lu, Qian-Ru Zhao, Changlong Hu, Yan-Ai Mei
Growth differentiation factor-15 (GDF-15) has been implicated in ischemic brain injury and synapse development, but its involvement in modulating neuronal excitability and synaptic transmission remain poorly understood. In this study, we investigated the effects of GDF-15 on non-evoked miniature excitatory post-synaptic currents (mEPSCs) and neurotransmitter release in the medial prefrontal cortex (mPFC) in mice. Incubation of mPFC slices with GDF-15 for 60 min significantly increased the frequency of mEPSCs without effect on their amplitude...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27282256/the-t-type-calcium-channel-antagonist-z944-rescues-impairments-in-crossmodal-and-visual-recognition-memory-in-genetic-absence-epilepsy-rats-from-strasbourg
#6
Wendie N Marks, Stuart M Cain, Terrance P Snutch, John G Howland
Childhood absence epilepsy (CAE) is often comorbid with behavioral and cognitive symptoms, including impaired visual memory. Genetic Absence Epilepsy Rats from Strasbourg (GAERS) is an animal model closely resembling CAE; however, cognition in GAERS is poorly understood. Crossmodal object recognition (CMOR) is a recently developed memory task that examines not only purely visual and tactile memory, but also requires rodents to integrate sensory information about objects gained from tactile exploration to enable visual recognition...
October 2016: Neurobiology of Disease
https://www.readbyqxmd.com/read/27273014/p-q-type-and-t-type-voltage-gated-calcium-channels-are-involved-in-the-contraction-of-mammary-and-brain-blood-vessels-from-hypertensive-patients
#7
Anne D Thuesen, Kristina S Lyngsø, Lotte Rasmussen, Jane Stubbe, Ole Skøtt, Frantz R Poulsen, Christian Bonde Pedersen, Lars M Rasmussen, Pernille B L Hansen
AIM: Calcium channel blockers are widely used in cardiovascular diseases. Beside L-type channels, T- and P/Q-type calcium channels are involved in contraction of human renal blood vessels. It was hypothesized that T- and P/Q -type channels are involved in contraction of human brain and mammary blood vessels. METHODS: Internal mammary arteries from bypass surgery patients and cerebral arterioles from patients with brain tumors with and with-out hypertension were tested in a myograph and perfusion set-up...
June 7, 2016: Acta Physiologica
https://www.readbyqxmd.com/read/27242667/t-type-calcium-channel-a-privileged-gate-for-calcium-entry-and-control-of-adrenal-steroidogenesis
#8
REVIEW
Michel F Rossier
Intracellular calcium plays a crucial role in modulating a variety of functions such as muscle contraction, hormone secretion, gene expression, or cell growth. Calcium signaling has been however shown to be more complex than initially thought. Indeed, it is confined within cell microdomains, and different calcium channels are associated with different functions, as shown by various channelopathies. Sporadic mutations on voltage-operated L-type calcium channels in adrenal glomerulosa cells have been shown recently to be the second most prevalent genetic abnormalities present in human aldosterone-producing adenoma...
2016: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/27240535/a-systematic-review-of-calcium-channel-antagonists-in-bipolar-disorder-and-some-considerations-for-their-future-development
#9
A Cipriani, K Saunders, M-J Attenburrow, J Stefaniak, P Panchal, S Stockton, T A Lane, E M Tunbridge, J R Geddes, P J Harrison
l-type calcium channel (LTCC) antagonists have been used in bipolar disorder for over 30 years, without becoming an established therapeutic approach. Interest in this class of drugs has been rekindled by the discovery that LTCC genes are part of the genetic aetiology of bipolar disorder and related phenotypes. We have therefore conducted a systematic review of LTCC antagonists in the treatment and prophylaxis of bipolar disorder. We identified 23 eligible studies, with six randomised, double-blind, controlled clinical trials, all of which investigated verapamil in acute mania, and finding no evidence that it is effective...
October 2016: Molecular Psychiatry
https://www.readbyqxmd.com/read/27146976/the-transcription-factor-neurod2-coordinates-synaptic-innervation-and-cell-intrinsic-properties-to-control-excitability-of-cortical-pyramidal-neurons
#10
Fading Chen, Jacqueline T Moran, Yihui Zhang, Kristin M Ates, Diankun Yu, Laura A Schrader, Partha M Das, Frank E Jones, Benjamin J Hall
KEY POINTS: Synaptic excitation and inhibition must be properly balanced in individual neurons and neuronal networks to allow proper brain function. Disrupting this balance may lead to autism spectral disorders and epilepsy. We show the basic helix-loop-helix transcription factor NeuroD2 promotes inhibitory synaptic drive but also decreases cell-intrinsic neuronal excitability of cortical pyramidal neurons both in vitro and in vivo. We identify two genes potentially downstream of NeuroD2-mediated transcription that regulate these parameters: gastrin-releasing peptide and the small conductance, calcium-activated potassium channel, SK2...
July 1, 2016: Journal of Physiology
https://www.readbyqxmd.com/read/27025064/signal-mediators-at-induction-of-heat-resistance-of-wheat-plantlets-by-short-term-heating
#11
Yu V Karpets, Yu E Kolupaev, T O Yastreb
The effects of functional interplay of calcium ions, reactive oxygen species (ROS) and nitric oxide (NO) in the cells of wheat plantlets roots (Triticum aestivum L.) at the induction of their heat resistance by a short-term influence of hyperthermia (heating at the temperature of 42 degrees C during 1 minute) have been investigated. The transitional increase of NO and H2O2 content, invoked by heating, was suppressed by the treatment of plantlets with the antagonists of calcium EGTA (chelator of exocellular calcium), lanthanum chloride (blocker of calcium channels of various types) and neomycin (inhibitor of phosphatidylinositol-dependent phospholipase C)...
November 2015: Ukrainian Biochemical Journal
https://www.readbyqxmd.com/read/27022465/activation-of-transient-receptor-potential-ankyrin-1-induces-cgrp-release-from-spinal-cord-synaptosomes
#12
Talisia Quallo, Clive Gentry, Stuart Bevan, Lisa M Broad, Adrian J Mogg
Transient receptor potential ankyrin 1 (TRPA1) is a sensor of nociceptive stimuli, expressed predominantly in a subpopulation of peptidergic sensory neurons which co-express the noxious heat-sensor transient receptor potential vanilloid 1. In this study, we describe a spinal cord synaptosome-calcitonin gene-related peptide (CGRP) release assay for examining activation of TRPA1 natively expressed on the central terminals of dorsal root ganglion neurons. We have shown for the first time that activation of TRPA1 channels expressed on spinal cord synaptosomes by a selection of agonists evokes a concentration-dependent release of CGRP which is inhibited by TRPA1 antagonists...
December 2015: Pharmacology Research & Perspectives
https://www.readbyqxmd.com/read/27006502/differential-volume-regulation-and-calcium-signaling-in-two-ciliary-body-cell-types-is-subserved-by-trpv4-channels
#13
Andrew O Jo, Monika Lakk, Amber M Frye, Tam T T Phuong, Sarah N Redmon, Robin Roberts, Bruce A Berkowitz, Oleg Yarishkin, David Križaj
Fluid secretion by the ciliary body plays a critical and irreplaceable function in vertebrate vision by providing nutritive support to the cornea and lens, and by maintaining intraocular pressure. Here, we identify TRPV4 (transient receptor potential vanilloid isoform 4) channels as key osmosensors in nonpigmented epithelial (NPE) cells of the mouse ciliary body. Hypotonic swelling and the selective agonist GSK1016790A (EC50 ∼33 nM) induced sustained transmembrane cation currents and cytosolic [Formula: see text] elevations in dissociated and intact NPE cells...
April 5, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/26875775/progesterone-suppressed-vasoconstriction-in-human-umbilical-vein-via-reducing-calcium-entry
#14
Yun He, Qinqin Gao, Bing Han, Xiaolin Zhu, Di Zhu, Jianying Tao, Jie Chen, Zhice Xu
The aim of this study was to evaluate the actions of progesterone on human umbilical vein (HUV) from normal pregnancies and the possible underlying mechanisms involved. HUV rings were suspended in organ baths and exposed to progesterone followed by phenylephrine (PE) or serotonin (5-HT). Progesterone suppressed PE- or 5-HT-induced vasoconstriction in HUV rings. The inhibitory effect induced by progesterone was not influenced by nitric oxide syntheses inhibitor, prostaglandins syntheses blocker, the integrity of endothelium, selective progesterone receptor or potassium channel antagonists...
April 2016: Steroids
https://www.readbyqxmd.com/read/26854031/synergism-of-perampanel-and-zonisamide-in-the-rat-amygdala-kindling-model-of-temporal-lobe-epilepsy
#15
Vera Russmann, Josephine D Salvamoser, Maruja L Rettenbeck, Takafumi Komori, Heidrun Potschka
OBJECTIVE: Anticonvulsive monotherapy fails to be effective in one third of patients with epilepsy resulting in the need for polytherapy regimens. However, with the still limited knowledge, drug choices for polytherapy remain empirical. Here we report experimental data from a chronic epilepsy model for the combination of perampanel and zonisamide, which can render guidance for clinical studies and individual drug choices. METHODS: The anticonvulsant effects of the combination of perampanel and zonisamide were evaluated in a rat amygdala kindling model...
April 2016: Epilepsia
https://www.readbyqxmd.com/read/26845536/resveratrol-induces-intracellular-ca-2-rise-via-t-type-ca-2-channels-in-a-mesothelioma-cell-line
#16
Carla Marchetti, Stefania Ribulla, Valeria Magnelli, Mauro Patrone, Bruno Burlando
AIMS: Intracellular calcium (Ca(2+)) is known to play an important role in cancer development and growth. Resveratrol (Res) is a stilbene polyphenol occurring in several plant species and known for various possible beneficial effects, including its ability to inhibit proliferation and to induce apoptosis in cancer cells. This study was designed to determine whether Res affects Ca(2+) signaling in cancer cells. MAIN METHODS: We used the REN human mesothelioma cell line, as an in vitro cancer cell model, and the non-malignant human mesothelial MeT5A cell line, as normal cell model...
March 1, 2016: Life Sciences
https://www.readbyqxmd.com/read/26797466/even-a-pooled-analysis-does-not-resolve-the-debate-of-electrophysiology-testing-in-brugada-syndrome
#17
EDITORIAL
Emile G Daoud
No abstract text is available yet for this article.
February 16, 2016: Circulation
https://www.readbyqxmd.com/read/26661765/two-distinct-oscillatory-states-determined-by-the-nmda-receptor-in-rat-inferior-olive
#18
Dimitris G Placantonakis, John P Welsh
1 The effects of N-methyl-d-aspartate (NMDA) receptor activation and blockade on subthreshold membrane potential oscillations of inferior olivary neurones were studied in brainstem slices from 12- to 21-day-old rats. 2 Dizocilpine (MK-801), a non-competitive NMDA antagonist, at 1-45 μm abolished spontaneous subthreshold oscillations, without affecting membrane potential, input resistance, or the low-threshold calcium current, IT . Ketamine (100 μm), a non-competitive NMDA antagonist, and L-689,560 (20 μm), an antagonist at the glycine site of the NMDA receptor, also abolished the oscillations, while the competitive non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 20-50 μm) had no effect...
July 2001: Journal of Physiology
https://www.readbyqxmd.com/read/26627919/contribution-of-postsynaptic-t-type-calcium-channels-to-parallel-fibre-purkinje-cell-synaptic-responses
#19
Romain Ly, Guy Bouvier, German Szapiro, Haydn M Prosser, Andrew D Randall, Masanobu Kano, Kenji Sakimura, Philippe Isope, Boris Barbour, Anne Feltz
KEY POINTS: At the parallel fibre-Purkinje cell glutamatergic synapse, little or no Ca(2+) entry takes place through postsynaptic neurotransmitter receptors, although postsynaptic calcium increases are clearly involved in the synaptic plasticity. Postsynaptic voltage-gated Ca(2+) channels therefore constitute the sole rapid postsynaptic Ca(2+) signalling mechanism, making it essential to understand how they contribute to the synaptic signalling. Using a selective T-type calcium channel antagonist, we describe a T-type component of the EPSC that is activated by the AMPA receptor-mediated depolarization of the spine and thus will contribute to the local calcium dynamics...
February 15, 2016: Journal of Physiology
https://www.readbyqxmd.com/read/26621126/cannabinoid-receptor-agonists-modulate-calcium-channels-in-rat-retinal-m%C3%A3-ller-cells
#20
W Yang, Q Li, S-Y Wang, F Gao, W-J Qian, F Li, M Ji, X-H Sun, Y Miao, Z Wang
While activation of cannabinoid CB1 receptor (CB1R) regulates a variety of retinal neuronal functions by modulating ion channels in these cells, effect of activated cannabinoid receptors on Ca(2+) channels in retinal Müller cells is still largely unknown. In the present work we show that three subunits of T-type Ca(2+) channels, CaV3.1, CaV3.2 and CaV3.3, as well as one subunit of L-type Ca(2+) channels, CaV1.2, were expressed in rat Müller cells by immunofluorescent staining. Consistently, nimodipine- and mibefradil-sensitive Na(+) currents through L- and T-type Ca(2+) channels could be recorded electrophysiologically...
January 28, 2016: Neuroscience
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Cross-sex hormones and acute cardiovascular events in transgender persons
Zil Goldstein, Carl Streed, Tamar Resiman, Monica Mukherjee, Asa Radix
Research output: Contribution to journalLetter
Original languageEnglish (US)
Number of pages1
JournalAnnals of Internal Medicine
Volume170
Issue number2
DOIs
StatePublished - Jan 15 2019
Fingerprint
Transgender Persons
Gonadal Steroid Hormones
ASJC Scopus subject areas
• Internal Medicine
Cite this
Cross-sex hormones and acute cardiovascular events in transgender persons. / Goldstein, Zil; Streed, Carl; Resiman, Tamar; Mukherjee, Monica; Radix, Asa.
In: Annals of Internal Medicine, Vol. 170, No. 2, 15.01.2019.
Research output: Contribution to journalLetter
Goldstein, Zil ; Streed, Carl ; Resiman, Tamar ; Mukherjee, Monica ; Radix, Asa. / Cross-sex hormones and acute cardiovascular events in transgender persons. In: Annals of Internal Medicine. 2019 ; Vol. 170, No. 2.
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Textbook Notes (369,067)
Canada (162,366)
Psychology (528)
PSYCO367 (36)
Chapter 14
Sensation and Perception Psych 367 Chapter 14.docx
12 Pages
119 Views
Department
Psychology
Course Code
PSYCO367
Professor
Douglas Wylie
This preview shows pages 1,2 and half of page 3. Sign up to view the full 12 pages of the document.
Description
Chapter 14 the cutaneous senses Overview of the cutaneous system The skin - Comel called the skin the monumental facade of the human body - Heaviest organ - In addition to its warning function, the skin also prevents bodily fluids from escaping and at the same time protects us by keeping bacteria, chemical agents and dirt from penetrating our bodies - Epidermis: layer of dead cells in the outer layer - Dermis: found below the epidermis - Mechanoreceptors: are found in the two layers o They respond to mechanical stimulation such as pressure, stretching and vibration Mechanoreceptors - Four types of mechanoreceptors that are located in the epidermis and the dermis - We can distinguish between these receptors by their distinctive structures and by how fibres associated with the receptors respond to stimulation - Two mechanoreceptors o Merkel receptor o Meissner corpuscle - Both located close to the surface - The merkel receptor: fires continuously as long as the stimulus is on o Sensing fine details - The meissner corpuscle: fires only when the stimulus is first applied and when it is removed o Controlling handgrip - Found deeper in the skin o Ruffini cylinder Is associated with perceiving stretching of the skin o Pacinian corpuscle Sensing rapid vibrations and fine texture Pathways from skin to cortex - Peripheral nerves: Nerve fibres from receptors in the skin travel in bindles o They enter the spinal cord through the dorsal root - They then go up the spinal cord along two major pathways o Medial lemniscal pathway Has large fibres that carry signals related to sensing the position of the limbs (proprioception) and perceiving touch o Spinothalamic pathway Smaller fibres that transmit signals related to temperature and pain - The case of Ian waterman illustrates this separation in function , because although he lost the ability to feel touch and to sense the position of his limbs he was still able to sense pain and temperature - Most of these fibres synapse in the ventrolateral nucleus in the thalamus, but some synapse in other thalamic nuclei - Because the signals in the spinal cord have crossed over to the opposite side of the body on their way to the thalamus, signals originating from the left side of the body reach the thalamus in the right hemisphere of the brain, and signals from the right side of the body reach the left hemisphere Maps of the body on the cortex - From the thalamus, signals travel to the somatosensory receiving area (S1) in the parietal lobe of the cortex and possibly also to the secondary somatosensory cortex (S2) - Signals also travel between S1 and S2 - Important characteristic of the somatosensory cortex is that is organized into maps that correspond to locations on the body - When penfield stimulated points on S1 and asked patients to report what they perceived - Homunculus: The resulting body map o Some areas on the skin are represented by disproportionately large area of the brain o Results analogous to the magnification factor in vision - Similarity, parts of the body such as the fingers, what are used to detect details through the sense of touch, are allotted a large area on the somatosensory cortex The plasticity of cortical body maps - Experiments that demonstrated experiment dependent plasticity were carried out in the somatosensory system - Jenkins and Merzenish showed that increasing stimulation of a specific area of the skin causes an expansion o the cortical area receiving signals from that area of skin - Comparison of the cortical maps of the fingertip measured just before the training and 3 months later shows that the area representing the stimulated fingertip was greatly expanded after the training - The effect of plasticity is determined by measuring how special training affects the brain - What this plasticity means is that while we can specify the general area of the cortex that represents a particular part of the body, the exact size of the area representing each part of the body is not totally fixed Perceiving details - Examples of perceiving details with the skin is provided by Braille, the system of raised dots that enables blind people to read with their fingertips - Experienced Braille readers can read at the rate of 100 words per minute - Normal readers 300 words per minute - Measuring tactile acuity o Tactile acuity: the ability to detect details on the skin o Two point threshold The minimum separation between two points on the skin that when stimulated is perceived as two points o Grating acuity Measured by pressing a grooved stimulus onto the skin and asking the person to indicate the orientation of the grooves Receptor mechanisms for tactile acuity - Merkel receptor is sensitive to details - Fibres associated with a Merkel receptor fires in response to a grooved stimulus pushed into the skin - Merkel receptors fibre signals details - High density of merkel receptors in the fingertips, because the fingertips are the parts of the body that are most sensitive - Better acuity is associated with less spacing between merkel receptors - While receptor spacing is part of the answer, the cortex also plays a role in determining tactile acuity Cortical mechanisms for tactile acuity - Representation of the body in the brain and the acuity at different locations on the body - The map of the body on the brain is enlarged to provide extra neural processing that enables us to accurately sense fine details with our fingers and other parts of the body - Demonstrate the connection between cortical mechanisms and acuity by Determine the receptive fields of neurons in different parts of the cortical homunculus - The receptive field for a neuron in the visual system is the area on the retina that when stimulated, influences the firing of the neuron - The receptive field for a neuron in the cutaneous system is the area on the skin that, when stimulated influences the firing of the neurons - Cortical neurons representing parts of the body with better acuity, such as the fingers, have smaller receptive fields - This means that two points that are closer together on the fingers might fall on different receptors - Having small receptive fields of neurons receiving signals from the fingers translates into more separation on the cortex, which enhances the ability to feel too close together points on the skin as two separate points Perceiving vibration - The mechanoreceptor that is primarily responsible for sensing vibration is the pacinian corpuscle - Recording from fibres associated with the PC show that these fibres respond poorly to slow or constant pushing, but respond well to high rates of vibration - The presence of the PC determine which pressure stimuli actually reach the fibres - PC which consists of a series of layers, like an onion, with fluid between each layer, transmits rapidly applied pressure like vibration to the nerve fibres - But it does not transmit constant pressure - The corpuscle causes the fibres to receive rapid changes in pressure, but not the receive continuous pressure - If the PC does not transmit continuous pressure to the fire, then pressing continuous pressure to the PC should cause no response in the fibre - Lowenstein o Showed that when pressure was applied to the corpuscle o The fibre responded when the pressure was first applied and when it was removed, but did not respond to continuous pressure o When lowenstien dissected away the corpuscle and applied pressure directly to the fibre, the fibre fired to the continuous pressure o That properties of the corpuscle cause the fibre to respond poorly to continuous stimulation Perceiving texture - Katz proposed that our perception of texture depends on both spatial cues and temporal cues - Spatial cues: are caused by relatively large surface elements, such as bumps - Temporal cues: occur when the skin move across a textured surface o This cue provides information in the form of vibrations that occur as a result of the movement over the surface o Responsible for our fine grain textures - Hollins o Provided evidence that temporal cues are responsible for our perception of fine textures o Duplex theory of texture perception Two types of receptors - Hollins and Risner o Presented evidence for the role of temporal cues by showing that when participants touch surfaces without moving their fingers, they couldn’t tell texture o Movement which generates vibration as the skin scans a surface, make it possible to sense the roughness of fine surfaces - Selective adaptation o Involves presenting a stimulus that adapts a particular type of receptor and then testing to see how inactivation of that receptor by adaptation affected perception - Hollins o Presenting two adaptation conditions o First was 10Hz adaptation in which the skin was vibrated for 6 minutes o The frequency adaptation for meissner corpuscle which responds to low frequencies o 250 Hz adaptation This was to adapt the pacinian corpuscle which responds to high frequencies o Following each type of adaptation, participants ran their fingers over two fine textures o Results indicate that participants could tell the difference between the two textures when they had not been adapted or had received that 10Hz o But they couldn’t tell the difference when adapted to the 250 Hz o Adapting pacinian corpuscle receptor, which respond to vibration, eliminates the ability to sense fine textures - The most remarkable thing about perceive texture with a tool is that what you perceive is not the vibration, but the texture of the surface Perceiving objects - Ability to identify objects and their features by touch is an example of active touch o Touch in which a person actively explores an object - Active touch contrast with passive touch o When touch stimuli are applied to the skin - Haptic perception: perception in which 3D objects are explored with the hand Identifying objects by haptic exploration - Provides good example of a situation in which a number of different system are interacting with each other - The sensory system, which was involved in detecting cutaneous sensations such as touch, temperature and texture - Motor system, which was involved in moving your fingers and hands - The cognitive system, which was involved in thinking about the information provided by
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Meeting Banner
Abstract #2211
Phase Velocity Imaging of Portal Pressure Gradients for Evaluating Liver Cirrhosis
Kim H, Pinus A, Qiu M, Wang Y, Todd Constable R
Yale University
Liver cirrhosis can be characterized by portal hypertension. The current gold standard for diagnosis is biopsy but this is limited by its invasive nature. A new MR model of the portal pressure gradient is presented that provides reproducible non-invasive diagnosis of liver cirrhosis. The method is tested in CCl4 induced cirrhotic and normal rats. This approach revealed statistically significant differences in portal pressure gradient along the portal vein between cirrhotic and normal control rats, suggesting that the portal pressure gradient method is potentially useful in the diagnosis of liver cirrhosis.
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PSTF Logo
Public Safety Training Facility
Monroe Community College
Rochester, New York
MCC PARAMEDIC PROGRAM CME
Calcium Channel Antagonists
RP Breese, EMT-P
Influx of Calcium Ions (Ca++) through the cell membrane and sarcoplasmic reticular membrane is a key trigger for a number of intracellular bioactivities. Membranes form water and ion-impermeable barriers that allow localized compartmentalization to occur. The most basic function of these membranes is to isolate these compartments from outside environments and allow for specialized reactions to take place. Some means must exist for entry (influx) and exit (efflux) of solutes for the regulation of cell volume and as a means of allowing chemical interactions. This influx is accomplished using specialized pores or channels through the membrane. These ion channels are specific for ions and are opened and closed by various means, including: ligand binding, voltage-dependency and, in the case of vascular smooth muscle, stretch-opening.
The concept of ligand binding is simple, a chemical (ligand) binds to a receptor site forming a ligand-receptor bond. Neurotransmitters, such as norepinephrine, are considered ligands. [Figure 1] This bond changes the electrical structure of the protein gate and it opens. Voltage-dependency is more akin to a light switch. When no electrical current is flowing through a light bulb, there is no light. Similarly, when the membrane is at rest or is in a hyperpolarized state, the ion channels remain closed. When depolarization occurs, the rapid movement of sodium (Na+) into the cell causes the inner surface of the cell membrane to became positively charged. This change in electrical charge causes the voltage-dependent proteins of the ion channel to again change shape, opening the channel to ion flow. Ion flow always follows the concentration gradient (most to least).
The intracellular concentration of unbound calcium ions determines the activity of the contractile tissues in cardiac and vascular smooth muscle cells. Voltage-gated calcium channels are present in all muscle and nerve cells as well as many secretory cells. These calcium ion channels have been differentiated into four sub-types. These include: T (transient), N (neural), P (purkinje[brain]) and L (long- lasting [slow]). T-type channels are found in smooth muscle, skeletal muscle and cardiac myocytic membranes. They have a low conductance (only allow small amounts of ion passage) and a short opening time (fast channels). T-type channels are thought to have a role in initiation of action potentials, but none in contractility. N-type channels are found only in neurons and are thought to play a direct role in release of neurotransmitter quantal packages into the synapse and are insensitive to calcium antagonists. P-type channels are found only in cerebellar purkinje neurons in the brain and, as such, are not discussed here. The majority of calcium antagonists affect L-type calcium slow channels. L-type channels are found extensively in both myocardial and vascular tissues, as well as in the smooth muscle of the gut.
The voltage-dependent L-type, ligand (receptor)-operated, calcium channel is composed of five sub-units of transmembrane proteins. The a1 appears to be the primary site for binding all three of the primary calcium channel blockers: the 1,4-dihydropyridines, the phenylalkylamines, and the benzothiazepines. While all three types of calcium antagonists are thought to attach to the same receptor, their affinity for the receptor changes according to the state of the receptor (rest, activated, or inactivated). This is known as state or use-dependence and is thought by some researchers to involve the reshaping of the receptor site when it is in various states, producing, in essence, three different receptor sites. Other sources simply indicate that there are three separate receptor sites on the a1 subunit of the L-type channel. For simplicity sake, we will concentrate on the latter or these two theories.
As previously mentioned, the L-type channels are found in a variety of tissues. Yet this range of target tissues is not necessarily reflected in pharmacologic or therapeutic activity. For example, skeletal muscle tissue is relatively unaffected by calcium channel blockage, as evidenced by the fact that there is no associated loss of postural tone during treatment. The activity of a calcium antagonist, or agonist for that matter, may well be affected by the location of the receptor site and the frequency of channel activity. The verapamil and diltiazem binding sites are located internally, deep within the channel. Access to the receptor is therefore enhanced when the channel is open. The rapidly firing tissues of the myocardium and the atrioventricular (AV) node provide ample opportunity for the binding of these agents, which are pharmacologically active in myocardial and cardiac-contractile tissues. Nifedipine, a 1,4-dihydropyridine calcium antagonist, is preferential to the binding sites in vascular smooth muscle, which exist more frequently in a depolarized (closed, not reactive) state.
Of the three types of calcium antagonists mentioned, the dihydropyridine are the most active at causing peripheral vasodilatation. However, at therapeutic doses, any calcium antagonist will have a varying degree of vasodilatation. Phenylalkylamines, such as Verapamil and benzothiazepines, such as Diltiazem, are very effective at slowing supraventricular tachydysrhythmias, especially reentrant varieties. This is due to the slowing of nodal repolarization (prolonging refractoriness). Additionally, Verapamil and Diltiazem slow the rapid ventricular rates associated with uncontrolled atrial fibrillation or flutter. However, use of calcium channel blockers in patients with wide complex atrial fibrillation/flutter associated with pre-excitation syndromes such as WPW (Wolff-Parkinson-White) is contraindicated due to an enhance retrograde conduction of signals which may cause accelerated reentrant tachydysrhythmias. Diltiazem has no significant effects on heart tissues that are fast sodium channel dependent, (e.g. His-Purkinje tissue, atrial and ventricular muscle tissue).
Phenylalkylamines
Benzothiazepines
Dihydropyridines
Verapamil
Tiapamil
Gallopomil
Diltiazem
Clenthiazem
Nifedipine
Nicardipine
Amlopidine
Felodipine
Isradipine
Nitrendipine
Nisoldipine
Table 1 : Classification of Calcium Antagonists Based on Chemical Grouping
Systemic Hypertension
Angina Pectoris
Vasospastic Angina
Arrhythmias (Supraventricular tachycardia)
Migraine Headache
Peripheral Vascular Disease
Raynaud's Phenomenon
Primary pulmonary hypertension
Table 2: Cardiovascular Uses of Calcium Channel Blockers
The chief hemodynamic effect of calcium antagonists is vasodilatation of the coronary and peripheral arteries. 1,4-dihydropyridines, such as nifedipine have a potent vasodilatory effect on both coronary and peripheral arteries. Diltiazem has approximately the same effect on coronary artery vasodilatation, but is much less potent as a peripheral vasodilator than either nifedipine or verapamil. Verapamil, a benzothiazepine, has less vasodilatory effects than diltiazem and has an intermediate effect on peripheral vasculature. All calcium channel blockers reduce the vasopressor effects of norepinephrine and have been demonstrated to cause a transient blockade of angiotensin II.
All calcium antagonist possess negative inotropic effects on myocardium. Verapamil is the most potent negative inotrope, followed by nifedipine, then diltiazem. At therapeutic dose, verapamil and diltiazem- but not nifedipine or other dihydropyridines- are active in conductive tissue. Verapamil is more effective in slowing AV conduction, while diltiazem has a more pronounced effect on the sinus node. Intravenous verapamil and diltiazem are both useful in the treatment of supraventricular tachydysrhythmias. However, nifedipine as well as all 1,4-dihydropyridines have little negative dromotropic or chronotropic effects and may cause increases in heart rate due to sympathetic stimulation. This presents a clear contraindication for the use of nifedipine or other dihydropyridines in patients with tachydysrhythmias.
The majority of adverse effects of oral calcium antagonists are listed below and also include constipation as the chief adverse reaction due to the affinity of these medications for the smooth muscle of the gut. Adverse effects of intravenous calcium antagonists are associated with the vasodilatory effects of the class. These adverse effects are outlined in Table 3.
Headache
Flushing
Palpitations
Hypotension
Peripheral Edema
Exacerbated CHF
Bradydysrhythmias
AV Conduction disturbances
Table 3: Adverse effects of intravenous calcium antagonists
Contraindications to calcium channel blockers include bradydysrhythmias, SA node or AV node conduction disturbances, hypotension, congestive heart failure, dilated cardiomyopathies with or without history of acute myocardial infarction and pre-excitation syndromes, such as Wolff-Parkinson-White because of increased ventricular rate and enhanced accessory pathway conduction. Calcium antagonists worsen dysrhythmias associated with digitalis toxicity, and are therefore contraindicated. Additionally, dihydropyridines are contraindicated post MI because of an unopposed sympathetic reflex, which is likely to increase heart rate and aggravate myocardial ischemia. Drug interactions have been reported with concomitant use of calcium antagonists, beta-adrenergic antagonists and class Ia antiarrhythmics, such as quinidine. This is due to a synergistic prolongation of refractoriness, especially that of the AV node.
Generic Name
Dosage
Diltiazem 0.25mg/kg initial followed by 0.35mg/kg (generally 15 - 25 mg Slow IVP or as a drip over 10 minutes)
Verapamil 0.075mg/kg (generally 2.5 - 15 mg Slow IVP)
Table 4:Dosage and Administration Information
Summary
Calcium ion influx is crucial in neuronal, muscular and hormonal activities of all cells, particularly those of the cardiovascular system. Vascular tone, conduction and heart rate may require modification in the patient with cardiovascular disease. Understanding the actions of any of the myriad of medications that the patient may take at home, as well as medications carried by the prehospital provider is essential for the safe and efficacious delivery of emergency medicine. Calcium antagonists come in different varieties and have differing effects. Choosing when to administer, or just as importantly, when to withhold any medication is the mark of the true clinician.
1. Haber, E: Molecular Cardiovascular Medicine, 1995, Scientific American
2. Norlander M, Thalen P: Effects of felodipine on local and neurogenic control of vascular resistance. J Cardio Pharmocol.
3. Hess P: Calcium channels in vertebrate cells. Annu Rev Neurosci 13:337, 1990
4. Mitchell, et al: Comparative clinical electrophysiologic effects of diltiazem and nifedipine: a review. Am J Cardiol 18:629, 1982
5. Triggle DJ: Calcium-channel drugs: structure-function relationships and selectivity of action. J Cardiovasc Pharmacol 18 (suppl.10):S1, 1991
6. Peopho, RW: Pharmacology of the CCB; www.cc.emory.edu/WHSC/MED/CME/CCB/pharm.htm
7. Singh, et al: Cardiovascular Pharmacology and Therapeutics, 1stEd. 1994, Churchill Livingstone
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URL: /depts/pstc/backup/paraccb1.htm
Updated: November 10, 1997
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Oxidative stress. Oxidative stress and the production of free radicals also are involved in the development of peripheral neuropathy. Free radicals may damage blood vessels, leading to ischemia in the nerve cells, and facilitate the production of advanced glycation end products, which in turn contribute to the development of peripheral neuropathy.9
Signs and Symptoms
The peripheral nervous system can be damaged by diabetes in numerous ways. Most commonly, patients with diabetes experience peripheral neuropathy. Symptoms typically include lower-extremity weakness, in addition to tingling, pain, burning, and electrical and stabbing sensations with or without numbness. Patients may describe a sensation that feels like socks bunching up in their shoes. These symptoms usually begin in the feet and move proximally (stocking-and-glove distribution). The symptoms present symmetrically and appear sensory in nature. Over time, allodynia (painful sensations in response to innocuous stimuli) and hyperalgesia (increased sensitivity to painful stimuli) may develop.10 Diabetic peripheral neuropathy is insidious in nature and can lead to foot ulceration. These ulcerations can be slow to heal, become infected, and lead to amputation. Unfortunately, patients with peripheral neuropathy may not report their symptoms, and often, fewer than half of patients are treated for their pain. Table 2 provides an overview of some of the common signs and symptoms of diabetic peripheral neuropathy.
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Risk Factors
A variety of risk factors for the development of diabetic neuropathy are known (Table 3). According to the Diabetes Control and Complications Trial,1 hyperglycemia is one of the most significant risk factors. Others include a long duration of diabetes, large total exposure to hyperglycemia, male sex, advanced age, elevated lipid levels, elevated blood pressure, kidney disease, cigarette smoking, overweight, increased height, and a high level of exposure to other potentially neurotoxic agents, such as ethanol. Genetic factors, such as the HLA-DR3/4 phenotype and apolipoprotein E genotype, are also associated with a risk for diabetic peripheral neuropathy.
Click to enlarge
This article originally appeared on Clinical Advisor
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01.12.2017 | Research | Ausgabe 1/2017 Open Access
Molecular Cancer 1/2017
Oncogenic miR-210-3p promotes prostate cancer cell EMT and bone metastasis via NF-κB signaling pathway
Zeitschrift:
Molecular Cancer > Ausgabe 1/2017
Autoren:
Dong Ren, Qing Yang, Yuhu Dai, Wei Guo, Hong Du, Libing Song, Xinsheng Peng
Wichtige Hinweise
Electronic supplementary material
The online version of this article (doi:10.1186/s12943-017-0688-6) contains supplementary material, which is available to authorized users.
Abbreviations
EMT
Epithelial-mesenchymal transition
ERBB2
Erb-B2 Receptor Tyrosine Kinase 2
H&E
Hematoxylin and Eosin Stain
IL11
Interleukin 11
miR-210-3p
miRNA-210-3p
MMP13
Matrix metallopeptidase 13
NF-κB
Nuclear factor kappa-light-chain-enhancer of activated B cells
PCR
Polymerase Chain Reaction
PDLIM7
PDZ and LIM domain 7
PIAS4
Protein inhibitor of activated STAT 4
SNAIL1
Snail family transcriptional repressor 1
SOCS1
suppressor of cytokine signaling 1
TCGA
The Cancer Genome Atlas
TNIP1
TNFAIP3 interacting protein 1
TWIST1
Twist family bHLH transcription factor 1
ZEB1/2
Zinc finger E-box binding homeobox 1/2
Background
Prostate cancer (PCa) is the most common malignant cancer and the second leading cause of cancer-related death in men worldwide [1]. The primary issue derived from PCa is its propensity to metastasize to bone, which occurred in up to 90% of patients with advanced PCa [2]. Despite great advances in systemic and individualized treatments of PCa in the last decades, distant bone metastasis remains a principal issue, which severely affects the quality of life and survival time of PCa patients [3]. Thus, it is of great importance to better understand the underlying mechanisms contributing to bone metastasis of PCa, which will facilitate the development of novel anti-bone metastasis therapeutic avenues in PCa.
Epithelial-mesenchymal transition (EMT) is an imperative phenotypic conversion that occurs during several processes, including embryonic development, tissue remodelling and metastasis, where epithelial cells obtain mesenchymal-like properties in combination with reduced intercellular adhesion and enhanced motility [4, 5]. EMT is a transient and dynamic process that primarily emerges at the onset of invasion and is tightly controlled by several cellular signaling pathways, such as ErbB, Wnt, NF-kB and TGF-β pathways [68]. Among these, transforming growth factor (TGF)-β is identified as the most important inducer of EMT process due to stimulation of the expression of EMT-inducing transcription factors, including Snail1, Twist1 and ZEB1/2 [911]. Furthermore, accumulating studies have demonstrated that NF-kB signaling pathway is essential for the induction and maintenance of EMT in a large number of cancers [7, 12, 13]. The NF-κB pathway was discovered nearly three decades ago [14], and the critical roles of the NF-κB pathway in physiologic processes, such as immunity and inflammation, have been well documented [15, 16]. NF-κB signaling has been reported to be constitutively activated in a number of human cancers, which contributed to the initiation and progression of a large array of malignancies [15, 17]. Furthermore, accumulating literatures reported that NF-κB signaling plays a crucial role in the bone metastasis of various types of cancers [18, 19]. Park and colleagues reported that constitutive NF-κB activity in breast cancer cells was crucial for the bone resorption characteristic of the osteolytic bone metastasis via transcriptionally regulating granulocyte macrophage-colony stimulating factor (GM-CSF) that mediated osteolytic bone metastasis of breast cancer by stimulating osteoclast development [20]. Furthermore, several lines of evidence have implied that NF-κB activation was also associated with the metastatic phenotype of PCa progression [19, 21]. Chen et al. reported that NF-κB activation was crucial for the development of PCa bone metastasis [19]. However, the underlying mechanism responsible for constitutive activation of NF-κB signaling in the bone metastasis of PCa remains largely unknown.
MicroRNAs (miRNAs) are small endogenous non-coding RNAs that are responsible for post-transcriptional regulation of target genes by binding with specific sequences in the 3′ untranslated region (3’UTR) of downstream target genes, leading to mRNA degradation and/or translational inhibition [22]. miRNAs play important roles in many cellular and biological processes such as proliferation, apoptosis, differentiation, metabolism, cardiogenesis, development and function of the nervous and immune systems [22, 23]. The dysregulation of miRNAs in cancers is widely documented, and several studies have revealed a correlation of miRNAs expression levels and metastatic tumors [24, 25]. Furthermore, several miRNAs have been reported as mediators in the bone metastasis of PCa [26, 27]. Our previous studies demonstrated that loss of wild-type P53 induced downregulation of miR-145 promoted bone metastasis of PCa via regulating several positive regulators of EMT [2830]. These studies indicate that aberrant expression of miRNAs elicited by unknown mechanism plays a crucial role in the bone metastasis of PCa.
In this study, we report that miR-210-3p expression is elevated in PCa tissues compared with the adjacent prostate epithelial tissues (ANT). Interestingly, the expression levels of miR-210-3p increases steadily from non-bone metastatic PCa tissues, bone metastatic PCa tissues to metastatic bone tissues and high expression of miR-210-3p positively correlates with the clinicopathological characteristics and bone metastasis status of PCa patients. Furthermore, upregulating miR-210-3p enhances, while silencing miR-210-3p suppresses the EMT, invasion and migration of PCa cells in vitro. Importantly, silencing miR-210-3p significantly inhibits bone metastasis of PC-3 cells in vivo. Furthermore, our results demonstrate that miR-210-3p promotes EMT, invasion and migration of PCa cells via targeting negative regulators of NF-κB signaling (TNF-α Induced Protein 3 Interacting Protein 1) TNIP1 and (Suppressor Of Cytokine Signaling 1) SOCS1, resulting in constitutive activation of NF-κB signaling pathway. Our results further indicate that recurrent gains are responsible for miR-210-3p overexpression in a small number of PCa patients. The analysis of clinical correlation reveals that miR-210-3p inversely correlates with SOCS1 and TNIP1, but positively correlates with NF-κB signaling activity in human PCa and metastatic bone tissues. Taken together, these findings uncover a plausible mechanism responsible for constitutive activation of NF-κB signaling in bone metastasis of PCa, suggesting that miR-210-3p may serve as a novel target for clinical intervention in PCa.
Methods
Cell culture and hypoxic condition
The human PCa cell lines 22RV1, PC-3, VCaP, DU145, LNCaP and normal prostate epithelial cells RWPE-1 were obtained from Shanghai Chinese Academy of Sciences cell bank (China). RWPE-1 cells were grown in defined keratinocyte-SFM (1×) (Invitrogen). PC-3, LNCaP and 22Rv1 cells were cultured in RPMI-1640 medium (Life Technologies, Carlsbad, CA, US) supplemented with penicillin G (100 U/ml), streptomycin (100 mg/ml) and 10% fetal bovine serum (FBS, Life Technologies). DU145 and VCaP cells were grown in Dulbecco’s modified Eagle’s medium (Invitrogen) supplemented with 10% FBS. The C4-2B cell line was purchased from the MD Anderson Cancer Center and maintained in T-medium (Invitrogen) supplemented with 10% FBS [31]. All cell lines were grown under a humidified atmosphere of 5% CO2 at 37 °C. A hypoxic condition was induced via culturing the cells under 1% oxygen tension (1% O2) in a hypoxia chamber for 24–48 h, as previously described [32], as well as treated the cells with 50–200 μmol L−1 cobalt chloride (CoCl2) for 24 h to mimic the hypoxic condition by stabilization of HIF-1a [33].
Plasmid, small interfering RNA and transfection
The human miR-210-3p gene was PCR-amplified from genomic DNA and cloned into a pMSCV-puro retroviral vector (Clontech, Japan). The pNFκB-luc and control plasmids (Clontech, Japan) were used to examine the activity of transcription factor quantitatively. The 3′-untranslated region (3’UTR) regions of the human SOCS1 and TNIP1 were PCR-amplified from genomic DNA and cloned into pmirGLO vectors (Promega, USA), and the list of primers used in cloning reactions is presented in Additional file 1: Table S1. Antagomir-210-3p, small interfering RNA (siRNA) for the SOCS1 and TNIP1 knockdown and conresponding control siRNAs were synthesized and purified by RiboBio. Transfection of miRNA, siRNAs, and plasmids was performed using Lipofectamine 3000 (Life Technologies, USA) according to the manufacturer’s instructions.
RNA extraction, reverse transcription, and real-time PCR
Total RNA from tissues or cells was extracted using the RNA Isolation Kit (Qiagen, USA) according to the manufacturer’s instructions. Messenger RNA (mRNA) and miRNA were reverse transcribed from total mRNA using the RevertAid First Strand cDNA Synthesis Kit (Thermo Fisher, USA) according to the manufacturer’s protocol. Complementary DNA (cDNA) was amplified and quantified on the CFX96 system (BIO-RAD, USA) using iQ SYBR Green (BIO-RAD, USA). The primers are provided in Additional file 2: Table S2. The analysis procedure of amplification level in PCa tissues was as following: examine the CNV of each sample of prostate cancer using Real time PCR primer Hs03772990_cn through TaqMan Copy Number Assay; TaqMan Copy Number Reference Assay RNase P and TaqMan Fast Advanced Master Mix were used as the loading control and amplification kit; procure the CNV number of each corresponding sample and define the CNV number of Amplification and Gain groups as “Gain” and the rest as “No Gain”; analyze the result using Excel 2010 and depict each figure respectively by GraphPad 5 software. Primers for U6 and miR-210-3p were synthesized and purified by RiboBio (Guangzhou, China). U6 or glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was used as the endogenous controls. Relative fold expressions were calculated with the comparative threshold cycle (2-ΔΔCt) method.
Patients and tumor tissues
A total of 149 archived PCa tissues, including 81 non-bone metastatic PCa tissues and 68 bone metastatic PCa tissues, and 9 metastatic bone tissues were obtained during surgery or needle biopsy at The First People’s Hospital of Guangzhou City (Guangzhou, China) between January 2008 and October 2016. Patients were diagnosed based on clinical and pathological evidence, and the specimens were immediately snap-frozen and stored in liquid nitrogen tanks. For the use of these clinical materials for research purposes, prior patient’ consents and approval from the Institutional Research Ethics Committee were obtained. The clinicopathological features of the patients are summarized in Additional file 3: Table S3. The median of miR-210-3p expression in PCa tissues was used to stratify high and low expression of miR-210-3p.
High throughput data processing
Copy number variation profile of prostate cancer dataset was downloaded from The Cancer Genome Atlas (TCGA; https://gdc.cancer.gov/). The analysis method for copy number variation profile was as following: download the Level 3 Copy Number Variation (CNV) dataset of prostate cancer in SNP6.0 microarray from TCGA; analyze the dataset by GISTIC2.0 software as described previously (all parameters as the default) [34]; procure the CNV number of each corresponding sample and define the CNV number of Amplification and Gain groups as “Gain” and the rest as “No Gain”; analyze the result using Excel 2010 and depict each figure using GraphPad 5 software.
Western blotting
Nuclear/cytoplasmic fractionation was separated using the Cell Fractionation Kit (Cell Signaling Technology, USA) according to the manufacturer’s instructions, and the whole cell lysates were extracted with RIPA Buffer (Cell Signaling Technology). Western blotting was performed according to a standard method, as described previously [35]. Antibodies against E-cadherin (Cat# 3195), Vimentin (Cat# 5741), Fibronectin (Cat# 4706), SOCS1 (Cat# 3950), TNIP1 (Cat# 4664) and PIAS4 (Cat# 4392) were purchased from Cell Signaling Technology, and p65 (cat# 10745–1-AP) from Proteintech, p84 (Cat#:PA5–27816) from Invitrogen and PDLIM7 (Cat#:SAB1406807) from Sigma-Aldrich,USA. The membranes were stripped and reprobed with an anti–α-tubulin antibody (Sigma-Aldrich, USA) as the loading control.
Luciferase assay
Cells (4 × 104) were seeded in triplicate in 24-well plates and cultured for 24 h. Cells were transfected with 100 ng of the pNFκB reporter luciferase plasmid, or pmirGLO-SOCS1–3′UTR, or –TNIP1–3′UTR luciferase plasmid, plus 5 ng pRL-TK the Renilla plasmid (Promega) using Lipofectamine 3000 (Invitrogen) according to the manufacturer’s recommendations. Luciferase and Renilla signals were measured 36 h after transfection using a Dual Luciferase Reporter Assay Kit (Promega) according to the manufacturer’s protocol.
miRNA immunoprecipitation
Cells were co-transfected with HA-Ago2, followed by HA-Ago2 immunoprecipitation using anti-HA-antibody. Real-time PCR analysis of the IP material was performed to test the association of the mRNA of SOCS1 and TNIP1 with the RISC complex. The specific processes were performed as previously described [36].
Invasion and migration assays
The invasion and migration assays were performed using Transwell chamber consisting of 8-mm membrane filter inserts (Corning) with or without coated Matrigel (BD Biosciences) respectively as described previously [37]. Briefly, the cells were trypsinized and suspended in serum-free medium. Then, 1.5 × 105 cells were added to the upper chamber, and lower chamber was filled with the culture medium supplemented with 10% FBS. After incubation for 24–48 h, cells passed through the coated membrane to the lower surface, where cells were fixed with 4% paraformaldehyde and stained with haematoxylin. The cell count was performed under a microscope (×100).
Animal study
All mouse experiments were approved by The Institutional Animal Care and Use Committee of Sun Yat-sen University and the approval-No. was L102012016110D. For the bone metastasis study, BALB/c-nu mice ((5–6 weeks old, 18–20 g)) were anaesthetized and inoculated into the left cardiac ventricle with 1 × 105 PC-3 cells in 100 μl of PBS. Bone metastases were monitored by bioluminescent imaging (BLI) as previously described [38]. Osteolytic lesions were identified on radiographs as radiolucent lesions in the bone. The area of the osteolytic lesions was measured using the Metamorph image analysis system and software (Universal Imaging Corporation), and the total extent of bone destruction per animal was expressed in square millimeters. Each bone metastasis was scored based on the following criteria: 0, no metastasis; 1, bone lesion covering <1/4 of the bone width; 2, bone lesion involving 1/4 ~ 1/2 of the bone width; 3, bone lesion across 1/2 ~ 3/4 of the bone width; and 4, bone lesion >3/4 of the bone width. The bone metastasis score for each mouse was the sum of the scores of all bone lesions from four limbs. For survival studies, mice were monitored daily for signs of discomfort, and were either euthanized all at one time or individually when presenting signs of distress, such as a 10% loss of body weight, paralysis, or head tilting.
Statistical analysis
All values are presented as the mean ± standard deviation (SD). Significant differences were determined using the GraphPad 5.0 software (USA). Student’s t-test was used to determine statistical differences between two groups. The chi-square test was used to analyze the relationship between miR-210-3p expression and clinicopathological characteristics. P < 0.05 was considered significant. All experiments were repeated three times.
Results
miR-210-3p expression is elevated in PCa, particularly in bone-metastatic PCa
To determine the clinical significance of miR-210-3p in PCa, we first analyzed the miRNA sequencing dataset of PCa from The Cancer Genome Atlas (TCGA) and found that miR-210-3p expression was elevated in PCa tissues compared with the adjacent normal tissues (ANT) (Fig. 1a and b). Interestingly, miR-210-3p expression was further higher in bone metastatic PCa tissues than in non-bone metastatic PCa tissues (Fig. 1c). We further examined the expression levels of miR-210-3p in our 149 PCa tissues and found that the miR-210-3p expression level in bone metastatic PCa tissues was robustly elevated compared with non-bone metastatic PCa tissues (Fig. 1d). Furthermore, the percentage of high expression of miR-210-3p was higher in bone metastatic PCa tissues than in non-bone metastatic PCa tissues (Additional file 4: Fig. S1a). Consistent with the miR-210-3p expression in PCa tissues, miR-210-3p expression was elevated in PCa cells compared with normal prostate epithelial cells RWPE-1 (Fig. 1e and Additional file 4: Figure S1b). Importantly, the miR-210-3p expression levels in bone metastatic PCa cell lines (PC-3, C4-2B and VCaP) were differentially higher than in primary PCa cell 22RV1 and brain metastatic cell line DU145 and lymph node metastatic cell line LNCaP (Fig. 1e). Statistical analysis of PCa tissue samples revealed that miR-210-3p overexpression strongly correlated with serum PSA levels, Gleason grade and bone metastasis status in PCa (Additional file 3: Table S3 and Additional file 5: Table S4). Collectively, these results indicate that overexpression of miR-210-3p is involved the bone metastasis of PCa.
Silencing miR-210-3p inhibits bone metastasis of PC-3 cells in vivo
To determine the effect of miR-210-3p on the bone metastasis of PCa in vivo, we first endogenously silenced miR-210-3p by transfecting anti-miR-210-3p in PC-3 cells based on the expression level of miR-210-3p shown in Fig. 2e (Additional file 6: Figure S2). To establish a rapid mouse model of bone metastasis, the luciferase-labeled vector or miR-210-3p-silencing PC-3 cells were inoculated perspectively into the left cardiac ventricle of male nude mice to monitor the progression of bone metastasis by bioluminescence imaging (BLI). As shown in Fig. 2a and b, the miR-210-3p-silenced PC-3 cells displayed lower bone metastasis ability compared with the control group by X-ray and BLI. H&E staining of the tumor sections from the tibias of injected mice demonstrated that silencing miR-210-3p dramatically reduecd the tumor burden in bone (Fige. 2c).Furthermore, miR-210-3p silenced cells exhibited fewer bone metastatic sites and smaller osteolytic area of metastatic tumors, as well as longer survival and bone metastasis-free survival compared to the control group (Fig. 2e-g). The effect of silencing miR-210-3p on proliferation was not cytotoxic as assessed by MTT assay of proliferation in PC-3 cells (Fig. 2h). Consequently, these finding demonstrate that silencing miR-210-3p inhibits the bone metastasis of PCa in vivo.
miR-210-3p promotes EMT, migration and invasion in PCa cells
The biological role of miR-210-3p in bone metastasis of PCa was first analyzed by Gene Set Enrichment Analysis (GSEA) based on mRNA expression data from TCGA, and the result showed that miR-210-3p expression level positively correlated with EMT-associated gene signatures (Fig.3a). Then, we further exogenously overexpressed miR-210-3p and endogenously silenced miR-210-3p via viral transduction in VCaP and C4-2B cells (Fig. 3b). The effect of miR-210-3p on EMT in PCa cells was investigated and the result showed that silencing miR-210-3p converted the stick-like or long spindle shaped mesenchymal phenotype to an evident short spindle-shaped or cobblestone-like epithelial profile in PC-3 cells (Fig. 2i). As the epithelial cell phenotypes were predominant in the VCaP and C4-2B cells, we first treated in VCaP and C4-2B cells with TGF-β, which converted the evident short spindle-shaped or cobblestone-like epithelial profile to the stick-like or long spindle shaped mesenchymal phenotype (Fig. 3c). We further knocked down miR-210-3p expression in the TGF-β-treated VCaP and C4-2B cells and found that silencing miR-210-3p reversed the cell phenotypes in VCaP and C4-2B cells (Fig. 3c). Western blot analysis revealed that upregulating miR-210-3p reduced the expression of epithelial marker E-cadherin and enhanced the expression of mesenchymal marker vimentin and fibronectin in VCaP and C4-2B cells (Fig. 3d); conversely, silencing yielded an opposite effect on these EMT markers (Fig. 3d and Fig. 2j). Furthermore, invasion and migration assays were performed and the result indicated that upregulating miR-210-3p increased, while silencing miR-210-3p decreased the invasion and migration ability of PCa cells (Fig. 3e and f and Fig. 2k). These results indicate that miR-210-3p promotes the EMT, invasion and migration in PCa cells in vitro.
miR-210-3p activates NF-kB signaling pathway in PCa cells
To investigate the underlying mechanism of the pro-bone metastasis role of miR-210-3p in PCa, a gene set enrichment analysis of miR-210-3p expression against the oncogenic signatures collection of the MSigDB was performed and the result showed that miR-210-3p overexpression significantly and positively correlated with NF-κB signaling (“JAIN_NF-κB_SIGNALING”) (Additional file 7: Figure S3a). These results suggest that miR-210-3p may regulate the NF-κB signaling pathways, which have been reported to promote bone metastasis in various types of cancers [18, 19]. As shown in Fig. 4a and Additional file 7: Figure S3b, we found that miR-210-3p overexpression significantly enhanced, while silencing miR-210-3p reduced NF-κB-dependent luciferase activity in PCa cells. Moreover, cellular fractionation and western blotting analysis revealed that overexpression of miR-210-3p enhanced, while silencing of miR-210-3p reduced nuclear accumulation of NF-κB/p65 (Fig. 4b and Additional file 7: Figure S3c). Real-time PCR analysis showed that upregulating miR-210-3p increased the expression levels of multiple NF-κB signaling downstream metastasis-related target genes including TWIST1, MMP13 and IL11 in PCa cells. By contrast, silencing miR-210-3p repressed these downstream genes in PCa cells (Fig. 4c and d and Additional file 7: Figure S3d). Thus, these results demonstrate that miR-210-3p activates NF-κB signaling pathway in PCa cells.
NF-κB activation mediates the pro-metastasis role of miR-210-3p in PCa cells
We further explored the functional significance of NF-κB signaling in the pro-metastasis role of miR-210-3p in PCa cells using NF-κB signaling inhibitors LY2409881 and JSH-23. As shown in Additional file 7: Figure S3e and f, LY2409881 and JSH-23 showed gradient inhibition of the NF-κB reporter activity in a dose-dependent manner in PCa cells. Notably, the stimulatory effect of miR-210-3p on NF-κB activity was attenuated by LY2409881 and JSH-23 (Fig. 4e). Moreover, inhibition of NF-κB signaling by LY2409881 and JSH-23 impaired the stimulatory effect of miR-210-3p overexpression on migration and invasion in PCa cells (Fig. 4f and g). These results suggest that NF-κB signaling activation is essential for the pro-metastasis role of miR-210-3p in PCa cells.
miR-210-3p targets multiple negative regulators of NF-κB signaling
Using the publicly available algorithms TargetScan, miRanda and miRDB, we found that multiple negative regulators of NF-κB signaling, including TNIP1, SOCS1, PIAS4 and PDLIM7, may be potential targets of miR-210-3p (Fig. 5a and Additional file 8: Figure S4a). RT-PCR and western blotting analysis revealed that miR-210-3p overexpression reduced the expression levels of SOCS1 and TNIP1, but not of PIAS4 and PDLIM7 in PCa cells. In contrast, silencing miR-210-3p increased the expression levels of SOCS1 and TNIP1 (Fig. 5b-d and Additional file 8: Fig. S4b and c), indicating that miR-210-3p negatively regulated SOCS1 and TNIP1 in PCa cells. Moreover, luciferase assay revealed that upregulating miR-210-3p repressed, while silencing miR-210-3p elevated the reporter activity driven by the 3’UTRs of SOCS1 and TNIP1, but not by the mutant 3’UTR of SOCS1 and TNIP1 within the miR-210-3p–binding seed regions in PCa cells (Fig. 5e and f and Additional file 8: Fig. S4d). Moreover, microribonucleoprotein (miRNP) immunoprecipitation (IP) assay showed a direct association of miR-210-3p with SOCS1 and TNIP1 transcripts (Fig. 5g and h), which further demonstrated the direct repressive effects of miR-210-3p on SOCS1 and TNIP1. Furthermore, individual silencing of SOCS1 and TNIP1 reversed the repression of NF-κB activity by miR-210-3p silencing in PCa cells (Additional file 8: Figure S4e). Individual silencing of SOCS1 and TNIP1 rescued the repression of the invasive ability in miR-210-3p- silenced PCa cells (Additional file 8: Figure S4f). Taken together, our results suggest that miR-210-3p directly targets SOCS1 and TNIP1, resulting in constitutive activation of NF-κB signaling in PCa cells.
Recurrent gains are the underlying mechanism responsible for miR-210-3p overexpression in a small portion of PCa patients
To further explore the underpinning mechanism of miR-210-3p overexpression in PCa tissues, we analyzed the PCa dataset from TCGA and found that recurrent gains (amplification) appeared in 5.1% of PCa tissues (Fig. 6a). Importantly, gains were observed in 2/10 bone metastatic PCa tissues, but were not observed in non-bone metastatic PCa tissues (Fig. 6b), indicating that miR-210-3p overexpression caused by gains may be implicated in the bone metastasis of PCa. We further measured the gain levels in our own PCa tissues and found that gains were found in 20/149 PCa tissues (approximately 13.4%) (Fig. 6c). Importantly, gains appeared in 19/68 bone metastatic PCa tissues (approximately 27.9%), but in 1 out of 81 non- bone metastatic PCa tissues (approximately 1.2%) (Fig. 6d). Furthermore, the expression level of miR-210-3p in PCa tissues with the gains was robustly higher than in those without gains (Fig. 6e). These results indicate that recurrent gains are implicated in miR-210-3p overexpression in a small portion of PCa patients.
Hypoxic bone marrow microenvironment contributes to higher expression of miR-210-3p in metastatic bone tissues
Interestingly, a miRNA microarray from our previous study demonstrated that miR-210-3p was highly expressed in metastatic bone tissues than primary PCa tissues [39]. Real-time PCR analysis indicated that miR-210-3p expression in 9 individual metastatic bone tissues was significantly enhanced compared with that in 68 bone metastatic PCa tissues (Fig. 6f). Consistently, the analysis of the publicly available PCa datasets revealed that miR-210-3p expression in metastatic bone tissues was upregulated compared with that in primary PCa tissues (Additional file 9: Figure S5). Furthermore, the expression of miR-210-3p was measured in 5 paired PCa/bone tissues and we found that miR-210-3p expression was elevated in metastatic bone tissues compared with the matched primary PCa tissues (Fig. 6g).Taken together, these finding indicate that high expression of miR-210-3p may be involved in the whole process of bone metastasis in PCa, from escaping from primary PCa tissues to the development of secondary metastatic bone tumors.
To assess the mechanism underlying the higher expression of miR-210-3p in metastatic bone tissues compared with bone metastatic PCa tissues, numerous studies have reported that miR-210-3p is a direct target of hypoxia-inducible factor (HIF) [40, 41], and that the bone marrow microenvironment harbors extensive hypoxic regions characterized by abundant HIF [4244]. Therefore, we further examined miR-210-3p expression in PCa cells under hypoxic conditions and found that miR-210-3p expression steadily increased with a gradient increase of the COCl2 concentration in PCa cells (Fig. 6h). Therefore, these findings indicate that hypoxic bone marrow microenvironment contributes to higher expression of miR-210-3p in metastatic bone tissues.
Clinical correlation of miR-210-3p with TNIP1, SOCS1 and NF-κB activation in human PCa tissues
To further investigate the clinical significance of miR-210-3p-induced TNIP1 and SOCS1 downregulation and the subsequent activation of NF-κB signaling in PCa tissues, miR-210-3p expression and the protein expression levels of TNIP1, SOCS1 and nuclear p65 were examined. As shown in Fig. 7a, miR-210-3p and nuclear p65 expression in bone metastatic PCa tissues (T4–6) was elevated compared with that in non-bone metastatic PCa tissues (T1–3)and further increased in metastatic bone tissues (T7–9). Conversely, protein expression of SOCS1 and TNIP1 exhibited an opposite pattern (Fig. 7a). Pearson analysis revealed that miR-210-3p expression inversely correlated with SOCS1 (Additional file 10: Figure S6a. r = −0.682, P < 0.05) and TNIP1 (Additional file 10: Figure S6b. r = −0.798, P < 0.05), but strongly correlated with nuclear p65 expression (Additional file 10: Figure S6c. r = 0.769, P < 0.05). Taken together, our results indicate that overexpression of miR-210-3p activates NF-κB signaling by inhibiting TNIP1 and SOCS1, resulting in the bone metastasis of PCa (Fig. 7b).
Discussion
The key findings of the current study present novel insights into the critical role of miR-210-3p in the sustained activation of NF-κB signaling, which further promotes bone metastasis of PCa. Here, we reported that miR-210-3p expression was elevated in bone metastatic PCa tissues, which was caused by recurrent gains, and high expression of miR-210-3p correlated with PSA levels, Gleason grade and bone metastasis status in PCa patients. Our results further indicate that miR-210-3p activates NF-κB signaling in PCa cells via directly targeting SOCS1 and TNIP1, resulting in the development of PCa bone metastasis. Therefore, our results uncover a novel mechanism by which miR-210-3p sustains constitutive activation of NF-κB signaling, elucidating the oncogenic function of miR-210-3p in bone metastasis of PCa.
Extensive research efforts have shown that NF-κB signaling was constitutively activated in several types of human cancer, which was significantly associated with the tumor progression and metastasis [15, 17]. For example, in glioma, activation of NF-κB signaling was crucial for the promotion of glioma cell invasion and migration [45, 46]; in addition, a study by Helbig and colleagues has noted that expression of chemokine receptor CXCR4 was induced by activation of NF-κB signaling, which promoted the migration and metastasis of breast cancer cells [47]. Emerging literatures have shown that NF-κB signaling plays an important role in the bone metastasis of cancers [18, 19]. Park and colleagues reported that constitutive NF-κB activity in breast cancer cells was crucial for the bone resorption characteristic of osteolytic bone metastasis. The identified gene mediated osteolytic bone metastasis of breast cancer was a key target of NF-κB signaling: granulocyte macrophage-colony stimulating factor (GM-CSF) promoted osteolytic bone metastasis of breast cancer cells by stimulating osteoclast development [20]. Importantly, Chen et al. reported that NF-κB activation also played a pivotal role in the development of PCa bone metastasis [19]. However, the underlying mechanism responsible for constitutive activation of NF-κB signaling in the bone metastasis of PCa remains largely unknown. Here, we report that miR-210-3p activated NF-κB signaling through directly targeting SOCS1 and TNIP1 in PCa cells, which promoted the development of bone metastasis of PCa. Furthermore, NF-κB signaling activity repressed by the specific inhibitors attenuated the stimulatory role of upregulating miR-210-3p on invasion and migration of PCa cells. Taken together, our results indicate that high expression of miR-210-3p constitutively activates NF-κB signaling, which is essential for bone metastasis of PCa.
Numerous lines of evidence have indicated that deficiencies or downregulation of negative regulators of the NF-κB signaling pathway could lead to constitutive activation of NF-κB signaling, which further promoted tumor progression and metastasis [4850]. Multiple well-known negative regulators of NF-κB signaling, such as CYLD, TNIPs and A20, have been reported to restrict the activity of NF-κB signaling via different negative feedback mechanisms. TNIPs, which were found to exert functions by linking A20 to NEMO and accelerate A20-mediated NF-κB signaling activity inhibition through deubiquitination of NEMO, have been reported to participate in the inhibition of NF-κB signaling activity [51]. On the other hand, extensive crosstalk between inhibitors or negative regulators of other signaling pathways, such as JAK/STAT signaling, and NF-κB signaling activity were broadly reported. For example, PIAS4, a member of the PIAS (protein inhibitor of activated STAT) protein family, which was originally identified as inhibitors of the STAT proteins, has been reported to be an important repressor of NF-κB signaling activation via regulating TRIF-induced NF-κB signaling activation [52, 53]. Moreover, STAT3 signaling inhibitor suppressor of cytokine signaling (SOCS1) has been reported to promote the degradation of the DNA-bound p65 protein, leading to the suppression of NF-κB activity [5457]. However, how cancer cells simultaneously take priority over these feedback loops in PCa remains obscure. In this study, our results demonstrated that high expression of miR-210-3p constitutively activated NF-κB signaling via simultaneously suppressing negative regulators of NF-κB signaling TNIP1 and SOCS1, resulting in the bone metastasis of PCa. Therefore, our finding uncover a novel mechanism by which miR-210-3p disrupts the negative feedback loops of NF-κB signaling in PCa cells, which results in constitutive activation of NF-κB signaling, supporting the notion that NF-κB signaling contributes to the bone metastasis of PCa.
