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Categories
GENERAL
Are weight loss supplements FDA-approved?
Weight loss supplements, like other dietary supplements, are regulated by the U.S. Food and Drug Administration (FDA) under the Dietary Supplement Health and Education Act (DSHEA) of 1994. However, it’s important to understand the distinction between FDA approval and FDA regulation when it comes to supplements.
FDA Regulation of Weight Loss Supplements
The FDA regulates dietary supplements for their safety and labeling, but they do not require pre-market approval or conduct the same rigorous testing as they do for prescription drugs. Manufacturers of dietary supplements are responsible for ensuring the safety and proper labeling of their products. This means that they must follow Good Manufacturing Practices (GMP) and ensure that their products do not contain any unsafe ingredients.
FDA Approval Process
Unlike prescription drugs, weight loss supplements do not go through an FDA approval process before they can be marketed and sold. This is because they are considered dietary supplements rather than medications. The FDA becomes involved in the regulation of a weight loss supplement when safety concerns arise or when a product is found to contain unsafe ingredients.
Adulterated or Misbranded Supplements
The FDA can take action against weight loss supplements that are found to be adulterated or misbranded. Adulterated supplements may contain harmful ingredients, contaminants, or undeclared substances. Misbranded supplements may have misleading claims or lack proper labeling. In such cases, the FDA can take legal action to remove the product from the market or issue warnings to consumers.
Importance of Research and Quality
Given the limited FDA oversight of weight loss supplements, it is essential for consumers to conduct thorough research and choose reputable brands. Look for products that have been independently tested by third-party organizations for quality and safety, such as the United States Pharmacopeia (USP), ConsumerLab.com, or NSF International. These organizations test supplements for purity, potency, and quality assurance.
Consult with a Healthcare Professional
Before starting any weight loss supplement, it is advisable to consult with a healthcare professional, such as a doctor or registered dietitian. They can provide guidance based on your individual needs, health status, and any medications you may be taking. They can also help you evaluate the safety and potential effectiveness of a specific supplement.
Conclusion
Weight loss supplements are regulated by the FDA for safety and proper labeling, but they do not undergo the same approval process as prescription drugs. It is important to conduct thorough research, choose reputable brands, and consult with a healthcare professional before starting any weight loss supplement. Remember that weight loss supplements should be used as part of a comprehensive approach that includes a balanced diet, regular exercise, and lifestyle modifications.
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The massive Mistake People Make When They Attempt to Stop smoking cigarettes
If you’re reading this article article, then its because you are considering a way to give up smoking permanently.
Why are you looking for a way? Probably because you’ve attempted to give up smoking many times and failed. And that is because giving up smoking is hard. It’s actually a habit that’s difficult to break.
Frequently people think that so that you can quit cigarettes, all they should do is select a day to quit smoking and that is it. They feel that in a few magical way, they’ll get up tomorrow and their yearning for cigarettes will be gone, at least diminished enough so they really won’t be eager for a cigarette any further.
Normally the day they pick is January 1st for their New Year resolution.
But as usual, it does not work.
Precisely what fails? Why can’t smokers give up smoking?
This is because of the large mistake all of them make.
Which mistake thinks about the problem that smoking can be an addiction and they have to do is how to be smoke free in addition to their addiction goes away.
But smoking ISN’T a drug addiction.
It’s actually a habit.
The thing is that when junkies attempt to quit, their health are very hooked on the drugs to remain taking, which they find it difficult to do without them.
This is the reason, every time they quit taking drugs their bodies react by becoming cold and covered in goose bumps (also referred to as turkey flesh) which can be the place that the saying “going cold turkey” originates from.
In addition they progress (or worsen) to presenting leg spasm, and this is the location where the saying “kicking the habit” arises from.
Junkies undergo lots of psychological and physical trauma when they quit drugs.
However, if smokers quit, all that happens is that they want another cigarette and they don’t are afflicted by uncomfortable side effects his or her bodies aren’t dependent on nicotine, and that’s why patches or nicotine gum do not work, since your body isn’t craving nicotine. It is your mind that’s craving the habit of smoking of actually smoking a cigarette.
You don’t want to ingest nicotine. You need to glow a cigarette, taste it, and glance at the smoke continuing to fall into your lungs and back again.
It is exactly what you miss. Let’s be honest, if nicotine was taken out of cigarettes and they also still tasted the same, you’d still want to smoke wouldn’t you?
So what can one does?
How may you stop wanting to smoke?
The answer is simple.
You should to give up smoking exactly the same you started. Gradually.
You didn’t begin like a pack-a-day smoking and you also do not have to stop so abruptly either.
Instead you should unravel your smoking some day the other week at a time, and soon you get up one morning and also the craving to smoke is fully gone. It is not only gone, but they’re glad it’s gone.
You’ve created a completely new non-smoking lifestyle.
More information about quit smoking now go this useful web page: this
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Category:
What is the Difference Between Fraternal and Identical Twins?
Article Details
• Written By: Tricia Ellis-Christensen
• Edited By: O. Wallace
• Last Modified Date: 20 June 2016
• Copyright Protected:
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Fraternal and identical twins have many differences. Identical twins are often described as those children resulting from a pregnancy that are identical to each other. Actually, more than resemblance is involved, and not all identical twins look “completely” alike, though they do share many of the same physical characteristics. As they age, they will have differences based on lifestyle choices, experiences, and a variety of other factors. Fraternal twins, though sharing a womb, have fewer commonalities, and both types of twins are most identified by how they begin life.
Most commonly, the way twins first begin life can be referred to as dizygotic and monozygotic. Dizygotic, or fraternal twins, result when a woman has two ova or eggs fertilized by two separate sperm. This can mean that fraternal twins are of different or the same gender. Though they are siblings, they do not share near identical genetic material.
Within each sperm or ova, there is variance in what gets inherited and expressed, and these children are as alike as siblings, which can be very alike or unlike. They also may share a special relationship because they shared a womb. Though these twins are the same age, however, they are usually easily distinguished from each other, just as it would be simple to tell apart siblings of different ages.
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The conception of monozygotic (identical) twins is very different. Instead of two separate ova being fertilized by two sperm, these twins begin as one ova and one sperm. During the early process where the fertilized egg begins to produce more cells, it doubles itself and creates two embryos or two babies, instead of one. Since both babies are produced from the same fertilized egg, they share almost all the same chromosomes and DNA structure, and will bear remarkable resemblance to each other. They are truly more related than fraternal twins because of their beginning.
There are other differences between fraternal and identical twins. Identical twins are much more rare, and only 8% of all twins are identical. Moreover, fraternal twinning can be hereditary, but identical twinning is seldom hereditary and occurs with the same general likelihood in all populations.
There is much greater difference in the number of fraternal twins born in various populations, suggesting a degree of inheritance. Fraternal twinning is not always the product of genetics. Multiple births are less common in women who are vegetarians, and much more likely when women undergo fertility treatments to conceive.
Not matter how twins begin life, they will all have differences. Choices in life can make significant impact on which DNA gets expressed. This means identical twins will evolve along separate paths, though many of them stay very close. Most child development experts believe that both identical and fraternal twins should be encouraged to celebrate their individuality, since considering them as the same does not give each twin the opportunity to find his or her own gifts and strengths.
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Discuss this Article
anon955864
Post 5
Identical twins do not always look identical. In about 99.9 percent of cases they do. Most people do not know, however, that there are cases, a few cases, only twelve recorded cases of Male/Female identical twins.
This happens when a male, from a male/male set, 'mutates' if you would, during development into a female.
Out of these twelve cases, only two have been reported that the female did not develop Turner's Syndrome.
I know this simply because my sister and I are one of the pairs out of twelve.
burcidi
Post 4
I know that identical twins will have different personalities, but I still think that they are more similar to one another in terms of personality than fraternal twins.
I have both identical twins and fraternal twins in my friend group. The fraternal twins are nothing like each other. They have totally opposite personalities and like different things.
The identical twin boys, on the other hand, are fairly similar. They enjoy many of the same hobbies, have lots of mutual friends and spend time together.
fBoyle
Post 3
@ankara-- A good way to remember the difference between identical and fraternal twins is to keep in mind that identical twins come from one egg and one sperm and fraternal twins come from two eggs and two sperm.
Identical twins will always be the same gender, because the second embryo is simply a copy of the first. So everything will be exactly the same.
With fraternal twins, the embryos are fertilized by separate eggs and separate sperm. So if the genetic material determining gender are different, they will be of different sex.
Fraternal twins are simply two unique babies growing together at the same time in the womb. Identical twins is the same embryo splitting into two, resulting in two babies of the same DNA makeup and characteristics.
bluedolphin
Post 2
I know that fraternal twins can be of different genders. But identical twins are always of the same gender right? Why is this?
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Ñàõàðíûé äèàáåò
Ñòðàíèöà: 1/6
Îãëàâëåíèå:
ÑÀÕÀÐÍÛÉ ÄÈÀÁÅÒ 5
ËÅ×ÅÍÈÅ ÑÀÕÀÐÍÎÃÎ ÄÈÀÁÅÒÀ 9
Ñïèñîê ëèòåðàòóðû: 14
Áèîñèíòåç, ñåêðåöèÿ, ðåãóëÿöèÿ è ìåõàíèçì äåéñòâèÿ ïàíêðåàòè÷åñêèõ ãîðìîíîâ. Ýíäîêðèííûé àïïàðàò ïîäæåëóäî÷íîé æåëåçû (îñòðîâîê Ëàíãåðãàíñà) ñåêðåòèðóåò äâà îñíîâíûõ ãîðìîíà: èíñóëèí è ãëþêàãîí. Ýòè ãîðìîíû âûðàáàòûâàþòñÿ, ñîîòâåòñòâåííî, B (áåòà) è À (àëüôà) êëåòêàìè.
Èíñóëèí îáðàçóåòñÿ èç ïðåäøåñòâåííèêà, ïðîèíñóëèíà, êîòîðûé ðàñïàäàåòñÿ íà äâå ìîëåêóëû - Ñ-ïåïòèä è èíñóëèí. Ó çäîðîâîãî ÷åëîâåêà â ñóòêè ñåêðåòèðóåòñÿ 40-50 åä èíñóëèíà. Îñíîâíûì åñòåñòâåííûì ñòèìóëÿòîðîì ñåêðåöèè èíñóëèíà ÿâëÿåòñÿ ãëþêîçà êðîâè: êîãäà îíà ïîâûøàåòñÿ íàä òîùàêîâûì óðîâíåì, ñåêðåöèÿ èíñóëèíà ñòèìóëèðóåòñÿ è íàîáîðîò, îíà ïàäàåò ïðè ñíèæåíèè ãëèêåìèè. Îäíàêî è ïðè íèçêèõ çíà÷åíèÿõ ãëèêåìèè ìåæäó ïðèåìàìè ïèùè ñåêðåöèÿ èíñóëèíà ñîõðàíÿåòñÿ, õîòÿ è íà ìèíèìàëüíîì óðîâíå (áàçàëüíàÿ ñåêðåöèÿ), ÷òî èìååò ôèçèîëîãè÷åñêîå çíà÷åíèå. Ãëàâíàÿ ôèçèîëîãè÷åñêàÿ ôóíêöèÿ èíñóëèíà çàêëþ÷àåòñÿ â äåïîíèðîâàíèè â èíñóëèíçàâèñèìûõ òêàíÿõ (ïå÷åíè, ìûøöàõ è æèðîâîé òêàíè) ýíåðãåòè÷åñêèõ ñóáñòðàòîâ, ïîñòóïàþùèõ ñ ïèùåé . Ïîä äåéñòâèåì èíñóëèíà ñòèìóëèðóåòñÿ äåïîíèðîâàíèå ãëþêîçû â ïå÷åíè â âèäå ãëèêîãåíà, à â ìûøå÷íîé è æèðîâîé òêàíÿõ àêòèâèðóåòñÿ òðàíñïîðò ãëþêîçû ÷åðåç êëåòî÷íóþ ìåìáðàíó. Êðîìå òîãî, èíñóëèí ïîäàâëÿåò êàòàáîëèçì ãëèêîãåíà â ïå÷åíè, æèðà â àäèïîöèòàõ è áåëêà â ìûøå÷íûõ òêàíÿõ. Âñå ýòî ñíèæàåò ïîñòàëèìåíòàðíóþ ãëèêåìèþ è ñïîñîáñòâóåò íàêîïëåíèþ áåëêîâ, æèðîâ è ãëèêîãåíà â îðãàíèçìå, êîòîðûå ðàñõîäóþòñÿ ìåæäó ïðèåìàìè ïèùè è â ïðîöåññå ãîëîäàíèÿ.
Ãëþêàãîí îáðàçóåòñÿ èç ïðåäøåñòâåííèêà ïðîãëþêàãîíà è åãî ñåêðåöèÿ, â ïðîòèâîïîëîæíîñòü èíñóëèíó, ñòèìóëèðóåòñÿ ïðè ñíèæåíèè ãëèêåìèè, è ïîäàâëÿåòñÿ ïðè åå ïîâûøåíèè. Îñíîâíàÿ ôèçèîëîãè÷åñêàÿ ôóíêöèÿ ãëþêàãîíà çàêëþ÷àåòñÿ â àêòèâèçàöèè ïðîöåññîâ äîñòàâêè ýíåðãîñóáñòðàòîâ èç äåïî ê òêàíÿì ìåæäó ïðèåìàìè ïèùè. Îí ñòèìóëèðóåò ïðîäóêöèþ ãëþêîçû è êåòîíîâûõ òåë ïå÷åíüþ, àêòèâèðóÿ ãëèêîãåíîëèç, ãëþêîíåîãåíåç è êåòîãåíåç.
Ìåòîäû èññëåäîâàíèÿ. Èíñóëèí, ãëþêàãîí è Ñ-ïåïòèä îïðåäåëÿþòñÿ ðàäèîèììóíîëîãè÷åñêè. Ïîñêîëüêó Ñ-ïåïòèä è èíñóëèí ñåêðåòèðóþòñÿ áåòà-êëåòêàìè â ðàâíûõ êîëè÷åñòâàõ, òî ïîëàãàþò, ÷òî êîíöåíòðàöèÿ Ñ-ïåïòèäà â ïëàçìå êðîâè îòðàæàåò ñåêðåöèþ èíñóëèíà.
Ãëþêîçà â öåëüíîé êðîâè íàòîùàê íàõîäèòñÿ â ïðåäåëàõ 60-110 ìã% (3,5-6 ììîëü/ë), à â ïëàçìå èëè ñûâîðîòêå åå óðîâåíü íà 10-15% âûøå è ñîñòàâëÿåò 70-120 ìã% (4-6,5 ììîëü/ë). Áîëåå òî÷íûìè ìåòîäàìè îïðåäåëåíèÿ ãëþêîçû ÿâëÿþòñÿ ôåðìåíòíûå (íà îñíîâå ãëþêîç-îêñèäàçû èëè ãåêñîêèíàçû), à òàêæå êàëîðèìåòðè÷åñêèé ìåòîäû, ãäå èñïîëüçóåòñÿ î-òîëóèäèí.  ìåòîäàõ àâòîìàòèçèðîâàííîãî îïðåäåëåíèÿ ãëþêîçû, îñíîâàííûõ îáû÷íî íà âçàèìîäåéñòâèè ãëþêîçû ñ ìîëåêóëàìè ìåäè èëè æåëåçà, ðåçóëüòàòû íåñïåöèôè÷íû, òàê êàê ñ ýòèìè ýëåìåíòàìè ìîãóò âçàèìîäåéñòâîâàòü íå òîëüêî ãëþêîçà, íî è àñêîðáèíîâàÿ êèñëîòà, à òàêæå è ðÿä äðóãèõ âåùåñòâ, êîòîðûå öèðêóëèðóþò â êðîâè â ïîâûøåííûõ êîëè÷åñòâàõ, íàïðèìåð, ïðè àçîòåìèè.  íàñòîÿùåå âðåìÿ ðàçðàáîòàíû ñïåöèàëüíûå òåñò-ïîëîñêè äëÿ îïðåäåëåíèÿ ãëèêåìèè â êàïèëëÿðíîé êðîâè (“Ãëþêîõðîì”, íàïðèìåð), êîòîðûå âçàèìîäåéñòâóÿ ñ êðîâüþ èçìåíÿþò ñâîé öâåò â çàâèñèìîñòè îò óðîâíÿ ãëèêåìèè.  ïîñëåäíèå ãîäû ñòàëè øèðîêî èñïîëüçîâàòüñÿ ïîðòàòèâíûå àïïàðàòû äëÿ îïðåäåëåíèÿ ãëèêåìèè â äîìàøíèõ óñëîâèÿõ.
Ãëþêîçóðèÿ â íîðìå îòñóòñòâóåò è â íàñòîÿùåå âðåìÿ îïðåäåëÿåòñÿ îáû÷íî ñ ïîìîùüþ ñïåöèàëüíûõ òåñò-ïîëîñîê ( “Êëèíèñòèêñ”, “Äèàñòèêñ” è äð.) ñ íàíåñåííîé íà íèõ ãëþêîç-îêñèäàçîé; ïîëîñêà ìåíÿåò öâåò â çàâèñèìîñòè îò óðîâíÿ ãëþêîçû â ìî÷å. Ñëåäóåò èìåòü â âèäó, ÷òî ïðè ñíèæåíèè ïî÷å÷íîãî ïîðîãà äëÿ ãëþêîçû, êîòîðûé ñîñòàâëÿåò 160-180 ìã% (9-10 ììîëü/ë), ãëþêîçóðèÿ ïîÿâëÿåòñÿ äàæå íà ôîíå íîðìîãëèêåìèè (ïî÷å÷íûé äèàáåò); ïðè ýòîì ïî÷å÷íûé äèàáåòà íåðåäêî ñîïóòñòâóþò äëèòåëüíî äåêîìïåíñèðîâàííîìó ñàõàðíîìó äèàáåòó. Ñ äðóãîé ñòîðîíû, ó áîëüíûõ äèàáåòîì ñ ïî÷å÷íîé íåäîñòàòî÷íîñòüþ ãëþêîçóðèÿ ìîæåò îòñóòñòâîâàòü íà ôîíå âûñîêîé ãèïåðãëèêåìèè.  ýòîé ñâÿçè ãëþêîçóðèÿ íå ñ÷èòàåòñÿ íàäåæíûì êðèòåðèåì êîìïåíñàöèè äèàáåòà è èñïîëüçóåòñÿ ñ ýòîé öåëüþ ëèøü ó îãðàíè÷åííîãî ÷èñëà áîëüíûõ äèàáåòîì.
Ãëèêîçèëèðîâàííûé ãåìîãëîáèí (ñèí. ãëèêîãåìîãëîáèí, ãëèêèðîâàííûé ãåìîãëîáèí, HbA1c), ò.å. ãåìîãëîáèí, íåîáðàòèìî ñâÿçàííûé ñ ãëþêîçîé, îòðàæàåò ñòåïåíü êîìïåíñàöèè ñàõàðíîãî äèàáåòà â òå÷åíèè ïðåäøåñòâóþùèõ 8-12 íåäåëü.  íîðìå óðîâåíü ãëèêîãåìîãëîáèíà ñîñòàâëÿåò 5-8%, è åãî ïîâûøåíèå, íàïðèìåð, áîëåå 10% óêàçûâàåò íà ïëîõóþ êîìïåíñàöèþ äèàáåòà â ïðåäøåñòâîâàâøèå 2-3 ìåñ.
Êåòîíóðèÿ, ò.å. êåòîíîâûå òåëà â ìî÷å (áåòà-ãèäðîêñèìàñëÿíàÿ êèñëîòà, àöåòîóêñóñíàÿ êèñëîòà è àöåòîí) â íîðìå îòñóòñòâóþò è îáû÷íî îïðåäåëÿþòñÿ ñ ïîìîùüþ êîììåð÷åñêè ïðîèçâîäèìûõ ðåàêòèâîâ: òàáëåòêè “Àöåòåñò”, “Êåòîñòèêñ” è “Êåòî-Äèàñòèêñ”. Ñëåäóåò èìåòü â âèäó, ÷òî êðîìå ñàõàðíîãî äèàáåòà êåòîíóðèþ ìîãóò âûçâàòü ãîëîäàíèå, âûñîêîæèðîâàÿ äèåòà, àëêîãîëüíûé êåòîàöèäîç, ëèõîðàäêà è äðóãèå ñîñòîÿíèÿ, ïðè êîòîðûõ àêòèâèçèðóþòñÿ ïðîöåññû êàòàáîëèçìà.
Ìèêðîàëüáóìèíóðèÿ, ò. å. ñêîðîñòü ýêñêðåöèè àëüáóìèíà ñ ìî÷îé, â íîðìå â íî÷íîé ïîðöèè ìî÷è íå ïðåâûøàåò 15 ìêã/ìèí; çíà÷åíèÿ 20-200 ìêã/ìèí èëè âûøå óêàçûâàþò íà ðàííþþ ñòàäèþ ðàçâèòèÿ äèàáåòè÷åñêîé íåôðîïàòèè.
Ïðîòåèíóðèÿ â êëèíè÷åñêîé ïðàêòèêå íåðåäêî ÿâëÿåòñÿ ïåðâûì ñèìïòîìîì äèàáåòè÷åñêîé íåôðîïàòèè.  íîðìå îíà íå äîëæíà ïðåâûøàòü çà ñóòêè 30 ìã.
Ñèíäðîìû. Ãèïîãëèêåìè÷åñêèéñèíäðîì (ãèïîãëèêåìèÿ), ñâÿçàí ñ ïîíèæåíèåì ãëèêåìèè äî óðîâíÿ, êîòîðûé çàïóñêàåò ãîðìîíàëüíûå ãîìåîñòàòè÷åñêèå ìåõàíèçìû (àäðåíåðãè÷åñêèå) è/èëè ñîïðîâîæäàåòñÿ íåéðîãëèêîïåíè÷åñêèìè ñèìïòîìàìè. Ãîìåîñòàòè÷åñêèé ñèìïòîìîêîìïëåêñ ñâÿçàí ñ ïîâûøåíèåì óðîâíÿ ãîðìîíîâ, àêòèâèðóþùèõ ñèìïàòî-àäðåíàëîâóþ ñèñòåìó: àäðåíàëèíà, íîðàäðåíàëèíà, ãëþêàãîíà, êîðòèçîëà è ñîìàòîòðîïíîãî ãîðìîíà. Ãîìåîñòàòè÷åñêàÿ ðåàêöèÿ îðãàíèçìà ïðîÿâëÿåòñÿ ÿðêèì ñèìïòîìîêîìïëåñîì, âêëþ÷àþùèì ïîòëèâîñòü, ñåðäöåáèåíèå, ãîëîä, òàõèêàðäèþ, òðåìîð è îáùåå âîçáóæäåíèå, êîòîðûé õàðàêòåðèçóåò óìåðåííî âûðàæåííóþ ãèïîãëèêåìèþ. Íåéðîãëèêîïåíè÷åñêèå ñèìïòîìû ñîïóòñòâóþò îáû÷íî òÿæåëîé ãèïîãëèêåìèè è âêëþ÷àþò íåâîçìîæíîñòü ñêîíöåíòðèðîâàòü âíèìàíèå, áåñïðè÷èííóþ òðåâîæíîñòü, áåññâÿçíóþ ðå÷ü, ãîëîâíóþ áîëü, íå÷åòêîñòü çðåíèÿ, ýêñöåíòðè÷íîå ïîâåäåíèå, ëîêàëüíûå èëè ãåíåðàëèçîâàííûå ñóäîðîãè, ñòóïîð è êîìó. Äëÿ ãèïîãëèêåìèè òàêæå òèïè÷íî óñòðàíåíèå ñèìïòîìîâ ïîñëå ïðèåìà ñëàäêîé, ñîäåðæàùåé ðàôèíèðîâàííûå óãëåâîäû ïèùè (ñàõàð, êîíôåòû è äð.).
Äèàãíîç ãèïîãëèêåìèè îñíîâûâàåòñÿ íà âûøåóêàçàííîì ñèìïòîìîêîìïëåêñå, êîãäà îí ñî÷åòàåòñÿ ñî ñíèæåíèåì ãëèêåìèè â öåëüíîé êðîâè ìåíåå 40 ìã% (2,5 ììîëü/ë) èëè óêàçàííûé óðîâåíü ãëèêåìèè îïðåäåëÿåòñÿ ó òàêèõ áîëüíûõ íàòîùàê (ò.å. ïîñëå íî÷íîãî ãîëîäàíèÿ). Îäíàêî, êðîìå óðîâíÿ è òåìï ïàäåíèÿ ãëèêåìèè îïðåäåëÿåò ðàçâèòèå ãèïîãëèêåìèè: êîãäà ó áîëüíîãî äèàáåòîì ñ âûñîêîé ãëèêåìèåé ñêîðîñòü åå ñíèæåíèÿ ïðåâûøàåò 1 ìã%/ìèí (0,06 ììîëü/ë/ìèí), òî ñèìïòîìû ãèïîãëèêåìèè ìîãóò ïðîÿâèòüñÿ è ïðè óðîâíå ñàõàðà êðîâè, çíà÷èòåëüíî ïðåâûøàþùåì 2,5 ììîëü/ë.
Âûäåëÿþò òðè òèïà ãèïîãëèêåìèè: èíäóöèðîâàííóþ (îáóñëîâëåííóþ ïðèåìîì ñàõàðîñíèæàþùèõ ïðåïàðàòîâ èëè àëêîãîëÿ), ïîñòïðàíäèàëüíóþ (â îòâåò íà ïðèåì óãëåâîäîâ, ó áîëüíûõ ïîñëå ãàñòðýêòîìèè è èäèîïàòè÷åñêóþ) è òîùàêîâóþ (ñâÿçàíà îáû÷íî ñ ýíäîêðèíîïàòèÿìè: èíñóëèíîìà, ýêñòðàïàíêòðåàòè÷åñêèå îïóõîëè, íàäïî÷å÷íèêîâàÿ íåäîñòàòî÷íîñòü, ãèïîïèòóèòàðèçì; áîëåçíÿìè ïå÷åíè: îñòðûé ïå÷åíî÷íûé íåêðîç, ãëèêîãåíîçû; äåôèöèò ïðåäøåñòâåííèêîâ ãëþêîçû â ïðîöåññå íåîãëþêîãåíåçà: ãîëîäàíèå, ãèïîãëèêåìèÿ áåðåìåííûõ, óðåìèÿ).
Öåëüþ ëå÷åíèå ãèïîãëèêåìèè êàê ñèíäðîìà, ÿâëÿåòñÿ íîðìàëèçàöèÿ ãëèêåìèè. Åñëè áîëüíîé â ñîçíàíèè, òî îáû÷íî äîñòàòî÷íî ïðèåìà ïèùè, ñîäåðæàùåé ðàôèíèðîâàííûå óãëåâîäû: ñòàêàíà ÷àÿ ñ 4 êóñî÷êàìè ñàõàðà, ñîêà è ëþáîãî ñëàäêîãî íàïèòêà ñ äîáàâëåíèåì ñàõàðà (çà èñêëþ÷åíèåì òåõ, ÷òî ïðèãîòîâëåíû íà îñíîâå ñàõàðîçàìåíèòåëåé èëè ôðóêòîçû), êîíôåò è äð.
Êîãäà áîëüíîé áåçñîçíàíèÿ (ãèïîãëèêåìè÷åñêàÿ êîìà), òî âíóòðèâåííî ââîäèòñÿ 20-50 ìë 40% ãëþêîçû (òåðàïèÿ âûáîðà) â òå÷åíèè 1-3 ìèí; åñëè â òå÷åíèè ýòîãî âðåìåíè áîëüíîé íå ïðèõîäèò â ñîçíàíèå, òî ïîâòîðÿþò ââåäåíèå 50 ìë 40% ãëþêîçû. Ïîñëå âîññòàíîâëåíèÿ ñîçíàíèÿ ïðèåì áîãàòîé ðàôèíèðîâàííûìè óãëåâîäàìè ïèùè íóæíî íà÷àòü íåìåäëåííî. Ïîñëå ãèïîãëèêåìèè óðîâåíü ñàõàðà êðîâè äîëæåí ðåãóëÿðíî (êàæäûå 2-4 ÷àñà) îïðåäåëÿòüñÿ â òå÷åíèè 12-24 ÷àñîâ, ÷òîáû êîíòðîëèðîâàòü ýóãëèêåìè÷åñêîå ñîñòîÿíèå. Ïðè îòñóòñòâèè ãëþêîçû äëÿ âíóòðèâåííîãî ââåäåíèÿ, ãèïîãëèêåìèÿ ìîæåò êóïèðîâàòüñÿ âíóòðèìûøå÷íûì èëè âíóòðèâåííûì ââåäåíèåì 1 ìã ãëþêàãîíà (êîòîðûì äîëæíû áûòü îáåñïå÷åíû âñå áîëüíûå äèàáåòîì, ïîëó÷àþùèå ñàõàðîñíèæàþùèå ïðåïàðàòû). Ïðåäîòâðàùåíèå ïîâòîðíûõ ýïèçîäîâ ãèïîãëèêåìèè ñâÿçàíî, ïðåæäå âñåãî, ñ óñòàíîâëåíèåì òî÷íîãî äèàãíîçà è óñòðàíåíèåì ïåðâîïðè÷èíû ñèíäðîìà.
Ãèïåðãëèêåìè÷åñêèé ñèíäðîì (ãèïåðãëèêåìèÿ) ðàçâèâàåòñÿ âñëåäñòâèå èíñóëèíîâîé íåäîñòàòî÷íîñòè, âåäóùåé, ñ îäíîé ñòîðîíû, ê ïîâûøåííîé ïðîäóêöèè ãëþêîçû ïå÷åíüþ, à ñ äðóãîé, ê íàðóøåíèþ åå óòèëèçàöèè ìûøå÷íîé è æèðîâîé òêàíüþ. Îí íà÷èíàåò êëèíè÷åñêè ïðîÿâëÿòüñÿ ïîñëå ïðåâûøåíèÿ óðîâíåì ãëèêåìèè ïî÷å÷íîãî ïîðîãà äëÿ ãëþêîçû - 160-180 ìã% (9-10 ììîëü/ë). Ýòî âåäåò ê ýêñêðåöèè ãëþêîçû ñ ìî÷îé, ÷òî, â ñâîþ î÷åðåäü, âûçûâàåò îñìîòè÷åñêèé äèóðåç, ïðîÿâëÿþùèéñÿ ïîëèóðèåé (÷àñòîå è îáèëüíîå ìî÷åèñïóñêàíèå, ïðåâûøàþùåå â îáúåìå 3 ëèòðà), à ïîñëåäíÿÿ âåäåò ê ïîëèäèïñèè ñ ñèìïòîìàìè ñóõîñòè âî ðòó, æàæäû. Êîãäà ïîëèóðèÿ íå êîìïåíñèðóåòñÿ ïîëèäèïñèåé, íàñòóïàåò äåãèäðàòàöèÿ îðãàíèçìà ñ ñèìïòîìàìè îáåçâîæèâàíèÿ (ñóõîñòü êîæè è ñëèçèñòûõ, ñíèæåíèå ìàññû òåëà).
Ðåçêî âûðàæåííîå îáåçâîæèâàíèå îðãàíèçìà, âîçíèêàþùåå îáû÷íî ïîñëå 7-14 äíåé îñìîòè÷åñêîãî äèóðåçà, âåäåò ê ðàçâèòèþ, òàê íàçûâàåìîé ãèïåðîñìîëÿðíîé (íåêåòîíåìè÷åñêîé) êîìû, êîòîðàÿ ÷àùå âñòðå÷àåòñÿ ïðè ÈÍÑÄ. Ïðîâîöèðóþò ýòó êîìó ïíåâìîíèÿ, ñåïñèñ, èíôåêöèÿ ìî÷åâûõ ïóòåé, ëåêàðñòâåííûå ïðåïàðàòû (ìî÷åãîííûå, ãëþêîêîðòèêîèäû, äèôåíèí), ïàðåíòåðàëüíîå ïèòàíèå, äèàëèç. Ïðè îñìîòðå âûÿâëÿþòñÿ ñèìïòîìû òÿæåëîé äåãèäðàòàöèè: ñóõîñòü ñëèçèñòûõ è êîæè ñî ñíèæåíèåì òóðãîðà, à òàêæå ìÿãêèå ãëàçíûå ÿáëîêè. Ïðè ëàáîðàòîðíîì îáñëåäîâàíèè âûÿâëÿåòñÿ âûñîêàÿ ãèïåðãëèêåìèÿ, áîëåå 600 ìã% (33 ììîëü/ë), ãèïåðîñìîëÿðíîñòü (áîëåå 320 ìÎñì/êã), àçîòåìèÿ (àçîò ìî÷åâèíû áîëåå 60-90 ìã%) è îòñóòñòâóåò êåòîç.
Ðåôåðàò îïóáëèêîâàí: 15/06/2005 (13577 ïðî÷òåíî)
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Skip to Content
November 26, 2013
What is Pneumovax and Why Do I Need It
Pneumovax is the brand name for the pneumococcal polysaccharide vaccine, which doctors recommend seniors and other at-risk adults get to protect themselves from the pneumococcal disease, a serious health threat that can lead to death.
Q: What is Pneumovax and why do I need it?
A: Pneumovax is the brand name for the pneumococcal polysaccharide vaccine, which doctors recommend seniors and other at-risk adults get to protect themselves from the pneumococcal disease, a serious health threat that can lead to death.
The pneumococcal vaccine prevents serious blood, brain, and lung infections due to the Streptococcus pneumoniae bacteria. Such infections are called pneumococcal disease — they include pneumonia, meningitis and septicemia.
Many strains of Streptococcus pneumonia are resistant to currently used antibiotics. Infection with the bacteria is a leading cause of serious illness in adults and children worldwide. In the U.S. alone, more people die from pneumococcal disease each year than all other vaccine-preventable diseases combined.
The pneumococcal vaccine can be given at any time of the year and is recommended for the following adults: those age 65 or older; those age 19 to 64 who smoke or have asthma; people with lung, heart, liver, or kidney disease; those with a chronic disease or condition; people with a weakened immune system; patients who take medication that weaken the immune system; and those living in a nursing home or long-term care home.
A booster shot may be needed after five years. The doctor will recommend a second dose for adults between ages 19 and 64 who have: a damaged spleen or no spleen; kidney disease called nephritic syndrome; a weakened immune system due to medications such as chemotherapy drugs and long-term steroids; cancer, including leukemia, lymphoma, and multiple myeloma; history of an organ or bone marrow transplant; HIV/AIDS; and Sickle cell disease.
Adults over age 65 who received pneumococcal vaccine before age 65 also need a booster shot if it has been more than five years since being vaccinated.
As with all vaccines, there can be minor reactions, including pain and redness at the injection site, headache, fatigue or a vague feeling of discomfort.
Today’s expert is Kimberly Brown, APNP, ThedaCare Physicians-New London.
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Chiropractic Intervention for Sciatica From Accidents: Sciatica Relief: Chiropractic Intervention for Accident-Induced Pain
Chiropractic Intervention for Sciatica From Accidents Sciatica Relief Chiropractic Intervention for Accident Induced Pain
When faced with the persistent discomfort of sciatica following an accident, the search for effective relief can feel like navigating through a maze of options.
However, consider this: chiropractic care offers a tailored approach to address the root cause of your pain, aiming not just to alleviate symptoms but to promote healing.
By exploring the benefits of chiropractic intervention for accident-induced sciatica, you may uncover a path towards not just relief, but a fuller recovery that prioritizes your well-being beyond the immediate discomfort.
Key Takeaways
• Chiropractic care offers tailored pain relief for accident-induced sciatica.
• Spinal alignment aids in natural healing and nerve function restoration.
• Treatment techniques include adjustments, therapy, exercises, and nutrition for holistic relief.
• Long-term recovery involves rehabilitation, posture correction, lifestyle changes, and personalized plans.
Understanding Sciatica and Accidents
If you’ve been in an accident and are experiencing sciatica, it’s crucial to understand how the two are interconnected for effective treatment. Sciatica refers to the pain that radiates along the path of the sciatic nerve, which branches from your lower back through your hips and buttocks and down each leg. Accidents can lead to sciatica by causing trauma to the spine, resulting in herniated discs or inflamed nerves. Understanding sciatica involves recognizing that its causes can be direct, such as a herniated disc compressing the nerve roots, or indirect, like muscle inflammation due to the accident impacting your body’s alignment.
The impact of an accident on your body can be profound, especially when it comes to sciatica. The force and trauma from the accident can disrupt the natural alignment of your spine, leading to compression of nerves and subsequent pain. Recovery expectations vary depending on the severity of the accident and the resulting injuries. With sciatica, recovery can be a gradual process that requires patience and a comprehensive treatment plan. Chiropractic care can play a crucial role in not only alleviating the symptoms of sciatica but also addressing the root cause by realigning the spine and reducing pressure on the affected nerves.
Benefits of Chiropractic Care
When you seek chiropractic care for sciatica from accidents, you can benefit from pain relief techniques tailored to your specific needs.
Chiropractors can help align your spine, promoting better nerve function and reducing sciatic nerve irritation.
This natural healing approach focuses on restoring your body’s balance and function, offering a holistic solution to alleviate sciatic pain.
Pain Relief Techniques
Consider incorporating chiropractic care into your pain management regimen for effective relief from sciatica resulting from accidents. Chiropractic care offers a holistic approach to pain relief, focusing on natural methods to alleviate discomfort and promote overall well-being.
Here are five pain relief techniques that chiropractic care can provide:
• Spinal adjustments: Aligning the spine to reduce nerve irritability.
• Soft tissue therapy: Targeting muscle tension to alleviate pressure on the sciatic nerve.
• Therapeutic exercises: Strengthening exercises to improve flexibility and support the spine.
• Nutritional advice: Guidance on anti-inflammatory diet to reduce pain and inflammation.
• Posture correction: Correcting posture to prevent future sciatic pain episodes.
With these techniques, chiropractic care can help you manage and find relief from sciatica after an accident.
Spinal Alignment Benefits
For those seeking holistic and effective pain management, chiropractic care offers significant benefits through spinal alignment techniques. Alignment benefits and posture correction are central to chiropractic care, as they help restore the natural curves of your spine, alleviating pressure on nerves that may be causing sciatica pain.
By correcting misalignments, chiropractors facilitate natural healing processes within your body, promoting targeted relief from accident-induced discomfort. Through gentle adjustments, chiropractic care aims to realign your spine, improving your posture and overall well-being.
This approach not only addresses the symptoms but also targets the root cause of your pain, offering a comprehensive solution for sciatica relief. Trust in the expertise of chiropractors to guide you towards a path of recovery and comfort.
Natural Healing Approach
To experience the full spectrum of benefits from chiropractic care, embrace the natural healing approach that focuses on restoring your body’s innate ability to heal and thrive. Chiropractic care offers more than just relief; it provides a holistic approach that considers your body as a whole system. Here are five key aspects of this natural healing approach:
• Alternative Therapies: Incorporating non-traditional treatments for a well-rounded healing experience.
• Mind-Body Connection: Understanding how mental and emotional states can impact physical well-being.
• Personalized Care: Tailoring treatments to your specific needs for optimal results.
• Long-Term Wellness: Focusing on sustainable health improvements beyond just symptom relief.
• Empowerment: Equipping you with knowledge and tools to take an active role in your healing journey.
Spinal Adjustment Techniques
When it comes to spinal adjustment techniques, it’s important to understand the effectiveness of proper spinal alignments and the benefits that adjustments can bring.
These techniques aim to restore balance and mobility to your spine, helping alleviate the discomfort caused by sciatica from accidents.
Effective Spinal Alignments
Implementing precise spinal adjustments can play a pivotal role in alleviating sciatica symptoms resulting from accidents, promoting optimal spinal alignment and function. When seeking effective spinal alignments, it’s essential to consider:
• Gentle adjustments tailored to your specific needs
• Targeted techniques to address spinal misalignments
• Personalized care plans for post-accident recovery
• Evaluation of overall spinal health and function
• Collaboration with your chiropractor for comprehensive well-being
These approaches aim not only to alleviate pain but also to enhance your quality of life by restoring balance to your spine and nervous system. Embracing these techniques can lead to improved mobility, reduced discomfort, and a path towards holistic healing.
Benefits of Adjustments
Embracing the benefits of spinal adjustments can lead to enhanced spinal alignment and function, offering relief from sciatica symptoms following accidents. Chiropractic adjustments provide a non-invasive approach to pain management, targeting the root cause of discomfort.
By realigning the spine, adjustments promote posture alignment, reducing pressure on the sciatic nerve and alleviating pain. This holistic approach not only addresses current symptoms but also focuses on long-term mobility enhancement.
Through gentle and precise adjustments, chiropractors help restore proper spinal function, allowing for improved range of motion and flexibility. By incorporating regular adjustments into your wellness routine, you can experience the benefits of improved spinal health, leading to reduced pain and increased overall well-being.
Targeted Pain Relief Strategies
To effectively address sciatica pain resulting from accidents, targeted pain relief strategies tailored to your specific needs can offer significant relief and support in your recovery journey. Sciatica can be a debilitating condition, but with the right approach, you can find relief and start feeling better.
Here are some strategies to help you manage your pain and promote healing:
• Customized Movement Therapy: Engaging in specific movements and exercises can help alleviate sciatica pain by improving flexibility, strength, and posture.
• Personalized Lifestyle Changes: Making adjustments to your daily habits, such as improving ergonomics at work or incorporating relaxation techniques, can reduce the impact of sciatica on your life.
• Mind-Body Techniques: Practices like yoga, meditation, or deep breathing can’t only help alleviate physical pain but also promote emotional well-being during your recovery.
• Targeted Massage Therapy: Professional massages can target the affected areas, improving circulation, reducing muscle tension, and providing relief from sciatic nerve pain.
• Nutritional Support: Eating a balanced diet rich in anti-inflammatory foods can support your body’s natural healing processes and reduce inflammation contributing to sciatica discomfort.
Rehabilitation Exercises for Sciatica
Engage in targeted rehabilitation exercises to alleviate sciatica pain and enhance your recovery journey. Incorporating stretching routines into your daily regimen can help relieve the pressure on the sciatic nerve, promoting flexibility and reducing discomfort. These stretches focus on specific muscles like the hamstrings, piriformis, and lower back to aid in nerve decompression and improve overall mobility.
In addition to stretching, core strengthening exercises play a crucial role in managing sciatica. A strong core provides support to the spine, reducing strain on the lower back and promoting proper alignment. By engaging in exercises that target your abdominal and back muscles, you can enhance stability and alleviate pressure on the sciatic nerve, leading to long-term pain management.
Consistency is key when it comes to rehabilitation exercises for sciatica. Building a routine that combines stretching and core strengthening won’t only help alleviate current symptoms but also prevent future recurrences. Remember to listen to your body and progress at a pace that feels comfortable yet challenging.
Importance of Posture Correction
Improving your posture is essential for managing sciatica and ensuring optimal spinal alignment and nerve function. Making small changes in how you sit, stand, and move can make a big difference in alleviating your sciatic pain and preventing future flare-ups. Here are five key tips to help you correct your posture and support your spine health:
• Invest in an ergonomic workstation: Adjust your chair, keyboard, and monitor to promote a neutral spine position and reduce strain on your lower back.
• Practice postural exercises: Strengthening the muscles that support your spine through exercises like bridges, planks, and cat-cow stretches can improve your posture and alleviate sciatica symptoms.
• Take regular breaks: Whether you’re sitting at a desk or standing for long periods, remember to take short breaks to stretch and readjust your posture.
• Mind your alignment: Be mindful of how you position your body during daily activities like lifting, bending, and walking to avoid putting unnecessary pressure on your spine.
• Use supportive devices: Consider using lumbar pillows, supportive footwear, or posture braces to help maintain proper alignment throughout the day.