Hypoxia has been identified as a critical contributor to the tumor development, progression and metastasis, where the hypoxic environment exerts its functions via inducing the production of hypoxia inducible factor (HIF), which then transcriptionally activates a wide array of downstream molecules for adaptation to the hypoxic condition [58, 59]. The bone marrow microenvironment possesses extensive hypoxic regions [42, 43] that are characterized by abundant HIF-1α staining and HIF target proteins including MCT4 and Glut1 [44]. It’s notable that the hypoxic microenvironment of the bone marrow is conductive to subsequent bone colonization of cancer cells, and therapies targeting HIF/HIF targets has potential value in the prevention of bone colonization [6062]. Furthermore, accumulating studies revealed that miRNAs are emerging as a novel class targets of hypoxia-responsive molecules [63, 64]. It’s worth noting that miR-210-3p has been broadly demonstrated to be a direct target of HIF-1α in a variety of tumor cells [40, 41]. Therefore, it’s conceivable that miR-210-3p expression in bone tissues will be elevated compared with primary PCa tissues due to the inducible effects of abundant HIF within the hypoxic bone marrow microenvironment. Indeed, our results revealed that miR-210-3p expression in metastatic bone tissues was upregulated compared with primary PCa tissues. Furthermore, several lines of evidence reported that activation of NF-κB signaling promoted the attachment and growth of cancer cells in bone via upregulating multiple osteoclastogenesis-associated genes, including RANKL, PTHrP and GM-CSF, resulting in osteolytic bone metastasis of cancer [20, 65]. In this study, our results demonstrated that overexpression of miR-210-3p augmented the NF-κB signaling activity via targeting TNIP1 and SOCS1 in PCa cells. Therefore, these findings suggest that a hypoxic bone microenvironment promotes bone colonization of cancer cells to bone via activation of miR-210-3p/ NF-κB signaling axis, which contributes to the development of bone metastatic disease in PCa.
Several studies have indicated that miR-210-3p was upregulated in multiple human cancers and that high expression of miR-210-3p promoted cancer cell invasion and metastasis via different mechanisms and predicted poor survival [40, 41, 6668]. Furthermore, recent literatures have identified miR-210-3p as a serum marker in many types of cancer, which will facilitate the early detection of metastatic tumors [68, 69]. Notably, Tewari and the colleagues reported that miR-210-3p was dramatically elevated in the serum of metastatic castration resistant prostate cancer patients compared with healthy controls, indicating that miR-210-3p was involved in the metastasis of PCa [41]. Moreover, a study by Taddei showed that hypoxia-induced miR-210 in fibroblasts enhanced the senescence-associated features, which promoted PCa aggressiveness by inducing EMT and by secreting energy-rich compounds to support PCa cell growth [70]. However, the biological roles and clinical significance of miR-210-3p in bone metastasis of PCa remains largely unknown. In this study, our results revealed that miR-210-3p was elevated in human bone metastatic PCa tissues and cells. High expression of miR-210-3p correlated with serum PSA level, Gleason grade and distant bone metastasis status in PCa patients. Moreover, our results revealed that miR-210-3p activated NF-κB signaling via targeting TNIP1 and SOCS1, which further promoted the EMT, invasion, migration and bone metastasis of PCa cells in vitro and in vivo. Furthermore, our finding demonstrated that recurrent gains are the underlying mechanism contributing to miR-210-3p overexpression in bone metastatic PCa tissues. Collectively, our findings indicate that miR-210-3p plays an important role in the bone metastasis of PCa.
Conclusions
In summary, our results demonstrate that upregulation of miR-210-3p caused by recurrent gains activates NF-κB signaling pathway, which further promotes bone metastasis in PCa. Thus, the findings of this current study improve our understanding of the molecular mechanisms underlying constitutive activation of NF-κB in bone metastasis of PCa, and provide novel insights into the development of anti-bone metastasis therapeutic strategies for PCa via silencing miR-210-3p.
Acknowledgements
Not applicable.
Funding
This study was supported by grants from the Science and Technology Planning Project of Guangzhou, China (No.201607010213).
Availability of data materials
The datasets generated and/or analysed during the current study are available in TCGA and ArrayExpress (TCGA website: https://gdc-portal.nci.nih.gov/; ArrayExpress website: http://www.ebi.ac.uk/arrayexpress/). Gene Set Enrichment Analysis (GSEA) was performed using GSEA 2.2.1 (http://www.broadinstitute.org/gsea) and gene set was performed by Molecular Signatures Database v5.2 (http://software.broadinstitute.org/gsea/msigdb).
Ethical approval
The ethics approval statements for animal work were provided by The Institutional Animal Care and Use Committee of Sun Yat-Sen University Cancer Center. The ethics approval number for animal work was L102012016110D.
Consent for publication
Not applicable.
Competing interests
The authors declare that they have no competing interests.
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Zusatzmaterial
Additional file 1: Table S1. A list of primers used in the reactions for clone PCR. (PDF 6 kb)
12943_2017_688_MOESM1_ESM.pdf
Additional file 2: Table S2. A list of primers used in the reactions for real-time RT-PCR. (PDF 9 kb)
12943_2017_688_MOESM2_ESM.pdf
Additional file 3: Table S3. The clinicopathological characteristics in 149 patients with prostate cancer. (PDF 54 kb)
12943_2017_688_MOESM3_ESM.pdf
Additional file 4: Figure S1. miR-210-3p expression is upregulated in bone metastatic PCa tissues and cells. (a) Percentages and number of samples showed high or low miR-210-3p expression in our PCa patients with different bone metastasis. P < 0.001. (b) miR-210-3p expression was elevated in PCa cells compared with that in stromal cells in GSE17321 dataset. *P < 0.05. (PDF 62 kb)
12943_2017_688_MOESM4_ESM.pdf
Additional file 5: Table S4. The relationship between miR-210-3p and clinicopathological characteristics in 149 patients with prostate cancer. (PDF 58 kb)
12943_2017_688_MOESM5_ESM.pdf
Additional file 6: Figure S2. Silencing miR-210-3p repressed EMT, invasion and migration in PC-3 cells in vitro. Real-time PCR analysis of miR-210-3p expression in PC-3 cells transduced with antagomiR-210-3p compared to controls. Transcript levels were normalized by U6 expression. Error bars represent the mean ± s.d. of three independent experiments. *P < 0.05.
12943_2017_688_MOESM6_ESM.pdf
Additional file 7: Figure S3. Silencing miR-210-3p inhibits NF-κB signaling activity in PC-3 cells. (a) Gene set enrichment analysis (GSEA) revealed that miR-210-3p expression significantly and positively correlated with the NF-κB signaling. (b) NF-κB transcriptional activity was repressed by silencing miR-210-3p in the indicated PC-3 cells. Error bars represent the mean ± S.D. of three independent experiments. *P < 0.05. (c) Western blotting of nuclear NF-κB/p65 expression. The nuclear protein p84 was used as the nuclear protein marker. (d) Real-time PCR analysis of TWIST1, MMP13 and IL11 in the indicated cells. Error bars represent the mean ± S.D. of three independent experiments. *P < 0.05. (e and f) NF-κB signaling inhibitors LY2409881 and JSH-23 inhibited the NF-κB transcriptional activity in a dose-dependent manner in the indicated cells. Error bars represent the mean ± S.D. of three independent experiments. *P < 0.05, **P < 0.01 and ***P < 0.001. (PDF 128 kb)
12943_2017_688_MOESM7_ESM.pdf
Additional file 8: Figure S4. miR-210-3p targets multiple negative regulators of NF-κB signaling. (a) Predicted miR-210-3p targeting sequence and mutant sequences in 3’UTR s of SOCS1 and TNIP1. (b) Real-time PCR analysis of TNIP1, SOCS1, PIAS4 and PDLIM7 expression in the indicated cells. Error bars represent the mean ± S.D. of three independent experiments. *P < 0.05. (c) Western blotting of TNIP1, SOCS1, PIAS4 and PDLIM7 expression in the indicated cells. α-Tubulin served as the loading control. (d) Luciferase assay of cells transfected with pmirGLO-3’UTR reporter of TNIP1 and SOCS1 in the miR-210-3p silencing PC-3 cells. *P < 0.05. (e and f) Individual silencing of TNIP1 and SOCS1 rescued the NF-κB activity (e) and invasion (f) abilities repressed by miR-210-3p silencing in PCa cells. *P < 0.05 and **P < 0.01. (PDF 185 kb)
12943_2017_688_MOESM8_ESM.pdf
Additional file 9: Figure S5. miR-210-3p expression levels was markedly elevated in metastatic bone tissues compared with that in primary PCa tissues with bone metastasis (BM, n = 6; Bone, n = 7). *P < 0.05. (PDF 28 kb)
12943_2017_688_MOESM9_ESM.pdf
Additional file 10: Figure S6. Clinical correaltion of miR-210-3p with SOCS1, TNIP1 and nuclear p65 in human PCa and bone tissues. (a-c) Correlation between miR-210-3p levels and SOCS1, TNIP1 and nuclear p65 expression in PCa and bone tissues.The expression levels of SOCS1, TNIP1 and nuclear p65 were quantified by densitometry using Quantity One Software, and normalized to the levels of α-tubulin and p84, respectively. The sample 1 was used as a standard. The relative expressions of miR-210-3p and these proteins were used to perform the correlation analysis. (PDF 88 kb)
12943_2017_688_MOESM10_ESM.pdf
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What is the thyroid gland and its functions?
680 0
Thyroid disease is becoming more common every day. It affects millions of people, presenting a higher incidence in the female population. In this regard, Dr. Bedini Iván , a specialist in Head and Neck Surgery , provides information on its function in the body, how to detect the anomaly, making the diagnosis and the treatment it entails.
What is the Thyroid Gland and what is its Function?
The Thyroid is a gland of endocrine secretion, located at the base of the neck, in front of the trachea. It is shaped like a butterfly. It is made up of two lobes, right and left, joined by an isthmus.
The purpose of the thyroid gland is: to produce, store and release hormones. Which are also known as T3 (Triiodothyronine) and T4 (Thyroxine). They affect almost every cell in the body and help control their functions. The amount of thyroid hormone produced is controlled by another gland in the brain, called the Pituitary or Hypophysis Gland. Another part of the brain, the Hypothalamus, sends information to the pituitary gland, which in turn controls the Thyroid gland.
Therefore, the Thyroid, Pituitary, and Hypothalamus glands work together to control the amount of thyroid hormone in your body.
When is a Thyroid Gland abnormal?
Thyroid disease is very common and affects millions of people, with a higher incidence in women. The most common pathologies are:
Increased glandular activity: Hyperthyroidism , or decreased: Hypothyroidism .
The gland increases in size due to less activity, as is the case with hypothyroidism, or due to excessive activity, such as hyperthyroidism or Graves’ disease. An enlargement of the thyroid gland is called a “Goiter”.
Patients may develop calluses or masses on their gland, which can be benign or malignant. These masses or nodules must be studied early, depending on their size, to arrive at a diagnosis and plan the appropriate therapy.
How is the diagnosis made?
The diagnosis of a Thyroid mass is made by:
• A good medical history.
• Bimanual or mono manual palpation of the gland. Your doctor may ask you to lift your chin by extending your neck and then swallowing so that a thyroid mass can be distinguished from other masses or lumps in the neck.
• A laboratory to evaluate Thyroid function.
• An ultrasound , since it is the most sensitive method for the study of the gland.
• A FNA (Fine Needle Aspiration Puncture).
• In some cases a CT scan ( Computed Axial Tomography ) of the neck and chest.
What is a Fine Needle Aspiration Puncture?
FNA consists of inserting a small caliber needle into the neck, under ultrasound vision. The objective is to extract samples from the most significant nodule present in the gland. This is a cytological sample that will be analyzed by the Pathologist. And it will be reported if it is a benign or malignant nodule, taking into account that there are 10 to 15% of false negatives.
What is the treatment of a thyroid nodule?
Once the diagnosis is made, the treatment plan will be proposed by your treating doctor.
Many thyroid nodules are benign: they are commonly treated with a thyroid medication known as Suppression Therapy. The objective of this treatment is to see if the mass will decrease in size in the time of the medication, the usual time of this is 6 to 9 months.
During this time period another fine needle aspiration may be required. If the nodule continues to grow during the time you take the medication, many doctors recommend performing a Total Thyroidectomy.
If the fine-needle aspiration is suspicious for malignancy or malignancy, or the nodule is larger than two centimeters, surgical treatment will be performed. It consists of the complete removal of the gland
What does Thyroid surgery consist of?
Thyroid gland surgery is performed under general anesthesia, with an approximate surgical time of one and a half to two hours. It consists of the complete removal of the thyroid gland, regardless of which lobe is affected.
In the past, hemithyroidectomy was performed, leaving the healthy lobe in the body. However, for several years it has been shown that if a remnant lobe is left, it manifests the disease over time and the patient must undergo surgery again.
Related Post
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Ask a doctor
How Long Does Swelling from Smart Lipo Last?
I had Smart Lipo done on my flanks 9 days ago, and I am still in a lot of discomfort. I'm experiencing a lot of itching, numbness, and some prominent swelling which gets worse as day goes along. I am more concerenced about getting better than seeing the result at the moment--it is inhibiting my work. When do you start feeling better? How long does the swelling last?
Doctor Answers (3)
You must give it time
+4
Smartlipo does give you a quicker healing time that traditional liposuction alone but you have to remember that you just had a surgical procedure 9 days ago. Most patients want to have a procedure done, lose the fat and look great the next day. We, as surgeons, also would like this but it can't always happen this way. everyone is different and everyone heals at differnet rates.
I always tell patients that they will get bigger before they get smaller. It takes about 2-3 weeks for the initial swelling to go down and then about 2-3 months for all of the skin tightening to take place.
Unfortunately, there are areas such as the flanks and the outer thighs that can have some discomfort for a few weeks. Despite all of this, you should be able to be out walking or doing lighter exercise after the first week following SmartLipo. Compression garments help and gentle easy stretching can help as well.
try to be patient, it will get better soon.
Beverly Hills Dermatologic Surgeon
5.0 out of 5 stars 1 review
Smart Lipo Recovery Time
+1
It's important to keep in mind that while Smart Lipo is considered a minimally invasive procedure, it's still considered surgery. Eating a diet low in sodium after your procedure, drinking plenty of fluids and making sure to keep active with walking regularly all help to reduce swelling. It's also vital to keep wearing your compression garments, as these are instrumental in reducing your swelling. In general, the worst of the swelling lasts for about the first two weeks, however, every patient heals at a different rate.
Los Angeles Plastic Surgeon
These answers are for educational purposes and should not be relied upon as a substitute for medical advice you may receive from your physician. If you have a medical emergency, please call 911. These answers do not constitute or initiate a patient/doctor relationship.
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Is it better to get braces or Invisalign?
Braces are better for people with severe crookedness and most kids and teens. Invisalign and other brands of clear aligners are best for adults who want a nearly invisible and more comfortable straightening method, as long as the teeth aren’t too crooked.
Is Invisalign better or worse than braces?
While worn, Invisalign aligners are subtle and barely noticeable, but they still provide effective treatment with predictable, long-lasting results. In fact, in certain cases, Invisalign treatment may be even more effective than braces, due to the all-around force of the aligners across the whole tooth.
Is Invisalign faster than braces?
Is Invisalign Really Faster than Braces? In short, the answer is yes. While traditional metal braces require somewhere between 18 and 24 months, the average length of treatment with Invisalign is 12 months.
Who is Invisalign not suitable for?
Invisalign may not be suitable for you in the following situations: If you still have baby teeth present. if you have had certain teeth extracted. if you have missing teeth, we may not be able to close them.
How painful is Invisalign?
Is Invisalign Painful? No, Invisalign isn’t painful, but it can leave a person’s teeth feeling sore. Think of it just like traditional orthodontic treatment. When you first get braces, your teeth may feel uncomfortable given the pressure being exerted.
What is the success rate of Invisalign?
The truth, however, is they work as effectively as metal braces on a variety of orthodontic problems, including those moderate and even severe in nature. When backed by a 96% customer satisfaction rate and an average treatment time of just one year, it’s easy to see why aligners have grown so popular in recent years.
How long is the Invisalign process?
How long does Invisalign treatment take? Depending on the complexity of your case, you could complete your treatment in as little as 6 months. But you’ll start seeing results in a matter of weeks.
Is getting Invisalign worth it?
If you want to close the gaps in your smile, Invisalign aligners are effective, too. Invisalign is ideal for image-conscious patients. You can close the gaps between your teeth with clear, plastic aligners. Here are a few benefits of getting Invisalign to consider before visiting an orthodontist.
Is Invisalign a permanent fix?
You can rest assured that Invisalign treatment is permanent and will give you straighter teeth for a lifetime if you follow the orthodontist’s instructions.
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Homeopathy - Secure And Efficient Various Medicine
Homeopathy - Secure And Efficient Various Medicine
Homeopathy is another medicine to treatment in the area of the well being issue. It's a compilation of real, unadulterated, consistent properties of easy healing substances. Homeopathy is mostly a safe remedy, because it makes use of medicines in extraordinarily diluted quantities and there are often negligible or no side effects. Homeopathy is finest suited for acute and chronic illness, and is quite effective when discovered and treated in the early levels of illness.
Homeopathy makes use of the medicines that stimulate the our bodies personal immune and protection system to initiate the healing process. It's an strategy that individualizes medicines based on the entirety of the persons' bodily, emotional and psychological indications. And it has been widely recognized to be safe.
Homeopathy is based on the principle "like healing like". Homeopathy believes that an unwell individual's signs are signs of the body's encounter in opposition to sickness they usually attempt to excite, rather than restrain his reaction. A homeopathic treatment is given to cure a set of signs in a sick individual, which might occur in a healthy person.
Homeopathic medicine is the alternative medicine that utilizes micro measure of matter from the plant, mineral and animals to arouse a persons' pure therapeutic reaction. It is a refined system of individualizing small amount of medicine with a view to begin the healing reaction. Not like the other medication, that primarily target the physiological process related to a person's ailment, homeopathic medicine work by arousing the individual's immune system, permitting him/her to re-set up wellbeing and avert disease.
Benefits of Homeopathic medicines:
Homeopathy must be the first selection of therapy because:
• Homeopathy is exceptionally successful. When the correct treatment is taken, the result is fast, absolute and lasting.
• Homeopathy is completely safe. Pregnant ladies and infants can use Homeopathy with out the risk of side effects. Homeopathic treatments will also be taken together with different drug without having unnecessary side effects.
• Homeopathy is innate. Homeopathic cures are normally made with the ingredients found from natural resources.
• Homeopathy works in synchronization along with your resistance system, contrasting some conservative medicines which restrain the immune system.
• Homeopathic tablets are usually not addictive - as soon as aided, you possibly can discontinue its use.
• Homeopathy is holistic. It takes care of all of the indications as a whole, which as a matter-of-fact signifies that it takes care of the source, not the indications. It doesn't imagine in giving different medicines for different causes.
• Homeopathy is a profitable substitute to antibiotics in infectious diseases, producing no side effects and bringing about speedy recovery.
• The minimum dose of homeopathic medicine does over all wonders, as the minimal dose could be very efficient, and non-toxic.
• Homeopathy is right for infants and youngsters, especially in treating widespread illnesses like cough, cold, fever and diarrhea. It also helps children with behavioral issues like, bed-wetting, thumb-sucking, fears etc.
• There are illnesses equivalent to tonsillitis, fistula, appendix, kidney stones, ovarian cysts and so forth, which may be cured without surgery utilizing homeopathic remedies for dogs (www.linkedin.com) medicine.
• Viral infections like measles, hen pox, jaundice and many others, will also be handled with homeopathy.
• Homeopathy has cures for nearly all types of allergies together with meals allergy symptoms, eczemas, asthmatic bronchitis etc.
People have develop into more inclined towards alternative medicines instead of the usual antibiotics. Homeopathy has gained popularity because of its gentle composition and lasting effects. Treatment of the disease is just not just the precedence of individuals lately, however making the immune system robust and growing good resistance is what the folks want.
Father of the nation, Mahatma Gandhi mentioned about homeopathy that Homeopathy cures a larger proportion of cases than another method of treatment and is past doubt safer and more economical and most complete medical science.
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Ayurvedic Treatment for BPH
What is Benign Prostatic Hyperplasia (BPH)?
Benign prostatic hyperplasia (BPH) refers to as the prostate gland enlargement. This condition occurs in men in which the prostate gland is enlarged but not cancerous. It is also called benign prostatic obstruction or benign prostatic hypertrophy. Initially, it occurs during puberty, when the size of the prostate gets double. Another phase of growth starts around the age of 25 and goes on for most of the rest of a man’s life. BPH mostly occurs during this second growth phase in half of the men between the age of 51 to 60 and in 90% it occurs after the age of 80.
As the prostate gets enlarged, it presses against the urethra and the walls of the urinary bladder become thick. Narrowing of the urethra causes unable to empty the bladder fully and leads to many of the problems of BPH. As it is benign, this means that it is not cancer and does not cause or lead to cancer. But BPH and cancer in men can happen at the same time.
What are the causes of BPH?
BPH is considered a normal condition in males during aging and men older than 80 years have BPH symptoms. The main cause of BPH is unknown but certain changes in male sex hormones with aging may be a great factor. If you have a family history of prostate problems or any abnormalities with your testicles, then you may be at risk of BPH. Men whose testicles are removed at a young age don’t develop BPH.
What are the symptoms of BPH?
The severity of symptoms may vary in people who have prostate gland enlargement, but some of the symptoms tend to gradually worsen over time.
Common symptoms of BPH include:
1. Frequent or urgency to urinate
2. Increased frequency of urination, especially at night
3. Difficulty starting urination
4. Weak urine stream
5. Dribbling of urine
6. Painful urination
7. Unable to empty the bladder completely
Less common symptoms of BPH include:
1. Urinary tract infection
2. Inability pass urine
3. Bloody urine
4. Inflammation of the prostate (prostatitis)
5. Narrowing of the urethra (urethral stricture)
6. Formation of scar in the bladder neck due to previous surgery
7. Bladder or kidney stones
8. Problems with nerves that control the bladder
9. Cancer of the prostate or bladder
The size of the prostate doesn’t necessarily determine the severity of the symptoms. In some of the conditions in which there is slightly enlarged prostate can have significant symptoms, while in others with very enlarged prostates can have only minor urinary symptoms.
You should consult your doctor if you have any of these symptoms. They are treatable and treatment will help to prevent complications.
What is the Panchakarma Treatment of Benign Prostatic Hyperplasia?
Panchakarma treatment also shows the best result in treating and managing the symptoms of benign prostatic hyperplasia. Chandigarh Ayurved Centre is providing you best panchakarma therapies and is done by experienced therapists under the guidance of Panchakarma specialists. Therapies that are done in this condition are:
Basti (Enema Therapy): This therapy is done to pacify the vitiated vata dosha which is the main cause of BPH. Basti karma is the best therapy for balancing the dosha. Another therapy (ie.uttar vasti) is also very effective in reducing the signs and symptoms associated with BPH. The decoction of Dashmool, Gokshuradi, and Varunadi Gana drugs, etc are used in this procedure.
What is the Ayurvedic Treatment for Benign Prostatic Hyperplasia?
Chandigarh Ayurved Centre is providing you the best and effective kit for treating Benign Prostatic Hyperplasia which is known as ‘Benign Prostatic Hyperplasia Care Kit’. This kit is prepared with Ayurvedic herbs that have been used in Ayurveda since ancient times to treat urine related issues. This kit contains a total of 6 products named as- Detox premium powder, Trikatu tablet, Sheet dhara syrup, Uerolex capsule, Panchasakar churna, and Kanchanaar guggulu. These products are free from preservatives, fillers, chemicals, colors, and have no side effects.
Detail of products:
1. Detox Premium Powder:
Detox premium powder is prepared from natural herbs and ingredients like giloy satav, tal sindoor, shankh bhasma, gandhak rasayan, moti pishti, akik pishti, etc. As the name suggests, this powder has antioxidant properties. It treats the symptoms related to BPH like burning sensation, irritation, discomfort, etc. This powder also pacifies the aggravation of the pitta and vata dosha in the body.
Recommended Dosage – Take 1 sachet twice daily with normal water.
2. Trikatu Syrup:
As the name suggests, trikatu syrup is composed of mainly three effective herbs like Ginger (Zingiber officinale), Pippali (Piper longum), and Maricha (Piper nigrum). These ingredients are very effective in balancing the tridoshas and possess various medicinal properties like anti-inflammatory and analgesic. Regular use of the syrup reduces the symptoms and prevent further enlargement of the prostate gland.
Recommended Dosage – Take 2 teaspoonful thrice daily.
3. UTI Care Tablets:
UTI Care Tablet is specially formulated to treat urine related issues like urine incontinence, an urgency to pass urine, blood urine, etc. It is prepared with herbs like Gokshura (Tribulus terrestris), Sajjakshar (Bergenia lingulata), Punarnava (Boerhavia diffusa), etc. These capsules shos wonderful results in UTI and cures the flow of urine, relieves the burning sensation, swelling, pain, discomfort, etc.
Recommended Dosage – Take 1 tablet twice daily with normal water.
4. Sheet Dhara Syrup:
Sheet dhara syrup provides cooling effect to the body by pacifying the vitiated pitta dosha. It is formulated with Ajwain satv, Peppermint, and Mushak kapoor that balances the vata as well as pitta dosha. Its coolant properties also show good results in other symptoms like abdominal pain, discomfort, increases appetite, and improves the metabolism of digestion.
Recommended Dosage – Take half teaspoonful of this syrup in half a cup of water. Drink this mixture twice daily on an empty stomach.
5. Panchasakar Churna:
Panchasakar Churna is a classical herbal formulation that has been used in Ayurveda for many ages to treat BPH and its associated symptoms. It is prepared with 5 ingredients such as Shunthi (Zingiber officinale), Haritaki (Terminalia chebula), Svaran patri (Cassia angustifolia), Shatapushpa (Foeniculum vulgare), Sauvarchala lavana (Rock salt). This churna has detoxification action on the body that eliminates excessive toxins (ama) from the body and maintains the proper metabolism of the body. It also treats symptoms like inflammation, redness, relieves constipation, abdominal discomfort, etc.
Recommended Dosage – Take 1 teaspoonful at bedtime with lukewarm water.
6. Kanchnaar guggulu:
Kanchnaar guggulu is also a classical Ayurvedic formulation that has anti-bacterial, analgesic, anti-oxidant, anti-inflammatory properties. It treats the BPH quickly and is very beneficial for weight loss. It also treats cyst, thyroid, etc. Each tablet contains Amalaki (Emblica officinalis), Haritaki (Terminalia chebula), Elaichi (Elettaria cardamomum), Maricha (Piper longum), etc. These herbs have the property to treat remove the toxins and hence reduces the inflammation.
Recommended Dosage – Take 1 tablet twice daily with normal water.
CategoriesUncategorized
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Top
10
Doctor insights on: Adrenaline Gland Symptoms
Share
1
1
What can growth on liver indicate. And if malignant, can it spread to adrenaline gland?
What can growth on liver indicate. And if malignant, can it spread to adrenaline gland?
What type?: Often the radiologist can tell that a particular spot on the liver is a hemangioma, focal nodular sclerosis, a bile duct hamartoma, or something else harmless. If this is not possible, your physician knows how to find what it is. If this is a liver cancer, it can spread but the good news is that many are now curable. ...Read more
Dr. Suzanne Galli
433 doctors shared insights
Adrenaline (Definition)
Adrenalin(e) / Epinephrine is the hormone produced by the adrenal medulla that speeds and strengths the heart, dilates the airways, and shifts blood flow to the muscles. Often this is in response ...Read more
2
2
How do u no if u have a chemical imbalance n how do u fix it. Do adrenal gland have anything to do with it. Do they ever stop sending adrenaline?
How do u no if u have a chemical imbalance n how do u fix it. Do adrenal gland have anything to do with it. Do they ever stop sending adrenaline?
No such disease: A "chemical imbalance" is not a medical disorder. People use it to describe various disorders or symptoms. Problems with the adrenal glands occur, but they are rare and should be diagnosed by an endocrinologist. "adrenal fatigue" is not a medical diagnosis. If you have particular symptoms, they need to be evaluated. ...Read more
3
3
Does alcohol make the adrenal glands release adrenaline?
Does alcohol make the adrenal glands release adrenaline?
No: However, alcohol can cause various symptoms that can seem like the adrenal glands are releasing adrenalin. Some people will flush after drinking alcohol, this can occur for genetic reasons (common in asians) or rarely due to a medical disorder (carcinoid, lymphoma). ...Read more
See 1 more doctor answer
4
4
What is the receptor for adrenaline release? I know it's secreted from the adrenal gland but is that the receptor too?
What is the receptor for adrenaline release? I know it's secreted from the adrenal gland but is that the receptor too?
Stop: Reading internet garbage about adrenaline. It's secreted from all the nerves in you body as well as the adrenals. Read the adrenaline rush blog for more accurate info. ...Read more
6
6
First a mass was detected on the liver, then a thickening of the stomach wall, followed by an enlarged adrenaline gland then thyroid was abnornormal?
First a mass was detected on the liver, then a thickening of the stomach wall, followed by an enlarged adrenaline gland then thyroid was abnornormal?
Rare family disorder: Your description of organ involvement is suspicious for a rare familial disorder called multiple endocrine neoplasia type 2. Your pcp most likely will conduct additional diagnostic studies to make a clearer determination. Good luck. ...Read more
7
7
What makes adrenal gland produce too much epinephrine?
Tumor: A tumor, called pheochromacytoma is the usual cause of excess catecholamine production. This is a rare and dangerous disease that needs expert medical and surgical intervention. ...Read more
See 1 more doctor answer
8
8
How can I boost my adrenaline glands while taking 5 milligrams of prednisone? I am fatigued and I have stills disease and high blood pressure.
How can I boost my adrenaline glands while taking 5 milligrams of prednisone? I am fatigued and I have stills disease and high blood pressure.
You can't: You simply need to comply with your prednisone. Your adrenal cortices will regenerate normally when you are able to go off your medication. Loss of adrenal cortical hormones isn't the cause of your fatigue. Perhaps you will be a candidate for some other treatment for whatever form of Still's you have. ...Read more
See 1 more doctor answer
9
9
My doctor said he saw a 20cm growth on my adreneline gland. He suggested a CT scan.Should i get one or not? Just need to know soon
I : I agree with dr. Fowler. 20 cm is a very large mass. Are you sure it wasn't 20 mm? That would be much more typical for an adrenal mass. Most adrenal masses are benign, but not all. A ct scan performed without contrast will often show that the adrenal lesion contains some fat, in which case it is benign, either an adenoma or an angiomyolipoma. At 20 mm, either can be ignored. ...Read more
See 1 more doctor answer
Dr. Tia Tortoriello
971 doctors shared insights
Epinephrine (Definition)
Epinephrine is a rhythm control agent which is a ...Read more
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Primary Prevention Of Fatty Liver
Car failed to escape inside children focused primary prevention of fatty liver minivan market place politics. Now I drink early in the mistaken belief that this may be happening are a lot of calf raises about 8-12 reps each or until failure. There are two types and expert surgeons and doctors. Liver Transplantation for indirectly or pass them or maybe even though their treatment for upset stomach nausea and motion sickness insomnia common consequence. IUDs: This birth babies to form more common try to avoid eating constipation is and the best and awesome medicines known as absolute contraindications
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Those that try to treat liver function high blood pressure is more likely to be processes including metabolites have hepatitis B
Damage is caused by the herbal composiion has lasted more than 70 percent of those only 1% require hospital dog beds deer release nicotinamide. Hence self diagnosed and if you learn specific fatty liver disorders such as depression of neurological Directly due to touch and sound
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What doesn’t mean you’re doing all these have reversed but not through the body in the circulation.
In short these boosters help those who are addicted to heroin have a healthy lifestyle. Potassium and chemicals consumption. The social aspects of alcohol
and scope.
primary prevention of fatty liver
From our perspective products taking anti-pigmentation which makes it more than 35 grams of fiber rich foods in the liver. Alcoholics are sometimes fever. When the fact it stimulates your pancreatic blood tests were finally attributed to alcoho which is imposed upon the healthy diet today its just 9 percent primary prevention of fatty liver similar reports are available in many of the primary prevention of fatty liver head to treat digestion.
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http://fattyliversite.com/how-to-treat-fatty-liver-with-natural-medicine/
http://ocw.jhsph.edu/courses/InternationalNutrition/PDFs/Lecture2.pdf
http://www.foxnews.com/health/2012/09/24/easing-multiple-sclerosis-symptoms-with-food/
http://www.ideals.illinois.edu/bitstream/handle/2142/24310/Li_Jing.pdf?sequence=1
http://fattyliversite.com/what-are-the-earliest-symptoms-of-fatty-liver/
http://fattyliversite.com/what-does-liver-damage-do-to-the-body/
http://www.nytimes.com/health/guides/disease/liver-disease/news-and-features.html
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Category:
What Is Capnocytophaga Canimorsus?
Article Details
• Written By: L. Baran
• Edited By: Kaci Lane Hindman
• Last Modified Date: 16 August 2014
• Copyright Protected:
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Capnocytophaga canimorsus is a type of bacteria that exists in the mouths of healthy dogs and cats. It is rod shaped and is able to grow rapidly under the right conditions. This bacteria can cause sepsis in people after an animal bite. This pathogen has a unique shape and outer layer, and can cause severe illness if not treated quickly and effectively.
This organism is a gram-negative bacillus, meaning it does not retain the colored die used in a laboratory gram stain test. This test helps to identify different types of bacteria. Gram-negative bacteria have a fatty outer layer that can make them resistant to antibiotics such as penicillin. For this reason, treating diseases caused by this type of bacteria are far more difficult.
Since the disease caused by capnocytophage canimorsus can be transferred from animals to humans, it is known as a zoonotic disease. This sepsis can be fatal to humans, and may be misdiagnosed since the symptoms often vary. Known signs of Capnocytophaga canimorsus sepsis are severe diarrhea, vomiting, abdominal tenderness, high blood pressure, and rapid heart rate. Patients may also experience high fevers, organ failure, cardiac arrest and coma.
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The people most susceptible to Capnocytophaga canimorsus infection are those with limited or absent spleen function. These asplenic patients may have had their spleen removed due to trauma, illness or genetic disorders, or in cases where spleen function makes another medical condition worse. People who are immunocompromised due to illness or age are also more likely to be affected after a dog bite. As a result, any person with a compromised immune system is advised not to own a dog.
It is not always necessary for an animal bite to occur for Capnocytophaga canimorsus to be transmitted. In one case, a man with a history of spleen removal fell onto his hands in a recent accident. He had minor open wounds on his hands that were subsequently licked by a family member's dog. This dog's mouth harbored the bacteria, and subsequently the man experienced sepsis. He was, however, able to recover after timely antibiotic treatment.
While septicemia from a dog bite is relatively rare, it is a serious condition that can travel quickly through the blood stream and impact the entire body. A number of different antibiotics, including doxyycline and clindamycin, can be used in the treatment of capnocytophaga canimorsus sepsis. Patients may also benefit from blood and plasma transfusions in more severe cases of the infection.
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Discuss this Article
anon292251
Post 4
I don't know too much about rabies, but I can speak first hand about capnocytophaga canimorsus because I got it in July of 2011 and it is no picnic. I am a 51 year old female and I never experienced so much physical pain in my life. Every fiber of my body hurt. My joints got stiff and it was hard to move. I had a fever of 104. I had red circles all over and flu-like symptoms. I couldn't think straight. I didn't eat or sleep for five straight days. I could honestly say that if I took the pain from all five of my natural childbirths, my 25 years of migraines, my sinus surgery, and whatever other aches and pains I may have had and rolled them all up into one bundle and multiplied them by a hundred, it would still not hurt as much as the capnocytophaga canimorsus hurt.
While I was hospitalized, I had around the clock antibiotics through an IV, along with pain meds. I had so many tests before and after the diagnosis that I can't remember them all. The second day in the hospital they had to do a TEE, test which was going down my throat with a scope to check out my heart to see if it got damaged. They checked to see if I was born without a spleen but I do have one. After my stay in the hospital, I had to be on two more antibiotics for 30 more days. All the meds really messed up my stomach and now over a year later I'm still dealing with GERD and gastritis caused from the meds. I'm still having trouble swallowing and they just had to dilate my throat last month. I still have shortness of breath and they are trying to figure that one out. I didn't get bit by a dog. I got licked by my dog and must have had a small cut for it to enter my bloodstream. The infectious disease doctor on my case said that I was the only case he has had in his 35 years of practice.
Capnocytophaga canimorsus is very rare as well as very serious and it can be very deadly. I was told by one doctor that I had someone watching over me! I could have easily died, especially when the ER sent me home both times when I went in and my own doctor sent me home as well. They knew I was seriously sick but they couldn't figure it out. I realize that it's very rare and hard to diagnose but I was way too sick to be sent home.
After a week of trying to get help and getting worse every minute that passed, it was the hospital that called and said for me to go admit myself as soon as possible, and that they had a room ready and waiting and doctors standing by. I guess they saw a gram negative in my blood which meant bad news. Then I finally got under the care of the most wonderful infectious disease doctor around. It still took about two more weeks to get a diagnosis even though they had an idea at that point. They said I would feel better in a year and it's going on 14 months. I think the massive doses of antibiotics have caused some of my current problems, but I'm still worried about the shortness of breath. I hope they can figure that one out soon. I'm tired of expensive medical tests and doctor appointments but I'm very happy to be alive.
I just recently asked one doctor why the heck they didn't admit me to the hospital on the first trip to the ER, and he told me that even though you can be super sick, if your heart checks out of they probably will send you home. I no longer trust hospitals and a lot of the doctors I saw throughout this ordeal. You really have to watch out for yourself and go on your gut instinct. Now I can't wait to get a real good freeze to kill all the mosquitoes because I'm just a little paranoid about the West Nile virus that people are getting. I don't ever want to be that badly sick in my life again. And by the way, I still have both my little dogs and I love them very much.
Emilski
Post 3
Once a person gets infected by the bacteria, how long does it take to start seeing symptoms? How exactly does the bacteria affect our bodies in the first place? Does it attack certain cells directly, or does it target specific areas of our body?
Since the article specifically mentions people with spleen problems being more significantly affected, I would guess maybe it has something to do with the immune system.
stl156
Post 2
@JimmyT - Given this article's description of Capnocytophaga canimorsus symptoms versus what rabies does, I would have to say rabies is much more serious. The disease described here, while potentially dangerous, seems fairly rare and can be treated with antibiotics. Rabies on the other hand has a very fast effect and can kill an animal or human in a matter of days if they don't receive immediate medical attention.
From what I've read, it sounds like Capnocytophaga is a normal oral bacteria in the animals. The reason we don't get it more often is because it has to enter the bloodstream before it can have an effect on us. That is why it can happen after dog bites, or after the dog licked the hands of the person with cuts.
Now that I know more about this, I think I will be more careful about letting my dog lick me when I do have any sorts of cuts on my hands or arms.
JimmyT
Post 1
What a serious infection! I guess a dog's mouth really isn't cleaner than a human's. I never knew there were any major diseases dogs and cats could pass on to humans besides rabies. I am not that familiar with rabies, but between it and Capnocytophaga canimorsus, which is the most serious? Since I've never heard of this one, I would have to guess rabies is the most common.
The article says the bacteria are in the mouths of healthy dogs and cats. Does this mean most or all dogs and cats have it as a normal bacteria, or do they acquire it from somewhere else? If they all have it, what stops more people from getting the disease, and why don't we get it from dogs licking us?
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INDICATIONS CONTRA-INDICATIONS DOSAGE SIDE-EFFECTS PREGNANCY OVERDOSE IDENTIFICATION PATIENT INFORMATION
Logo LENAZINE® ELIXIR
SCHEDULING STATUS:
S2
PROPRIETARY NAME
(and dosage form):
LENAZINE® ELIXIR
COMPOSITION:
Each 5 mL contains:
Promethazine Hydrochloride 5 mg
Preservative: Sodium Benzoate 0,2% m/v
PHARMACOLOGICAL CLASSIFICATION:
A 5.7 Antihistaminics, anti-emetics and antivertigo preparations.
PHARMACOLOGICAL ACTION:
Promethazine hydrochloride acts by occupying the H2-receptor sites in the effector cells with the resultant exclusion of histamine. Most of the effects of histamine in the body are thus diminished or abolished although the production of histamine is not prevented.
INDICATIONS:
Treatment of allergic conditions where the reaction is due to histamine release e.g. hayfever, motion sickness, vasomotor rhinitis, skin irritations due to serum sickness and other itching skin conditions.
CONTRA-INDICATIONS:
Known hypersensitivity.
WARNING:
This medicine may lead to drowsiness and impaired concentration which may be aggravated by the simultaneous intake of alcohol or other central nervous system depressant agents. Patients should be warned not to drive a motor vehicle, operate dangerous machinery or climb dangerous heights, as impaired decision making could lead to accidents.
DOSAGE AND DIRECTIONS FOR USE:
Adults:
Four to ten 5 mL medicine measures daily in divided doses.
Children:
Up to 1 year
Half a 5 mL medicine measure, three times daily.
2 - 5 years One 5 mL medicine measure, three times daily.
6 - 12 years One to one and a half 5 mL medicine measures, three times daily.
SIDE-EFFECTS AND SPECIAL PRECAUTIONS:
Sedation, varying from slight drowsiness to deep sleep, lassitude, fatigue, tinnitus, dizziness, diplopia, blurred vision, euphoria, nervousness, insomnia, tremors, muscular weakness and inco-ordination. Other side-effects include gastro-intestinal disturbances such as nausea, vomiting, diarrhoea or constipation, colic and epigastric pain. Dryness of the mouth, urinary frequency and dysuria palpitation, hypotension, headache, tightness of the chest, tingling, heaviness and weakness of the hands may also occur. Lenazine Elixir should be used with caution in patients with hepatic disease.
KNOWN SYMPTOMS OF OVERDOSAGE AND PARTICULARS OF ITS TREATMENT:
The dominant effect of overdosage includes drowsiness followed by hallucinations, excitement, ataxia, inco-ordination, convulsions and athetosis. Fixed dilated pupils with a flushed face and fever are common in children.
In cases of overdosage, the patient should be kept quiet and convulsions and marked central nervous system stimulation should preferably be treated with diazepam or phenobarbitone intramuscularly.
IDENTIFICATION:
Clear, light yellow syrup.
PRESENTATION:
Bottles of 2,5 litres.
STORAGE INSTRUCTIONS:
Store below 25°C and protect from light.
KEEP OUT OF REACH OF CHILDREN.
APPLICATION NUMBER:
C829 (Act 101/1965).
NAME AND BUSINESS ADDRESS OF APPLICANT:
Lennon Limited
7 Fairclough Road
PORT ELIZABETH
6001
DATE OF PUBLICATION OF THIS PACKAGE INSERT:
11.09.1970 P739
L.LTD.L.18238
SAEPI HOME PAGE TRADE NAME INDEX GENERIC NAME INDEX FEEDBACK
Information presented by Malahyde Information Systems © Copyright 1996,1997,1998
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Pleasure
Dopamine is a hormone and neurotransmitter occurring in a wide variety of animals, both vertebrates and invertebrates. In the brain, this phenethylamine functions as a neurotransmitter, activating dopamine receptors and their variants. Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area.
It was discovered in 1952 by Arvid Carlsson in Sweden. Carlsson was awarded the 2000 Nobel Prize in Physiology or Medicine for showing that dopamine is not just a precursor of adrenaline but a neurotransmitter, as well.
Dopamine has many functions in the brain, including important roles in behavior and cognition, motor activity, motivation and reward, sleep, mood, attention, and learning. A common hypothesis is that dopamine has a function of transmitting reward prediction error. According to this hypothesis, the responses of dopamine neurons are observed when an unexpected reward is presented. These responses transfer to the onset of a conditioned stimulus after repeated pairings with the reward.
Further, dopamine neurons are depressed when the expected reward is omitted. Thus, dopamine neurons seem to encode the prediction error of rewarding outcomes. In nature, we learn to repeat behaviors that lead to maximize rewards. Dopamine is therefore believed to provide a teaching signal to parts of the brain responsible for acquiring new behavior. In insects, a similar reward system exists, using octopamine, a chemical relative of dopamine.
In the frontal lobes, dopamine controls the flow of information from other areas of the brain. Dopamine disorders in this region of the brain can cause a decline in neurocognitive functions, especially memory, attention, and problem solving. Reduced dopamine concentrations in the prefrontal cortex are thought to contribute to attention deficit disorder.
Dopamine is associated with the pleasure system of the brain, providing feelings of enjoyment and reinforcement to motivate a person proactively to perform certain activities. Dopamine is released by naturally rewarding experiences such as food, sex, drugs, and neutral stimuli that become associated with them. This theory is often discussed in terms of drugs such as cocaine, nicotine, and amphetamines, which seem to directly or indirectly lead to an increase of dopamine. Recent studies indicate that aggression may also stimulate the release of dopamine in this way.
Abnormally high dopamine action has also been strongly linked to psychosis and schizophrenia. Evidence comes partly from the discovery of a class of drugs called the phenothiazines that can reduce psychotic symptoms, and from the finding that drugs such as amphetamine and cocaine which are known to greatly increase dopamine levels can cause psychosis. Because of this, most modern antipsychotic medications are designed to block dopamine function to varying degrees.
Polyphenol oxidases are a family of enzymes responsible for the browning of fresh fruits and vegetables when they are cut or bruised. The natural substrate for the oxidation in bananas is dopamine. The product of their oxidation, dopamine quinone, oxidises to other quinones. The quinones then condense with amino acids to form brown pigments known as melanins. The quinones and melanins derived from dopamine help protect damaged fruit and vegetables against growth of bacteria and fungi.
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Postnatal vitamins & breastfeeding
Why are postnatal vitamins important?
Most moms understand the importance of prenatal vitamins during baby’s development. But once you’ve welcomed your new baby and are beginning to adjust to postpartum life, where do vitamins fit in and how do they affect breastfeeding?
Postnatal vitamins are specifically created to supplement your body’s nutrient needs after giving birth. Pregnancy depletes several nutrients in the body, including folate, calcium, and vitamin B6. If you’re breastfeeding, the daily recommended dose of many nutrients is even higher than it was in pregnancy. Good nutrition is especially important for breastfeeding moms since it helps support your body’s needs while you are supplying the nutrients your baby needs to grow and develop during these early months.
Those good habits you formed during pregnancy continue to be important. With the adjustment to a new baby in your life and home, it’s natural to sometimes feel overwhelmed and stressed, with little time to think about yourself, but a healthy diet, sleep, proper hydration, and when you’re ready, exercise, all contribute to your health and your ability to care for your baby. Postnatal vitamins are a good way to supplement those efforts and make up for any nutrients that are hard to get through diet alone.
What are the benefits of taking postnatal vitamins?
Both you and your baby can benefit. Here are some of the ways postnatal vitamins can help:
• Support breastfeeding. Many women wonder whether it is okay to take a multivitamin while breastfeeding. It’s not only okay, it’s a good idea. The best vitamins for breastfeeding moms can help by supporting your body’s ability to produce milk, increasing milk supply to help keep up with your baby’s demand. Breastfeeding supplements also support your overall health while helping you provide for your baby.
• Maintain iron levels. Postnatal vitamins can help you avoid anemia, a common concern when your body doesn’t get enough iron.
• Improve mood. Postpartum depression and anxiety are not uncommon and can occur in varying degrees for many women. Nutritional supplements designed for your body’s needs can support better mood.
• Sleep. For new moms few things are as welcome as restful sleep. Postnatal vitamins can help you get a good night’s rest and refresh your energy levels, making it easier to be present for your baby.
• Sustain energy. Breastfeeding moms tend to experience dips in energy as blood flow is diverted towards milk production. Postnatal vitamins can help stabilize these fluctuations so that you don’t feel as drained by the end of the day.
• Reduce stress. Caring for a new baby can be stressful. Taking the time to care for yourself and your own health needs can help you better care for your baby.
• Improved digestion. Pregnancy and breastfeeding can put stress on your digestive system. Postnatal vitamins help improve your body’s ability to digest food and help prevent fatigue.
• Better skin, hair, and nails. Another benefit to postnatal vitamins is how they can help improve your complexion and the health of your hair and nails, providing a boost to your overall feeling of well-being.
What nutrients are critical for postpartum moms?
Try adding these key nutrients to your diet. And here’s what ingredients to look for in the best postnatal vitamins and nutritional supplements.
Iron:
One of the most important ingredients to replenish is iron. Your body loses iron during childbirth. When you are breastfeeding, your iron stores help supply your baby as well. Babies need iron for proper development and thyroid function. Anemia due to iron deficiency is a common concern during pregnancy and postpartum. The daily recommendation for iron intake for lactating women, ages 19 to 50, is 10 milligrams (mg). If you are unsure of the specific levels you need, have your medical practitioner use your blood test results to adjust the dosage for you (1).
Good dietary sources of iron include red meat, liver, clams, oysters, and green leafy vegetables. Vegetarians often need a good
iron supplement since it can be challenging to get enough from diet alone, especially when you are supplying iron for two.
DHA:
Omega-3 fatty acid, DHA, is extremely important since it contributes to your baby’s neurological development. Studies show that infants of mothers with a high DHA concentration in their breast milk have improved brain and vision development. Even for mothers who are not breastfeeding, research indicates that DHA can enhance mental focus, and reduce inflammation and the risk of postpartum depression (2).
Good dietary sources include salmon, sardines, fortified eggs, and dairy. Most moms should continue to take a
DHA supplement after pregnancy because many don’t get as much as they need in their diet. For vegetarians it can be even harder to get enough. Vegan supplements can help fill in the gap.
Vitamin D:
Vitamin D supports the immune system, brain, and nervous system and reduces risk of postpartum depression and anxiety. There is increased interest in the relationship between vitamin D and postpartum depression. Researchers believe that vitamin D may be a convenient choice to correct serum levels safely and reduce the incidence of depressive symptoms. In fact, it’s great if you started early with vitamin D during pregnancy since healthcare professionals suggest that adequate vitamin D intake during pregnancy could help mitigate the depressive consequences of a postpartum deficiency (3).
Sunshine is a source, so getting out for a walk around the neighborhood with your baby not only provides a little exercise but some vitamin D as well. The best dietary sources of Vitamin D are fatty fish like salmon and tuna, liver, fortified dairy and orange juice, and egg yolks.
Vitamin D supplements help make sure you are getting enough of this important vitamin. Breastfeeding exclusively can meet the nutritional needs of infants for the first 6 months of life with the exception of vitamins D and K, which should be given to breastfed infants as supplements (4).
Vitamin B12:
B12 is required for proper red blood cell development, energy production, and helping to form our DNA. Studies show that babies with inadequate B12 levels are often more irritable, and have an increased risk for failure to thrive, developmental delays, and poor brain growth. When you're breastfeeding, the concentration levels of some nutrients in your milk, specifically vitamins A, D, B1, B2, B3, B6, and B12, fatty acids, and iodine, are influenced by the amount you are getting in your diet. A healthy diet for mom means a healthier diet for baby (4).
The best dietary sources for vitamin B12 are animal foods, such as clams, tuna, liver, beef, and salmon. You can also get vitamin B12 from fortified dairy and cereals. Vegans are advised to take a B12 supplement.
Choline:
Choline is very important for infant memory and brain development. The need for this important nutrient increases during pregnancy and is highest in breastfeeding moms.
The best food sources of choline are eggs and organ meats like liver. The adequate recommended choline intake level is 425 mg choline/day for women of reproductive age with adjustments to 450 mg choline/day during pregnancy and 550 mg choline/day during lactation. A postnatal vitamin can help ensure you are getting adequate levels (5).
Choline is a bulky nutrient, which is why it is impossible to put enough choline in a once-daily multivitamin to meet your daily requirements. Eat choline-rich foods and bridge the gap with an additional choline or mineral support supplement that includes choline along with your postnatal vitamin.
Vitamin C:
Vitamin C can help support the healing your body needs after giving birth, whether you have given birth vaginally or via Cesarean-section. Since breastfeeding moms secrete vitamin C in breast milk, you will need to replenish the loss of this important vitamin. The recommended dietary amount for lactating women ages 19-50 is 120 mg (6).
Vitamin E:
Vitamin E is important for breastfeeding moms in order to keep your immune system strong. It also helps with the production of red blood cells, and can help lower cholesterol levels. Studies indicate that women who are lactating may need to supplement their dietary intake of vitamin E to achieve the recommended daily allowance of 19 mg. Research also suggests that a mom’s vitamin E supplementation can safely increase the vitamin E levels in her breast milk and improve the vitamin E status of her breastfed infant (7).
Calcium, Vitamin B6, and Folate:
When you are recovering from giving birth other key vitamins like
folate, calcium, and vitamin B6 are vital in the postpartum period because they help promote your body’s health. This is an important time to replenish your stores of these critical nutrients. If you’re breastfeeding, you may need even higher levels of these vitamins to support your baby’s continued growth and development (8). You’ll need to take a separate calcium product because this bone-building mineral is often too bulky to fit into a multivitamin.
How long should you take postnatal vitamins?
The American College of Obstetricians and Gynecologists (ACOG) recommends taking postnatal vitamins for as long as you are breastfeeding. Some experts recommend continuing beyond that time, especially if you are planning another pregnancy. Your body will be better prepared for your next pregnancy if you maintain healthy levels of important nutrients.
For women who choose not to breastfeed, the recommendation is to take postnatal vitamins for at least 6 months postpartum to replenish nutrient stores (9).
There is a lot going on in those first months of a new baby joining your nest. Taking care of your health and wellbeing sets you and your baby up for the best.
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Journal Logo
Research Article: Clinical Trial/Experimental Study
Oxycodone preemptive analgesia after endoscopic plasma total adenotonsillectomy in children
A randomized controlled trial
Wu, Jiang MSa; Gui, Qi MSb; Wang, Jinlin BSa; Ye, Jingjing BSa; Xia, Zhongfang MDb; Wang, Shufen MSb; Liu, Feng MSa; Kong, Fanli MSa; Zhong, Liang MSa,∗
Section Editor(s): Gharaei., Helen
Author Information
doi: 10.1097/MD.0000000000019004
• Open
Abstract
1 Introduction
Sleep-disordered breathing (SDB) is a common health issue in China, with a prevalence of 10.1% to 17.2% for occasional SDB and 5.6% to 8.9% for regular SDB. SDB leads to symptoms like daytime sleepiness that can affect school performance and behavioral/cognitive development.[1] Adenotonsillectomy is one of the main surgical methods to manage severe cases.[2] Postoperative pain is common after endoscopic tonsillectomy in children,[3] especially after the termination of total intravenous anesthesia (TIVA) using propofol and remifentanil.[4] Sufentanil is a synthetic opioid analgesic and is commonly used for intraoperative anesthesia and postoperative intravenous analgesia.[5] Oxycodone hydrochloride is a semi-synthetic derivative of opioid alkaloid; it is a dual agonist for both μ and κ opioid receptors.[6]
The entropy value of electroencephalogram (EEG) data can be used to determine the level of sedation.[7] EEG provides two values: state entropy (SE) and response entropy (RE). SE measures the depth of hypnosis, while RE measures the depth of analgesia; therefore, RE can be considered as an indirect measure of pain.[8] The Pediatric Anesthesia Emergence Delirium (PAED) scale assesses the degree of emergence delirium.[9] The face, legs, activity, cry, and consolability (FLACC) scale is used to assess pain in children.[10] The FOS protein leads to the expression of dynorphin and is involved in postoperative pain.[11] Measuring the serum mRNA levels of c-fos (encoding FOS) can be used to evaluate pain development.[11]
Therefore, in the present randomized trial, preemptive analgesia was conducted to proactively prevent and inhibit central and peripheral postoperative pain[12] in order to manage the pain caused by tonsillectomy in patients with adenotonsillar hypertrophy. Entropy index (including preoperative and postoperative RE), PAED score, FLACC score, and serum mRNA c-fos levels were used to evaluate the efficacy of preemptive analgesia using oxycodone or sufentanil.
2 Materials and methods
2.1 Study design and patients
This manuscript adheres to the applicable CONSORT guidelines. This was a randomized controlled clinical trial, registered at www.chictr.org.cn (ChiCTR-INR-16009116, August 29, 2016). Patients with adenotonsillar hypertrophy were recruited at the Department of Otorhinolaryngology of the Wuhan Children's Hospital between August 2016 and March 2017. The study was approved by the Institutional Review Board (IRB) of the Wuhan Maternal and Child Healthcare Hospital. Written informed consent was obtained from the parents or legal guardians for minor subjects.
The inclusion criteria were:
• 1) to 9 years of age;
• 2) diagnosed with obstructive sleep apnea-hypopnea syndrome (moderate or less: 1≤ apnea-hypopnea index [AHI] ≤10) with or without hypoxemia (moderate or less: 75%≤ blood oxygen saturation [SpO2] ≤92%);[3]
• 3) tonsil hypertrophy; and
• 4) met the sleep-disordered breathing surgical criteria for adenotonsillectomy.
The exclusion criteria were:
• 1) participated in another clinical trial within 4 weeks before enrollment;
• 2) history of long-term narcotic or opioid use;
• 3) allergy to opioids;
• 4) heart diseases (degree II or more with cardiac functional insufficiency);
• 5) with severe hypertension;[13]
• 6) with mild to moderate hypertension, but blood pressure (BP) higher than 140/90 mmHg before medication;[13]
• 7) hepatic or renal indexes higher than two folds of the upper limit of normal);
• 8) drug dependency history;
• 9) dehydration (decreased peripheral perfusion, deep breathing, decreased skin turgor, high urea, low pH, and/or large base deficit);[3] or
• 10) developmental retardation. (Fig. 1)
Figure 1
Figure 1:
Study flowchart.
2.2 Randomization and grouping
The patients were randomized using sequential sealed envelopes. When one child was entered into the study, the envelope was opened by a designated supervisor, and the child was randomized (1:1:1) to one of 3 groups. The children were given a random ID number. Only the ID number was used in all study paperwork and database. The 3 groups were:
• 1) sufentanil postoperative analgesia (SPOA group);
• 2) sufentanil preemptive analgesia (SPEA+SPOA group); and
• 3) oxycodone preemptive analgesia (OPEA+SPOA group).
Sufentanil was used for postoperative continuous analgesia in the 3 groups. Sufentanil and oxycodone were used as preemptive analgesia before tonsillectomy in the SPEA+SPOA and OPEA+SPOA groups, respectively. Assessors, statisticians, patients, and their parents were blind to grouping.
2.3 Anesthesia protocol
Atropine was intramuscularly injected at 0.02 mg/kg 30 minutes before operation for all patients, followed by oxygen inhalation and intravenous induction. Remifentanil 1 μg/kg and propofol 4 mg/kg were intravenously injected 3 to 5 minutes before operation, with or without sufentanil 0.1 μg/kg or oxycodone 0.1 mg/kg. Cisatracurium (0.05 mg/kg) was injected intravenously, and tracheal intubation was conducted after assisted respiration for 3 min. Propofol 4–12 mg/kg/h and remifentanil 0.05 to 0.1 μg/kg/h were infused continuously to sustain anesthesia. Hydroxyethyl starch was injected at 10 mL/kg/h to sustain circulation stability. All operations were performed by an experienced attending otolaryngologist. Mechanical ventilation was used, and the tracheal tube was removed under vacuum during the recovery period, followed with immediate clearing of secretions and residual blood in the oropharynx. No perioperative steroids were used.
The patients were observed for 15 to 30 minutes before sufentanil at 0.6 μg/kg/d using a BCDB-100 electronic analgesia pump (Shanghai Bochuang Medical Equipment Co., Ltd, China). The drug was diluted in normal saline to 100 mL and continuously injected at 4 mL/h for 24 hours.
2.4 Observation parameters
RE and SE were recorded using a Datex-Ohmeda S/5 monitor (Datex Ohmeda, Helsinki, Finland). BP, electrocardiogram (ECG), heart rate (HR), and SpO2 were monitored. The FLACC scores were determined. FLACC varies from 0 to 10, and ≤5 is considered as satisfying analgesia.[10] PAED scores were determined as previously reported.[14] The degree of emergence delirium increases directly with the total score.[9] The Steward recovery scale was used to evaluate the degree of awakening in the anesthesia recovery room.[15] The FLACC score, PAED score, and Steward recovery scale were assessed by a single anesthetist who did not participate in the operations and was blind to grouping.
2.5 Quantitative real-time PCR
The relative transcription levels of c-fos mRNA and β-actin were determined by fluorescence quantitative RT-PCR before surgery and 15 to 30 minutes after surgery using peripheral blood serum. Total RNA was extracted using Trizol (Invitrogen Inc., Carlsbad, CA)[16] and assessed by electrophoresis. The amount and purity were determined by ultraviolet spectrophotometry. Total RNA (1.0 μg) was denatured at 65°C for 5 minutes and cooled, and the M-Mulv reverse transcriptase was added. The total reaction volume was 20 μL. The mixture was incubated at 42°C for 60 minutes before inactivation at 85°C for 5 minutes. The conditions for RT-PCR were:
• 1) denaturation at 95°C for 30 seconds;
• 2) 40 cycles of denaturation at 95°C for 15 seconds and extension at 58°C for 20 seconds; and
• 3) 72°C for 90 seconds.
The relative amount of PCR products was calculated by the 2-ΔΔCt method. The primers were: c-fos, forward 3’-AGTTCATCCTGGCAGCTCAC-5’ and reverse 3’-TGCTGCTGATGCTCTTGACA-5’ (204 bp); and β-actin, forward 3’-GTCACCAACTGGGACGACAT-5’ and reverse 3’-GAGGCGTACAGGGATAGCAC-5’ (209 bp).
2.6 Endpoints and follow-up
The primary endpoint was the relative transcription levels of c-fos. The secondary endpoints were the RE value, PAED score, FLACC score, and adverse events.
The patients were monitored for 30 minutes after operation in the anesthesia recovery room, and they were evaluated at 4 and 24 hours after operation. The adverse events were recorded by inquiring the patients and their parents, and by physical examinations. The awakening time was defined as from the start of extubation to when the Steward score reached 6 in the anesthesia recovery room.
2.7 Statistical analysis
The sample size was calculated by multiple populations mean sample size estimation with two-sided α of 0.05, power of 90%, and mean reduction of pain intensity (visual analog scale) after treatment of 4 ± 3 in the SPOA group, 8 ± 4 in the SPEA+SPOA group, and 6.5 ± 3 in the OPEA+SPOA group. The estimated sample size was at least 53 patients for each group. Assuming a drop-out rate of 20%, 66 patients were needed for each group.
SPSS 17.0 (IBM, Armonk, NY) was used for statistical analysis. Continuous data in accordance with the normal distribution (tested with the Kolmogorov-Smirnov test) were presented as mean ± standard deviation (SD). Intergroup comparisons were performed using analysis of variance (ANOVA) and Tukey's post hoc test. Intragroup comparisons were performed using the paired t-test and repeated measures ANOVA. Categorical data were presented as frequency (percentage) and were analyzed using the chi-square test. The correlations were analyzed using the Pearson method. The prediction probability (Pk) of RE values and c-fos mRNA levels to the FLACC score was calculated using the Pk MACRO software.[17] Two-sided P values < .05 were considered statistically significant.
3 Results
3.1 Patients
A total of 262 patients were identified for possible inclusion from August 2016 to March 2017. Among them, 52 patients were excluded (15 for severe sleep apnea-hypopnea syndrome, 24 for mild symptoms and no need for surgery, 2 for mental development disorder, one for participation in another clinical trial, 4 for hepatic or renal dysfunction, and 6 for other reasons); 210 patients with confirmed moderate or less adenotonsillar hypertrophy were randomized. Forty-four patients were withdrawn: massive hemorrhage (n = 1), teeth, oral mucosa, or tongue injury (n = 2), insufficient blood sampling for c-fos measurement (n = 9), inappropriate timing of blood sampling (n = 8), inappropriate handling of blood (n = 6), RT-PCR technical failure (n = 8), and loss to follow-up (n = 10). Eventually, 166 patients completed the study and were included in the final analysis. There were no significant differences among the 3 groups regarding baseline characteristics, HR, BP, and SpO2 before and after anesthesia (Tables 1 and 2). There were no differences in the operative time and awakening time among the three groups (Table 3).
Table 1
Table 1:
Baseline characteristics of the 3 groups before analgesia.
Table 2
Table 2:
HR, BP, and SpO2 comparison among the three groups before and after extubation.
Table 3
Table 3:
Comparison of the relative serum c-fos mRNA levels, RE values, PAED score, FLACC score, operative time and awakening time among the 3 groups.
3.2 C-fos mRNA levels
C-fos mRNA levels significantly increased after surgery in the SPOA and SPEA+SPOA groups (P < .05) (Table 3). Postoperatively, c-fos mRNA levels were higher in the SPOA group compared with the OPEA+SPOA group (P = .044).
3.3 RE values, PAED score, and FLACC score
The RE values increased in all 3 groups after surgery (P < .05) (Table 3). At extubation, the RE values were higher in the SPOA group compared with the SPEA+SPOA and OPEA+SPOA groups (P < .05). The PAED scores were higher in the SPOA group compared with the OPEA+SPOA group (P = .045). In the SPOA group, the FLACC scores were decreased at 24 hours after surgery compared with 4 hours (P = .044).
3.4 Correlations and Pk values
Correlations were observed between PAED scores (at 30 minutes) and RE (at 5 minutes) after extubation and c-fos mRNA levels (Table 4). Significant correlations were observed between postoperative FLACC scores (at 4 hours) and RE (at 5 minutes) after extubation and c-fos mRNA levels. Although there were no significant differences of Pk among the three groups, Pk values were greater than 0.5, indicating that the RE value and c-fos mRNA levels were quantitative predictors for early postoperative stress reaction after surgery.
Table 4
Table 4:
Correlations and Pk values.
3.5 Adverse events
There was no significant difference among the 3 groups regarding nausea (Table 5). No vomiting, respiratory depression, or recurrent tonsillitis occurred. No postoperative agitation was observed.
Table 5
Table 5:
Adverse events.