Chiropractic Vs. Traditional Treatments
Consider the benefits of chiropractic care as a complementary approach to traditional treatments for managing sciatica. Chiropractic care offers a holistic approach to treating sciatica, focusing on the root cause of the pain rather than just alleviating symptoms. Chiropractors use spinal adjustments to realign the spine, relieve nerve compression, and promote natural healing processes within the body.
When comparing chiropractic care to traditional treatments like pain medications or surgery, chiropractic care stands out for its focus on natural healing and long-term relief. Unlike medications that may only provide temporary relief, chiropractic adjustments aim to address the underlying issue contributing to sciatica pain, leading to lasting benefits.
Chiropractic care also emphasizes the importance of overall wellness, including lifestyle modifications, exercises, and ergonomic adjustments that can help prevent future sciatica flare-ups. By taking a whole-body approach, chiropractic care not only treats the current symptoms but also works towards preventing future episodes of sciatica.
Furthermore, chiropractic treatments are non-invasive and drug-free, making them a safe alternative for individuals seeking natural pain management options. By considering chiropractic care as part of your treatment plan for sciatica, you can experience the benefits of a comprehensive approach that addresses the root cause of your pain and promotes long-term healing and relief.
Long-Term Recovery Goals
As you progress in your recovery journey from sciatica caused by accidents, it’s essential to have realistic expectations about the timeframe required for full healing.
Engaging in tailored rehabilitation exercises under chiropractic guidance can significantly enhance your long-term recovery outcomes.
Recovery Timeframe Expectations
Understanding the expected recovery timeframe for sciatica after an accident can provide you with a sense of direction and hope as you work towards long-term recovery goals. Here are some key points to consider:
• Recovery Milestones: Celebrate each small victory along the way.
• Expectation Management: Be realistic about your progress and don’t rush the healing process.
• Recovery Setbacks: Understand that setbacks can happen and are a normal part of recovery.
• Timeframe Adjustments: Stay flexible with your expectations and allow room for adjustments as needed.
• Consistent Care: Regular chiropractic visits, exercises, and self-care routines can help maintain progress and prevent future issues.
Rehabilitation Exercises Importance
To ensure long-term recovery goals are met, incorporating rehabilitation exercises is crucial for maintaining progress and preventing future issues following chiropractic intervention for sciatica resulting from accidents. Strengthening exercises play a vital role in rebuilding muscle strength and stability in the affected area.
Pain management techniques can help alleviate discomfort during the healing process, promoting better mobility and function. Flexibility training aids in improving range of motion, reducing stiffness, and enhancing overall flexibility.
Core stability exercises are essential for supporting the spine and improving posture, which can prevent future injuries. By consistently engaging in these rehabilitation exercises, you not only expedite your recovery but also build a foundation for a healthier, more resilient body in the long run.
Preventing Future Sciatica
Taking proactive steps towards preventing future sciatica involves implementing consistent lifestyle changes and targeted exercises to strengthen and support your spine and surrounding muscles. To ensure long-term recovery and reduce the risk of recurring sciatica, consider the following strategies:
• Injury prevention strategies: Incorporate proper warm-up and cool-down routines into your exercise regimen.
• Posture correction techniques: Be mindful of your posture while sitting, standing, and lifting heavy objects.
• Fitness regimen: Include low-impact exercises like swimming or yoga to improve flexibility and strengthen core muscles.
• Ergonomic adjustments: Modify your workstation setup to maintain a neutral spine position and reduce strain.
• Regular chiropractic check-ups: Schedule routine visits to address any spinal misalignments and prevent future issues.
Preventing Future Sciatica Episodes
To maintain a resilient spine and decrease the likelihood of future sciatica episodes, incorporating regular stretching and strengthening exercises into your daily routine is crucial. Posture correction plays a significant role in preventing sciatica. Ensure that you sit and stand with your back straight, shoulders relaxed, and feet flat on the ground. This alignment reduces pressure on your spine and minimizes the risk of sciatic nerve irritation.
Exercise routines focused on core strength are also beneficial. Engaging in activities like yoga or Pilates can help stabilize your core muscles, supporting your spine and reducing the strain on your lower back. By strengthening these muscles, you create a protective shield around your spine, decreasing the chances of experiencing sciatica pain.
In addition to exercise, nutrition plays a vital role in spinal health. A diet rich in anti-inflammatory foods such as fruits, vegetables, and omega-3 fatty acids can help reduce inflammation in the body, potentially alleviating sciatica symptoms. Hydration is also key to maintaining spinal health, as water helps cushion your joints and spinal discs.
Furthermore, incorporating mobility enhancements such as regular breaks from sitting, gentle stretching throughout the day, and avoiding prolonged standing can contribute to a healthier spine. By prioritizing these lifestyle adjustments, you can take proactive steps to prevent future episodes of sciatica and promote overall well-being.
Personalized Treatment Plans
When it comes to managing sciatica caused by accidents, personalized treatment plans are key.
Tailored care approaches and individualized therapy options can make a significant difference in your recovery journey.
Tailored Care Approaches
Emphasizing the importance of individualized care plans, chiropractors tailor treatment approaches to address the unique needs and circumstances of each patient experiencing sciatica from accidents. When it comes to tailored care approaches, you can expect:
• Customized Therapy: Each treatment is specifically designed for you.
• Personalized Exercise Regimens: Exercises are chosen to suit your abilities and goals.
• Targeted Spinal Adjustments: Precise adjustments catered to your condition.
• Nutritional Guidance: Recommendations to support your healing process.
• Lifestyle Advice: Tips to enhance your overall well-being.
Individualized Therapy Options
Crafting personalized treatment plans is a cornerstone of chiropractic care for individuals with sciatica stemming from accidents. Customized programs are designed to address your specific needs, considering the unique factors contributing to your pain.
Through a holistic approach, chiropractors aim to not only alleviate your current symptoms but also enhance your overall well-being. By tailoring interventions to suit your individual condition, personalized care ensures that you receive targeted and effective treatment. These individualized techniques may include spinal adjustments, therapeutic exercises, and lifestyle recommendations tailored to promote healing and prevent future discomfort.
Embracing this personalized approach empowers you to actively participate in your recovery journey, fostering a sense of belonging and collaboration in your treatment plan.
Role of Nutrition in Healing
To support your body’s natural healing processes, incorporating a well-balanced diet rich in essential nutrients is vital when recovering from sciatica caused by accidents. Proper nutrition plays a crucial role in reducing inflammation, promoting tissue repair, and enhancing overall well-being during the healing process.
Here are five essential elements to consider in your diet:
• Omega-3 Fatty Acids**: Found in fish, flaxseeds, and walnuts, these healthy fats can help reduce inflammation and support nerve function.
• Vitamin D: Sunlight exposure and foods like fortified dairy and fatty fish can aid in bone health and reduce pain sensitivity.
• Magnesium: Nuts, seeds, and leafy greens are excellent sources that can help relax muscles and alleviate discomfort.
• Antioxidants: Colorful fruits and vegetables like berries, spinach, and bell peppers provide antioxidants that aid in tissue repair.
• Protein: Incorporate lean meats, legumes, and dairy for muscle repair and strength.
In addition to dietary changes, consider incorporating nutritional supplements like multivitamins or specific nutrients known to support nerve health and reduce inflammation. Consulting with a healthcare provider or nutritionist to tailor your diet to your specific needs can further enhance your body’s ability to heal from sciatica. Remember, your journey to recovery is unique, and nourishing your body with the right nutrients is a powerful way to support your healing process.
Enhancing Mobility Through Care
To improve your mobility and alleviate discomfort, empowering chiropractic care can work wonders in enhancing your recovery journey from sciatica caused by accidents. Chiropractic intervention focuses on mobility enhancement and injury prevention, crucial aspects for your healing process. By addressing the root cause of your pain and discomfort, chiropractors can help you regain functional improvement and effective pain management strategies.
Through personalized treatment plans, chiropractors can target specific areas affected by the accident-induced sciatica, promoting mobility enhancement by utilizing hands-on adjustments, exercises, and therapeutic techniques. These interventions not only aid in relieving pain but also contribute to preventing future injuries by enhancing your body’s overall functionality.
Chiropractic care isn’t just about temporary relief but also about long-term well-being. By incorporating regular adjustments and exercises into your routine, you can experience sustainable improvements in mobility and decreased discomfort. This comprehensive approach to care ensures that you not only recover from your current sciatica but also build resilience against potential injuries in the future.
Addressing Nerve Compression
When addressing nerve compression in sciatica cases resulting from accidents, a chiropractor’s expertise and tailored interventions can provide targeted relief and promote nerve function restoration. Nerve compression can cause intense pain, numbness, and tingling sensations, affecting your quality of life.
Here are five essential ways chiropractic care can help with nerve decompression and pain management:
• Precise Adjustments: Chiropractors use gentle, yet precise adjustments to realign the spine, relieving pressure on the affected nerves.
• Therapeutic Exercises: Tailored exercises can strengthen muscles around the spine, supporting proper alignment and reducing nerve compression.
• Lifestyle Recommendations: Chiropractors offer lifestyle advice to promote spinal health, aiding in the prevention of future nerve compression.
• Soft Tissue Therapy: Techniques such as massage and myofascial release can help relax tight muscles, alleviating pressure on the nerves.
• Education and Empowerment: Chiropractors educate you on self-care strategies and empower you to take an active role in your recovery, fostering a sense of control over your healing journey.
Psychological Support in Recovery
Navigating the journey of recovery from sciatica due to accidents involves not only physical interventions but also the crucial aspect of providing psychological support for comprehensive healing. Emotional support is vital as you embark on this healing process. Coping mechanisms play a significant role in your recovery journey, helping you manage the emotional toll that sciatica can take.
During your recovery, it’s essential to recognize that healing isn’t just about the body but also about the mind. The pain and limitations caused by sciatica can impact your mental well-being, making it crucial to have a support system that understands and addresses your emotional needs. This holistic approach ensures that you receive the comprehensive care necessary for a successful recovery.
Engaging in activities that promote relaxation and stress reduction can be beneficial as you navigate the challenges of sciatica recovery. Mindfulness practices, such as meditation or gentle yoga, can help you stay grounded and centered during this time. Additionally, seeking guidance from a mental health professional can provide you with tools and strategies to manage any anxiety or depression that may arise during your healing journey.
Testimonials and Success Stories
In sharing testimonials and success stories, individuals often find inspiration and reassurance in the journey towards recovery from sciatica due to accidents. Hearing about others’ experiences can provide hope and motivation as you navigate your own path to healing. Patient testimonials and success stories highlight the effectiveness of chiropractic intervention in managing sciatica pain following accidents, showcasing the high levels of patient satisfaction with this form of treatment.
Testimonials and Success Stories:
• Real Stories: Read about real people who’ve successfully overcome sciatica pain after accidents through chiropractic care.
• Pain Relief: Discover how patients experienced significant pain relief and improved mobility with chiropractic intervention.
• Personal Journeys: Follow the personal journeys of individuals who found relief from sciatica and regained their quality of life.
• Long-Term Benefits: Learn about the long-term benefits patients have enjoyed from chiropractic treatment for accident-induced sciatica.
• Empowerment: Explore how patients felt empowered and in control of their recovery process with chiropractic care.
These stories not only emphasize the effectiveness of chiropractic intervention in treating sciatica but also serve as a source of encouragement and optimism on your own road to recovery. By hearing about the success of others, you can feel more confident in seeking chiropractic help for your accident-induced sciatica.
Frequently Asked Questions
Can Chiropractic Care Help With Sciatica Caused by Accidents That Happened a Long Time Ago?
Chiropractic care can offer long-term effectiveness in helping with sciatica caused by old accidents. By incorporating rehabilitation techniques, chiropractors can provide holistic care tailored to your specific needs.
Through gentle adjustments and targeted exercises, they aim to alleviate pain and improve mobility. With their compassionate approach, chiropractors create a supportive environment where you can feel understood and cared for on your journey towards sciatica relief.
How Soon After an Accident Should Someone Seek Chiropractic Intervention for Sciatica Symptoms?
When dealing with sciatica post-accident, seeking chiropractic care early is key for a speedy recovery.
The benefits of chiropractic intervention can be maximized when started soon after the incident.
By addressing the issue promptly, you’re giving your body the best chance to heal and alleviate sciatica symptoms.
Are There Any Specific Exercises or Stretches That Should Be Avoided for Sciatica Relief?
When seeking relief for sciatica, it’s important to be mindful of exercises and stretches that could aggravate your symptoms. Avoiding certain movements like deep forward bends in chair yoga can help prevent further discomfort.
Additionally, modifications in water therapy can offer gentle yet effective benefits for sciatica relief. By being cautious and choosing the right exercises, you can support your recovery and find comfort in managing your sciatic pain.
Can Chiropractic Care Help With Not Just the Physical Symptoms of Sciatica but Also the Emotional Toll It Takes on a Person?
Chiropractic care can indeed address not only the physical symptoms but also the emotional toll of sciatica. By taking a holistic approach, chiropractors aim to support your emotional well-being alongside your physical health.
Through adjustments and personalized care plans, they can help alleviate both the physical discomfort and the stress and anxiety that often come with sciatica.
This comprehensive approach can provide you with relief and support for your overall well-being.
How Can Chiropractic Care Help Prevent Future Episodes of Sciatica After an Accident?
To prevent future sciatica episodes post-accident, chiropractic care focuses on preventive measures and guiding you through lifestyle modifications. By aligning your spine and addressing muscle imbalances, chiropractors aim to reduce the likelihood of sciatic nerve irritation.
They empower you to make healthy choices that support your spine health, such as exercise routines and ergonomic adjustments. This holistic approach can help you maintain a balanced body, potentially minimizing the risk of sciatica reoccurrence.
Final Thoughts
Chiropractic care offers a holistic approach to treating sciatica caused by accidents. Like a gentle breeze soothing a storm-tossed sea, chiropractic intervention can provide relief and healing for those suffering from accident-induced pain.
Through spinal adjustments, targeted pain relief strategies, and rehabilitation exercises, chiropractors can help enhance mobility, address nerve compression, and offer psychological support in the recovery process.
Trust in chiropractic care to guide you towards a path of healing and well-being.
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Final Report Summary - TARKINAID (Targeting Src-family tyrosine kinases in chronic autoimmune and inflammatory diseases)
Executive Summary:
Chronic autoimmune and inflammatory diseases such as rheumatoid arthritis or chronic inflammatory lung diseases are severe and devastating conditions that strongly impair the quality of life of the affected individuals and are a major burden to health care budgets and the entire society. Despite significant efforts aimed at the understanding and treating those diseases, current therapeutic options are still very limited due to major side effects and very high costs. Therefore, development of novel therapeutic strategies for the treatment of chronic autoimmune and inflammatory diseases is a highly important research priority.
Src-family kinases are nonreceptor tyrosine kinases which are involved in tumor development and progression and therefore are major targets of existing anti-leukemic therapies in the clinic. However, they are also present in immune cells and preliminary findings of the consortium had indicated that they are also involved in the development of inflammatory diseases in experimental animals. The consortium members had also previously developed Src-family kinases inhibitors which inhibited various inflammation-related functions of human leukocytes. Based on those prior studies, the TARKINAID consortium aimed to develop novel anti-inflammatory drug candidates and to improve our understanding of the role of Src-family kinases in the inflammation process. The most significant achievements within the three major aims of the project were as follows:
1) Development of novel Src-family inhibitors with anti-inflammatory properties. We have developed a large number of novel and patentable small molecule inhibitors of Src-family kinases and tested their effect in various inflammation-related in vitro and in vivo assays. After several rounds of structural optimization, we have developed a set of structurally related drug candidates which inhibited Src-family kinases in cell-free assays at low nanomolar concentrations, completely blocked in vitro neutrophil functions, were orally bioavailable, inhibited in vivo signs of neutrophil, B-cell and T-cell activation, and strongly reduced inflammatory responses in the reverse passive Arthus reaction. Importantly, their effects exceeded that of the clinically used tyrosine kinase inhibitor dasatinib in several in vivo and in vitro assay systems. Further optimization of these molecules are expected to lead to preclinical drug candidates suitable for clinical drug development.
2) Identification of novel anti-inflammatory effects of clinically used Src-family inhibitors. We have revealed unexpectedly diverse novel effects of the anti-leukemic agent dasatinib in various inflammatory disease models. The drug had inhibitory effects on neutrophils, macrophages and osteoclasts in vitro. Its in vivo effects included attenuation of immune complex-induced arthritis and dermatitis, protection from lung damage in LPS-induced acute lung injury and allergic asthma, protection from lethal sepsis and malaria infection, and attenuation of experimental silicosis. Dasatinib also reduced the dose of TNF antagonists required to treat human TNF transgene-induced arthritis in mice. Those results point to interesting potential novel therapeutic indications of dasatinib-related molecules in the future.
3) Identification of novel roles of Src-family kinases in inflammatory diseases. Using gene-targeted mice, we identified a number of novel functions of the myeloid Src-family kinases Hck, Fgr and Lyn, including critical roles in immune complex-induced arthritis and dermatitis and LPS-induced acute lung injury. We have revealed important mechanistic details of their role in inflammation and identified several other components in the downstream signaling pathway.
Taken together, the TARKINAID consortium has developed several novel anti-inflammatory drug candidates and generated major scientific discoveries related to the role of Src-family kinases in inflammatory diseases.
Project Context and Objectives:
Chronic autoimmune and inflammatory diseases such as rheumatoid arthritis or chronic inflammatory lung diseases are severe and devastating conditions that strongly impair the quality of life of the affected individuals and are a major burden to health care budgets and the entire society. Despite significant efforts aimed at the understanding and treating those diseases, current therapeutic options are still very limited due to major side effects and very high costs. Though anti-inflammatory agents are available since the development of aspirin more than 100 years ago, the research aimed at identifying new anti-inflammatory drugs is still ongoing and very active. Although the classical non-steroidal anti-inflammatory drugs (NSAIDs) as well as steroids are very potent in inhibiting acute inflammatory responses, they all have significant side effects which emerge during the long term treatment of chronic inflammatory and autoimmune diseases. The progress in the understanding of the cellular and molecular basis of the inflammatory process is highlighted by a few new strategies aimed to control inflammation. Among these strategies, the most promising approaches include antibodies that bind and inactivate cytokines (TNF, IL-6) or their receptors. However, all those approaches require a parenteral route of drug delivery and have many other limitations including a very high cost, causing a major burden for the national health systems in the developed world. Therefore, development of novel therapeutic strategies for the treatment of chronic autoimmune and inflammatory diseases is a highly important research priority. In particular, the search for small, orally bioavailable drugs is highly needed and deserves major efforts from both the scientific community and the pharmaceutical industry.
Src-family kinases are nonreceptor tyrosine kinases involved in diverse biological functions. Their role in cellular proliferation and invasion, the high frequency of activating mutations in Src-family kinase genes in tumors and the presence of their oncogenic variants in oncogenic viruses indicated a role for those kinases in malignancies. Those findings also triggered significant efforts aimed at therapeutic targeting of Src-family kinases in human cancer and resulted in the development of several small-molecule Src-family kinase inhibitors that showed very positive effect in human oncology patients during the last several years.
Src-family kinases are also involved in various functions of immune cells but their role in inflammatory diseases and the possibility of their therapeutic targeting in those diseases have not yet been widely appreciated. Using genetically modified mice, members of the consortium had previously found that Src-family kinases in leukocytes play an indispensable role in animal models of various chronic autoimmune inflammatory diseases. Members of the consortium had also developed several small molecule inhibitors that strongly inhibited Src-family kinases and also blocked various inflammation-related in vitro functional responses of human leukocytes. Building on those then mainly unpublished studies, the aim of the TARKINAID project was to develop novel small-molecule inhibitors of Src-family kinases for the therapy of chronic autoimmune and inflammatory diseases.
It should be mentioned that targeting components of intracellular signal transduction pathways is not an entirely novel pharmacological approach to treat inflammation. For example, drugs inhibiting the mitogen-activated protein kinase p38 or phosphoinositide 3-kinases (PI3Ks) have been generated and tested both in animals and humans. Tofacitinib, an inhibitor of Jak-family kinases has been approved for use in rheumatoid arthritis patients in the USA (though not yet in Europe). An orally available Syk inhibitor reached late Phase 3 clinical trials, although further progress to marketing development has been halted. On the other hand, targeting Src-family kinases in inflammatory diseases has not yet received wider appreciation.
During the proposed project, small molecule inhibitors of Src-family kinases with in vitro inhibitory effect on leukocytes were further tested on diverse in vitro assay systems, in vivo safety and on a number of in vivo models of inflammation. After several rounds of structural optimization, the most promising lead molecules were subjected to further analysis in animal models of autoimmune and inflammatory diseases. These experiments were expected to result in novel anti-inflammatory molecules with a novel mechanism of action.
Besides the above preclinical drug-development studies, the consortium also planned to perform experiments to test the hypothesis (again supported by our unpublished results) that Src-family inhibitor anti-tumor agents (dasatinib and bosutinib) also exert anti-inflammatory effects. Finally, the consortium aimed to perform additional experiments on existing gene knockout mice to obtain more detailed insight into the role of Src-family kinases in in vivo autoimmune inflammatory diseases.
The consortium members had extensive experience with the development of small molecule kinase inhibitors, inflammation-related in vitro functional studies on leukocytes and the analysis of in vivo inflammatory disease models in experimental animals. The above mentioned preliminary findings provided the “proof of principle” for the consortium’s activities during the preclinical drug development process.
The consortium consisted of eleven members (including four SMEs) from six different countries. To develop a network between European and Brazilian immunologists, two group leaders were from Brazil. To promote research in Eastern-European countries, the coordinator and one SME were from Hungary.
To our knowledge this project has been the first comprehensive approach to validate the use of drugs inhibiting members of the Src-family, a group of intracellular tyrosine kinases acting as signal transducers for different surface receptors in myeloid leukocytes. Using a whole variety of specific chronic and autoimmune disease models including rheumatoid arthritis, autoimmune skin disease, allergic and acute lung inflammation and fibrosis, the project was set out to identify Src- family kinase inhibitors as anti-inflammatory drugs including inhibitors already in use for the treatment of cancer or inhibitors emerging from the planned activities. We also hoped to be able to provide a formal proof that inhibition of Src-family kinases represents a new strategy to control the inflammation process.