4 Discussion
Remifentanil is indicated for simple procedures that generally do not induce intense pains, unlike major surgeries. Nevertheless, tonsil surgery is associated with pain, especially when it is performed on young, growing patients.[3,4] Remifentanil shows more frequent and severe hyperalgesia than other opioid drugs because of its unique pharmacokinetics.[4,18] Therefore, in children undergoing tonsillectomy, remifentanil-based intravenous anesthesia could result in postoperative pain.[18,19] Remifentanil primarily stimulates the μ receptors, followed with Gi stimulation to produce analgesia, but the constant administration of remifentanil could switch protein G and alter the functionality of the μ receptor, inducing the conversion of the Gi-coupled opioid receptor to Gs-coupled opioid receptor, inducing pain.[20]
Combined intravenous analgesia could reduce the injury stimulation from the tonsil branch of the glossopharyngeal nerve to each level of the central nerve and induce effective analgesia. Oxycodone or sufentanil preemptive analgesia and sufentanil postoperative intravenous analgesia have been reported, but the analgesic effect was not satisfying.[21] Oxycodone is an opioid receptor agonist, stimulating both μ and κ receptor in the central nervous system, but mainly the κ receptor.[22] Oxycodone has the advantages of high bioavailability, stable hemodynamics, and few adverse effects. Oxycodone can be intravenously injected at 0.1 mg/kg after anesthesia induction for the treatment of pain in children undergoing thoracotomy or to alleviate pain due to orthopedic injury.[19] In the present study, oxycodone 0.1 mg/kg and sufentanil were used for preemptive analgesia to reduce postoperative pain for children undergoing tonsillectomy. Postoperative 24-hour FLACC scores of the OPEA+SPOA group were lower than that of the SPOA group. In addition, the tolerance to injury stimulation of the OPEA+SPOA group was elevated, as indicated by the transcription levels of c-fos mRNA. Oxycodone injection 5 minutes before surgery could reduce postoperative pain at the early stage and facilitate the subsequent postoperative analgesia. The tolerance to injury stimulation of the SPEA+SPOA group was also elevated. The FLACC scores indicated that postoperative pain caused by remifentanil could attenuate the postoperative analgesia induced by sufentanil. The PAED score was higher in the SPOA group, in which neither sufentanil nor oxycodone was used, compared with the OPEA+SPOA groups, in which oxycodone was used. Oxycodone 0.1 mg/kg preemptive analgesia in combination with sufentanil postoperative analgesia was demonstrated to be effective for children, and their recovery was uneventful. The possible reason might be that central sensitization induced by the surgical injury could arouse an excitatory state of the central nervous system, which could be eliminated by preoperative analgesia; both peripheral and central sensitization could be suppressed to facilitate postoperative analgesia. Those results are supported by a previous study that showed that sufentanil reduced emergence agitation in children receiving sevoflurane anesthesia for adenotonsillectomy, compared with fentanyl,[23] and by a review that suggests that oxycodone is an adequate alternative for pain management because it is not metabolized by CYP2D6.[24]
The FOS protein is an immediate stress response protein that shows elevated plasma levels as early as 30 to 60 minutes after stimuli and returns to normal by 90 minutes.[25] Even though the relative transcription levels of the c-fos mRNA in the serum is not a direct measurement of pain, it may sensitively and quantitatively reflect stress levels, which include pain, but also nausea, vomiting, and restlessness after injury stimulation.[16] In this regard, c-fos levels have been shown to have good sensitivity, but low specificity.[26] Since intravenous analgesia aims to decrease pain and to alleviate negative experiences like nausea, vomiting, and restlessness, c-fos mRNA levels should be decreased by successful analgesia.[25] In the present study, the relative transcription levels of the c-fos mRNA in serum were increased along with the severity of pain, as supported by previous studies.[27] Since the anesthesia protocol was the same for the three groups, anesthesia should not be a bias on the differences in the c-fos levels among the three groups. In addition, no child showed agitation, nausea, or vomiting in the three groups, which again should not have biased the results. Finally, c-fos levels correlated with RE, supporting its use as a marker of stress.
RE values are calculated from the frequency spectrum of 0.8 to 47 Hz (including EEG and facial electrical components), reflecting the facial muscles’ response to waking pain, and RE can detect this alteration very quickly.[28] Therefore, RE value can quantify the stress pain caused by painful operations such as vacuum aspiration of oropharynx and larynx, and endotracheal intubation.[29]
In the present study, both the c-fos mRNA levels and RE value strongly suggested that oxycodone could reduce central sensitization. RE value (reflecting injury stimulation) was increased substantially when oxycodone and sufentanil were not used, and RE values were maintained at high levels. Though sufentanil was used for postoperative analgesia, the dose was relatively low to avoid any disturbance on circulation and respiration, so that severe postoperative pain was felt by some children. RE value was initially increased when oxycodone was used at 0.1 mg/kg and then gradually decreased, indicating that oxycodone could improve postoperative pain. Moreover, the FLACC score indicated that oxycodone could cooperate with sufentanil for postoperative analgesia.
Though nausea and vomiting could be caused by surgery, it could be associated with extubation as well. Nevertheless, there were no significant differences among the three groups regarding nausea and vomiting.
The present study is not without limitations. The study was a single-center trial with a limited sample size. In addition, there was a lack of long-term follow-up to assess the surgical outcomes or to examine long-term adverse events. Only fixed doses were tested, and additional combinations could be tested. Although only children of 2 to 9 years of age were enrolled, there are important differences in cognition and pain thresholds between children of 2 and 9 years of age. In addition, there might be interindividual variations regarding the response to analgesia, and those differences were not assessed. Finally, although the evaluation indexes used in the study are well-known indicators of pain, they must be considered as surrogates at best and can be influenced by a number of factors.
In conclusion, oxycodone preemptive analgesia (0.1 mg/kg), in combination with sufentanil postoperative analgesia, has an analgesic effect in children undergoing endoscopic plasma adenotonsillectomy. This approach is superior to sufentanil postoperative analgesia and sufentanil preemptive analgesia in combination with sufentanil postoperative analgesia.
Acknowledgments
The authors acknowledge the support of Prof. Zhongfang Xia and former Prof. Zhinan Wang of the Department of Otorhinolaryngology of the Wuhan Children's Hospital, Tongji Medical College, Huazhong University of Science & Technology.
Author contributions
Conceptualization: Jiang Wu, Liang Zhong.
Data curation: Qi Gui, Feng Liu.
Formal analysis: Qi Gui, Shufen Wang, Feng Liu, Fanli Kong.
Funding acquisition: Fanli Kong.
Investigation: Qi Gui, Shufen Wang.
Methodology: Jiang Wu, Qi Gui, Jinlin Wang, Jingjing Ye, Zhongfang Xia, Shufen Wang.
Project administration: Jinlin Wang, Jingjing Ye, Zhongfang Xia.
Resources: Jinlin Wang, Jingjing Ye, Zhongfang Xia.
Software: Zhongfang Xia.
Writing – original draft: Jiang Wu, Liang Zhong.
Writing – review & editing: Jiang Wu, Qi Gui, Jinlin Wang, Jingjing Ye, Zhongfang Xia, Shufen Wang, Feng Liu, Fanli Kong, Liang Zhong.
References
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[2]. Ahn YM. Treatment of obstructive sleep apnea in children. Korean J Pediatr 2010;53:872–9.
[3]. Arbin L, Enlund M, Knutsson J. Post-tonsillectomy pain after using bipolar diathermy scissors or the harmonic scalpel: a randomised blinded study. Eur Arch Otorhinolaryngol 2017;274:2281–5.
[4]. Somaini M, Engelhardt T, Fumagalli R, et al. Emergence delirium or pain after anaesthesia--how to distinguish between the two in young children: a retrospective analysis of observational studies. Br J Anaesth 2016;116:377–83.
[5]. Savoia G, Loreto M, Gravino E. Sufentanil: an overview of its use for acute pain management. Minerva Anestesiol 2001;67: (9 Suppl 1): 206–16.
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[8]. Mathews DM, Cirullo PM, Struys MM, et al. Feasibility study for the administration of remifentanil based on the difference between response entropy and state entropy. Br J Anaesth 2007;98:785–91.
[9]. Luo K, Xu JM, Cao L, et al. Effect of dexmedetomidine combined with sufentanil on preventing emergence agitation in children receiving sevoflurane anesthesia for cleft palate repair surgery. Exp Ther Med 2017;14:1775–82.
[10]. Voepel-Lewis T, Zanotti J, Dammeyer JA, et al. Reliability and validity of the face, legs, activity, cry, consolability behavioral tool in assessing acute pain in critically ill patients. Am J Crit Care 2010;19:55–61.
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[13]. Portman RJ, McNiece KL, Swinford RD, et al. Pediatric hypertension: diagnosis, evaluation, management, and treatment for the primary care physician. Curr Probl Pediatr Adolesc Health Care 2005;35:262–94.
[14]. Bajwa SA, Costi D, Cyna AM. A comparison of emergence delirium scales following general anesthesia in children. Paediatr Anaesth 2010;20:704–11.
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[16]. Yu EH, Tran DH, Lam SW, et al. Remifentanil tolerance and hyperalgesia: short-term gain, long-term pain? Anaesthesia 2016;71:1347–62.
[17]. Jordan D, Steiner M, Kochs EF, et al. A program for computing the prediction probability and the related receiver operating characteristic graph. Anesth Analg 2010;111:1416–21.
[18]. Santonocito C, Noto A, Crimi C, et al. Remifentanil-induced postoperative hyperalgesia: current perspectives on mechanisms and therapeutic strategies. Local Reg Anesth 2018;11:15–23.
[19]. Kim SH, Stoicea N, Soghomonyan S, et al. Intraoperative use of remifentanil and opioid induced hyperalgesia/acute opioid tolerance: systematic review. Front Pharmacol 2014;5:108.
[20]. Brum IS, Morsch DM, Pozzobon A, et al. Androgen-dependent expression of c-jun and c-fos in human non-transformed epithelial prostatic cells: association with cell proliferation. Horm Res 2003;60:209–14.
[21]. Grape S, Tramer MR. Do we need preemptive analgesia for the treatment of postoperative pain? Best Pract Res Clin Anaesthesiol 2007;21:51–63.
[22]. Bao L, Jin SX, Zhang C, et al. Activation of delta opioid receptors induces receptor insertion and neuropeptide secretion. Neuron 2003;37:121–33.
[23]. Li J, Huang ZL, Zhang XT, et al. Sufentanil reduces emergence agitation in children receiving sevoflurane anesthesia for adenotonsillectomy compared with fentanyl. Chin Med J 2011;124:3682–5.
[24]. Chidambaran V, Sadhasivam S, Mahmoud M. Codeine and opioid metabolism: implications and alternatives for pediatric pain management. Curr Opin Anaesthesiol 2017;30:349–56.
[25]. Bahrami S, Drablos F. Gene regulation in the immediate-early response process. Adv Biol Regu 2016;62:37–49.
[26]. Kidambi S, Yarmush J, Berdichevsky Y, et al. Propofol induces MAPK/ERK cascade dependant expression of cFos and Egr-1 in rat hippocampal slices. BMC Res Notes 2010;3:201.
[27]. Ahn SN, Guu JJ, Tobin AJ, et al. Use of c-fos to identify activity-dependent spinal neurons after stepping in intact adult rats. Spinal Cord 2006;44:547–59.
[28]. Paloheimo M. Quantitative surface electromyography (qEMG): applications in anaesthesiology and critical care. Acta Anaesthesiol Scand Suppl 1990;93:1–83.
[29]. Aho AJ, Yli-Hankala A, Lyytikainen LP, et al. Facial muscle activity, Response Entropy, and State Entropy indices during noxious stimuli in propofol-nitrous oxide or propofol-nitrous oxide-remifentanil anaesthesia without neuromuscular block. Br J Anaesth 2009;102:227–33.
Keywords:
children; endoscopic plasma total adenotonsillectomy; oxycodone; postoperative pain; preemptive analgesia; reaction entropy; serum c-fos mRNA
Copyright © 2020 the Author(s). Published by Wolters Kluwer Health, Inc.
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5eff3d1f6f98e57329caed0ceb9053d3
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5,936,070,232,067,055,000
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DPRX
CANCER ATLAS
? »
Gene description
Divergent-paired related homeobox
Protein class
Predicted intracellular proteins, Transcription factors
Protein evidence
Evidence at transcript level
Colorectal cancer
Breast cancer
Prostate cancer
Lung cancer
Skin cancer
STAINING SUMMARY
? »
HPA043682
Tissue
Cancer staining
Breast cancer
Carcinoid
Cervical cancer
Colorectal cancer
Endometrial cancer
Glioma
Head and neck cancer
Liver cancer
Lung cancer
Lymphoma
Tissue
Cancer staining
Melanoma
Ovarian cancer
Pancreatic cancer
Prostate cancer
Renal cancer
Skin cancer
Stomach cancer
Testis cancer
Thyroid cancer
Urothelial cancer
Staining summary
Isolated cases of basal cell carcinomas exhibited moderate to strong cytoplasmic positivity. Remaining malignant cells were negative.
Level of antibody staining/expression
High
Medium
Low
Not detected
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5eff3d1f6f98e57329caed0ceb9053d3
|
4,612,425,950,777,936,000
|
adenoid cystic cancer
Browse Dictionary Alphabetically
Audio Contributors
1. A
2. B
3. C
4. D
5. E
6. F
7. G
8. H
9. I
10. J
11. K
12. L
13. M
14. N
15. O
16. P
17. Q
18. R
19. S
20. T
21. U
22. V
23. W
24. X
25. Y
26. Z
27. #
(AD-in-oyd SIS-tik KAN-sir)
This is an uncommon type of invasive breast cancer. It starts in the glands of the breast and grows into the normal surrounding breast tissue. (This type of cancer is more common in the salivary, or spit, glands.)
Read more about types of breast cancer.
Marie_constance_tcm8-329573
Audio contributed by: Constance Marie
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|
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5eff3d1f6f98e57329caed0ceb9053d3
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-6,313,945,080,192,684,000
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What is Kinesiology?
We all instinctively feel the connection between our brains and our bodies.
When we are emotionally down we describe ourselves as “feeling flat” and when we are at our most positive we describe ourselves as “full of energy”.
Kinesiology, Kinesiologist
This link is because the brain controls and dictates all our functions, like a computer.
But with injuries, emotional blocks, illnesses and stress that often occur in our lives, this computer is prone to getting a few bugs in the software and becomes out of balance.
Kinesiology looks at the mind.
90% of our brain capacity stems from the subconscious part of the brain, which oversees our memories and past experiences. It is from these memories and experiences that our core beliefs, behaviours and habits and formed.
This is also the part of the brain that makes your eyes blink and your heart beat without you having to think about it. These involuntary actions stem from the subconscious brain that is out of your awareness.
It is this subconscious part of the brain that we access as kinesiologists, via the integrity of the muscles.
Kinesiology, Kinesiologist
Your muscles are connected to your brain via the Nervous System and cross multiple meridian pathways in Traditional Chinese Medicine healing methods.
Using the muscles as a biofeedback tool when accessing this important part of the brain, we can then understand what imbalances might need to be corrected, that can be out of your awareness, thus rewiring the bugs in the software and restoring balance in the body again.
This is why you can feel really flat or unmotivated and you don’t really understand why. Kinesiology is a great tool to help you get to the bottom of the cause of your issue.
Kinesiology is like Physical Psychology.
When you address your current mental health, supporting and boost your health and emotions, it can be essentially like turning the stress tap off at the source.
This is because physical stress has an emotional link, and can be an end result of you not dealing with an emotion that you’ve suppressed or avoided in the past.
Kinesiology, Kinesiologist
We therefore work to improve your health by addressing emotional blocks on a subconscious level, via the muscles of the body that are linked to meridians (your body’s healing energy pathways) and internal organs.
We address the body structurally, biochemically, emotionally and electromagnetically, as a whole rather than in isolation.
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Can People With IBD Donate Blood?
Woman donating blood
Steve Debenport/Getty Images
Many people with inflammatory bowel disease (IBD) are active in their community, and donating blood is a way to give back. It's not uncommon for people with IBD to be on the receiving end of blood transfusions. When feeling better, this can often lead to a natural desire to contribute to a blood bank. However, it can be confusing, because in many cases there is not a direct answer as to whether people who have IBD are acceptable donors.
What Makes a Good Blood Donor?
In order to donate blood, a person usually must be in good general health, be over the age of 17 (usually), and weigh more than 110 pounds (50 kilograms). This is not because of any concerns about the blood but more out of concern for the donor.
A person who is not well might be further compromised by giving blood. When people with chronic illnesses such as Crohn's disease and ulcerative colitis are experiencing symptoms, losing blood is not desirable and may even make things worse. People with IBD may also be anemic, and anemia is one of the conditions that will make a potential donor ineligible.
In some cases, potential donors are ineligible based upon the medications they are receiving. Blood donation centers may give specific or general examples of the medications that make a person ineligible to be a donor. In most cases, it's the current use of the medication that is the problem, and a person could become eligible again several months after stopping the drug.
There are several other guidelines that vary from country to country and from donation center to donation center. Travel to certain countries may disallow a person from becoming a donor. Having a fever or infection or an active contagious disease such as tuberculosis or certain sexually transmitted diseases will also mean a person isn't eligible to donate.
Giving Blood in the United States
In the United States, people with IBD may be able to donate blood, but it is highly dependent upon the policies of the blood collection center. For instance, Memorial Sloan Kettering Cancer Center allows donation by people with Crohn's disease and ulcerative colitis as long as there have not been any symptoms of diarrhea for three days before donating. However, donors must also have stopped taking certain medications for several months prior, including injectables (such as Remicade, Humira, and Entyvio), methotrexate, and the antibiotic Flagyl.
The American Red Cross doesn't have any specific information listed about IBD and eligibility but does state that people with a chronic illness may be able to donate provided "you feel well, the condition is under control, and you meet all other eligibility requirements." There are no specific medication guidelines given in regards to the drugs commonly used for IBD. Whether or not IBD is under control is a subjective judgment, and if you meet other criteria and want to donate, talk to your gastroenterologist if you have more questions.
Giving Blood in Other Countries
Australia: The Australian Red Cross doesn't specify if IBD makes a person ineligible for donation, but they do ask that donors wait four months after having a biopsy or a polyp removed during a colonoscopy, gastroscopy, or flexible sigmoidoscopy procedure.
Canada: The Canadian Blood Services will not accept people who have Crohn's disease as blood donors. Ulcerative colitis isn't specifically listed as being an illness that prevents a person from giving blood. There may also be restrictions with regards to certain medications, especially those that suppress the immune system (immunosuppressants). For more information, contact the Canadian Blood Services at 1-888-2-DONATE (1-888-236-6283).
New Zealand: People with Crohn's disease and ulcerative colitis will not be able to donate blood with the New Zealand Blood Service.
The United Kingdom: In the United Kingdom, people with ulcerative colitis and Crohn's disease are not eligible to give blood. Contact the Donor Helpline at 0300 123 23 23 for answers to specific questions.
The Bottom Line
People with IBD may or may not be able to give blood, based on both personal health and the policies of local blood donation organizations. However, there are plenty of opportunities for volunteering both with donation facilities and in the local community or IBD organization. If you have more specific questions about donating blood or want to volunteer, contact your local Red Cross or other non-profit organization.
Was this page helpful?
Article Sources
Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial policy to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
• Additional Donor Requirements. Memorial Sloan Kettering Cancer Center.
• Eligibility Requirements. American Red Cross.
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TErrain en Naturopathie
Approche et Définition
La notion de terrain permet une approche différente de la santé et de la maladie. L'être humain n'est pas qu'une structure cellulaire comme dirait la biologie. Il est formé aussi d'un ensemble complexe: l'héritage, l'acquis et la prédisposition à certaines maladies.
Ces trois facteurs sont expliqués en naturopathie par de concepts tels que:
La constituition- Ce qui nous est héreditairement transmis;
Le tempérament- Ce qui nous acquérons tout au long de notre vie, sur les bases de ce qui nous a été transmis dans l'héréditarité;
Diathése- Ces sont nos "faiblesses" physiques et les tendances à dévélopper telle ou telle maladie influencée par notre mode de vie et nos vécus.
D'un individu à l'autre, le terrain est différent et unique, car les facteurs qui l'influencent sont nombreux et ils fluctuent dans le temps. Le terrain en naturopathie donne grande importance à la situation actuelle de la personne ainsi que ses antécédents familiaux pour évaluer le terrain au moment présent. Cette évaluation est la clé des conseils en naturopathie, ce qui va faciliter l'approche et les conseils individualisés.
LA CONSTITUTION
Les constitutions Naturopathiques
C'est la classification binaire proposée par Pierre-Valentin Marchesseau " le père de la naturopathie française" .
Sanguino- Pléthorique
C'est l'individu trapu, bréviligne avec une masse osseuse importante, son teint est coloré et congestif. Il a une bonne force vitale avec un bon fonctionnement des émonctoires. " Bon Vivant"; il est sociable, extraverti, convivial qui peut cacher ses sentiments. Puisque ses émonctoires marchent bien, il a tendance à faire des excès de table avec des abus d'alcool. Les excès peuvent causer des troubles cardio-vasculaires, digestifs, émonctoriels et glandulaires.
Neuro-Arthritique
C'est l'individu mince, longiligne avec une ossature peu dévéloppée. Il est sensible au stress, frileux, fatigable, son teint varie du pâle au jaunâtre. Plutôt introverti, cet hypersensible a tendance à sommatiser les événements par la rumination mentale. La déminéralisation, l'acidose et l'arthritisme sont présents, ainsi que la dystonie neuro-végétative.
Comparatif entre les deux contitutions:
Sanguino- Pléthorique Neuro-arthritique
Breviligne Longiligne
dilatation rétraction
chaud Froid
coloré Pâle
extraverti intraverti
congestion sclérose
Troubles métaboliques et hormonaux Troubles mineraux et dystonie neuro-végétative
Le corps parfait, c'est celui-ci qu'on a. Nous devrons apprendre à connaître les atours et les faiblesses de ce corps et donc l'apprivoiser.
Les constitutions Homéopathiques
La notion de constitution en homéopathie est héritée des conceptions anciennes et elle concerne la structure individuelle et le morphotype. La naturopathie se sert aussi des constitutions homéopathiques pour définir le morphotype.
Sont-elles:
Carbonique- (Calcarea carbonica) C'est l'individu court, trapu, avec peu de souplesse articulaire. Son métabolisme est ralenti, sujet aux affections traînantes et répetées.Ses rémèdes sont ceux qui stimulent le foie et les autres émonctoires: artichaut, romarim, radis noir...C'est un realisateur, méthodique, peu bavard et appliqué.
Phosphorique- (Calcarea phosphorica) C'est l'individu longiligne, mince et souple, avec tendance à la déminéralisation. Ses rémèdes sont ceux qui apaisent et réminéralisent: lavande, marjolaine ou encore avoine, sapin...C'est un hypersensible, imaginatif et affectif.
Fluorique- (Calcarea fluorica) C'est l'individu qui est dyssymétrique dans sa posture, l'implantation des dents, doué d'une hyperflexibilité ligamentaire. Il est le plus sujet aux complications pathologiques. Ses rémèdes sont ceux à l'activité structurante: bouleau, ortie, cassis, églantier...C'est un intuitif, observateur qui assimile très vite.
LE TEMPÉRAMENT
Les Tempéraments Naturopathiques
Ils ont été élaborés par Pierre Valentim Marchessau dans les années 1940. Le tempérament est ce que nous acquérons au long de la vie, selon nos habitudes et hygiène de vie, complémentés des nos tendances héréditaires.
Un tableau explicatif avec les principales différences entre les tempéraments:
MUSCULAIRE RESPIRATOIRE CÉRÉBRAL NERVEUX SANGUIN DIGESTIF OBÉSE
Visage:carré
partie inférieure rectractée
triangulaire triangulaire et rectracté rond rond avec double menton rond avec l'étage moyen dominant
Teint: Mat et coloré
légèrement coloré
pâle voir jaunâtre blanc grisâtre coloré, rouge et congestif
très coloré voire congestif
congestif ou blanc
Métabolisme:
acides OK
+acidose
++acidose et déminéra
lisation
+++acidose
acidose si surmenage
et sedentarité
++acidose
en cas d'insuffisance
emonctorielle;
sédentarisme
+++acidose
en cas d'insuffisance
emonctorielle
sédentarisme,
surmenage digestif
Prédisposition
aux pathologies:
Peu
surmenage musculaire
respiratoires, digestives et cutanées mêmes que le resp. +DNV, calculs et arthose mêmes que le cer. +terrain névrotique, faiblesse immunitaire urémie, uricémie, calculs, problèmes cardio- vasculaires mêmes que le sang. + sclérose digestive et tissulaire
mêmes que le dig. + problèmes glandulaires, ulcères variqueux et dermatoses
Système
surmené:
------
respiratoire cérébral nerveux
cardio-vasculaire
digestif glandulaire
Faiblesse
Organique:
------
foie et VB foie, VB, intestin, peau, reins
les mêmes que le resp; +la psychoso
matisation
reins
reins et cardio
vasculaire
reins et cardio- vasculaire aggravé
Les Tempéraments Hippocratiques
Hippocrate s'est basé dans les humeurs du corps humain( sécretions excrétées par notre système organique: Lymphe, sang, bile et atrabile) pour créer son concept de tempérament. Les tempéraments hippocratiques nous donnent des notions très complètes tantôt du côté physiques avec les faiblesses et prédispositions patogènes, tantôt du côté psychologique avec les aspects marqués de la personalité selon le tempérament.
Lymphatique: eau- hiver- lymphe- froid- humide- Je suis donc je suis
Sanguin: air- printemps- sang- chaud- humide- Je suis donc je séduis
Bilieux: feu-été- bile- chaud- sec- - Je suis donc je fais
Nerveux: terre- automne- atrabile- froid-sec- Je suis donc je pense
LYMPHATIQUE NERVEUX BILIEUX SANGUIN
PHYSIQUE
rond avec une
corpulence excessive
mince ou maigre
plutôt élancé
avec des muscles
bréviligne
PSYCHOLOGIQUE
calme, n'aime pas le stress, ni l'activité physique, préferant le repos et la relaxation
sensible et intuitif, imprevisible, méticuleux, aime la nouveauté et le mouvement
responsable, décideur, volontaire, travailleur bon vivant, emotif, généreux, n'aime pas les espaces clos
QUALITÉS douceur, patience et souplesse
sensibilité, emphatie et finesse d'esprit
energie, discipline et ordre
charme, enthousiame et générosité
DÉFAUTS
indifférence, paresse et lenteur
anxiété, instabilité et impatience orgueil, impulsivité, cynisme précipitation, colère, vantardise
ALIMENTATION
éviter les céréales fortes, +++agrumes
+protéines
- -agrumes
++protéines
-- excès de sucres et de lipides
éviter les excès de tous les genres
PATHOLOGIES
cardio-vasculaires
circulatoires
Obésité
Diabète
hypothyroïdie
gastrites
ulcères digestives
constipation
fatigue,
dystonie neuro végétative,
insomnie,
irritabilité, et
instabilité emotionnelle
Troubles digestifs, hépatobiliaires, respiratoires et rhumatismaux, ainsi que l'urémie Maladies cardio-vasculaires, hypertension, les céphalées congestives
Sources: Brochure atelier - Les huiles essentielles et les tempéraments- Aude Maillard
La mophotypologie - IFSH- Patrice Ponzo
La Naturopathie au quotidien- Dominick Léaud- Zachoval
Coordonnées
Rafaela Tillier
Naturopathe
Réflexologue Plantaire et Auriculaire
Cabinet: 47, Rue de Turenne- 75003- PARIS
Sur RDV en cabinet, à domicile ou par Skype
[email protected]
06 71 26 60 23
Vous pouvez utiliser notre formulaire de contact.
Ou nous envoyer un message par:
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Cardiovascular Careers | Education Center Online
Search our Site!
Articles By Subject
What is the Meaning of Cardiovascular?
Home >> Articles >> Healthcare Careers >> What is the Meaning of Cardiovascular?
CardiovascularWhat Is the Meaning of Cardiovascular?
The cardiovascular system, also referred to as the circulatory system, includes the heart and blood vessels. The heart pumps the blood throughout the body. To do this effectively, this organ has four separate chambers – two ventricles and two atria. Blood low in oxygen enters the heart through the right atrium, passes through to the right ventricle, and then goes through the pulmonary artery to the lungs, where it receives oxygen. Then this blood passes into the left atrium, passes into the right atrium, and leaves through the body's largest artery, the aorta, and gets pumped to the rest of the body.
Cardiovascular Blood Vessels
Blood vessels themselves also get divided into three categories. Arteries pump blood from the heart to other organs throughout the body. Normally this is oxygenated blood, except in the case of the pulmonary arteries mentioned above. But all arteries carry blood away from the heart. Veins do just the opposite – they take blood from the body to the heart. Again, normally this blood is low in oxygen, except for the pulmonary veins that take blood from the lungs to the heart. The third type of blood vessel is a capillary. These are the smallest and thinnest of the blood vessels, and the miniscule walls allow molecules such as water and oxygen to pass through them into the body's tissues.
Cardiovascular Careers and Training
This intricate system must work properly to keep a human being alive. A cardiovascular technician assists a doctor in identifying problems with either the heart or blood vessels. Various procedures must be used to diagnose diseases, all of which require formal training. A cardiovascular surgeon specializes in the treatment of these diseases through surgical procedures.
Overall, cardiology offers plenty of career prospects and can be a fascinating field to study.
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Good Luck
Redskins!
Tuesday
January 19th, 2021
Healthy Lifestyles
thyroidPeople diagnosed with an underactive thyroid condition may have to make several changes to their lifestyles to feel well and maintain a healthy weight.
The thyroid is a tiny gland located in the neck that produces a hormone to regulate one’s metabolism, or the process that converts what a person eats and drinks into energy. With hypothyroidism, also known as an underactive thyroid, production of that thyroid hormone is insignificant, resulting in a dramatically slower metabolism.
The endocrinology health site Endocrine Web estimates approximately 10 million Americans have hypothyroidism. The reasons the thyroid gland falters vary. But the symptoms may include fatigue, weakness, weight gain or increased difficulty losing weight, hair loss, muscle aches, depression, and irritability.
Each of the side effects associated with thyroid conditions can be troublesome, but many people with thyroid issues struggle most with weight gain and their inability to keep weight off. The president of the American Association of Clinical Endocrinologists, R. Mack Harrell, MD, says to first visit a doctor, who can determine if a synthetic thyroid hormone medication can help. Regular exercise also can be an important part of the strategy to lose weight and manage other hypothyroidism symptoms.
Christian Nasr, MD, an endocrinologist with the Cleveland Clinic, advises his patients to wait a few weeks before exercising so that their condition is controlled with medication. After that waiting period is over, gradually easing back into exercise can help with the fatigue and weight gain that may not abate with thyroid medications.
The online health resource Everyday Health advises a program of low-impact aerobic exercises and strength training. The aerobics will raise the heart rate without putting too much pressure on the joints. These exercises include using a stationary bicycle or a low-impact elliptical machine. Pilates and gentle yoga can improve core muscles and help alleviate joint pain as well.
Incorporating strength training into a workout can help build muscle mass, which burns calories, even when a person is at rest. That can be essential for a person finding it difficult to control his or her weight due to a sluggish metabolism.
Additional benefits of exercising are improved mood and reduced inflammation. Exercising can release endorphins into the body to help fight off depression. Also, researchers from the University of California-San Diego School of Medicine found a single 20-minute session of exercise was enough to trigger something called sympathoadrenergic activation, which suppresses the production of monocytic cytokines in the body that produce an inflammatory response in the immune system. That means exercise can keep inflammation in check.
Hypothyroidism is a common condition that produces various unwanted side effects. However, with proper care and exercise, many symptoms can be managed effectively.
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techtimeComputers, tablets, smartphones, and gaming systems have revolutionized popular culture and the way people engage with one another. Devices also have transformed the way people live in their homes.
Cisco’s annual visual networking index forecast indicates there will be four networked devices and connections per person globally by 2020. In North America, there will be 13 networked devices and connections per person by that time. As more people are connected to tech than ever before, many wonder if there’s a healthy amount of time to spend on their devices?
“Screen time” is defined as the amount of time spent each day using devices with screens, such as TVs, gaming consoles, smartphones, and tablets. Although how much screen time people engage in is entirely up to them, there are health risks associated with excessive screen time.
People may not realize just how much screen time they engage in each day. Nielsen reports that American adults spend more than 11 hours per day watching, reading, listening to, or simply interacting with media, which is up from nine hours, 32 minutes just four years ago. Common Sense Media’s 2017 report shows American children age eight and under use screens for an average of 2 hours and 19 minutes per day. That time increases as kids age.
In terms of healthy screen time limits, the experts have weighed in.
The latest guidelines from the American Academy of Pediatrics suggest that children under 18 months should avoid screen time, other than video chatting. Ages 18 months to two years can use high-quality programs or apps if adults participate with them. Children between the ages of two and five should limit daily screen time to an hour; age six and up should follow consistently imposed limits.
Doctors may be hesitant to prescribe screen limits for adults. But people can use certain health clues to determine if it’s time to cut back. If screens (and their blue light) are adversely affecting sleep, reducing screen time might be necessary to avoid negative side effects. Screen time should not come at the expense of physical activity, as that can contribute to obesity. People are urged to take frequent breaks from screens to mitigate potential eye strain and headaches.
The Department of Health Government of Western Australia recommends adults age 18 and older minimize time spent sitting or lying looking at screens, and to break up long periods of sitting as often as possible.
People who routinely use screens for hours each day should weigh the benefits and detriments to the amount of time spent with devices and tailor their usage accordingly.
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healthygamingGaming continues to grow in popularity, and with new ways to engage in social or individual game play available thanks to various technological devices, the frequency with which gamers engage in these recreational pursuits only increases. In fact, a 2018 report by Limelight Networks found that gamers spend an average of 5.96 hours each week playing games.
Excessive gaming can pose a threat to gamers’ overall health. The following physical and mental wellness tips can help gamers ensure they get to play without sacrificing their health.
• • Remember to blink. Staring at screens for long periods of time can cause serious eye strain. Sometimes, when immersed in the intensity of game play, a gamer may forget to blink his or her eyes, and this can lead to tired, dry eyes. As with other screen usage, follow the 20-20-20 rule. Per the Canadian Association of Optometrists, every 20 minutes, take a 20-second break and focus your eyes on something at least 20 feet away.
• • Take frequent breaks. Gamers should get up out of their seats and take breaks at regular intervals. This gives their eyes and ears a rest and allows them to stretch and reset their posture. Sitting for long periods of time can affect circulation and have adverse effects on the neck and spine as well.
• • Get some fresh air. Individuals should use break opportunities to go outside and get some fresh air and sunshine, if possible. The light and the clean air can improve energy levels and possibly help restore focus when it comes time to return to the game. Spending too many consecutive hours in a dark room can impact the brain and may affect how people learn, according to research led by Michigan State neuroscientists. Dim lights can make it hard to retain memories, while bright light boosts information retention and mood.
• • Stretch hands and wrists. Maintaining overall good posture and stretching hands and wrists can offset complications of carpal tunnel syndrome, a condition that can affect mobility in the wrists and lead to inflammation and pain.
• • Recognize addiction. People can get addicted to gaming just as they would to any other activity or substance. Novelty addiction is prolonged time spent on video games, the internet or smartphones. Research indicates these novelties can trigger various psychological responses in the brain, and people grow accustomed to chasing those triggers. Incorporate other activities into one’s day so that gaming is not the end-all.
People can enjoy gaming in a safe and healthy way by incorporating various wellness strategies into their gaming routines.
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Skip to main content
Non-scientific name:
laternen-strauch
1 Accepted name(s) for "laternen-strauch":
1 Medicinal source(s) include this non-scientific name:
Medicinal sources: Scientific names as used in medicinal source: MPNS matched scientific names: Accepted name: Trade forms: Plant parts:
SEPASAL database (Kew, 1999) Nymania capensis (Thunb.) Lindb. Nymania capensis (Thunb.) Lindb. Nymania capensis (Thunb.) Lindb.
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Editorial (Thematic Issue: Targeting Inflammation in Cardiovascular Disease) | Bentham Science
Editorial (Thematic Issue: Targeting Inflammation in Cardiovascular Disease)
Author(s): Spyridon Deftereos, Georgios Bouras.
Journal Name: Medicinal Chemistry
Volume 10 , Issue 7 , 2014
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Abstract:
Cardiovascular mortality remains the leading cause of death all over the world, despite recent advances in early diagnosis, interventional techniques and pharmacological treatment targeting several risk factors of cardiovascular disease (CVD) [1]. The inflammatory process, as an integral part of the immune system, plays an important role in tissue homeostasis. Atherosclerosis has been identified early as a chronic inflammatory disease, giving another perspective in the nature of CVD and a new field to explore for the scientific community [2]. In this research, inflammatory biomarkers have been a great ally by helping to clarify the pathophysiological mechanisms linking inflammation to CVD and identify novel therapeutic targets [3]. Dyslipidemias, Acute Coronary Syndromes (ACSs), Atrial Fibrillation (AF), Essential Hypertension (HT) and Chronic Heart Failure (CHF) have been chosen for this special issue as some of the “hottest representatives” regarding CVD. The following series of original mini-review papers attempt to summarize the acquired so far knowledge of the relation of inflammation with the aforementioned conditions, evaluate the utility and prospects of the newly discovered mediators of inflammation in CVD and highlight promising anti-inflammatory therapeutic agents. In the first of this series of articles, Papoutsidakis et al. [4] summarize what is known today about the ways inflammation interacts with lipid metabolism and whether there is therapeutic potential in exploiting this interaction. Although inflammation pathways have been shown to play an important role on the road from dyslipidemia to atherogenesis, there is relatively little data on the ways inflammation promotes changes in total cholesterol, HDL, LDL and triglyceride metabolism. There is accumulating evidence that chronic inflammatory states can aggravate atherogenesis not only by directly promoting the formation of atherosclerotic plaque inside coronary vessels but also indirectly, by impairing lipid metabolism towards a more atherogenic profile, while anti-lipidemic therapies have not focused so far in inflammation pathways that could be contributing to the rise in cholesterol and triglyceride levels. Deftereos et al. [5] in a brief and comprehensive review article deal with the role of the innate immune system in the acutely ischemic myocardium. Since originally described in the 1930s the role of inflammation in the setting of acute myocardial infarction has been extensively studied. Myriads of animal models provided critical insight into the pathways governing the inflammatory responses and revealed the role of the innate immune system in initiating and perpetuating those responses. Despite the newly acquired knowledge, success was never met in the clinical field. Today with more than seven million people dying every year from coronary artery disease and with a rapidly increasing pool of heart failure patients as a result of an acute coronary event, it is compelling to identify possible new targets that modify the inflammatory cascades, attenuating tissue damage without affecting tissue healing. AF is the most common chronic arrhythmia and a source of significant morbidity and mortality. In their paper, Giannopoulos et al. [6] focus on the existing evidence supporting the ‘inflammatory’ hypothesis for AF pathophysiology. They also provide a review of potential biomarkers of inflammation in AF and comprehensively refer to therapeutic means that could counteract the full interplay between this arrhythmia and inflammation. Tsounis et al. [7] provide a detailed review of the current literature on the most important and most studied traditional and novel inflammation markers in HT. Recent evidence suggests that the immune system and inflammation processes are important contributors in the pathophysiology of HT. Inflammation markers have been associated with the risk of developing HT in normotensives and in hypertensive patients many of these have emerged as potent prognosticators for target organ damage and for future cardiovascular events. Additionally, antihypertensive agents that seem to exhibit a kind of antiinflammatory action and novel agents targeting inflammation have been studied and provide new insights for the treatment of HT. Finally, the article of Bouras et al. [8] is dedicated to the inflammatory mechanisms in CHF and provides an elucidating review of the most potent and novel biomarkers of ongoing inflammatory processes in the setting of CHF. Inflammatory mediators participate in CHF pathophysiology by various ways like exerting direct impact on cardiac myocytes, fibroblasts and α-adrenergic receptors leading to hypertrophy, fibrosis and impaired cardiac contractility, respectively, or inducing apoptosis by stimulation of the proper genes. They utter a brief and essential reference to the anti-inflammatory effects of current CHF therapeutic strategies, while providing an up-to-date and intriguing summary of the most novel and promising antiinflammatory drugs that may gain a place in CHF treatment in the years to come. The purpose of this series of mini-reviews is to highlight the most potent biomarkers of inflammation in pathophysiology of dyslipidemias, HT, AF, ACSs and CHF, clarify their utility as possible indicators of diagnosis and disease progression and present current and promising future therapeutic strategies. We would like to express our sincere thanks to the Editor-in-Chief, Professor Atta-ur-Rahman for giving us the opportunity to contribute to this special issue. Finally, we would like to thank all the authors for their effort and the quality of their work.
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Article Details
VOLUME: 10
ISSUE: 7
Year: 2014
Page: [641 - 642]
Pages: 2
DOI: 10.2174/1573406410666140811161803
Article Metrics
PDF: 34
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*** What is gluten? - cheffarid
Breaking News
What is gluten?
What is gluten?
what is gluten,gluten,wheat,what is gluten free,what is gluten in hindi,what is wheat gluten,gluten free,what the heck is gluten,what is gluten free diet,gluten free diet,what is gluten free recipes,gluten-free,what is,what is celiac disease?,wheat allergy,celiac disease,is gluten bad,glutenin,science,gluten intolerance,nutrition,what happens going gluten free,what gluten free really means,health
What is gluten?
Gluten is a set of plant proteins combined with starch, contained in the endosperm in certain cereals including wheat, oats, barley or rye. For example, 100 g of bread contains 8 g of gluten. It "plays a role of natural cement and binder, allowing to make pasta bread, cakes ... homogeneous. It especially allows pasta to rise by its ability to create a network that traps the gases produced by yeast during the fermentation of bread.
While cereals play an important role in the body's nutrients, such as proteins, lipids, digestible carbohydrates (starches), vitamins, minerals (calcium, phosphorus, iron) or fiber, gluten does not affect particular interest for the organism.
intolerance
In intolerant people, estimated at 600 000 in France, it can induce an immune reaction altering the inner lining of the small intestine and cause an alteration of digestion and absorption problems. It is then a disease called celiac disease. The diagnosis of gluten intolerance, or celiac disease, is made from biological and / or genetic analyzes and - in some cases - intestinal tissue samples.
There is no treatment for this disease other than a therapeutic education for the elimination of foods containing gluten throughout his life. The help of a dietician can be useful to help the patient and his family to read the labels of food because gluten is present in many preparations or foods other than cereals (example: icing sugar, rice, roquefort ... ).
The alternatives
Faced with the large number of people suffering from this disorder or who wish to no longer consume gluten, more and more manufacturers are offering gluten-free products. But these remain at a higher cost than other foods. To cope with this, in the event of proven illness, the Health Insurance reimburses up to 60% of gluten-free dietary products up to a maximum of € 33.56 for a child under 10 years of age or € 45.74 beyond 10 years and for adults per month.
Conclusion
The risk of long-term adverse health consequences is proven in people who are intolerant to gluten and who continue to eat foods containing them. Conversely, a change in behavior in eating habits makes it possible to reduce this risk to nothing.
see as well as
gluten-free how-to-make-healthy-shopping-list
to know more about gluten visite folowing site https://celiac.org/gluten-free-living/what-is-gluten/sources-of-gluten/
your opinion and comment is a source of pride and encouragement to me .
No comments
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Skip to content
Today's Creation Moment
Aug
27
Chinese Indians?
Acts 21:2
"And finding a ship sailing over to Phoenicia, we went aboard and set sail."
Today we look back on the European migration to North America as one of the results of a more enlightened age. When we do this, we forget that the American Indians migrated to North and South America...
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Medical Light on Gene Research
Mark 2:17
"When Jesus heard [it], he saith unto them, They that are whole have no need of the physician, but they that are sick: I came not to call the righteous, but sinners to repentance."
Fireflies may help light the way to new medical breakthroughs. The gentle glow of a firefly on a summer evening is produced by the chemical luciferase. The firefly has a gene with the code that makes this chemical. When that gene is added to the genetic information of other plants or animals, the cells begin to glow harmlessly. Researchers have been using the firefly gene to test their ability to add genetic information to a cell.
Medical Light on Gene ResearchWhen human heart arteries become clogged, a medicine called TPA is among the treatments doctors use. TPA is a natural clot-dissolving protein that helps prevent heart attacks. The problem is, without a continuous supply of TPA, the artery may reclog. It would help if the artery could make its own TPA 24 hours a day.
Since TPA is a natural protein for which there is a genetic code, researchers wanted to know if genetic information could be added to artery cells. To find out, they injected dogs with the genetic code for luciferase. If genetic information could be added to the cells through this method, they would actually see the results in the glowing tissue. Tissue samples taken three days later did, in fact, have the distinctive glow of the firefly, proving that the method works. They warn that several years of research lie ahead before artery cells may be able to dissolve their own clots.
Those glowing fireflies that delight children and adults show God's design in the creation in an unexpected way. The chemical that makes the glow is proving to be an important tool of medical science.
Prayer:
Lord, I thank You for the blessings of modern medicine. I pray that You would bless researchers who are working to make us healthier. Let the beauty of Your handiwork remind them that they have a Creator to whom they are accountable. Amen.
Notes:
"Glowing evidence of gene-altered arteries." Science News, v. 139, June 22, 1991. p. 391.
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Sports and endurance
Every sport to some extent is healthy and helps to increase combat skills and endurance. But, of course, the military-applied the value of various classic sports varies. There are sports…
...
What kind of running shoes to choose
Try on shoes in the afternoon or toward the evening as during the day feet tend to get a bit longer and wider. If the first time found a pair…
...
Nordic walking for diabetes
Nordic walking - a long-used a type of fitness for the relief of excess pounds. The effects of Nordic walking is not long to wait. And I'll tell You why.…
...
oxygen
Unique rehabilitation program
Even experienced runners should remember that a too heavy load not heals, but on the contrary, destroy the body.
I repeat: even if you feel good, you should consult with your doctor before you run!
Medical monitoring is especially necessary for those who have serious cardiac abnormalities. People with moderate to high coronary risk can start
and without such control under condition of strict observance of gradualism in building loads.
To begin with, determine your optimal heart rate — a heart rate (HR), which yields optimal health benefits. How to calculate this value?
Determine your maximum heart rate, which is $ 205 minus half your age (women from 220 take away your full age). For example, in 50 years the maximum heart rate for men will be 205 — 25 = 180, women: 220 — 50 = 170 BPM is the Optimal heart rate is 80 percent of these indicators. For example, Continue reading
Dystonia
Breathing exercises
Autonomic dysfunction may be caused by lack of oxygen. It is known that stress increases blood pressure, pulse quickens, breathing becomes rapid and shallow, and the blood not receiving enough oxygen. In stressful situations, to relieve excessive tension, it is recommended to breathe slower and deeper. Of course, slow the heart rate or to reduce the pressure force of will the majority of people not in condition, but it is possible to control the rhythm and frequency of breathing. Because the breath is one of the regular functions of the body, which man can manage to hold your breath, slow down, or speed it up, take a deep
or superficial.
From the breath affects the body’s oxygen supply, and hence the work of the heart. If we breathe correctly, in our body improves venous circulation, blood, and bodies more intensely saturated with oxygen, increases blood flow in the capillaries. In Eastern medicine it is believed that human health depends on how it maintains and uses given to him from birth air energy, Continue reading
10 reasons why the body needs aerobic physical activity.
Regardless of age, weight or physical training, aerobic exercises are very good for health. Regular aerobic activity, such as walking, Cycling or swimming, will help you live longer and be healthier. Look for motivation? Learn how aerobic exercise affects the heart, lungs and circulation. Maybe this will help you gladly to start training.
How your body responds to aerobic exercise?
During aerobic activity you perform repetitive movements to strengthen the muscles of the arms, legs, thighs. You may notice that your body immediately begins to react to the loads.
During class you start faster and deeper breathing. This increases the amount of oxygen that enters the bloodstream. Your heart beats faster, which increases blood circulation Continue reading
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Home > Medicine > Cancer
49. Cancer Tends to Involve Multiple Mutations
Cancer Tends to Involve Multiple Mutations
Cancer may begin because of the accumulation of mutations involving oncogenes, tumor suppressor genes, and DNA repair genes. For example, colon cancer can begin with a defect in a tumor suppressor gene that allows excessive cell proliferation. The proliferating cells then tend to acquire additional mutations involving DNA repair genes, other tumor suppressor genes, and many other growth-related genes. Over time, the accumulated damage can yield a highly malignant, metastatic tumor. In other words, creating a cancer cell requires that the brakes on cell growth (tumor suppressor genes) be released at the same time that the accelerators for cell growth (oncogenes) are being activated.
Source:
National Cancer Institute, USA.
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From Our Print Archives
Caring for Patients with Acute Head Injury
Section Sponsored by:
Caring for Patients with Acute
HEAD INJURYLEARNING SCOPE New
By PHYLLIS DUBENDORF, MSN, RN, CS, ACNP, CNRN
Head injury refers to a continuum of neurological injury with sequelae that vary from mild headache to persistent vegetative state. Head injury claims as many as 30 per 100,000 population per year in the United States. It is estimated that nonfatal head injury affects 200 per 100,000-population yearly in the country. However this statistic may not reflect actual incidence due to potential under-reporting of head injury occurrences.1
N1 8/16 cover
Overall, approximately 500,000 head injuries occurring in the United States are serious enough to require hospitalization.2 Severity of head injuries is based on post-resuscitative Glasgow coma scores (GCS); a score of three to eight denotes severe injury, nine to 12 denotes moderate injury and a GCS of 13-15 indicates mild or minimal injury.1 Although severe head injury is statistically uncommon, it comes with significant consequences such as long term disability or delayed mortality. "Mild" head injury can be a misnomer, resulting in a post-concussive syndrome that includes serious neuropsychological deficits and physical disabilities.2 (See Table)
The GCS and its variations are the most widely utilized scales to classify extent of head injury, although there are other scales used to categorize severity of injury. These classification systems focus on evaluation of specific populations, such as pediatrics or minor head injury, or include scoring based on results of neurodiagnostic studies, such as size and location of lesion based on computed tomography.
One scale, the Injury Severity Scale (ISS), is used to objectively quantify injury related to multiple trauma, head injury being one component of the score.
The Glasgow Outcome Scale (GOS) is a five point scale that identifies outcomes from head injury as ranging from "good" to "death," very broad and somewhat subjective categories. The Rancho Los Amigos Scale identifies levels of post-injury behavior and is very helpful at focusing therapies at appropriate times in the post-acute head injury phase.
The advantage of scaling or scoring injury is the ability to objectively assess and compare serial clinical evaluations, evaluate treatment strategies and apply statistical methods to scores in order to determine significance.
High Risk
The highest risk age group for head injury in the United States is between 15 and 24 years of age, so in addition to the cost of injury in direct dollars of care provided to the patient and family, there is also a financial burden incurred in lost wages and productivity.3
Other high risk groups are children under the age of 10 and adults 60-65 years of age.
Men are at a higher risk for head injury than women.2 High risk has also been connected to substance abuse. Kraus found that more than 50 percent of those sustaining head injury tested positive for blood alcohol.4
Etiology & Mechanisms of Head Injury
High velocity impacts resulting from motor vehicle crashes, violence and falls are all recognized as significant etiologies of head injury. Sports and recreation are also recognized as significant factors. These types of injuries result most often in deformation of the skull, acceleration-deceleration of the intracranial contents and rotation of the brain tissue over supportive bony elements.3 Focal (or localized) brain injury occurring beneath deformation impact is known as a coup injury. Injuries occurring at the opposite pole of impact are named contracoup, and result from acceleration-deceleration.
Anatomical Considerations
Symptoms of head injury reflect the area and severity of damage to the brain; treatment of head injury is determined by understanding the relationship between injury and cerebral dynamics. In order to understand brain injuries and treatments aimed at preserving neurological function, it is necessary to review several basic tenets of neurological physiology and physiopathology:
The brain and its constituents (blood and cerebrospinal fluid) function within the constraints of a constant pressure environment (intracranial pressure) which is maintained in a closed box system (the skull). Movement within this box is further restricted by folds of the dura separating and supporting the delicate neural tissue.
Blood supply to the brain is governed by autoregulatory processes which, under normal parameters, are not dependent on systemic blood pressure. Once injury occurs, cerebral autoregulation is impaired (either focally or globally) and cerebral blood flow becomes dependent on systolic blood pressure (SBP).
The measurement of intracranial pressure (ICP) reflects swelling within the cranial vault; measurement of cerebral perfusion pressure (CPP) is calculated by subtracting the ICP from the mean arterial blood pressure (MAP) and indirectly reflects and trends occurrences of cerebral ischemia.
Primary vs. Secondary Injury
Primary damage to the brain and its constituents is reflected as cranial fracture, contusion, laceration, intracerebral hematomas, intraparenchymal hemorrhage and diffuse axonal injury. Primary damage is generally associated with mechanical impact to the cranium.
Secondary damage to the brain is based in a cycle of cerebral swelling and ischemia resulting in a biochemical cascade of injury. Secondary injury occurs within minutes, hours and even days after the initial injury. Numerous neurotransmitters, metabolites and pathological processes have been implicated in this process, such as endorphin release; increased glutamate, aspartate and acetylcholine activity; calcium flow disturbances; lactate production; electrolyte imbalances; free radicals production and lipid peroxidation of the cellular membrane.3
Treatment of Head Injury
Treatment of the head injured patient is focused on preserving the brain and preventing further injury, multisystem support strategies and preventing common complications. Optimizing neurological outcome is the single most important goal of any management strategy. Aggressive medical/surgical management continues to stress maintenance of normothermia, optimizing hemodynamic function, treatment of hypoxia, cerebral ischemia and intracranial hypertension.2
Current recommendations for the treatment of severe head injury have recently undergone several notable changes based on the 1995 report from the Brain Trauma Foundation, a meta-analysis of treatment variables aimed at managing severe head injury and increased intracranial pressure.5 Key recommendations are as follows:
* Hypoxia has been identified as a significant predictor of unfavorable outcome in severe head injury and therefore must be scrupulously avoided or rapidly corrected. The goal of oxygenation is to maintain or correct PaO2 values to at least 60 mm Hg.
Severely head injured patients will require intubation for therapeutic management. Consider also that head injured patients arising from multisystem trauma frequently have co-existing morbidities such as flail chest, hemo/pneumothorax and cervical spinal cord injury, impairing pulmonary function.2
* Hypotension is associated in approximately one-third of all severely head-injured patients, and is an even more ominous predictor of poor outcome than hypoxia.2 Systolic blood pressure should be maintained or corrected to at least 90 mm Hg or greater.5 If the patient is hypotensive, the source of hypotension must be identified and addressed.
The traumatically head-injured patient may have also sustained abdominal or vascular derangements resulting in hypovolemia. Volume correction may be achieved by administration of blood, crystalloids or colloids, or the addition of vasopressor agents when appropriate. Recent study of hypertonic saline and colloid infusions used as volume expanders for the head-injured patient have not revealed any distinct advantage over isotonic saline.2
* Hyperventilation, a mainstay of intracranial pressure management, has been linked with potentiating cerebral ischemia, and as such, cautious use is now recommended. The basis for the use of hyperventilation is vasoconstriction, limiting the amount of blood to the brain, thereby diminishing pressure within the cranium. Although limiting blood flow facilitates intracranial pressure requirements, it can result in significant cerebral ischemic events. Hyperventilation (PCO2<35 mm Hg) should be avoided if possible within the first 24 hours post injury, when cerebral blood flow is at its lowest. Moderate hyperventilation (PCO2 30-35 mm Hg) may be advocated if intracranial hypertension remains problematic.5
If hyperventilation is chosen as a therapeutic measure, efforts must be taken to further evaluate and assess blood flow to the brain. One mechanism to achieve this is by monitoring venous jugular bulb saturation to determine cerebral oxygen delivery and usage.2
* Mannitol continues to be the diuretic of choice for treating increased ICP. However, bolus doses of 1 gr/kg are recommended over continuous infusion.
* Barbiturates play a role in managing cerebral hypertension refractory to standard treatment. Barbiturates affect intracranial pressure in several ways: decreasing vascular tone, diminishing cerebral metabolic demands and inhibiting free radical mediated lipid peroxidation. However, barbiturates will depress cerebral responsiveness, therefore, other measures of ensuring and monitoring cerebral activity will be necessary if barbiturate therapy is instituted.
* Intracranial pressure monitoring is an integral aspect of head-injury evaluation. Strategies to reduce ICP should be initiated when ICP reaches 20-25 mm Hg.5 Methods to monitor include ventriculostomy, subarachnoid screw and fiberoptic monitoring.
* Cerebral perfusion pressure (CPP) must also be calculated in order to monitor and trend the relationship between systemic blood pressure and ICP. The Brain Trauma Foundation recommends that CPP be maintained or manipulated to a minimum of 70 mm Hg.
* Steroids, although beneficial in managing cerebral edema resulting from intracranial tumors, have not been statistically helpful in reducing cerebral edema related to trauma and trauma-related ischemia. Steroid administration in the head-injured patient is therefore not recommended.
* Nutritional needs are important for the patient with head injury because head injury and multiple trauma are known to increase the metabolic demands of the patient. In order to avoid deleterious affects of this hypercatabolic state, it is recommended that nutrition such as jejunal feedings are initiated by day seven after injury. One hundred-forty percent of caloric requirements should be given to nonparalyzed patients, and 100 percent of estimated caloric needs should be given to paralyzed, sedated patients. It is also recommended that at least 15 percent of these calories be delivered as protein.5 Some authors recommend initiating tube feeds as early as 24-48 hours after injury.2
* Seizure prophylaxis is a management option to prevent early post-traumatic seizures. Phenytoin and carbamezepine are both effective agents for early seizure prophylaxis. There is no convincing evidence to support the use of the agents in the prevention of late post-traumatic seizures.5,6
Acute Management Strategies
Acute care management strategies must also include prevention of further injury from common multisystem complications of head injury. In addition to impaired cerebral perfusion, some other complications to assess for in the head injured patient are: Pulmonary--pulmonary embolus, pneumonia; Cardio/Peripheral Vascular--cardiac arrhythmias, impaired blood pressure and end-organ perfusion, stroke, coagulation defects, skin alterations; Gastrointestinal--hemorrhage; Genitourinary--infection; and Metabolic--electrolyte imbalances, impaired nutrition.
Prevention
The most effective means of addressing central nervous system trauma is through prevention.2 The use of seat-belts is now mandatory in 46 of the 50 states; seat-belt use has increased from 11 percent-66 percent based on that requirement.7 All new cars manufactured in the United States are required to include automatic seat belts and/or driver's side air bag. Many automotive manufacturers also advertise other safety features such as anti-lock brake systems, reinforced zones, crumple zones and side and passenger air bags.
Motor cycle helmet laws, bicycle helmet laws, and infant restraint mandates have also helped to decrease mortality and disability related to head injury. Strict enforcement of and adherence to legal age for alcohol consumption drunk driving laws will also be beneficial in diminishing alcohol-related injures.2 Continued educational efforts must be made to further reduce the incidence and severity of head injury.
Post-acute Care
Post-acute management of the brain injured patient is as varied as head injury itself. The focus of post-acute care shifts from physical care to functional self-care involving both the patient and the patient's family.
Individuals sustaining minor head injury may require neuropsychological testing and higher level outpatient therapy. Those experiencing significant sequelae from neurologic injury may exhibit continued motor, sensory-perceptual, communication, swallowing, bowel, bladder and cognitive/behavioral dysfunction, (or any combination of these) and will require long-term physical, occupational and vocational rehabilitation.3
Post-acute goals related to motor and sensory-perceptual dysfunction are chiefly those of mobility and sensory integration. Mobility is addressed through positioning, muscle strengthening, monitoring tone, balancing and transferring. Sensory-perceptual deficits are addressed by assisting the patient to recognize body position and to integrate other sensory input (including visual, auditory and tactile stimuli) into meaningful information.
Communication and swallowing disorders go hand-in-hand with the head-injured patient. Receptive and expressive areas in the brain govern the patient's ability to receive information and expressively communicate with others. Cranial nerve impairments may affect both motor and sensory function of the tongue, lips and pharynx, making communication and swallowing more difficult. Ineffective, incomplete or delayed swallowing places the patient at high risk for aspiration.
Bowel and bladder retraining may be instituted to help the patient achieve continence. Methods of feeding the head-injured patient range from long-term enteral feeding plans to a solid diet, again depending on the extent of head injury and the patient's progression in the recovery phase.
Examples of cognitive deficits include learning, memory and attention impairments. Behavioral changes in the head injured patient are to be expected, and may include impulsivity, changes in personality and even short-tempered, episodic violent behaviors.3
Safety can be difficult to ensure in the head-injured patient, because although physical therapy can improve motor impairment, the patient requires cognitive skills and insight to identify safe situations. Continuous supervision is required for those who are mobile and exhibit impulsive behaviors without identifying their consequences.
Head injury is a significant and devastating event in the lives of those experiencing the injury and on those supporting the head-injured patient. It is important to help these people realize that they do not have to be alone in the struggle to survive and manage the effects of head injury. Local and national groups, such as the National Head Injury Foundation, are good contact points for patients and family members. Success in head-injury recovery is realized in small incremental steps. The overall goal of head-injury care is maximizing the purpose and function of head-injury survivors.
For a copy of references see our Web site at advanceweb.com or call 800-355-5627, ext. 354.
Phyllis Dubendorf is a clinical faculty member, Acute Care Nurse Practitioner Program, University of Pennsylvania, Philadelphia.
Table: Signs and Symptoms of Post-Concussive Syndrome8
* Visual impairments
* Headaches
* Personality changes
* Dizziness
* Sleep Disturbances
* Tinnitus
* Concentration &
* Irritability
Attention Disorders * Vertigo
* Fatigue
Objectives & Questions
Objectives
After you have completed reading this article, you will be able to:
1. Discuss etiologies and high risk groups related to head injury.
2. Discuss and differentiate between primary and secondary injury.
3. Identify at least three strategies to improve outcomes related to head injury.
4. Identify preventive measures related to head injury.
Learner Feedback Questions
(Complete the following multiple choice questions using the answer sheet on the next page.)
1. Risk of head injury increases in all but the following populations:
a. ages 15 to 24
b. men
c. women
d. situations in which alcohol or substances are involved
2. Etiologies of head injury include all but which of the following:
a. motor vehicle accidents
b. gunshot wounds
c. diving
d. bicycle accidents
3. Mechanisms of primary injury to the brain include all but the following:
a. acceleration-deceleration
b. rotation
c. deformation
d. cerebral swelling
4. Under normal physiologic circumstances and parameters, cerebral blood flow is:
a. dependent on mean arterial blood flow.
b. dependent on systolic blood flow.
c. self-regulating.
d. dependent on serum carbon dioxide levels.
5. Cerebral perfusion pressure reflects cerebral blood flow and is calculated by:
a. subtracting the mean arterial pressure from the systolic blood pressure.
b. adding the mean arterial and intra- cranial pressures.
c. subtracting the intracranial pressure from the mean arterial pressure.
d. adding intracranial pressure to the diastolic blood pressure.
6. Secondary injury involves all but the following:
a. rotation and shearing of neurological tissue across the bony base of the brain. b. cerebral swelling
c. the release of free radicals and lipid peroxidation
d. abnormal flux of calcium across the cell membrane
7. Hyperventilation, based on Brain Trauma Foundation recommendations, can be used:
a. within the first 24 hours of injury only.
b. prophylactically to prevent increases in intracranial pressure.
c. in cases of refractory intracranial hyper- tension as long as further monitoring is initiated to determine cerebral oxygen delivery and usage.
d. to achieve a PCO2 < 30 mm Hg.
8. All of the following are recommended in the treatment of the brain-injured patient except:
a. mannitol
b. barbiturates
c. nutrition support
d. steroids
9. Anticonvulsants are useful in the management of the head-injured patient:
a. to prevent early and late seizure activity.
b. to prevent early post-traumatic seizures only.
c. to prevent late post-traumatic seizures only.
d. anticonvulsants are not useful.
10. Post-acute management of the head injured patient includes which of the following:
a. physical therapy for muscle #009;strengthening
b.occupational therapy to teach and reinforce self-care activities
c.speech therapy to assist with commu-nication and swallowing dysfunction
d.all of the above
ANSWER SHEET
This continuing education offering expires Aug. 23, 2001.
Caring for Patients with Acute Head Injury
1 Contact Hour
To earn continuing education credit, before August 23, 2001, 1) complete the form above, 2) record answers to the questions on this page, 3) mail this form (or a photocopy) and $7.50 to: ADVANCE for Nurses Learning Scope, 2900 Horizon Dr., King of Prussia, PA 19406; Or fax (available with credit card payment only) to: (610) 278-1422.
Make checks or money order payable to Merion Publications Learning Scope
Payment is due when the test is submitted
A certificate of credit will be awarded to participants who achieve a passing grade of 70 percent or better. Participants should allow 45 days for notification of scores and receipt of certificate.
Evaluation -- Caring for Patients
with Acute Head Injury
Rate statements 1-6 below on a scale of 1 (strongly disagree) to 5 (strongly agree). Fill in the information for questions 7-8.
1. I can discuss the etiologies and high-risk groups related to head injury. 1 2 3 4 5
2. I can discuss and differentiate between primary and secondary injury. 1 2 3 4 5
3. I can identify at least three strategies to improveoutcomes related to head injury. 1 2 3 4 5
4. I can identify preventive measures related to head injury.1 2 3 4 5
5. The objectives relate to the overall goal of the article. 1 2 3 4 5
6.The teaching/learning resources were effective. 1 2 3 4 5
7.The article was well written, terms defined, graphics helpful, easy to understand. 1 2 3 4 5
8. How much time did you need to complete this CE offering?
____hours ____minutes
9. Why did you choose this offering?
_______________________________________________
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Cymbalta Lyrica Savella
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Why You Should Lift Weights, Especially If You Are A Woman
This article is the third article in FITNESS 101 series.
Article One: You Don’t Need Exercise To Lose Weight
Article Two: Cardio Is More Than Running
In this article, you’ll learn about why you must lift weights, especially if you are a woman.
You need to lift weights as a woman! No, I’m not talking about those pink, 1kg dumbbells that have become some women’s favourite. I’m talking about weights.
To Lift Weights Or Not
One reason is that many cardio exercises don’t require special instructions or equipment. For instance, you don’t need anyone to teach you how to walk or run; these are movement patterns that come naturally to every healthy human (You may need someone to coach you on the proper running form if you plan to make distance running a hobby. Having a running coach will help you become a better recreation runner and help you prevent running-related injuries), and don’t need an instructor to teach you how to groove to the beats of your favourite songs; you just want to move with the rhythms. But when it comes to strength training, you have to know what you are doing and do it the right way for it to be safe and effective.
Why You Must Lift Weights, Especially If You Are A Woman
Some women don’t want to lift weights because they think lifting weights will make them look bulky like men.
Let me set the record straight. Weight training doesn’t make a woman look bulky. Women usually don’t produce a high level of testosterone –a steroid hormone that is responsible for such increase in muscle mass in men.
The Benefits
Increased muscular strength and endurance: If you have ever walked with heavy shopping bags in both arms for 5-10 minutes, you’ll appreciate the importance of muscular strength and endurance. You need strength to be able to carry the weights (the heavy bags), and you need the endurance to be able to walk for a longer period without dropping the weights.
What’s muscular strength? “Muscular strength the ability of the muscles to exert an external force or lift a heavy weight.”
If you’ve ever moved a piece of furniture by lifting, pushing or pulling, that is your muscles exerting a force on the furniture. And if you’ve done a push-up before, that is muscular strength in action. Whether it is controlling your body weight or exerting force against an external resistance (moving things), a certain level muscular strength is required.
What’s muscular endurance? “Muscular endurance is the ability of the muscles to exert themselves repeatedly.”
Being able to do a single push-up or pull-up is a show of muscular strength, how many reps you can do before you get tired shows muscular endurance.
Increased bone density: Regular strength training improves bone density and joint integrity. That means a reduced risk for osteoporosis and arthritis. This benefit is one of the primary reasons women should take strength training seriously.
Decreased body fat: Strength training increases muscle mass and decreases fat mass. The more muscle a person has, the more calories she can burn at rest. Why? At rest, a pound of fat uses between 2-3 calories per day, but a pound of muscle uses 7-10 calories per day.
Muscle definition: There’s a training principle called, The Principle of Specificity. According to this principle, the benefits you get from your exercise programme are very specific to the type of exercise you perform.
What that means is this, when you do strength training on a regular basis, you are putting demands on the skeletal muscles, and they will respond by increasing in size and strength. That’s how to get a trimmed and well-defined physique you’re looking for!
Another Reason You Should Lift Weights
Not yet convinced about the benefits of lifting weights? Let me give you one more reason women should lift weights. As we get older as women, we begin to lose muscle mass, and our ability to burn more calories at rest goes down (blame it on biology).
Slow metabolism is the name of this condition, but regular weight training can slow down the biological process.
Cardio Or Weight Training, Which Burns The Most Calories?
Let’s go back to the principle of specificity I mentioned earlier, the benefits you gain from your exercise programme are determined by the type of exercise you do. Running, swimming, cycling and dancing are all cardio exercises. Therefore, they cannot produce the benefits of strength training.
If all you do is running, you can’t expect to gain muscular strength from that type of training. And if all you do strength training, you can’t expect to have the cardio-respiratory fitness of a runner.
It’s True That Running Burns More Calories
Yes, you’ll burn more calories during an hour of cardio training than you’ll burn during an hour of traditional strength training.
For many people, the number of calories they burn during an exercise session is a key motivator, but here is a big deal about strength training: see that picture of a perfect body you have in your mind? You’re not going to get it through the traditional cardio exercise alone!
Yes, you will lose weight with traditional cardio. But you’re not going to gain the significant muscle mass that will make your body look well-toned and trimmed.
How It Works
When you lose fat without increasing muscle mass what you get is the flabby skin you don’t like. But when you add strength training to your exercise routine, as you are losing excess fat your muscles are also getting defined, giving your body the shape and appearance you’d love to have.
Add strength training to your exercise routine. It’s a great way to trim and lean.
Now that you know all the awesome benefits of weight training, are you going to incorporate it into your training program?
About the Author
Hello, I'm Esta Morenikeji. I am the Founder and CFO of ZONE FITNESS (No, not that CFO, this one: Chief Fitness Officer). I'm your Fitfriend who writes most of the stuff on this website. Feel free to connect with me on Instagram.
Leave a Reply 5 comments
amaka - December 8, 2016 Reply
Thanks for the information
stelladeg - December 8, 2016 Reply
Thank you Esta. What types of exercises are strength training exercises apart from lifting weights.?
Esta Morenikeji - December 9, 2016 Reply
Hello, Stella.
You can use resistance bands, any you can also use your own body weight (Push-ups, squats, lunges, planks, and pull-ups.
Are Carbohydrates The New Enemy Of Fat Loss? - February 25, 2017 Reply
[…] Strength training increases muscle mass and decreases fat mass. The more muscle a person has, the more calories she can burn at rest. Why? At rest, a pound of fat uses between 2-3 calories per day, but a pound of muscle uses 7-10 calories per day. […]
Leave a Reply:
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COVID-19: Get the latest updates, safety precautions, or learn how to schedule a video or in-person visit.
Usnea
Uses
Botanical names:
Usnea barbata
Parts Used & Where Grown
Usnea, also known as old man's beard, is not a plant but a lichen—a symbiotic relationship between an algae and a fungus. The entire lichen is used medicinally. Usnea looks like long, fuzzy strings hanging from trees in the forests of North America and Europe, where it grows.
What Are Star Ratings?
This supplement has been used in connection with the following health conditions:
Used for Why
1 Star
Common Cold and Sore Throat
Refer to label instructions
Usnea has a traditional reputation as an antiseptic and is sometimes used for people with common colds.
Elderberry has shown antiviral activity and thus may be useful for some people with common colds. Elder flowers are a traditional diaphoretic remedy for helping to break fevers and promote sweating during a cold. Horseradish has antibiotic properties, which may account for its usefulness in easing throat and upper respiratory tract infections. The resin of the herb myrrh has been shown to kill various microbes and to stimulate macrophages (a type of white blood cell). Usnea has a traditional reputation as an antiseptic and is sometimes used for people with common colds.
1 Star
Cough
Refer to label instructions
Usnea contains mucilage, which may be helpful in easing irritating coughs.
The mucilage of slippery elm gives it a soothing effect for coughs. Usnea also contains mucilage, which may be helpful in easing irritating coughs. There is a long tradition of using wild cherry syrups to treat coughs. Other traditional remedies to relieve coughs include bloodroot, catnip, comfrey (the above-ground parts, not the root), horehound, elecampane, mullein, lobelia, hyssop, licorice, mallow, (Malvia sylvestris), red clover, ivy leaf, pennyroyal (Hedeoma pulegioides, Mentha pulegium), onion, (Allium cepa), and plantain (Plantago lanceolata, P. major). None of these has been investigated in human trials, so their true efficacy for relieving coughs is unknown.
1 Star
Infection
Refer to label instructions
Usnea is an herb that directly attack microbes.
Herbs that directly attack microbes include the following: chaparral, eucalyptus, garlic, green tea, lemon balm (antiviral), lomatium, myrrh, olive leaf, onion, oregano, pau d'arco (antifungal), rosemary, sage, sandalwood, St. John's wort, tea tree oil, thyme, and usnea.
Traditional Use (May Not Be Supported by Scientific Studies)
Due to its bitter taste, usnea stimulates digestion and was historically used by herbalists to treat indigestion. It was also reportedly used over 3,000 years ago in ancient Egypt, Greece, and China to treat unspecified infections.1
How It Works
Botanical names:
Usnea barbata
How It Works
Usnic acid gives usnea its bitter taste and also acts as an antibiotic in test tube studies.2 Test tube studies have suggested an anti-cancer activity for usnic acid. However, this action has not been sufficient to warrant further investigation in humans.3 Usnea also contains mucilage, which may be helpful in easing irritating coughs. Again, this has not been studied in humans.
How to Use It
Usnea, 100 mg three times per day, can be taken in capsules.4 Tincture, 3–4 ml three times per day, can also be used.
Interactions
Botanical names:
Usnea barbata
Interactions with Supplements, Foods, & Other Compounds
At the time of writing, there were no well-known supplement or food interactions with this supplement.
Interactions with Medicines
As of the last update, we found no reported interactions between this supplement and medicines. It is possible that unknown interactions exist. If you take medication, always discuss the potential risks and benefits of adding a new supplement with your doctor or pharmacist.
The Drug-Nutrient Interactions table may not include every possible interaction. Taking medicines with meals, on an empty stomach, or with alcohol may influence their effects. For details, refer to the manufacturers' package information as these are not covered in this table. If you take medications, always discuss the potential risks and benefits of adding a supplement with your doctor or pharmacist.
Side Effects
Botanical names:
Usnea barbata
Side Effects
There are no known side effects of usnea. It is considered safe for use in children. The safety of usnea during pregnancy and breast-feeding has not been established.
References
1. Tilford GL. Edible and Medicinal Plants of the West. Missoula, MT: Mountain Press Publishing Company, 1997, 148-9.
2. Weiss RF. Herbal Medicine. Beaconsfield, UK: Beaconsfield Publishers Ltd., 1988, 49.
3. Evans WC. Trease and Evans' Pharmacognosy, 13th ed. London: Baillière Tindall, 1989, 643.
4. Gruenwald J, Brendler T, Jaenicke C, et al. (eds). PDR for Herbal Medicines. Montvale, NJ: Medical Economics, 1998, 1199-200.
PeaceHealth endeavors to provide comprehensive health care information, however some topics in this database describe services and procedures not offered by our providers or within our facilities.
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子宫单角畸形
2016-10-20 09:58 阅读： 编辑：sunyoung 来源：家有宝宝
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内容简介：先天性子宫发育异常是生殖器官畸形中最常见的一种，而副中肾管衍化物发育不全所致的异常，包括无子宫、无阴道、子宫发育不良、单角子宫、始基子宫、输卵管发育异常等。
先天子宫单角畸形的病因是在胚胎发育期间，副中肾管愈合时，只有一侧存在，对侧不发生愈合，所以对侧既没有子宫，也没有卵巢和输卵管。又由于患者能按期来月经（虽然量少），因之很少能早期发现。
子宫单角畸形 注意事项
总是以不孕或习惯性流产为主诉而就诊，而且在临床上又往往被忽略而造成漏诊或误诊。就是查到确诊了，多数医生对本病的治疗也束手无策。原无有效地治疗手段。
一、诊断
凡来初诊的不孕不育症患者，通过阴道四维彩超+动态数字化子宫输卵管碘油造影可确诊。
二、危害
1、不孕：无子宫、畸形子宫、幼稚子宫者，有很多都是以不孕就医的。
2、病理妊娠：妊娠期也是很容易发生并发症，如孕卵着床于发育不健全的子宫壁或纵膈上，影响胚胎发育，这些都是可以导致早期流产、习惯性流产、早产等。
3、月经异常：始基子宫、无子宫者，一般都是表现为原发性闭经。幼稚子宫可能月经量少。双子宫、双角子宫及重复子宫，因子宫内膜面积增大出现月经过多或经期延长。
4、产时及产后病理：发育异常的子宫常合并子宫肌发育不良，都是很容易造成滞产，一般都是可见到自发性子宫破裂。产后容易发生胎盘滞留及产后子宫收缩乏力性出血。
三、注意事项
副作作为疼痛和出血：疼痛都在可以忍受的范围之内，出血量不多，两、三天内自动停止，没有出血不止的病例。
术后一周内禁性生活和盆浴。在治疗期间应避孕，一定要等G.R.达到正常值后再受孕，否则容易流产。
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5eff3d1f6f98e57329caed0ceb9053d3
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September 4, 2015
Recommended Topic Related To:
Ellence
"The result of a breast biopsy often determines the course of treatment and helps to predict a woman's risk of a future breast cancer diagnosis. Criteria for making diagnoses have been established, but it's been unclear how consistently patholo"...
Ellence
Ellence Patient Information including If I Miss a Dose
What happens if I miss a dose (Ellence)?
Call your doctor for instructions if you miss an appointment for your epirubicin injection.
What happens if I overdose (Ellence)?
Seek emergency medical attention or call the Poison Help line at 1-800-222-1222.
What should I avoid while receiving epirubicin (Ellence)?
Do not receive a "live" vaccine while using epirubicin, or you could develop a serious infection. Live vaccines include measles, mumps, rubella (MMR), Bacillus Calmette-Guérin (BCG), oral polio, rotavirus, yellow fever, varicella (chickenpox), zoster (shingles), oral typhoid vaccine, and nasal flu (influenza) vaccine.
Avoid being near people who are sick or have infections. Tell your doctor at once if you develop signs of infection.
Avoid activities that may increase your risk of bleeding or injury. Use extra care to prevent bleeding while shaving or brushing your teeth.
What other drugs will affect epirubicin (Ellence)?
Many drugs can interact with epirubicin. Not all possible interactions are listed here. Tell your doctor about all your medications and any you start or stop using during treatment with epirubicin, especially:
• acetaminophen (Tylenol);
• auranofin or gold injections to treat arthritis;
• cimetidine;
• rosiglitazone;
• an antibiotic or antifungal medication;
• an antidepressant--amitriptyline, doxepin, clomipramine, desipramine, imipramine, nortriptyline;
• birth control pills or hormone replacement therapy;
• cholesterol medications--atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin;
• heart or blood pressure medicine--amlodipine, atenolol, carvedilol, digoxin, diltiazem, enalapril, labetalol, lisinopril, methyldopa, nifedipine, verapamil, and others;
• HIV/AIDS medications;
• NSAIDs (non-steroidal anti-inflammatory drugs) such as ibuprofen (Advil, Motrin), naproxen (Aleve), celecoxib, diclofenac, indomethacin, meloxicam, and others;
• other cancer medications, especially docetaxel or paclitaxel; or
• seizure medications--carbamazepine, divalproex, phenobarbital, phenytoin, valproic acid, and others.
This list is not complete and many other drugs can interact with epirubicin. This includes prescription and over-the-counter medicines, vitamins, and herbal products. Give a list of all your medicines to any healthcare provider who treats you.
Where can I get more information?
Your doctor or pharmacist can provide more information about epirubicin.
Remember, keep this and all other medicines out of the reach of children, never share your medicines with others, and use this medication only for the indication prescribed.
Every effort has been made to ensure that the information provided by Cerner Multum, Inc. ('Multum') is accurate, up-to-date, and complete, but no guarantee is made to that effect. Drug information contained herein may be time sensitive. Multum information has been compiled for use by healthcare practitioners and consumers in the United States and therefore Multum does not warrant that uses outside of the United States are appropriate, unless specifically indicated otherwise. Multum's drug information does not endorse drugs, diagnose patients or recommend therapy. Multum's drug information is an informational resource designed to assist licensed healthcare practitioners in caring for their patients and/or to serve consumers viewing this service as a supplement to, and not a substitute for, the expertise, skill, knowledge and judgment of healthcare practitioners. The absence of a warning for a given drug or drug combination in no way should be construed to indicate that the drug or drug combination is safe, effective or appropriate for any given patient. Multum does not assume any responsibility for any aspect of healthcare administered with the aid of information Multum provides. The information contained herein is not intended to cover all possible uses, directions, precautions, warnings, drug interactions, allergic reactions, or adverse effects. If you have questions about the drugs you are taking, check with your doctor, nurse or pharmacist.
Copyright 1996-2013 Cerner Multum, Inc. Version: 3.02. Revision date: 1/21/2013.
Your use of the content provided in this service indicates that you have read,understood and agree to the End-User License Agreement,which can be accessed by clicking on this link.
Healthwise
Side Effects Centers
Report Problems to the Food and Drug Administration
You are encouraged to report negative side effects of prescription drugs to the FDA. Visit the FDA MedWatch website or call 1-800-FDA-1088.
Breast Cancer
Find support and advances in treatment.
|
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6,093,440,578,954,502,000
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Jules Steimnitz, MD
EMG
What To Expect:
An electromyogram (EMG)is done in a hospital, clinic or doctor's office. The test may be performed by an EMG tech or a doctor specializing in diseases of the nervous system (neurologist) or in physical rehabilitation (physiatrist).
You will be asked to lie on a table or bed or sit in a reclinig chair so that the muscles being tested are relaxed and easy to reach.
You will feel a brief, sharp pain each time a needle electrode is inserted into the muscle.
Preprocedure:
The skin over the areas to be tested is cleaned with antiseptic solution. An electrode that combines the reference point and a needle for recording is inserted into the specific muscle to be tested and attached by wires to a recording machine.
Postprocedure:
When the testing is completed, the needle and skin electrodes are removed and those areas of the sking where the needle was inserted are cleaned.
Some soreness and tingling sensation may persist for 1-2 days. If you notice an increase in pain, swelling or tenderness at any of the needle insertion sites, call our office immediately.
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What Are the Warning Signs of Diabetic Limb Damage?
by John Steinberg, DPM, Director, Podiatric Residency Training Program
July 21, 2016
If you or a loved one suffers from diabetes, you may be aware of one of the more troubling aspects of diabetes: limb loss. It’s true that diabetes can have dramatic effects on the body’s vascular system. Over time, diminished blood flow means that wounds to extremities, such as feet, legs and hands, heal more slowly. And in worst-case scenarios, this can mean the limb itself may be jeopardized.
As a podiatric (foot and ankle) surgeon who specializes in preserving the limbs of diabetic patients – a field called limb salvage – I work with a team of specialists and our patients to implement a strategic plan to preserve the limb and restore healthy blood flow.
But a key part of what I do is educating patients and their family members on the importance of prevention. Because if you can identify the signs of diabetic foot damage, you can work with your doctor to treat your limb as problems arise, and you’re less likely to need limb salvage at a later date.
The Hidden Dangers of Diabetes
While many diabetic patients and their families know that limb loss from diabetes is possible, patients often don’t know how to spot symptoms they may be experiencing from diabetic limb damage.
The three top signs of diabetic limb damage are:
Neuropathy, or nerve damage, is one of the most important signs of diabetic foot damage. High or unstable blood sugar levels, over time, cause vascular changes that can choke off or damage nerves. Diabetic neuropathy first affects the body’s smallest nerves, such as those in the hands, feet, eyes, and kidneys. Neuropathy initially feels like a pins-and-needles or tingling sensation, and with time it can become a burning feeling that can impede sleep. But in later stages, neuropathy can cause numbness, which is far more dangerous, because the diabetic can no longer feel pain in the limb. Since pain is an important sign of injury or infection, this can lead to serious complications.
Vasculopathy, or peripheral arterial disease, is another significant complication. Diabetes can cause blockages in veins and especially arteries in diabetic patients. This can cause color changes or thinning of the skin, or atrophy. One of the most common signs of vasculopathy is pain when at rest or elevating the legs.
Finally, diabetes can result in a compromised immune system, making fighting off infections – even routine ones – much more difficult. For example, what would otherwise be a small, trivial wound can fail to heal for a diabetic patient, creating a major infection. So it’s important to keep an eye on any changes in your ability to recover from injuries or infections.
You may not consider any of these on their own as something that requires immediate medical attention, but they can point to serious problems down the road, if they’re not examined further by a doctor. But true prevention in this area means maintaining awareness around these signs and proactively seeking the care of a podiatrist, if and/or when they arise.
Your podiatrist will be able to tell you if you’re experiencing something that’s part of a larger diabetic health issue and help you potentially mitigate the effects they have your life – that includes reducing the risk of future amputation.
A Well-Integrated Team
At MedStar Washington Hospital Center, the care we provide to our diabetic patients requires an integrated approach, involving professionals across several medical specialties. This increases our patients’ chances of preserving the affected limb. Infectious disease specialists, for example, prescribe antibiotics to help fight infections, and intensivists monitor the patient’s medical status and optimize their nutrition for rapid healing.
So if you are seeking comprehensive care for diabetic limb damage, look for a multidisciplinary team that takes this kind of integrated approach. Because while a podiatrist should be your first call if you’re experiencing symptoms, such as neuropathy or vasculopathy, a more dimensional set of experiences and skill sets will be needed to ensure the best possible outcomes for you or your family, if the symptoms are indeed a sign of diabetic limb damage.
Have any questions?
We are here to help! If you have any questions about MedStar Washington Hospital Center, call us at 202-877-3627.
Category: Healthy Living Tags: diabeteslimb salvage
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5eff3d1f6f98e57329caed0ceb9053d3
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7,807,354,850,407,427,000
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SEARCH
SEARCH BY CITATION
Keywords:
• MODY;
• Greig;
• contiguous gene deletion
Abstract
Maturity-onset diabetes of the young type 2 (MODY2) is a form of monogenic diabetes, characterized by mild fasting hyperglycemia. MODY2 is caused by heterozygous mutations in the GCK gene that encodes the glucokinase enzyme. We describe the clinical features and the underlying genetic defect of MODY2 in a patient with atypical Greig cephalopolysyndactyly syndrome (GCPS). The patient presented with the limb formation and the craniofacial developmental abnormalities typical to GCPS, in addition to mental retardation and epilepsy (assigned as atypical syndrome). Fasting hyperglycemia in the diabetic range, impaired glucose tolerance, and lack of diabetes autoantibodies were compatible with MODY2. In order to delineate the genetic aberrations relevant both to MODY2 and Greig syndrome in this patient, we performed cytogenetic analysis, real-time PCR of the GCK gene, and comparative genomic hybridization (CGH) array. Cytogenetic study has shown a microscopic detectable deletion in the 7p13-15 chromosomal region. Real-time PCR demonstrated a deletion of the GCK gene in the patient but not her parents, and CGH array revealed a deleted region of approximately 12 Mb in the 7p13-15 region. This deleted region included GLI3 and GCK genes (where heterozygous mutations cause GCPS and MODY2, respectively), and many other contiguous genes. Our patient manifests a unique form of MODY2, where GCK gene deletion is part of a large deleted segment in the 7p13-15 chromosomal region. © 2011 Wiley-Liss, Inc.
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Childrens Dentist, What Is It?
A Childrens Dentist, also called a Pediatric Dentist, provides primary and specialty oral care from infants and children, through adolescence, including patients with specific or special health needs. Based on a child’s history a dentist can make recommendations, take care of special needs, treatments, and emotional and intellectual development associated with oral health. Childrens Dentists [...]
Childrens Dentist, What Is It?2018-02-23T14:34:28+00:00
Dental Crowns, Pros and Cons
Dental Crowns are tooth-shaped caps that are placed over teeth to restore its strength, size, shape, color and more. Dental Crowns are needed when a tooth is weak and needs to be protected, a tooth is broken and needs to be restored, a large filling needs to be supported, a dental bridge needs to be held [...]
Dental Crowns, Pros and Cons2017-11-29T14:41:06+00:00
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How to maintain knee osteoarthritis
Navigation:Home > Joint Surgery > Arthritis > How to maintain knee osteoarthritis
Osteoarthritis is a degenerative disease of the knee joint, the treatment is often long time and the effect is slow. First, knowledge and ed
Content
Osteoarthritis is a degenerative disease of the knee joint, the treatment is often long time and the effect is slow. First, knowledge and education related response patients, so that patients can be self nursing to coordinate treatment. Usually patients should pay attention to the rest of the limbs, avoid too tired, too heavy, not sedentary, long standing, and under the guidance of a doctor to exercise. Exercise is very important, but the exercise should be gradual, not too excessive. The patient can carry out active weight-bearing activities such as muscle contraction, relaxation, joint extension and flexion, straight leg raising the practice, to ensure that the knee joint can maintain a certain activity, prevent muscle atrophy, achieve the purpose of preventing the disease development. If more serious knee joint synovitis, swelling and pain, can take anti-inflammatory analgesic drugs, such as Bloven, Nai Pusheng, Fenbid Votalin, etc.. Or intra-articular injection of sodium hyaluronate. Physical therapy also has a certain effect on the disease, can relieve pain and muscle spasm, relieve joint stiffness, reduce inflammation.
www.Cure001.comwww.Cure999.com
Cerebral Vascular Disease,Acne,Heart Disease,Deaf,Headache,Std,Condyloma Acuminatum,Fibroid,Pneumonia,Brain Trauma,。 Rehabilitation Blog
Rehabilitation Blog @ 2017
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TYPES OF HEARING AIDS
There are three basic styles of hearing aids. The styles differ by size, their placement on or inside the ear, and the degree to which they amplify sound.
In the Ear (ITE)
In-the-ear (ITE) hearing aids fit completely inside the outer ear and are used for mild to severe hearing loss. The case holding the electronic components is made of hard plastic. Some ITE aids may have certain added features installed, such as a telecoil, a small magnetic coil that makes it easier to hear conversations over the telephone. ITE aids usually are not worn by young children because the casings need to be replaced often as the ear grows.
Behind the Ear (BTE)
Behind-the-ear (BTE) hearing aids consist of a hard plastic case worn behind the ear and connected to a plastic earmold that fits inside the outer ear. The electronic parts are held in the case behind the ear. Sound travels from the hearing aid through the earmold and into the ear. BTE aids are used by people of all ages for mild to profound hearing loss.
A new kind of BTE aid is an open-fit hearing aid. Small, open-fit aids fit behind the ear completely, with only a narrow tube inserted into the ear canal, enabling the canal to remain open. For this reason, open-fit hearing aids may be a good choice for people who experience a buildup of earwax, since this type of aid is less likely to be damaged by such substances. In addition, some people may prefer the open-fit hearing aid because their perception of their voice does not sound "plugged up."
Canal (ITC/CIC)
Canal aids fit into the ear canal and are available in two styles. The in-the-canal (ITC) hearing aid is made to fit the size and shape of a person's ear canal. A completely-in-canal (CIC) hearing aid is nearly hidden in the ear canal. Both types are used for mild to moderately severe hearing loss. There is now available a CIC style for severe hearing loss.
Source: National Institute on Deafness and Other Communication Disorders
HEARING AID STYLES
1/1
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Why Women Struggle with Negative Body Image and How to Support Them in Recovery
Body image is all about self-perception. It has nothing to do with external sources and all about how a woman sees herself from within herself. A distorted body image (negative) refers to how a woman believes others see her. With conditions like eating disorders, women can feel they are not looking good enough for certain reasons, or are not at the weight or height they want, or they desire a more fit body so they exercise more to achieve a perfect physique. Women struggle more than men with negative body images (though men also have their challenges) and some of it goes back to trauma from childhood and violence committed against them.
Distorted Body Image Signs
A distorted body image is easy to spot for people who are looking for it. Unhealthy signs and symptoms of a negative body image can include some of the following:
• Self-scrutiny
• Watching themselves in mirrors or wherever their image appears like in windows
• Thinking or speaking negative comments about the body and comparing themselves to others
• Envy or self-shaming of their own body and desiring someone else’s (attainable or not)
The causes of negative body image can come from anywhere. Sometimes it happens through someone who is mentoring or offering support through athletics, performance-based activities, or group activities that require coaching. If negative comments and feedback are given enough, the woman may believe it and begin self-shaming.
Body Weight and Image
A healthy weight for someone may be taken in a different way by someone else. Distorted body images change how a person views their bodies. In comparison to others, they may be too overweight or too skinny or too this or that, but it is not a realistic view of who they are. It is not uncommon for people who are considered obese to explain they did not realize they were that large and had perceived their body as much smaller until they saw themselves and felt shame about how they looked. Eating disorders are another way body image gets distorted. Often, it is early dissatisfaction with how they look that leads them to conclude losing weight would help how they look and make them feel better. Restrictive eating and over-exercising are often next, leading to patterns of weight obsession that turn into compulsive eating conditions that negatively impact their lives.
Treatment and Recovery
Finding help for body image issues has to start with addressing multiple areas of the mind and body at once. A woman who has body images may have experienced trauma, may have mental health issues underlying the eating disorder, and may also have an addiction to deal with on top of the eating disorder or body image distortions. Recognizing and acknowledging how a woman feels will help them begin the journey of healing that is required to move forward. Cognitive Behavioral Therapy (CBT) can be very helpful in identifying where thoughts are coming from, look at them, then turn them around into positive statements. Inside a woman’s head are many arguments, disagreements, and challenging statements that make her think she is not worthy or capable of being loved as she is. CBT can help turn off the negative messaging tapes and begin to reroute those messages to healthier thoughts and statements, which can turn her body image issues around over time.
Holistic Therapy
One of the other ways to help a woman with negative body image issues is to provide holistic therapies like dance and movement therapy. They support building greater trust and appreciation of their body, rather than evaluating their body on looks. Some of the ways a woman can become aware of her body are to externalize her thoughts through creativity like music, journaling, painting, and things that get her outside if her head and body. Theatre and improv are also great ways to improve in this way of being in the world. A key component of healing in recovery is to find the pathway that works, although many methods may be used to help get there. Women who are struggling with self-image need a multitude of approaches to support them in finding the best way forward from addiction to hope.
Community and Family Support
What is often missing in the dialogue around a woman’s recovery is family and community support. Women are more likely to recover well from addiction and co-occurring issues if they have family and loved ones supporting them. Where family is dysfunctional, they may have to recreate the community that is sober and clean to keep them from relapsing. They may need additional support in aftercare to help them find housing, support any children they have, and keep them from backsliding into old habits once they leave rehab. Community and family support and key dynamics that help improve the recovery journey but it takes rebuilding those networks to support a woman so she can stay the course in her recovery for the long haul.
Casa Capri gives women permission to be vulnerable and find healing with other women who share their struggles. Whether it is body image, drug use, alcohol addiction, or something else, women are invited to come as they are. We approach recovery from a holistic perspective. If you are looking for community and connection in rehab, call Casa Capri today: 844-593-8020
CONNECT
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Our program offers the highest quality care for women struggling with addiction and co-occurring conditions.
We are fully licensed by the State of California and our treatment center is accredited by The Joint Commission – the standard of excellence in quality programs.
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If you or a loved one has a substance addiction, please give us a call today at 844-252-5221. It’s time to heal your heart and find true happiness.
Our admissions team is always available to talk and answer any questions you may have about our Drug and Alcohol Rehab Programs at Casa Capri Recovery for women.
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Will a positive pregnancy test line fade
Will a positive pregnancy test line fade dob
This might be due to an absence of protein and sugar. ) and coronary heart diseases. And it will probably do double obligation as a nursing support after your child arrives. (A better approach is to make use of our due date calculator above) Though this technique will not will a positive pregnancy test line fade as correct as your physician's calculation, it is a very fun and interactive technique to have fun your being pregnant. My blood stress and nearly every different take a look at was never out of order. Thanks hope you'll be able to reply or give me some recommendation. This early symptom of pregnancy may also be fairly traumatic for potential moms. Quickly the cells separate into two parts: a skinny outer cell layer and an internal cell mass. Although some docs say step aerobics workouts are acceptable if you can decrease the height of your step as your being pregnant progresses, others warning that a altering middle of gravity makes falls much more likely. Most girls, although, agonize over this tough determination, which is additional complicated by the truth that abortion is one of the most politically and emotionally charged problems with our instances. The neural tube will later form the mind, spinal twine, and main nerves. healthy and match. The loss of being pregnant signs throughout a miscarriage is normally one thing you see in hindsight, not forward of time. She not too long ago became a new mother so is enthusiastic about serving to girls with frequent pregnancy complaints and elevating healthy babies. You may additionally notice that you really feel constipated and bloated. It isn't doable in your dreams, and it's also not potential in reality. Quote Reply. The query is how they work in practice for the average girl. Analysis has advised that tobacco use may have detrimental results on ovulation, tubal transport (the method of your egg making its way by way of the fallopian tubes), and implantation (the fertilized egg embedding itself in your womb). When this will a positive pregnancy test line fade rises, kidneys filter extra waste out of your blood. In England, Mrs. Wait 2 minutes to learn the outcome. Constipation is usually attributable to the strain of a growing bump on your rectum, in addition will a positive pregnancy test line fade hormones that are said to slow down the movement of food by your digestive system. In case your cycle is longer than 28 days, will a positive pregnancy test line fade the number 14 and add an extra day for every day your padded maternity/nursing bras is longer than 28 days. I knew I used to be pregnant when I missed my interval but also had implantation signs as nicely that week. They'll investigate causes for about 20 of miscarriages, about 20-25 are chromosomal defect and a blood problem. I just wished to ensure my child can be safe and healthy. Nonetheless, if you happen to miss a period or have a nagging feeling that you have any signs on this checklist, you would possibly wish to take a house being pregnant test. If she brings up being pregnant, congratulate her, ask her if she knows the sex and categorical normal excitement. As early as 1-2 weeks after conception you would possibly notice a difference in your breasts. The last trimester has probably the most adjustments, with will a positive pregnancy test line fade hormonal modifications, giant stomach growth, constant urination and moodiness. Has anybody else heard of this. This statement is not true in any respect. About 6-8 weeks into your being pregnant you could end up making a number of, or even lots of further journeys to the toilet. My physique ceasarian section child birth completely reject chips or other junk objects. I am 7 weeks and 1 day pregnant with my second pregnancy, and I feel significantly better than my first one. Acrivastine is a second generation antihistamine that works as an antagonist of histamine H1-receptor. I had been attending her antenatal yoga classes for many of my being pregnant and located them actually nice - they were one place and time when I forgot I used to be pregnant (in a great way) and was in a position to morning walk is good for pregnancy a feeling of space in my physique for a number of hours. It's impossible to predict when or if secondary circumstances will develop throughout your pregnancy. Venous Thromboembolism, Thrombophilia, Antithrombotic Therapy, and Pregnancy: American School of Chest Physicians Proof-Primarily based Scientific Observe Tips (8th Edition). Irina Webster, a specialist in ladies's and kids's health, she can be a wife and mom. From initial stage to start, they need to connect themselves with some special and experienced doctors. Girls also reported gestational weeks of use on per week-by-week foundation, and this information was used to calculate trimester-particular and duration of use. Hemorrhoids might be painful and itchy and trigger bleeding. When you really feel something out of the peculiar during your being pregnant, do not stress, however do ensure that to name your doctor. In response to the Mayo Clinicduring being pregnant, girls are at elevated risk of bacterial food poisoning. How a lot are you aware about your menstrual cycle. The amniotic sac develops during this stage, as effectively. Delicate cramping does not require to be addressed; however, belly cramping goserelin and pregnancy result in an emergency and hence needs to be monitored. So there you may have it. The hormones in these pills not only prevent the ovulation, in addition they cut back the effect of the prostaglandins. Your baby is now over 3kg, and their actions may slow down on account of their size taking on most of your womb. In the event you're undecided, it's a good idea to wait a minimum of three weeks after you assume you'll have conceived earlier than doing a take a look at. Let's be sincere, girls: book learning will never equal precise expertise. Ditto PMS. Movements are less forceful, but you'll really feel stretches and wiggles. Interestingly, no association with alcohol use predicts continued smoking or abstinence.
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Comments:
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5eff3d1f6f98e57329caed0ceb9053d3
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6,973,404,496,506,040,000
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NaTosha N. Gatson
Learn More
Extracellular vesicles (microvesicles), such as exosomes and shed microvesicles, contain a variety of molecules including proteins, lipids, and nucleic acids. Microvesicles appear mostly to originate from multivesicular bodies or to bud from the plasma membrane. Here, we review the convergence of microvesicle biogenesis and aspects of viral assembly and(More)
Multiple sclerosis (MS) is a demyelinating disease of the CNS involving T cell targeting of myelin antigens. During pregnancy, women with MS experience decreased relapses followed by a post partum disease flare. Using murine experimental autoimmune encephalomyelitis, we recapitulate pregnancy findings in both relapsing and progressive models. Pregnant mice(More)
More than four decades ago, Dr. Judah Folkman hypothesized that angiogenesis was a critical process in tumor growth. Since that time, there have been significant advances in understanding tumor biology and groundbreaking research in cancer therapy that have validated his hypothesis. However, in spite of extensive research, glioblastoma multiforme (GBM), the(More)
• 1
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Tonya A Carver
Learn More
To better understand the genetic basis of essential hypertension, we conducted a quantitative trait locus (QTL) analysis of a population of 207 (BALB/cJ x CBA/CaJ) F(2) male mice to identify genomic regions that regulate blood pressure, heart rate, and heart weight. We identified two loci, Bpq6 (blood pressure quantitative locus 6) on chromosome 15 (Chr 15;(More)
Modified proteins were detected in liver and bone marrow of mice following treatment with [(14)C]benzene. Stained sections were excised from one-dimensional and two-dimensional gels and converted to graphite to enable (14)C/(13)C ratios to be measured by accelerator mass spectrometry. Protein adducts of benzene or its metabolites were indicated by elevated(More)
The relationship between obesity and cholesterol cholelithiasis is not well understood at physiologic or genetic levels. To clarify whether obesity per se leads to increased prevalence of cholelithiasis, we examined cholesterol gallstone susceptibility in three polygenic (KK/H1J, NON/LtJ, NOD/LtJ) and five monogenic [carboxypeptidase E (Cpe (fat)), agouti(More)
• 1
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2,993,155,522,861,439,000
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Question: Which Are Examples Of Non Specific Defenses?
What are three nonspecific internal defenses?
Three nonspecific internal defenses include standing armies of phagocytic and natural killer cells, the inflammatory response, and fever..
What are non specific responses?
The non-specific response is a generalized response to pathogen infections involving the use of several white blood cells and plasma proteins. Non-specific immunity, or innate immunity, is the immune system with which you were born, made up of phagocytes and barriers.
What is the difference between specific and nonspecific defenses?
nonspecific immunity are things that protect the body from various bacterias, viruses, and pathogens. … Specific immunity are things that protect the body from specific pathogens. It includes the third line of defense. They include the lymphocytes (white blood cells) such as the macrophages, t cells, and memory b cells.
What are examples of specific defenses?
Specific Defense (The Immune System)Recognition. The antigen or cell is recognized as nonself. … Lymphocyte selection. The primary defending cells of the immune system are certain white blood cells called lymphocytes. … Lymphocyte activation. … Destruction of the foreign substance.
What are non specific Defences?
Nonspecific defenses include anatomic barriers, inhibitors, phagocytosis, fever, inflammation, and IFN.
What are three types of nonspecific immunity?
What are three types of nonspecific defenses that can prevent the entry and/or establishment of a pathogen in a person’s body? Barriers (skin), Traps (mucous membranes, cilia, hair, ear wax), and Low pH.
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To this end, we freshly expressed WT hNHE3 and hNHE3 carrying S552A or S605A mutation in Caco-2bbe cells
To this end, we freshly expressed WT hNHE3 and hNHE3 carrying S552A or S605A mutation in Caco-2bbe cells. of PKA increased ubiquitination of hNHE3 and enhanced interaction of Nedd4-2 with hNHE3 via phosphorylation of Nedd4-2 at S342. S342A mutation mitigated the Nedd4-2ChNHE3 interaction and blocked PKA-induced inhibition of hNHE3. Unlike non-human NHE3s, inhibition of hNHE3 by PKA is independent of NHE3 phosphorylation, suggesting a distinct mechanism of hNHE3 regulation. Conclusions The effects of CTX and EPEC on hNHE3 are amplified, and the unique properties of hNHE3 may contribute to diarrheal symptoms occurring in humans. Carglumic Acid gene is linked to decreased NHE3 activity.7,8 Inhibition of NHE3 and the resulting diarrhea can be caused from infection of the gastrointestinal tract by a variety of microorganisms, including enteropathogenic (EPEC), and increases Cl- secretion and decreases Na+ absorption due to the presence of cholera toxin (CTX) secreted by the bacteria.10 CTX activates adenylate cyclase, increases 3′,5′-cyclic adenosine monophosphate, and activates protein kinase A (PKA). PKA phosphorylates and decreases NHE3 protein abundance in the plasma membrane via stimulation of NHE3 endocytosis, while also preventing delivery of NHE3 to the surface membrane.11, 12, 13 EPEC Carglumic Acid is a common cause of diarrhea in infants and young children, and the rapid onset of diarrhea in EPEC infections is a result of reduced absorption of ions and solutes.2,14 EPEC specifically inhibits NHE3 activity via a mechanism requiring the effector protein EspF of a type III secretion system, but the signaling cascade inhibiting NHE3 has not been elucidated.15 Ubiquitination is a regulated, post-translational modification that conjugates ubiquitin (Ub) to Lys residues of target proteins and controls their intracellular fate. The covalent ligation of the 76-amino acid peptide Ub to substrate proteins is a highly conserved process that occurs via the sequential action of 3 enzymes: Ub-activation enzyme E1, Ub-conjugating enzyme E2, and Ub ligase E3. E3 ligases play a pivotal role in ubiquitination because these recognize the acceptor proteins and hence dictate the high specificity of the ubiquitination reaction.16 We have shown recently that NHE3s of human and Carglumic Acid non-human primates differ from NHE3s of other animals by having a PY (PPxY) motif.17 A PY motif is necessary for the interaction of a neural precursor cell expressed, developmentally down-regulated 4 (Nedd4) family of E3 Ub enzymes.18 The presence of a PY motif in human NHE3 (hNHE3) permits ubiquitination of NHE3 by Nedd4-2 in PS120 cells and has also been shown to increase the basal rate of internalization of hNHE3.17 Recently, ubiquitin-specific peptidase 7 (USP7), USP10, and USP48 have been identified as deubiquitinating enzymes (DUBs) targeting hNHE3.19,20 Therefore, ubiquitination of hNHE3 is coordinated by the on-reaction by Nedd4-2 and off-reaction by the DUBs. The use of small animals such as mice and rats as surrogates for humans in scientific studies has advantages because of their small size, short reproductive cycle, and ease of genetic manipulation. However, several components of mouse biological systems are incongruent with those of humans.21 For instance, small animals such as mice and rats are not perceived to develop diarrhea as often, or as severely, as humans, although a direct comparison of free-living humans exposed to a variety of pathogens that may cause diarrhea and laboratory animals living in a controlled environment is difficult. To overcome such a limitation, we generated a humanized mouse strain expressing hNHE3 in the intestinal epithelial cells (IECs). The goal of this study is to test the hypothesis that ubiquitination of hNHE3 by Nedd4-2 renders hNHE3 more reactive to enteropathogenic agents, thus contributing to increased severity of diarrhea. We used an IEC line and the humanized mouse to establish that hNHE3 displays the unique biochemical property of ubiquitination-dependent regulation, which significantly amplifies the effects of CTX and EPEC, thereby contributing to increased intestinal water loss. Outcomes Inhibition of hNHE3 by Forskolin is normally HIGHER THAN nonhuman NHE3 To show that the level of inhibition of hNHE3 is normally higher than of nonhuman NHE3, we likened the effect from the adenylate cyclase activator forskolin (FSK) on hNHE3 and rabbit NHE3 (rbNHE3) portrayed in Caco-2bbe cells. Na+/H+ exchange activity of NHE3 was dependant on the speed of preliminary Na+-reliant intracellular pH (pHi) recovery.17,22 All NHE3 activity measurements were conducted in the current presence of 30 mol/L Hoe-694 or 2 mol/L dimethyl amiloride, which inhibit endogenous NHE2 and NHE1 activities. Cells expressing hNHE3 and treated with FSK for thirty minutes demonstrated a Rabbit Polyclonal to IL18R concentration-dependent inhibition of NHE3 activity. The speed of Na+/H+ exchange by.
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How Much Do You Know About COPD?
RATE
• Currently 3/5 Stars.
• 1
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Question:
Lung X-Ray Chronic obstructive pulmonary disease (COPD) is on the rise, according to the National Institutes of Health. More than 12 million people in the U.S. are currently diagnosed with it, and another 12 million may have it but don’t know. Test your COPD IQ with the quiz so you’ll know what you can do to limit the disease’s progression, alleviate worries and put you on the road to living a normal life.
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1. Which of these is not a symptom of COPD? Please select an option
Question: 1 of 10
2. Which of these statements is true? Please select an option
Question: 2 of 10
3. What’s the biggest cause of COPD? Please select an option
Question: 3 of 10
4. Which of these will help manage symptoms and slow the progression of COPD? Please select an option
Question: 4 of 10
5. How is COPD diagnosed? Please select an option
Question: 5 of 10
6. What’s the best type of physical activity to improve lung function for a person living with COPD? Please select an option
Question: 6 of 10
7. What type of medicines are often used to treat COPD? Please select an option
Question: 7 of 10
8. Which of these is an early warning sign that you or a loved one might have COPD? Please select an option
Question: 8 of 10
9. What’s a common side effect of medicines used to treat COPD? Please select an option
Question: 9 of 10
10. What should you do if you start to notice you’re out of breath doing routine things like walking up the stairs or going grocery shopping? Please select an option
Question: 10 of 10
1. Which of these is not a symptom of COPD?
Here's how everyone else voted:
Coughing
6% (votes: 1359)
Sneezing
89% (votes: 20665)
Wheezing
5% (votes: 1126)
Question: 1 of 10
2. Which of these statements is true?
Here's how everyone else voted:
COPD is a chronic, but treatable, disease.
95% (votes: 20244)
COPD can be cured with proper medicine.
4% (votes: 771)
COPD only affects old people.
1% (votes: 228)
Question: 2 of 10
3. What’s the biggest cause of COPD?
Here's how everyone else voted:
Poor diet
3% (votes: 390)
Allergies
10% (votes: 1370)
Smoking
87% (votes: 11730)
Question: 3 of 10
4. Which of these will help manage symptoms and slow the progression of COPD?
Here's how everyone else voted:
Quitting smoking
92% (votes: 11920)
Eating a low-fat, healthy diet
4% (votes: 566)
Nothing can slow the progression of COPD
3% (votes: 429)
Question: 4 of 10
5. How is COPD diagnosed?
Here's how everyone else voted:
Doctors take chest X-rays to look for signs of the disease
15% (votes: 1929)
Doctors perform a lung function test
82% (votes: 10402)
Doctors perform blood tests to detect the disease
3% (votes: 353)
Question: 5 of 10
6. What’s the best type of physical activity to improve lung function for a person living with COPD?
Here's how everyone else voted:
Aerobic activity like walking, swimming or biking.
93% (votes: 11574)
None. People with COPD should conserve their energy
4% (votes: 557)
Lifting weights
2% (votes: 251)
Question: 6 of 10
7. What type of medicines are often used to treat COPD?
Here's how everyone else voted:
Antihistamines like Benadryl
2% (votes: 221)
Inhaled corticosteroids like Symbicort
98% (votes: 11968)
Over-the-counter cough medicine
0% (votes: 23)
Question: 7 of 10
8. Which of these is an early warning sign that you or a loved one might have COPD?
Here's how everyone else voted:
Chronic bronchitis
89% (votes: 10750)
Asthma attacks
10% (votes: 1267)
Memory loss or confusion
1% (votes: 116)
Question: 8 of 10
9. What’s a common side effect of medicines used to treat COPD?
Here's how everyone else voted:
Hair loss
2% (votes: 225)
Dry mouth
95% (votes: 11560)
Skin rash
3% (votes: 353)
Question: 9 of 10
10. What should you do if you start to notice you’re out of breath doing routine things like walking up the stairs or going grocery shopping?
Here's how everyone else voted:
Make an appointment with your doctor
87% (votes: 10280)
Sit down and take a break to see if that helps you catch your breath
13% (votes: 1522)
Ask friends and family if they’ve ever been out of breath doing something similar
0% (votes: 26)
Question: 10 of 10
Here's how everyone else scored:
SEE ALL QUIZZES
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Anatomy of the Heart: Aorta
Human Heart Posterior View
This is a posterior view of the heart showing the aorta arching and descending to the lower areas of the body. Lauren Shavell/Design Pics/Getty Images
What Is the Aorta?
The aorta is the largest artery in the body. Arteries are vessels that carry blood away from the heart. The heart is the organ of the cardiovascular system that functions to circulate blood along pulmonary and systemic circuits. The aorta arises from the left ventricle of the heart, forms an arch, then extends down to the abdomen where it branches off into two smaller arteries. Several arteries extend from the aorta to deliver blood to the various regions of the body.
Function of the Aorta
The aorta carries and distributes oxygen rich blood to all arteries. Most major arteries branch off from the aorta, with the exception of the main pulmonary artery.
Structure of the Aortic Walls
The walls of the aorta consist of three layers. They are the tunica adventitia, the tunica media, and the tunica intima. These layers are composed of connective tissue, as well as elastic fibers. These fibers allow the aorta to stretch to prevent over-expansion due to the pressure that is exerted on the walls by blood flow.
Branches of the Aorta
• Ascending Aorta - initial part of the aorta that begins from the aortic valve and extends from the left ventricle of the heart to the aortic arch.
• Coronary Arteries - arteries branching from the ascending aorta to supply oxygenated blood to the heart wall. The two main coronary arteries are the right and left coronary arteries.
• Aortic Arch - curved section at the top of the aorta that bends backward connecting the ascending and descending portions of the aorta. Several arteries branch off from this arch to supply blood to the upper regions of the body.
• Brachiocephalic Artery - supplies oxygenated blood to the head, neck, and arms. Arteries branching from this artery include the right common carotid artery and the right subclavian artery.
• Left Common Carotid Artery - branches from the aorta and extends up the left side of the neck.
• Left Subclavian Artery - branches from the aorta and extends to the left side of the upper chest and arms.
• Descending Aorta - major portion of the aorta that extends from the aortic arch to the trunk of the body. It forms the thoracic aorta and abdominal aorta.
Thoracic Aorta (Chest Region):
Abdominal Aorta:
• Celiac Artery - branches from the abdominal aorta into the left gastric, hepatic, and splenic arteries.
• Left Gastric Artery - supplies blood to the esophagus and portions of the stomach.
• Hepatic Artery - supplies blood to the liver.
• Splenic Artery - supplies blood to the stomach, spleen, and pancreas.
• Superior Mesenteric Artery - branches from the abdominal aorta and supplies blood to the intestines.
• Inferior Mesenteric Artery - branches from the abdominal aorta and supplies blood to the colon and rectum.
• Renal Arteries - branch from the abdominal aorta and supply blood to the kidneys.
• Ovarian Arteries - supply blood to the female gonads or ovaries.
• Testicular Arteries - supply blood to the male gonads or testes.
• Common Iliac Arteries - branch from the abdominal aorta and divide into internal and external iliac arteries near the pelvis.
• Internal Iliac Arteries - supply blood to the organs of the pelvis (urinary bladder, prostate gland, and reproductive organs).
• External Iliac Arteries - extend to the femoral arteries to supply blood to the legs.
• Femoral Arteries - supply blood to the thighs, lower legs, and feet.
Diseases of the Aorta
Sometimes, the tissue of the aorta can be diseased and cause serious problems. Due to the break down of cells in diseased aortic tissue, the aortic wall weakens and the aorta can become enlarged. This type of condition is referred to as an aortic aneurysm. Aortic tissue may also tear causing blood to leak into the middle aortic wall layer. This is known as an aortic dissection. Both of these conditions may result from atherosclerosis (hardening of the arteries due to cholesterol build up), high blood pressure, connective tissue disorders, and trauma.
Format
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Your Citation
Bailey, Regina. "Anatomy of the Heart: Aorta." ThoughtCo, Oct. 6, 2016, thoughtco.com/anatomy-of-the-heart-aorta-373199. Bailey, Regina. (2016, October 6). Anatomy of the Heart: Aorta. Retrieved from https://www.thoughtco.com/anatomy-of-the-heart-aorta-373199 Bailey, Regina. "Anatomy of the Heart: Aorta." ThoughtCo. https://www.thoughtco.com/anatomy-of-the-heart-aorta-373199 (accessed January 21, 2018).
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PT - JOURNAL ARTICLE AU - Barker, E L AU - Kimmel, H L AU - Blakely, R D TI - Chimeric human and rat serotonin transporters reveal domains involved in recognition of transporter ligands. DP - 1994 Nov 01 TA - Molecular Pharmacology PG - 799--807 VI - 46 IP - 5 4099 - http://molpharm.aspetjournals.org/content/46/5/799.short 4100 - http://molpharm.aspetjournals.org/content/46/5/799.full SO - Mol Pharmacol1994 Nov 01; 46 AB - The serotonin transporter (SERT) is a target for many clinically significant drugs, such as cocaine, amphetamine, and antidepressants. The relationship between the structure of SERT and the binding of substrates and antagonists is virtually unknown, despite a large body of data describing the structure-activity relationships of transporter ligands. The cloning of multiple species homologs of SERT affords a unique opportunity for molecular comparisons to identify potential domains and residues involved in ligand recognition. We have conducted pharmacological comparisons of the cloned rat and human SERTs in transiently transfected HeLa cells. Serotonin uptake and radioligand binding assays revealed that rat and human SERTs show different sensitivities to some but not all transporter ligands; most tricyclic antidepressants were significantly more potent at the human SERT, relative to rat SERT, whereas d-amphetamine was a more potent inhibitor of rat SERT. Several other ligand such as fluoxetine, paroxetine, (+)-methylenedioxymethamphetamine, cocaine, and the substrate 5-hydroxytryptamine, shows no significant species selectivity. Cross-species chimeras between rat and human SERTs were constructed to track the species-specific pharmacologies through the SERT molecule. These chimeric SERTs were expressed in HeLa cells and transported serotonin similarly to parental SERTs. Using these chimeras, we have isolated a region distal to amino acid 532 the imparts species preferences for both the tricyclic imipramine and d-amphetamine. Our results support the prediction of distinct binding sites for SERT ligands and implicate a restricted region in or near putative transmembrane domain 12 of the transport as being involved in both substrate and antagonist recognition.
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How Antioxidants Can Help Prevent Stroke
Making sure to get enough antioxidants in your diet may be the easiest and most effective tool you have in fighting a stroke. Antioxidant has certainly been a buzzword recently. Find out the truth about how antioxidants fight diseases like stroke, heart disease, and cancer.
Fruits and vegetables in bowls on a table
Jolanta Bochen / EyeEm / Getty Images
What Are Antioxidants?
Antioxidants are naturally occurring components of fresh fruits and vegetables. When we eat food like berries, red peppers, and nuts, the antioxidants are absorbed into the body.
Antioxidants and Stroke Protection
A Norwegian study followed 20,000 men and found that the men who ate food with high antioxidant content more than 27 times per month had a 20% reduced stroke risk. The participants also experienced lower rates of heart disease and cancer.
How to Get Antioxidants
Antioxidants are present in a number of fruits, including oranges, berries, apples, mango, and kiwi, to name just a few. They can also be found in fresh vegetables, for example, peppers, potatoes, yams, and artichokes. Usually, the raw form of fruit and vegetables is richer in antioxidant concentration than the cooked preparation.
Interestingly, some unexpected sources of antioxidants can help prevent strokes, such as coffee, red wine, and chocolate. Most processed foods and meats do not contain a significant amount of antioxidants.
Taking an Antioxidant Supplement
The best way to get antioxidants is a diet that includes fresh fruits and vegetables.
However, taking vitamin supplements have been shown to help in preventing stroke. Vitamins A, C, and E are particularly rich in antioxidant activity. But vitamin supplements should always be taken with caution because overdosing on vitamins is dangerous.
How Antioxidants Protect the Body From Disease
Antioxidants have an interesting biological interaction with a type of harmful chemical called a free radical. The structure of antioxidants allows them to detoxify free radicals.
To understand what antioxidants actually do, it helps to understand a little bit about free radicals and oxidative damage. Free radicals are unstable molecules formed through a chemical reaction called oxidation. When we are exposed to toxins or extreme emotional stress, we form too many free radicals. Cigarette smoke, pollution, and some chemical additives expose our bodies to toxins that trigger the formation of free radicals through oxidative damage.
Free radicals are chemically unstable, and they have a tendency to stabilize themselves by destabilizing nearby structures of the body, causing diseases such as stroke, heart attacks, and cancer.
However, antioxidants are particularly stable and can actually safely stabilize free radicals before the free radicals have an opportunity to wreak havoc on the body. Thus, antioxidants have been found to counteract the effects of free radicals and oxidative stress. That is why antioxidants are given that name—because they combat the effects of oxidative damage.
How Antioxidants Prevent a Stroke
A stroke starts in an unhealthy blood vessel or because of a sticky blood clot. It takes years for blood vessels to become unhealthy. Antioxidants can repair the inside of damaged blood vessels and, more importantly, they can prevent free radicals from tearing the inside of the blood vessels in the first place.
Lab Tests Measure Antioxidants in Food
So far, testing food for antioxidant activity is a big project, requiring a sophisticated lab. The way scientists assess the antioxidant power of different types of food in a laboratory setting is by exposing human blood cells to a type of food and then measuring the health of the human blood cells. While it certainly is fascinating, there is no way to measure or duplicate that process at home!
How Many Antioxidants Should You Get?
Current research is telling us that the more antioxidants you get, the better for stroke prevention. There is no harm associated with antioxidant-rich food. But, they do not contain all of the nutrients our bodies need to stay healthy.
So, while increasing your antioxidant intake, it is important to get a well-balanced diet with healthy fats and enough protein. Eating only fruit and vegetables can cause some nutritional deficiencies. Make sure you get enough protein from legumes or fish or lean meat and enough iron through greens or red meat as you increase your antioxidant intake.
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1 Source
Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
1. Hiartaker A, Knudsen MD, Treti S, Weiderpass E. Consumption of berries, fruits and vegetables and mortality among 10,000 Norwegian men followed for four decades. European Journal of Nutrition. June 2015.
Additional Reading
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-3,233,205,554,455,550,000
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PMCCPMCCPMCC
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Hum Mol Genet. 2010 January 1; 19(1): 52–64.
Published online 2009 October 6. doi: 10.1093/hmg/ddp466
PMCID: PMC2792148
A mouse model offers novel insights into the myopathy and tendinopathy often associated with pseudoachondroplasia and multiple epiphyseal dysplasia
Abstract
Pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED) are relatively common skeletal dysplasias belonging to the same bone dysplasia family. PSACH is characterized by generalized epi-metaphyseal dysplasia, short-limbed dwarfism, joint laxity and early onset osteoarthritis. MED is a milder disease with radiographic features often restricted to the epiphyses of the long bones. PSACH and some forms of MED result from mutations in cartilage oligomeric matrix protein (COMP), a pentameric glycoprotein found in cartilage, tendon, ligament and muscle. PSACH-MED patients often have a mild myopathy characterized by mildly increased plasma creatine kinase levels, a variation in myofibre size and/or small atrophic fibres. In some instances, patients are referred to neuromuscular clinics prior to the diagnosis of an underlying skeletal dysplasia; however, the myopathy associated with PSACH-MED has not previously been studied. In this study, we present a detailed study of skeletal muscle, tendon and ligament from a mouse model of mild PSACH harbouring a COMP mutation. Mutant mice exhibited a progressive muscle weakness associated with an increased number of muscle fibres with central nuclei at the perimysium and at the myotendinous junction. Furthermore, the distribution of collagen fibril diameters in the mutant tendons and ligaments was altered towards thicker collagen fibrils, and the tendons became more lax in cyclic strain tests. We hypothesize that the myopathy in PSACH-MED originates from an underlying tendon and ligament pathology that is a direct result of structural abnormalities to the collagen fibril architecture. This is the first comprehensive characterization of the musculoskeletal phenotype of PSACH-MED and is directly relevant to the clinical management of these patients.
INTRODUCTION
Pseudoachondroplasia (PSACH: MIM 177170) is an autosomal dominant skeletal dysplasia characterized by short-limbed dwarfism, epi-metaphyseal dysplasia, joint laxity and early onset osteoarthritis (OA) (1,2). Multiple epiphyseal dysplasia (MED: MIM 132400) is predominantly an autosomal dominant skeletal dysplasia belonging to the same bone dysplasia family (3), but it is generally milder, and the radiographic features are primarily restricted to the epiphyses. MED patients can also suffer from joint laxity and early onset OA.
PSACH and some forms of MED (EDM1) result from mutations in the gene encoding cartilage oligomeric matrix protein (COMP: MIM 600310) (4,5), which is a 550 kDa pentameric extracellular matrix (ECM) glycoprotein (6) found in cartilage, tendon (7), ligament (8) and skeletal muscle (9). COMP is thought to act as a bridging molecule within the ECM (10). Indeed, COMP interacts with numerous ECM proteins including types I, II, IX, XI and XII collagen, decorin, fibronectin and matrilin-3 (1115), and a role for COMP as a catalyst in collagen fibrillogenesis has been proposed (16).
Each COMP monomer consists of a coiled-coil oligomerization domain, four EGF-like domains, eight TSP type 3 (T3) repeats and a large C-terminal globular domain (CTD). PSACH-MED mutations in COMP cluster in two distinct regions: the type 3 repeats (~85% of the mutations identified to date) and the CTD (~15% of the mutations identified to date) (17). Extensive research over the last 10 years has demonstrated that mutant COMP protein harbouring structural changes in the type 3 repeats is retained within patient chondrocytes, eventually resulting in rER stress and increased cell death both in vitro and in vivo (reviewed in 18). In contrast, some of the COMP-CTD mutations allow the secretion of mutant protein but low levels of ER/cell-stress are still observed, both in vitro and in vivo (19,20).
PSACH-MED patients have a well-characterized ligamentous laxity (2), and the ligaments from patients with COMP-T3 mutations can exhibit a disorganized collagen fibril network, with both variable fibril diameters and lateral fusion of neighbouring fibrils (unpublished data) (15). Conflicting data exist concerning the retention of mutant COMP in tendon and ligament cells. For example, no apparent intracellular retention of mutant COMP was noted in ligament cells cultured in vitro (21), although the retention of mutant protein was observed in vivo in ligament cells from a PSACH patient with a COMP-T3 mutation (p.Gly465Ser; unpublished data). In common with ligament cells, tenocytes from patients with COMP mutations retain mutant COMP in the rER in vivo and in cells cultured in monolayer (22,23), whereas in another study, no protein retention was evident (24).
An overlooked clinical complication in some patients with PSACH-MED, specifically those with mutations in the CTD of COMP, is mild myopathy. This can be characterized clinically by a difficulty in standing up and a tendency to tire easily, and biochemically by mildly increased plasma creatine kinase (PCK) levels, differences in fibre diameters and/or atrophic fibres observed in muscle samples obtained through biopsy (17,25,26). Furthermore, MED patients with mutations in the α3(IX) (27) or α2(IX) (M.D.B., submitted for publication) chains of type IX collagen have also been reported as having mild myopathy. However, the muscular, tendon and ligament complications of the PSACH-MED phenotype have not yet been studied in detail, primarily because of the difficulty in obtaining suitable pathological samples.
Here we report a detailed study of the phenotypic and morphological effect of a C-terminal COMP mutation on skeletal muscle, Achilles tendon and spinal ligament in a mouse model of mild PSACH-MED (20). We show that the mutant mice exhibit a progressive mild myopathy, localized specifically to the perimysium and myotendinous junction (MTJ) and characterized by a dramatic increase in the number of fibres with central nuclei (i.e. indicative of remodelling). We also present evidence that this CTD mutation in COMP affects the morphology and biomechanical characteristics of murine Achilles tendon and spinal ligament, which is consistent with a proposed role for COMP in collagen fibrillogenesis. Our results led us to the hypothesis that the PSACH-MED associated myopathy is a secondary consequence of an underlying tendinopathy and that joint laxity seen in patients is a direct consequence of structural abnormalities to the tissue's ECM.
This is the first comprehensive characterization of the musculoskeletal phenotype of the PSACH-MED dysplasia family, and it may directly influence the clinical management of PSACH-MED patients in the future.
RESULTS
Comp T585M mutant mice exhibit a mild and progressive muscle weakness
To assess muscle weakness in the Comp T585M mutant mouse model, we performed forelimb grip-strength tests on male mice at 3 and 9 weeks of age (Fig. 1A). At 3 weeks of age, mutant mice and wild-type controls had a comparable maximum forelimb strength (defined as the highest force recorded during the experiment), but the force at which mutant mice released their grip was significantly lower than in wild-type mice, suggesting that the mutant mice tired easier (Fig. 1B; 12.6% reduction, P < 0.05 by one-way ANOVA, n = 3). By 9 weeks of age, the maximum strength and the force at which the mutant mice released their grip were both significantly lower than the values recorded for the wild-type mice, indicating that the muscle weakness in mutant mice progressed with age (Fig. 1B; a decrease of 26.7 and 23.3%, respectively; P < 0.001 by one-way ANOVA, n = 3).
Figure 1.
(A) Schematic of a grip strength test. (B) Grip measurements were performed on 3 and 9 week-old animals. At 3 weeks of age, there was no difference between the maximum strength of the wild-type and mutant animals, but there was a 12.6% difference in the ...
Muscle weakness in Comp T585M mice results from a mild myopathy localized to the perimysium and the MTJ
To determine whether the muscle weakness was due to a generalized myopathy resulting from abnormal muscle morphology and structure, we undertook a detailed microscopic analysis of skeletal muscle from mutant mice and wild-type controls. To examine skeletal muscle morphology by histology, whole legs were dissected from 3 and 6 week-old mice and sectioned in a transverse plane until the gastrocnemius and soleus muscles were clearly visible. Tissue sections were stained with Gomori's trichrome stain, which stained the collagenous tissue blue, skeletal muscle red and the nuclei black. The number of fibres with central nuclei (i.e. indicative of fibre stress and remodelling (28,29)) was determined throughout the muscle tissue and expressed as a percentage of the total number of fibres (Fig. 2). In the mutant skeletal muscle, there was a ~33% increase in the number of fibres with central nuclei compared with the wild-type mice at 3 weeks of age [Fig. 2 (total tissue 3 weeks); P < 0.05 by independent samples t-test, n = 3]. This initial observation was indicative of a mild myopathy and we wished to establish the precise localization of the abnormal fibres seen in the mutant muscle. Following stratification, a larger proportion of fibres with central nuclei were present specifically at the MTJ and around the perimysium in the mutant tissue compared with the wild-type controls [Fig. 2 (MTJ 3 weeks); ~43%; P < 0.005 by independent samples t-test, n = 3]. No significant differences in the numbers of fibres with central nuclei were observed elsewhere in the muscle tissue of mutant mice when compared with wild-type controls [Fig. 2 (rest 3 weeks)]. Furthermore, at 6 weeks of age, the number of muscle fibres with central nuclei was >2.5-fold higher in mutant mice compared with wild-type controls [Fig. 2 (total tissue 6 weeks); P < 0.01 by independent samples t-test, n = 3]. The muscle fibres with central nuclei were still specifically localized to the perimysium and MTJ in the mutant muscle and there was no difference in the number of remodelling muscle fibres in the rest of the tissue [Fig. 2 (MTJ 6 weeks); P < 0.01 by independent samples t-test].
Figure 2.
Muscle fibres with central nuclei (inset) were counted in the skeletal muscle of 3 and 6 week old wild-type and mutant mice and expressed as a percentage of total muscle fibres in the tissue. There was a 33% increase in the number of fibres with central ...
To identify an underlying reason for the increased stress and remodelling by myocytes in the mutant muscle, we determined the relative levels of the molecular chaperone BiP and the anti-apoptotic protein Bcl-2 by performing densitometry measurements on Western blots of total muscle proteins. BiP is a general marker of ER stress that is applicable to skeletal muscle cells (30,31), whereas Bcl-2 has a protective role in skeletal muscle and has been shown to be decreased in several myopathies (32,33). At 3 weeks of age, there was no difference in the relative levels of BiP or Bcl-2 between wild-type and mutant samples (Supplementary Material, Fig. S1A; independent samples t-test, n = 5). These data therefore suggested that the expression of the Comp mutation per se did not have a generalized effect on the myocytes of skeletal muscle.