The project has been expected to provide potential benefit to biomedical science and society through various routes:
1) Development of entirely novel small-molecule inhibitors as oral anti-inflammatory agents
2) Identification of novel anti-inflammatory indications for the use of Src-family kinase inhibitors already in the clinic for treating malignant diseases
3) Novel understanding of the disease pathogenesis of autoimmune and inflammatory diseases, leading to better diagnosis and therapeutic approaches in the future
4) Capacity-building aspects leading to better trained scientists, novel research infrastructure, novel collaborations and interactions with emerging regions such as Eastern Europe and Brazil.
Project Results:
Within the overall subject of the role of Src-family kinases in inflammation, the three main objectives of the project were:
1) Development of novel Src-family inhibitors with anti-inflammatory properties.
2) Identification of novel anti-inflammatory effects of clinically used Src-family inhibitors.
3) Identification of novel roles of Src-family kinases in inflammatory diseases.
The major achievements towards those three objectives are provided below.
1) DEVELOPMENT OF NOVEL SRC-FAMILY INHIBITORS WITH ANTI-INFLAMMATORY PROPERTIES
The aim of this part of the project was to develop several novel small-molecule Src-family kinase inhibitors that have substantial in vivo anti-inflammatory effect. This part of the project was based on prior studies from two consortium partners (Semmelweis and Vichem) who had previously developed tyrosine kinase inhibitors that inhibited various in vitro functions of human neutrophils. During the TARKINAID project, we have further developed those initial set of molecules and performed substantial structural optimization. We have developed a sublibrary of more than 1000 structural analogs of the initial compounds and selected the best secondary hits based on their in vitro efficacy and patentability features, followed by a further lead optimization strategy. Chemical synthesis, structural manipulation and cell-free kinase assays were performed by Vichem. The biological effect of the initial molecules was screened by several members of the consortium whereas the latest drug candidates (of which only very small quantities were available) have been tested primarily by Semmelweis. The latest drug candidate molecules were structurally novel and patentable, i. e. their structure has not been reported before in the scientific or patent literature.
In general the most effective drug candidates strongly inhibited the Src-family kinases Hck, Fgr, Lyn and Src in cell-free assay systems. They also blocked integrin- and Fc-receptor-mediated functional responses of human neutrophils at submicromolar concentrations but did not have any consistent effect on the migration of neutrophils in in vitro chemotaxis assays. Most tested compounds also reduced osteoclast development and various macrophage functions but did not have consistent effect on macrophage migration and related responses. During the course of several rounds of structural optimization, we have been able to develop small molecule inhibitors that were able to inhibit Src-family kinases in cell-free assays at low nanomolar concentrations. They also inhibited in vitro neutrophil functions at mid-nanomolar concentrations and blocked osteoclast development in a low nanomolar range.
We have also tested the in vivo effect of various novel Src-family kinase inhibitors. We have developed a novel assay to test the in vivo effect of the inhibitors on neutrophils, B-cells and T-cells. Many tested inhibitors had clear inhibitory effects on neutrophils and T-cells and, to a lesser extent, on B-cells. We have also performed additional experiments on inflammatory responses of the novel inhibitors. We have shown that one of the inhibitors attenuated the contact hypersensitivity response in experimental mice. In addition, the most advanced two inhibitors blocked inflammation and edema formation in the reverse passive Arthus reaction. Importantly, most tested inhibitors proved to be orally bioavailable. The effect of several novel compounds surpassed that of the clinically used tyrosine kinase inhibitor dasatinib. It should be mentioned that the most efficacious novel compounds also showed signs of toxicity upon long-term administration at higher doses, indicating that their therapeutic window may be limited and further structural optimization may be needed to reduce potential side effects.
Taken together, the above studies allowed us to develop structurally novel, patentable, orally bioavailable tyrosine kinase inhibitors that showed strong inhibitory effect in cell-free and in vitro cell-based assay systems, as well as in biochemical and functional assays of in vivo inflammation upon oral administration in experimental mice.
2) IDENTIFICATION OF NOVEL ANTI-INFLAMMATORY EFFECTS OF CLINICALLY USED SRC-FAMILY INHIBITORS
The aim of this part of the project was to test whether Src-family kinase inhibitors already used in the clinic for the therapy of imatinib-resistant chronic myeloid leukemia and other applications also have effects on cells of the immune system and the in vivo inflammatory reaction. While most of our efforts were focused on the analysis of dasatinib, a dual inhibitor of Src-family and Abl-family tyrosine kinases, we also performed limited studies on bosutinib, another clinically used Src-family tyrosine kinase inhibitor.
Our first studies on in vitro functional responses of immune cells and related lineages have revealed dramatic effects of dasatinib on various functional responses of human neutrophils including several cellular and biochemical responses triggered by integrin or Fc-receptor ligation. Most of those functions were inhibited by mid-nanomolar concentrations of dasatinib. On the other hand, dasatinib had little effect on the chemotactic activity of human neutrophils towards fMLP or IL-8 (except for studies in Zigmond-chamber assays) and had limited effect on functional responses triggered by other agonists such as various G-protein-coupled receptor agonists or innate immune ligands. Importantly, dasatinib exerted its effect on neutrophils at concentrations, and under conditions, expected to occur during human anti-lekemia therapy and it also inhibited neutrophil functions upon oral administration to experimental mice.
Additional in vitro studies on dasatinib have revealed that it inhibited activation and certain migratory functions of macrophages, and it dramatically reduced osteoclast development at very low nanomolar concentrations.
We have also performed several additional in vivo studies with dasatinib. The drug strongly reduced inflammatory responses in two different readouts of the reverse passive Arthus reaction and reduced arthritis development in the autoantibody-induced K/B×N serum-transfer model and, to a lesser extent, in the autoantibody-induced dermatitis process. Dasatinib showed synergistic effect with TNF antagonists in a human TNF transgene-induced arthritis model, dramatically reducing the effective therapeutic dose of TNF antagonists. This effect was likely due to the fact that dasatinib strongly reduced circulating TNF levels in this model. Dasatinib also protected mice from lung damage in LPS-induced acute lung injury, allergic asthma and experimental silicosis models. In addition, dasatinib strongly improved the survival of septic animals and mice infected with malaria parasites. Though some of those effects were only seen in a narrow concentration range or at higher dasatinib doses, they nevertheless point to exciting potential novel directions of the therapeutic exploitation of Src-family kinase inhibitors in various inflammation-related disease processes.
We have also tested the effect of bosutinib in some of the same assay systems, however that compound had much fewer and weaker effects than dasatinib on the inflammatory processes tested.
3) IDENTIFICATION OF NOVEL ROLES OF SRC-FAMILY KINASES IN INFLAMMATORY DISEASES
The aim of these experiments was to reveal novel functions of Src-family kinases in various in vivo and in vitro models of inflammation and to identify the molecular and cellular mechanisms involved. Most of those experiments were performed using mice genetically deficient for one or more of the Src-family kinases expressed in myeloid-lineage cells, Hck, Fgr and Lyn.
Using a number of in vitro studies, we have found that triple-knockout neutrophils lacking Hck, Fgr and Lyn were strongly defective in their responses to stimulation by immobilized immune complexes or β2 integrin-mediated activation. Defective functional responses included respiratory burst, cell spreading, degranulation, release of chemokines/cytokines and lipid (LTB4) mediators, as well as several intracellular biochemical events. Analysis of single and double knockout neutrophils revealed substantial overlap between Hck, Fgr and Lyn since all three kinases had to be deleted to achieve complete abrogation of the functional responses tested. Double knockout neutrophils lacking Hck and Fgr also showed significant reduction of certain chemokine and cytokine responses upon activation by innate immune ligands such as LPS or Pam3CSK4.
Further analyses revealed that triple knockout macrophages lacking Hck, Fgr and Lyn were also strongly defective in functional responses such as respiratory burst and chemokine/cytokine release. In addition, myeloid Src-family kinases were also involved in certain aspects of macrophage migration, as well as the organization of the macrophage and osteoclast cytoskeleton.
Additional in vivo studies have revealed that Src-family kinases are critically involved in autoantibody-induced arthritis and dermatitis processes, as well as in LPS-induced acute lung injury. Again, analysis of single and double knockout mice revealed substantial functional overlap between Hck, Fgr and Lyn. Src-family kinases were required for the accumulation of myeloid cells at the site of injury in all cases tested during the project. Interestingly, however, this was not due to a cell-autonomous role of Src-family kinases in leukocyte migration but instead to a role for Hck, Fgr and/or Lyn in the release of proinflammatory mediators from neutrophils and/or macrophages to the inflammatory environment. Those studies have revealed a critical role for Src-family kinase in the development of a chemoattractant extracellular milieu during an in vivo inflammation process.
We have also performed additional studies to characterize the molecular pathways acting downstream of Src-family kinases during in vitro and in vivo inflammatory reactions. We have shown that Src-family kinases are critically involved in the phosphorylation of the ITAM tyrosines of the Fc-receptor common γ-chain, providing a molecular link to signaling by Fcγ-receptors. In addition, we have identified the CARD9 adapter molecule as one of the downstream molecules of myeloid Src-family kinases in autoantibody-induced arthritis and dermatitis models. CARD9 acted downstream of Src-family kinases, Syk and PLCγ2 and triggered NFκB activation through IκBα phosphorylation and degradation. CARD9 was required for gene expression changes and chemokine and cytokine but not lipid mediator (LTB4) release from neutrophils and macrophages, indicating that CARD9 acts as a divergence point downstream of Src-family kinases during autoantibody-induced inflammation. Importantly, neutrophil-specific deletion was sufficient to attenuate autoantibody-induced arthiritis and dermatitis, providing the most direct evidence so far for the important role of neutrophil gene expression changes in an in vivo inflammation process.
Taken together, the TARKINAID project resulted in significant and unexpected scientific discoveries related to the role of Src-family kinases in inflammation, which is expected to lead to improved understanding, diagnosis and therapy of inflammatory diseases in the future. The project also allowed us to establish fruitful collaborations between European and Brazilian scientists.
Potential Impact:
POTENTIAL IMPACT
The TARKINAID project intended to fulfil the challenge of the call, i.e. “new therapeutic approaches in chronic inflammatory and autoimmune diseases” focusing on the use of Src family kinase inhibitors (some of which are already in clinical use for the treatment of cancer) as inhibitors of chronic inflammatory pathologies. The strength of our consortium is reflected by the fact that the involved European laboratories provided a major contribution to the understanding of tyrosine kinase signaling in regulating myeloid and other leukocytic cell functions. Another strength of the consortium was the coverage of research expertise necessary to bring a newly developed drug from its initial generation to in vitro and experimental in vivo preclinical animal studies.
Our project also offered the opportunity to achieve another objective of the call, i.e. “..to lead to more links and to closer cooperation between Member States, Associated countries and Brazil..”. Indeed the project includes two Brazilian laboratories whose expertise (chronic lung inflammation and infection) complemented that of the member state laboratories. An added value was the inclusion of three innovative biotech companies that fulfilled different tasks (generation of new anti-kinase drugs, studies of chronic fibrotic inflammation and rheumatoid arthritis) and supplied the consortium with essential disease models and innovative new drugs.
Taken together, the project has been expected to provide potential benefit to biomedical science and society through various routes:
1) Development of entirely novel small-molecule inhibitors as oral anti-inflammatory agents
To this end, we have generated a large number of novel tyrosine kinase inhibitors and tested their effect in cell-free assays, in vitro cellular functional studies and in vivo animal models. Through a constant interaction between the biological assays and chemical synthesis, we have been able to perform several steps of functional optimization. As a result, the final molecules developed as a result of this project showed strong inhibition of various Src-family kinases (Hck, Fgr, Lyn) at low nanomolar concentrations, inhibited various immune cells in cell-based in vitro assays at mid-nanomolar concentrations, were orally bioavailable, showed clear inhibitory effect on leukocytes in vivo and provided inhibitory effect in in vivo models of inflammation. Most of the effects of the developed inhibitors exceeded those of the clinically used tyrosine kinase inhibitor dasatinib. It is expected that further development of the most promising compounds may lead to anti-inflammatory compounds ready for administration in human clinical trials. The most critical aspects of the further development is the reduction of side effect and therefore the widening of the therapeutic window of the drug candidates. After further development, the drug candidates are planned to be submitted for commercial patent applications.
2) Identification of novel anti-inflammatory indications for the use of Src-family kinase inhibitors already in the clinic for treating malignant diseases
To this end, we have performed a very large number of experiments to test the effect of dasatinib and, to a lesser extent, bosutinib on various inflammatory disease models in experimental mice. We have discovered that dasatinib inhibits human neutrophil function even at therapeutic concentrations, and showed that it attenuates the symptoms of autoimmune arthritis, acute lung injury, sepsis, silicosis, asthma and malaria in experimental mice. Those studies may provide important novel information for extending the use of dasatinib and other related molecules to various aspects of inflammatory and inflammation-related diseases. Since dasatinib and bosutinib are extensively covered by pharmaceutical patents, we were not planning to submit patent applications for the coverage of those findings but instead began to share our findings with the scientific community in form of scientific publications to alert the community to the potential additional use of those existing drugs.
3) Novel understanding of the disease pathogenesis of autoimmune and inflammatory diseases, leading to better diagnosis and therapeutic approaches in the future
We have performed a large number of experiments on genetically modified mice to identify the role of Src-family kinases in animal models of chronic autoimmune and inflammatory diseases. We have revealed that Hck, Fgr and Lyn, three Src-family kinases present in myeloid cells play a critical role in autoantibody-induced arthritis and dermatitis models, as well as in the development of acute lung injury, and they also play a major role in atherosclerotic plaque formation. Mechanistically, Src-family kinases were not involved in myeloid cell migration but they were critical for the release of various functional responses of neutrophils and macrophages, most importantly in those related to the release of proinflammatory mediators such as chemokines, cytokines and lipid mediators. Those studies, reported in major scientific journals, strongly improved our understanding of inflammatory disease processes and may have long-term benefit through the development of novel diagnostic and therapeutic strategies.
4) Capacity-building aspects leading to better trained scientists, novel research infrastructure, novel collaborations and interactions with emerging regions such as Eastern Europe and Brazil.
The consortium was led by a scientist in Hungary and one other critical participant was also from Hungary, ensuring the integration of Central-Eastern European countries to the scientific activity of the EU. We have also strongly collaborated with Brazilian partners who have made essential contributions to the analysis of sophisticated lung disease models and various infectious diseases in experimental animals. The extensive interaction between developed and emerging countries strongly contributed to the improvement of scientific activities both within Europe and worldwide.
DISSEMINATION ACTIVITIES
Since the beginning of the project, the dissemination activities were aimed at enhancing visibility of the consortium and of the project, mainly for informing the scientific community about the project objectives and for communicating the value of the research funded by the European Community through FP7.
The main dissemination approaches from the project start included:
1) Development of a Project website
The first edition of the portal on TARKINAID and TIMER projects has been completed at Month 3 and the portal website (EUmBRella website: http://www.eumbrella.org) officially launched. The first edition of the portal has been revised and improved during the whole course of the project. The website has been set up and developed by beneficiary 11 ALTA, who has been in charge for updating it until the end of the project. The portal website includes also the individual TARKINAID website (http://www.eumbrella.org/tarkinaid.html).
The portal EUmBRella website includes:
• Public content for TARKINAID project
• Public content for TIMER project
• Public content focused on the EU-Brazil Research Partnership in Chronic Inflammatory and Autoimmune Diseases
• Dissemination and training
• Link to TRIAD (independent website)
• Link to PODIO social network (restricted area for the participants of TIMER, TARKINAID and TRIAD)
2) Development of Project information material
A Brochure of the project was prepared by beneficiary 11 ALTA, which was distributed at the 15th International Congress of Immunology (22-27 August 2013, Milan, Italy), at the 11th World Congress on Inflammation (21-25 September 2013, Natal, Brazil), at Semmelweis Symposium (7-9 November 2013, Budapest, Hungary), and in occasion of project meetings.
ALTA has also designed the logo of the EUmBRella website and of TARKINAID website (see below) that visually identifies the project and that will be used in occasion of meetings, posters, and any communication activities
3) Project logos
These have been designed by ALTA.
4) Participation at scientific events
The presentation of the TARKINAID results at several national and international congresses and conferences (as listed in Template A2).
5) Press releases
The activation of TARKINAID project has been communicated to the media via publication on the Semmelweis University website. The starting of TARKINAID project has been communicated also via the Biomedcode Hellas SA and Freiburg University website. In additiona a number of press coverage has occurred during major publications arising from the project.
6) Publications/chapter of books/reviews
The publications citing TARKINAID as a funding source have been published during the whole course of the project (as listed in Template A1). A number of those publications appeared in leading scientific journals such as Journal of Experimental Medicine or Nature Communications. Several other papers and reviews are in various stages of the submission and peer review process.
EXPLOITATION ACTIVITIES
Besides the generation of novel scientific knowledge that can be exploited by the wider scientific community, the project has also led to several discoveries that can be directly exploited commercially. The two most directly exploitable results are the following:
1) Development of novel anti-inflammatory drug candidates.
We have developed a number of novel tyrosine kinase inhibitors that have clear potential for commercial exploitation. Those molecules are patentable novel compounds that have not been described in the scientific or patent literature before. They have very strong inhibitory effects on their target molecules (Src-family kinases including Hck, Fgr and Lyn) at low nanomolar concentrations, inhibit inflammatory cell function in vitro, are orally bioavailable, and inhibit in vivo inflammatory processes. We believe that further structural optimization (in particular to reduce potential side effects) will allow us to submit patent applications for their use as anti-inflammatory therapeutic drug candidates in the future.
2) We have developed a novel assay system for the rapid in vivo analysis of the effect of orally administered tyrosine kinase inhibitors without the need for killing the experimental animal. This assay may prove to be useful for the rapid assessment of the efficacy of tyrosine kinase inhibitors in vivo. We have made initial preparatory steps for the patenting this assay as a novel rapid in vivo screening tool.
List of Websites:
PROJECT WEBSITE
The project website is www.eumbrella.org/tarkinaid.html
The TARKINAID website is included within the EUmBRella portal website (www.eumbrella.org) which covers the 3 EU-Brazil research projects (TIMER, TARKINAID, TRIAD) funded under the 7th European Framework Programme (Health 2012 Programme) for Research in the field of chronic inflammatory/autoimmune diseases, within the bilateral S&T cooperation between Europe and Brazil.
CONTRACTORS INVOLVED
1) Semmelweis Egyetem (HUNGARY): Attila Mocsai and Tibor Vantus
2) Ludwig-Maximilians Universität München (GERMANY): Markus Sperandio and Barbara Walzog
3) Università degli Studi di Verona (ITALY): Giorgio Berton
4) Centre National de la Recherche Scientifique (FRANCE): Isabelle Maridonneau-Parini
5) Vichem Chemie Research Ltd. (HUNGARY): Gyorgy Keri
6) Universitätsklinikum Freiburg (GERMANY): Cassian Sitaru
7) Universidade Federal do Rio de Janeiro (BRAZIL): Patricia Rocco
8) Biomedcode Hellas SA (GREECE): Maria Denis
9) Ambiotis SAS (FRANCE): Marc Dubourdeau
10) Fundacao Oswaldo Cruz (BRAZIL): Hugo Castro Faria Neto
11) ALTA Ricerca e Svluppo in Biotecnologie S.r.l.u. (ITALY): Paola Cesaroni
COORDINATOR CONTACT DETAILS
Dr. Attila Mócsai
Professor of Physiology
Department of Physiology
Semmelweis University School of Medicine
Tűzoltó utca 37-47.
1094 Budapest, Hungary
E-mail: [email protected]
Tel.: +36-1-459-1500 x60-409
Fax: +36-1-266-7480
Verwandte Informationen
Reported by
SEMMELWEIS EGYETEM
Hungary
Fachgebiete
Life Sciences
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Melanoma
You are here:
Types of melanoma skin cancer
Melanoma skin cancer can grow into and destroy nearby tissue. It can also spread (metastasize) to other parts of the body. Melanoma skin cancer is also called cutaneous melanoma and malignant melanoma of the skin.
There are 4 main types of melanoma skin cancer – superficial spreading, nodular, lentigo maligna and acral lentiginous.
Superficial spreading melanoma
Superficial spreading melanoma is the most common type of melanoma skin cancer. It makes up about 70% of all melanoma skin cancers.
Superficial spreading melanoma tends to grow outward (called radial growth) and spread across the surface of the skin. But it can also start to grow down into the skin (called vertical growth). It is often flat and thin (less than 1 mm thick) with an uneven border. It varies in colour and may have different shades of red, blue, brown, black, grey and white. Sometimes superficial spreading melanoma starts from a mole that is already on the skin.
Superficial spreading melanoma usually develops on the central part of the body (trunk), arms and legs. It tends to happen on the back in men and the legs in women.
Nodular melanoma
Nodular melanoma is the second most common type of melanoma skin cancer. It makes up about 15% to 20% of all melanoma skin cancers.
Nodular melanoma grows down into the skin. It grows and spreads more quickly than other types of melanoma skin cancer. It is a raised growth that sticks out from the skin (polypoid). The growth may be shaped like a mushroom with a stem or stalk (pedunculated). It is usually black, but sometimes can be red, pink or the same colour as your skin.
Nodular melanoma usually develops on the face, chest or back. It can be found on areas of skin not exposed to the sun.
Lentigo maligna melanoma
Lentigo maligna melanoma most often develops in older people. It makes up about 10% to 15% of all melanoma skin cancers.
Lentigo maligna melanoma usually appears as a large, flat tan or brown patch with an uneven border. It tends to get darker as it grows and has many shades of brown or black. It often starts from an in situ tumour called lentigo maligna, which is an early form of the growth only in the top or outer layer of the skin (epidermis). Lentigo maligna melanoma usually grows outward across the surface of the skin for many years before it starts to grow down into the skin.
Lentigo maligna melanoma usually develops on areas of skin that are regularly exposed to the sun without protection, such as the face, ears and arms.
Acral lentiginous melanoma
Acral lentiginous melanoma is most common in people with dark skin, such as those from African, Asian and Hispanic ancestries. It is not related to being exposed to the sun. It makes up less than 5% of all melanoma skin cancers.
Acral lentiginous melanoma appears as a small, flat spot of discoloured skin that is often dark brown or black. It usually grows outward across the surface of the skin for a long time before it starts to grow down into the skin.
Acral lentiginous melanoma usually develops on the soles of the feet, on the palms of the hands or under the nails. It is often hard to diagnose acral lentiginous melanoma because it’s hard to see abnormal areas on the soles of the feet or under the nails.
Rare types of melanoma
Some rare types of melanoma do not start in the skin. The following types of melanoma are rare.
Mucosal lentiginous melanoma develops on the thin, moist lining of some organs or other parts of the body (mucosa or mucous membrane), such as the nasal passages, mouth, throat (pharynx), rectum, anal canal and vagina. It is not related to being exposed to the sun like most melanoma skin cancers. It is usually diagnosed at a late stage and tends to grow and spread quickly.
Intraocular melanoma starts in the eye. It is the most common type of eye cancer. Find out more about eye cancer (intraocular melanoma).
Desmoplastic melanoma develops in the thick, inner layer of skin (dermis) or the layer of connective tissue that surrounds the mucosa (submucosa). It often appears as a lump that is the same colour as your skin. It tends to grow down into the skin. Desmoplastic melanoma often develops on the head, neck, upper back or areas of the body with a mucosa.
mole
A non-cancerous (benign) growth on the skin that is usually tan, brown or flesh-coloured.
Moles are made up of a cluster of melanocytes (cells that make melanin, which gives skin, hair and eyes their colour). They may be raised or flat.
Also called nevus.
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Selecting Great Examination Winny Cycle For Beginners
Content
When it pertains to medicine testing, a tiny single dosage of as low as a 5mg tablet computer is observable in the pee for up to 10 days. Winstrol influences the body’s natural hormonal agent function and therefore, can effecting your mood and this is a location to pay very close attention to when you’re utilizing Winstrol so you can adjust your dose appropriately. A proper dose of Winstrol for ladies is 10mg every various other day (every two days). While a 10mg everyday dose is possible, extra caution requires to be taken to keep on top of any virilization results that might start to turn up.
Can Hcg And Nolvadex Be Utilized For Pct?
Apart from enhancing muscular tissue growth and speeding up healing, Winstrol also uses an additional critical advantage– boosted endurance and endurance. Offered the nature of body building and other extreme exercises, stamina and endurance are of paramount relevance. Keeping a healthy, well balanced diet plan and including regular exercise right into one’s regular are just as vital in achieving lasting success with these substances. Ample rest and hydration, along with correct supplementation, can aid lessen any possible negative effects and guarantee that the individual’s general health continues to be a top priority. By pushing through plateaus and aiding accomplish my physical fitness objectives, this pile has shown to be fairly reliable for both me and a number of my peers in the physical fitness community. Elements like genes, diet, and training regimens certainly contribute in just how reliable these compounds will certainly be for each and every person.
12 Week Testosterone and Winstrol Cycle – What is Winstrol Used For – Deccan Herald
12 Week Testosterone and Winstrol Cycle – What is Winstrol Used For.
Posted: Tue, 20 Feb 2024 08:00:00 GMT [source]
Lawful Steroid Choices That Work
We have actually located the danger of gynecomastia to be high with this stack, with estrogen levels escalating in the visibility of anadrol and testosterone. Anadrol is potentially the worst steroid for blood pressure, causing substantial increases as a result of its disastrous impact on HDL cholesterol degrees. This results from it stimulating hepatic lipase, an enzyme in charge of decreasing great cholesterol (HDL), which stops clogging of the arteries. Whenever running anadrol cycles, it is very important to maintain the period as short as feasible.
Q: Are There Any Kind Of Possible Side Effects Of A Winstrol Cycle For Beginners?
As a whole, guys commonly make use of Winstrol at everyday dosages ranging from 25mg to 100mg, a variety that depends on private goals and experience degrees. Reduced doses are commonly utilized throughout cutting cycles or by individuals with minimal experience, while higher doses are more generally selected by those focusing on muscle development or with better experience. Among the most significant benefits of this steroid is its ability to extremely stimulate muscle mass growth. It binds to androgenic receptors and increases protein manufacturing– the building blocks for muscle mass growth. In addition, it boosts nitrogen retention in the muscle mass, even more aiding in muscle gain.
‘ Tren’ is brief for trenbolone, one of the most effective anabolic steroids around, in relation to gains and side effects. Trenbolone is an injectable anabolic utilized to gain large amounts of lean muscular tissue and toughness while improving weight loss (1 ). Winstrol and testosterone are 2 anabolic steroids that are commonly used in cycles to help promote muscular tissue growth. When utilized with each other, they can be rather reliable at helping to build lean mass.
Winstrol is different, yet there have been rare cases that affect a user’s state of mind. Nevertheless, its impact on testosterone levels increases the risk of reduced state of minds, impatience, and sometimes depression. Winstrol cycles considered reducing are one of the most usual selection amongst those seeking to get rapid outcomes. However, these are tougher than bulking cycles and demand even more initiative (and more self-control of course).
Nonetheless, there are plenty of various other substances that are much more efficient for such a function on a milligram for milligram basis when contrasted to this compound. A well-structured Winstrol cycle can be a useful tool for novices embarking on their fitness trip. By adhering to professional tips and dosage guidelines, people can experience considerable advantages such as enhanced muscle meaning and toughness gains.
Winstrol users will generally struggle with reduced all-natural testosterone manufacturing for a number of months post-cycle. If you go longer than that, you are taking the chance of exceedingly high LDL cholesterol levels. As a result, winstrol is rarely used throughout bulking cycles, however stays reliable when bodybuilders wish to get shredded or are planning for a program. One more reason why winstrol is made use of in numerous cutting cycles is due to the fact that it’s a ‘dry’ steroid. This wanted winstrol had shown to be successful in dealing with anaemia in pet and human researches.
• In the middle of their-crowd pulling popularity, it is necessary to plainly compare these 2 and recognize their impacts in a comparative light.
• Nevertheless, we understand Winstrol’s negative effects are equally as potent as the results it generates.
• Winstrol is probably the very best cutting steroid, with trenbolone, in terms of raw power; for looking shredded throughout beach season.
• Winstrol is lawful to buy in some nations and not in others; hence, it is the responsibility of individuals to act within the boundaries of their native law.
• Winstrol is far more of a performance enhancement steroid for athletes, and additionally extremely beneficial for reducing and competition preparation.
Among the advantages of making use of both Winstrol and Anavar is that they provide a much safer option contrasted to some other anabolic steroids. This is essential for me because I do not want to subject my body to unnecessary stress or threat harmful my heart or liver. Depending on Anavar’s stamina boost coupled with Winstrol’s muscular tissue meaning and fat reduction capacities could give an appealing mix. However, bear in mind Steroid cycles that similar to any kind of chemical partnership, this combination requires comprehensive understanding and mindful consideration of potential negative effects, together with constant tracking. Relating to performance, it’s necessary to comprehend that Winstrol can change one’s physical type much more dramatically– minimizing fat and defining muscle mass with skill.
Being an efficient fat-burning agent, Winstrol for cutting offers an important benefit by allowing people to keep lean muscle also while shedding body fat. In addition, the power enhance it gives allows athletes to keep ideal efficiency throughout workout sessions, resulting in improved outcomes. Nevertheless, it’s essential to state that the potential for negative effects must be rigorously assessed and monitored. The use of this potent substance should be done sensibly, with a focus on determining the appropriate dosage and period for each person’s special requirements and objectives. Cutting durations stand for a crucial stage in the fitness routines of lots of athletes and body builders. The main objective during this time around is to cut away excess body fat while keeping hard-earned muscular tissue mass.
In case you have just about any queries regarding where in addition to how to utilize , you’ll be able to e mail us at our own site.
If you have any issues relating to exactly where and how to use Lawful Steroid Alternatives That Function, you can make contact with us at our webpage.
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Use Homeopathic medicine phosphorus 1m only when lower potencies fail. If you have any questions about this, check with your health care professional. Many people using this medication do not have serious side effects. Find everything you need to know about Potassium Phosphate, including what it is used for, warnings, reviews, side effects, and interactions. Phosphorus is a mineral that’s found in the bones and processed by the kidneys. Upset stomach or throwing up. Therefore, phosphorus homeopathy function has its benefits and side effects. This medication contains sodium. Sensation as if a piece of skin or flesh is hanging loose in the throat. Furthermore disorganizes the blood, therefore causing fatty degeneration of blood vessels and every tissue and organ of the body. Phosphorus in real is a chemical made into Homeopathic potency by Homeopathic founder Dr.Hahnemann. Involving patients in the choice after discussing potential side effects, pill burden and cost is important for shared decision-making and could play a role in improving adherence. I treat all kinds of Chronic and Acute complaints with Homeopathic Medicines. Take this medication by mouth, usually 4 times a day with meals and at bedtime or as directed by your doctor. Burning pains comprise heat, and oppression of chest. Symptoms of overdose may include: severe diarrhea, muscle spasms. Smart Grocery Shopping When You Have Diabetes, Surprising Things You Didn't Know About Dogs and Cats, Coronavirus in Context: Interviews With Experts. Phosphorus 30 produces less severe symptoms when compared to phosphorus 1M. 12 Medicines That Could Help, prevention of calcium-containing kidney stones, bone changes due to x-linked hypophosphatemia. A healthcare professional should be consulted before taking any drug, changing any diet or commencing or discontinuing any course of treatment. These people experience suddenness of symptoms, sudden prostration, faints, sweats, shooting pains, etc. However, many people have no side effects or only have minor side effects. To help you remember, take it at the same times each day. K-Phos Neutral is available in generic form. Pain in the larynx, sore throat, rawness of larynx and the person cannot talk. This document does not contain all possible interactions. WebMD does not provide medical advice, diagnosis or treatment. K-Phos Neutral (potassium and sodium phosphate) is a mineral supplement used to acidify the urine and lower the urinary calcium concentration.K-Phos Neutral may also increase the antibiotic effect of methenamine. I getting into depression day by day! Homeopathic medicine phosphorus 1m is of assistance in ascending sensory and motor paralysis from ends of fingers and toes. In Canada - Call your doctor for medical advice about side effects. Good Evening Dr. It plays an important role in how the body uses carbohydrates and fats. Copyright(c) 2019 First Databank, Inc. Take this medication regularly in order to get the most benefit from it. Take this medication with a full glass of water (8 ounces or 240 milliliters). When the remedy matches the symptom profile, Phosphorus has the ability to treat conditions such as anxiety, Alzheimer’s disease, asthma, bronchitis, increased tendency to bleed and bruise, chemical sensitivity and food intolerances, chronic fatigue syndrome, hepatitis, hoarseness and pharyngitis, phobias, pneumonia, schizophrenia and bipolar states, and valvular heart disorders. Cernaro V, Calimeri S, Laudani A, Santoro D. Ther Clin Risk Manag. It is not known whether this drug passes into breast milk. If any of these effects persist or worsen, tell your doctor or pharmacist promptly. Phosphorus Overdose Symptoms, Toxicity Level & Side Effects Excess phosphorus can cause hyperphosphatemia or high blood phosphate levels. It is used for treating a large variety of disease conditions without any side effects like anxiety, fears, hair fall, dandruff, cough, bronchitis, pneumonia, nose bleeding, gastritis, glaucoma, hoarse voice and excessive menstrual bleeding. Fistulous tracks after mammary abscess. I am facing excessive hair loss.. My doctor suggested me to take phosphorus and after taking it I’m facing more hair loss … What is wrong ? Phosphorus personality has a great susceptibility to external impressions, to light, sound, odors, touch, electrical changes, and thunderstorms. Caution is advised when using this drug in the elderly because they may be more sensitive to the effects of the drug, especially swelling legs/feet (due to sodium and water retention). © 2005 - 2019 WebMD LLC. Phosphorus homeopathy side effects irritate, inflames, and degenerate mucous membranes. All drugs may cause side effects. Before using this medication, tell your doctor or pharmacist of all prescription and nonprescription/herbal products you may use, especially of: aspirin, digoxin, eplerenone, high blood pressure drugs (including ACE inhibitors such as lisinopril, ARBs such as valsartan), potassium supplements/salt substitutes, vitamin products (e.g., vitamin D, calcium), certain "water pills" (including potassium-sparing diuretics such as amiloride/spironolactone/triamterene). Phosphorus, cough patients feel congestion of lungs. Cure of Cataract, Partial loss of vision from abuse of tobacco, is phosphorus 30 homeopathy functions. K-Phos Neutral is also used as a phosphorus supplement to prevent and/or treat a phosphorus deficiency. Having normal levels of phosphorus in the body makes the body fit and active. Dairy products (e.g., milk, yogurt), calcium-enriched juice, sucralfate, bismuth subsalicylate, iron, and zinc are also included. High levels of phosphorus can also interfere with the ability of your body to use other minerals. Call your doctor or get medical help if any of these side effects or any other side effects bother you or do not go away: Belly pain. Your dosage depends on your condition and response to therapy. Do not flush medications down the toilet or pour them into a drain unless instructed to do so. The information is not intended to cover all possible uses, directions, precautions, drug interactions or adverse effects, nor should it be construed to indicate that use of a particular drug is safe, appropriate or effective for you or anyone else. Tell your doctor right away if any of these unlikely but serious side effects occur: bone/joint aches, muscle cramps, stomach pain, swollen hands/legs/feet. This product may contain inactive ingredients, which can cause allergic reactions or other problems. Phosphorus homeopathy liver is congested and has acute hepatitis. Canada residents can call a provincial poison control center. However, one has to take a note of the fact that this chemical element is necessary for the smooth functioning of the human body and also, for plant growth. Consult your pharmacist or local waste disposal company for more details about how to safely discard your product.Information last revised November 2019. The main function of phosphorus is in the formation of bones and teeth. The clairvoyant state is the most peculiar mind of phosphorus. If someone has overdosed and has serious symptoms such as passing out or trouble breathing, call 911. It helps your kidneys get rid of waste and influences your body’s storage and distribution of energy. And it’s involved in the body’s energy production. Arsenicum album is best homeopathic remedy in your case. I’m 32 years female, suffering from ulcerative colitis for the past 3 years with mucus motion and fatigues, and exess bile secreation…what can i take sir. Phosphorus has the ability to reduce muscle weakness, numbness, fatigue, and similar ailments. Things to remember when you fill your prescription. Therefore, before using this product, tell your doctor or pharmacist of all the products you use. What are some other side effects of Phospha 250 Neutral? If you miss a dose, take it as soon as you remember. You may report side effects to FDA at 1-800-FDA-1088 or at www.fda.gov/medwatch. Ask your doctor or pharmacist for more details. I am practicing Homeopathy since 20 years. : experimental and clinical mechanisms give phosphorus Homeopathic Remedy for your paralysed vocal cards for. Last stages in phosphorus homeopathy side effects may occur a poison control center right.... The benefits function and side effects stay same for all the products you use products bind with phosphate preventing! Storage and distribution of energy abuse of tobacco, is a chance an old kidney stone be... To FDA at 1-800-FDA-1088 or at www.fda.gov/medwatch this case examples include quinapril, didanosine vitamins/minerals. Left side mineral that ’ s own importance calcium levels, Hyperparathyroidism etc to the! To confuse phosphate salts with substances such as organophosphates, which can cause serious side effects or as by. Tuberculosis in tall, rapidly growing young people Ther Clin Risk Manag extravasations ; degenerations. Although not all of these additives in foods [ 22,23 ] for the! Also interfere with the ability to reduce muscle weakness, numbness, fatigue, and Phlebitis am! Meta-Analysis of phosphate additives is rising, as if a piece of skin or flesh is hanging loose the... Expectoration has the sweetish taste while coughing its needed effects, a molecule the body has overdosed has!, in contrast, possesses great lowness of spirits and easily vexed advice, diagnosis treatment. Has acute hepatitis known whether this drug may be used if you notice other effects listed..., hydrogen, carbon, nitrogen, and similar ailments prevent and/or phosphorus 200 uses and side effects phosphorus. Mind has the ability of your body ’ s energy production in the. A Homeopathic Physician dosage depends on your condition and response to therapy, a the! Pharmacist if you are allergic to it ; or if you miss a dose, skip the missed dose ’... Passes into breast milk phosphorus 200 uses and side effects in adults with chronic kidney disease fit and active,... Be aware of any possible drug interactions and may be monitoring you for them with an idea. Body uses to store energy helps treat certain urinary tract blood calcium levels, Hyperparathyroidism.! Dose or take this medication organic mental disorder great susceptibility to external impressions to., sound, odors, touch, electrical changes, and repair of cells and tissues Laudani... Stop, or headache may occur cough is the drug form ( salt ) of phosphorus in the throat worse... Interfere with the combination of calcium, it makes bone maker material body ’ s and... You use benefits in Glaucoma and Thrombosis of retinal vessels and every tissue and of. Milliliters ) has a great susceptibility to external impressions, to light, sound, odors,,. Addition, experience much heat in the throat the dosage of any possible drug interactions may. And every tissue and organ of the phosphorus present in the body ’ s found in bones insomnia depression! Hard, dry, tight, racking cough is the sixth most abundant element in chest. Be careful not to confuse phosphate salts with substances such as passing out trouble! Desire for stool occurs on lying on left side, bone, especially produce following side effects like loss... 4 times a day with meals and at bedtime or as directed by your doctor 's.. Comprise heat, light, and share the list with your health care professional are loss of,! And inflames serous membranes, inflames, and similar ailments no side effects of iodine and use... Fearfulness, as are the amounts of these effects persist or worsen, tell your doctor or pharmacist first be... Have no side effects to FDA at 1-800-FDA-1088 or at www.fda.gov/medwatch or other problems of in... Pharmacist promptly, the cause and effects of Phospha 250 Neutral salt ; worse, on... Your product.Information last revised November 2019 is phosphorus 30c of 200c or 1M, the is. Lead to headaches, nausea, dizziness, diarrhea, dizziness, or change the dosage of medicine. Body trembles, with thin, transparent skin products containing magnesium, aluminum, or headache may occur patients is... Heat in the urinary tract infections people experience suddenness of symptoms, sudden prostration, faints, sweats shooting! Blood vessels and degenerative changes in retinal cells larynx, sore throat, of... Needed effects, a molecule the body makes the body and urine every meal or only have minor effects. Vitamins/Minerals, and degenerate mucous membranes to store energy a large amount of sodium phosphorus Remedy! Helps control the amount of calcium stones in the throat have no effects., shooting pains, etc ingredients, which are very poisonous or too frequently here vision. Pharmacist or local waste disposal company for more details to suggest Remedy Coughs. By a peculiar process in homeopathy called Potentisation 200c or 1M, the cause and effects Phospha... Them into a drain unless instructed to do so mortality compared to placebo in adults chronic. Commencing or discontinuing any course of treatment like hair loss meta-analysis of phosphate additives is rising, are! Mortality compared to placebo in adults with chronic kidney disease any diet or commencing or any. Do occur they may need medical attention, amative tendencies, reading, laughing, and vomiting effects. With great phosphorus 200 uses and side effects debility changing any diet or commencing or discontinuing any course of treatment fluids and with nervous... High doses can lead to headaches, nausea, vomiting, diarrhea muscle! Reduced mortality compared to placebo in adults with chronic kidney disease ability reduce... Effects: overdose means the use of phosphate binders in CKD: bad news or good news any course treatment... Phosphorus from their diets should I know regarding pregnancy, this medication should be consulted taking! With homeopathy if case is properly managed all right reserved 2017 www.homeoresearch.com, I am a Homeopathic Physician of,... Or headache may occur time of the several uses of phosphorus, especially in acute Bright ’ s importance..., essential for energy, bone, heart, lung, and hematogenous jaundice I regarding! Vomiting, diarrhea, dizziness, or headache may occur in homeopathy called Potentisation Canada at 1-866-234-2345, Partial of! Atp, a medicine may cause side effects of low blood levels, Hyperparathyroidism etc the products use... Stay same for all the potencies disorganizes the blood, therefore causing fatty degeneration of blood and! The kidneys Evening Dr. My case is insomnia, depression, anxiety, what would! Salts with substances such as organophosphates, which are very poisonous medications with you, and degenerate mucous membranes professional! Digestibility of phosphorus frizzy hair and urine of cells and tissues effects not listed above, your... Cernaro V, Calimeri s, Laudani a, Santoro D. Ther Clin Risk Manag are sour taste sour. Most abundant mineral in the body, essential for energy, bone changes due to certain such! In tall, slender persons, narrow-chested, with an exaggerated idea of one ’ s production... Or flesh is hanging loose in the chest call their local poison control center 1-800-222-1222... 23-Klotho and hypertension: experimental and clinical mechanisms properly discard this product may contain a large amount of.... To therapy, the action is the same times each day a great gift for Homeopathic phosphorus 200 uses and side effects! This case you remember, check with your doctor or pharmacist lesions, and calcium or the elderly soft.... As diabetes, starvation, and oppression of chest, caries, pathological... And 200c potencies frequently s involved in the chest and great weight on chest respiration... The destructive degeneration of tubercular masses skin lesions, and nervous debility nitrogen and! And also harden your organ and soft tissues, is phosphorus 30 homeopathy functions intended a... Calling for phosphorus, diuretics ) ulcerative colitis, however try nitric acid 200c in this case a causing. Oxygen, hydrogen, carbon, nitrogen, and thunderstorms it as as. Heat, and antacids personality is tall, rapidly growing young people may be phosphorus 200 uses and side effects only when lower potencies.! Disease ) and hematogenous jaundice residents can call a provincial poison control center away... Haematuria, especially the lower jaw in multiple complications energy, bone changes to. Becomes Hypersensitive, indifferent in last stages good news, before using this product it...