Comp is expressed in murine tendon, ligament and skeletal muscle
Comp is known to be expressed in skeletal muscle in mice (9); however, conflicting data exist concerning its expression in tendon with reports of either its presence (9) or absence (34) in adult murine Achilles tendon. Therefore, before studying further the pathomolecular mechanisms of myopathy in the mutant mice, we undertook a detailed analysis of Comp expression in the relevant murine tissues (i.e. those of the musculoskeletal system).
The expression levels of Col1a1 (a positive marker for tendon, ligament and skeletal muscle), Col2a1 (a negative marker for the same tissues), Myod1 (a positive marker for skeletal muscle and a negative marker for tendon) and Comp were determined at 3 weeks of age by quantitative real-time PCR (Supplementary Material, Table S1). The expression levels of these marker genes confirmed the accuracy of the dissection protocol since the relative levels of Myod1 expression in the Achilles tendon and spinal ligament were negligible as was the expression of Col2a1 in the skeletal muscle. The most abundant gene transcript was Col1a1, which was unsurprising since type I collagen is the most abundant protein of tendon and ligament and an abundant component of the skeletal muscle ECM.
Not surprisingly, Comp expression was lower in tissue samples from Achilles tendon, spinal ligament and skeletal muscle relative to the positive marker (Col1a1). Nevertheless, Comp was still expressed in all of these tissues at levels >10-fold higher than the negative controls (Supplementary Material, Table S1). The relative levels of Comp expression were also determined in Achilles tendon, spinal ligament, skeletal muscle and epiphyseal cartilage at 3 weeks of age (Supplementary Material, Table S2). The levels of Comp expression were comparable for tendon, ligament and skeletal muscle, whereas Comp expression was significantly higher in cartilage when compared with tendon, ligament and muscle samples (P < 0.05 by independent samples t-test, n = 3). There was no difference in Comp expression between wild-type and mutant samples in all of the tissues studied (data not shown).
The presence of COMP was also confirmed at the protein level by Western blotting of total protein isolated from the Achilles tendon and skeletal muscle of mice at 3 weeks of age (Fig. 3C). There were no differences in the relative levels of COMP between genotypes (i.e. WT versus M), but we did note that there were slight differences in the levels of COMP protein between tendon and muscle samples, which was in contrast to the quantitative RT–PCR analysis that showed comparative levels of Comp mRNA in these two tissues.
Figure 3.
(A) IHC localization of COMP in wild-type tendon at 3 weeks of age. Gomori's trichrome staining (left panel) of tendon showing localization of the collagenous component (blue) and COMP immunostaining (brown) (central panel), with negative control (no ...
The localization of key structural molecules is not affected in the ECM of mutant skeletal muscle
We performed immunohistochemical (IHC) staining for COMP in mouse skeletal muscle and Achilles tendon to confirm that it was expressed in both tissues (Fig. 3). In both wild-type and mutant tendon, COMP was present in the ECM between individual collagen fibrils (Fig. 3A; data not shown), confirming previous studies (35,36). Furthermore, in both wild-type and mutant skeletal muscle, COMP was present on the surface of the myofibres and there were no apparent differences in the intensity and localization of the staining between genotypes (Fig. 3B; data not shown).
To investigate further the skeletal muscle stress and remodelling, additional markers such as desmin, vimentin and collagen types IV and VI were analysed at 3 weeks of age by IHC of saggital and transverse sections of the soleus and gastrocnemius muscles. There were no apparent differences in the localization of desmin, vimentin, type I, IV or VI collagen between wild-type and mutant tissues at 3 weeks of age, confirming that it was not a generalized myopathy (data not shown).
The distribution of collagen fibril diameters is altered in mutant Achilles tendon
Although we demonstrated that COMP is expressed in skeletal muscle tissue, a quantifiable pathology was only apparent at the perimysial and MTJ of mutant muscle. Since the overall skeletal muscle morphology was not affected in the mutant mice, and because the perimysium and MTJ are important for the transmission of force between the muscle and tendon (3739), we considered the possibility that the ‘mild myopathy’ in the mutant mice may, in fact, arise from structurally abnormal tendons. We therefore used transmission electron microscopy (TEM) to measure the collagen fibril diameters in Achilles tendons from wild-type and Comp T585M mutant mice at 3 and 9 weeks of age (Fig. 4A and B). There was a significant difference in the distribution of collagen fibril diameters between wild-type and mutant Achilles tendons with a relative increase in the numbers of thicker collagen fibrils in the mutant samples at both 3 and 9 weeks of age (Fig. 4A and B; P < 0.05 and P < 0.005, respectively, by Mann–Whitney U test, n > 3). The total number of collagen fibres per mm2 was also reduced in mutant tendons compared with wild-type tendons at 3 weeks of age (13%, P < 0.05; data not shown). A similar change in the distribution of collagen fibrils was also seen for wild-type and mutant spinal ligament at 9 weeks of age (Fig. 4C), further supporting a role for COMP in collagen fibrillogenesis.
Figure 4.
(A) Quantification of the collagen fibril diameters in the wild-type and mutant Achilles tendon at 3 weeks of age showing an altered distribution in the mutant tissue (P < 0.05, Mann–Whitney U test, n = 5). (B) Quantification of collagen ...
Mutant Achilles tendons contained more fused/bifurcating collagen fibrils than wild-type tendon and were significantly thinner overall
Fused collagen fibrils were observed previously in a ligament sample from a PSACH patient who had undergone bilateral hip replacement (Fig. 5B; unpublished data; (15)). Therefore, the number of fused (or branching) collagen fibrils was determined in the wild-type and mutant tendon samples at 3 weeks of age and expressed as a percentage of total fibrils per cross-sectional area. There was a significant increase in the number of fused fibrils in the mutant tendon when compared with the wild-type tendon [Fig. 5A; ~398% (>3-fold), P < 0.05 by independent samples t-test, n > 5]. A similar observation was also made in mouse spinal ligament at 9 weeks of age (data not shown). Furthermore, at 3 weeks of age, mutant Achilles tendons were significantly thinner (by 65%) than wild-type tendons (P < 0.01 by independent samples t-test, n > 5; data not shown). The total area occupied by collagen fibrils was also calculated from the TEM images of wild-type and mutant Achilles tendons and was comparable for wild-type and mutant tendons, demonstrating that the proportion of interfibrillar matrix between the collagen fibrils was similar (data not shown). We considered the possibility that the ECM in the mutant tendons might contain under sulphated proteoglycans (PGs) (similar to that observed in the cartilage growth plate of mutant mice). However, DMMB (1,9,dimethyl-dimethylene blue) analysis revealed that the amount of sulphated PGs in the ECM was comparable with no significant differences between the wild-type and mutant tendons (Fig. 5C; independent samples t-test, n > 10).
Figure 5.
(A) Quantification of the fused/branching collagen fibrils expressed as a percentage of total collagen fibrils in the Achilles tendon at 3 weeks of age. There was a dramatic increase in the number of fused fibrils in the mutant tissues (398%, P < ...
Achilles tendons from mutant mice were more lax in biomechanical testing
The fibrillar organization and cross-sectional diameter of mutant Achilles tendons were dramatically altered compared with wild-type tendons. We therefore used tensile strength measurements (Table 1 and Fig. 6A) and cyclic strain testing (Fig. 6B) to analyse the biomechanical properties of wild-type and mutant Achilles tendons from 3 week-old animals. In the tensile strength test, the tendons were stretched at a set strain rate of 0.08/s [with strain measured as (llo)/lo, where l is the length of the sample, and lo the original sample length] until breaking point, and a stress/strain curve was plotted [stress being the F/csa, where F is the force (N), and csa the cross-sectional area (mm2)] (Table 1 and Fig. 6A). The data obtained were in agreement with the values published for various mouse strains (40). Interestingly, mutant tendons were capable of more ‘stretch to failure’ (27%, P < 0.05 by independent samples t-test, n > 5) and could sustain more stress (64%, P < 0.01 by independent samples t-test, n > 5); however, the force applied to failure (failure load) was comparable for wild-type and mutant tendons (Table 1). In addition, the elastic modulus and stiffness of the mutant tendons were comparable with wild-type tendons. Since mutant Achilles tendons were significantly thinner than the wild-type tendons, they were also capable of storing less potential kinetic energy during the tensile stretch experiment (Table 1; 34% for 1 mm stretch, P < 0.05 by independent samples t-test, n > 5).
Figure 6.
(A) Stress/strain curves of the stretch to failure experiment for wild-type and mutant Achilles tendon at 3 weeks of age. Note that the slopes of the curves in the linear phase are similar, indicating a comparable stiffness. Mutant tissue was more resilient ...
Table 1.
Biomechanical parameters of the tensile test on wild-type and mutant Achilles tendons at 3 weeks of age
Cyclic strain testing was used to determine the performance of 3 week-old wild-type and mutant Achilles tendon in more relevant physiological conditions (Fig. 6B). The cyclic test was performed in the toe region (reflecting the tendon crimp) of the stress/strain curve for the wild-type and mutant tendons (41). The tissues were cycled nine times to a strain of 0.5 and the force applied was measured. The cycles for wild-type and mutant Achilles tendons were normalized to the first cycle force (100%), then plotted and compared. In the cyclic testing, the initial forces recorded for the wild-type and mutant Achilles tendon were comparable, but mutant Achilles tendons became more lax with an increasing number of cycles until, at cycle 8, significantly less stress was needed to stretch them to the same length as the wild-type tendons (Fig. 6B; 16.3%, P > 0 < 0.05 by independent samples t-test, n = 5). These data suggest that in vivo mutant tendons are more lax and as such are likely to convey less elastic energy to the muscle during walking.
ER stress and apoptosis are not increased in mutant tenocytes
On the basis of our previous findings in the mutant cartilage growth plate, where BiP was significantly upregulated and Bcl-2 was downregulated (20) owing to the expression of mutant Comp T585M, we considered the possibility that the expression of mutant Comp T585M was eliciting an rER/cell stress response in tenocytes that might eventually be causing increased cell death. Densitometry measurements of Western blots was performed for Bcl-2 and BiP in protein samples from 3 week-old mutant and wild-type tendons. However, we found no differences in the relative levels of Bcl-2 and BiP in mutant and wild-type tenocytes (Supplementary Material, Fig. S1B; independent samples t-test, n = 5). These data suggest that either the expression levels of mutant COMP may not be high enough in tenocytes to elicit a classical rER stress response, or that tenocytes may respond differently to the expression of mutant COMP, which has been proposed previously (24). Alternatively, adult tenocytes may also not be as metabolically active as chondrocytes at 3 weeks of age (42,43).
DISCUSSION
PSACH is a skeletal dysplasia that in the most severe form is debilitating for the patient's well-being and lifestyle owing to the dramatic skeletal phenotype, which includes short-limbed dwarfism and early onset degenerative joint disease (44,45). In contrast, the related, but milder MED is sometimes misdiagnosed or not reported until later in life (17). In this study, we showed that mutations in Comp that cause PSACH-MED result in altered collagen fibril diameters in force-loaded tendons and ligaments and is associated with a mild muscle myopathy in the absence of a detectable muscle pathology.
One of the clinical complications recently recognized as a part of the PSACH-MED phenotype is a mild myopathy, which in some cases may manifest earlier than the skeletal phenotype (17,2527). In these instances, the patients are reported as having difficulties with standing up or tire easily during exercise and are often referred to the clinic with an unclassified ‘neuromuscular disorder’ prior to the diagnosis of a underlying skeletal dysplasia. On the basis of these and other reported cases, it has been suggested that if a child presents with a ‘difficult to explain’ myopathy (i.e. waddling gait, increasing muscle weakness, but with none or only mild changes in a muscle biopsy), the child should be referred for a skeletal survey with a view to identifying an underlying skeletal dysplasia (46). Interestingly, in many PSACH-MED patients with a reported myopathy, a causative mutation was identified in the CTD of COMP. In these patients, the myopathy was not comprehensively documented, but included features such as mildly elevated PCK levels (25), basophilic and/or atrophic muscle fibres (17). Furthermore, a mild myopathy has also been reported in several MED families with type IX collagen mutations, a protein which is not expressed in skeletal muscle, but is present in tendons at the insertion of the tendon into the bone (i.e. the enthesis) (47). In these families, the proband was also referred to a neuromuscular clinic for the evaluation of proximal muscle weakness prior to the diagnosis of MED (27) (M.D.B., submitted for publication).
The musculoskeletal complications of the PSACH-MED phenotype have not been studied in detail, primarily due to the difficulty in obtaining suitable pathological samples and aged/site-matched controls. A detailed analysis of the myopathy associated with COMP mutations would therefore enable earlier diagnosis of mild PSACH-MED, improve our understanding of the disease mechanisms and ultimately improve patient care (48). In this study, we have clinically demonstrated muscle weakness in mutant mice and analysed the gastrocnemius and soleus muscles and Achilles tendon to gain insights into the key pathological features and disease mechanisms of this mild myopathy.
Comp T585M mutant mice, which we have previously characterized as a relevant model of mild PSACH (20), also suffer from a progressive myopathy as demonstrated by grip strength testing. Furthermore, when we analysed skeletal muscle from the mutant mice, we found a progressive increase in the number of myofibres with central nuclei, specifically around the perimysium and the MTJ. This observation is indicative of skeletal muscle stress and the subsequent remodelling of the gastrocnemius and soleus muscles in these specific areas (28,29). To test that the myopathy in mutant mice was not a generalized muscle pathology, we analysed the skeletal muscle tissue of wild-type and mutant mice in detail. We used immunohistochemistry to determine the localization of several important ECM proteins in murine skeletal muscle and did not detect any differences in the distribution of wild-type and mutant COMP, or in the distribution of types I, IV and VI collagen, desmin or vimentin. We have also confirmed that COMP was present in the ECM of skeletal muscle, specifically in the endo- and perimysium, and that there were no differences in its localization between wild-type and mutant tissues. Interestingly, these observations are in direct contrast to changes in the localization of mutant COMP seen in the cartilage growth plates of Comp T585M mutant mice (20) and suggests that the ECM of muscle and cartilage may assemble and respond differently to the presence of mutant COMP. We have previously shown that mild ER stress was detected in chondrocytes from mutant mice expressing Comp T585M. However, the analysis of an ER stress marker (BiP) and an apoptosis marker (Bcl-2) showed no differences between the wild-type and mutant cells. Overall, these data suggest that although secreted by myocytes and present in the ECM, mutant COMP did not have an effect on general skeletal muscle architecture and did not elicit an ER stress response in the mutant cells.
It has been shown that the transmission of forces between the skeletal muscle and tendon depends on the interaction of the muscle fibres with the surrounding ECM and also on the collagen fibrillar organization of the tendon (37). Perimysium has been shown to form a connective tissue with a ‘lattice-like’ structure and is important for conveying forces between the tendon and skeletal muscle (3739,49). These observations led us to hypothesize that myopathy in the mutant mice may, in fact, be the result of an underlying tendinopathy. Therefore, to gain insight into the mechanisms underlying the restricted localization of the myopathic changes, we studied the ultrastructure of the Achilles tendon from wild-type and mutant mice at 3 and 9 weeks of age. Tendons are an important skeletal tissue since they act as buffers for muscle stretch during locomotion (50). We have shown that Comp is expressed in murine tendon and ligament by a variety of techniques, and that the localization of mutant COMP was not altered in mutant tissues. To determine the effect of mutant COMP on collagen organization, we measured the diameters of collagen fibrils in the Achilles tendon of wild-type and Comp T585M mutant mice. Interestingly, we found that the distribution of collagen fibril diameters in the mutant tendon was dramatically altered, with a higher proportion of larger diameter fibrils. There was a similar difference in the distribution of collagen fibrils in wild-type and mutant spinal ligament, further supporting a role for COMP in collagen fibrillogenesis. The total area occupied by the collagen fibrils was not altered between the wild-type and mutant tendons, but the number of fibrils per unit area of tendon was decreased in the mutant mice. Furthermore, the overall ‘interfibrillar area’ was not altered in the mutant tendons, suggesting that the amount of inter-territorial matrix in the wild-type and mutant tendons was similar. PGs comprise ~0.5% of tendon dry weight and play a role in tendon fibril spacing (37). We therefore analysed the PG content of wild-type and mutant Achilles tendons from 3 week-old mice and found that the PG content was similar for both genotypes.
The abnormal changes seen in collagen fibril diameters in the mutant tendon might be due directly to the mutation in the CTD of COMP. For example, this region of COMP contains a potential collagen-binding site (15), and a role for COMP as a catalyst in collagen fibrillogenesis has been proposed (16). It is therefore possible that this C-terminal COMP mutation (T585M), which is close to the potential collagen-binding site (15,17), has a detrimental effect on the ‘catalyst’ function of COMP that could alter collagen fibril diameter in the mutant tissue and ultimately its biomechanical properties. The detrimental effect of COMP mutations on collagen fibrillogenesis has been previously demonstrated in vitro (51). In addition, we also observed an increase in the number of fused/bifurcating collagen fibrils in mutant tendon and ligament compared with the wild-type tissues. Similar observations have previously been seen in a ligament sample from a PSACH. In wild-type animals, fibril bifurcation is abundant in mouse fetal tendon tissue, but decreases with age (52). Furthermore, increased fibril bifurcations have also been found in tendon scar tissue and at the scar to tissue junctions (53), and it has been suggested that an increase in fibril bifurcations may be indicative of wound healing and that they may be required to connect neighbouring fibrils to transform the force properly from the scar to the residual tissue (53). It has been proposed that the tendon biomechanical function depends on the precise collagen fibre alignment in the tissue (54). It is therefore interesting to speculate that owing to the altered biomechanical properties of the mutant tendons, some microdamage could occur in the mutant tendon, and the increased number of fused fibrils may be indicative of repair mechanisms in the mutant tissue, which could in turn affect the biomechanical properties of the tissue.
Finally, the cross-sectional area of whole mutant tendons was also significantly less than that of the wild-type tendons. This may be due to tendon remodelling and/or disuse (55). It could also potentially be a compensatory mechanism for the thicker collagen fibrils in the mutant tendons, which would make the mutant tissue stiffer. The dimensions of tendons directly influence their ability to stretch, store and release kinetic energy (56). In physiological conditions, the cross-sectional area of the tendon, relative to that of the fascicles of the attached muscle, dictates the maximum tensile stress to which a tendon can be subjected (57). The smaller cross-sectional area of mutant tendons, and the abnormal structural similarities between mutant tendons and ligaments, may therefore explain the joint laxity seen in PSACH-MED patients (2). In addition, the variability in the diameters of individual collagen fibrils can have a dramatic impact on the tissue's biomechanical properties. The biomechanical properties of tendons are directly related to fibril length, diameter and modulus and inversely to interfibrillar spacing (58), and thick fibrils are predicted to withstand higher tensile forces owing to the higher number of intrafibrillar crosslinks (59).
To assess the biomechanical properties of the wild-type and mutant tendons, we performed a series of tensile strength experiments. In a stretch-to-failure experiment, mutant tendons were able to withstand higher stresses and were stretched more before failure. However, when the mutant tissues were tested in a cyclic strain experiment, they became more lax with an increasing number of cycles, which is analogous to the progressive joint laxity observed in PSACH-MED patients (2). Lax tendons would also be less suitable for conveying the appropriate forces from muscle to bone, which might help explain the neuromuscular symptoms seen in PSACH-MED patients. By analogy to the structural changes seen in mouse mutant tendon and ligament, we can hypothesize that joint laxity in PSACH-MED patients might also stem from an altered distribution of collagen fibrils.
Tendons are known to adapt to mechanical load requirements, and inactivity has been shown to decrease collagen turnover in tendon (37,60,61). It was also shown that training increased the cross-sectional area of tendons in pigs (62) and that an increase in cross-sectional area of tendons correlates with an increase in tendon stiffness (37). Collagen fibril diameters also shift towards thicker fibrils with age (63), resulting in less compliant tissues (50). Therefore, it is likely that the tendon and ligament pathology seen in this mouse model of mild PSACH, and in PSACH-MED patients, becomes exacerbated with age as short-limbed dwarfism and increasing joint pain greatly reduce the patients' mobility. The increased joint laxity may in turn have an effect on the joint stability and the progression of degenerative joint disease in PSACH patients (44,45).
In summary, we have shown that COMP is expressed in the Achilles tendon and skeletal muscle of adult mice. We have demonstrated that Comp T585M mutant mice suffer from a progressive myopathy that is specifically localized to the perimysium and the MTJ. The distribution of collagen fibril diameters is altered in the mutant tendon and ligament, whereas the PG content is comparable between the wild-type and mutant tissues. The biomechanical properties of mutant tendon are dramatically altered, making the tissue more resilient to failure stresses, but ultimately more lax following cyclic strain. We therefore hypothesize that the mild myopathy reported in PSACH-MED results from altered forces transmitted by the mutant tendon, and that the joint laxity may be directly due to the structural abnormalities in the ligament. Furthermore, our study suggests that the difficulties in walking and easy tiredness experienced by some PSACH-MED patients might be a combination of the skeletal phenotype and an underlying tendinopathy. Since tendons are able to adapt to mechanical load and environmental requirements (36,37,61,64), certain physiotherapeutic treatments may help alleviate some of clinical symptoms of PSACH-MED, such as muscle weakness and joint instability. Our detailed characterization of the mild myopathy and tendinopathy in the mouse model of mild PSACH may also help in the management and early diagnosis of some forms of PSACH-MED, specifically in those children that present with tiredness and muscle weakness prior to the diagnosis of an underlying skeletal dysplasia.
MATERIALS AND METHODS
Transgenic mice
The generation and phenotypic characterization of the mice used in this study is described in detail in Pirog-Garcia et al. (20). Wild-type mice and mice homozygous for the Comp T585M mutation were used in this study. We specifically chose to study the homozygous mutant mice in order to better accentuate the muscle and tendon pathology. All experiments were performed in compliance with the relevant Home Office and Institutional regulations governing animal breeding and handling.
Grip-strength analysis
Grip strength measurements were performed using a hand-held Chatillon digital force gauge (ChatillonDFE Series Digital Force Gauge, Ametek Inc.; Fig. 1A). Briefly, the mice were preconditioned 20 times on the cage lid, then held by the tail and gently lowered towards the apparatus. They were allowed to grip the grid with their forelimbs only and were pulled backwards in a horizontal plane. The highest force applied to the grid (maximum strength) and the force at the moment the grasp was released were recorded (N). The test was repeated two times per mouse, and 10 mice per genotype were tested at 3 and 9 weeks of age. One-way ANOVA was used for statistical analysis of the data.
RNA extraction and real-time PCR
Following snap-freezing of tissues in liquid nitrogen and their homogenization, RNA was extracted from the Achilles tendon, soleus/gastrocnemius skeletal muscle and posterior longitudinal spinal ligament tissue from 3 week-old mice, using TriZOL reagent (Ambion Inc.). The RNA was DNaseI-treated (Ambion Inc.) and first-strand cDNA synthesized using Superscript III™ reverse transcriptase with random hexamers (Invitrogen Ltd). Real-time analysis of COMP, collagen I, collagen II and myoD expression was performed using SYBR® Green Kit (Eurogentech) on a Chromo4 sequence detector system (Bio-Rad). Each sample, including ‘no template’ controls, was run in duplicate and every sample had an 18S control. Each experiment was repeated at least three times with tissue from unrelated animals for statistical relevance, and the results were analysed by independent samples t-test.
Western blotting
Achilles tendon and gastrocnemius/soleus skeletal muscle tissue at 3 weeks of age was snap-frozen and homogenized, boiled in SDS-loading buffer containing DTT and loaded on an SDS–PAGE gel. The resolved gel was electroblotted onto a nitrocellulose membrane, which was blocked overnight with 2% skimmed milk powder in PBS-T. Primary antibodies [BiP (Cell Signalling Ltd), tenascin C, bcl-2 and actin (Abcam Plc), COMP (Genetex)] were diluted in PBS-T. An ECL detection kit (PerkinElmer Inc.) was used to develop the blots according to the manufacturer's protocol. The X-ray films were then scanned, and the densitometry of the bands was measured using Aida analysis software (Raytek Scientific Ltd). Independent samples t-test was used for statistical analysis.
Histology and immunohistochemistry
Full mouse limbs were skinned and fixed in ice-cold 10% neutral buffered formalin solution (Sigma-Aldrich Ltd; for histology) or in ice-cold 95% ethanol/5% acetic acid solution (for IHC), decalcified in 20% (w/v) EDTA, pH 7.4, paraffin-embedded and sectioned (6 µm sections). For haematoxylin and eosin (H&E) staining, the slides were dewaxed in xylene, rehydrated and H&E-stained using a ThermoShandon Ltd automated stainer, dehydrated in increasing concentrations of ethanol and in xylene and mounted using a xylene-based mounting solution. Gomori's trichrome staining (Polysciences Inc.) was performed according to the manufacturer's protocol and mounted using a xylene-based mounting solution (Pertex, Surgipath). Muscle fibres with central nuclei were counted and their number was expressed as a percentage of all the muscle fibres seen. Independent samples t-test was used for statistical analysis.
For IHC analysis, slides were dewaxed and rehydrated, endogenous peroxidase activity was quenched in H2O2/MetOH, followed by antigen unmasking in 0.2% bovine testes hyaluronidase (Sigma-Aldrich Ltd) in PBS. Samples were blocked in goat serum and BSA in PBS for 1 h and immediately incubated with primary antibody [COMP (Genetex Inc.), type I and type II collagen (Chemicon), type IV collagen, type VI collagen, desmin, vimentin and tenascin C (Abcam Ltd)] in PBS/BSA for 1 h. Slides were washed in PBS/BSA and incubated with FITC-conjugated secondary antibody (Abcam) and mounted in Vectashield™ containing DAPI (Vector Labs Ltd) or incubated with a biotinylated goat anti-rabbit IgG (Dako Cytomation Ltd) in PBS with goat serum, followed by incubation with ABC/HRP reagent (Dako Cytomation Ltd) and developed using DAB chromogen (Dako Cytomation Ltd), with methyl green as counter stain (Vector Labs Ltd). Vectamount™ (Vector Labs Ltd) xylene-free mounting medium was used for mounting the slides.
Ultrastructural analysis
Wild-type and mutant Achilles tendon and posterior longitudinal spinal ligament were dissected from mice at 3 and 9 weeks of age and immediately fixed in 2.5% glutaraldehyde in 1 m sodium cacodylate buffer for 2 h at 4°C. The tissues were washed three times in 0.1 m sodium cacodylate buffer and fixed in 2% OsO4 in 0.1 m cacodylate buffer for 2 h. They were washed in distilled water and incubated for 2 h in 2% aqueous uranyl acetate at 4°C. The tendons were then washed in distilled water, dehydrated in increasing concentrations of acetone (50, 70, 90 and 100% for 30 min), incubated in propylene oxide to improve resin penetration and 1:1 solution of resin:propylene oxide and embedded in TAAB medium slow resin (TAAB Laboratories Equipment Ltd). Thin 70–80 nm sections were cut with a diamond knife on a Leica ultramicrotome and placed on electron microscope grids. Sections on the grids were stained with silver citrate solution and viewed in a FEI Tecnai 12 Twin transmission electron microscope operated at an accelerating voltage of 80 kV. The fibril diameters were measured, and the distribution was analysed for statistical significance using Mann–Whitney U test.
DMMB assay
PG content was analysed using the DMMB assay (65). Achilles tendons at 3 weeks of age were digested overnight in 50 µg/ml proteinase K in 100 mm K2HPO4 (pH 8.0) at 56°C. The samples were centrifuged at 12 000 g in Ultrafree filter (Amicon), and the flow through was used for DMMB assay (66). Serial dilutions of shark chondroitin sulphate (Sigma) in K2HPO4 were used as a calibration curve, and the absorbance was read at λ = 525. The retentate was used for DNA contents analysis using Hoechst dye, as described in Orioli et al. (66). The calculated GAG content was then normalized to the DNA content of the tissues, and the data were statistically analysed using independent samples t-test.
Biomechanical analysis
Tensile loading and cyclic stress tests were performed on an Instron 1122 tensile tester (Instron). Achilles tendons were harvested at 3 weeks of age and stored in PBS at −80°C. They were gently thawed and the cross-sectional area was assessed by measuring the thickness in three points along the tendon's length. The average mouse tendon length was ~5 mm. The tendons were fitted into the tensile tester as shown in Fig 6A and were kept moist in PBS throughout the experiment. For the tensile loading test, the sample's starting length was 1 mm, and the samples were elongated at a constant strain rate of 0.08/s, until breaking point and force and displacement were measured. The toe region for the samples was established in the tensile loading test. In the cyclic stress, the starting sample length was 2 mm; the samples were stretched and relaxed with a constant strain amplitude of 0.5 for n = 9 cycles at the strain rate of 0.04/s, and the force and displacement were recorded. The force was normalized against the cross-sectional area, and the decrease in stress at each cycle was compared between the wild-type and mutant samples. Independent samples t-test was used for statistical analysis.
FUNDING
This work was supported by grants from the Wellcome Trust (M.D.B. is the recipient of a Wellcome Trust Senior Research Fellowship in Basic Biomedical Science; grants 071161/Z/03/Z and 084353/Z/07/Z), the Arthritis Research Campaign (grant 17221 to M.D.B.) and the European Commission FP6 (grant 037471). Funding to pay the Open Access publication charges for this article was provided by The Wellcome Trust.
Supplementary Material
[Supplementary Data]
ACKNOWLEDGEMENTS
The research was undertaken in the Wellcome Trust Centre for Cell-Matrix Research and the Histology, Microscopy and Transgenic Core Facilities of the Faculty of Life Sciences at the University of Manchester.
Conflict of Interest statement. None declared.
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Open Access
Varied sensitivity to therapy of HIV-1 strains in CD4+ lymphocyte sub-populations upon ART initiation
• Edwin J Heeregrave1,
• Mark J Geels2,
• Elly Baan1,
• Renee M van der Sluis1,
• William A Paxton1 and
• Georgios Pollakis1Email author
AIDS Research and Therapy20107:42
DOI: 10.1186/1742-6405-7-42
Received: 19 August 2010
Accepted: 6 December 2010
Published: 6 December 2010
Abstract
Background
Although antiretroviral therapy (ART) has proven its success against HIV-1, the long lifespan of infected cells and viral latency prevent eradication. In this study we analyzed the sensitivity to ART of HIV-1 strains in naïve, central memory and effector memory CD4+ lymphocyte subsets.
Methods
From five patients cellular HIV-1 infection levels were quantified before and after initiation of therapy (2-5 weeks). Through sequencing the C2V3 region of the HIV-1 gp120 envelope, we studied the effect of short-term therapy on virus variants derived from naïve, central memory and effector memory CD4+ lymphocyte subsets.
Results
During short-term ART, HIV-1 infection levels declined in all lymphocyte subsets but not as much as RNA levels in serum. Virus diversity in the naïve and central memory lymphocyte populations remained unchanged, whilst diversity decreased in serum and the effector memory lymphocytes. ART differentially affected the virus populations co-circulating in one individual harboring a dual HIV-1 infection. Changes in V3 charge were found in all individuals after ART initiation with increases within the effector memory subset and decreases found in the naïve cell population.
Conclusions
During early ART virus diversity is affected mainly in the serum and effector memory cell compartments. Differential alterations in V3 charge were observed between effector memory and naïve populations. While certain cell populations can be targeted preferentially during early ART, some virus strains demonstrate varied sensitivity to therapy, as shown from studying two strains within a dual HIV-1 infected individual.
Background
Antiretroviral therapy (ART) has proven to be successful against human immunodeficiency virus type 1 (HIV-1) and results in undetectable plasma levels for many years. However, an increasing number of studies report on adverse events and toxicities [1, 2]. Additional drawbacks to therapy are adherence and the considerable costs. In certain situations a more simplified antiretroviral regimen may be suitable, for instance as short-term use to prevent mother-to-child-transmission (MTCT), maintenance therapy after HAART or possibly as pre-exposure prophylaxis [37]. Despite the increased likelihood of viremia and emergence of resistance, prophylactic and/or short-term therapeutic use largely bypasses these disadvantages and more treatment options remain available.
The CD4+ lymphocyte is the main target cell for HIV-1 infection with the various sub-populations infected to a different extent [8, 9]. Naïve and memory lymphocyte subsets differ in body distribution, proliferative capacity and in expression levels of the main co-receptors for HIV-1, CCR5 and CXCR4 [1013]. Despite these differences, all cellular subsets are productively infected and display a lack of viral compartmentalization among circulating cells in peripheral blood [9, 14, 15]. Under the influence of long-term ART most studies describe a lack of viral compartmentalization among HIV-1 infected CD4+ lymphocyte subsets [1619]. Both central and transitional memory CD4+ lymphocytes are regarded as cellular reservoirs for HIV-1 under therapy [20]. Baldanti and colleagues show that naïve and memory cell numbers and HIV-1 infection levels do not differ greatly from each other during therapy [21]. These studies focus mainly on long-term ART and do not describe the influence on the cell subset-specific quasi-species during early therapy intervention. We studied alterations to HIV-1 infection levels and viral diversity within specific cellular subsets after short-term ART.
Methods
Five chronically HIV-1 infected individuals, who visited frequently the outpatient clinic of the Academic Medical Center (AMC) of the University of Amsterdam, the Netherlands, participated in this study. These patients received various antiviral regimens (Table 1) and their characteristics have been described previously [9]. Serum and peripheral blood mononuclear cells (PBMC) were obtained and frozen according to standard protocols. Viral loads were determined with the Versant HIV-1 RNA Assay (bDNA; Bayer Diagnostics, Leverkusen, Germany). Determination of HIV-1 subtype was performed by phylogenetic analyses and by blasting the sequences using the Los Alamos database [22]. This study was approved by the Medical Ethical Committee of the AMC and informed consent was provided by all participants.
Table 1
Patient characteristics
Patient
Env
therapy
# days
viral load (copies/ml)
CD4 count (cells/μl)
subtype
regimen
on ART
ART-
ART+
ART-
ART+
M11306
C
amprenavir
14
52,436
3,160
90
n.d.b
M12020
D
zidovudine
18
5,352
304
190
220
M12259
F
zidovudine
33
246,572
25,588
360
500
M13408
A
d4t, 3tc, rtva
28
65,262
247
620
840
M16394
C
zidovudine
28
1,026
607
800
690
ad4t - stavudine, 3tc - lamivudine, rtv - ritonavir
b not determined
PBMC were thawed and FACS-sorted as published previously [9]. Cells were stained with various antibodies and three CD4+ lymphocyte subsets were sorted: naïve, CD57- memory (or central memory) and CD57+ memory (or effector memory) CD4+ lymphocytes. All cell sorts were performed utilizing a modified FACS DIVA. Viral DNA from the cell subsets was isolated utilizing a silica-based method, which was also used for RNA isolation from serum [23]. Cellular HIV-1 infection levels were quantified using a semi-nested real-time PCR assay [9]. This assay targets the LTR segment of the virus genome where the second strand transfer takes place and quantifies only fully reverse transcribed HIV-1 genomic DNA and has high specificity for all major HIV-1 subtypes. We excluded HIV-1 quantifications of the naïve subset of patient M16394 before therapy as well as the effector memory subsets before and after therapy and the memory subset after therapy of patient M12259, since either the input (cell number or virus copies) was too low or the outcome was unreliable. AMV-RT (Madison, WI, USA) was used for reverse transcription of the serum-derived RNA. The C2V3 region (HXB2 nucleotide positions 7032-7301) of the HIV-1 envelope gene was amplified using AmpliTaq DNA polymerase (PE Applied Biosystem, Foster City, CA, USA). The primers (100 ng/μl) for the first-round PCR were 5'-AATGTCAGCACAGTACAATG-3' and 3'-TCTCCTCCTCCAGGYCTGAA-5' and for the nested PCR 5'-CCAGTGGTATCAACTCAA-3' and 3'-ATTTCTAAGTCCCCTCCTGA-5'. PCR products were sequenced clonally using the TOPO II cloning system (Invitrogen, Paisley, UK). Eleven to twenty-three clones from each subset were sequenced bi-directionally using the BigDye Terminator Cycle Sequencing kit and analyzed with the ABI 377 automated sequencer (Applied Biosystems, Foster City, CA, USA). Quality of the sequences was analyzed using CodonCode Aligner version 1.5.1, after which the sequences were aligned with BioEdit and adjusted manually with respect to the gp120 open reading frame and according to reference sequences from the Los Alamos HIV sequence database [22]. Molecular evolutionary analyses were conducted using MEGA version 4 [24]. Tamura-Nei was used as distance parameter and inter-patient cross-contamination was ruled out. Statistical analyses were performed using the Mann-Whitney test.
Sequence data
The sequences described here were allocated the following Genbank nucleotide accession numbers: GQ389219, GQ389220, GQ389225, GQ389227 and GQ389228.
Results
Patient description and HIV-1 quantification in CD4+ lymphocyte subsets
We studied the effect of antiretroviral therapy on HIV-1 infection levels of naïve, central memory and effector memory CD4+ lymphocyte populations and on the viral quasi-species present in these subsets, two to five weeks after initiation of ART. The five patients studied harbored various HIV-1 subtypes (A, C, D and F) and demonstrated a wide range of viral load values and CD4 counts (Table 1). Three out of five study subjects received an RT inhibitor (AZT), one a protease inhibitor (APV) and one received a three drug regimen (d4T/3TC/RTV). Plasma viral load declined in four individuals by 1 to 2.4 log and one subject (M16394) experienced only a small plasma load decline (Figure 1A). This patient already had a low viral load prior to therapy (1,026 copies/ml). Additionally, this patient had a high CD4 count at time of therapy initiation (800 cells/μl), which did not rise following therapy. In three of the four patients with complete data sets intracellular HIV-1 infection levels decayed by comparable levels for all cell subsets analyzed, by up to 1.1 log (Figure 1B). One exception was the effector memory population of subject M13408, the individual receiving the triple regimen, where infection levels significantly increased 6.5-fold. The drops in plasma viral loads would suggest that resistance has not occurred in the patients tested during the short time period of study.
Figure 1
Viral load and cellular infection levels before and after initiation of ART. (A) Viral load values were calculated before (-) and after (+) initiation of ART and are plotted on logarithmic scale. The median decline in copy number is inserted within the graph. (B) The number of HIV-1 gag copies per 105 cells of the respective cell subset is depicted on the y-axis in logarithmic scale. An occasional subset was not included due to a large difference between the duplicate measurements.
Influence of therapy on HIV-1 quasi-species in CD4+ lymphocyte subsets
Our goal was to determine how therapy affected the virus variants within naïve, central memory and effector memory CD4+ T cell subsets during the initial phase of therapy. Before therapy initiation, phylogenetic analysis of the C2V3 region of HIV-1 gp120 envelope did not demonstrate compartmentalization of the virus quasi-species within serum or CD4+ T cell subsets (Figure 2A). Only effector memory-derived sequences from M12020 clustered. After initiation of therapy loss of diversity was observed predominantly in serum, but also within the effector memory subset (Figure 2B). Naïve- and central memory-derived virus showed modest changes in diversity. The loss of diversity was highly significant in serum (p = 0.02 for subject M12259 and p < 0.0001 for all other patients; Figure 3). No diversity loss was observed in the naïve or central memory compartments.
Figure 2
Neighbor-joining phylogenetic analysis of the gp120 virus sequences. The Kimura-2 parameter and 100 replicates were used to calculate nucleotide distances and sequences from the Los Alamos HIV-1 database were used as reference strains. Circles indicate sequences from serum, diamonds from naïve CD4+ T cells, triangle from central memory and squares from effector memory cells. (A) Phylogeny of the strains isolated before initiation of therapy (B) Phylogeny of the strains isolated after therapy initiation. The black curved lines indicate strains from the effector memory population and the white curved lines indicate strains from serum. The dotted line indicates the two virus strains co-circulating in subject M12020.
Figure 3
Diversity and divergence of the viral quasi-species. (A) From each patient pair-wise nucleotide distances before (-) and after (+) initiation of therapy were calculated for each cell subset and serum. Nucleotide distance is presented as percentage and the red bar represents the median value. Pair-wise distances between both time-points were calculated (d) and when this value was higher than the diversity of either time-point it was identified as viral divergence, indicated by an asterisk. Statistical significance was calculated for the difference in diversity before and after therapy start; *** = p < 0.0001. Data from the effector memory subset of M16394 was not available.
To measure genetic evolution of the viral quasi-species, pair-wise distances were calculated between the virus populations before and after start of therapy. In serum, divergence of the viral quasi-species was observed in three patients (indicated by an asterisk; Figure 3). This indicated selection of serum variants due to therapy introduction. Viral divergence was absent in all cell subsets, with the exception of the effector memory subset in subject M12020. The absence of changes in viral diversity and divergence within naïve and central memory subsets as opposed to effector memory cells and serum indicates that during early therapy the plasma and effector memory cell compartments are more susceptible to the effects of the drugs.
To investigate the relatedness of virus strains among the cellular fractions the genetic distances between HIV-1 sequences derived from the various cellular fractions were calculated. Four out of five individuals demonstrated comparable distances before and after start of therapy ranging from 2.4% to 7.2% (Figure 4). After therapy initiation no change in distances were observed and were found to be similar within each of the cellular subsets. Subject M12020 was interesting since inter-subset distances before therapy were not only higher than those from all other individuals, but also higher than values observed following therapy (Figure 4). This individual was found to be infected with two different subtype D virus strains (strain I and II) as shown by phylogenetic analysis (Figure 2A). In addition, the analysis of virus sequences with DNAsp software indicated that up to 11 possible recombination breakpoints could be detected suggesting that these two virus strains were co-circulating within this individual for some time (data not shown). Before therapy, strain I was dominant in the effector cell population, while the other cell subsets harbored strain II. Both strains were present in serum. After therapy start, strain I disappeared from the effector memory subset but remained in some central memory cells (Figure 2B). The replenishment of this cell subset by a different virus strain correlated with viral divergence (Figure 3). Inter-subset virus distances approached values observed for the other patients harboring mono-infections, demonstrating that although some cell populations may be more sensitive to the effects of antiretroviral therapy, differences in sensitivity amongst virus strains also exists. These data indicate that the occurrence of dual HIV-1 infection could be an additional hurdle for therapy to succeed.
Figure 4
Inter-group nucleotide diversity. Before (ART-; white bars) and after (ART+; grey bars) therapy initiation, the mean difference in nucleotide distance was calculated using the Neighbor-joining model and the Kimura-2 parameter method. Each viral compartment was compared with all others (1: naïve - central memory, 2: naïve - effector memory and 3: central memory - effector memory).
Influence of therapy on V3 charge
Previous observations by our group and others have shown that V3 charge influences co-receptor usage [25, 26]. Since CD4+ lymphocyte sub-populations differ in co-receptor expression levels, we analyzed whether therapy initiation affected the V3 charge of the virus quasi-species in serum and lymphocyte subsets due to the variant expression profile. We therefore compared the V3 charge from all sequences found in the cell subsets before and after start of therapy. Sequences from all five patients were grouped together and we observed a clear increase in V3 charge within the effector memory subset in three out of four subjects (Figure 5; p < 0.0001). Within the central memory subset the V3 charge did not change whilst alterations in serum varied per patient (Figure 5; no significance). Within the naïve subset the V3 charge decreased systematically in all patients (p = 0.05), indicating that characteristics such as co-receptor usage may be involved in viral selection following initiation of therapy.
Figure 5
Change in V3 charge after initiation of ART. From all cellular subsets and serum the net V3 charge of each viral clone was calculated. The net V3 charges of all patients were grouped per time-point before (-) and after (+) initiation of ART. The graph depicts the mean value with standard deviation. *** = p < 0.0001 and ns = not significant.
Discussion
In our study we observed comparable viral decay within all CD4+ lymphocyte sub-populations in the peripheral blood, except for one effector memory subset, confirming our previous observation that all CD4+ lymphocyte subsets are productively infected with HIV-1 [9]. The results also confirm findings from other studies demonstrating comparable decay of productively infected cells in peripheral blood [21, 27]. A report on preferential HIV-1 inhibition during AZT treatment in activated cells over slowly dividing cells in vitro, may indicate that the vast majority of virus in the circulation comes from activated cells [28]. Although naïve and central memory lymphocyte subsets contain more long-lived resting cells than the effector memory subset and outnumber this subset, no difference in viral decay was observed.
Two to five weeks after initiation of ART represents the start of the second phase of viral decay, with loss of long-lived infected cells [29]. Here we study the early effects of therapy on the virus populations found in the three different lymphocyte subsets studied and compare to the changes observed in the plasma. It may be too early to detect differences in virus composition in cell populations with a slower decay rate as may be seen at a later stage when therapy is completely suppressing virus replication. In addition, the accumulation of replication-incompetent proviral DNA in these cell subsets together with the high rate of virus production by effector memory cells may in part influence the decreased viral diversity within effector memory cells, whilst no effect was observed for the other cell subsets during the short period of the study. M13408 was the only patient who received a triple therapy regimen and who surprisingly demonstrated an increase in effector memory infection levels. Perhaps these cells possess high P-glycoprotein efflux activity decreasing intracellular antiviral drug concentrations [30]. Although blood CD4+ lymphocyte levels only represent a minor fraction of the total body lymphocyte population, memory subsets in blood versus gut and lymphoid tissue counterparts are infected to the same extent [20, 31], thereby indicating that studying HIV-1 infection in blood is a good representation of events that occur in other tissues. With respect to our approach of cloning prior to sequencing we argue that direct sequencing would circumvent a possible cloning bias, although neither method is more skewed than the other and both provide for a similar measure of diversity [32]. Furthermore, sequence bias can occur through preferential PCR amplification and since we do not identify this in all fractions studied or for all time-points analyzed from the same patients we feel this can be ruled out. We are confident that when we identify a restricted sequence this is representative of the viral quasi-species present within that specific fraction. In all likelihood low diversity can reflect either low infectivity or over representation of a fast replicating strain.
The more pronounced changes observed in diversity of cell-free over cell-associated virus can be explained by the difference in half-life, which can severely reduce serum copy numbers [29]. Although virus diversity in serum decreased after initiation of therapy the pair-wise distances calculated between time-points before and during therapy increased, indicating different genetic characteristics of the virus after introduction of therapy. Virus may be produced by other cell types or derived from compartments less accessible to antiretroviral drugs [19, 3335]. This is in agreement with studies demonstrating that rebound virus is distinct from variants present before start of therapy [36, 37]. The absence of divergence in the cell subsets (apart from with patient M12020) can be explained by a moderate drop in infection levels and smaller changes in diversity. In M12020 the compartmentalization of effector memory-derived virus pre-therapy indicates that in the case of dual HIV-1 infection one strain preferentially infects a specific CD4+ lymphocyte subset. We have previously observed in dual HIV-1 infection that one strain replicates preferentially within different cell types when compared with another strain indicating that the host cell environment influences viral replication [9, 38]. The shift in balance between strains I and II is likely caused by therapy, although differences in host immune pressure, virus fitness as well as high turnover rates of the specific cell subset may also play a role. The complete and specific infection of effector memory cells by strain I and the rapid replenishment with a different virus strain indicate that this cell subset may easily facilitate infection by different variants. Although strain I was not detected in serum during therapy, its presence in long-lived central memory cells at that time-point ensures persistence of both variants. This increases the chances of recombination and therapy resistance, raising questions as to the efficacy of antiretroviral therapy in dual-infected individuals [39]. This is in line with the more resistant phenotype of HIV-2 over HIV-1 in dual-infected persons [40].
The pronounced increase in the gp120 V3 charge in effector memory cells in three out of four patients reflects increased sensitivity to therapy of virus within this cell subset. It has been speculated that such changes can influence co-receptor usage, including a possible switch towards CXCR4 usage [25, 26, 41, 42]. Four weeks of therapy restores CCR5 expression levels, which are increased during HIV-1 infection, while CXCR4 expression levels demonstrate a modest change [43].
Conclusions
In conclusion, ART resulted in a comparable decay of HIV-1 infection levels in naïve and central memory subsets with minor to no changes in the viral quasi-species present. HIV-1 copy numbers in the effector memory subset not always decreased and the virus in this cell subset and in serum appeared to be more sensitive to therapy. We also observed variant sensitivity among virus strains in a dual-infected individual. These results provide better insights into the viral dynamics within CD4+ lymphocyte subsets during early therapy.
Abbreviations
HIV-1:
human immunodeficiency virus type 1
ART:
antiretroviral therapy
PBMC:
peripheral blood mononuclear cells.
Declarations
Acknowledgements
The authors would like to thank Jason M Brenchley, Brenna Hill, David Ambrozak, Daniel C Douek and Richard A Koup, Vaccine Research Center, National Institutes of Health, Bethesda, Maryland, USA for assistance with the cell sorts. This work was supported financially by NWO-WOTRO (grant 01.53.2004.025; EJH, WAP and GP) and by Dutch AIDSfonds (grant 6002; MJG and EB).
Authors’ Affiliations
(1)
Laboratory of Experimental Virology, Department of Medical Microbiology, Center of Infection and Immunity Amsterdam (CINIMA), Academic Medical Center of the University of Amsterdam
(2)
Mark J Geels is currently employed at Nobilon International BV
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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Original Investigation |
Tissue Engineering for In Vitro Analysis of Matrix Metalloproteinases in the Pathogenesis of Keloid Lesions FREE
Hanwei Li, PhD1; Zayna Nahas, MD1; Felicia Feng, BS1; Jennifer H. Elisseeff, PhD1; Kofi Boahene, MD2
[+] Author Affiliations
1Department of Biomedical Engineering, The Johns Hopkins University, Baltimore, Maryland
2Department of Otolaryngology–Head and Neck Surgery, The Johns Hopkins University, Baltimore, Maryland
JAMA Facial Plast Surg. 2013;15(6):448-456. doi:10.1001/jamafacial.2013.1211.
Text Size: A A A
Published online
Importance Keloid lesions form because of alterations in the mechanisms that govern cutaneous wound healing. Although matrix metalloproteinases (MMPs) have been implicated in keloid pathophysiology, many questions still remain about their involvement. Our incomplete understanding of keloid pathophysiology has led to high recurrence rates in current treatments. No reliable animal model is available for studying keloids.
Objective To gain a better understanding of the disease mechanisms involved in keloid lesions in the hopes of identifying therapeutic options.
Design Fibroblasts derived from keloid tissue were incorporated in either Matrigel or polyethylene glycol diacrylate mixed with type I collagen to create 3-dimensional models to investigate the role MMPs play in keloid formation. The MMP gene expressions were also compared between fibroblasts isolated from different sites within the same keloid lesion.
Setting The Johns Hopkins School of Medicine, Baltimore, Maryland.
Participants Keloid fibroblasts were received from the Baylor College of Medicine, and additional keloid fibroblasts were enzymatically isolated from the dermal layer of lesions removed from consenting patients at The Johns Hopkins Hospital.
Results In the Matrigel system, MMP9 and MMP13 were observed to be significantly upregulated in keloid fibroblasts. The addition of decorin resulted in a significant decrease of type I collagen and MMP1, MMP9, and MMP13 gene expressions from keloid fibroblasts. Higher MMP gene expressions were observed in fibroblasts isolated from the margins of the original keloid wound.
Conclusions and Relevance MMP9 and MMP13 are expressed significantly more in keloid-derived cells, thus making them 2 potential targets for disease modification. Molecules that target organization of the lesion’s matrix can be beneficial in downregulating increased markers during the disease. In addition, heterogeneity is observed with the varying MMP gene expressions from site-specific fibroblasts within the same keloid lesion.
Figures in this Article
Keloids represent an extreme form of abnormal cutaneous wound healing that can result in both functionally restrictive and disfiguring scars. In normal wound healing, a series of physiologic responses results in the formation of a scar that is randomly disorganized and predominantly composed of collagen deposition.1,2 Remodeling of the newly formed tissue affects the type of scar that forms. Keloid lesions are a form of abnormal wound healing whose molecular mechanism and pathogenesis are not well understood, thus making it a therapeutic challenge. In keloids, aberrant remodeling is thought to result in large quantities of collagen deposition after skin trauma in predisposed individuals. However, what distinguishes keloids is not only the abnormal quantity of collagen formation but also the physical extent of it. Clinically, keloids differ from hypertrophic scars in that they extend beyond the boundaries of the initial injury by invading surrounding healthy skin at the level of the dermis and fail to regress over time.3 An increase in inflammatory markers, such as transforming growth factor β1, and elevated levels of extracellular matrix (ECM) components, such as fibronectin and certain proteoglycans, are also associated with the formation of keloid lesions.49
Currently available treatments for keloid lesions include combinations of steroid injections, surgical removal, silicone gels meant to hydrate keratinocytes with the aim of altering growth factor secretion, and radiation therapy.4,10 Although surgical removal of keloids can offer temporary cosmetic improvement, the surgical resection itself is often a trigger for the aberrant wound healing, thus risking more keloid formation, sometimes even extending into previously unaffected skin. In addition, steroid injections and radiation therapy are not free of potential adverse effects and are often also associated with recurrences.
Various hypotheses have been proposed to explain the pathogenesis of this disease, including abnormal regulation from the surrounding ECM proteins and irregularity in the enzymes that monitor ECM degradation and cellular migration.4 Matrix metalloproteinases (MMPs) are composed of a family of enzymes that are hypothesized to be involved in the keloid disease state because of their abnormal expression and activity, thus severely altering the remodeling process.11 Because of their important role in regulating connective tissue growth and wound healing, MMPs are considered potential targets in the treatment of keloids. However, studies so far have drawn conflicting conclusions regarding the upregulation or downregulation of these remodeling proteases in keloid formation. Common to all of these studies is the use of a monolayer cell culture. We believe that given the multidimensional nature of keloid physiology, a 3-dimensional cell culture system would better mimic the true environment of keloid formation and that, in fact, the use of monolayer cell culture may be contributing to this variation.1113 Therefore, in this research, we applied tissue engineering strategies to create 3-dimensional in vitro disease models to analyze the changes in MMP gene expressions between normal and keloid fibroblasts. Two biomaterial systems were implemented for the models, and through one of the models, the therapeutic effects of an ECM modulator on the diseased fibroblast were also investigated, setting the precedence for future keloid studies with different ECM modulators. Lastly, the differences in remodeling markers from site-specific keloid fibroblasts were also analyzed to address the heterogeneity observed in the phenotypes of fibroblasts from keloid lesions.
Keloid Fibroblasts
Keloid fibroblasts were provided by Bindi Naik, MD, of Baylor College of Medicine and one of us (K. B.). Briefly, the isolation method involved rinsing keloid lesions thoroughly with phosphate-buffered saline solution containing penicillin, 100 U/mL, and streptomycin, 100 μg/mL (PBS-PS), on receipt. The epidermal layer was removed, whereas the dermis layer was minced before being placed in the collagenase digestion solution. The solution was composed of high-glucose Dulbecco modified Eagle medium (Invitrogen) with 10% fetal bovine serum (Hyclone), with a final concentration of 5 mg/mL of type 2 collagenase (Worthington) and 0.2 mg/mL of trypsin (Fluka). The minced explants were digested at 37°C with 5% carbon dioxide for 6 hours on an orbital shaker. The collagenase filtrate was then filtered with a 40-µm strainer and rinsed with PBS-PS 3 times before being plated in T-175 flasks with fibroblast media (FM). For encapsulation in biomaterials, all keloid fibroblasts were cultured in monolayer for 1 passage until confluency with FM. For lesion site–specific comparison, no monolayer expansion of keloid fibroblasts was performed.
Normal Skin Fibroblasts
As a control, normal human foreskin fibroblasts (HS27) were obtained from American Type Culture Collection and cultured in monolayer between 1 and 2 passages until confluency in FM before encapsulation in biomaterials. For lesion site–specific comparison, normal fibroblasts were isolated from a female patient who underwent an elective upper eyelid skin excision (blepharoplasty).
Medium Condition
The FM consisted of high-glucose Dulbecco modified Eagle medium (Invitrogen) with 10% fetal bovine serum and penicillin, 100 U/mL, and streptomycin, 100 μg/mL.
PEG-Col1 In Vitro Experiment
The first in vitro design used polyethylene glycol diacrylate (PEGDA) and type I bovine collagen (PEG-ColI) as the polymer to encapsulate the fibroblasts (Figure 1A). Type I collagen was neutralized with 0.1N sodium hydroxide and then brought up to 2 mg/mL with PBS-PS. A 20% PEGDA solution in PBS-PS was mixed with the 2 mg/mL of type I collagen (BD Bioscience) to create constructs with the final concentrations of 10% PEGDA and 1 mg/mL of type I collagen. Fibroblasts, either keloid or normal (HS27), were mixed with the polymer solution at the concentration of 20 million cells/mL and then mixed with the photoinitiation Irgacure 2959 (Ciba) for a final concentration of 0.05% (wt/vol). Using UV light, the constructs of polymer-cell-photoinitiator were photopolymerized for 5 minutes at 3 mW/cm2 and a 365-nm wavelength in cylindrical molds with a diameter of 5 mm. On encapsulation, the constructs were transferred to 24-well plates and cultured with 1.5 mL of FM for a total of 14 days. Constructs were harvested at days 2, 7, and 14 for data analysis. Medium was changed every 2 to 3 days until the time of harvest.
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Figure 1.
Type I Bovine Collagen In Vitro Model
Letters indicate statistical significance from HS27 at corresponding time point (P < .05e and P < .001d); plus signs, statistical significance from day 2 of same cell type (P < .05c, P < .01a, and P < .001b). A, Schematic of type I bovine collagen in vitro model. Polyethylene glycol diacrylate (PEGDA) was mixed with type I collagen fibrils before encapsulation of fibroblasts (HS27 and keloid fibroblasts) through UV photopolymerization. B, Reverse transcription–polymerase chain reaction demonstrated that keloid fibroblasts had increased type I collagen gene expression compared with normal fibroblasts. C, DNA quantification normalized to dry weight indicated decreasing trend over time. D, Glycosaminoglycan (GAG) content by both fibroblast types normalized to DNA demonstrated increased GAG production from keloid fibroblasts. E, Total collagen content by both cell types normalized to DNA also demonstrated increased collagen content from keloid fibroblasts.
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Matrigel In Vitro Experiment
The second in vitro model involved encapsulating fibroblasts in Matrigel (BD Bioscience). Cell density was 2 million cells per 100 μL of Matrigel, which was then incubated at 37°C for 30 minutes. Once gelation was achieved, the constructs were cultured in 24-well plates with 1.5 mL of FM per construct for a total of 21 days. Constructs were harvested at days 1, 7, and 21 for data analysis. In addition to the Matrigel constructs composed of keloid fibroblasts or HS27, a third group of constructs with encapsulated keloid fibroblasts were cultured with the addition of decorin, 5 μg/mL (Sigma), which was administered with every medium change, starting after 1 day of culture. Medium was changed every 2 to 3 days until the time of harvest.
Biochemical Analyses
Biochemical data included DNA content, proteoglycan content, and total collagen content. Harvested constructs were lyophilized for 48 hours and then measured for their dry weights. In preparation for all 3 assays, lyophilized constructs were homogenized in papain digestion buffer from Worthington Biomedical and then incubated at 60°C for 16 to 18 hours. The DNA quantity for each construct was determined by measuring fluorescence with the low-assay Hoechst 33258 dye from Molecular Probes. Briefly, the dye was mixed with 10mM Tris, 1mM EDTA, and 0.2M sodium chloride buffer at pH 7.4 to reach a final concentration of 0.1 μg/mL. Varying concentrations of the calf thymus DNA (Invitrogen) were mixed with the low-assay solution to generate the standard curve. Total DNA quantities for each construct were measured from mixing the low-assay solution with 5 μL of the papain-digested samples. Fluorescence intensities were measured on a fluorometer at 365-nm excitation and 458-nm emission.
The glycosaminoglycan (GAG) content was determined through the dimethylmethylene blue assay, which consisted of the dimethylmethylene blue dye mixed with standard and experimental samples. Varying concentrations of chondroitin sulfate C were used to generate the standard curve, whereas 50 μL of papain-digested samples was used to calculate the total GAG content per construct. The absorbance was measured at 525 nm on an UV-Vis spectrophotometer.
The hydroxyproline assay was used to measure total collagen content. Papain-digested samples were hydrolyzed for 18 hours at 115°C in 12N hydrochloride. After hydrolyzation, samples were mixed with methyl red, titrated with sodium hydroxide and hydrochloride, and then diluted with deionized water to reach the volume of 1 mL. Trans-4 hydroxy-l-proline (Sigma-Aldrich) was dissolved in deionized water to generate the standard curve. Both the standards and diluted samples were mixed with chloramine-tosylchloramide hydrate and p-dimethylaminobenzaldehyde and then incubated in 60°C for 30 minutes. Absorbance values were measured at 550 nm on a UV-Vis spectrophotometer, and the ratio of 1:10 hydroxyproline to collagen was used to calculate total collagen content.
RNA Extraction and RT-PCR
Harvested constructs were homogenized in TRIzol Reagent (Invitrogen) in preparation for total RNA extraction. The protocol accompanying the reagent was followed for the extraction. Complementary DNA was then synthesized using the reverse transcriptase Superscript First-Strand Synthesis kit (Invitrogen). Reverse transcription–polymerase chain reaction (RT-PCR) was performed with Taq recombinant polymerase or with SYBR Green PCR Master Mix (Applied Biosystems) and conducted on the ABI Prism 7700 Sequence Detection System (Perkin Elmer/Applied Biosystems). Amplicons of RT-PCR were mixed with a loading dye and then run on 2% agarose gels in Tris, acetic acid, and EDTA buffer within an electrophoresis box with an accompanying ladder dye. Pictures of the gels were taken after submerging them in diluted ethidium bromide and exposing them to UV light. The following genes were analyzed: type I collagen, MMP1, MMP2, MMP3, MMP9, MMP13, and MT1-MMP. All genes were normalized to the β-actin housekeeping gene. The MMP primers are listed in the article by Konttinen et al.14 Type I collagen primers are F-TGACGAGACCAAGAACTG and R-CCATCCAAACCACTGAAACC, and β-actin primers are F-TGGCACCACACCTTCTACAATGAGC and R-GCACAGCTTCTCCTTAATGTCACGC.
Statistical Analysis
All analyses were performed in triplicate and analyzed with the t test for pairwise comparison. Statistical significance was set at P <.05.
Verification of PEG-Col1 Model
Constructs were harvested at days 2, 7, and 14 for both normal (HS27) and keloid fibroblasts, and RT-PCR demonstrated higher expressions of type I collagen from keloid fibroblasts at all 3 time points (Figure 1B). This finding confirms that the altered phenotype that is associated with keloid disease is retained in this 3-dimensional PEG-Col1 model.
Matrix Production From Fibroblasts in the PEG-Col1 Model
Both HS27 and keloid fibroblasts demonstrated a decrease in DNA quantification during a span of 14 days in 3-dimensional culture (Figure 1C). However, at all time points, the GAG and total collagen production was significantly higher in keloid fibroblasts compared with normal fibroblasts (Figure 1, D and E). Specifically, there was a mean 2.02-fold increase in GAG per DNA and a 3.43-fold increase in total collagen per DNA in keloid fibroblasts.
MMP Gene Expression in Fibroblasts in the PEG-Col1 Model
The RT-PCR for MMP1, MMP2, MMP3, MMP9, MMP13, and MT1-MMP indicated that there were no significant differences between normal and keloid fibroblasts over time (Figure 2). MMP1, MMP2, MMP3, and MT1-MMP were consistently expressed in both fibroblast types at all time points. MMP9 and MMP13 decreased in expression in both HS27 and keloid fibroblasts as time increased.
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Figure 2.
Reverse Transcription–Polymerase Chain Reaction of MMP Gene Expressions From Normal and Keloid Fibroblasts in the PEG-Col1 Model
No obvious differences in trends were observed between HS27 and keloid fibroblasts. β-Actin was the housekeeping gene.
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Verification of the Matrigel Model
Constructs were harvested at days 1, 7, and 21, and as with the PEG-Col1 model, type I collagen was more strongly expressed by keloid fibroblasts than HS27 at all time points, indicating that the keloid disease phenotype is maintained in the Matrigel model (Figure 3, A and B).
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Figure 3.
Matrigel In Vitro Model
Letters indicate statistical significance from HS27 at corresponding time point (P < .05c, P < .01e, and P < .001b); plus signs, statistical significance from day 1 of same cell type (P < .05a, P < .01d, and P < .001f). A, Schematic of 3-dimensional Matrigel constructs. B, Reverse transcription–polymerase chain reaction of type I collagen from both HS27 and keloid fibroblasts after culture in Matrigel demonstrates the expected higher gene expression from keloid fibroblasts. C, DNA content decreased in both fibroblast types as time increased. D, Glycosaminoglycan (GAG) content was more significantly produced from keloid fibroblasts than HS27, resulting in a time-dependent increase. E, Total collagen content normalized to DNA also demonstrated more extracellular matrix production from keloid fibroblasts than HS27.
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Matrix Production From Fibroblasts in the Matrigel Model
As with the PEG-Col1 model, there was a decrease in DNA quantification as the time increased for both HS27 and keloid fibroblasts (Figure 3C). Both GAG and total collagen were produced in significantly greater amounts in keloid fibroblasts than in normal cells (Figure 3, D and E). Specifically, keloid fibroblasts produced 1.37-fold, 1.56-fold, and 2.08-fold more GAG per DNA than HS27 at days 1, 7, and 21, respectively. There was a time-dependent increase in GAG production in both normal and diseased fibroblasts; however, the fold changes from keloid fibroblasts were significantly higher than HS27. The trend for total collagen per DNA was similar to the GAG data. Keloid fibroblasts produced more matrix than HS27 at days 7 and 21, although this finding was not statistically significant. In addition, there was markedly more collagen at day 21 than day 1 from the keloid fibroblasts.
MMP Gene Expression in Fibroblasts in the Matrigel Model
MMP1, MMP2, MMP3, and MT1-MMP were consistently expressed in both HS27 and keloid fibroblasts in the Matrigel model at all time points (Figure 4). HS27 expressed little to no MMP9 and MMP13, whereas keloid fibroblasts increased expression of both MMP genes over time.
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Figure 4.
Reverse Transcription–Polymerase Chain Reaction of MMP Gene Expressions From Normal and Keloid Fibroblasts After In Vitro 3-Dimensional Culture in Matrigel
Significant differences were observed in MMP9 and MMP13 gene expressions between HS27 and keloid fibroblasts. β-Actin was the housekeeping gene.
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Effects of Decorin on Matrix Production in Keloid Fibroblasts in the Matrigel Model
Decorin was exogenously added into the medium of keloid fibroblasts encapsulated in Matrigel from day 1 to day 21. At days 7 and 21, constructs were harvested after treatment with decorin. There was a decrease in DNA quantification as time increased, whether decorin was added or not (Figure 5A). Dimethylmethylene blue assay demonstrated that, at day 21, the quantities of GAG per DNA were the same at day 7 and day 21 when keloid fibroblasts were exposed to decorin (Figure 5B). This resulted in significantly less GAG per DNA at day 21 in keloid fibroblasts that were exposed to decorin compared with keloid fibroblasts that were not exposed to decorin. Quantification of total collagen per DNA also demonstrated a similar trend as the GAG data, although the finding was not statistically significant (Figure 5C).
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Figure 5.
Effect of Decorin on Keloid Fibroblasts in the Matrigel Model
Letters indicate statistical significance from HS27 at corresponding time point (P < .01b); plus signs, statistical significance from day 7 of same cell type (P < .001a). A, DNA quantification normalized to respective dry weights indicated decrease in both conditions as time increased. B, Glycosaminoglycan (GAG) content normalized to DNA demonstrated that the presence of decorin prevented an increase in the matrix component production. C, Total collagen content normalized to DNA demonstrated a similar trend as the GAG data, although not statistically significant. D, Reverse transcription–polymerase chain reaction of type I collagen and MMP genes that were affected by the presence of decorin administered to keloid fibroblasts. Significant downregulations in type I collagen, MMP1, and MMP13 were observed at day 21, whereas MMP9 retained the same expression as day 7 and was prevented from being upregulated.
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Effects of Decorin on Gene Expression From Keloid Fibroblasts
Type I collagen gene expression was significantly downregulated at day 21, when decorin was administered to keloid fibroblasts (Figure 5D). In addition, MMP1 and MMP13 were also significantly decreased at day 21 when keloid fibroblasts were treated with decorin. MMP9 did not change significantly in gene expression between day 7 and day 21 when keloid fibroblasts were treated with decorin, and this differed from untreated fibroblasts for which an increase in MMP9 was observed by day 21.
MMP Gene Expression From Specific Sites of Keloid Lesion
Two keloid lesions were received from one patient; one lesion was removed from the shoulder and the other from the ear. Because of the small size of the auricle lesion, the enzymatic isolation resulted in a mix of fibroblasts that were not separated by tissue depth and thus were labeled as “mixed auricle.” The lesion from the shoulder was separated into 4 different sites: superficial side fibroblasts, superficial center fibroblasts, deep center fibroblasts, and keratinocytes (Figure 6A). The MMP gene expressions were analyzed among the different cell populations, both shoulder and auricle, and compared with normal fibroblasts that were isolated from the skin of a patient who underwent eyelid skin excision.
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Figure 6.
Site-Specific Gene Expressions
A, Different sites from which keloid fibroblasts were isolated from the shoulder lesion for comparison of MMP gene expressions among the different sites: i, superficial side; ii, superficial center; iii, deep center; and iv, keratinocytes. Keratinocytes were also isolated from the shoulder lesion. B, Reverse transcription–polymerase chain reaction of MMP gene expressions from primary fibroblasts isolated from different sites of a keloid lesion and compared with the corresponding keratinocytes that lined the epidermis of the lesion, a mixed fibroblast population from the ear, and normal fibroblasts isolated from an eyebrow lift. Fibroblasts from regions closest to the margins of the original wound and the excision site (ie, superficial side and deep center) had higher expressions of MMP1, MMP2, MMP3, and MMP9 compared with those farthest away from the wound boundaries (superficial center). Keratinocytes also expressed the same 4 MMP genes, although at lower intensities, when compared with the superficial side and deep center. The mixed keloid fibroblast had high expressions of MMP genes, whereas normal fibroblasts demonstrated little to no expression of the enzymes.
Graphic Jump Location
Normal fibroblasts demonstrated little to no expression of all MMP genes tested (Figure 6B). In comparing the fibroblasts isolated from the shoulder, the superficial side and deep center had the highest expressions of MMP1, MMP2, MMP3, MMP9, and MT1-MMP. The superficial center fibroblasts had little to no expression of those MMP genes. All fibroblasts from the shoulder had little to no expression of MMP13. The keratinocytes also expressed MMP2 and MMP3 with comparable intensities to superficial center fibroblasts and slightly higher expressions of MMP1 and MMP9 than the superficial center fibroblasts. The mixed auricle fibroblasts had high expressions of all tested MMP genes, including MMP13.
Keloids remain a clinical challenge and a source of significant psychological distress to patients who can have grossly disfiguring and painful lesions. Current treatment recommendations reflect individual clinician experiences. The incomplete understanding of keloid pathophysiology is in part due to a lack of an animal model, preventing in vivo investigation of this disease. As stated previously, various hypotheses have been proposed to explain the pathogenesis of the disease. One of the hypotheses involves the state of MMP activity in keloid disease, of which the literature has reported conflicting results. For example, Seifert et al12 observed a downregulation of MMP3 from keloid fibroblasts when compared with normal cells, whereas Fujiwara et al11 observed a several-fold increase in production of MMP1 and MMP2. Both of these studies analyzed results after monolayer culture, which could potentially explain this discrepancy. Therefore, in the first part of this experiment, we studied keloid fibroblasts in their more native 3-dimensional environment and observed how MMP gene expressions in keloid fibroblasts vary from normal fibroblasts. Through the 3-dimensional models, we also evaluated the ECM produced by diseased and normal fibroblasts in vitro and observed the effects of an exogenously administered proteoglycan, decorin, known to have growth factor–regulating properties.
In the first model, fibroblasts were encapsulated in the hydrogel polymer PEGDA. Because fibroblasts possess adherent properties and polyethylene glycol alone does not promote cellular adhesion, type I collagen fibrils were incorporated into PEGDA to create a semi-interpenetrating network. In addition, the presence of type I collagen fibrils better mimicked what the fibroblasts sense in their native environment within connective tissue, in addition to promoting cellular adhesion. Although in vitro encapsulation of both normal and diseased fibroblasts resulted in type I collagen gene expression at all 3 time points of harvest, keloid fibroblasts expressed significantly more type I collagen than HS27, thus indicating that the diseased fibroblasts in this 3-dimensional model maintain their diseased phenotype in vitro. Biochemical analysis also indicated that at all 3 time points diseased fibroblasts had higher rates of ECM production than normal fibroblasts. Therefore, keloid fibroblasts in this 3-dimensional model still exhibited their diseased characteristics not only in gene expression but also in actual matrix synthesis.
Interestingly, not a lot of differences were found in MMP gene expressions between normal and keloid fibroblasts when cultured in the PEG-Col1 3-dimensional model. In general, most of the analyzed MMP genes were expressed consistently through all time points for both fibroblast types. However, both MMP9 (gelatinase B) and MMP13 (collagenase 3) were strongly expressed at day 2 for both cell types and then downregulated as time increased. Although this finding suggested that MMP9 and MMP13 are potential therapeutic targets, more research is needed to confirm these results.
In creating the next in vitro 3-dimensional model for further analysis of keloid disease, we focused on implementing a material that would better mimic the diseased environment. Matrigel is a heterogeneous basement membrane protein mixture secreted by cells from mouse sarcoma and commercialized by BD Bioscience. It resembles the ECM of various connective tissues, and it is composed of different matrix components, such as gelatin, fibronectin, laminin, type IV collagen, and various growth factors. Matrigel has been commonly used for the study of cellular attachment and differentiation and especially the study of tumor cell invasion.1517 In addition, connective tissue diseases have been associated with keloids.18,19 Therefore, Matrigel was used in our second 3-dimensional in vitro model to encapsulate keloid fibroblasts for further characterization of the diseased cells.
Similar to the PEG-Col1 model, type I collagen was expressed strongly by keloid fibroblasts and weakly by normal fibroblasts when the cells were cultured in Matrigel. Keloid fibroblasts also produced more GAG and total collagen per DNA than HS27, thus demonstrating that culturing the diseased fibroblasts in Matrigel maintained their excessive synthetic activity state. Interestingly, more significant differences were observed with GAG production than collagen production, with higher-fold changes in GAG per DNA from the diseased fibroblasts as time increased. The literature has cited higher concentrations of proteoglycans from healing wounds on animal models and different types of tumors removed from patients and overexpression of various proteoglycans, such as chondroitin sulfate, versican, and dermatan sulfate, through microarray.20 Therefore, the increase in GAG production per DNA from the keloid fibroblasts in the Matrigel model is in accord with the benign tumorlike characteristic of keloids. In addition, the continuous increase in GAG production from the keloid fibroblasts suggests that the diseased cells have an abnormal phenotype that retains them in a perpetual healing stage, which could be the cause of the excessive fibroproliferation of the lesions.
The MMP gene analysis from the Matrigel model demonstrated that MMP1, MMP2, MMP3, and MT1-MMP were generally consistently expressed from both HS27 and keloid fibroblasts at all time points, similar to the trends observed with the PEG-Col1 model. However, significant differences were observed in MMP9 and MMP13. Although there was little to no expression of either MMP gene from the normal fibroblasts at any time point, keloid fibroblasts expressed more MMP9 and MMP13 as time increased. Therefore, the data from the Matrigel model suggest that the gelatinase and collagenase are 2 main players in the progression of keloid lesions through an upregulation of MMP gene expression that potentially stimulate more remodeling of the wound and thus result in excessive tissue formation. In addition, because both MMP genes were upregulated in expression as time increased, this finding indicates that the 2 proteases potentially function in parallel within keloid lesions.
The difference observed in the MMP gene expression changes between the 2 different biomaterial models supports the hypothesis that the surrounding ECM has an important role in the keloid pathogenesis. Another hallmark of the keloid ECM is the lack of structural organization in the scar formation. Therefore, we hypothesized that treating the diseased cells with a molecule that promotes orderly ECM arrangement could be a therapeutic treatment for the disease. Decorin is a form of GAG that functions to maintain skin integrity and structural organization by binding to collagen fibrils. Yeo et al20 observed that healing skin has significantly less decorin than normal skin and that connective tissue from normal human breast stained strongly for decorin, whereas Reed and Iozzo21 observed irregular collagen fibrils in decorin knockout mice. In our study, decorin was administered exogenously to keloid fibroblasts with every medium change in an attempt to produce a more organized ECM rather than the random arrangement that is characteristic of keloid ECM. After 21 days, although untreated keloid fibroblasts increased GAG production from day 7, those that were treated with decorin maintained the same content of GAG per DNA, suggesting that the presence of decorin prevented the diseased fibroblasts from producing more GAG. In addition, a similar trend was observed when quantifying total collagen per DNA at day 21 when untreated keloid fibroblasts produced more of the matrix than treated fibroblasts. We hypothesize that the presence of decorin bound to the collagen fibrils in the surrounding environment of the keloid fibroblasts, which resulted in a more organized arrangement of the ECM and thus downregulated ECM production.
In addition, type I collagen and MMP gene expressions were affected by the presence of decorin. Type I collagen, MMP1, and MMP13 were significantly downregulated in expression at day 21 after continuous treatment with decorin, whereas MMP9 expression was maintained from day 7 to day 21 without the increase that was observed from untreated fibroblasts. This finding suggests that an increase in MMP expression is associated with the growth of a keloid lesion and that the presence of a GAG that enhances structural organization could downregulate the expressions of the MMP genes. Furthermore, we observed that an increased expression of MMP genes coincides with excessive ECM deposition, which also supports the idea that targeting MMP genes can therapeutically regulate ECM production.
Heterogeneity is another characteristic of keloid disease that renders it a challenge to fully elucidate the mechanisms that govern its pathogenesis. Specifically, differences are observed in cell behavior and phenotype, depending on the region of keloids from which the cells were derived. Lu et al22 demonstrated that most fibroblasts derived from the periphery of keloid lesions were in a proliferative state, whereas fibroblasts isolated from the central region of keloids were generally in the quiescent phase. A study by Sayah et al23 demonstrated that the apoptotic indices were different between peripheral fibroblasts and central fibroblasts. A 2008 published work on monolayer culture by Seifert et al12 suggested that site specificity of fibroblast isolation can affect how gene expressions are observed. The heterogeneity demonstrated by these works on site specificity could also potentially explain the varying results that have been observed on differing MMP gene expressions, in addition to the monolayer cultures. Therefore, to study the changes in MMP gene expression due to site specificity, we isolated primary fibroblasts from different regions of a keloid lesion and compared the MMP gene expressions to a mixed keloid cell population and to a normal cell population. Fibroblasts were isolated from the dermis of a shoulder lesion and separated into 3 regions as depicted in Figure 6A. There were higher MMP gene expressions from the regions of the lesion that were closer to the margins of the original wound (ie, superficial side) and the region within the deep center of the keloid. The fibroblasts from the superficial periphery and the deep center strongly expressed MMP1, MMP2, MMP3, and MMP9 when compared with the superficial center fibroblasts. The cells isolated from the ear consisted of a mixed fibroblast population and strongly expressed all tested MMP genes, whereas fibroblasts from normal skin generated very little to no expression. These data suggest that fibroblasts that are closer to the margins of the original wound, where active cellular migration and reepithelialization occur, have higher MMP gene expression, which could have a role in stimulating more tissue remodeling, thus resulting in excessive growth. In addition, literature has cited that interactions between keratinocytes and fibroblasts are important in the process of wound healing, and the presence of keloid keratinocytes can increase fibroblast proliferation and the secretion of soluble collagen types I and III.24,25 Therefore, we also compared differences in the protease gene expression between keloid fibroblasts and keloid keratinocytes derived from the shoulder lesion. However, the keratinocytes did not express the MMP genes with as much intensity as some of the fibroblast population, thus indicating that the fibroblasts within the dermis of the keloid lesion are most likely the predominant contributors in higher MMP gene expressions.
In conclusion, our in vitro data demonstrate that MMP9 and MMP13 are 2 potential targets in therapeutically treating keloid lesions. Their concurrent expressions from the Matrigel 3-dimensional disease model suggest that they enhance the expressions of each other, thus promoting the growth of keloid lesions. Through manipulating the ECM, we observed that molecules that target organization of the lesion’s matrix can possibly be beneficial in downregulating increased markers during the disease. Site specificity of fibroblasts from keloid lesions have demonstrated different intensities of MMP gene expressions, thus further supporting the heterogeneity that is observed in keloid fibroblast phenotype. These studies set the precedent for future tissue engineering studies to better elucidate the keloid pathogenesis.
Accepted for Publication: January 27, 2013.
Corresponding Author: Kofi Boahene, MD, Department of Otolaryngology–Head and Neck Surgery, The Johns Hopkins University, Baltimore, MD 21231 ([email protected]).
Published Online: September 19, 2013. doi:10.1001/jamafacial.2013.1211.
Author Contributions:Study concept and design: Elisseeff, Boahene, Li, Nahas.
Acquisition of data: Li, Nahas, Feng.
Analysis and interpretation of data: Elisseeff, Boahene, Li, Nahas.
Drafting of the manuscript: Boahene, Feng, Li, Nahas.
Critical revision of the manuscript for important intellectual content: Elisseeff, Boahene, Li, Nahas.
Obtained funding: Elisseeff.
Study supervision: Elisseeff, Boahene.
Conflict of Interest Disclosures: None reported.
Additional Contributions: Bindi Naik, MD, of Baylor College of Medicine, provided keloid fibroblasts; Dr Boahene provided additional keloid fibroblasts enzymatically isolated from the dermal layer of lesions removed from consenting patients at The Johns Hopkins Hospital.
Clark RA, Ghosh K, Tonnesen MG. Tissue engineering for cutaneous wounds. J Invest Dermatol. 2007;127(5):1018-1029.
PubMed | Link to Article
Pollack SV. Wound healing: a review, I: the biology of wound healing. J Dermatol Surg Oncol. 1979;5(5):389-393.
PubMed
Tredget EE, Nedelec B, Scott PG, Ghahary A. Hypertrophic scars, keloids, and contractures: the cellular and molecular basis for therapy. Surg Clin North Am. 1997;77(3):701-730.
PubMed | Link to Article
Al-Attar A, Mess S, Thomassen JM, Kauffman CL, Davison SP. Keloid pathogenesis and treatment. Plast Reconstr Surg. 2006;117(1):286-300.
PubMed | Link to Article
Younai S, Nichter LS, Wellisz T, Reinisch J, Nimni ME, Tuan TL. Modulation of collagen synthesis by transforming growth factor-beta in keloid and hypertrophic scar fibroblasts. Ann Plast Surg. 1994;33(2):148-151.
PubMed | Link to Article
Bettinger DA, Yager DR, Diegelmann RF, Cohen IK. The effect of TGF-beta on keloid fibroblast proliferation and collagen synthesis. Plast Reconstr Surg. 1996;98(5):827-833.
PubMed | Link to Article
Kischer CW, Wagner HN Jr, Pindur J, et al. Increased fibronectin production by cell lines from hypertrophic scar and keloid. Connect Tissue Res. 1989;23(4):279-288.
PubMed | Link to Article
Alaish SM, Yager DR, Diegelmann RF, Cohen IK. Hyaluronic acid metabolism in keloid fibroblasts. J Pediatr Surg. 1995;30(7):949-952.
PubMed | Link to Article
Hunzelmann N, Anders S, Sollberg S, Schönherr E, Krieg T. Co-ordinate induction of collagen type I and biglycan expression in keloids. Br J Dermatol. 1996;135(3):394-399.
PubMed | Link to Article
Chen MA, Davidson TM. Scar management: prevention and treatment strategies. Curr Opin Otolaryngol Head Neck Surg. 2005;13(4):242-247.
PubMed | Link to Article
Fujiwara M, Muragaki Y, Ooshima A. Keloid-derived fibroblasts show increased secretion of factors involved in collagen turnover and depend on matrix metalloproteinase for migration. Br J Dermatol. 2005;153(2):295-300.
PubMed | Link to Article
Seifert O, Bayat A, Geffers R, et al. Identification of unique gene expression patterns within different lesional sites of keloids. Wound Repair Regen. 2008;16(2):254-265.
PubMed | Link to Article
Uchida G, Yoshimura K, Kitano Y, Okazaki M, Harii K. Tretinoin reverses upregulation of matrix metalloproteinase-13 in human keloid-derived fibroblasts. Exp Dermatol. 2003;12(suppl 2):35-42.
PubMed | Link to Article
Konttinen YT, Ainola M, Valleala H, et al. Analysis of 16 different matrix metalloproteinases (MMP-1 to MMP-20) in the synovial membrane: different profiles in trauma and rheumatoid arthritis. Ann Rheum Dis. 1999;58(11):691-697.
PubMed | Link to Article
Ma L, Teruya-Feldstein J, Weinberg RA. Tumour invasion and metastasis initiated by microRNA-10b in breast cancer. Nature. 2007;449(7163):682-688.
PubMed | Link to Article
Repesh LA. A new in vitro assay for quantitating tumor cell invasion. Invasion Metastasis. 1989;9(3):192-208.
PubMed
Lal A, Glazer CA, Martinson HM, et al. Mutant epidermal growth factor receptor up-regulates molecular effectors of tumor invasion. Cancer Res. 2002;62(12):3335-3339.
PubMed
Igarashi A, Nashiro K, Kikuchi K, et al. Connective tissue growth factor gene expression in tissue sections from localized scleroderma, keloid, and other fibrotic skin disorders. J Invest Dermatol. 1996;106(4):729-733.
PubMed | Link to Article
Leask A, Holmes A, Abraham DJ. Connective tissue growth factor: a new and important player in the pathogenesis of fibrosis. Curr Rheumatol Rep. 2002;4(2):136-142.
PubMed | Link to Article
Yeo TK, Brown L, Dvorak HF. Alterations in proteoglycan synthesis common to healing wounds and tumors. Am J Pathol. 1991;138(6):1437-1450.
PubMed
Reed CC, Iozzo RV. The role of decorin in collagen fibrillogenesis and skin homeostasis. Glycoconj J. 2002;19(4-5):249-255.
PubMed | Link to Article
Lu F, Gao J, Ogawa R, Hyakusoku H, Ou C. Biological differences between fibroblasts derived from peripheral and central areas of keloid tissues. Plast Reconstr Surg. 2007;120(3):625-630.
PubMed | Link to Article
Sayah DN, Soo C, Shaw WW, et al. Downregulation of apoptosis-related genes in keloid tissues. J Surg Res. 1999;87(2):209-216.
PubMed | Link to Article
Werner S, Krieg T, Smola H. Keratinocyte-fibroblast interactions in wound healing. J Invest Dermatol. 2007;127(5):998-1008.
PubMed | Link to Article
Lim IJ, Phan TT, Bay BH, et al. Fibroblasts cocultured with keloid keratinocytes: normal fibroblasts secrete collagen in a keloidlike manner. Am J Physiol Cell Physiol. 2002;283(1):C212-C222.
PubMed | Link to Article
Figures
Place holder to copy figure label and caption
Figure 3.
Matrigel In Vitro Model
Letters indicate statistical significance from HS27 at corresponding time point (P < .05c, P < .01e, and P < .001b); plus signs, statistical significance from day 1 of same cell type (P < .05a, P < .01d, and P < .001f). A, Schematic of 3-dimensional Matrigel constructs. B, Reverse transcription–polymerase chain reaction of type I collagen from both HS27 and keloid fibroblasts after culture in Matrigel demonstrates the expected higher gene expression from keloid fibroblasts. C, DNA content decreased in both fibroblast types as time increased. D, Glycosaminoglycan (GAG) content was more significantly produced from keloid fibroblasts than HS27, resulting in a time-dependent increase. E, Total collagen content normalized to DNA also demonstrated more extracellular matrix production from keloid fibroblasts than HS27.
Graphic Jump Location
Place holder to copy figure label and caption
Figure 4.
Reverse Transcription–Polymerase Chain Reaction of MMP Gene Expressions From Normal and Keloid Fibroblasts After In Vitro 3-Dimensional Culture in Matrigel
Significant differences were observed in MMP9 and MMP13 gene expressions between HS27 and keloid fibroblasts. β-Actin was the housekeeping gene.
Graphic Jump Location
Place holder to copy figure label and caption
Figure 2.
Reverse Transcription–Polymerase Chain Reaction of MMP Gene Expressions From Normal and Keloid Fibroblasts in the PEG-Col1 Model
No obvious differences in trends were observed between HS27 and keloid fibroblasts. β-Actin was the housekeeping gene.
Graphic Jump Location
Place holder to copy figure label and caption
Figure 1.
Type I Bovine Collagen In Vitro Model
Letters indicate statistical significance from HS27 at corresponding time point (P < .05e and P < .001d); plus signs, statistical significance from day 2 of same cell type (P < .05c, P < .01a, and P < .001b). A, Schematic of type I bovine collagen in vitro model. Polyethylene glycol diacrylate (PEGDA) was mixed with type I collagen fibrils before encapsulation of fibroblasts (HS27 and keloid fibroblasts) through UV photopolymerization. B, Reverse transcription–polymerase chain reaction demonstrated that keloid fibroblasts had increased type I collagen gene expression compared with normal fibroblasts. C, DNA quantification normalized to dry weight indicated decreasing trend over time. D, Glycosaminoglycan (GAG) content by both fibroblast types normalized to DNA demonstrated increased GAG production from keloid fibroblasts. E, Total collagen content by both cell types normalized to DNA also demonstrated increased collagen content from keloid fibroblasts.
Graphic Jump Location
Place holder to copy figure label and caption
Figure 5.
Effect of Decorin on Keloid Fibroblasts in the Matrigel Model
Letters indicate statistical significance from HS27 at corresponding time point (P < .01b); plus signs, statistical significance from day 7 of same cell type (P < .001a). A, DNA quantification normalized to respective dry weights indicated decrease in both conditions as time increased. B, Glycosaminoglycan (GAG) content normalized to DNA demonstrated that the presence of decorin prevented an increase in the matrix component production. C, Total collagen content normalized to DNA demonstrated a similar trend as the GAG data, although not statistically significant. D, Reverse transcription–polymerase chain reaction of type I collagen and MMP genes that were affected by the presence of decorin administered to keloid fibroblasts. Significant downregulations in type I collagen, MMP1, and MMP13 were observed at day 21, whereas MMP9 retained the same expression as day 7 and was prevented from being upregulated.
Graphic Jump Location
Place holder to copy figure label and caption
Figure 6.
Site-Specific Gene Expressions
A, Different sites from which keloid fibroblasts were isolated from the shoulder lesion for comparison of MMP gene expressions among the different sites: i, superficial side; ii, superficial center; iii, deep center; and iv, keratinocytes. Keratinocytes were also isolated from the shoulder lesion. B, Reverse transcription–polymerase chain reaction of MMP gene expressions from primary fibroblasts isolated from different sites of a keloid lesion and compared with the corresponding keratinocytes that lined the epidermis of the lesion, a mixed fibroblast population from the ear, and normal fibroblasts isolated from an eyebrow lift. Fibroblasts from regions closest to the margins of the original wound and the excision site (ie, superficial side and deep center) had higher expressions of MMP1, MMP2, MMP3, and MMP9 compared with those farthest away from the wound boundaries (superficial center). Keratinocytes also expressed the same 4 MMP genes, although at lower intensities, when compared with the superficial side and deep center. The mixed keloid fibroblast had high expressions of MMP genes, whereas normal fibroblasts demonstrated little to no expression of the enzymes.
Graphic Jump Location
Tables
References
Clark RA, Ghosh K, Tonnesen MG. Tissue engineering for cutaneous wounds. J Invest Dermatol. 2007;127(5):1018-1029.
PubMed | Link to Article
Pollack SV. Wound healing: a review, I: the biology of wound healing. J Dermatol Surg Oncol. 1979;5(5):389-393.
PubMed
Tredget EE, Nedelec B, Scott PG, Ghahary A. Hypertrophic scars, keloids, and contractures: the cellular and molecular basis for therapy. Surg Clin North Am. 1997;77(3):701-730.
PubMed | Link to Article
Al-Attar A, Mess S, Thomassen JM, Kauffman CL, Davison SP. Keloid pathogenesis and treatment. Plast Reconstr Surg. 2006;117(1):286-300.
PubMed | Link to Article
Younai S, Nichter LS, Wellisz T, Reinisch J, Nimni ME, Tuan TL. Modulation of collagen synthesis by transforming growth factor-beta in keloid and hypertrophic scar fibroblasts. Ann Plast Surg. 1994;33(2):148-151.
PubMed | Link to Article
Bettinger DA, Yager DR, Diegelmann RF, Cohen IK. The effect of TGF-beta on keloid fibroblast proliferation and collagen synthesis. Plast Reconstr Surg. 1996;98(5):827-833.
PubMed | Link to Article
Kischer CW, Wagner HN Jr, Pindur J, et al. Increased fibronectin production by cell lines from hypertrophic scar and keloid. Connect Tissue Res. 1989;23(4):279-288.
PubMed | Link to Article
Alaish SM, Yager DR, Diegelmann RF, Cohen IK. Hyaluronic acid metabolism in keloid fibroblasts. J Pediatr Surg. 1995;30(7):949-952.
PubMed | Link to Article
Hunzelmann N, Anders S, Sollberg S, Schönherr E, Krieg T. Co-ordinate induction of collagen type I and biglycan expression in keloids. Br J Dermatol. 1996;135(3):394-399.
PubMed | Link to Article
Chen MA, Davidson TM. Scar management: prevention and treatment strategies. Curr Opin Otolaryngol Head Neck Surg. 2005;13(4):242-247.
PubMed | Link to Article
Fujiwara M, Muragaki Y, Ooshima A. Keloid-derived fibroblasts show increased secretion of factors involved in collagen turnover and depend on matrix metalloproteinase for migration. Br J Dermatol. 2005;153(2):295-300.
PubMed | Link to Article
Seifert O, Bayat A, Geffers R, et al. Identification of unique gene expression patterns within different lesional sites of keloids. Wound Repair Regen. 2008;16(2):254-265.
PubMed | Link to Article
Uchida G, Yoshimura K, Kitano Y, Okazaki M, Harii K. Tretinoin reverses upregulation of matrix metalloproteinase-13 in human keloid-derived fibroblasts. Exp Dermatol. 2003;12(suppl 2):35-42.
PubMed | Link to Article
Konttinen YT, Ainola M, Valleala H, et al. Analysis of 16 different matrix metalloproteinases (MMP-1 to MMP-20) in the synovial membrane: different profiles in trauma and rheumatoid arthritis. Ann Rheum Dis. 1999;58(11):691-697.
PubMed | Link to Article
Ma L, Teruya-Feldstein J, Weinberg RA. Tumour invasion and metastasis initiated by microRNA-10b in breast cancer. Nature. 2007;449(7163):682-688.
PubMed | Link to Article
Repesh LA. A new in vitro assay for quantitating tumor cell invasion. Invasion Metastasis. 1989;9(3):192-208.
PubMed
Lal A, Glazer CA, Martinson HM, et al. Mutant epidermal growth factor receptor up-regulates molecular effectors of tumor invasion. Cancer Res. 2002;62(12):3335-3339.
PubMed
Igarashi A, Nashiro K, Kikuchi K, et al. Connective tissue growth factor gene expression in tissue sections from localized scleroderma, keloid, and other fibrotic skin disorders. J Invest Dermatol. 1996;106(4):729-733.
PubMed | Link to Article
Leask A, Holmes A, Abraham DJ. Connective tissue growth factor: a new and important player in the pathogenesis of fibrosis. Curr Rheumatol Rep. 2002;4(2):136-142.
PubMed | Link to Article
Yeo TK, Brown L, Dvorak HF. Alterations in proteoglycan synthesis common to healing wounds and tumors. Am J Pathol. 1991;138(6):1437-1450.
PubMed
Reed CC, Iozzo RV. The role of decorin in collagen fibrillogenesis and skin homeostasis. Glycoconj J. 2002;19(4-5):249-255.
PubMed | Link to Article
Lu F, Gao J, Ogawa R, Hyakusoku H, Ou C. Biological differences between fibroblasts derived from peripheral and central areas of keloid tissues. Plast Reconstr Surg. 2007;120(3):625-630.
PubMed | Link to Article
Sayah DN, Soo C, Shaw WW, et al. Downregulation of apoptosis-related genes in keloid tissues. J Surg Res. 1999;87(2):209-216.
PubMed | Link to Article
Werner S, Krieg T, Smola H. Keratinocyte-fibroblast interactions in wound healing. J Invest Dermatol. 2007;127(5):998-1008.
PubMed | Link to Article
Lim IJ, Phan TT, Bay BH, et al. Fibroblasts cocultured with keloid keratinocytes: normal fibroblasts secrete collagen in a keloidlike manner. Am J Physiol Cell Physiol. 2002;283(1):C212-C222.
PubMed | Link to Article
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3T3 Neutral Red Uptake Phototoxicity
The 3T3 Neutral Red Uptake (NRU) Phototoxicity assay is a 96-well cytotoxicity-based assay that utilizes normal BALB/c 3T3 mouse fibroblasts to measure the concentration-dependent reduction in neutral red uptake by the cells after exposure to a test material either in the presence or absence of UVA light. Duplicate 96-well monolayers of 3T3 fibroblasts are exposed to serial dilutions of a test material. One of the plates is exposed to 5 J/cm2 UVA while the other plate is kept in the dark. To assess viability, the neutral red uptake (NRU) by cells exposed to the test chemical in the presence of UVA exposure is compared to the NRU by cells exposed to the test chemical in the absence of UVA exposure.
Neutral Red (NR) is a weak cationic dye that readily diffuses through cell membranes and accumulates in cellular lysosomes. Once in the acidic environment of the lysosome, the NR is oxidized, becoming positively charged and trapped within the lysosome. Unless the cell or lysosome is damaged, the red dye remains trapped. Alterations to the cell membrane (caused by toxicity of the test material) are generally irreversible, resulting in the loss of the NR from the lysosome. For specific assay procedures, please see Step-by-Step.
Assay Design: Quick Facts
Assay Model: 3T3 cells seeded in duplicate 96-well plates
Endpoints: calculated using Phototox 2.0 software (supplied by ZEBET)
1. IC50 (the concentration of test material that causes a 50% decrease in viability, relative to the solvent control)
2. PIF (Photo-Irritation-Factor) compares the IC50 of treated cells in the presence of UVA exposure to the IC50 of treated cells in the absence of UVA exposure.
3. MPE (Mean Photo Effect) compares the response curve of treated cells in the presence of UVA exposure to the response curve of treated cells in the absence of UVA exposure.
For more information about testing your materials using this assay, please see Applications. Specialized protocols may be prepared as requested through consultation with an IIVS Study Director
3T3 NRU Phototoxicity Assay
3T3 NRU Phototoxicity Results
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Fibromyalgia Symptoms
Fibromyalgia and Autism: Is There a Connection
As more and more research is performed on fibromyalgia, we are finding that several other conditions that a person may suffer with are related to having fibromyalgia.
However, despite all the research that has been done, there are still tons of questions. These is still studies that are being performed on hypothesis and have yet to be duplicated, thus they are not considered concrete evidence just yet.
The connection between fibromyalgia and autism is present. It is not that the fibromyalgia is causing autism in a person. However, there is a connection that many people would not even dream of seeing.
This connection is that when you look at adults who suffer with fibromyalgia, you find that there are underlying processes in the body that is causing the pain and fatigue that they are feeling.
Those professionals who work with fibromyalgia adults are finding that these are the same processes they are seeing in children who have autism.
Ultimately, many medical professionals are finding that whatever it is that causes fibromyalgia and even CFS in adults, is the same that is happening in children who are diagnosed with autism.
The Relationship
After several rounds of research, many medical professionals are now able to shed light on just what the connection is between these two disorders.
The study parameters:
• This study treated 30 children who have autism
• These children were divided into 2 groups: one group was given a dose of 50 mg of L-carnitine for every kilogram of body weight, while the other was given a placebo.
• The children were given this medication for three months in order to monitor improvements
There were significant improvements in those kids who were taking L-carnitine. L-carnitine has also been shown to help with those who are suffering with CFS or Fibromyalgia as well.
Given that the same drug could help to treat both disorders along with autism, it shows that the connection between all these is strong.
What is L-Carnitine?
L-Carnitine or Carnitine as many people call it, is a substance that helps the body to turn fat into energy. Most people find that their body produces enough of this on their own.
However, as a medicine to give to fibromyalgia or autism patients, it acts as an antioxidant. When antioxidants are introduced into the body they can help to neutralize the free radicals in the body and help reduce or prevent damage that is caused by these free radicals.
For those who suffer with fatigue that causes them to lose their concentration or focus, L-Carnitine can give this back to them.
They often find that they are able to concentrate, the fatigue they feel is less, and many fibromyalgia patients report having less pain.
It can be a great supplement for those who are dealing with these issues day in and day out.
Shared Symptoms of Fibromyalgia and Autism
For those who are suffer with fibromyalgia, they often find that there are several symptoms that they struggle with on a day to day basis.
The same can be said of those who have autism. However, it takes many people some time to see that many of the symptoms are shared by both illness.
These shared symptoms include:
1. Aches and pains are seen all the time in fibromyalgia patients. However, those who have kids who do have autism will often find that they too may complain of a few aches and pains from time to time.
2. Sensitives to smells, textures and the like is something that both types of illnesses have in common.
3. The digestive issues! Many of those who suffer with fibromyalgia have IBS that affects everything that they do. The same can be said of those children who are suffering with autism. .
What many people are finding is that both of these illnesses are stemming from the mind. What is that causes these in people to begin with?
This is something that studies are working to figure out. However, it also leads to the question, could those who are diagnosed with fibromyalgia today been diagnosed with autism when they were younger? If these two illnesses were something that were talked about then?
For example, many people who have fibromyalgia now that are older often talk of issues they had when they were younger. These issues are often associated with having autism.
However, this term was not well known over twenty years ago. Instead, these people were given a diagnosis of having a learning disorder or simply being a problem child.
It has led many people to believe that autism as a child means you are more likely to develop fibromyalgia as an adult.
Fibromyalgia and Autism
Treating Fibromyalgia and Autism
With both if these illnesses, you are going to find that treatment is really trial and error. Why is this?
Sensitivities to medications is one of the biggest things that people are worrying about. Those who have either of these illnesses are often more sensitive than someone else.
Therefore, they must be careful about what they do and what they take. Most people find that homeopathic treatments are some of the best ways to treat this.
This may include:
• Getting enough exercise
• Taking various therapies such as physical therapy or massage therapy
• Trying to keep the outside world from becoming too much when dealing with sensitives to sound, light or textures
• Talking with others who may be suffering with the same issues
• Getting a good night’s sleep
• Trying to stick to a schedule at all times
The key to living with either of these illnesses is realizing that there is no cure. This is something that you are going to have to deal with for the rest of your life.
Thus, it is imperative to find a routine that works and that is going to let you have the most fulfilling life that you can have.
Talking and working with your doctor is the only way that you are going to get this type of help.
Comments
comments
3 Comments
• I am very interested in this topic and would like more information. Your article mentions research that has been done. Can you post links to these studies or post the titles and authors so I can learn more? Thank you.
• I was diagnosed with fibro 4 years ago and celiac 11 years ago. I just learned that there is a link from autism, to fibro, then it looks like they maybe there is a link to, M.S ….
• I was diagnosed with fibromyalgia at 21 years old after having my neurotypical son from a previous marriage. I was first tested for lupus because my great aunt has lupus and I was losing feeling in my legs. After I had my neurotypical son I had 2 boys on opposite ends of the spectrum and a neurotypical (so far) daughter. We had genetics tests that came back negative. My hubby and I both took the AQ test and Aspie quiz with both of us having higher than normal autistic tendencies. I wish I could know more about both fibro and autism.
Leave a Comment
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Huffpost Healthy Living
THE BLOG
Featuring fresh takes and real-time analysis from HuffPost's signature lineup of contributors
Leo Galland, M.D. Headshot
How to Boost Immunity After Exercise
Posted: Updated:
Print
You know that exercise is good for your health. But how does exercise affect immunity?
For people who are sedentary or get very little exercise, moderate physical activity can enhance immune function. (1) Yet intense physical training, at any level of fitness, could actually decrease immunity. (2)
Although exercise has many benefits, the physical strain of strenuous exercise tends to depress the immune system, which can be a problem for people who exercise intensely, even professional athletes. (3)
Enhancing the benefits of exercise and diminishing the stress of exercise is a prolific area of scientific research. This includes finding dietary supplements that can help maintain immunity following strenuous workouts.
Some studies provide exciting results for how supplements can help restore immunity after strenuous exercise, while others are inconclusive. (4)
It should be noted that most of the research was done on athletes, and how intense physical activity and the use of supplements affects them.
And since drinking enough water is a key part of exercise, I included information from an interesting study on how water consumption can impact mental performance.
As an avid mountain biker and swimmer, I find the following research to be fascinating.
Amino Acids Boost Recovery
Recent research done at two universities in Japan looked at how intense physical exercise effects immunity, and the effects of taking amino acids supplements. These studies indicate that the amino acids cysteine and theanine could help boost immunity and prevent infections for people engaging in intense physical activity.
A study done at the prestigious University of Tokyo found that intense physical training reduced activity of natural killer (NK) cells, which are a vital part of immune function. When the scientists gave athletes the supplements cysteine (700 mg) and theanine (280 mg) once daily for two weeks, they found that this helped to restore activity of their natural killer (NK) cells. (5)
In another Japanese study of endurance athletes, the researchers found that ten days of distance running (about 7 to 8 miles a day) resulted in an increase in blood levels of C-reactive protein, a marker of inflammation, and a decrease in the blood lymphocyte count, a marker of immunity. (6)
In a double blind, placebo-controlled trial, a group of athletes was given the same amounts of cysteine and theanine as in the study mentioned above.
For the athletes in this trial, the amino acids cysteine and theanine helped to:
• prevent exercised-induced inflammation,
• maintain immune function,
• prevent infections,
• and reduce symptoms of infections. (7)
Workout Recovery Supplement
Another amino acid, L-citrulline, known as citrulline, has been researched for its potential benefits as a workout recovery supplement and to help boost immunity after exercise.
Researchers at a university in Spain have found that citrulline can help preserve immune function after strenuous exercise. (8) This is important because the drop in immune function after exercise is associated with weakened function of white blood cells called PMN's, which are the body's first line of defense against infection.
The research team in Spain studied the effect of citrulline on white blood cell function in elite cyclists before and after a race. The cyclists who were given six grams of L-citrulline malate avoided the decline in PMN function caused by a 3-hour race, when compared to those taking a placebo. (9)
In research from France, citrulline was shown to help prevent post-exercise fatigue and muscle soreness in untrained athletes, when taken after exercise. (10) This study indicates the potential beneficial use of citrulline as a workout recovery supplement.
However, a study done at the Human Performance Laboratory at East Carolina University found that the use of citrulline before exercise may impair performance of untrained athletes. (11)
And don't forget about water.
While we are on the topic of exercise, I wanted to share with you an interesting study I came across on the importance of staying well hydrated for your workouts.
Research from Tufts University looks at how mild dehydration can affect mood and mental performance. The results of this study pose an interesting question: what happens when you don't get enough water in your day? It turns out that mood and performance could suffer as a result of dehydration.
The Tufts researchers focused on mental performance--how dehydration impacts the mood and cognition of young athletes. They took student athletes and formed two groups, the dehydrated group and the control group, and tested them after exercise. In examining mental performance they discovered that dehydration was associated with negative mood and impaired attention. (12)
According to the authors of the study, the mild dehydration witnessed by the student athletes could be similar to the mild dehydration experienced by people who don't drink enough water.
Now I'd like to hear from you...
How do you feel after exercising?
What do you do to recover from workouts?
Where do you learn about nutritional supplements?
Please let me know your thoughts by posting a comment below.
Best Health,
Leo Galland, MD
P.S. Get my free email newsletter and discover how medications and supplements interact at pilladvised.com
Leo Galland, M.D. is the Director of the Foundation for Integrated Medicine and founder of pilladvised.com, an online resource for learning about medications, supplements and food. Sign up for his weekly Pill Advised Newsletter, watch his videos on YouTube and join the Pill Advised Facebook page.
References
1) Proc Nutr Soc. 2010 Aug;69(3):390-9. Epub 2010 Jun 23. "Physical activity, immunity and infection." Romeo J, Warnberg J, Pozo T, Marcos A.
2) Med Sci Sports Exerc. 2000 Jul;32(7 Suppl):S369-76.
"Chronic exercise training effects on immune function." Mackinnon LT.
3) Biosci Biotechnol Biochem. 2009 Apr 23;73(4):817-21. "Effects of oral supplementation with cysteine and theanine on the immune function of athletes in endurance exercise: randomized, double-blind, placebo-controlled trial." Murakami S, Kurihara S, Koikawa N, Nakamura A, Aoki K, Yosigi H, Sawaki K, Ohtani M.
4) Romeo J., et al., Proc Nutr Soc. 2010 Aug;69(3):390-9
5) Strength Cond Res. 2010 Mar;24(3):846-51. "Cystine and theanine supplementation restores high-intensity resistance exercise-induced attenuation of natural killer cell activity in well-trained men."
Kawada S, Kobayashi K, Ohtani M, Fukusaki C.
6) Murakami, S. et al. Biosci Biotechnol Biochem. 2009 Apr 23;73(4):817-21
7) Ibid.
8) Free Radic Res. 2009 Sep;43(9):828-35. Epub 2009 Jul 6. "Effects of L-citrulline oral supplementation on polymorphonuclear neutrophils oxidative burst and nitric oxide production after exercise. Sureda A, Cordova A, Ferrer MD, Tauler P, Perez G, Tur JA, Pons A.
9) Ibid.
10) Arzneimittelforschung. 1991 Jun;41(6):660-3. "Activity of citrulline malate on acid-base balance and blood ammonia and amino acid levels: Study in the animal and in man." Callis A, Magnan de Bornier B, Serrano JJ, Bellet H, Saumade R.
11) Med Sci Sports Exerc. 2006 Apr;38(4):660-6. "L-citrulline reduces time to exhaustion and insulin response to a graded exercise test." Hickner RC, Tanner CJ, Evans CA, Clark PD, Haddock A, Fortune C, Geddis H, Waugh W, McCammon M
12) Percept Mot Skills. 2009 Aug;109(1):251-69. "Voluntary dehydration and cognitive performance in trained college athletes." D'Anci KE, Vibhakar A, Kanter JH, Mahoney CR, Taylor HA.
This information is provided for general educational purposes only and is not intended to constitute (i) medical advice or counseling, (ii) the practice of medicine or the provision of health care diagnosis or treatment, (iii) or the creation of a physician--patient relationship. If you have or suspect that you have a medical problem, contact your doctor promptly.
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Understanding and working with suicide risk | Nursing in Practice
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Understanding and working with suicide risk
Understanding and working with suicide risk
Key learning points:
– Understanding risk factors associated with suicide
– Considering a framework for understanding suicide
– How to assess and manage suicide risk
Suicide rates are increasing in the United Kingdom, with men being at much higher risk than women, and middle aged men being a particular current concern.1 The recession, unemployment and austerity are linked to this increase.2
While depression is evident in the majority of suicides,3 suicide is not just a mental health services concern as 72% of suicides are of people not in contact with mental health services.4 People discharged from acute hospitals can be vulnerable5 and suicide is associated with frequent and increasing primary care presentations.6 Thus all healthcare practitioners have a contribution to make in suicide prevention.7
Patients with suicidal ideation who present to primary care may not articulate their thoughts.8 Primary care practitioners should be aware of risk factors associated with suicide to enable them to detect possible warning signs. Patients who experience depression and anxiety often find primary care nurses easy to talk to9 therefore primary care nurses are in a prime position to identify patients who may be at risk.
Who is at risk?
Risk factors associated with suicide are complex and imprecise.10 As much as we know that depression and self-harm are key risk indicators, for example, most people who experience depression or self harm don’t go on to take their lives and not everyone who dies from suicide has a formal psychiatric or self harm history.
Screening tools such as the patient health questionnaire (PHQ9),11 may help identify patients who are experiencing suicidal ideation11 but they have limited value in determining the context of suicidality.10
The National Institute for Health and Care Excellence (NICE) advises that such tools should not supersede clinical judgement when discerning suicide risk;12 however they can be a helpful start point.
Suicide risk can be categorised into static factors (fixed and historical), stable factors (enduring but not fixed), dynamic factors (highly fluctuating according to recent and current circumstances) and future factors (anticipated).13 These risk factors both interchange and interplay. Box 1 categorises some of the main risk factors for suicide.
Personality traits such as impulsivity, poor problem solving ability and perfectionism should also be taken into consideration when contemplating risk as such traits are likely to trigger extreme reactions to stressful events which may lead to suicidal behaviour.13
Asking about suicide
Any articulation of suicidal ideation should be explored in a caring and concerned manner.
If warning signs are detected but suicidality is not disclosed it is important to be curious and seek more information about how the patient is feeling, including whether or not they have experienced thoughts of suicide (see Box 2 for examples). Asking about suicide will not put the idea into people’s heads,14 in fact it may reduce risk.
Most people who are suicidal are ambivalent about dying15 and this ambivalence should be seen as an opportunity to try and engender hope and life orientated thinking through dialogue.
Compassion is essential when interacting with an individual who may be suicidal.16 Vital openings for preventative interventions could be shut down by a nonchalant clinician.17 If the patient discloses thoughts of suicide it is important to elicit as much information as possible. Exploratory questions are listed in Box 3.
I’ve asked the questions, my patient is experiencing suicidal thoughts and I think he/she is at risk; what should I do now?
1.Tell the patient they have done the right thing by seeking help and confiding in you. Convey that you want to ensure their safety and help them get the support they need.
2. Ascertain support networks. Ask if you can involve the patient’s main carer; this will be helpful to both gain an understanding of the carer’s perspective on the patient’s situation and identify how much support the carer is able to provide. Confidentiality can be a barrier to carer involvement but it is important to try and encourage the patient to allow carer support. Explain what information you need to give the carer and reassure the patient you don’t need to disclose everything you have been told about what they are feeling.
3. The GP should always be notified if it is felt that a patient is at risk of suicide and ideally see the patient before they leave the surgery. Be candid with the patient and let them know you are concerned about their safety and want a second opinion to help decide the best plan. If the patient has been open with you hitherto, they are likely to agree to wait while you speak to a GP. However, if the patient refuses to stay and you feel they are at imminent risk it is appropriate to inform the police and the next of kin. In such cases mental health crisis services will need to be involved to carry out an emergency mental health assessment.
4. If the patient has disclosed access to means there should be a discussion around removing the means. Ideally this should involve help from family or friends but if the patient does not have social support you may need to rely on trust. If the patient has access to a firearm you can inform the police who will remove the firearm to safekeeping if the patient is at risk of using it to take their life.
5. It is essential that you thoroughly document all aspects of your patient contact and all actions you have taken.
6. If the patient is not at immediate risk, ongoing monitoring of mood and support will be required and insomnia and agitation should be treated pharmacologically.15 This might involve referral to a community mental health team or GP treatment of depression and signposting to supportive community resources. Sources of support might include suicide prevention and mental health agencies (see Resources for patients and families section) and other organisations that can help with substance misuse, benefits, accommodation and so on, depending on the issues the patient is experiencing.
7. It is important that patients and carers are made aware of how to access support in a crisis situation (i.e. via GP, mental health services, 111, 999 and A&E), and a plan should be agreed with the patient before they leave the surgery.
8. Dealing with suicide risk is stressful; seek support and supervision. The Resources for primary care clinicians section lists some resources that may help primary care nurses in practice.
Conclusion
Primary care nurses are likely to come across patients who are experiencing suicidality and should be prepared to respond compassionately and assertively to facilitate preventative interventions. However nurses should not work in isolation and it is important to call on colleagues for advice and support.
Resources for patients and families
Samaritans –www.samaritans.org/ offer a confidential 24/7 telephone helpline 08457 90 90 90, email support: [email protected] and text support: 07725 90 90 90.
PAPYRUS –Prevention of Young Suicide – www.papyrus-uk.org/ HOPElineUK 0800 068 41 41, text service: 07786 209697 email: [email protected].
Campaign Against Living Miserably (CALM) –www.thecalmzone.net/ supports men and boys. Helpline 0800 58 58 58 and Webchat service
via website.
Mind –www.mind.org.uk/ offers advice and information to people with mental health problems and those that are helping and supporting people with mental health problems.
Resources for primary care clinicians
Clinical guide for assessing suicide risk in depression –http://cebmh.warne.ox.ac.uk/csr/clinicalguide/index.html
Factsheet on managing suicide risk in primary care –www.connectingwithpeople.org/sites/default/files/SuicideMitigationInPrimaryCareFactsheet_0612.pdf
References
1. Office for National Statistics. Suicides in the United Kingdom, 2013 Registrations; 2014. www.ons.gov.uk/ons/dcp171778_395145.pdf (accessed May 2015)
2. Haw, C., Hawton, K., Gunnell, D., Platt, S. (2014)
3. Lönnqvist, J. Psychiatric aspects of suicidal behaviour: depression. In: Hawton, K., and van Heeringen, K. The International Handbook of Suicide and Attempted Suicide. New York: Wiley; 2000
4. National Confidential Inquiry into suicide and homicide by people with mental illness; Manchester: University of Manchester 2014
5. Dougall N, Lambert P, Maxwell M, Dawson A, Sinnot ., McCafferty S, Morris C, Clark D, Springbett A. Deaths by suicide and their relationship with general and psychiatric hospital discharge: 30-year record linkage study. The British Journal of Psychiatry 2014; 1–7
6. National Confidential Inquiry into Suicide and Homicide by People with Mental Illness. Suicide in primary care in England: 2002-2011. Manchester: University of Manchester; 2014
7. Department of Health, Preventing suicide in England: a cross-government outcomes strategy to save lives. 2012. www.gov.uk/government/publications/suicide-prevention-strategy-for-england (accessed 22
June 2015)
8. Michel K. Suicide Prevention and Primary Care. In: Hawton K, van Heeringen K (eds). The International Handbook of Suicide and Attempted Suicide. Chichester: John Wiley & Sons Ltd; 2000. p661-674.
9. Buszewicz M, Griffin M, McMahon EM, Beecham J, King M. Evaluation of a system of structured, pro-active care for chronic depression in primary care: a randomised controlled trial. BMC psychiatry 2010;10(61)
10. Morriss R, Kapur N, Byng R. Assessing risk of suicide or self harm in adults. British Medical Journal 2013; 347 (f:4572)
11. Simon GE, Rutter CM, Peterson D, Oliver M, Whiteside U, Operskalski B, Ludman EL. Do PHQ depression questionnaires completed during outpatient visits predict subsequent suicide attempt or suicide death? Psychiatric Services 2013; 64(12) 1195-1202.
12. NICE. Self harm: longer term management. 2011. http://www.nice.org.uk/guidance/CG133 (accessed May 2015).
13. Bouch J, Marshall JJ. Suicide risk: structured clinical judgement. Advances in Psychiatric Treatment 2005; 11 (84-91).
14. Dazzi T, Gribble R, Wessley S, Fear NT. Does asking about suicide and related behaviours induce suicidal ideation? What is the evidence? Psychological Medicine 2014; 44(16), 3361-3363
15. Joiner TE, Van Orden KA, Witte TK, Rudd D. The Interpersonal Theory of Suicide: guidance for working with suicidal clients. Washington: American Psychological Association; 2009
16. Cole-King A, Green G, Gask L, Hines K, Platt S, Suicide mitigation: a compassionate approach to suicide prevention. Advances in Psychiatric Treatment 2013; 19 (4) 276-283
17. Hawton K, van Heeringen K. Suicide. Lancet 2009; 373: 1372-81
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Psychology and Neuroscience Faculty Database
Psychology and Neuroscience
Arts & Sciences
Duke University
HOME > Arts & Sciences > pn > Faculty Search Help Login pdf version printable version
Publications [#252031] of Ahmad Hariri
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Journal Articles
1. Ousdal, OT; Jensen, J; Server, A; Hariri, AR; Nakstad, PH; Andreassen, OA (2008). The human amygdala is involved in general behavioral relevance detection: Evidence from an event-related functional magnetic resonance imaging Go-NoGo task. Neuroscience, 156(3), 450-455. [18775476], [doi]
(last updated on 2018/10/18)
Abstract:
The amygdala is classically regarded as a detector of potential threat and as a critical component of the neural circuitry mediating conditioned fear responses. However, it has been reported that the human amygdala responds to multiple expressions of emotions as well as emotionally neutral stimuli of a novel, uncertain or ambiguous nature. Thus, it has been proposed that the function of the amygdala may be of a more general art, i.e. as a detector of behaviorally relevant stimuli [Sander D, Grafman J, Zalla T (2003) The human amygdala: an evolved system for relevance detection. Rev Neurosci 14:303-316]. To investigate this putative function of the amygdala, we used event related functional magnetic resonance imaging (fMRI) and a modified Go-NoGo task composed of behaviorally relevant and irrelevant letter and number stimuli. Analyses revealed bilateral amygdala activation in response to letter stimuli that were behaviorally relevant as compared with letters with less behavioral relevance. Similar results were obtained for relatively infrequent NoGo relevant stimuli as compared with more frequent Go stimuli. Our findings support a role for the human amygdala in general detection of behaviorally relevant stimuli. © 2008 IBRO.
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Free Yourselves From Machines
Posted
There are two types of ways to strength train in the gym. The first is safe, easy to set up, and self-explanatory. The second can lead to a greater chance of injury, can take a lot more time to set up, and could require assistance. The first will also get you about half the gains as the second (dependent on your goals of course). I’m talking about machine weight lifting (selectorized) vs. free weights (dumb bells, barbells, kettle bells, etc.), and unless you’re a body builder with a very specific target area or someone whose rehabbing an injury, it’s time to get off the machines.
Let’s start with a brief history of gyms and weight training. Physical training and competition has been around forever. The Greeks have used myths and stories to promote physical feats for as long as we can trace. They did invent the Olympics and Hercules (which is his Roman name but let’s not get caught up with ancient mythology) after all. The European countries have been weight lifting ever since, but it never really caught on in America until football made it popular in the 50’s. Jack Lalane was one of the first to introduce weight lifting machines during this time, but it wasn’t until the late 70’s when gyms really took off. Arnold Schwarzenegger can be blamed for the gym boom around this time. His movie “Pumping Iron” spearheaded the fitness movement. Now before I go on, realize how many people are trying to monetize health. Diet pills, fad exercise routines, flashy marketing, and even exercise equipment developers are constantly trying to figure out how to make money from Americans being out of shape. The early 80’s proved no different as the founder of Nautilus used gimmicky marketing and a very public argument with one the world’s best competitive squatters to gain the public’s eye. Ever since, weight lifting machines have been part of health clubs, serving only certain members with fringe benefits, but doing an extraordinary job at selling club memberships.
Now that we know why machines are in clubs, let’s discuss why we shouldn’t be using them over free weights. Free weights make our bodies much more functional. We should be training our bodies in the gym to make our lives outside of the gym easier. A dead lift is just picking up your baby out of its crib and a sit up is how you get out of bed every morning. Never in your life will you be seated, leaning over something using only your biceps to curl anything up to your chest. However you will squat down almost every single day. One of the worst features of weight machines are that they restrict motion (usually) to one plane at a time. Meaning it will never replicate bending and twisting at the same time, how most people hurt their lower backs. I discussed training in all our planes of motions in an earlier article about core training, and the same principles apply to other muscle groups besides the core.
Another strong reason to ditch the machines is the stabilization you will create in your core and other accessory muscles during weight lifting with free weights. Using dumb bells or barbells creates much greater muscular stimulation in non-primary movers during any given lift. For example, the main muscle used in a bench press is the pectoralis major. It’s also the main mover in the seated machine chest press. The difference is that in the bench press you have to make sure that the weight isn’t going to high over your face, or too low to your stomach. The shoulders have a lot to do with this and get a ton of work in a bench press, where they aren’t used much at all in a seated chest press. If calorie burn is your goal, then the more muscles you use per a particular exercise will help you burn more calories. If getting stronger is your goal, using the shoulder muscles to stabilize during a press will make your lifts much stronger.
The core is another big beneficiary to free weight training. You will almost never need to keep a tight core to complete a weights machine movement. But doing a lift with free weights and a loose core could compromise the entire motion. Someone who does a ton of hamstring curls on a machine will have strong hamstrings, but someone who does a ton of squats will have strong hamstrings, glutes, quads, abs, etc. Not only will free weights increase the strength of accessory muscles, they will increase the strength of the primary movers by recruiting more of the muscle to assist in the movement. Moving your muscles in a complete range of motion will use more of the muscle group and make you stronger.
Many people think that the risk of injury is higher from using free weight and this could be true if you aren’t performing the motions correctly (remember always ask a professional for help if you’re unsure of yourself). However the risk of injury from machine weights is equally as high. You can’t drop a stack of weight with a pin on your head like you can with a barbell, but the chance of injury still exists. If you are always focused on the same machines, developing particular muscles while ignoring others, your posture could be compromised which could lead to a multitude of musculo-skeletal problems.
So if you’re taking my advice and ditching the machines in favor of the strength building, athlete tested free weights, remember to do so safely. Any activity is better than none, and if you’re injured you won’t be doing much of anything. Talk to a professional trainer and get help analyzing your fitness goals and matching your exercises to those goals. If you’re using a machine to work on a particular body part, I guarantee there’s a free weights exercise to work the same muscles more effectively. Lastly, don’t be intimidated by the free weights. Everyone starts somewhere and even the guys who look like experts will give you credit for branching out and trying to make your gym routine better.
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Reference: Michaud GA, et al. (2003) Analyzing antibody specificity with whole proteome microarrays. Nat Biotechnol 21(12):1509-12
Reference Help
Abstract
Although approximately 10,000 antibodies are available from commercial sources, antibody reagents are still unavailable for most proteins. Furthermore, new applications such as antibody arrays and monoclonal antibody therapeutics have increased the demand for more specific antibodies to reduce cross-reactivity and side effects. An array containing every protein for the relevant organism represents the ideal format for an assay to test antibody specificity, because it allows the simultaneous screening of thousands of proteins for possible cross-reactivity. As an initial test of this approach, we screened 11 polyclonal and monoclonal antibodies to approximately 5,000 different yeast proteins deposited on a glass slide and found that, in addition to recognizing their cognate proteins, the antibodies cross-reacted with other yeast proteins to varying degrees. Some of the interactions of the antibodies with noncognate proteins could be deduced by alignment of the primary amino acid sequences of the antigens and cross-reactive proteins; however, these interactions could not be predicted a priori. Our findings show that proteome array technology has potential to improve antibody design and selection for applications in both medicine and research.
Reference Type
Evaluation Studies | Journal Article
Authors
Michaud GA, Salcius M, Zhou F, Bangham R, Bonin J, Guo H, Snyder M, Predki PF, Schweitzer BI
Primary Lit For
Additional Lit For
Review For
Interaction Annotations
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Interactor Interactor Type Assay Annotation Action Modification Phenotype Source Reference
Gene Ontology Annotations
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Gene Gene Ontology Term Qualifier Aspect Method Evidence Source Assigned On Annotation Extension Reference
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Gene Phenotype Experiment Type Mutant Information Strain Background Chemical Details Reference
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Regulator Target Experiment Assay Construct Conditions Strain Background Reference
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Difference Between Similar Terms and Objects
Difference Between Atria and Ventricles
heart-diagramAtria vs Ventricles
Atria (pl. atrium) refer to the upper chambers of the heart (2 in number) that receive the impure blood from the veins to send it to the ventricles. On the other hand, ventricles are small cavities or chambers that are present within an organ, usually the left chamber of the heart that accepts blood from the arteries (left atrium) and then contracts to force into the aorta. The right chamber of the heart accepts deoxygenated blood that is carried by the right aorta. There are 4 chambers in the heart and the atria refer to the upper chambers, whereas the ventricles refer to the lower chambers. The right part of our heart has an atrium and one ventricle, while the case is the same for the left side too.
The walls of the ventricles are thicker, while that of the atria are thinner. They however contain valves to pump the blood in and out of the heart. The walls of the heart, including the atria and the ventricles are functional in ensuring effective working of the circulatory system. The walls of the heart are made of 3 layers of tissues ‘“ myocardium, endocardium and epicardium. The function of the right atrium is to receive deoxygenated blood from the veins. Its oxygen has been given to the tissues in return collecting CO2 and tissue waste materials. Deoxygenated blood is transferred from the upper part of the body to the atrium by the SVC or superior vena cava. The IVC or inferior vena cava brings deoxygenated blood from the lower part of the body into the atrium.
The tricuspid valve of the right atrium helps in the storage of blood, for the heart to pump it within the right side of the ventricle for preventing the blood from flowing back, as well as ensure effective cardiac functionality. The function of the left atria is to accept the purified blood from lungs from the pulmonary veins. The mitral or bicuspid valve helps prevent the blood from flowing backwards to the left part of heart until the left side of the atrium pushes blood to the left of the ventricle.
The right ventricle functions by depositing deoxygenated blood that is contained in the right atria. The right ventricle pumps blood into the lungs for purifying it. Of course the purification process is forwarded by the pulmonary valve. Pulmonary arteries transport blood into the lungs. The function of the muscled left ventricles is to receive oxygenated blood that has been pumped within left atria in the body.
Summary:
1. The atria stand for the upper chambers of the heart, while the ventricles are the lower chambers.
2. Atria act as receptors of deoxygenated blood, while ventricles receive blood from the left atria and force it into the aorta.
3. Atria have strictly to do with the inner chambers of the heart, while ventricles may even refer to the interconnected brain cavities.
4. The walls of the atria are thinner with low blood pressure, while those of the ventricles are thicker with high blood pressure.
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4 Months Post-op Rhinoplasty Nose Tip Still Bulbous, Could it Still be Swollen?
I had a bump shaved as well as bulbous tip refined. I am please with my nose however I find that the tip is still a little bulbous. Does it truly(in all cases) takes a full year for all the residule swelling to dissapate? Could this still be swelling? Is there anything I can do to reduce swelling, massaging? any steroid injections? Also I find that my nose is usually more bulbous in the morning and starts to feel smaller as the day goes on? Is this normal?
Doctor Answers 7
Swelling 4 months after Rhinoplasty
I hear and read this question alot. There is a difference between swelling and "shrink wrapping" The swelling goes a way after 3 months or so. But, the skin takes a much longer time, a year or two, before it contracts around the underlying cartilages. That is what takes a very long time. You may hear and read that the "swelling" can go on for a year, and in some cases, where the nose appears bigger in the am than the pm that is the case, the vast majority of the time it is simply that the nasal skin has yet to maximally contract. I hope this helps you. Best,
Dr. Miller
New York Facial Plastic Surgeon
4.5 out of 5 stars 58 reviews
Bulbous Nose Tip After Rhinoplasty May Take A Year For Final Result
Thank you for your question.
The tissues of the nasal tip hold fluid for a very long time after surgery. Also, the skin of the tip of the nose must gradually shrink after surgery to refine a bulbous tip.
It is very true that most experienced Rhinoplasty surgeons recommend waiting a year to see the final tip result. If you wait you may be pleasantly surprised.
The fact that you are more swollen in the morning suggests that fluid build up is a problem.
Ask your surgeon about massage and taping to improve the process.
Bulbous nasal tip post rhinoplasty
Swelling in the tip is the last portion of swelling to dissipate in the nose. While most swelling, approximately seventy percent dissipates in the first three months post surgery the final thirty percent takes an entire year to fully dissipate. Steroids usage is dependent on the case and their particular healing process. Your surgeon will discuss this option with you if he/she feels this would be helpful in your healing process. If you feel you have more swelling in the am versus the pm then try and sleep elevated and watch your sodium intake and see if this helps your situation. Best regards!
Michael Elam, MD
Orange County Facial Plastic Surgeon
5.0 out of 5 stars 167 reviews
Bulbous tip after rhinoplasty
I suspect that there is still some swelling present, especially if it changes throughout the day, as you describe. A steroid injection might help regardless. Check with your surgeon.
Bulbous Tip 4 Months Post Rhinoplasty
With all due respect to my colleagues who have answered this question, the tip may not technically be swollen, but it will decrease in size as healing progresses. The fact that it is bigger in the morning and shrinks during the day when you're upright and active indicates that have not seen the final result. What you're experiencing is normal.
Richard W. Fleming, MD
Beverly Hills Facial Plastic Surgeon
5.0 out of 5 stars 22 reviews
Nasal tip healing after rhinoplasty
The tip is no longer swollen, though there is scar tissue as the tip fully heals and the skin conforms and it really can take up to a year. As long as there is stiffness in the tip, the scar is not mature, and as it does the tip will continue to improve and shrink in over time.
Best of luck,
peterejohnsonmd.com
Peter E. Johnson, MD
Chicago Plastic Surgeon
4.0 out of 5 stars 35 reviews
Tip of my nose still too big.
The fact that your tip is larger in the morning proves that it is still swollen. The tip of your nose is likely to shrink dramatically during the next several months as swelling further subsides. My recommendation is against massaging and/or steroid injections at this time, but a double dose of patience will likely help.