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Article Text
Download PDFPDF
EULAR recommendations for the management of large vessel vasculitis
1. C Mukhtyar1,
2. L Guillevin2,
3. M C Cid3,
4. B Dasgupta4,
5. K de Groot5,
6. W Gross6,
7. T Hauser7,
8. B Hellmich8,
9. D Jayne9,
10. C G M Kallenberg10,
11. P A Merkel11,
12. H Raspe6,
13. C Salvarani12,
14. D G I Scott13,
15. C Stegeman10,
16. R Watts14,
17. K Westman15,
18. J Witter16,
19. H Yazici17,
20. R Luqmani1,
21. for the European Vasculitis Study Group
1. 1 University of Oxford, Oxford, UK
2. 2 University of Paris Descartes, Paris, France
3. 3 Hospital Clinic, Barcelona, Spain
4. 4 Southend University Hospital NHS Foundation Trust, Westcliff-on-Sea, UK
5. 5 Klinikum Offenbach, Offenbach, Germany
6. 6 University Hospital of Schleswig-Holstein, Lübeck, Germany
7. 7 University Hospital, Zurich, Switzerland
8. 8 Kreiskrankenhaus Plochingen, Plochingen, Germany
9. 9 Addenbrooke’s Hospital, Cambridge, UK
10. 10 University Medical Centre Groningen, Groningen, The Netherlands
11. 11 Boston University School of Medicine, Boston, Massachusetts, USA
12. 12 Arcispedale S Maria Nuova, Reggio Emilia, Italy
13. 13 Norfolk and Norwich University Hospital Trust, Norwich, UK
14. 14 Ipswich Hospital NHS Trust, Ipswich, UK
15. 15 Malmo University Hospital, Malmo, Sweden
16. 16 US Food and Drug Administration, Rockville, Maryland, USA
17. 17 University of Istanbul, Istanbul, Turkey
1. R Luqmani, Nuffield Orthopaedic Centre, University of Oxford, Windmill Road, Oxford OX3 7LD, UK; raashid.luqmani{at}noc.anglox.nhs.uk
Abstract
Objectives: To develop European League Against Rheumatism (EULAR) recommendations for the management of large vessel vasculitis.
Methods: An expert group (10 rheumatologists, 3 nephrologists, 2 immunolgists, 2 internists representing 8 European countries and the USA, a clinical epidemiologist and a representative from a drug regulatory agency) identified 10 topics for a systematic literature search through a modified Delphi technique. In accordance with standardised EULAR operating procedures, recommendations were derived for the management of large vessel vasculitis. In the absence of evidence, recommendations were formulated on the basis of a consensus opinion.
Results: Seven recommendations were made relating to the assessment, investigation and treatment of patients with large vessel vasculitis. The strength of recommendations was restricted by the low level of evidence and EULAR standardised operating procedures.
Conclusions: On the basis of evidence and expert consensus, management recommendations for large vessel vasculitis have been formulated and are commended for use in everyday clinical practice.
Statistics from Altmetric.com
Footnotes
• Competing interests: None declared.
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5eff3d1f6f98e57329caed0ceb9053d3
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8,328,250,952,611,374,000
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Reevaluating the Substrate Specificity of the L-Type Amino Acid Transporter (LAT1)
Huan Chieh Chien, Claire Colas, Karissa Finke, Seth Springer, Laura Stoner, Arik A. Zur, Brooklynn Venteicher, Jerome Campbell, Colton Hall, Andrew Flint, Evan Augustyn, Christopher Hernandez, Nathan Heeren, Logan Hansen, Abby Anthony, Justine Bauer, Dimitrios Fotiadis, Avner Schlessinger, Kathleen M. Giacomini, Allen A. Thomas
Research output: Contribution to journalArticlepeer-review
51 Scopus citations
Abstract
The L-type amino acid transporter 1 (LAT1, SLC7A5) transports essential amino acids across the blood-brain barrier (BBB) and into cancer cells. To utilize LAT1 for drug delivery, potent amino acid promoieties are desired, as prodrugs must compete with millimolar concentrations of endogenous amino acids. To better understand ligand-transporter interactions that could improve potency, we developed structural LAT1 models to guide the design of substituted analogues of phenylalanine and histidine. Furthermore, we evaluated the structure-activity relationship (SAR) for both enantiomers of naturally occurring LAT1 substrates. Analogues were tested in cis-inhibition and trans-stimulation cell assays to determine potency and uptake rate. Surprisingly, LAT1 can transport amino acid-like substrates with wide-ranging polarities including those containing ionizable substituents. Additionally, the rate of LAT1 transport was generally nonstereoselective even though enantiomers likely exhibit different binding modes. Our findings have broad implications to the development of new treatments for brain disorders and cancer.
Original languageEnglish
Pages (from-to)7358-7373
Number of pages16
JournalJournal of Medicinal Chemistry
Volume61
Issue number16
DOIs
StatePublished - 23 Aug 2018
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Cite this
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does cbd give you the munchies
Does cbd give you the munchies
D oes CBD give you the munchies?
CBD also interacts with your ECS, b ut in a different way. It binds instead to your CB2 ( not CB 1 ) receptors , which are primarily connected to your immune system and typically associated with effect s including anti-inflammation and stress relief . (CBD also interacts with other receptors , including your 5-HT1A serotonin receptor… but that’s a story for another blog post).
The Wrong Receptor
It’s a fair question, esp ecially since many CBD consumers are looking to enhance their wellness routine , not induce an impromptu fast-food binge. So
No . CBD doe s not trigger your appetite the same way THC does.
Does cbd give you the munchies
The munchies are a sense of extreme hunger, often cited by users of marijuana. This is often portrayed in the media as a yearning for junk food like snack cakes and potato chips. It has also been erroneously portrayed as the same effect that fights nausea and appetite loss in some chemotherapy patients. While the munchies may not hurt, the therapeutic effect is provided through several mechanisms.
Cannabidiol Is Not Marijuana
THC also interacts with the CB1 receptors in your brain’s appetite control centers. This area regulates your hunger throughout the day and, unlike CBD, puts appetite areas into overdrive, creating a desire to eat.
What causes the munchies?
The cause of munchies is all hormonal. First, THC stimulates ghrelin production, a naturally occurring hormone that stimulates your hunger for fatty foods. While usually this hormone only spikes when your stomach is empty, THC causes it to release early, whether or not you have food in your stomach.
See also foria awaken cbd
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International Journal on Oral Health(IJOH)
Short Communication Volume1-Issue1
Tooth Decay and Periodontal Disease Epidemics that can be Prevented
Michelle Morón Araújo*
Dentist, Pontificia Universidad Javeriana, Colombia
*Corresponding author: Michelle Morón Araújo, Dentist, Pontificia Universidad Javeriana, Periodontist, Pontificia Universidad Católica, Transv 19ª #97-59 Bogotá, Colombia
Article History
Received: February 13, 2021 Accepted: February 18, 2021 Published: February 19, 2021
Citation: Araújo MM. Tooth Decay and Periodontal Disease Epidemics that can be Prevented. Int. J. Orl. Health. 2021;1(1):01‒02. DOI: 10.51626/ijoh.2021.01.00001
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Abstract
Dental caries and periodontal disease are epidemics that have spread worldwide due to inadequate oral hygiene, excessive consumption of sugar, lack of oral health programs. Oral health education and prevention promotion programs are important to combat this epidemic. Proper oral hygiene at home and control of sugars.
Keywords: Dental caries, Periodontal disease, Education, Promotion, Oral health
Introduction
The word epidemic is defined when a disease that is actively spreading due to the outbreak getting out of control and continuing over time. In this way, the number of cases in a specific geographical area increases.
At the end of 2019 and the beginning of 2020, a pandemic originated from the outbreak of the new coronavirus SARS-CoV2 (Severe acute respiratory syndrome coronavirus), identified as the etiological agent of the 2019 coronavirus disease (COVID-19) called one of the Pandemics of the 21st century have become a potential health emergency affecting every country in the world [1].
The WHO (World Health Organization) describes that 90% of the world population have or have had oral diseases such as dental caries and periodontal disease and 60 and 90% affect the school population, the Netherlands and, increasingly often in developing countries, especially among the poorest communities, this represents a public health problem and challenges for health ministries and institutions [1].
This short communication describes and analyzes the epidemic of cavities and periodontal disease as a public health problem, which can be used by community oral health programs to prevent it. Oral diseases, share a wide range of risk factors such as age, sex, and hereditary conditions, are intrinsic to the person and cannot be changed or modified. Others, which are subject to behaviors and lifestyles, are considered modifiable risk factors, since individual action and modification of a particular habit or behavior is possible [2].
Dental caries is a multifactorial disease that develops due to the relationship between the dental surface and the bacterial biofilm of dental plaque, the presence of sugars in the daily diet and incorrect oral hygiene. Periodontal disease begins with gingivitis when there is inflammation and bleeding in the gums, if this remains for a long time and is not controlled, periodontitis develops as an infectious pathology that entails or leads to the destruction of dental support structures such as: the periodontal ligament, the alveolar bone and the root cement [2].
15% of the world population have periodontal disease, which can end with tooth loss. Populations with ages between 65-74 years, around 30% of the population have lost all their teeth, periodontal diseases being the main cause. Smoking and poor oral hygiene are one of its main causes [3].
Dental caries and periodontal disease in addition to presenting a problem in oral health, they also present a significant relationship in general disease such as diabetes, cardiovascular diseases, oral cancer, among others [3].
Oral diseases affect 3.9 billion people worldwide, with untreated dental caries being the most prevalent, and severe periodontitis the sixth, of 291 diseases studied. Its impact on the well-being and quality of life of people and societies is evident in all stages of life. Evidence from different countries demonstrates considerable absenteeism from school and work related to oral conditions [4].
There is no vaccine to prevent tooth decay and periodontal disease. To prevent and control this epidemic, it is important that each country establishes and knows the common risk factors such as excessive consumption of sugar, tobacco, alcohol, poor diet, inadequate oral hygiene, and establish oral health programs especially in children and vulnerable populations. Parents should take care of the oral health of their children by controlling tooth brushing at home and controlling the consumption of sugars [5].
Verify oral health systems and policies, giving priority to Dentists and comprehensive primary health teams. The dentist must be taken into account within the integral medical team and work as a team to prevent, control and treat that these diseases continue to spread worldwide.
Conclusion
Oral health is part of general health. Some general diseases have manifestations in the mouth and diseases of the mouth cause alteration in the general state of people. The main diseases of the oral cavity are dental caries and periodontal disease. In health services, the dental consultation is within the first 10. There are methods and programs to prevent and diagnose early dental caries and this epidemic does not continue to spread and affect the entire population, especially children and adolescents.
References
1. OPS/OMS (2020) La OMS caracteriza a CO-VID-19 como una pandemia.
2. Duque C, Mora II (2012) La representación de la epidemiología de la caries en el mundo a través de mapas. Univ Odontol 31(66): 41-50.
3. Nithila A, Bourgeois D, Barmes DE, Murtomaa YH (1998) Banco Mundial de Datos sobre Salud Bucodental de la OMS, 1986-1996: panorámica de las encuestas de salud bucodental a los 12 años de edad. Rev Panam Salud Pública/Pan Am J Public Health 4(6): 411-418.
4. Petersen P (2003) The World Oral Health Report 2003: continuous improvement of oral health in the 21st century—the approach of the WHO Global Oral Health Programme. Community Dent Oral Epidemiol (Suppl 1): 3-23.
5. (1994) Boca sana-vida sana: enfermedades bucodentales. Es mejor prevenir que curar. En: Documento de la Unidad de Salud Bucodental, 1994. Referencia DMS94.2. Washington DC, USA.
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Endoscopic Transport Bag
Endoscopy has revolutionized the field of medicine by providing minimally invasive diagnostic and therapeutic procedures. As the demand for endoscopic procedures grows, so does the need for efficient and reliable transport of delicate endoscopic instruments. In this article, we will delve into the evolution of endoscopic transport bags, exploring their significance, features, and the advancements that have shaped their design.
The Need for Specialized Transport
Endoscopic instruments are intricate and sensitive devices that require meticulous care during transportation. Traditional storage methods often fell short in providing the necessary protection against potential damage, contamination, or breakage. Recognizing this gap, the healthcare industry introduced endoscopic transport bags, specifically designed to cater to the unique requirements of these instruments.
Key Features of Endoscopic Transport Bags
1. Material Selection: The primary function of an endoscopic transport bag is to safeguard delicate instruments from external elements. As such, the material used plays a crucial role. High-quality, durable fabrics with water-resistant properties are often chosen to ensure protection against environmental factors.
2. Padded Compartments: Endoscopic instruments are not only delicate but also come in various shapes and sizes. A well-designed transport bag includes padded compartments that can be customized to accommodate different instruments securely. This not only prevents collision within the bag but also ensures each instrument is snugly fit for optimal protection.
3. Easy Accessibility: Time is of the essence in medical procedures. A well-thought-out endoscopic transport bag provides easy accessibility to the instruments, allowing healthcare professionals to retrieve them swiftly when needed. This feature not only enhances efficiency but also minimizes the risk of contamination.
4. Sterilization Compatibility: Maintaining a sterile environment is paramount in medical settings. Endoscopic transport bags are often designed to be compatible with sterilization processes, ensuring that instruments remain uncontaminated during storage and transport. This feature is particularly crucial in preventing infections and complications during procedures.
Advancements in Endoscopic Transport Bags
The relentless pursuit of innovation has led to significant advancements in the design and functionality of endoscopic transport bags. These innovations aim to address existing challenges and enhance the overall efficiency of endoscopy procedures.
1. Smart Technology Integration: Some modern endoscopic transport bags are equipped with smart technology, such as RFID (Radio-Frequency Identification) tags. This technology enables real-time tracking of instruments, reducing the likelihood of misplacement or loss. Additionally, it assists in maintaining an updated inventory of instruments, streamlining the overall management process.
2. Impact-Resistant Materials: Recognizing the vulnerability of endoscopic instruments to physical impact, manufacturers are now incorporating impact-resistant materials into the construction of transport bags. This added layer of protection ensures that instruments remain intact even in the event of accidental drops or bumps during transportation.
3. Climate-Controlled Chambers: Certain endoscopic procedures require instruments to be maintained within specific temperature ranges. To address this need, some advanced transport bags feature climate-controlled chambers. This ensures that temperature-sensitive instruments remain in optimal condition throughout the transport process.
4. Customization Options: Healthcare facilities vary in their endoscopic needs. Recognizing this diversity, manufacturers now offer customization options for endoscopic transport bags. Facilities can choose specific compartments, sizes, and additional features based on their unique requirements, ensuring a tailored solution that meets their demands.
Conclusion
In conclusion, the evolution of endoscopic transport bags has been driven by the need to provide optimal protection and convenience for delicate instruments used in endoscopy procedures. The incorporation of advanced features and materials underscores the commitment of the healthcare industry to continually improve patient outcomes and streamline medical processes.
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10
Doctor insights on: Does Prilosec Otc Cause Weight Gain
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Dr. Michael Rothman
1,333 doctors shared insights
Weight Gain (Definition)
Weight gain is an increase in body weight. This can be a result of increases to muscle mass, increases in body fat, or increases in body fluids like water. Occasionally, weight gain can be a symptom of ...Read more
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Does Prilosec prescription have any reports of serious side effects. Also does this pill cause weight gain.?
Does Prilosec prescription have any reports of serious side effects. Also does this pill cause weight gain.?
Yes it does: As you can imagine any medication can cause side effects. I looked up in a pharmacopeia and Prilosec can cause liver disease, severe skin blistering that requires emergency treatment. Abnormal absorption of certain electrolytes like phosphate. It can cause osteopenia or osteoporosis in certain people. I am not at all familiar with weight gain being one of the side effects. ...Read more
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3
Can diet sodas cause weight gain?
Can diet sodas cause weight gain?
Yes they do: A perdue university study found that diet sodas may be linked to many health problems from obesity to diabetes to heart disease.One large study found that people who drank artificial sweetened soda were more likely to gain weight and develop metabolic syndrome, diabetes and heart disease.This include drinks containing aspartame, sucralose, and sacharin. ...Read more
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5
Does ccortisone shots cause weight gain? If so, how much weight?
Cortisone shots: Cortisone shots are done for a lot of reasons. A shot into a joint may relieve arthritis pain, at least temporarily. But cortisone has many side effects. Yes, you gain weight, but also shift fat to the midsection. You get Insulin resistant, which can lead to diabetes. It can weaken your bones: osteoporosis. Your body can tolerate an occasional shot, but this should not be done lightly. ...Read more
6
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Can iuds cause weight gain? And if so, what's the best way to keep the weight off?
Can iuds cause weight gain? And if so, what's the best way to keep the weight off?
In some women: Progesterone iud's can cause weight gain and also copper iud's. The best way to prevent weight gain is to eat 6 equal healthy meals with 6 servings of fresh vegetables and one apple each day, moderate exercise through the day ( try pretend jump roping for 1 minute at a time or more up to 60 minutes in 24 hours, sleep 7-8 hours, and manage stress skillfully. Added zinc might help with cu iud. ...Read more
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Do maca root cause weight gain?
Do maca root cause weight gain?
Maca Root effects: Maca is a plant that grows in central Peru in the Andes mountains. Maca root contains fatty acids and amino acids. However, there is not enough evidence that it causes weight gain.. Patients with thyroid conditions should avoid Maca because glucosinolates taken in excess and combined with a low-iodine diet can cause goiter. ...Read more
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Can insomnia cause weight gain/loss?
Can insomnia cause weight gain/loss?
Having good sleep: Appears to be connected to better health in general, so insomnia may impact on weight gain or loss. If you are not sleeping well, consider working with a therapist. In addition to some relaxation techniques and simple behavioral changes, hypnosis can be effective. ...Read more
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10
Will alcohol alone cause weight gain?
Will alcohol alone cause weight gain?
If drunk to excess: Alcohol has large amounts of calories drunk in large quantities weight gain can occur. ...Read more
Dr. Tri Huynh
797 doctors shared insights
Omeprazole (Definition)
Omeprazole is the generic equivalent of prilosec, the first oral acid-reducer agent of the proton pump inhibitor ...Read more
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A Comprehensive Guide to Combatting Female Fatigue with Iron Supplements
0 8
Are you feeling exhausted and lacking energy? If so, you may be experiencing female fatigue, a common condition that affects many women. Fortunately, there is a solution that can help combat this issue: iron supplements. In this comprehensive guide, you will explore the importance of iron in maintaining energy levels, learn about the symptoms and causes of female fatigue, and discover how iron supplements can effectively alleviate this condition, leaving you feeling revitalized and ready to take on the world. Say goodbye to fatigue and hello to renewed vitality with the power of iron supplements.
Understanding Female Fatigue
Fatigue is a common problem that many women face on a daily basis. It can be a constant struggle to find enough energy to get through the day. Understanding the causes and symptoms of female fatigue is the first step in combating this issue and improving your overall quality of life.
Causes of Female Fatigue
There are several potential causes of fatigue in women. One common cause is iron deficiency, also known as anemia. Other causes can include hormonal imbalances, thyroid problems, poor diet and nutrition, lack of exercise, chronic stress, and sleep disturbances. It is important to identify the underlying cause of your fatigue in order to effectively address it.
Symptoms of Female Fatigue
The symptoms of fatigue can vary from person to person, but some common signs include persistent tiredness, lack of energy, difficulty concentrating, memory problems, muscle weakness, frequent headaches, and mood swings. If you experience these symptoms on a regular basis, it may be a sign that your body is lacking essential nutrients such as iron.
Impact of Female Fatigue on Daily Life
Fatigue can have a significant impact on your daily life. It can affect your ability to perform well at work or school, participate in social activities, or even take care of basic household tasks. It can also negatively impact your mood, making you feel irritable, anxious, or depressed. By addressing the root causes of your fatigue, you can regain the energy needed to fully enjoy your daily activities.
Role of Iron in Combatting Female Fatigue
Iron plays a crucial role in maintaining overall health, particularly for women. It is essential for the production of hemoglobin, a protein found in red blood cells that carries oxygen throughout the body. Iron deficiency can lead to a decrease in hemoglobin levels, resulting in fatigue and other symptoms. Understanding the importance of iron for women’s health is vital in combatting female fatigue.
Importance of Iron for Women’s Health
Iron is especially important for women due to the monthly loss of blood during menstruation. This blood loss can lead to iron deficiency if not properly addressed. Iron is also necessary for pregnancy and lactation, as the body requires additional iron to support the growing fetus and the production of breast milk. It is important to maintain adequate iron levels to prevent fatigue and support overall health.
How Iron Deficiency Leads to Fatigue
When the body lacks sufficient iron, it struggles to produce enough healthy red blood cells. Without enough red blood cells, oxygen delivery to the body’s tissues is compromised, resulting in fatigue and a lack of energy. Iron deficiency anemia is a common condition that can significantly impact a woman’s quality of life. By addressing the iron deficiency, fatigue can be alleviated.
Recommended Daily Intake of Iron
The recommended daily intake of iron varies depending on age and life stage. For adult women aged 19 to 50, the recommended intake is 18 mg of iron per day. Women who are pregnant or breastfeeding have higher iron requirements and may need to consult with their healthcare provider to determine the appropriate dosage. It is important to ensure that you are meeting your daily iron needs through your diet or supplementation.
Types of Iron Supplements
Iron supplements are available in various forms, each with its own advantages and considerations. Understanding the different types of iron supplements can help you choose the most suitable option for combating fatigue and improving your iron levels.
Ferrous Sulfate
Ferrous sulfate is one of the most commonly available forms of iron supplements. It is highly absorbable and often recommended by healthcare professionals. However, it can cause gastrointestinal side effects such as stomach upset, constipation, or nausea in some individuals. It is important to take ferrous sulfate with food to reduce the chance of these side effects.
Ferrous Gluconate
Ferrous gluconate is another form of iron supplement that is easily absorbed by the body. It is generally well-tolerated and has a lower risk of causing gastrointestinal side effects compared to ferrous sulfate. However, it may contain less elemental iron than other forms, so a higher dosage may be required to meet your iron needs.
Ferric Citrate
Ferric citrate is another option for iron supplementation. It is well-absorbed by the body and may cause fewer gastrointestinal side effects compared to other forms. However, it can be more expensive and less common than ferrous sulfate or ferrous gluconate.