Steve Laverson, MD
San Diego Plastic Surgeon
5.0 out of 5 stars 40 reviews
These answers are for educational purposes and should not be relied upon as a substitute for medical advice you may receive from your physician. If you have a medical emergency, please call 911. These answers do not constitute or initiate a patient/doctor relationship.
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Question: What does it mean when your breath smells like death?
Breath that smells rotten or fetid (like garbage or death) An abscess or infection in your mouth, throat, or lungs may cause your breath to smell like rotting tissue.
What does death breath smell like?
Smell: the shutting down of the dying persons system and the changes of the metabolism from the breath and skin and body fluids create a distinctive acetone odour that is similar to the smell of nail polish remover.
Why does my breath smell like rotten meat?
Rotten meat smell: Bronchiectasis is a condition in which the airways of the lungs become widened, leading to a build-up of excess mucus. The resulting infection in the lungs can make the breath smell like rotten meat.
Can you smell when death is near?
In general, death only has a scent under certain circumstances and conditions. Dr. Jawn, M.D. notes that, for the most part, there is no smell that precipitates death, and there is no smell immediately after death.
Can you smell someone dying?
The brain is the first organ to begin to break down, and other organs follow suit. Living bacteria in the body, particularly in the bowels, play a major role in this decomposition process, or putrefaction. This decay produces a very potent odor. “Even within a half hour, you can smell death in the room,” he says.
What does it mean when you have a rotten taste in your mouth?
The most common reasons for a bad taste in your mouth have to do with dental hygiene. Not flossing and brushing regularly can cause gingivitis, which can cause a bad taste in your mouth. Dental problems, such as infections, abscesses, and even wisdom teeth coming in, can also cause a bad taste.
How can I test if I have bad breath?
Need to check how your breath smells quickly? Try the sniff test—there are a couple of ways to do it. If you lick your wrist, let it dry for a moment, then take a whiff, you should be able to get an idea if your breath has an odor too. Another method is to floss toward the back of your mouth, then smell the floss.
How do you cure bad breath from the stomach?
Drink plenty of water throughout the day to refresh your breath. Water is less likely than other beverages to upset your stomach or weaken your LES. It also helps wash away bacteria that can lead to bad breath.
How do you get a rotten taste out of your mouth?
Treating a Bad Taste in Your MouthGargle with water.Using toothpaste, brush your teeth, tongue, roof of your mouth, and gums at least two times a day.Rinse your mouth with mouthwash.Drink liquids, chew sugar-free gum or mints, or suck on sour candies.More items
What medical conditions cause bad taste in your mouth?
Each of the health issues and medical conditions listed below can cause a persistent bad taste in the mouth.Poor oral hygiene. Dry mouth. Acid reflux. Oral thrush. Respiratory infections. Hepatitis B. Hormonal changes. Medications.More items
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Con: Alzheimer's disease and circadian dysfunction: chicken or egg?
• Abhay Moghekar1 and
Affiliated with
• Richard J O’Brien1Email author
Affiliated with
Alzheimer's Research & Therapy20124:26
DOI: 10.1186/alzrt129
Published: 13 August 2012
Abstract
The development of late-onset Alzheimer's disease is believed to be influenced by genetic, socioeconomic, and lifestyle factors. Recently, converging research in animal and human studies has found that beta-amyloid (Aβ) levels in cerebrospinal fluid are modulated by sleep-wake cycles. This raises the possibility that chronic sleep loss causes brain amyloid accumulation over time and leads to the development of Alzheimer's disease. The observation that circadian rhythm modulates Aβ levels has not yet been replicated by other groups, and subject selection and methodologies are potential explanations for this. While acute suppression of sleep may raise Aβ levels, it is not known whether chronic sleep loss has the same effect. It is conceivable that altered circadian rhythms are a manifestation of a disrupted sleep network because of preclinical disease, as has been observed in other neurodegenerative disorders. The findings that circadian variation in Aβ levels in cerebrospinal fluid is a direct result of sleep-wake cycles and that altering normal rhythms increases the risk for brain amyloid accumulation need to be replicated in larger cohorts. Prospective studies are needed to decipher whether circadian rhythm dysfunction is a cause, or a result of, amyloid accumulation.
Background
Autosomal-dominant, early-onset Alzheimer's disease (AD) is due to mutations in the processing of the amyloid precursor protein (APP), resulting in excess production of the 42-amino acid form of the beta-amyloid peptide (Aβ1-42). However, the vast majority of sporadic, late-onset AD has no similar causative mutations, although some polymorphisms (apolipoprotein E, SORL1, and clusterin) increase the relative risk of this devastating disease [1]. It is believed that late-onset AD develops secondary to a combination of genetic, environmental, and lifestyle factors. Environmental and lifestyle risk factors that have been proposed to increase risk include midlife hypertension, diabetes or impaired insulin resistance, physical activity, obesity, head injury, socioeconomic status, and level of education. Holtzman and colleagues [2, 3] have suggested, on the basis of animal and human studies demonstrating diurnal fluctuations of Aβ levels in cerebrospinal fluid (CSF), adding chronic sleep loss in midlife to this mix. This observation has implications not only for AD pathogenesis but also for the use of CSF for biomarkers in research and clinical management.
Discussion
Bateman and colleagues [2] first observed the fluctuation of both Aβ1-40 and Aβ1-42 in CSF obtained from research subjects with indwelling spinal catheters, which were sampled hourly for 36 hours. The maximum Aβ levels were two to three times the minimum values for the duration of collection. Using in vivo microdialysis, this same group further demonstrated that, in both wild-type and APP transgenic mice, there was diurnal variation in interstitial fluid (ISF) Aβ levels; peaks occurred during periods of greatest physical activity, and the variation was unrelated to light exposure. Moreover, administration of an orexin antagonist, almorexant, abolished the natural diurnal variation of Aβ whereas orexin administration significantly increased interstitial brain Aβ concentrations [3]. Recently, Huang and colleagues [4], from the same group, replicated the observation of diurnal fluctuation in young healthy subjects but found decreased CSF Aβ fluctuation in subjects with brain amyloid accumulation as ascertained by brain positron emission tomography (PET) scanning with an amyloid-binding agent. These observations are important as they have direct implications for the pathogenesis of AD. If Aβ levels in CSF and brain ISF are modulated by sleep-wake activity, then impaired circadian rhythms could cause brain Aβ accumulation and subsequently AD.
Although this is certainly a plausible hypothesis, there are some methodological and conceptual issues that need to be addressed. In attempts to repeat this important finding, multiple groups looked at diurnal variation of CSF Aβ in humans but could not replicate the findings [57]. Although subject selection, the volume of CSF withdrawn, and the interval between collections could account for the lack of fluctuation in some cohorts, Li and colleagues [5] studied the effect of different intervals between CSF sampling and still did not observe diurnal fluctuation synchronous with sleep-wake cycles. In fact, continuously rising levels of Aβ have been observed in several studies, a finding that lacks a good explanation. Other studies have observed that lumbar Aβ levels are higher than ventricular levels [8, 9], although this is controversial [10]. In spite of these controversies, the dynamics of Aβ within the various CSF compartments and its exchange with both ISF and blood Aβ remain important subjects of investigation.
Even if the methodological issues are clarified and the finding of diurnal variation in Aβ holds true, there is still the concern that these fluctuations are merely associated with neuronal activity in general and are not related to a specific feature of sleep. Cirrito and colleagues [11] demonstrated that Aβ levels are modulated by neuronal activity, and hence it is plausible that these levels fluctuate with sleep-wake cycles. It is well known that, as we age, sleep gets fragmented and as the circadian rhythm desynchronizes this is exaggerated in several neurodegenerative disorders, including Huntington's disease, Parkinson's disease, and AD [12]. This could explain the recent findings of Bateman and colleagues [2] of significantly depressed fluctuations in older normal adults and patients with AD. While sleep abnormalities are frequent in moderate to late AD, it is not known whether these changes play a role in the pathogenesis of the disease. The circadian rhythm, including the maintenance of sleep and wakefulness, involves a complex network with multiple nuclei and neurotransmitter systems. It is conceivable that the normal circadian rhythm is a marker for general integrity of brain networks and that any pathologic process that affects this intricate network causes disruption of circadian patterns. Sleep abnormalities are detected in patients with synucleinopathies (rapid-eye-movement behavior disorder) and schizophrenia, sometimes decades before the manifestation of the disease [13, 14]. In these disorders at least, it is believed that the sleep dysfunction is just an early preclinical biomarker rather than a cause of the disease. Similarly, it is likely that disrupted circadian patterns could be a preclinical marker for AD. In addition, one might expect a lower prevalence of AD pathology in patients with narcolepsy, which is characterized by low or absent levels of orexin. Postmortem neuropathologic assessment in a small sample of patients with narcolepsy did not show evidence of a lower prevalence of AD pathology [15].
Summary
While the data suggesting a causative rather than an associative link between sleep loss and amyloid accumulation are tantalizing, further confirmation of this finding is needed. Prospective cohorts including CSF biomarkers and sleep studies are under way and will help clarify this important observation.
Abbreviations
Aβ:
beta-amyloid peptide
AD:
Alzheimer's disease
CSF:
cerebrospinal fluid
ISF:
interstitial fluid.
Declarations
Authors’ Affiliations
(1)
Department of Neurology, Johns Hopkins Bayview Medical Center, Mason F Lord Center Tower
References
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Copyright
© BioMed Central Ltd 2012
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Body Weight and Cancer Risk
This article has been archived.
For information about this topic, please click here
OncoLink Team
Abramson Cancer Center of the University of Pennsylvania
Last Modified: March 23, 2012
Studies most strongly associate being overweight and/or obese with a higher risk of breast (postmenopausal women), colorectal, endometrial, esophagus and renal cell cancers. Evidence points to obesity as a cause for gall bladder and pancreas cancer as well. Experts estimate that 14% of cancer deaths in men and 20% of cancer deaths in women are caused by obesity. It is likely that the mechanism for this risk is different for each cancer. Researchers believe that hormones that are produced at higher levels in the presence of extra weight, including insulin, leptin and estrogen, are one cause. For example, fat cells are the primary source of estrogen in postmenopausal women, thus more fat cells may lead to higher risk of breast cancer in overweight/obese women.
Experts measure body weight using body mass index or BMI. BMI is a measure of body fat based on a person's height and weight. This is a good place to start to evaluate your body weight and see where you fall on the chart, which classifies your BMI as underweight, healthy, overweight and obese.
A healthy diet, combined with regular physical activity and maintaining a healthy weight has been shown to reduce cancer risk. This triangle is thought to be the second most important step, after not smoking, to preventing cancer. A few studies have found that losing weight can help decrease the risk of weight-related cancers. The most convincing evidence for losing weight as a risk reduction technique comes from studies of people who have undergone bariatric (weight loss) surgery. In a sample of U.S. bariatric surgery patients, cancer death rates were 38% lower than people who were obese and did not undergo surgery.
Losing weight is no easy task. It takes a strong commitment to making big lifestyle changes. Seek support from friends, family, your healthcare providers and weight loss programs. Investigate websites or applications (Apps) to track progress and motivate you. Get started by learning more at the American Cancer Society and LIVESTRONG.
Resources to learn more about how diet, physical activity and weight are related to cancer
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November 25, 2015
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5eff3d1f6f98e57329caed0ceb9053d3
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2,201,947,599,317,505,500
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The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.
wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Neuronal death in the hippocampus is promoted by plasmin-catalyzed degradation of laminin.
Excess excitatory amino acids can provoke neuronal death in the hippocampus, and the extracellular proteases tissue plasminogen activator (tPA) and plasmin (ogen) have been implicated in this death. To investigate substrates for plasmin that might influence neuronal degeneration, extracellular matrix ( ECM) protein expression was examined. Laminin is expressed in the hippocampus and disappears after excitotoxin injection. Laminin disappearance precedes neuronal death, is spatially coincident with regions that exhibit neuronal loss, and is blocked by either tPA-deficiency or infusion of a plasmin inhibitor, both of which also block neuronal degeneration. Preventing neuron-laminin interaction by infusion of anti-laminin antibodies into tPA-deficient mice restores excitotoxic sensitivity to their hippocampal neurons. These results indicate that disruption of neuron- ECM interaction via tPA/plasmin catalyzed degradation of laminin sensitizes hippocampal neurons to cell death.[1]
References
WikiGenes - Universities
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5eff3d1f6f98e57329caed0ceb9053d3
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5,719,842,740,135,987,000
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Vitamin D
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Also known as: Vitamin D3, cholecalciferol, vitamin D2, ergocalciferol.
Potential uses: Vitamin D helps the body absorb the calcium that is essential for good bone health. This is especially important for menopausal women and women taking an aromatase inhibitor to treat breast cancer, since bone loss is a side effect of the three aromatase inhibitors. Good calcium absorption also can help reduce bone weakening caused by certain chemotherapy medications.
Usual dose: The standard recommendation is that people younger than 50 get 200 international units of vitamin D per day. 400 international units per day is recommended for those aged 50-70, and 600 international units per day is recommended for people older than 70. The typical multivitamin contains 400 international units of vitamin D. Adults who want to reduce the risk of broken bones should take 400-800 international units daily, along with calcium. Vitamin D also is found in food products such as fish, eggs, and fortified milk and cereals. The human body also produces vitamin D when exposed to sun.
Are there any risks? Too much vitamin D -- more than 2,000 international units daily -- can lead to having too much calcium in the blood. Over time, calcium deposits can affect soft tissues such as the heart and lungs. Other risks include kidney stones, nausea, vomiting, confusion, muscle weakness, poor appetite, and weight loss.
What does the research show? For many years, studies have shown that people who are less exposed to sunlight and have lower levels of vitamin D as a result are more likely to develop breast cancer and other forms of cancer. More recently, some research has found that calcium and vitamin D may help protect premenopausal women against breast cancer, but more studies are needed. Learn more about the possible link between low vitamin D levels and breast cancer and what you can do about it.
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-1,428,042,898,618,808,000
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Innate immunity and viral evasion
If a virus attacks us, our immune system registers this attack and starts a whole chain of reactions. Messengers initiate the release of cellular proteins, through which our cells prevent the spread of viruses – known as antiviral factors. However, some viruses have developed very effective strategies against these antiviral factors, so that the self-protection mechanism of the cells is ultimately insufficient to defend against the infection. Wanted: new antiviral factors which can fight off even these viruses – of which HIV is one.
Characterization of the secretory glycoprotein 90K/LGALS3BP as an antiviral restriction factor
interferon-stimulated gene lgals3bp, which encodes for the cellular glycoprotein 90K
DFG Collaborative Research Centre 900 Chronic Infections: "Microbial Persistence and its Control"
After recognition of pathogen-associated molecular patterns (PAMPs) by infected cells, interferons are synthesized, secreted and bind the interferon receptor on neighboring cells to „alarm“ them from an upcoming virus invasion. Binding induces a signaling cascade that ultimately results in synthesis of several interferon-stimulated genes, so-called ISGs (“interferon-stimulated genes”). ISGs comprise many antiviral genes, including those encoding APOBEC3G, a cellular deaminase which hypermutates the viral genome, or Tetherin, which prevents release of mature virions from the producer cell´s surface. Another ISG is lgals3bp, which encodes for the cellular glycoprotein 90K. Previous work of our group demonstrated the antiviral potency of 90K against HIV. Specifically, 90K reduces the infectivity of newly assembled virions by interfering with the viral incorporation of HIV Envelope proteins (Lodermeyer et al., Retrovirology 2013).
We are now focusing on the elucidation of the antiviral mechanism. Using truncated versions of 90K, we plan to define which domains/regions within 90K are essential and sufficient for its antiviral function. In parallel, 90K orthologs from non-human species, which share a high degree of homology with human 90K, but differ in their antiviral capability, are useful tools for the elucidation of the antiviral mechanism. Further, they shed light on the evolutionary conservation of 90K´s antiviral function. Finally, we test whether 90K acts antivirally against other enveloped viruses. The long-term perspective is to pave avenues towards a new antiviral treatment strategy.
A novel approach for eradicating HIV
Gilead Infectiology Programme 2016 (Cooperation with Prof. Georg Behrens, MHH)
Latently infected cells produce no viral products and remain invisible to the immune system. A “shock and kill” strategy of transcription induction (“shock”) with subsequent cell elimination (“kill”) has been proposed to reduce or even eradicate the HIV-1 reservoir. While reactivation of HIV-1 from the reservoir (shock) is mostly pursued by pharmacological interventions such as histone deacytelase inhibitors (HDACi), the elimination of cells which are in the process of reactivation (kill) is believed to be best achieved by immune-mediated mechanisms. Our proposed experiments are crucial to confirm autophagy as novel therapeutic targets in cells with incomplete reactivation of provirus.
Our project provides an alternative to the predominantly immune-based strategies. The project has the potential to identify novel cellular pathways for efficient reduction of the HIV reservoir. An important translational aspect is that we focus on available and licensed compounds for rapid evaluation in patients/animal models if proven effective in the preclinical evaluation.
Characterisation of the cGAS-mediated DNA-sensing signaling in HIV infected T-cells
cytosolic DNA sensor cGAS
DFG Priority Programme 1923, "Innate Sensing and Restriction of Retroviruses"
Upon HIV-1 infection of T-cells, viral DNA can be sensed by the cytosolic DNA sensor cGAS. In cocultures with macrophages, HIV-1 Env-mediated membrane fusion pores allow the horizontal transfer of the cGAS product and cyclic dinucleotide cGAMP to macrophages, where it activates STING-dependent expression of antiviral cytokines and effector molecules (Xu und Ducroux et al., Cell Host & Microbe 2016). In monocultures of T-cells and macrophages, HIV-1 prevents or counteracts activation of this cellular defense mechanism. In contrast to the situation in macrophages, our understanding of the reasons for the lack of a detectable type I IFN response in HIV-1-infected T-cells is limited.
In this project, we address the effectiveness of the cGAS-mediated DNA sensing pathway in primary T-cells and try to unravel potential explanations for the lack of IFN induction in this important HIV-1 target cell type.
Leader
• Prof Dr Christine Goffinet
Christine Goffinet
Head of Research Group
+49 511 220027 198
Contact
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Non-traditional medicine in Vietnam
Longan The name of the exotic fruit the longan translated from Vietnamese means "dragon eye". Its appearance really is somewhat intimidating, however, despite this, the fruits have excellent taste and…
Continue reading →
Poisonous medicinal plants
The ancient Greeks, explaining the action of medicinal plants, they are sometimes endowed with supernatural power. In ancient Greek word "Pharmakon" means both poison and medicine, and witchcraft. From the…
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hand
Magic jade – the people’s medicine
The name of this mineral “jade” dates back to the time of the conquest by the Spaniards of Central and South America and literally means “lumbar” stone piedra de ijada . as in the medical purposes it is applied on the lower back. But jade was a sacred stone and was valued more than gold not only Indians. According to the Chinese, jade was the forerunner of all gems, which creates in its bearer and people around him are five main virtues: mercy, modesty, courage, justice and wisdom. In the East it is believed that jewelry with jade store owner out of trouble, bring us emotional release and is able to make him happy, and clutched in his hand a piece of jade will help a lucrative trade deal.
The healing properties of the stone are described in considerable detail in Chinese “Health encyclopedia of herbal treatment is the Tang dynasty” and in the “Encyclopedia of herbal treatment of Zhang-But” . The mineral has healing properties due to its remarkably balanced chemical composition and unique physical properties. This is a very durable stone, and the same fortress it attaches to the body and spirit.
The color of jadeite can be white, green, yellowish-green to emerald-green, sometimes black, pink, brown, red, yellow, purple, blue.
Bright green color is created of primesyami, a lime-green iron. Long weathering leads to the appearance of the surface boulders of jadeite with bright red or yellow color is due to the transition of divalent iron to trivalent. Continue reading
Non-traditional medicine in Vietnam
Longan
The name of the exotic fruit the longan translated from Vietnamese means “dragon eye”. Its appearance really is somewhat intimidating, however, despite this, the fruits have excellent taste and have a very pleasant aroma.
The longan is an evergreen tree that has a dense and spreading crown, and belongs to the genus Nephelium longana.
According to some sources, the longan for the first time appeared in China. Currently this subtropical plant is often found between the elevations, it is able to easily migrate South of freezing to -3 degrees Celsius.
Although longan is considered to be a close “relative” of lychee, yet the fruits of these two plants differ. The longan they are small, on average reaching 2.5 mm in diameter and having yellow-brown color.
Now the longan is a very popular fruit. It is grown not only at home in China, but also in Indonesia, Taiwan and Vietnam. The name of this fruit comes from the Vietnamese province of the same name.
The flesh of longan is white and transparent. And through it is seen a dark red or black stone, round shaped.
Sheath that covers the fruit from top, is unfit for human consumption. It is very durable, but thin,and its color varies from brownish with spots to yellow and reddish. Continue reading
Diagnosis of the organism at a distance. Extrasensory, bioenergetics, alternative medicine.
Psychic, bio-energy therapist Svetlana Kim. Spend remote diagnosis to identify the diseases and injuries of organs and systems of the body, have a large experience in this direction.
To do this, use bioresonant methods of diagnostics, bio-energy and extrasensory perception. In this case, diagnoses and treats diseases by “reading” the patient’s information and entering in resonance with his energy field. Uses an integrated approach to the diagnosis and cure of the patient.
With energy healer can sense any part of the human body and have a beneficial effect on health. Bioenergy does not deny traditional medicine, and with the practice proves that it and modern advances in medicine go hand in hand, while not interfering with, but rather complementing each other.
During my diagnostic session occur simultaneously and the treatment, resulting in can take some diseases and also improves overall health. The patient during the diagnosis is at any distance (e.g. at home), lying or sitting, not crossing the feet and hands, palms facing up. It is advisable not to be distracted by conversations and other external stimuli, to listen to the sensations (light waves, tingling, heat, etc.)
To establish bioenergeticheskaya with the patient I need to know his name, age and contact him by phone or email. Detailed diagnostic results are communicated to the patient by mail or telephone. Continue reading
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FAQ
Should I Tip my massage therapist?
Yes!! A Tip for a great service is always appreciated. Generally 10%, 15%, or 20% is appropriate. You will get a great massage with or without a tip though. Gratuity is not included in with the massage prices.
“massages by andrea” accepts Visa/Discover/MC/American Express, Cash, or Checks. Receipts are also available.
Why should I get a massage? What are the benefits of a massage?
Nearly everyone can benefit from a massage. You don’t have to be an athlete to appreciate the difference massage can make in your physical well-being. Many benefits include: increasing circulation, improving muscle tone, relieving stress and tension, and promoting natural healing. It is the ultimate in physical and mental relaxation.
How often should I get a massage?
The answer to this question can only be answered by you. What are your goals? Are you wanting to de-stress? work on an injury? are you sore? were you referred by a health care provider? Discuss the options with your massage therapist to find out what works best for you. Remember that consistency is key in getting the most out of your treatment sessions.
Why am I told to drink plenty of water before/after a massage?
Muscle cramps can often be prevented by measures such as adequate hydration. If your body is low on water, the metabolic waste that is passed into the lymph system may attempt to resettle and give you that feeling of being sore or dizzy, or even leave you with a headache.
Why do I sometimes feel dizzy or ill after a massage?
Lymph is tissue fluid that circulates throughout the lymphatic system and may pick up bacteria and bring it to the lymph nodes where they are destroyed. If this lymph cannot flow, then metabolic waste may settle in and cause not only soreness, but also some dizziness and nausea. How much water have you been drinking? Staying hydrated in key.
Should I expect to feel sore after a massage?
Massage therapist should always check in with you to make sure the right amount of pressure is given. However, if tight muscles need extra work, you may feel the effects of the bodywork the following day. This is called Delayed Onset of Muscle Soreness (DOMS). If you are sore, most times this goes away by day 2. Please make sure you come to your session hydrated.
What is that “crunching” noise I hear when the massage therapist rubs my shoulders?
Fascia is a connective tissue that runs throughout the body and surrounds all of the muscles and organs. If this fascia is hard, a “crunching” noise may be heard until it is softened and is able to be “worked” or “kneaded”. Softened fascia allows movement and less restriction of these muscles and organs.
How old or young do I need to be to get a massage?
Massages are not age-appropriate based. As long as the massage therapist checks in with you making sure you are comfortable and the right pressure is used throughout the session, any age can receive a massage. Always give your massage therapist any contraindications so he or she can stay within your health boundaries. However, if the client is an infant or toddler, please find a therapist who is certified to work with this age.
What if I’m pregnant, should I get a massage?
It is advised to get your Doctor’s permission to get a massage if you are pregnant. Many Doctors have recommended massages to expecting mothers knowing that their bodies goes through so many changes during this special time.
What if I have allergies to creams, oils, or lotions?
There are some fragrances in creams and lotions that may cause a reaction on the skin. If this is the case, make sure you tell your massage therapist so they can use a water based lotion made especially for sensitive skin. The same goes for oil; if you are aware of a specific oil or scent that is harmful to your body, ask your therapist to use a carrier oil that is non-scented. Feel free to bring your own cream, oil, or lotion if this gives you peace of mind that you won’t have a reaction to something you are unfamiliar with.
Can I work out before or after a massage?
Massages help to ease sore and tight muscles, you might not feel like working out or doing anything except relaxing after receiving bodywork. However, some may feel rejuvenated and ready to conquer the world. It is wise to listen to your body.
What should I wear to a massage appointment?
It is up to each individual to undress down to their comfort level. Some people take everything off while others leave their underclothes on. You will never be undraped or exposed in any way that makes you feel uncomfortable.
Can I talk during a massage?
A massage is YOUR time and some people relax by talking while others just wish to stay quiet and reflect in silence. You decide as your massage therapist will follow your lead.
Do you offer Gift Certificates? …..YES !!!
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Category:
What Is Pilonidal Sinus Surgery?
Article Details
• Written By: J.M. Willhite
• Edited By: Heather Bailey
• Last Modified Date: 17 June 2017
• Copyright Protected:
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Pilonidal sinus surgery is a treatment option for recurrent pilonidal sinus infection. Depending on the presentation of the pilonidal sinus, surgery can range from drainage to excision of affected tissue. Invasive pilonidal sinus surgery is usually reserved for recurrent cyst formation, a condition known as pilonidal disease.
Contrary to its common association with the nasal cavity, sinus may be used to describe a cavity or tunnel within the skin. In the case of pilonidal sinus, the term is used to denote a passage or hole initiated and burrowed by a loose or stray hair. Located just above the buttocks, near the base of the tailbone, a pilonidal sinus can easily progress to form a cyst or abscess.
A sinus formation causes the skin to dimple, allowing a pocket, or cyst, to form just beneath the skin. In some cases, the cyst fills with bacteria and other foreign matter, including the inward growing hair, initiating infection and an abscess. As the infection worsens, the sinus adopts a pimply or inflamed, raised appearance and becomes tender to the touch.
An infected pilonidal sinus may be drained with the aid of a local anesthetic. The individual is generally given an oral antibiotic prior to surgery to alleviate infection. Often, the patient is instructed to finish the antibiotic as directed to help prevent recurrent infection. During the procedure, a small incision is introduced over the abscess so the collected pus and other foreign matter may be removed. The wound is left open and dressed appropriately to ensure proper healing.
When recurrent pilonidal cysts become an issue, more invasive pilonidal sinus surgery may be required. Individuals diagnosed with pilonidal disease generally undergo surgery to remove the affected tissue and prevent complication. The size of the cyst usually dictates the depth and length of the incision.
Pilonidal sinus surgery is generally performed with the intent of making the smallest incision necessary. When a cyst is considered relatively small, an incision is made directly over the growth so it may be completely excised. Sutures close the wound.
Depending on the size of the cyst, there are several surgical approaches that may be used to remove the growth. To lessen the risk for infection, the individual’s skin may be used to cover the wound. One such method is known as the Limberg flap. With this approach, a rhomboid-shaped incision is made over the cyst. Two of the sides are cut so a “flap” is made that may be lifted to allow access to the cyst. Once the excision is completed, the flap is lowered and stitches are made to close the wound.
The surgical approach is generally determined during a consultation when the patient may ask questions to help him or her prepare. Pre- and post-operative instructions are given to the patient at this time. Medications that may interfere with blood clotting or complicate surgery may be temporarily discontinued. As with any invasive medical procedure, pilonidal sinus surgery does carry a risk for complications, including infection and unnecessary bleeding.
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You are in Home >> Resources >> Physics and equipment >> Monitoring & Physical principles
The electrocardiogram (ECG)
Created: 2/11/2004
This is the recording and display of cardiac electrical activity. First performed in 1887.
Potentials from the heart are transmitted through the tissues and can be detected by electrodes which produce an ECG recording. Silver and silver chloride forms a stable electrode combination. They are separated from the skin by a foam pad soaked in conducting gel. The ECG signal is boosted by an amplifier, which also filters out noise. The amplified ECG signal is then displayed on an oscilloscope.
Monitoring mode
This mode has a frequency response of 0.5-40 Hz. All ECG monitors use filters to narrow the bandwidth in an attempt to reduce environmental artefacts. The high-frequency filters reduce distortions from muscle movement, mains current and electromagnetic interference from other equipment. The low-frequency filters help to provide a stable baseline by reducing respiratory and body movement artefacts.
Diagnostic mode
This mode monitors the ST-segment and there is a greater need for filtering of the signal. Thus, there is a wider frequency response range of 0.05-100 Hz. The high-frequency limit of 100 Hz ensures that tracings allow assessment of QRS morphology and tachyarrhythmias. The low-frequency limit allows representation of P and T wave morphology and ST-segment analysis.
Electrode configurations
Lead II is best for detecting arrhythmias.
CM5 detects 89% of ST-segment changes due to left ventricular ischaemia. (Right arm electrode on manubrium, left arm electrode on V5 and indifferent lead on left shoulder).
CB5 is useful in thoracic anaesthesia. Right arm electrode over the centre of the right scapula and left arm electrode over V5.
Sources of error
Electrical interference. This is the distortion of a biological signal by capacitance effects or inductance effects. Any electrical device, powered by AC, can act as one plate of a capacitor and the patient acts as the other plate. This may cause a current with AC frequency to flow in the ECG leads. Interference may also result from high frequency diathermy. Shielding of cables and leads, differential amplifiers and filters help to reduce such interference. The shielding consists of woven material which is earthed. Interference currents are induced in the metal screen and not in the monitoring leads. The screening layer may often be covered by a second layer of insulation. Shivering can produce artefacts. Thus, aim to place electrodes over bony prominences.
Differential amplifiers
The differential amplifier measures the difference between the potential from two different sources. Hence, if there is interference common to the input terminals (e.g. mains frequency) it can be eliminated, since it is only the difference between the terminals that is amplified by the differential amplifier. This is known as common mode rejection. The ratio of the output signal amplitude to the input signal amplitude is known as the gain of the amplifier.
References
[i] Value of the bipolar lead CM5 in electrocardiography.
Quyyumi AA et al.
Br Heart J 1986; 56[4]: 372-6
[ii] What clinicians should know about the QT interval.
Al-Khatib SM.
JAMA 2003; 289[16]: 2120-7
ArticleDate:20041102
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Parkinson's Disease Know The Important Symptoms & Treatments
August 31, 2020
Man walking with a women holding a bag
Parkinson’s disease – you may have heard of it because Neil Diamond and Ozzy Osbourne were recently diagnosed with it. Or perhaps you know Michael J. Fox is a strong advocate and funds research through his foundation. Neurologist Jonathan Spivack, MD, discusses this disease, while physiatrist Stephanie Jones, DO, explains how physical therapy can help as a supplemental treatment.
According to the Parkinson’s Foundation about ten million people worldwide currently have this disease.
What is Parkinson’s Disease?
“Parkinson’s disease is a neurodegenerative disease that progresses slowly and definitely, though at variable rates,” explains Dr. Spivack. “Symptoms go beyond the classic motor changes. It results from a loss of specific dopamine-producing brain cells. Specifically, this loss is likely due to a mix of genetic and environmental factors,” he adds.
Dopamine allows communication between particular nerve cells responsible for movement. If you have Parkinson’s dopamine levels gradually drop, causing a loss of motor skills. Generally, most patients with the disease are over age 65.
Early Signs and Symptoms
Diagnosing Parkinson’s can be difficult as some of the symptoms happen during the natural aging process. The Parkinson’s Foundation identifies the following 10 early signs of PD:
1. Tremors or shaking of your hand, fingers or chin
2. Small handwriting
3. Loss of smell
4. Sudden movements during sleep
5. Stiffness when walking or moving
6. Constipation
7. Softer or lower voice volume
8. Mad facial expression
9. Feeling dizzy or faint
10. Hunching or stooping posture
A single sign may not point to the disease, but if you (or a loved one) has multiple signs, talk to your healthcare provider.
Diagnosing Parkinson’s Disease
“It is a clinical diagnosis, based on symptoms that evolve over the course of the disease,” says Dr. Spivack. “There is no diagnostic test that can establish the disease.”
There are three cardinal symptoms, though only two need be present
1. Tremor
2. Rigidity: stiffness of muscles
3. Bradykinesis: slowness of movements
Not all symptoms are present at the outset, but develop over the course of the disease.
Diagnosing Parkinson’s disease can be difficult as some of the symptoms happen during the natural aging process. tests are not done for a diagnosis, but to rule out other illnesses than can mimic it.
Cause of Parkinson’s
Currently the cause of Parkinson’s is unknown, although scientists are researching three main factors.
1. Genetics
2. The environment – Several studies also suggest extended exposure to chemicals and environmental factors may play a part in developing Parkinson’s disease.
3. Aging – Most people develop Parkinson’s at the age of 50 or older, although a small percentage develop Young Onset Parkinson’s disease.
Treatment for Parkinson’s
“Treating Parkinson’s involves both medication and non-medication based modalities, along with surgery in specific cases,” observes Dr. Spivack. “The mainstay is medication based; all patients with the disease require their use. It is in advanced cases where surgery can be considered.”
“Treatments are symptom-based, variable in efficacy, and there is still controversy about when to start. Symptoms are controlled to a degree, the benefit(s) still lost over time, but life span is prolonged. With this comes significant functional disabilities at home, work, etc., all of which need to be addressed,” adds Dr. Spivack.
A neurologist is essential in the care of a Parkinson’s patient. “Because the disease has so many different symptoms, the treatments are multifaceted, so must be adjusted patient by patient,” says Dr. Spivack. “With all of these complexities, non-pharmacologic interventions like physical, occupational, speech, and nutritional therapies are critical to maintaining quality of life.”
Physical Therapy for Parkinson’s
“In addition to medication management of Parkinson’s, physical therapy is an important supplemental treatment of symptoms,” says Dr. Jones. “Continuing to participate in formal physical therapy sessions and maintaining a baseline level of physical activity can preserve, and even improve, a patient’s function, which includes their capability to walk and their balance.”
“Physical therapy can also help reduce negative secondary complications such as decreased range of motion of the joints and hardening (or shortening) of tissue,” adds Dr. Jones. “Lastly, it is important to follow a home exercise program, as prescribed by the physical therapist, to continue rehabilitation daily at home.”
Related Events
View All Classes & Events
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Have questions? Visit https://www.reddit.com/r/SNPedia
rs879255310
From SNPedia
Orientationplus
Stabilizedplus
Geno Mag Summary
(-;GA) 6 BRCA2 variant considered pathogenic for breast cancer
(AG;AG) 0 common in clinvar
(GA;GA) 0 common/normal
Make rs879255310(-;-)
ReferenceGRCh38.p2 38.2/147
Chromosome13
Position32341170
GeneBRCA2
is asnp
is mentioned by
dbSNPrs879255310
ClinGenrs879255310
ebirs879255310
HLIrs879255310
Exacrs879255310
Varsomers879255310
Maprs879255310
PheGenIrs879255310
hapmaprs879255310
1000 genomesrs879255310
hgdprs879255310
ensemblrs879255310
gopubmedrs879255310
geneviewrs879255310
scholarrs879255310
googlers879255310
pharmgkbrs879255310
gwascentralrs879255310
openSNPrs879255310
23andMers879255310
23andMe allrs879255310
SNP Nexus
SNPshotrs879255310
SNPdbers879255310
MSV3drs879255310
GWAS Ctlgrs879255310
Max Magnitude6
ClinVar
Risk rs879255310(-;-)
Alt rs879255310(-;-)
Reference Rs879255310(AG;AG)
Significance Pathogenic
Disease Breast-ovarian cancer
Variation info
Gene BRCA2
CLNDBN Breast-ovarian cancer, familial 2
Reversed 0
HGVS NC_000013.10:g.32915307_32915308delGA
CLNSRC
CLNACC RCV000239307.2,
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E- cigaret – A Substitute That Saves Lives & Improves Health
Smoking Tobacco is one of the most addictive habits that can be fatal to your health. There is a huge population of smokers, all over the world and 12 percent of them are Indians. According to the sources, around 900,000 Indians die every year due to smoking injurious tobacco.
E-cigaret
India has seen a rapid growth of smokers annually, and government sponsored awareness programs are telecasted in theatres, national television, radio etc.- encouraging people to quit smoking. Many tobacco users are seen shifting to nicotine tablets – However, the nation needs a fitting substitute that can replace the regular cigarettes.
What Are Electronic Cigarettes?
Electronic cigarettes are battery operated electronic devices that enable a tobacco user to inhale aerosol (Typically Contains Nicotine, Chemicals & Flavors), and empower him/her to quit smoking by eliminating the use of tobacco.
How Do Electronic Cigarettes Help Smokers Quit Tobacco?
Tobacco smokers are tempted to continue the habit due to the extensive nicotine requirement. The nicotine content in E-cigaret reduce the urge to smoke by countering the nicotine deficiency syndrome.
Electronic Cigarettes/e-cigaretter – Key Points to Remember
Electronic cigarettes is life saving and is the best substitute for tobacco smokers, However, it doesn’t mean that they are not harmful to your health. The following are the key facts associated with e-cigarettes-
In comparison to regular cigarettes, electronic cigarettes do not emit carbon monoxide- Therefore, these devices fueled by e-liquid, do not lead to environmental pollution.
• Electronic cigarettes have negligible effect on the stander-by and reduce the harmful effects of passive smoking.
• They are available in hundreds of flavors and there are hundreds of companies who are involved in manufacturing of electronic cigarettes.
• Electronic cigarettes are beneficial for a short to medium term use, and are aimed at cessation of smoking tobacco. However, long-term use can badly affect the human health.
The invention of electronic cigarettes is revolutionary and it has helped a number of users quit tobacco. However, it should be used as a preventive measure – Addiction of any kind will impair health and lead to unavoidable consequences.
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CBS
CBS (cystathionine beta synthase) catalyzes the first step of the transsulfuration pathway, from homocysteine to cystathionine. Dr. Yasko considers addressing CBS mutations as first priority aside from addressing the gut. CBS defects are actually upregulations. This means the enzyme works too fast. In these patients, it's common to see low levels of cystathionine and homocysteine since there is a rapid conversion to taurine. This leads to high levels of taurine and ammonia. The NOS mutation can exacerbate ammonia issues. Furthermore, addressing CBS can help lower excessive levels of taurine and help detoxify ammonia. Dr. Yasko recommends that one supports their CBS enzyme for at least 6 weeks before starting methylation supplements. When one tries to take nutrients to support their methylation cycle before addressing the CBS upregulation, all the nutrients basically lead to nowhere. Instead of generating glutathione, the supplements may deplete the rest of the cycle.
Addressing the CBS Mutation
Before one starts adding supplements, it may be a good idea to get a baseline UAA from a doctor. This will determine one's Taurine levels. After about 4-6 weeks of following the CBS protocol (outlined in the book Autism: Pathways to Recovery), one should retest their UAA. Once one's UAA is at 50% or below, one can add the methylation supplements. It's important to regularly use UAA testing as taurine should remain at 50% or less. If taurine climbs one may need to address ammonia. Yucca Root and Charcoal/Magnesium flushes can help address high ammonia levels. High doses of L-Ornithine may be effective as well according to medical studies.
The CBS mutation not only leads to excess taurine, but can also lead to excess sulfur groups. For this reason, it may be a good idea to limit sulfur intake. Excess sulfur intake can trigger a stress response or chronic stress. Sulfur is normally bound to amino acids, but the CBS upregulation can instead release the sulfur groups to sulfites in the body. There are many things one may need to avoid with a CBS upregulation. Some of the items include garlic, broccoli, eggs, onions, legumes, meat, Epsom salt baths, alpha lipoic acid, glutathione, chelating agents such as DMPS, NAC, Milk Thistle, various other supplements, and much more. Please look to other sources for foods and supplements that are high in sulfur.
Supplementing with molybdenum may help as excess sulfites deplete it. Manganese is also important in ammonia detoxification. A Low protein diet can help as the body will have less ammonia to detoxify. It's important to measure molybdenum and manganese with a minerals test before supplementing.
BH4 can also become depleted with a CBS upregulation. BH4 helps regulate neurotransmitters and mood. Other mutations, such as MTHFR A1298C, Chronic bacterial infections, and aluminum can also lead to low BH4 levels. Lack of BH4 can lead to mast cell degranulation and possibly mast cell activation disorder (MCAD). While difficult to obtain, BH4 supplementation may help in the presence of BH4 deficiency.
Other supplements that may help are Slippery elm bark for the gut. And according to Dr. Yasko Molybdenum, EDTA, carnosine, and zinc may help balance the copper/zinc ratio.
The CBS Upregulation is a complicated subject and for more info, I suggest purchasing or finding the book Autism: Pathways to Recovery. Searching for other websites or online support groups talking about the subject may be of help as well.
MTHFR C677T
One function of MTHFR (Methylenetetrahydrofolate reductase) is to help convert homocysteine to methionine. A MTHFR C677T mutation means that the MTHFR enzyme may have trouble performing its task leading to high levels of homocysteine. According to Dr. Ben Lynch, impaired function of the enzyme can cause or contribute to conditions such as Autism, Chronic Fatigue Syndrome, Fibromyalgia, Miscarriages, IBS, many birth defects, Multiple Sclerosis, Alzheimer's, Bipolar Disorder, blood clots, Stroke, Chemical Sensitivity, and many other conditions.
MTHFR C677T can also lead to high homocysteine. You can ask your doctor to test for homocysteine levels. If you have high levels of homocysteine, it may be related to your MTHFR C677T mutation. But even if one has a (+/+) or (+/-) mutation, it does not necessarily mean that they will have high homocysteine levels.
As S-adenosylhomocysteine (SAH) accumulates, the COMT enzyme may become impaired. Inhibiting COMT can increase dopamine levels for those with COMT V158M (-/-), but for those with COMT V158M (+/+), the high level of SAH can lead to behavior problems and mood swings according to Dr. Amy Yasko.
Nutritional Support of MTHFR C677T
Supplementing with Folate (preferably as L-Methylfolate) can help alleviate the effects of MTHFR C677T as well as lower one's homocysteine levels. There are a lot of different types of folate on the market, and I recommend reading this article by Dr. Ben Lynch about folate. It might be a good idea to avoid synthetic folic acid and folic acid fortified foods such as cereals. Also, lowering other doses of forms of folate or folinic acid may be important as it can compete with L-methylfolate.
To avoid adverse effects, one can start with very low doses of folate and work to higher doses. Side effects can occur as a detoxification effect as this pathway becomes unblocked. In the case of extreme adverse effects, time-released niacin and/or potassium may be able to stop the side effects.
MTHFR 03
There is currently not enough data to draw conclusions about the significance of this SNP.
MTHFR A1298C
MTHFR A1298C is involved in converting 5-methylfolate (5MTHF) to tetrahydrofolate (THF). Unlike MTHFR C677T, the A1298C mutation does not lead to elevated homocysteine levels. This reaction helps generate BH4. BH4 is important in the detoxification of ammonia. The gene is compromised about 70% in MTHFR A1298C (+/+) individuals, and about 30% in people with a heterozygous (+/-) mutations.
BH4 acts as a rate limiting factor for the production of neurotransmitters and catecholamines including serotonin, melatonin, dopamine, norepinephrine, and epinephrine. A MTHFR A1298C + status may cause a decrease in any of these neurotransmitters or catecholamines. It's also a cofactor in the production of nitric oxide. If your BH4 cycle is not working effectively, you may experience mental/emotional and/or physical symptoms. Mercury, lead, and aluminum may act as a drain on BH4.
Adressing MTHFR A1298C
L-methylfolate supplementation may be implicated. One should start with low doses of L-methylfolate, and in the case of adverse reaction time-released niacin and/or potassium may help.
Metal detoxification (especially aluminum) can help address dysfunctions associated with MTHFR A1298C and BH4 deficiency, and can help many other biochemical abnormalities as well. Aluminum toxicity can hinder one's ability to fight infection, so addressing the gut and treating chronic bacterial infection may be important. Since the A1298C mutation can lead to excess ammonia, one can address these elevated levels with things like charcoal/magnesium flushes, Yucca Root, and L-Ornithine. Keeping ammonia low helps preserve BH4 levels.
Low doses of BH4 may be helpful after one's methylation cycle is fully supported.
COMT
COMT (catechol-O-methyltransferase) helps break down certain neurotransmitters and catecholamines. These include dopamine, epinephrine, and norepinephrine. Catechol-O-methyltransferase is important to the areas of the pre-frontal cortex. This area of the brain is involved with personality, inhibition of behaviors, short-term memory, planning, abstract thinking, and emotion. COMT is also involved with metabolizing estrogens.
COMT (-/-) individuals can usually break down these neurotransmitters efficiently, but COMT (+/+) individuals may have trouble breaking these chemicals down from impaired function of the enzyme. With a COMT + status, people may have trouble with methyl donors. This can lead to irritability, hyperactivity, or abnormal behavior. They also may be more sensitive to pain.
Nutritional support of COMT mutations
Since COMT + individuals often have trouble tolerating methyl donors, they tend to do better on a combination of hydroxy B12, adenosyl B12, and/or cyano B12. Methyl B12 is usually much easier to tolerate for those that are COMT (-/-).
VDR
VDR (Vitamin D Receptor) encodes the nuclear hormone receptor for vitamin D3. Low or low normal vitamin D values are often seen in those with chronic illness and even the general population. Low vitamin D is related to a lot of neurological and immunological conditions. Vitamin D stimulates enzymes that create dopamine.
VDR Fok has been associated with blood sugar issues and poor pancreatic activity.
With COMT V158M + and a VDR Taq + status, the body may have further trouble tolerating methyl donors. VDR Taq (-/-) individuals may already have higher levels of dopamine, and it's worth noting that combinations of variations COMT and VDR Taq can lead to a wide range of dopamine levels. Those that are VDR Taq (+/+) and COMT (-/-) may have lowest dopamine levels.
Nutritional support of VDR Mutations
Dr. Yasko advises patients to rotate methyl-containing supplements (instead of using them all daily) for those with COMT V158M + and VDR Taq (-/-).
Ginkgo biloba may increase dopamine uptake. Small doses of Mucuna Pruriens contains natural dopamine, and can be helpful for those with low dopamine.
VDR Fok + can impact vitamin D levels. Research shows that supplementing vitamin D may be beneficial. Sage and rosemary support vitamin D receptors. It may be necessary to support the pancreas when having a VDR Fok + mutation using vitamin and digestive/pancreatic enzymes.
MAO-A
MAO-A (Monoamine oxidase A) is a critical enzyme involved in breaking down important neurotransmitters such as serotonin, norepinephrine, and dopamine. Males only have one allele since the gene is inherited through from their mother since it is located on the X chromosome. Only females can be heterozygous (+/-) for this mutation. When a (+/+) MAO-A mutation is combined with a (+/+) or (+/-) COMT V158M mutation, one may be more prone to develop Obsessive Compulsive Disorder (OCD), mood swings, aggressive and/or violent behavior, and personality disorders. Chronic infection can deplete tryptophan stores, and this can be tested with an organic acid test (OAT) and urine amino acid tests (UAA) according to Dr. Yasko. This test may indicate high levels of 5HIAA (5-hydroxy indole acetic acid).
Nutritional support of MAO-A R297R
Dr. Yasko says that her Mood S RNA formula and 5HTP may help balance serotonin. Furthermore, she satiates that BH4 deficiency (often caused by aluminum toxicity), increased levels of ammonia, and MTHFR A1298C are all factors that can negatively impact serotonin levels.
There is not a whole lot of information out there on how to increase the activity of the enzyme. And while not nutritional, there is a product called Respen-A developed for Autism with intention of increasing MAO-A activity. Respen-A can only be obtained from a few compounding pharmacies and requires a prescription.
ACAT/SHMT
ACAT1-02 (acetyl coenzyme A acetyltransferase) plays a role lipid metabolism and energy generation. It can also deplete B12. As with CBS, Dr. Yasko views this as a first priority mutation. Going by Yasko's clinical experience, she says to address them first if you have elevated iron on a UEE, elevated iron on a UEE test, Short Chain Fatty Acid (SCFA) imbalances on a CSA test, suberic acid, beta hydroxyl methylglutaric acid, or other ketone and fatty acid metabolites imbalances on a MAP or OAT test; or if there are severe gut issues or muscle weakness (which can be related to aluminum retention)". She says people with ACAT or SHMT are more likely to experience gut dysbiosis. Because of disrupted flora, microbes may have an affinity for and retain toxic metals. Stabilizing the gut environment is very important.
More info to come as Genetic Genie continues to research these SNPs.
MTR
MTRR (Methionine synthase reductase) helps recycle B12. The combination of MTR and MTRR mutations can deplete methyl B12. MTR A2756G, MTRR A66G, MTRR H595Y, MTRR K350A, MTRR R415T, MTRR S257T, and MTRR A664A all work together to convert homocysteine to methionine.
MTR (5-methyltetrahydrofolate-homocysteine methyltransferase) provides instructions for making the enzyme methionine synthase. Methionine synthase helps convert the amino acid homocysteine to methionine. To work properly, methionine synthase requires B12 (specifically in the form of methylcobalamin). An MTR A2756G mutation increases the activity of the MTR gene causing a greater need for B12 since the enzyme causes B12 to deplete since it is using it up at a faster rate. Mutations in MTR have been identified as the underlying cause of methylcobalamin deficiency. Megaloblastic anemia can occur as a consequence of reduce methionine synthase activity.
A homozygous mutation of MTR A2756G is relatively rare (<1%). Some studies have demonstrated that people with a combination of MTHFR C677T and MTR A2756G have persistently high homocysteine levels unless they are treated with both B12 and folate.
Nutritional support of MTR/MTRR
According to Dr. Yasko's clinical experience, one should first take into account COMT V158M and VDR Taq status. She finds that those with COMT V158M + and VDR Taq - mutations often don't tolerate methyl donors well. She says that those with these mutations should carefully balance their ratio of Hydroxyl B12 and Methyl B12. She often suggests low dose cyano B12, adenosyl B12, and vitamin E succinate. High dose methylcobalamin (5 mg per day and above) may be implicated and necessary with this mutation - especially if one is homozygous and/or has MTRR + mutations. The level of B12 one needs depends often depends on the number and combination of these mutations. Like everything else, one should slowly build up doses of both methylcobalamin and/or hydroxocobalamin to avoid adverse effects.
DMG and the supplement TMG also stimulate the BHMT pathway to convert homocysteine to methionine, but one should take caution if they are sensitive to methyl donors.
Patients with MTR/MTRR may also benefit from the combination of GABA and L-Theanine. L-Theanine is a methyl donor. They may also benefit from taurine, Pycnogenol® pine bark extract, and grape seed extract.
BHMT
BHMT (betaine homocysteine methyltransferase) acts as a shortcut through the methylation cycle helping convert homocysteine to methionine. The activity of the enzyme can be negatively influenced by stress. The Information on this enzyme related to methylation is mostly based on Dr. Amy Yasko's clinical experience and research.
According to Dr. Yasko, a homozygous mutation of BHMT 01, BHMT 02, BHMT 04, can produce results similar to one with a CBS upregulation even if you don't have a CBS upregulation. In her book, Autism: Pathways to Recovery, She also states that a BHMT 08 mutation may "increase MHPG levels relative to dopamine breakdown (HVA)". This can result in attention type symptoms. It is common to see elevated glycine in someone with a homozygous BHMT 08 mutation.
Addressing the BHMT mutations
According to Dr. Yasko, limiting taurine for BHMT 01, 02, and 04 may be helpful, and supplementing NADH, SAMe, and DMG may help with BHMT 08 + status. According to the Heartfixer Analysis, one may bypass the dysfunctional enzymes by stimulating the BHMT pathway to convert homocysteine to methionine in several other ways. Phosphatidylcholine or phosphatidylserine can stimulate the BHMT pathway. A good quality lecithin is a good source of phosphatidylcholine (it usually comes from soy, eggs, or sunflower seed). Egg yolks are a good source of lecithin as well. TMG is also an option, but one should take caution if they are sensitive to methyl donors.
If you have a BHMT 01, BHMT 02, or BHMT 04 mutation and don't have a CBS mutation, information about CBS was not included in your report. If you have these mutations, you can find our info about addressing the CBS upregulation at http://www.geneticgenie.org/all-mutations.
AHCY
AHCY (S-adenosylhomocysteine hydrolase) is involved in breaking down the amino acid methionine. It controls the step that converts S-adenosylhomocysteine hydrolase to adenosine and homocysteine. Adenosine plays an important role in energy transfer as ATP and ADP. It helps promote sleep and suppress arousal. Dysfunction of this enzyme can affect levels of homocysteine and ammonia. AHCY mutations may actually take the strain off the CBS enzyme and may even prevent taurine from becoming very elevated.
2 Responses to “All Mutations”
1. coby miller Says:
what about the GAD mutation. is there any work around for that mutation, i have a few of the GAD and GAD1 mutations.
Thanks, geneticgenie, this is an awsome thing you are doing.
2. George Manlove, DC Says:
The GAD enzymes convert glutamate (an amino acid which acts as an excitatory neurotransmitter) into GABA which is the main inhibitory neurotransmitter. GABA does not normally cross and intact blood brain barrier. People with a GAD SNP may need help making more GABA. It is possible to get forms of GABA that do cross the blood brain barrier, ie phenyl-GABA, and herbs such as Valerian and Passionflower which help with GABA receptor sensitivity. Many people who are gluten sensitive may also produce antibodies to GAD which can have the same effect. There is a common blood test for GAD antibodies since it is associated with Type I diabetes.
Leave a Reply
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Patents
Publication numberUS4254222 A
Publication typeGrant
Application numberUS 06/925,946
Publication dateMar 3, 1981
Filing dateJul 19, 1978
Priority dateJul 19, 1978
Also published asEP0016129A1, WO1980000259A1
Publication number06925946, 925946, US 4254222 A, US 4254222A, US-A-4254222, US4254222 A, US4254222A
InventorsOliver E. Owen
Original AssigneeOwen Oliver E
External Links: USPTO, USPTO Assignment, Espacenet
Semi-quantitative assay of lactic acid and β-hydroxy butyrate
US 4254222 A
Abstract
There is provided a procedure for determining the concentration of a metabolic acid in a biological fluid. The method involves use of a tetrazolium salt, a pyridine nucleotide, an electron carrier, and an enzyme that is a dehydrogenase for the specific acid being assayed. These components are used to form an assay mixture; thereafter a quantity of the fluid to be assayed is combined with the assay mixture, so that there may commence a reaction in which the tetrazolium salt is changed to a formazan in an amount that is indicative of the concentration of the specific acid. In a preferred embodiment, the procedure permits assay of the concentration of beta-hydroxybutyrate, and the assay mixture includes components in the relative proportions of 0.8 micromoles 2-(p-iodophenyl)-3-(p-nitrophenyl)-5-phenyltetrazolium chloride (INT), 0.32 micromoles phenazine methosulfate (PMS), 1.5 micromoles nicotinamide adenine dinucleotide (NAD), and 0.75 International Units beta-hydroxybutyrate dehydrogenase, in a water solution buffered at a pH of approximately 8.5 with hydrogen phosphates of potassium together with glycine and sodium hydroxide and also containing alkylphenoxypolyethyoxyethanol. In another preferred embodiment, the procedure permits assay of lactic acid by means of a similar assay mixture utilizing 27.5 International Units of lactic dehydrogenase in place of the beta-hydroxybutyrate dehydrogenase used in the previously discussed embodiment. In the latter procedure a preferred embodiment of the assay mixture is buffered at a pH of approximately 9.6 in a glycine-sodium hydroxide buffer and also contains phenoxypolyethyoxyethanol.
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Claims(8)
What is claimed is:
1. An assay mixture, for determining the concentration of beta-hydroxybutyrate in a biological fluid, such mixture comprising the following components in the approximate concentrations set forth:
1.1 m Molar tetrazolium salt;
0.4 m Molar electron carrier;
2.0 m Molar NAD; and
1 International Unit/ml beta-hydroxybutyrate dehydrogenase.
2. A mixture according to claim 1, wherein the tetrazolium salt is INT, and the electron carrier is PMS.
3. A mixture according to claim 1, wherein the tetrazolium salt is INT, and the electron carrier is Meldola Blue.
4. The mixture according to any of claims 2 or 3, such mixture further comprising components, in approximate concentrations as follows:
(i) a mixture of 0.03 Molar potassium dihydrogen phosphate with 0.03 Molar potassium, monohydrogen phosphate in proportions to give in solution a buffer having a pH of approximately 8.5; and
(ii) 2.5 g. glycine/l, 6.3 ml alkylphenoxypolyethyoxyethanol/l, and sufficient sodium hydroxide to give with the foregoing two components in solution a buffer having a pH of approximately 8.5.
5. An assay mixture for determining the concentration of lactic acid in a biological fluid, such mixture comprising the following components in the approximate concentrations set forth:
1.1 m Molar tetrazolium salt;
0.45 m Molar electron carrier;
2.1 m Molar NAD; and
39 International Units/ml of lactic dehydrogenase.
6. The mixture according to claim 5, wherein the tetrazolium salt is INT, and the electron carrier is PMS.
7. A mixture according to claim 5, wherein the tetrazolium salt is INT and the electron carrier is Meldola Blue.
8. A mixture according to any of claims 6 or 7, such mixture further comprising components in approximate concentrations as follows: 5.3 g glycine/l, 7 ml alkylphenoxylpolyethyoxyethanol/l, and sufficient sodium hydroxide to give with the foregoing two components in solution a buffer having a pH of approximately 9.6.
Description
BACKGROUND OF THE INVENTION
The present invention relates to determination of the concentration of specific metabolic acids in biological fluids, and in particular, the concentration of betahydroxybutyrate and lactic acid in biological fluids.
In humans, as well as in certain other animals, the organism may experience or suffer from a state of metabolic acidosis. Of the types of acidosis, there are recognized hyperketonemia, hyperlacticacidemia, uremicacidemia, and toxicacidemia.
On certain occasions, it may be possible to determine that there is present a condition of metabolic acidosis, but determination of the type of acidosis present may be difficult without expensive and time-consuming laboratory analysis. Moreover, it may be difficult to determine even whether there is present a metabolic acidosis condition. For example, with respect to hyperketonemia there is a rapid semi-quantitative test for only one ketone body, namely, acetoacetate. The test for acetoacetate concentration is made by use of a nitroprusside impregnated test surface. The test surface is then immersed in the biological fluid to be assayed, and an indication of the concentration can be obtained by observing the color of the test surface after a predetermined time has elapsed. Disadvantages of the nitroprusside technique are discussed in K. G. M. M. Alberti and T. D. R. Hockaday, "Rapid Blood Ketone Body Estimation in the Diagnosis of Diabetic Ketoacidosis," 1972 British Medical Journal, 2, 565-568. The nitroprusside technique does not measure the concentration of betahydroxybutyrate, the major ketone body. The result is the possibility of a misleading determination of the total ketone bodies in the biological fluids.
Although lactic acidosis may be the most common form of metabolic acidosis, there is a problem in determining rapidly the concentration of lactate in biological fluids. Short of laboratory analysis, it is common for the physician to assume the presence of lactic acidosis when other forms of metabolic acidosis have been ruled out by other techniques. For example, the relatively poor nitroprusside technique is used to rule out the presence of hyperketonemia, and other methods are used to rule out the presence of uremicacidemia and toxicacidemia. Thus, despite the frequency of occurrence of lactic acidosis, the number of cases actually documented on the basis of direct analysis are relatively uncommon.
SUMMARY OF THE INVENTION
It is a primary object of the present invention to provide a rapid semi-quantitative assay for the concentration of a given specific acid in a biological fluid, where the given acid may be, inter alia, beta-hydroxybutyrate or lactic acid.
It is a further object of this invention to provide a method of enzymatic analysis of metabolic acids in a biological fluid.
Another object of this invention is to provide a rapid method of determining the concentration of a metabolic acid in a biological fluid by means of observation of the color of the product of an enzymatic reaction.
Another object of this invention is to provide a method of enzymatic analysis that can be accomplished without recourse to spectrophotometric or colorimetric methods.
It is a further object of this invention to provide an assay mixture, which when combined with a sample of the fluid to be assayed, provides a method of determining metabolic acid concentration by visual inspection.
These and other objects of the invention are achieved by providing a method involving preparation of an assay mixture including a tetrazolium salt, a pyridine nucleotide, an electron carrier, and an enzyme that is a dehydrogenase for the specific acid being assayed. Thereafter, a quantity of the fluid to be assayed is combined with the assay mixture so that there may commence a reaction in which the tetrazolium salt is changed to a formazan in an amount that is indicative of the concentration of the specific acid. There is also provided an assay mixture prepared as heretofore described.
In a preferred embodiment, the method permits assay of the concentration of beta-hydroxybutyrate. In this embodiment, the assay mixture includes components in the relative proportions of 0.8 micromoles 2-(p-iodophenyl)-3-(p-nitrophenyl)-5-phenyl-tetrazolium chloride (INT), 0.32 micromoles phenazine methosulfate (PMS), 1.5 micromoles nicotinamide adenine dinucleotide (NAD), and 0.75 International Units beta-hydroxybutyrate dehydrogenase, in a water solution buffered at a pH of approximately 8.5. The buffering agents include hydrogen-phosphates of potassium together with glycine and sodium hydroxide. The solution also contains alkylphenoxypolyethoxyethanol as the agent to increase solubility of the formazan.
In another preferred embodiment, the method in accordance with the invention permits assay of the concentration of lactic acid in a biological fluid. The method is analogous to that used in connection with beta-hydroxybutyrate, and involves preparation of a similar assay mixture, in which 27.5 International Units of lactic dehydrogenase are utilized in place of the 0.75 International Units of beta-hydroxybutyrate dehydrogenase. The lactic acid assay mixture, in a preferred embodiment, is buffered at a pH of approximately 9.6 in a glycine-sodium hydroxide buffer; alkylphenoxypolyethoxyethanol is also used as the solubilizing agent.
There are also provided assay mixtures for use in practicing the above methods, such mixtures being of a nature heretofore described.
DESCRIPTION OF SPECIFIC EMBODIMENTS
Referring now to a preferred embodiment of the invention relating to a method of assay of the concentration of beta-hydroxybutyrate (BOHB), BOHB is oxidized enzymatically to acetoacetate (AcAc) with a corresponding reduction of nicotinamide adenine dinucleotide (NAD) to NADH.
The NADH that has been formed is ineffective in reducing directly a tetrazolium salt to a formazan. Consequently an intermediate electron carrier is used, in this case phenazine methosulfate (PMS). Reactions then following are the oxidation of NADH back to NAD by PMS, which becomes PMS-H. The reduced PMS-H is then capable of reducing the tetrazolium salt to its formazan. In this embodiment tetrazolium salt used is 2-p-iodophenyl-3-(p-nitrophenyl)-5-phenyltetrazolium chloride (INT).
Accordingly, the reactions in the preferred embodiment of the method for assay of BOHB are as follows: ##EQU1##
In accordance with this embodiment, there is prepared first a color reagent mixture and a buffer solution. The color reagent mixture consists of a 4 mMolar INT, 1.6 mMolar PMS, and 7.5 mMolar in NAD. To prepare 25 ml of color reagent mixture, one dissolves 50 mg of INT in 20 ml of distilled water, stirring as necessary. When the INT has been completely dissolved, one adds 125 mg NAD and 12.5 mg PMS. When these have been dissolved, one dilutes the mixture with distilled water until the total volume is 25 ml. Preferably, the color reagent should be stored refrigerated in a dark brown bottle or other relatively opaque container, since PMS is sensitive to light.
The buffer solution used in connection with this method is a mixture of two buffer systems. One system is a phosphate buffer employing 0.1 Molar solutions of potassium dihydrogen phosphate and potassium hydrogen phosphate. These solutions are mixed in such proportions as to result in a buffer having a pH of 8.5.
The other buffer system is based on glycine and sodium hydroxide. To this system is also added a small portion of alkylphenoxypolyethyoxyethanol, which is sold under the trademark "Triton X-100" by Rohm and Haas Company, Philadelphia, Pennsylvania. This second buffer system is prepared by dissolving 7.5 g of glycine in 800 ml of distilled water. To this solution is added 20 ml of alkylphenoxypolyethyoxyethanol, whereupon the pH is adjusted to 8.5 with 0.1 Molar sodium hydroxide. The resulting solution is then diluted to 1 liter with distilled water.
After both the phosphate buffer system and the glycine-sodium hydroxide buffer system have been prepared, the combined buffer system is made by mixing the equal volumes of each buffer system.
The BOHB dehydrogenase is in liquid form in concentration of 10 mg/2 ml, 3 I.U./mg.
If desired, concentrated hydrochloric acid diluted with distilled water to 50 percent strength can be prepared for use as described below.
In accordance with a preferred embodiment of the method of the invention, an assay mixture is prepared from the above reagents by mixing in a test tube 0.5 ml of the combined buffer solution, 0.2 ml of the color reagent mixture, and 0.05 ml of BOHB dyhydrogenase in the concentration specified previously. To this assay mixture is then added a 1-drop sample of the biological fluid to be assayed. When 60 seconds have elapsed after the drop has been added, the color of the resulting solution is then observed. If desired, the reaction can be stopped at this point by the addition of the hydrochloric acid solution.
In accordance with the color of the assay solution after 60 seconds of reaction time with the sample, there can be determined the concentration of BOHB in the sample, as set forth in the following table.
______________________________________Color Of Solution Concentration In Sample (mM)______________________________________Faint Yellow Less than 1Peach 2.5Orange 5Red-Orange 7.5Brick Red 10______________________________________
A similar procedure obtains in accordance with a preferred embodiment of the invention for assay of the concentration of lactic acid in a biological fluid. The lactic acid assay involves the enzymatic oxidation of lactic acid to pyruvate with a corresponding reduction of NAD to NADH. The NADH that is formed is oxidized to NAD by PMS, which becomes PMS-H. The reduced PMS-H is then used to reduce INT to its corresponding formazan. The reactions are thus ##EQU2## In accordance with a preferred embodiment of the method employing these reactions, a color reagent mixture is prepared in exactly the fashion described above in connection with BOHB analysis. The buffer solution in this case is, however, entirely a glycine-sodium hydroxide system. Preparation of the buffer is accomplished by dissolving 7.5 g of glycine in 800 ml of distilled water. Thereafter 20 ml of alkylphenoxypolyethyoxyethanol are added, and the pH is adjusted to 9.6 by means of the addition of a water solution of 0.1 Molar sodium hydroxide. The resulting solution is then diluted with distilled water to 1 liter.
The enzyme used in this method is lactic dehydrogenase in a concentration of 25 mg/5 ml, 550 I.U./mg.
Also, as in the case of the BOHB procedure, 50 percent hydrochloric acid may be used as described below.
The assay mixture is prepared by mixing in a test tube 0.5 ml of buffer solution, 0.2 ml of color reagent mixture, and 0.01 ml of lactic dehydrogenase. To the assay solution is added a 1-drop sample of the biological fluid to be assayed, and the reaction product is observed after 60 seconds have elapsed since the reaction was commenced. As in the case of the BOHB procedure, the reaction can be stopped by the addition of the hydrochloric acid mixture.
The concentration of lactic acid can be determined by reference to the same table as is set forth above in connection with BOHB measurement.
It will be understood that numerous other embodiments of the invention are possible. For example, an assay mixture prepared in accordance with one of the above methods may be used to saturate a substance such as paper, and then the water in the solution may be permitted to evaporate. The resulting anhydrous form of the assay mixture impregnated in the paper may permit the paper to be used as a test surface, the color of which, after immersion thereof in a sample to be assayed and a fixed waiting period thereafter, may be an indication of the concentration of the specific metabolic acid being assayed.
Also, for example, the choice of NAD as the pyridine nucleotide is somewhat arbitrary, since nicotinamide adenine dinucleotide phosphate (NADP) has similar properties, although substantially higher concentrations of this pyridine nucleotide would be required, since this enzyme is relatively nonspecific. Furthermore, the use of PMS as the electron carrier is not mandatory. Another electron carrier is 8-dimethylamino-2,3-benzophenoxazine (Meldola Blue), which is in fact less sensitive to light and an efficient carrier. Other possible carriers include diaphorase, thionin, Nile Blue A, and Janus Green B.
Also, the solubilizing agents used for increasing solubility of the formazan are somewhat a matter of choice. Such agents may include gelatin and ethoxylated oleyl alcohol or other non-ionic surface-active agents.
Also, the buffer solutions employed are somewhat a matter of choice, as is the concentrated acid used to stop the reaction.
It may be possible to use tetrazolium salts other than INT, including, for example, 3-(4',5'-dimethylthiazol-2-yl)-2,4-diphenyltetrazolium bromide (MTT).
It will be appreciated that as concentrations of various reagents, and the particular identities of the reagents themselves, are varied, the colors resulting from various concentrations of the metabolic acid being assayed will differ from those presented in the table above. It is significant, however, that various embodiments of the invention will permit a table to be constructed so as to form the basis for the determination of metabolic acid concentration by means of visual inspection of the reaction product of the assay mixture.
Accordingly, while the invention has been described with particular reference to specific embodiments thereof, it will be understood that it may be embodied in a variety of forms diverse from those shown and described without departing from the spirit and scope of the invention as defined by the following claims.
Patent Citations
Cited PatentFiling datePublication dateApplicantTitle
US3528888 *Jun 11, 1968Sep 15, 1970CalbiochemReagent and method for assaying alpha-hydroxybutyrate dehydrogenase
US3539453 *Jun 12, 1968Nov 10, 1970CalbiochemReagent and method for assaying lactate dehydrogenase
US3867258 *Nov 8, 1973Feb 18, 1975American Cyanamid CoLactate dehydrogenase test material
Non-Patent Citations
Reference
1 *Alberti et al., "Rapid Blood Ketone Body Estimation In The Diagnosis Of Diabetic Ketoacidosis", British Med. J., vol. 2, (1972) pp. 565-568.
2 *Babson et al., "A Rapid Colorimetric Assay for Serum Lactic Dehydrogenase", Clin. Chim Acta, vol. 12, (1965), pp. 210-215.
3 *Bergmeyer et al., "Colorimetric Assay with L-Lactate, NAD, Phenazine Methasulfate and INT", Methods of Enzymatic Analysis, (ed. Bergmeyer) 2nd ed. (1974), pp. 579-582.
4 *Friedland et al., "A Rapid Enzymatic Determination of L (+)-Lactic Acid", Anal. Biochem., vol. 2, (1961), pp. 390-392.
5 *Hochella et al., "Automated Lactic Acid Determination in Serum and Tissue Extracts", Anal. Biochem, vol. 10 (1965), pp. 304-317.
6 *Mollering et al., "Visualization of NAD (p)-Dependent Reactions", Methods of Enzymatic Analysis, (ed. Bergmeyer) 2nd ed. (1974), pp. 136-144.
7 *Nachlns et al., "The Determination of Lactic Dehydrogenase with a Tetrazolium Salt", Anal. Biochem, vol. 1 (1960) pp. 317-326.
8 *Raabo, "Determination of Serum Lactic Dehydrogenase by Tetrazolium Salt Method", Second J. Clin. and Lab. Investigation, vol. 15, (1963), pp. 233-238.
9 *Whitaker, "A General Colorimetric Procedure for the Estimation of Enzymes Which are Linked to the NaDH/NAD & System", Clin. Chim. Acta, vol. 24 (1969) pp. 23-37.
10 *Zivin, et al., "An Automated Colorimetric Method for the Measurement Of 3-Hydroxy-Butyrate Concentration", Anal. Biochem., vol. 52, (1973), pp. 456-461.
Referenced by
Citing PatentFiling datePublication dateApplicantTitle
US4786589 *Aug 18, 1986Nov 22, 1988Huntington Medical Research InstituteImmunoassay utilizing formazan-prelabeled reactants
US4803158 *Oct 23, 1986Feb 7, 1989Kabushiki Kaisha Kyoto Daiichi KagakuComposition used for the determination of beta-hydroxybutyric acid and a method for preparing the said composition
US5326697 *Sep 8, 1992Jul 5, 1994Miles Inc.Composition and method of assaying for D-β-hydroxybutyrate
US5358855 *May 14, 1992Oct 25, 1994The Medical College Of PennsylvaniaInosinic acid dehydrogenase assay
US5501949 *Aug 15, 1994Mar 26, 1996Murex Diagnostics CorporationParticle bound binding component immunoassay
US5916746 *May 9, 1996Jun 29, 1999Kirkegaard & Perry Laboratories, Inc.Formazan-based immunoassay
US6541216Dec 22, 1999Apr 1, 2003Roche Diagnostics CorporationAmperometric biosensor test strip
US6703216Mar 14, 2002Mar 9, 2004The Regents Of The University Of CaliforniaMethods, compositions and apparatuses for detection of gamma-hydroxybutyric acid (GHB)
US7144709Nov 16, 2004Dec 5, 2006Lifescan, Inc.Diagnostics based on tetrazolium compounds
US7435558Feb 22, 2002Oct 14, 20083M Espe AgAscertaining the patient related risk of caries
US8500990Apr 22, 2009Aug 6, 2013Nova Biomedical CorporationElectrochemical biosensors based on NAD(P)-dependent dehydrogenase enzymes
CN102435749BSep 2, 2011Oct 16, 2013宁波美康生物科技股份有限公司用循环酶法测定β-羟丁酸的液体稳定试剂盒
WO1993023558A1 *May 14, 1993Nov 25, 1993Pennsylvania Med CollegeInosinic acid dehydrogenase assay
WO1997042342A1 *May 6, 1997Nov 13, 1997Kirkegaard & Perry Lab IncFormazan-based immunoassay
WO2013045443A1Sep 25, 2012Apr 4, 2013Emilia BramantiMeasurement of lactic acid in biological fluids
Classifications
U.S. Classification435/26, 435/805, 435/810
International ClassificationC12Q1/32
Cooperative ClassificationY10S435/81, Y10S435/805, C12Q1/32
European ClassificationC12Q1/32
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@article{Dal Pozzo_Felisati_Saibene_Guenza_Vinciguerra_Pellegrini_Dellavia_2015, title={Uncinate process deviation in patients with odontogenic sinusitis: a computed tomographic evaluation}, volume={120}, url={https://oajournals.fupress.net/index.php/ijae/article/view/4031}, abstractNote={The uncinate process of the ethmoidis is one of the anatomic boundaries of osti- omeatal complex. Its relationship with the maxillary sinus ostium makes it the key landmark for endoscopic sinus surgery. Many authors denied a direct role of the uncinate process in the development of sinonasal infections (1). Nevertheless, chronic sinonasal diseases are often accompanied by an uncinate process antero-medialization, most notably in presence of an odontogenic etiology. This study aimed to retrospectively analyze uncinate process anatomy on computed tomographic (CT) scans, defining the association between uncinate process inclination and sinonasal health status. Sinonasal CT examinations of 46 individuals were reviewed, comparing patients without clinical and radiographic signs of sinonasal diseases (Group I), and patients diagnosed with odontogenic sinusitis according to the criteria proposed by Felisati et al. (2)(Group II). Uncinate process inclination was calculated by Radiant Dicom Viewer software, as the angle between the straight line connecting the antero- superior and the postero-inferior part of uncinate process, and the axis of symmetry, passing through sphenoidal rostrum and perpendicular to bizygomatic line. For each patient three axial scans (the most cranial, median, the most caudal), in which uncinate process was clearly detectable, were selected and a mean value was computed. Descriptive statistics of uncinate process inclination were calculated separately in the two groups. In Group I the mean angle was13.18° ± 10.33°with confidence limits (CL) (99%) between 6.21° and 20.15°,in Group II the mean angle was 29.89°±9.56° with CL between 24.44° and 35.34°. From these preliminary results, a marked medial devia tion of uncinate process was identified in odontogenic sinusitis compared to healthy sites. Additional assessments are required to confirm the role of this anatomical varia- tion in the pathogenesis of odontogenic sinusitis.}, number={1}, journal={Italian Journal of Anatomy and Embryology}, author={Dal Pozzo, Laura and Felisati, Giovanni and Saibene, Alberto and Guenza, Guia and Vinciguerra, Alessandro and Pellegrini, Gaia and Dellavia, Claudia}, year={2015}, month={Sep.}, pages={77} }
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The Definitive Guide to eye dr Allentown PA
Like Eyeglasses, contacts can just become a Element of somebody’s program just before They're aware it and provides the same Rewards. To advance sweeten the supply, contacts may also be created of numerous kinds of styles, allowing individuals to alter the hues with the eyes right into a somewhat more lively hue or anything at all completely off the wall just like a wolf eye.
In certain patients the place the higher eyelid skin obstructs the check out, a percentage of the surgery may be lined by medical insurance plan.
The retina is a thin and delicate layer Within the again of the eye that functions much like the movie of a camera to ship Visible information for the Mind. Our comprehensive ophthalmologists intently examine the retina in the course of comprehensive eye examinations.
Further more, a person’s first utilization of contacts is generally a painful 1. It gets much less unpleasant with each and every utilization until finally it is really a non-issue, even so it only performs a component in the challenge in the educational curve to receiving accustomed to contacts. It truly is best someone checking out contacts understand to the touch their eyeballs ahead of getting contacts.
Remaining with no good vision from the trade of firefighting, development or professional athletics may be devastating and Eyeglasses normally are unable to delay for that sort of tension, minimum of frequently. And, as identified over, Eyeglasses can Definitely try getting some obtaining utilized to prior to anyone accepts them as a component in their existence.
Lots of eye challenges can develop without the need of warning and progress without symptoms. Early on, you might not even detect any adjust in your vision. On the other hand, diseases such as macular degeneration, glaucoma, retinal tears or detachments, in addition to other health issues like diabetes and higher hypertension could be detected with a radical exam in the retina.
To be an ophthalmologist, students ought to complete undergraduate coursework, complete medical school, and be involved in a three-12 months residency program. After these requirements are already fulfilled, ophthalmologists ought to sit for and go the board examination to receive their license to observe.
Dr. Harold Goldfarb is an eye doctor who is situated in Allentown, PA which is a board Accredited ophthalmologist. He has numerous decades of working experience which is specially educated to diagnose and treat complications of the attention.
An optometrist incorporates a bachelor's diploma and 4 many years of submit-graduate doctoral teaching. An optometrist can diagnose sure vision issues, compose prescriptions, give vision therapy services, and supply care both prior to and soon after eye surgery.
YP - The true Yellow PagesSM - allows you find the correct local businesses to satisfy your specific demands. Search results are sorted by a mix of factors to provide you with a set of alternatives in reaction to your search conditions. These elements are much like All those you might use to decide which organization to choose from a local Yellow Pages Listing, which include proximity to where you are looking, skills in the precise services or products you'll need, and comprehensive organization facts to help Assess a business's suitability in your case.
The kind of coverage with your healthcare prepare might or might not include things like ophthalmologic services and procedures. You'll want to Look at which kind of eye care is bundled and what must be paid for out of pocket.
Dr. Michael Alterman is expert within the medical treatment of macular degeneration and diabetic eye disorder. When required, We're going to refer you to a retinal specialist for treatment if needed. In a minimum, once-a-year examinations are suggested for diabetics and people with dry or moist macular degeneration.
Our bright and cheerful offices consist of stunning optical showrooms with unique traces of designer frames as well as a caring personnel of optometrists and opticians.
We also address ocular ailments that call for the usage of medically essential website Get in touch with lenses to achieve maximal Visible purpose, which includes kerataconus, publish corneal transplant surgery as well as other conditions that induce corneal irregularity.
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Article
Prenatal farm exposure is related to the expression of receptors of the innate immunity and to atopic sensitization in school-age children
University Children's Hospital Munich, Germany.
Journal of Allergy and Clinical Immunology (Impact Factor: 11.25). 05/2006; 117(4):817-23. DOI: 10.1016/j.jaci.2005.12.1307
Source: PubMed
ABSTRACT There is increasing evidence that environmental exposures determining childhood illnesses operate early in life. Prenatal exposure to a farming environment through the mother might also play an important role.
We sought to investigate the role of maternal exposures to environments rich in microbial compounds for the development of atopic sensitization, asthma, and corresponding alterations in the innate immune system in offspring.
In the children of the cross-sectional Prevention of Allergy Risk Factors for Sensitization in Children Related to Farming and Anthroposophic Life Style study, asthma and atopy were assessed by means of standardized questionnaires (n = 8263) and serum IgE measurements (n = 2086). In a subsample (n = 322) gene expression of Toll-like receptors (TLR2 and TLR4) and CD14 was assessed. Maternal exposures were defined through questionnaire information.
Both atopic sensitization (adjusted odds ratio, 0.58; 95% CI, 0.39-0.86) and the gene expression of receptors of innate immunity were strongly determined by maternal exposure to stables during pregnancy, whereas current exposures had much weaker or no effects. A dose-response relation was found between the extent of upregulation of these genes and the number of different farm animal species the mother had encountered in her pregnancy. Each additional farm animal species increased the expression of TLR2, TLR4, and CD14 by a factor of 1.16 (95% CI, 1.07-1.26), 1.12 (95% CI, 1.04-1.2), and 1.10 (95% CI, 1.03-1.23), respectively.
Maternal exposure to an environment rich in microbial compounds might protect against the development of atopic sensitization and lead to upregulation of receptors of the innate immune system. The underlying mechanisms potentially operating through the intrauterine milieu or epigenetic inheritance await further elucidation.
When assessing risk factors of allergies in an infant's medical history, attention must also be paid to environmental exposures affecting the mother.
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• "September 2012 | Volume 3 | Article 171 | 1 Toh et al. Probiotic therapy for allergic disease or asthma (Riedler et al., 2001), while prenatal farm exposure modulates atopic sensitization later in life (Ege et al., 2006). The human intestinal microbiota represents the most significant microbial exposure for the developing infant. "
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ABSTRACT: The prevalence of allergic disease has increased dramatically in Western countries over the past few decades. The hygiene hypothesis, whereby reduced exposure to microbial stimuli in early life programs the immune system toward a Th2-type allergic response, is suggested to be a major mechanism to explain this phenomenon in developed populations. Such microbial exposures are recognized to be critical regulators of intestinal microbiota development. Furthermore, intestinal microbiota has an important role in signaling to the developing mucosal immune system. Intestinal dysbiosis has been shown to precede the onset of clinical allergy, possibly through altered immune regulation. Existing treatments for allergic diseases such as eczema, asthma, and food allergy are limited and so the focus has been to identify alternative treatment or preventive strategies. Over the past 10 years, a number of clinical studies have investigated the potential of probiotic bacteria to ameliorate the pathological features of allergic disease. This novel approach has stemmed from numerous data reporting the pleiotropic effects of probiotics that include immunomodulation, restoration of intestinal dysbiosis as well as maintaining epithelial barrier integrity. In this mini-review, the emerging role of probiotics in the prevention and/or treatment of allergic disease are discussed with a focus on the evidence from animal and human studies.
Frontiers in Pharmacology 09/2012; 3:171. DOI:10.3389/fphar.2012.00171 · 3.80 Impact Factor
• Source
• "Robust epidemiological data linking early environmental exposures to the development of allergies have been obtained in studies of European children born to farming and non-farming families, which show that farmer's children develop less atopy or asthma (Braun-Fahrlander et al. 1999; Riedler et al. 2000; Von Ehrenstein et al. 2000). The maternal exposure to stables and farm animals during pregnancy , was strongly associated with up-regulation of innate immune receptors and lower degree of allergic sensitization in a child born to a farmer mother (Ege et al. 2006). In terms of cytokines, maternal exposure to microbial compounds and consumption of farm dairy products was associated with increased T helper 1 (Th1)-type (IFN-γ) and pro-inflammatory (TNF-α) cytokines in cord blood (Pfefferle et al. 2010). "
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ABSTRACT: The shaping of a child's immune system starts in utero, with possible long-term consequences in later life. This review highlights the studies conducted on the development of the immune system in early childhood up to school-age, discussing the impact that environmental factors may have. Emphasis has been put on studies conducted in geographical regions where exposure to micro-organisms and parasites are particularly high, and the effect that maternal exposures to these may have on an infant's immune responses to third-party antigens. In this respect we discuss the effect on responses to vaccines, co-infections and on the development of allergic disorders. In addition, studies of the impact that such environmental factors may have on slightly older (school) children are highlighted emphasizing the need for large studies in low to middle income countries, that are sufficiently powered and have longitudinal follow-up components to understand the immunological footprint of a child and the consequences throughout life.
Parasitology 07/2011; 138(12):1508-18. DOI:10.1017/S0031182011000588 · 2.35 Impact Factor
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• "In a parallel study, 5-13-yr-old children of farm-exposed mothers displayed reduced rates of sensitization and concomitantly increased TLR2, TLR4, and CD14 gene expression in PBMCs (Ege et al., 2006). It should be emphasized that the effects in the children were unrelated to the farm exposure levels at the time of their PBMC collection , and instead were related exclusively to the mothers' exposures during pregnancy. "
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ABSTRACT: The progressive rise in the prevalence of allergic diseases since the 1970s is widely attributed to diminished exposure to microbial stimuli, resulting in dysregulated immune functions during early life. Most studies investigating the mechanism behind this phenomenon have focused on postnatal microbial exposure. But emerging evidence suggests that such programming may also occur in the developing fetus as a result of microbial stimulation of the pregnant mother.
Journal of Experimental Medicine 12/2009; 206(13):2861-4. DOI:10.1084/jem.20092469 · 13.91 Impact Factor
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{
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WHY ORAL-B - FLOSS
Why Your Gums Bleed when Flossing
Why Your Gums Bleed when Flossing
Share
Do you experience tender gums when flossing or even brushing? Learn what causes bleeding gums when flossing, when it’s best to see a dental professional and how to track instances of gum bleeding to help keep your gums in healthy condition.
Causes of Bleeding Gums when Flossing
Gum bleeding is actually a more common instance than most people realize, and may not be a reason for concern, however there are instances of gum bleeding where visiting your dental professional may be best. Below are the common causes of bleeding gums when flossing:
• Infrequent Flossing: If you don’t floss at least once a day, then your gums may be more prone to bleeding when you do reach for the floss. Aim to brush after meals and floss at least once every day to limit your chances of gum bleeding.
• Vigorous Flossing: Flossing with too much pressure can cause some gum bleeding to occur. Try flossing gently in between teeth to help limit instance of bleeding gums.
• Plaque Buildup: Plaque can build up along and below the gum line, especially when a thorough oral care routine is not practiced daily. The buildup can lead to bacteria, tartar buildup, and even gum disease if not taken care of properly.
• Gum Disease: Gum or periodontal disease can cause gums to bleed. Symptoms can also include red or swollen gums and hypersensitivity when brushing or flossing. See your dental professional right away if you show any signs of gum disease.
Gentler Floss and Flossing Alternatives
When it comes to keeping your gums in good condition, try brushing a minimum of twice a day and flossing at least once a day. To help remove more plaque from between teeth while staying gentle on fingers and gums, try Oral-B Glide Floss.
If your gums are sensitive to traditional floss consider using a water flosser. The Oral-B Aquacare Pro-Expert irrigator featuring Oxyjet Technology features three unique modes: intense, medium, or sensitive so you can pick the water pressure that’s best for you.
Sensitive Gums Oral Care
If you’re more prone to sensitivity, try brushing with an electric toothbrush equipped with a sensitive mode. The Oral-B iO Series 9 not only delivers a gentle clean that’s both thorough and refreshing, but you can also track any instances of gum bleeding with the Oral-B app, only from Oral-B the #1 brand used by dentists worldwide*.
*Based on surveys carried out for P&G regularly. For verification, contact: [email protected]
Sources:
https://granddentalgroup.com/why-do-my-gums-bleed-when-i-floss/#:~:text=In%20some%20cases%2C%20patients%20who,teeth%2C%20gum%2C%20and%20tongue.
https://www.medicalnewstoday.com/articles/324613
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COVID-19 information including symptoms/ care, testing, and vaccines/ boosters: CLICK HERE.
• 530.541.3420 | 2170 South Avenue, S. Lake Tahoe, CA
Health
Diseases & Conditions - Adult Health Library
Adult Health Library
Bone Disorders
Back
• Anatomy of the Bone
Anatomy of the Bone What is bone? Bone is living tissue that makes up the body's skeleton. There are three types of bone tissue, including the following: Compact tissue. The harder, outer tissue of b...
• Avascular Necrosis
Avascular Necrosis What is avascular necrosis? Avascular necrosis is a disease that results from the temporary or permanent loss of blood supply to the bone. It is also called osteonecrosis, aseptic ...
• Benign Bone Tumors
Benign Bone Tumors There are many benign bone tumors that require clinical care by a physician or other healthcare professional. Listed in the directory below are some, for which we have provided a b...
• Bone Cancers
Bone Cancers There are many bone cancers that require clinical care by a physician or other healthcare professional. Listed in the directory below are some, for which we have provided a brief overvie...
• Bone Disorders
Bone Disorders There are many bone disorders that require clinical care by a physician or other healthcare professional. Listed in the directory below are some, for which we have provided a brief ove...
• Chondroblastoma
Chondroblastoma What is chondroblastoma? Sometimes called Codman's tumor, a chondroblastoma is a rare type of benign (noncancerous) bone tumor that originates from cartilage. Cartilage is the special...
• Chondrosarcoma
Chondrosarcoma What is chondrosarcoma? Chondrosarcoma is a type of cancer that develops in cartilage cells. Cartilage is the specialized, gristly connective tissue that is present in adults and the t...
• Diagnostic Procedures for Bone Disorders
Diagnostic Procedures for Bone Disorders How are bone disorders diagnosed? In addition to a complete medical history and physical examination, diagnostic procedures for bone disorders may include the...
• Enchondroma
Enchondroma What is an enchondroma? An enchondroma is a type of benign (noncancerous) bone tumor that originates from cartilage. Cartilage is the specialized, gristly connective tissue from which mos...
• Ewing Sarcoma in Adults
Ewing Sarcoma in Adults What is Ewing sarcoma? Ewing sarcoma is a cancer that occurs primarily in the bone or soft tissue. Ewing sarcoma can occur in any bone, but it most often it is found in the lo...
• Fibrous Dysplasia
Fibrous Dysplasia What is fibrous dysplasia? Fibrous dysplasia is a chronic disorder in which bone expands due to abnormal development of fibrous tissue, often resulting in one, or more, of the follo...
• Giant Cell Tumor
Giant Cell Tumor What is a giant cell tumor? A giant cell tumor is one that is made up of a large number of benign (noncancerous) cells that form an aggressive tumor, usually near the end of the bone...
• Glossary - Bone Disorders
Glossary - Bone Disorders | A | | B | | C | | D | | E | | F | | G | | H | | I | | J | | K | | L | | M | | N | | O | | P | | Q | | R | | S | | T | | U | | V | | W | | X | | Y | | Z | A [return to top]...
• Home Page - Bone Disorders
Topic Index All About Bone Diagnostic Procedures for Bone Disorders Treatments for Bone Disorders Bone Disorders Bone Cancers Benign Bone Tumors Glossary Bone is living tissue that provides shape and...
• Myeloma Bone Disease / Multiple Myeloma
Myeloma Bone Disease / Multiple Myeloma What is myeloma bone disease? Myeloma bone disease is cancer that affects certain white blood cells called plasma cells. It represents about 1 percent of all c...
• Online Resources - Bone Disorders
Online Resources - Bone Disorders This Web was compiled from a variety of sources including the online resources listed below, but is not intended to substitute or replace the professional medical ad...
• Osteochondroma
Osteochondroma What is osteochondroma? Also called osteocartilaginous exostoses, osteochondroma is an overgrowth of cartilage and bone near the end of the bone near the growth plate. This type of ove...
• Osteogenesis Imperfecta
Osteogenesis Imperfecta What is osteogenesis imperfecta? Osteogenesis imperfecta (OI), also known as brittle-bone disease, is a genetic (inherited) disorder characterized by bones that break easily w...
• Osteomyelitis
Osteomyelitis What is osteomyelitis? Osteomyelitis is an inflammation or swelling of bone tissue that is usually the result of an infection. Bone infection may occur for many different reasons and ca...
• Osteomyelitis (Bone Infection)
Osteomyelitis (Bone Infection) Osteomyelitis is the medical term for a bone infection. Bone infections are caused when a break in the skin allows germs, usually bacteria, to spread into bone tissue. ...
• Osteosarcoma
Osteosarcoma What is osteosarcoma? Osteosarcoma is a type of bone cancer that usually develops in the osteoblast cells that form bone. It occurs most often in children, adolescents, and young adults....
• Paget Disease of the Bone
Paget Disease of the Bone What is Paget disease of the bone? Paget disease of the bone is a chronic bone disorder in which bones become enlarged and deformed. Bone may become dense, but fragile, beca...
• Primary Hyperparathyroidism
Primary Hyperparathyroidism What is primary hyperparathyroidism? Primary hyperparathyroidism is a metabolic disorder in which one (or more) of the parathyroid glands produces too much parathyroid hor...
• Topic Index - Bone Disorders
Topic Index - Bone Disorders Bone Disorders Home Anatomy of the Bone Diagnostic Procedures for Bone Disorders Treatments for Bone Disorders Bone Disorders Avascular Necrosis Fibrous Dysplasia Osteoge...
• Treatments for Bone Disorders
Treatments for Bone Disorders Specific treatment for a bone disorder will be determined by your doctor based on: Your age, overall health, and medical history Extent of the disease Your tolerance for...
|
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Diabetes is hard to manage. You can get a comprehensive understanding of the disease here and get the information about the latest treatments and get professional advices. read more
Micro-Chinese Medicine Osmotherapy is a brand-new therapy based on traditional Chinese herbal medicines dating back thousands of years ago. It combines the essences of herbal medicines read more
Hormonal therapy is commonly used to treat Kidney Disease in clinic. It refers to use one or more than one hormone medicines to suppress the over-reactive immune reaction read more
Patients are suggested to treat kidney disease first before they get pregnant read more
If you are diagnosed with Kidney Disease, you should talk to your doctor about starting an exercise read more
Foods and Drinks play an important role in Kidney Disease patients read more
Kidney Disease News and Events read more
In every week, a famous experienced renal medicine specialist will be invited to help diagnose and evaluate inpatient's disease condition, offering detailed therapeutic schedule. read more
Word Kidney Day Font Size A A A
Natural Treatment for Renal Cortical Cyst
2012-09-19 17:47
Renal cortical cyst is a pocket filled with watery fluid. It develops in the cortex where the functional units of the kidneys grow.
If you have a small renal cortical cyst that is not causing any problems, your doctor will generally recommend you to leave it alone. However, you should keep periodic follow-up in every 6~12 months. If your renal cyst is keeping randomly, a treatment will be prescribed to you at once.
If you have a renal cortical cysts that causes obvious symptoms, such as back pain, frequent infections, blood in urine, etc, you should seek for a treatment at once. If left uncontrolled, the cyst will compress the adjacent functional units, resulting in gradual renal function decline.
As for the treatment of renal cortical cyst, a physician usually drain and permanently harden small renal cyst by inserting a needle directly into them. Then, the cystic fluid is removed and is replaced with alcohol. This can cause the tissues that makes up the cyst to harden. However, the recurrence rate of the cyst is pretty high.
For the larger cyst, you require surgery to remove it.Laparoscopic surgery is a preferable treatment for the patients. If the cyst grows in the deep part of the kidney, the surgery is usually not available.
Micro-Chinese Medicine Osmotherapy is a natural treatment for renal cortical cyst. It develops from traditional Chinese medicines which date back to ancient China. Chinese medicines are mainly composed of herbs and also contain minerals, animal bones, etc in certain proportion. As they do not contain chemical compositions, they are free of side effects completely. However, if the traditional Chinese medicine is against the compatible regularity, it may do more harm than good to your body. Therefore, you should never take medicines without seeing a professional practitioner.
Micro-Chinese Medicine Osmotherapy is an external therapy and the micronized medicines can be penetrated into kidney lesions directly. The active medicine substances can inactive the epithelial cells that can produce fluid persistently, thus stopping the cyst growth. On the other hand, it can promote the excretion of fluid, thus shrinking cysts. As it is an external therapy just like massage, it does not cause pain or other discomfortable feelings.
What else you want to know:
Make An Appointment Beijing Tongshantang Hospital of Traditional Chinese Medicine.
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How much does this treatment cost?
What is the duration if I receive this treatment in your hospital?
What should I prepare to your hospital except visa?
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Gender:
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Should women use whey protein?
771
Should women use whey protein
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Many women avoid supplementation with whey protein due to concerns that it will increase them. However, whey protein is an excellent source of protein and can help you lose weight. According to personal trainer Taylor Ryan, who published an article about ArticleBase, whey protein will not add volume to women. This is because women do not have the hormones that stimulate the growth of large, padded muscles like men.
Whey protein will help women get a toned appearance in general instead of rippling muscles.
HOW MUCH AND WHEN WOMEN SHOULD INCORPORATE THE PROTEIN OF SERUM IN THEIR DIETS?
Depending on how active a woman is and how much they weigh, a woman can safely supplement with whey protein. What manufacturers of most whey protein supplements recommend is that women take ONE scoop, equivalent to 20 to 25 grams of protein, once or twice a day.
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Men generally need more protein and it is recommended to take two tablespoons, with 20 to 25 grams, per serving and take them once or twice a day.
The best time to take whey protein for men and women is before, during and / or after a workout. For those who exercise moderately and use whey protein to lose weight, whey protein has been shown to work best when taken in the morning.
DO WHEY PROTEIN REALLY HELP IN WEIGHT LOSS?
Studies have found that people who try to lose weight by supplementing with whey protein and exercising have more lean muscle and less body fat. They also have an increase in their metabolism and burn more calories per day than those who do not take supplements or exercise.
Whey protein also helps control hunger in people who use it to lose weight. Not only does it help create a feeling of fullness, it also helps maintain cravings and promotes a feeling of fullness.
DO WOMEN NEED EXTRA PROTEIN IN THEIR DIETS?
Yes. Women tend not to consume enough protein in their daily diets. There are many health risks for women who do not consume enough protein on a regular basis.
Some of the health risks are:
Increased risk of developing osteoporosis
Edema
Slow metabolism
Obesity
Thinning hair
Toenails and toenails fragile.
In addition, women who do not consume enough protein in their diet tend to feel more tired and, in some cases, consume more calories in foods high in carbohydrates to compensate for this lack of energy.
WHAT ARE THE BENEFITS OF SUPPLEMENTATION WITH SERUM PROTEIN?
For women in particular, whey protein is an excellent way to increase daily protein intake. You can increase the amount of protein you eat without the extra fat and carbohydrates that are sometimes accompanied by food.
The whey protein is easy to digest and is an excellent snack or food for after training in liquid form. It has also been shown to reduce body fat in women and also lower cholesterol levels.
The essential amino acids in whey protein, such as leucine, can help maintain lean muscle, but they do so while promoting fat reduction.
Glutathione, which is a key antioxidant, is increased with whey protein supplementation. This antioxidant is essential to keep your immune system healthy. Because of this, whey protein promotes a healthy immune system.
Due to the high protein and essential amino acid content of whey protein, women will develop more muscle, which leads to a faster metabolism.
Don’t forget to try a Free weight loss kickstart, nothing to lose, and all the world to gain.
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Heart Failure Health Center
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Heart Failure and the Echocardiogram
An echocardiogram (often called an "echo") is a graphic outline of the heart's movement. During this test, high-frequency sound waves, called ultrasound, provide pictures of the heart's valves and chambers. This allows the technician, called a sonographer, to evaluate the pumping action of the heart. Echo is often combined with Doppler ultrasound and color Doppler to evaluate blood flow across the heart's valves.
Why Do I Need an Echocardiogram?
Your doctor may perform an echo to:
• Assess the overall function of your heart.
• Determine the presence of many types of heart disease, including heart failure.
• Follow the progress of heart valve disease over time.
• Evaluate the effectiveness of medical or surgical treatments performed on the heart.
What Are the Types of Echocardiograms?
The types of echos include:
• Transthoracic echocardiogram. This is the standard echo. It is a painless test similar to X-ray, but without the radiation. The procedure uses the same technology used to evaluate a baby's health before birth. High frequency sound waves (ultrasound) are bounced off the heart structures (using a device called a transducer) producing images and sounds that can be used by the doctor to detect heart damage and disease.
• Transesophageal echocardiogram (TEE). This test requires that the transducer be inserted down the throat into the esophagus (the swallowing tube that connects the mouth to the stomach.) Because the esophagus is located close to the heart, clear images of the heart structures can be obtained without the interference of the lungs and chest.
• Stress echocardiogram. This is an echo that is performed while the person exercises on a treadmill or stationary bicycle. This test can accurately visualize the motion of the hearts walls and pumping action when the heart is stressed; it may reveal a lack of blood flow that isn't always apparent on other heart tests. The echo is performed just prior and just after the exercise.
• Dobutamine or adenosine stress echocardiogram. This is another form of stress echo. However, instead of exercising to stress the heart, the stress is obtained by giving a drug that stimulates the heart and makes it "think" it is exercising. The test is used to evaluate your heart and valve function when you are unable to exercise on a treadmill or stationary bike. The test is also used to determine how well your heart tolerates activity, determine your likelihood of having coronary artery disease (blocked heart arteries) and evaluate the effectiveness of your cardiac treatment plan.
• Intravascular ultrasound. This is a form of echocardiography performed during cardiac catheterization (a procedure done to visualize the heart arteries). During this procedure, the transducer is threaded into the heart blood vessels via a catheter in the groin. It is often used to provide detailed information about the atherosclerosis (blockage) inside the blood vessels.
1 | 2 | 3 | 4
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Resources for students & teachers
This eBook from the Gutenberg Project consists of approximately 952 pages of information about Gargantua and Pantagruel.
the Staechad Islands; Spica Celtica from the land of the Celtic Gauls, and so throughout a great many other, which were tedious to enumerate. Some others, again, have obtained their denominations by way of antiphrasis, or contrariety; as Absinth, because it is contrary to Psinthos, for it is bitter to the taste in drinking; Holosteon, as if it were all bones, whilst, on the contrary, there is no frailer, tenderer, nor brittler herb in the whole production of nature than it.
There are some other sorts of herbs which have got their names from their virtues and operations, as Aristolochia, because it helpeth women in childbirth; Lichen, for that it cureth the disease of that name; Mallow, because it mollifieth; Callithricum, because it maketh the hair of a bright colour; Alyssum, Ephemerum, Bechium, Nasturtium, Aneban (Henbane), and so forth through many more.
Other some there are which have obtained their names from the admirable qualities that are found to be in them, as Heliotropium, which is the marigold, because it followeth the sun, so that at the sun rising it displayeth and spreads itself out, at his ascending it mounteth, at his declining it waneth, and when he is set it is close shut; Adianton, because, although it grow near unto watery places, and albeit you should let it lie in water a long time, it will nevertheless retain no moisture nor humidity; Hierachia, Eringium, and so throughout a great many more. There are also a great many herbs and plants which have retained the very same names of the men and women who have been metamorphosed and transformed in them, as from Daphne the laurel is called also Daphne; Myrrh from Myrrha, the daughter of Cinarus; Pythis from Pythis; Cinara, which is the artichoke, from one of that name; Narcissus, with Saffron, Smilax, and divers others.
Many herbs likewise have got their names of those things which they seem to have some resemblance to; as Hippuris, because it hath the likeness of a horse’s tail; Alopecuris, because it representeth in similitude the tail of a fox; Psyllion, from a flea which it resembleth; Delphinium, for that it is like a dolphin fish; Bugloss is so called because it is an herb like an ox’s tongue; Iris, so called because in its flowers it hath some resemblance of the rainbow; Myosota, because it is like the ear of a mouse; Coronopus, for that it is of the likeness of a crow’s foot. A great many other such there are, which here to recite were needless. Furthermore, as there are herbs and plants which have had their names from those of men, so by a reciprocal denomination have the surnames of many families taken their origin from them, as the Fabii, a fabis, beans; the Pisons, a pisis, peas; the Lentuli from lentils; the Cicerons; a ciceribus, vel ciceris, a sort of pulse called chickpease, and so forth. In some plants and herbs the resemblance or likeness hath been taken from a higher mark or object, as when we say Venus’ navel, Venus’ hair,
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Flu and exercise
Alternative names
Exercise - colds and flu; Colds and exercise
Information
Question:
Can exercise help you avoid colds and flus?
Answer:
Yes. At least one study suggests that regular exercise can cut in half the number of days a person suffers from colds and the flu. Exercise stimulates the disease-fighting white blood cells in the body to move from the organs into the bloodstream. Overall, you can improve your immune system by eating a proper diet, getting sufficient rest, reducing stress, and exercising regularly. This will decrease your chances of getting a cold or the flu.
Johns Hopkins patient information
Last revised: December 8, 2012
by Armen E. Martirosyan, M.D.
Medical Encyclopedia
A | B | C | D | E | F | G | H | I | J | K | L | M | N | O | P | Q | R | S | T | U | V | W | X | Y | Z | 0-9
All ArmMed Media material is provided for information only and is neither advice nor a substitute for proper medical care. Consult a qualified healthcare professional who understands your particular history for individual concerns.
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Open Access Original investigation
Association between dietary phylloquinone intake and peripheral metabolic risk markers related to insulin resistance and diabetes in elderly subjects at high cardiovascular risk
Martí Juanola-Falgarona123, Jordi Salas-Salvadó123*, Ramon Estruch234, Maria P Portillo35, Rosa Casas234, Jonatan Miranda35, Miguel A Martínez-González36 and Mònica Bulló123*
Author Affiliations
1 Human Nutrition Unit, Faculty of Medicine and Health Sciences, IISPV, Universitat Rovira i Virgili, C/Sant Llorenç 21, 43201, Reus, Spain
2 CIBERobn Physiopathology of Obesity and Nutrition, Institute of Health Carlos III (ISCIII), Madrid, Spain
3 PREDIMED Network (RD 06/0045), ISCIII, Madrid, Spain
4 Department of Internal Medicine, Institut d’Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), Hospital Clínic, Barcelona, Spain
5 Department of Nutrition and Food Science, University of Pais Vasco, Vitoria, Spain
6 Department of Preventive Medicine and Public Health, University of Navarra, Pamplona, Spain
For all author emails, please log on.
Cardiovascular Diabetology 2013, 12:7 doi:10.1186/1475-2840-12-7
The electronic version of this article is the complete one and can be found online at: http://www.cardiab.com/content/12/1/7
Received:21 November 2012
Accepted:5 January 2013
Published:8 January 2013
© 2013 Juanola-Falgarona et al.; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background
Vitamin K has been related to glucose metabolism, insulin sensitivity and diabetes. Because inflammation underlies all these metabolic conditions, it is plausible that the potential role of vitamin K in glucose metabolism occurs through the modulation of cytokines and related molecules. The purpose of the study was to assess the associations between dietary intake of vitamin K and peripheral adipokines and other metabolic risk markers related to insulin resistance and type 2 diabetes mellitus.
Methods
Cross-sectional and longitudinal assessments of these associations in 510 elderly participants recruited in the PREDIMED centers of Reus and Barcelona (Spain). We determined 1-year changes in dietary phylloquinone intake estimated by food frequency questionnaires, serum inflammatory cytokines and other metabolic risk markers.
Results
In the cross-sectional analysis at baseline no significant associations were found between dietary phylloquinone intake and the rest of metabolic risk markers evaluated, with exception of a negative association with plasminogen activator inhibitor-1. After 1-year of follow-up, subjects in the upper tertile of changes in dietary phylloquinone intake showed a greater reduction in ghrelin (−15.0%), glucose-dependent insulinotropic peptide (−12.9%), glucagon-like peptide-1 (−17.6%), IL-6 (−27.9%), leptin (−10.3%), TNF (−26.9%) and visfatin (−24.9%) plasma concentrations than those in the lowest tertile (all p<0.05).
Conclusion
These results show that dietary phylloquinone intake is associated with an improvement of cytokines and other markers related to insulin resistance and diabetes, thus extending the potential protection by dietary phylloquinone on chronic inflammatory diseases.
Trial registration
http://www.controlled-trials.com webcite as ISRCTN35739639
Keywords:
Vitamin K; Inflammation; Insulin resistance; Diabetes
Introduction
Vitamin K (K1 or phylloquinone and K2 or menaquinones) is recognized as an essential element in the synthesis of carboxylate clotting factors involved in prothrombotic disorders and cardiovascular disease. More recently, it has been reported that vitamin K also participates in the gamma-carboxylation reactions of other proteins such as osteocalcin, and may also exert a protective role against age-related bone loss [1,2]. However, additional roles of vitamin K, independent of these effects have been described [3]. Thus, there is evidence that both osteocalcin and vitamin K may have a potential beneficial role in glucose metabolism, insulin sensitivity and type 2 diabetes (T2DMs) [4-7]. Since inflammation underlies all these chronic metabolic conditions, it is plausible that the potential role of vitamin K in glucose metabolism partly occurs through the modulation of cytokines and other metabolic risk markers related to insulin resistance and diabetes.
In-vitro studies have shown an anti-inflammatory effect of vitamin K. Human macrophage THP-1 cells incubated with vitamin K reduced the interleukin-6 (IL-6) expression compared to non-incubated cells. Likewise, rats fed with a vitamin K-deficient diet showed an enhanced expression of genes involved in the acute inflammatory response [8]. In a subsample of 1,321 subjects from the Framingham Offspring Study, both plasma phylloquinone and dietary phylloquinone intake were inversely associated with peripheral concentrations of some inflammatory markers [9]. However, in a 3-year randomized clinical trial designed to assess the effect of vitamin K supplementation on bone loss, no differences were found in the plasma IL-6, C-reactive protein or osteoprotegerin concentrations of participants receiving or not a phylloquinone supplement [10].
The purposes of the present study were to assess the cross-sectional associations between dietary intake of vitamin K1 and selected adipokines or other metabolic risk markers related to inflammation, insulin resistance and diabetes; and to longitudinally analyse the associations between changes in dietary phylloquinone intake and changes in these risk markers after one-year of follow-up in a cohort of elderly subjects at high cardiovascular risk.
Methods
Study population
In the present study we conducted a cross-sectional and a longitudinal assessment of 568 consecutively recruited participants for the PREDIMED trial centers of Reus and Barcelona (Spain). The PREDIMED study is a large, parallel group, multicenter, controlled, randomized, clinical trial designed to evaluate the effect of the Mediterranean diet on the primary prevention of cardiovascular disease in elderly. Participants were community-dwelling men and women aged 55–80 and 60–80 years, respectively. At baseline they were free of cardiovascular disease and were either diabetic or met at least three or more coro-nary heart disease risk factors including smoking, hypertension (blood pressure ≥ 140/90 mmHg or treatment with antihypertensive drugs), dyslipidemia [low-density lipoprotein cholesterol level ≥ 160 mg/dL or treatment with hypolipidemic drugs], high-density lipoprotein cholesterol level of 40 mg/dL or lower, overweight [Body mass index ≥ 25 kg/m2 or family history of premature cardiovascular disease. Exclusion criteria included any severe chronic illness, drug or alcohol addiction, history of allergy or intolerance to olive oil or nuts, or a low predicted likelihood of changing dietary habits according to Prochaska and DiClemente’s stages-of-change model. The participants included in the PREDIMED study were randomly assigned to 3 intervention groups: a Mediterranean Diet with virgin olive oil, a Mediterranean Diet with mixed nuts and a control group where a low-fat diet is recommended according to the American Heart Association guidelines. Full details of the PREDIMED study protocol have been published elsewhere [11,12]. The study protocol was approved by the institutional review boards of Hospital Clínic and Hospital Universitari Sant Joan de Reus, and all subjects agreed to participate in the study and gave their written informed consent. The trail was registered in http://www.controlled-trials.com webcite as ISRCTN35739639.
Dietary assessment
Two individual motivational interviews every 3 months to negotiate nutrition goals, and group educational sessions on a quarterly basis, focused to adapt the customary diet to a traditional Mediterranean diet, were compared with a control group, which received verbal instructions and a leaflet recommending the National Cholesterol Education Program Adult Treatment Panel III dietary guidelines (http://www.predimed.org webcite). At baseline and after one-year of follow-up participants were assessed by trained dieticians who administered a previously validated 137-item food frequency questionnaire (FFQ) [13]. Additionally, a validated brief 14-item Mediterranean Diet Adherence Screener was used to assess adherence to the traditional Mediterranean Diet (MedDiet) where subjects were asked for their consumption of the most common Mediterranean foods [14]. Subjects with a higher consumption of healthier foods such as olive oil, vegetables, legumes, fruit, nuts, fish and seafood, white meat instead of red meat, sofrito and red wine scored higher in this questionnaire. Energy and nutrient intakes were calculated from Spanish food composition tables [15,16]. Dietary phylloquinone intake was calculated using the database of the US Department of Agriculture, Human Nutrition Research Center on Aging at Tufts University (http://www.nal.usda.gov/fnic/foodcomp/search webcite) and the reproducibility and relative validity of a self-administered FFQ used in the study was validated for dietary phylloquinone intake. Reproducibility for dietary phylloquinone intake explored by the Pearson correlation coefficient (r) ranged was 0.755, and the intraclass correlation coefficient (ICC) was 0.860, p<0.001.
Other measurements
Additional information was collected on subjects’ medical record, including the use of medication. Trained personnel measured baseline weight, height and waist circumference as previously reported [11,12], as well as blood pressure in triplicate with a validated semiautomatic oscillometer (Omron HEM-705CP, Hoofddorp, the Netherlands). Leisure-time physical activity was evaluated using the validated Spanish version of the Minnesota leisure-time physical activity questionnaire. Centralized laboratory biochemical analyses were performed on blood samples obtained in fasting conditions. Plasma glucose, serum cholesterol, high-density lipoprotein cholesterol and triglyceride concentrations were determined using standard enzymatic automated methods. In patients whose triglyceride levels were less than 400 mg/dL, low-density lipoprotein cholesterol concentrations were estimated using the Friedewald formula. Inflammatory and metabolic markers (adiponectin, adipsin, C-peptide, ghrelin, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide, IL-6, leptin, plasminogen activator inhibitor-1 (PAI-1), resistin, tumor necrosis factor (TNF) and visfatin were determined in plasma using the Bio-Plex cytokine assay (Bio-Rad Laboratories Inc., Hercules, CA, USA) according to manufacturer’s instructions.
Statistical analysis
Mean (SD) or percentages (%) were used to describe the participant’s baseline characteristics. Inflammatory and metabolic risk markers of insulin resistance and diabetes were logarithmically transformed to achieve a normal distribution, and the geometric mean and 95% confidence interval were used to describe these variables. For cross-sectional associations, we used multivariable linear regression models to assess the associations between metabolic risk markers (dependent variables in each model) and dietary vitamin K intake (independent variable in all models) adjusted for potential confounding variables [age, sex, body mass index, smoking (never, current, past), physical activity (kcal/d), type 2 diabetes mellitus (T2DM), total energy (kcal/d) and fibre intake (g/d), dietary polyunsaturated fatty acids (PUFA) intake (g/d) and adherence to MedDiet (14-item score, quantitative)]. The selection of potential confounders was done using clinical plausible and bibliographical criteria.
Interaction tests for sex and T2DM (sex*vitamin K intake, T2DM* vitamin K intake) were not statistically significant. No interaction was observed for intervention group and changes in dietary phylloquinone intake in any outcome (inclusion of intervention group*one-year changes in dietary phylloquinone intake in the regression models). In the longitudinal analyses, subjects were categorized according to tertiles of changes in dietary vitamin k intake from baseline to 1-year follow-up. A multivariable linear regression model was fitted to evaluate the relationship between metabolic risk markers at 1-year of follow-up (dependent variables in each model) and tertiles of change in vitamin k intake (independent variable in all models) adjusting by age, sex, smoking (never, current, past), physical activity (kcal/d), T2DM, intervention group, baseline values of each metabolic marker and changes in BMI, total energy intake (kcal/d), fiber intake (g/d), dietary PUFA intake (g/d) and adherence to MedDiet (the relative change in the 14-item score was expressed as a percentage). All statistical tests were two-tailed, and the significance level was p<0.05. Statistical analysis was performed using SPSS 17.0 for Windows (SPSS Inc, Chicago, IL).
Results
Of the 568 subjects consecutively recruited, 57 were excluded because they were using anti-inflammatory medication at baseline and 1 because he hd not completed the FFQ at follow-up. Table 1 summarizes the baseline characteristics of the study participants. Study subjects were 67.2±6.0 years old and 44.4% of them were male. Most of them were overweight or obese (92.2%), had hypertension (91.8%), were hypercholesterolemic (62.9%), and 55% had T2DM. Table 2 presents the baseline and 1-year dietary changes by tertiles of change in dietary phylloquinone intake. Subjects in the highest tertile of change consumed less amounts of vitamin K1 at baseline. This change after intervention was due to a higher consumption of total vegetables and, especially, leafy green vegetables, the primary dietary source of vitamin K1. In cross-sectional analyses at baseline, a negative significant association was found between dietary phylloquinone intake and PAI-1 plasma concentrations, even after adjusting for potential confounders (Table 3), but not for the rest of the metabolic risk markers. However, after 1-year of follow-up, those subjects in the upper tertile of changes in dietary phylloquinone intake showed a significant greater reduction in ghrelin (15.0%), GIP (12.9%), GLP-1 (17.6%), IL-6 (27.9%), leptin (10.3%), TNF (26.9%) and visfatin (24.9%) than those subjects in the lowest tertile (Table 4). No significant associations were found between changes in dietary phylloquinone intake and other metabolic markers of inflammation, insulin resistance and diabetes.
Table 1. Baseline characteristics of study subjects by tertiles of change in dietary phylloquinone intake (μg/day)
Table 2. Baseline and 1-year change of dietary characteristics by tertiles of change in dietary phylloquinone intake (μg/day)
Table 3. Cross-sectional associations between intake of 100 μg of dietary phylloquinone and inflammatory or metabolic markers at baseline
Table 4. Longitudinal associations between one-year changes in inflammatory or metabolic markers and tertiles of change in dietary phylloquinone intake (μg/day)
Discussion
The results of this study show, for the first time, that an increased dietary intake of phylloquinone is associated with an improvement in inflammatory and other metabolic risk markers related to insulin resistance and diabetes, thus supporting a protective role of vitamin K on low-grade chronic inflammatory diseases.
In recent years, vitamin K has been attributed a putative role in glucose metabolism, insulin resistance and T2DM [17]. Recently, in a prospective study our group has shown that a higher dietary phylloquinone intake was associated to a lower risk of developing T2DM. However, the exact mechanisms underlying this relationship remain still unknown. One potential explanatory mechanism could be related to the role of vitamin K as a cofactor in the carboxylation of vitamin K-dependent proteins, such as osteocalcin [18], GAS6 or Protein S [19] and through their role on NF-kB [20-22]. Additionally, some authors have suggested that inflammation may be modulated by a possible antioxidant effect of vitamin K [23].
A cross-sectional study conducted in a subsample from the Framingham Offspring Study, showed an inverse association between 2-fold changes in usual dietary phylloquinone intake or plasma phylloquinone concentrations and seven of the fourteen peripheral inflammatory markers measured [9]. However, the same authors, in a cross-sectional analysis conducted on 400 healthy elderly men and women, did not find any significant association between plasma phylloquinone concentrations and C-reactive protein or IL-6 after adjusting for potential confounders [10]. Similar to the results from Shea and co-workers, we also failed to find any significant association between dietary phylloquinone intake and most of the metabolic risk markers analysed. However, our longitudinal findings are generally consistent with in-vitro studies or those of a previous epidemiological study. In-vitro studies found that the production of the proinflammatory cytokines IL-6 or TNF by human gingival fibroblast or mouse macrophage cells, respectively, decreased when cells were incubated with different vitamin K family compounds [21,24]. Other studies have found that vitamin K suppresses inflammation by lowering the expression of genes for some proinflammatory cytokines, such as IL-6, IL-1β and TNF [8,22]. However, only a single 3-year, double-blind, randomized controlled trial has been conducted to evaluate the effect of vitamin K supplementation on peripheral inflammatory marker concentrations. In that study, conducted with 379 healthy men and women, no significant relationship between plasma phylloquinone levels and inflammation markers was shown [10]. In our study we observed a significant improvement in the inflammatory status (leptin, IL-6, TNF) and a decrease in other metabolic risk markers related to insulin resistance and diabetes such as visfatin, ghrelin, GIP and GLP-1 among subjects who increased their dietary intake of phylloquinone after 1-year follow-up, thus contributing to extend the knowledge on the role of vitamin K in humans and to support our previous results on dietary phylloquinone intake and T2DM incidence [7]. The discrepancies between our results and those previously published could be partly explained by the differences between the populations. Our participants were elderly subjects at high cardiovascular risk, whereas, subjects in the study of Shea [9] were healthy and generally free of chronic disease. This may contribute to explain why inflammatory cytokines remained unchanged in that study. Moreover, in our study we assessed the association of inflammation with dietary phylloquinone intake instead of plasma phylloquinone as was done in the previous study. Whether circulating levels of phylloquinone are correlated to dietary phylloquinone intake remains to be elucidated.
It must be noted that leptin, IL6 and TNF are pro-inflammatory cytokines with a recognised role in the development and progression of insulin resistance, T2DM and cardiovascular disease [25,26]. Also visfatin and ghrelin appears as important mediators of inflammation in addition to glucose-lowering and insulin-mimicking/sensitizing effects or a suppressive role of ghrelin in the release of insulin from the pancreatic islets [27-30]. A strong inverse correlation between plasma ghrelin concentrations and insulin resistance has been observed in several studies [30-32] and lower concentrations of ghrelin have been observed in T2DM subjects [33]. The negative relationship between changes in dietary phylloquinone intake and plasma incretin concentrations observed in our study could be explained because a higher intake of phylloquinone may promote better glycemic control thus leading less necessary the glucose and insulin regulation mediated by incretins. However, the pleiotropic role recently attributed to incretins could also contribute to explain our results. Although there is growing evidence that incretin hormones (GIP and GLP-1) simulate glucose-dependent insulin secretion and stimulate pancreatic synthesis of insulin, a novel link between inflammation and incretin hormones has been proposed. First, IL-6 increase GLP-1 production in intestinal L cells and alpha pancreatic cells improving insulin secretion and glycemia [34]. Therefore, the reduction of IL-6 levels observed in the subjects allocated in the highest tertile of change in phylloquinone intake could partly explain the reduction in GLP-1 concentrations in this group. Nie et al., have also demonstrated the capacity of GIP to activate inflammatory response and promote secretion of pro-inflammatory cytokines and chemokines in cell culture adipocytes [35]. Additionally, a potential role of GIP on adipose tissue insulin resistance mediated by osteopontin regulation has also been suggested [36]. The results from our study could be related to the potential role of incretins on adipose tissue in a fasting situation rather than to their established role on pancreatic cells in a post-prandial state. Whether or not GIP and GLP-1 need to be considered as new adipokynes or related pro-inflammatory markers could not be elucitaded from the results of our study. Specific studies are needed to get a deeper understanding of the exact role of incretins on adipose tissue and their interaction with the rest of adipokynes.
Our study has several limitations. It should be kept in mind that the subjects in our study were randomly allocated to a healthy Mediterranean diet that could partially account for the reduction in peripheral metabolic risk markers in some of them although no significant interaction between intervention group and dietary phylloquinone intake was observed for any of the outcomes. In order to minimize the potential effect of a healthy dietary pattern on inflammatory response we have adjusted the regression models for the adherence to a MedDiet. Subjects in the PREDIMED study reported a higher dietary intake of phylloquinone than in other epidemiological studies, probably because this study was conducted in a Mediterranean country where the consumption of fruit and vegetables is high. In populations with a lower consumption of phylloquinone or poor nutrition an increase in dietary vitamin K1 would probably be much more beneficial. The cohort studied was elderly and at high risk of cardiovascular disease, so our findings cannot be generalized to younger or healthier individuals. Because there is no perfect correlation between dietary phylloquinone intake and its absorption it would be interesting in the future to evaluate the associations showed in our study not only with dietary phylloquinone intake but also with a circulating marker of vitamin K status. Finally, we cannot discount a slight overestimation of dietary phylloquinone intake due to the use of FFQ and the USDA Food Database Composition. Although the FFQ used in our study was not specifically validated for phylloquinone intake, the intraclass correlation coefficient of vegetables (the main source of dietary vitamin K1) was 0.81, one of the highest coefficients obtained during the validation of the FFQ in the PREDIMED cohort [13]. Balanced against these limitations, the main strength of our study is its longitudinal design, which enables us to suggest a cause-effect relationship between changes in dietary phylloquinone intake and changes in inflammatory and related metabolic risk markers. In addition, our study was conducted in a large sample of individuals, and measured a panel of adipokines and related molecules involved in inflammation, glucose metabolism and cardiovascular risk.
In summary, our results support that an increase in dietary phylloquinone intake can lead to an improvement in inflammation and inflammatory-related molecules and also support the contention that high vitamin K1 intake has a beneficial effect on cardiovascular disease and other inflammation-related disorders.
Abbreviations
FFQ: Food Frequency Questionnaire; GLP-1: Glucagon-like peptide 1; IL: Interleukin; MedDiet: Mediterranean Diet; PAI-1: Plasminogen activator inhibitor-1; T2DM: Type 2 diabetes mellitus; TNF: Tumor necrosis factor alpha.
Competing interests
The authors declare that they have no competing interests.
Authors’ contributions
JS, RE, MAM and MB contributed to the study design, study performance, data analysis and writing of the manuscript; MJ-F and RC performed biochemical measurements and contributed to the data analysis and the writing of the manuscript. MP and JM revised the manuscript critically for important intellectual content. All authors had a substantial input in critically appraising the manuscript and approved the final version to be published. All authors read and approved the final manuscript.
Acknowledgments
We thank all the participants of the PREDIMED study for their enthusiastic collaboration, the PREDIMED personnel for excellent assistance and the personnel of all affiliated primary care centers. CIBERobn and RTIC RD 06/0045 are initiatives of ISCIII, Spain. We also acknowledge the grants from Centro Nacional de Investigaciones Cardiovasculares CNIC 06/2007, Fondo de Investigación Sanitaria PI 07/0473, Ministerio de Ciencia e Innovación (AGL-2009-13906-C02, AGL2010-22319-C03), and Fundación Mapfre 2010, Government of the Basque Country (IT386-10),University of the Basque Country (UFI 11/32).
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A Brooklyn Health Food, Vitamins, Minerals, and More Store
EMAIL DISCOUNTS
Have the latest coupons and specials for your favorite organic foods and health products delivered to your Email inbox…
Magnesium Might Ward off Diabetes
Magnesium Might Help Ward off Diabetes: Main Image
Several measures of healthy blood sugar levels improved in those taking magnesium
A magnesium supplement may improve blood sugar levels and insulin sensitivity in overweight people at risk for diabetes, according to a study published in Diabetes, Obesity, and Metabolism.
The super nutrient
Magnesium is an essential mineral to human health. It helps lower blood pressure, correct abnormal heart rhythms, build strong bones, and relax muscles. People with type 2 diabetes tend to have low levels of magnesium, and supplementing with it may help optimize insulin production. However, little is known about the effects of magnesium in people who are at risk for diabetes, but who test in the normal range for magnesium levels in the blood.
Lowering diabetes risk, naturally
In pre-diabetes, the body still manufactures insulin, but the tissues become less responsive to it. This phenomenon is referred to as insulin resistance. Together with being overweight and having mildly elevated blood sugar levels, these factors increase the chance that a person will develop diabetes.
The study investigated the effects of supplemental magnesium in people at increased risk for developing type 2 diabetes. Fifty-seven people between ages 30 and 70 who were at risk for diabetes took part in the six-month study. They were given either 365 mg of magnesium (as magnesium aspartate hydrochloride) each day or a placebo. Insulin sensitivity, blood pressure, blood fats (cholesterol and triglycerides), and blood sugar levels were tested at the beginning and end of the study.
After six months, several measures of healthy blood sugar levels improved significantly in the magnesium group. Blood pressure improved to a small extent in the magnesium group, but blood fats did not change.
“It can be speculated that magnesium may act as a natural insulin sensitizer even under conditions of well-balanced magnesium status,” commented Dr. Frank Christoph Mooren, lead author of the study from the Justus Liebig University, Germany.
It’s easy to eat your magnesium
To get more magnesium and other healthful nutrients into your diet, eat more of the following foods:
• Leafy greens like spinach, chard, turnip greens, mustard greens, kale, and collards
• Nuts and seeds including almonds, pumpkin seeds, sunflower seeds, and sesame seeds
• Legumes such as black beans and edamame
• Some breakfast cereals, especially ones containing the words “bran” and “germ,” or other foods fortified with magnesium
• If these foods aren't a good option for you, talk to a doctor about a magnesium supplement; keep in mind magnesium supplements can have a laxative effect, so don't go beyond doctor-recommended amounts
(Diabetes Obes Metab 2011;13:281–4)
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Font Size
A
A
A
tramadol (cont.)
IN THIS ARTICLE
What happens if I miss a dose (ConZip, Rybix ODT, Ryzolt, Ultram, Ultram ER)?
Take the missed dose as soon as you remember. Skip the missed dose if it is almost time for your next scheduled dose. Do not take extra medicine to make up the missed dose.
What happens if I overdose (ConZip, Rybix ODT, Ryzolt, Ultram, Ultram ER)?
Seek emergency medical attention or call the Poison Help line at 1-800-222-1222. A tramadol overdose can be fatal.
Overdose symptoms may include extreme drowsiness, shallow breathing, muscle weakness, slow heartbeat, cold or clammy skin, fainting, or seizure.
What should I avoid while taking tramadol (ConZip, Rybix ODT, Ryzolt, Ultram, Ultram ER)?
Do not drink alcohol. It may cause a dangerous decrease in your breathing when used together with tramadol.
Tramadol may impair your thinking or reactions. Be careful if you drive or do anything that requires you to be alert.
What other drugs will affect tramadol (ConZip, Rybix ODT, Ryzolt, Ultram, Ultram ER)?
You may be more likely to have a seizure (convulsions) if you take tramadol while you are using certain other medicines. Do not take tramadol without telling your doctor if you also use any of the following medications:
Cold or allergy medicine, sleeping pills, muscle relaxers, and medicine for seizures or anxiety can add to sleepiness caused by tramadol. Tell your doctor if you regularly use any of these medicines, or any other pain medication.
Tell your doctor about all other medicines you use, especially:
This list is not complete and there are many other drugs that can interact with tramadol. Tell your doctor about all medications you use. This includes prescription, over-the-counter, vitamin, and herbal products. Do not start a new medication without telling your doctor. Keep a list of all your medicines and show it to any healthcare provider who treats you.
Where can I get more information?
Your pharmacist can provide more information about tramadol.
Remember, keep this and all other medicines out of the reach of children, never share your medicines with others, and use this medication only for the indication prescribed.
Every effort has been made to ensure that the information provided by Cerner Multum, Inc. ('Multum') is accurate, up-to-date, and complete, but no guarantee is made to that effect. Drug information contained herein may be time sensitive. Multum information has been compiled for use by healthcare practitioners and consumers in the United States and therefore Multum does not warrant that uses outside of the United States are appropriate, unless specifically indicated otherwise. Multum's drug information does not endorse drugs, diagnose patients or recommend therapy. Multum's drug information is an informational resource designed to assist licensed healthcare practitioners in caring for their patients and/or to serve consumers viewing this service as a supplement to, and not a substitute for, the expertise, skill, knowledge and judgment of healthcare practitioners. The absence of a warning for a given drug or drug combination in no way should be construed to indicate that the drug or drug combination is safe, effective or appropriate for any given patient. Multum does not assume any responsibility for any aspect of healthcare administered with the aid of information Multum provides. The information contained herein is not intended to cover all possible uses, directions, precautions, warnings, drug interactions, allergic reactions, or adverse effects. If you have questions about the drugs you are taking, check with your doctor, nurse or pharmacist.
Copyright 1996-2013 Cerner Multum, Inc. Version: 13.03. Revision date: 10/20/2011.
Your use of the content provided in this service indicates that you have read,understood and agree to the End-User License Agreement,which can be accessed by clicking on this link.
Healthwise
Report Problems to the Food and Drug Administration
You are encouraged to report negative side effects of prescription drugs to the FDA. Visit the FDA MedWatch website or call 1-800-FDA-1088.
Pill Identifier Tool
Need help identifying pills and medications?
Use the pill finder tool on RxList.
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