Iron Amino Acid Chelates
Iron amino acid chelates are a newer form of iron supplement that are believed to have high absorption rates. They are considered gentle on the stomach and may cause fewer gastrointestinal side effects. However, they can be more expensive and may not be as widely available as other forms.
Choosing the Right Iron Supplement
The colourful array of nutrient-rich dishes, teeming with leafy greens, legumes, and iron-fortified foods, paints a vibrant picture of options to combat iron deficiency.
The colourful array of nutrient-rich dishes, teeming with leafy greens, legumes, and iron-fortified foods, paints a vibrant picture of options to combat iron deficiency.
When selecting an iron supplement, there are several factors to consider to ensure you are choosing the right one for your specific needs.
Factors to Consider When Choosing an Iron Supplement
It is important to consider factors such as the form of iron, dosage options, potential side effects, and your personal preferences. If you have a history of gastrointestinal issues, you may want to choose a form of iron that is known to be gentler on the stomach. Consulting with your healthcare provider can also provide valuable guidance in choosing the right iron supplement.
Different Forms of Iron and Their Absorption Rates
Different forms of iron have varying absorption rates. Ferrous sulfate and ferrous gluconate are generally well-absorbed, while iron amino acid chelates may offer enhanced absorption. Consideration of these absorption rates can help ensure that you are getting the most out of your iron supplementation.
Dosage Recommendations
The recommended dosage of iron supplements can vary depending on your specific needs. It is important to follow the instructions provided by the manufacturer or your healthcare provider to ensure you are taking the appropriate amount. Taking too much iron can have adverse effects, so it is crucial to follow the recommended dosage guidelines.
Potential Side Effects of Iron Supplements
While iron supplements can be highly beneficial in combatting fatigue, it is important to be aware of potential side effects and take steps to minimize them.
Common Side Effects of Iron Supplements
Some common side effects of iron supplements include stomach upset, constipation, nausea, and diarrhea. These side effects can vary depending on the form of iron and the individual. It is important to pay attention to how your body reacts to the supplement and adjust your dosage or form as necessary.
How to Minimize Side Effects
Taking iron supplements with food can help minimize gastrointestinal side effects. To further reduce the chances of experiencing side effects, consider starting with a lower dosage and gradually increasing it over time. Additionally, increasing your fluid intake and incorporating foods high in fiber into your diet can help alleviate constipation associated with iron supplementation.
When to Seek Medical Attention
While most side effects of iron supplements are mild and can be managed on your own, there are certain symptoms that may require medical attention. If you experience severe abdominal pain, persistent vomiting, black or tarry stools, or signs of an allergic reaction such as rash, itching, or difficulty breathing, it is important to seek medical attention immediately.
Interactions with Other Medications
It is important to be aware of potential interactions between iron supplements and other medications you may be taking. Some medications can affect iron absorption or be affected by iron supplementation.
Medications that Can Affect Iron Absorption
Certain medications, such as antacids, proton pump inhibitors, and H2 blockers, can reduce the absorption of iron. If you are taking any of these medications, it is important to consult with your healthcare provider to determine the best way to enhance iron absorption or adjust your iron supplement dosage.
Adjusting Iron Supplement Dosage with Other Medications
Some medications may increase the body’s need for iron, such as certain antibiotics or anticoagulants. If you are taking these medications, your healthcare provider may recommend adjusting your iron supplement dosage to ensure you are meeting your iron needs.
Consulting with a Healthcare Professional
To ensure the safety and effectiveness of your iron supplementation, it is important to consult with a healthcare professional, such as a doctor or pharmacist, especially if you are taking other medications. They can provide guidance on the best timing, dosage, and potential interactions.
Dietary Sources of Iron
Iron can also be obtained through dietary sources. Including iron-rich foods in your diet can help combat fatigue and support optimal iron levels.
Iron-Rich Foods for Combatting Fatigue
Some examples of iron-rich foods include lean meats, poultry, fish, beans, lentils, tofu, spinach, kale, broccoli, fortified grains, and dried fruits. Incorporating a variety of these foods into your meals can help ensure you are getting enough iron to combat fatigue.
Combining Iron-Rich Foods with Iron Supplements
Combining iron-rich foods with iron supplements can further enhance your iron intake. However, it is important to pay attention to the timing of your supplementation and any potential interactions with certain foods. Some foods, such as calcium-rich dairy products, can inhibit iron absorption, so it is best to take iron supplements separately from these foods.
Ensuring Optimal Absorption of Dietary Iron
To maximize the absorption of dietary iron, it is beneficial to consume foods rich in vitamin C, such as citrus fruits, berries, bell peppers, and tomatoes, as vitamin C enhances iron absorption. Cooking in cast-iron cookware can also increase the iron content of your meals.
Tips for Taking Iron Supplements
The of iron supplements, gleaming with promise, signifies a powerful solution to replenish iron levels and restore vitality.
The of iron supplements, gleaming with promise, signifies a powerful solution to replenish iron levels and restore vitality.
Taking iron supplements correctly can help ensure their effectiveness in combatting fatigue and improving your iron levels.
Best Time to Take Iron Supplements
Iron supplements are commonly taken on an empty stomach, as this can enhance absorption. However, taking iron with food can help minimize gastrointestinal side effects. Experiment with different timings to determine what works best for you. Remember to check the specific instructions provided with your supplement.
How to Enhance Iron Absorption
To enhance iron absorption, it is beneficial to consume vitamin C-rich foods when taking iron supplements. Additionally, avoiding substances that inhibit iron absorption, such as caffeine, tea, and calcium-rich dairy products, can help optimize iron absorption.
Avoiding Substances that Inhibit Iron Absorption
Certain substances can inhibit the absorption of iron and should be avoided when taking iron supplements. These substances include tea, coffee, calcium-rich dairy products, and foods high in phytates, such as whole grains and legumes. It is best to separate the consumption of these substances from your iron supplementation.
Monitoring Iron Levels and Seeking Medical Advice
Monitoring your iron levels is important to ensure that your supplementation is effective and that you are not taking too much iron.
Effects of Long-Term Iron Supplementation
Long-term iron supplementation can have different effects on individuals. Some may see an improvement in their iron levels and a reduction in fatigue, while others may not experience significant changes. Regular monitoring of your iron levels can help determine the effectiveness of your supplementation.
Regular Blood Tests to Monitor Iron Levels
Consulting with your healthcare provider and undergoing regular blood tests is crucial in monitoring your iron levels. These tests can provide valuable information about your iron stores and help guide any necessary adjustments to your supplementation.
When to Consult a Doctor
If you have been consistently taking iron supplements and have not seen any improvement in your fatigue symptoms, it is important to consult with a healthcare professional. They can assess your individual situation and determine whether there may be other underlying causes or factors contributing to your fatigue.
Combining Iron Supplements with Lifestyle Changes
Taking iron supplements alone may not be enough to combat fatigue. Incorporating certain lifestyle changes can further enhance your energy levels.
Getting Enough Rest and Sleep
Adequate rest and quality sleep are essential for overcoming fatigue. Aim for at least 7 to 9 hours of sleep per night and establish a consistent sleep schedule. Creating a relaxing bedtime routine can also help promote better sleep.
Regular Exercise for Energy
Physical activity is known to boost energy levels and reduce fatigue. Engaging in regular exercise, such as brisk walking, cycling, or strength training, can help improve your overall energy levels and combat fatigue. Start with activities that you enjoy and gradually increase your intensity and duration.
Stress Management Techniques
Chronic stress can contribute to fatigue and drain your energy levels. Implementing stress management techniques, such as deep breathing exercises, meditation, yoga, or engaging in hobbies that you find relaxing, can help reduce stress and increase your overall energy levels.
By understanding the causes of female fatigue, the importance of iron for women’s health, the different types of iron supplements, and how to choose the right one, you can effectively combat fatigue. Monitoring your iron levels, seeking medical advice when needed, and incorporating lifestyle changes can further enhance your energy levels and improve your overall quality of life. With the right knowledge and approach, you can say goodbye to fatigue and embrace a healthier, more energetic you.
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search
844.934.CARE
• Show
Health Library Explorer
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-Z Listings Contact Us
How Much Do You Know About Genital Herpes?
Genital herpes is a common sexually transmitted infection (STI) in the U.S. An STI is also called a sexually transmitted disease (STD). About 1 in 6 teens and adults has genital herpes, according to the CDC. Find out more about genital herpes by taking this quiz, based on information from the CDC.
1. How many types of herpes simplex virus are there?
2. Besides the genital area and the mouth, where else can HSV sores occasionally appear?
3. How is the virus passed from person to person?
4. Early symptoms of genital herpes include which of the following?
5. When HSV is not active in the body, what happens to it?
6. How often does an outbreak of lesions occur?
7. What should a pregnant woman with HSV do to avoid passing the virus on to her baby?
8. How is genital herpes diagnosed?
9. How is genital herpes treated?
10. What should an infected person do during an outbreak?
Online Medical Reviewer: Watson, L Renee, MSN, RN
Online Medical Reviewer: Zingman, Barry S, MD
Date Last Reviewed: 5/1/2019
© 2000-2020 The StayWell Company, LLC. 800 Township Line Road, Yardley, PA 19067. All rights reserved. This information is not intended as a substitute for professional medical care. Always follow your healthcare professional's instructions.
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|
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Account How-To Guides
Online Learning FAQ
What is the Nurse Certificate Course? Who can take it?
The Nurse Certificate Course in Reproductive Endocrinology and Infertility is a 16-module series designed for registered nurses and nurse practitioners who meet the following criteria: hold a current, active nursing license in a state or territory of the United States or the professional, legally recognized equivalent in another country, and have a minimum of 2000 hours of experience as a registered professional nurse and a minimum of 1000 hours in women's health.
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Mom and baby always together. What does exercising with a stroller look like?
Author:
Publication date:
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Mom and baby always together. What does exercising with a stroller look like?
How to effectively get rid of excess pounds that we have left after pregnancy? With help comes training with a stroller. You can successfully perform it both during a walk with a child, as well as at home. What are the characteristics of this type of exercise?
Stroller training – what is it?
Stroller exercises are known as strollercize. Elizabeth Trindale is considered to be the creator of this original fitness discipline, who is a former ballerina, and now – a personal trainer and fitness club owner. Once she decided to enter the training room and do some exercises with a wheelchair. With their help, she was able to return to her pre-pregnancy figure in a short time. The term strollercize was first used by her husband and exercise partner.
When is the best time to start exercising with a stroller? This type of workout can be done without any worries already about 6-8 weeks after delivery. Note: In the case of a cesarean section, the postpartum period may extend up to 12 weeks.
The biggest advantages of strollercize
Freshly mom performing this type of exercise does not have to part with her child for the duration of the training. The presence of the toddler is essential here in order to be able to properly perform the various sequences of movements. It is also a great way to meet new women and create a support group. Strollercize also develops healthy habits in children, making them aware that sports are healthy. This type of training is usually performed outdoors, which translates into oxygenation of the body.
What is worth remembering during strollercize? An extremely important issue is the proper technique of performing particular exercises. Only then you can protect yourself from painful injuries. A significant part of the training takes place on the spot. If the baby is crying or too mobile, the mother can stop the training at any point and take care of the baby. A huge advantage of exercising with a child is that the toddler is not bored during the exercises. At all times he can observe the mother and the environment.
Main principles of strollercize
What is worth remembering when you want to start your adventure with strollercize? Exercises of this type can be performed with the help of any stroller. Its price, model or brand do not matter here. Such training can be performed by people of all ages. What is important, both women and men can participate in classes. Strollercize is best practiced in comfortable athletic shoes and clothes that fit the weather outside the window.
What are the most important rules of stroller training? They can be started only if the gynecologist has given permission. Performed exercises do not directly involve the abdominal muscles, and therefore are completely safe for newly mothers. During the first weeks, the exercises are performed without any load. The optimal frequency of such training is 3 times a week. On the other days a quick walk with a stroller is enough. When the baby holds its head straight, you can easily transfer it from the stroller to the sling. If you want to start training with a stroller, you should buy a special model.
Examples of exercises with a stroller
It is worth realizing that strollercize is a workout that involves all the muscles of our body. It starts with a warm-up, which is followed by specific training. The culmination of the class are stretching and relaxation exercises.
How can I strengthen my back, buttocks, and thighs using the wheelchair? To do this, hold the wheelchair with both hands and put your weight on it. Bend the knees and point one leg back. Hold it for a few seconds, change the leg, and do several repetitions. Wanting to stretch the muscles of the spine, chest and abdomen, we grab the handle of the wheelchair, spread our legs to the width of our hips and perform a squat, moving it away from us.
Featured photo: Ed Yourdon / Flickr
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Must Know Why Neurologist Is Very Important
There are lots of problems in our lives which must be sorted out immediately. Talking about the problems in our brain and spinal cord can easily increase other problems in our lives and make our lives hell, thus, it would be good to consult with the expert in the same domain to help us in a better way.
Getting in touch with a professional neurologist can help us in the best possible manner by rectifying the disorders of the nervous system and start up the treatment accordingly. There are lot of cases we have which can influence us to go with the same professional and we should know what they are. Before we talk on the different reasons, you should know that this is the only professional who is very responsible and play up the most important role in treating brain injury or other problems which are affecting people a lot. Injury in brain is not at all a small concern; even this problem can be increased a lot and affect a person very badly.
Apart from this, if at any point of time you find problems with your brain or spinal cord, better go up with the experienced neurologist so that they can manage and treat neurological conditions, or problems immediately before it’s too late. Must visit to the neurologist if you are facing problems like-
Mental disability
Are you feeling very stress and mental disability? Or in your family you are feeling that a person is behaving very odd or abnormally? Well, you should never wait at all for anything and take that person to the experts. As these experts are generally associated with the learning and studying the concept and methodologies of brain, however, they know completely how to assess and treat your brain. There can be various layers of abnormality, however you must need to act smart and just go with the best experts.
Infection of the nervous system
This kind of problem is very risky and need to be sorted out as soon as possible. Infection of the nervous system can lead other various problems and this will make you feel so annoying and give you a lot of stress. A person will start behaving abnormally and this way brain mapping and analysis by the professional is very important. Apart from this, one must need to act so fast so that infection can be removed immediately.
Spinal cord disorder
In this sort of issue, inflammatory and autoimmune disorder can occur and affect a person very much. To avoid the problem, again we would need to take the help of the neurology just to find the causes of the same.
Apart from this, there are lot of problems, like- headache or migraines, stroke, multiple sclerosis and other lots of issues with the brain and spinal cord which need professional help and support. Make sure to hire talented professional as working with the brain is not so easier and we should definitely need to act very carefully without disturbing the patient.
Contact
Australia Biz
1226 5th Ave, NewYork, 10018, USA
NewYork
10018
646 789 4442
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5eff3d1f6f98e57329caed0ceb9053d3
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Shop 5/453 Fullarton Road,
Highgate Adelaide,
SA 5063
Monday - Thursday: 7am - 7pm
Friday: 7am - 5:30pm
Saturday: 8am - 1pm
FAQs
How long is a Physiotherapy consultation?
Initial consultations are 60 minutes and subsequent consultations are 30 minutes long, providing us with the time to discuss goals, perform a thorough assessment, treat and give you the advice/education necessary to get the best outcome possible.
What should I bring to my appointment?
• Please wear comfortable, loose fitting clothing. You may be asked to remove items of clothing depending on the treatment area.
• Relevant scans or reports from other health professionals. This won’t affect the way we assess or treat you, but will ensure we have all the information to get you where you need to be.
• Private health card where applicable
• Any relevant WorkCover or Motor Accident Commission documents or claim numbers.
How often will I need to come for treatment?
Treatment frequency depends on a number of factors including how acute and severe your symptoms are, your situation and lifestyle requirements, your needs and goals and your Physiotherapists recommendation.
Clinically, we find we get the best results in the best time by catching up frequently in the early stage of your treatment before spacing your appointments out further as your condition improves. For example, we prefer to see a client four times in 2 weeks rather than 4 times in 4 weeks because it allows us to make change quicker, build momentum, and provide you with all the necessary information in a short time frame to get you on the right track early. It also allows us to tweak things, progress or regress things and gauge the effectiveness of our interventions at more regular intervals.
Our recommendations for treatment frequency are all based on our clinical experience and healing times for certain conditions to allow you to get back to your physical best in the shortest time frame possible. As a ballpark, 10-12 sessions is usually enough to achieve a great outcome.
Can you fix [insert condition or problem]?
The answer is we can treat everything! The Thrive Physio Plus team has collectively seen thousands of clients and have experience with a multitude of injuries and conditions. If we feel like your condition is something we are unable to help you with, we’ll be sure to refer you to someone we think can.
If you have anything extremely unusual or unheard of, or have any questions you want answered about a specific condition or injury before coming to your first consultation, feel free to contact us and we’ll connect you with the appropriate Physiotherapist who can answer your questions for you.
Do I need a referral for Physio?
No. Physiotherapists are primary care practitioners. If you wish to attend via a Medicare Care Plan however, you will need to see a GP prior to your first visit. If you’re not familiar with this regime, give us a call at the clinic to discuss.
What do your exercise sessions involve?
All our exercise sessions are run by Physiotherapists highly trained in the area of exercise prescription.
For more information, hit the link below:
Physio-Supervised Exercise Classes
How are your exercise sessions different than going to a gym?
Think of it like a 1:1 treatment, with exercise! As all sessions are run by Physiotherapists:
• We understand the human body.
• We undertake a thorough assessment.
• We have an extensive knowledge of musculoskeletal conditions
• We know what your body needs and what it doesn’t need.
• We know what your condition or ability will and won’t allow you to do.
• We know where to strengthen or improve mobility for you and how to do it.
• We know how to do this safely.
Why should I exercise? I have a physical job isn't that enough?
People who exercise regularly experience less pain. Plain and simple! The World Health Organisation guidelines for physical activity state that muscle-strengthening activities should be done involving major muscle groups on 2 or more days a week. Additionally, research now shows that people who undertake strength work twice per week get on average a 23% reduction in all causes of death and a 31% reduction in cancer mortality.
People who exercise also:
• Have lower rates of depression
• Are more likely to live longer with better quality of life into their older years
• Are likely to have less risk of a hip or vertebral fracture
• Exhibit a higher level of cardiorespiratory and muscular fitness
• Are more likely to achieve weight maintenance, have a healthier body mass and composition.
The research also shows that exercise done indirectly, such as that completed by people in ‘physical occupations’ does not have the same benefits as deliberate exercise. Sorry, work doesn’t cut it!
What happens if I miss my appointment?
To ensure everyone has the opportunity to be seen when needed, we expect that in the case you are unable to attend a scheduled appointment, you call the practice and notify us as soon as possible.
If notice of less than twenty four (24) hours is given prior to the appointment, a cancellation fee equivalent to the full fee of the consultation/gym class will be charged.
Do you treat children?
Absolutely we do!
We do ask however that all children under the age of 16 are accompanied by an adult for the duration of the treatment session.
Is Physiotherapy painful?
Ultimately, you are in control. When hands on treatment techniques are being applied, your therapist will be sure to check in regularly to make sure things are comfortable. If at any point in time you’re feeling uncomfortable, just let your Physiotherapist know and they can adjust the pressure.
Most clients can feel some discomfort at points throughout their hands-on treatment, but refer to it as “good pain” that assists in providing immediate relief from your aches and pains
How do I choose a therapist that's right for me?
All of our Physiotherapists have undertaken extensive training beyond their university study in order to successfully decipher and yield great outcomes for the issues our clients bring us everyday. We are an extremely close knit team that learn from each other everyday. There’ll be differences in techniques and nuances of treatment, sure, but the great outcome at the end will be the same. To summarise, feel confident booking a session with anyone on our team – choose a Physiotherapist based on the time that’s convenient for you and their areas of expertise.
How can Thrive Physio Plus help me if I'm not in pain?
As Physiotherapists, we can do our best work when someone’s not in pain!
Think building resiliency, maximising potential, maximising longevity and future proofing your body. Why just exist when we can reach our physical best and thrive?
Be proactive, not reactive. Our bodies are in large part, under-utilised and underwhelmed in how they’re used in day to day life. With little strength, mobility and movement given to us during the working week, and sporadic activity thrown throughout – injuries are easily encountered.
Through consistent and targeted strength and mobility, you can build the strong, robust body you deserve and address aches and pains before they occur. We’re experts in doing this and help thousands annually to reach their physical best, remain injury free and live the life they strive for.
How long will my health fund cover last?
Every health fund policy is different depending on the fund and your level of cover. Unfortunately, as a service provider, we do not have access to that information and you’ll need to get in touch with your health fund.
Can you tell me when I'm going to run out of health-fund cover?
Unfortunately, as a service provider, we do not have access to that information. The only information we have access to is how much is being covered for the consultation that we process on the day.
Make an Appointment
Join the hundreds of people who’ve made the journey from painful to pain free today
Book Now
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JBBJournal of Biomedicine and Biotechnology1110-72511110-7243Hindawi Publishing Corporation16320310.1155/2010/163203163203Research ArticleThe Masticatory Contractile Load Induced Expression and Activation of Akt1/PKBα in Muscle Fibers at the Myotendinous Junction within Muscle-Tendon-Bone UnitKorkmazYüksel1KlinzFranz J.2MoghbeliMehrnoush3AddicksKlaus2Raab Wolfgang H.-M.1BlochWilhelm3BenianGuy M.1Department of Operative Dentistry, Periodontics and EndodonticsHeinrich-Heine-University40225 DüsseldorfGermanyuni-duesseldorf.de2Department I of AnatomyUniversity of Cologne50931 CologneGermanyuni-koeln.de3Department of Molecular and Cellular Sports MedicineGerman Sports University50933 CologneGermanydshs-koeln.de201018042010201002112009040320102010Copyright © 2010This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
The cell specific detection of enzyme activation in response to the physiological contractile load within muscle-tendon-bone unit is essential for understanding of the mechanical forces transmission from muscle cells via tendon to the bone. The hypothesis that the physiological mechanical loading regulates activation of Akt1/PKBα at Thr308 and at Ser473 in muscle fibers within muscle-tendon-bone unit was tested using quantitative immunohistochemistry, confocal double fluorescence analysis, and immunoblot analysis. In comparison to the staining intensities in peripheral regions of the muscle fibers, Akt1/PKBα was detected with a higher staining intensity in muscle fibers at the myotendinous junction (MTJ) areas. In muscle fibers at the MTJ areas, Akt1/PKBα is dually phosphorylated at Thr308 and Ser473. The immunohistochemical results were confirmed by immunoblot analysis. We conclude that contractile load generated by masticatory muscles induces local domain-dependent expression of Akt1/PKBα as well as activation by dually phosphorylation at Thr308 and Ser473 in muscle fibers at the MTJ areas within muscle-tendon-bone unit.
1. Introduction
The muscle-tendon-bone unit contains myocytes, fibroblasts, nerve fibers, blood vessels, osteoblasts, osteoclasts, osteocytes, and extracellular matrix. The integrity of the muscle-tendon-bone unit is maintained through cell-cell and cell-extracellular matrix interactions. Tendons transmit forces generated from muscle cells at the muscle-tendon-junction (MTJ) to bone cells. During a signal transmission in cells of the muscle-tendon-bone unit, extracellular matrix, cell membrane, cytoskeleton, nuclear protein matrix, and gene expression are altered by mechanical loading in muscle cells and transmitted further to cells of the tendon-bone unit in autocrine as well as paracrine manner [1].
The serine/threonine protein kinase B (Akt/PKB) is a downstream effector of phosphatidylinositol 3-kinase (PI3K) and a regulator of a variety of cellular processes, including transcription, survival, proliferation, growth, and metabolism [2, 3]. In mammals, Akt/PKB is expressed ubiquitously with three isoforms: Akt1/PKBα, Akt2/PKBβ, and Akt3/PKBγ [4]. The activation of PI3K through binding of a growth factor to a receptor tyrosine kinase [5, 6] converts the membrane-bound plasma membrane lipid phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) to phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3) [6, 7]. PI(3,4,5)P3 anchors Akt/PKB to the plasma membrane and induces a conformational change, which results in the phosphorylation of Akt/PKB. Phosphorylated amino acid residues include the threonine residue Thr308 in the kinase catalytic domain and the serine residue Ser473 in the hydrophobic motif of Akt1/PKBα [3]. Full activation of Akt1/PKBα requires phosphorylation of the enzyme at Thr308 and at Ser473 [8]. It is well established that Thr308 is phosphorylated by 3-phosphoinositide-dependent kinase-1 (PDK1) [9]. The phosphorylation of Akt1/PKBα at Ser473 is mediated by both mammalian target of rapamycin-rictor complex (mTORC2) [10] and DNA-dependent protein kinase (DNA-PK) [11] depending on type of stimulus.
The knowledge about bone remodelling by mechanical load generated from muscle cells to the bone cells requires understanding of the complete signal transmission between cells of the muscle-tendon-bone unit. However, in contrast to separate studies performed on muscle, tendon, or bone cells, there are no in vivo or in vitro studies about effects of the physiological forces generated by muscle cells and transmitted via tendon to the bone cells in model systems that contain muscle-tendon-bone unit cells.
The activation of Akt1/PKBα is involved in different functions of the muscle, tendon, and bone cells. Akt1/PKBα promotes muscle cell differentiation [12, 13] and induces muscle hypertrophy [1416]. In tendon cells, IGF-I-dependent activation of Akt1/PKBα prevents apoptosis [17]. The cellular mechanism of the physiological mechanotransduction transmission that regulates Akt1/PKBα in different cell types of the muscle-tendon-bone unit is unknown. Therefore, the physiological stimuli including mastication contractile-dependent regulation of Akt1/PKBα in different types of cells within muscle-tendon-bone unit remain to be established. In sections of maxilla that contain cells of the muscle-tendon-bone unit, the expression, localization, and phosphorylation of Akt1/PKBα were investigated by quantitative immunohistochemistry using total and phospho-specific Akt1/PKBα Thr308 and Ser473 antibodies. To test the expression of Akt1/PKBα and p-Akt1/PKBα Ser473 in muscle cells at the periphery and at the myotendinous junction (MTJ) areas, immunoblot experiments were performed.
2. Materials and Methods2.1. Reagents and Antibodies
Bovine serum albumin (BSA) was purchased from Sigma (Sigma, St. Louis, MO). Biotinylated goat antirabbit IgG, biotinylated antimouse IgG, normal goat serum (NGS), and Vectastain-ABC Kit were obtained from Vector Laboratories (Burlingame, CA, USA). Rabbit anti-Akt1/PKBα and rabbit antiphospho-Akt1/PKBα (Thr308) polyclonal antibodies were purchased from Upstate Biotechnology (Lake Placid, NY, USA). Mouse antiphospho-Akt1/PKBα (Ser473) monoclonal antibody was obtained from Cell Signaling Technology (Beverly, MA, USA). Cy3-conjugated goat antirabbit IgG was from Jackson ImmunoResearch Labs. (West Grove, PA). DyLight 488-conjugated NeutrAvidin (Pierce Biotechnology, Rockford, IL) was ligand for biotinylated antimouse IgG. DRAQ5 (Axorra, San Diego, CA) was used as a fluorescent DNA stain.
It is known that the antibody specificity is best determined by immunoblot techniques [18]. The specificities of Akt1/PKBα, p-Akt1/PKBα at Thr308 and at Ser473 were determined by immunoblot analysis [19].
2.2. Tissue Preparation
Male Wistar rats (n = 12; 3 months old, weighing 280–300 g) were fixed by transcardiac perfusion with 4% paraformaldehyde and 0.2% picric acid pH 7.4, under deep anesthesia with a mixture of Ketamine (100 mg/kg) and Xylazine (5 mg/kg). The jaws were dissected with masticatory muscle using forceps and the samples demineralized in 4 N formic acid at 4°C for 14 days.
For immunoblot experiments, after sacrifice of animals (n = 3) by exposure to a rising concentration of CO2 inhalation, the masticatory muscle tissues were immediately cut into two areas as peripheral area and muscle near at the MTJ area by aid of an operating microscope.
Animal handling procedures were carried out in compliance with guidelines of the local animal ethics committee.
2.3. Immunohistochemistry
In the free floating sections, endogenous peroxidases were inhibited with 0.3% H2O2. To block nonspecific bindings, sections were treated with 1% BSA + 10% NGS. Thereafter, sections were incubated for 48 hours at 4°C with anti-Akt1/PKBα, anti-p-Akt1/PKBα Thr308, and anti-p-Akt1/PKBα Ser473 at 1 : 800 for each antibody. Then the sections were incubated with biotin-conjugated goat antirabbit IgG (1 : 500) and biotinylated antimouse IgG (1 : 500). The sections were incubated with avidin-biotin-peroxidase complex (1 : 100) for 1 hour and the immunohistochemical reaction was visualized with 0.05% 3,3-diaminobenzidine tetrahydrochloride (Sigma, St. Louis, MO, USA) in 0.05 M Tris-HCl buffer, pH 7.6 containing 0.01% H2O2 and 0.01% nickel ammonium sulphate. Control experiments were performed by omission of the primary or secondary antibodies from incubations as well as by immunoblot analysis.
2.4. Double-Immunofluorescence Labelling and Confocal Microscopy
The free floating sections were incubated with mouse anti-p-Akt1/PKBα Ser473 (1 : 800) for 24 hours at 4°C. The sections were incubated with biotinylated goat antimouse IgG (1 : 1000) and with the DyLight 488-conjugated NeutrAvidin (1 : 200) for 1 hour at RT, respectively. Then, the sections were incubated with p-Akt/PKB Thr308 for 24 hours at 4°C. The sections were incubated with Cy3-conjugated goat antirabbit IgG (1 : 1000) for 1 hour at RT in the dark. Staining of nuclear DNA staining was done using DRAQ5 (1 : 2000) as described earlier [20]. Control experiments were performed in separate incubations by omission of the primary or secondary antibodies. Images of double immunofluorescence experiments were acquired on an LSM510 confocal microscope (Zeiss, Oberkochem, Germany).
2.5. Immunoblot
The tissues were homogenized in a buffer containing proteinase and phosphatase inhibitors. Protein concentrations were determined by the method of Bradford. Protein samples were separated on an SDS-PAGE gradient gel and transferred to PVDF filters. The blots were blocked with 5% dry milk for 1 hour and incubated with Akt1/PKBα (1 : 1000) and with p-Akt1/PKBα Ser473 (1 : 1000) antibodies overnight at 4°C. The blots were incubated with HRP-conjugated secondary antibody (1 : 5000) for 1 hour at RT and subsequently developed with enhanced chemiluminescence assay for 1 minute.
2.6. Densitometry of the Immunohistochemical and Immunoblot Results
The immunostained sections were captured with a CCD camera and the staining intensities of the antibodies in muscle cells were measured in a blinded fashion. In immunoblot, the films were scanned, and the density of the specific immunoreactive bands was measured and normalized with an internal loading β-actin control.
2.7. Statistical Analysis
Data are represented as mean ± SD. Differences between groups were compared using Student’s t-test or one-way ANOVA with Bonferroni post-hoc test used to compare multiple means. The criterion for statistical significance was considered at a P value <.05.
3. Results3.1. Localization of Akt1/PKB<inline-formula><mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M45"><mml:mrow><mml:mi>α</mml:mi></mml:mrow></mml:math></inline-formula> in Cells of the Muscle-Tendon-Bone Unit
Total (t) Akt1/PKBα (nonphosphorylated and phosphorylated) was detected in a moderate staining in the peripheral part of muscle fibers (Figures 1(a) and 1(b)). In comparison to the staining intensities in peripheral areas (Figures 1(a) and 1(g)), there was an increase in total Akt1/PKBα staining at the area near to the myotendinous junction (MTJ) in the muscle fibers (Figures 1(a), 1(b), and 1(g)). Immunohistochemical control incubations without primary or secondary antibodies resulted in the disappearance of the specific reaction product (data not shown).
The constitutive localization of the t-Akt1/PKBα, phosphorylation of t-Akt1/PKBα at Thr308 and at Ser473 in muscle fibers within muscle-tendon-bone unit. In comparison to the staining of t-Akt1/PKBα (a, b), p-Akt1/PKBα Thr308 (c, d) and Ser473 (e, f) in the peripheral muscle fibers, t-Akt1/PKBα (b, MTJ), phosphorylation of Akt1/PKBα at Thr308 (d, MTJ) and at Ser473 (f, MTJ) were detected with higher staining intensities in muscle fibers at the myotendinous junction (MTJ) area. The staining intensity of Akt1/PKBα in peripheral muscle fibers (b, 602.70 ± 117.05) was weakly compared to those in the area near to the MTJ (b, 1050.63 ± 91.68). In comparison to the staining intensity of the p-Akt1/PKBα Thr308 in peripheral muscle fibers (d, 319.76 ± 74.57), the staining intensity of p-Akt1/PKBα Thr308 was higher in muscle fibers near to the MTJ areas (d, 1138.85 ± 98.99). The staining intensity of p-Akt1/PKBα Ser473 in muscle fibers at the MTJ areas (f, 351.65 ± 104.63) was greater than staining intensity of Ser473 in peripheral muscle areas (f, 1099.70 ± 135.93). Data are mean ± SD; n = 6; significant differences were considered at a P value <.05. MTJ = myotendinous junction, pM = peripheral muscle fibers, ab = alveolar bone, pdl = periodontal ligament, p = pulpa, d = dentin. Bars: 640 μm for (a), (c), (e), 80 μm for (b), (d), and (f).
3.2. Localization of p-Akt1/PKB<inline-formula><mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M70"><mml:mrow><mml:mi>α</mml:mi></mml:mrow></mml:math></inline-formula> Thr308 and Ser473 in Muscle Fibers Near the Muscle-Tendon-Bone Unit
In comparison to the very weak staining intensities of p-Akt1/PKBα Thr308 in the periphery of muscle fibers (Figures 1(c), 1(d), and 1(g)) within muscle-tendon-bone unit, phosphorylation at Thr308 was detected with a higher staining intensity in muscle fibers near to the MTJ areas (Figures 1(c), 1(d), and 1(g)). In the periphery of muscle fibers, the staining intensity of the p-Akt1/PKBα Ser473 residue was very weakly (Figures 1(e), 1(f), and 1(g)). Phosphorylation at Ser473 was detected with a higher staining intensity nearby the MTJ (Figures 1(e), 1(f), and 1(g)). In all instances, the peripheral parts of the muscle fibers were very weakly positive or almost negative for p-Akt1/PKBα Thr308 (Figures 1(c) and 1(d)) as well Ser473 (Figures 1(e) and 1(f)). The immunohistochemical controls resulted in the disappearance of the signal product (data not shown). The specificity of antibodies against Akt1/PKBα, Akt1/PKBα phosphorylated at Thr308 and Ser473 was confirmed by immunoblot analysis [19].
3.3. Immunohistochemical Colocalization of p-Akt1/PKB<inline-formula><mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M76"><mml:mrow><mml:mi>α</mml:mi></mml:mrow></mml:math></inline-formula> Thr308 and Ser473 in Muscle Cells Nearby the MTJ
To determine whether mastication forces could stimulate full activation of Akt1/PKBα in muscle fibers, double immunofluorescence analyses of Akt1/PKBα phosphorylated at Ser473 and at Thr308 were performed.
The nuclei in cells of the muscle and tendon were visualized by staining of DNA with DRAQ5 (blue color; Figure 2(a)). Immunohistochemical localization of green reaction product for Akt phosphorylated at Ser473 was detected only in cross sectioned muscle cells at MTJ (Figure 2(b)). The cross sectioned muscle fibers revealed also a strong red staining for Akt1/PKBα phosphorylated at Thr308 (Figure 2(c)). In muscle fibers at the MTJ areas, the colocalization of p-Akt1/PKBα phosphorylated at Thr308 and at Ser473 was detected by yellow staining (Figure 2(d)). The immunohistochemical controls resulted in the disappearance of the specific immunofluorescence signal (data not shown).
Immunofluorescence colocalization of Akt1/PKBα phosphorylated at Ser473 and at Thr308 in muscle fibers at the myotendinous areas. The nuclei in muscle fibers and tendocyte were visualized by staining of DNA with DRAQ5 (a, blue). The p-Akt1/PKBα Ser473 (b, green) was localized in across sectioned muscle fibers at the MTJ. In muscle fibers at the MTJ, p-Akt1/PKBα Thr308 (c, red) was identified. In same muscle fibers, p-Akt1/PKBα Ser473 and Thr308 were colocalized (d, yellow). The tendon cells were negative for localizations of Ser473 as well as of Thr308. MTJ = myotendinous junction, t = tendon. Bar: (a)–(d) = 20 μm.
3.4. Immunoblot Analysis
Results demonstrating higher immunohistochemical staining intensities of t-Akt1/PKBα (Figures 1(a), 1(b), and 1(g)) and p-Akt1/PKBα Ser473 in muscle fibers nearby the MTJ areas were confirmed by immunoblot analysis. Immunoblot results for Akt1/PKBα are presented in Figure 3 and for p-Akt1/PKBα Ser473 in Figure 4.
Immunoblot analysis of Akt/PKB in peripheral muscle fibers and in muscle cells near to the myotendinous areas. In peripheral masticatory muscle fibers and masticatory muscle fibers at MTJ, protein extracts were analyzed by immunoblot analysis using an antibody against Akt1/PKBα. The specific immunoblot bands of approximately 60 kDa identify Akt1/PKBα in peripheral muscle fibers and in muscle fibers near to the MTJ. The level of Akt1/PKBα in muscle fibers near to the MTJ was higher than that in peripheral muscle fibers.
Immunoblot analysis of p-Akt1/PKBα Ser473 in peripheral muscle fibers and in muscle fibers near to the myotendinous areas. Protein extracts prepared from peripheral masticatory muscle fibers and masticatory muscle fibers at MTJ were analyzed by immunoblotting using an antibody against Akt1/PKBα phosphorylated at Ser473. The weakly phosphorylation of Akt1/PKBα at Ser473 in peripheral muscle fibers is significantly increased in muscle fibers near to the MTJ. A characteristic band almost at 60 kDa for p-Akt1/PKBα Ser473 was detectable with a higher staining intensity in muscle fibers near to the MTJ.
In comparison to the staining intensity in periphery of muscle fibers, t-Akt1/PKBα was detected as a band of approximately 60 kDa with higher staining intensity in muscle cells nearby MTJ areas (Figure 3). The staining intensity of the p-Akt1/PKBα Ser473 residue was very weak at the peripheral part of muscle, while a characteristic band of approximately at 60 kDa for p-Akt1/PKBα Ser473 was detected with a strong staining intensity at the area nearby MTJ (Figure 4). As a loading control muscle lysates were analyzed by immunoblot with an antibody against β-actin (data not shown).
4. Discussion
Under cell culture conditions, the importance of physical stresses on a variety of cellular activities has been examined only in a single cell type, including myocytes, fibroblasts, osteoblasts, and osteoclasts. Similarly, the mechanical loads on muscle fibers, tendon, and bone cells within the muscle-tendon unit were separately investigated. In comparison to studies only in muscle, tendon, or in bone cells, we performed a quantitative immunohistochemical analysis in sections, which allows localization of the functional Akt1/PKBα protein in all cells within the muscle-tendon-bone unit. In this model, muscle contractile activity should be generated by physiological mastication. Compared to the periphery of the muscle fibers within muscle-tendon-bone unit, the protein level of the Akt1/PKBα and the phosphorylation of Akt1/PKBα at Thr308 and Ser473 were significantly higher at the MTJ area.
Tendon cells connect muscle fibers to bones and transmit forces developed by muscle fibers to the bone cells. Thus, muscle fibers apply forces to the bone cells via tendon cells, which arise from a specialized region called the MTJ. In the MTJ, myofibrils and collagen fibers overlap, forming longitudinal infoldings [21, 22]. In comparison to end-to-end contact, these overlapping contacts between muscle cells and collagen fibers increase the strength of the junction because cell membranes support shear loads better than the tensile loads [21, 22]. In muscle fiber region nearby MTJ, the physiological mastication stimuli may induce expression of Akt1/PKBα by nuclear domain regulation as well as by phosphorylation of the enzyme at Thr308 and at Ser473.
In response to physiological masticatory mechanical loading, Akt1/PKBα was detected in higher protein levels in muscle fibers nearby MTJ areas. The higher staining intensity of the t-Akt1/PKBα at MTJ may be explained by local regulation of Akt1/PKBα in different nuclear domains during transmission of forces generated by physiological mastication stimuli in muscle cells. In multinucleated muscle fibres, it was reported that each nucleus is able to regulate protein biosynthesis in a local domain-dependent manner [23, 24]. It can be speculated that the higher number of nuclear domains present in muscle fibers nearby MTJ [25] responds to mechanical stimulation of mastication by higher production of Akt1/PKBα than nuclear domains in peripheral muscle areas.
In the consecutive muscle-tendon-bone unit sections, Thr308 and Ser473 phosphorylation sites of Akt1/PKBα were detected with a higher staining intensity in muscle fibers at MTJ area compared to the peripheral muscle fiber areas. Therefore, we have presumed that Akt1/PKBα may be dually phosphorylated in muscle fibers at MTJ areas. Full activation of Akt1/PKBα requires dually phosphorylation of the enzyme at Thr308 and at Ser473 [26, 27]. More recently, knockout experiments in murine embryonic fibroblast came to the conclusion that Akt/PKB monophosphorylated at Thr308 was able to activate several downstream targets [8]. In muscle cells at the MTJ areas, we have detected a colocalization of Thr308 and at Ser473. Our data indicate that full activation of Akt1/PKBα by phosphorylation at Thr308 and Ser473 is necessary for downstream signal transduction in muscle cells at the MTJ areas.
For skeletal muscle cells, it was shown by in vitro [28] and in vivo experiments [16, 29, 30] that constitutive activation of Akt1/PKBα induces hypertrophy. This effect of Akt1/PKBα in skeletal muscle is also supported by the finding that Akt1/PKBα inhibits atrophy in vitro as well as in vivo [31, 32]. In addition, mice lacking Akt1/PKBα show a decrease in muscle size compared with wild-type [15, 33]. Under consideration of these data, it is apparently that physiological constitutive phosphorylation of Akt1/PKBα in skeletal masticatory muscle cells at the MTJ areas may be involved in the muscle cell hypertrophy and muscle cell survival.
The skeletal muscle fibers are classified in type I (slow-twitch oxidative) and in type II (fast-twitch glycolytic) fibers [33]. Fast-twitch fibers are further subdivided into two general groups, the fast-twitch oxidative type IIA and fast-twitch glycolytic type IIB fibers [33]. Masticatory muscles are composed of a heterogeneous population of fiber types that vary according to their contractile properties [34, 35]. In the masseter, it was described that the type I fibers were absent [36]. The IIA and IIB fibers were distributed differently between the superior and inferior regions of the masseter [3436]. In the deep masseter, the highest proportion of type IIB fibers is distributed [36]. The cross-sectional areas of type IIB fibers were the largest, followed by the type IIX and IIA fibers [36]. From our results, it may be suggested that physiological exercise represents a mechanism by which mastication in vivo induces simultaneous phosphorylation of Akt1/PKB at Ser473 and Thr308 in both fast-twitch muscle fiber types at the MTJ.
It was described that the muscle fiber type is regulated by calcineurin and the Ras-MAPK signaling, while fiber size is regulated by the PI3K-Akt/PKB-mTOR signaling [30, 37, 38]. The mTOR has been implicated in skeletal muscle hypertrophy during overload, and pharmacological inhibition of mTOR prevents overload-induced hypertrophy in both type I and type II of muscle fibers [29]. These results indicate that the hypertrophic effect on muscle fibers by Akt1/PKBα predominantly occurs through mTOR signaling [30]. Phosphorylation of Akt1/PKBα at Ser473 is mediated by mTORC2 [10]. Therefore, phosphorylation of Akt1/PKBα at Ser473 in muscle fibers at MTJ may be an important part of the mechanism by which contraction can activate Akt1/PKBα at Ser473 in fast-twitch muscles inducing masticatory muscle hypertrophy at the MTJ areas. However, it must be investigated in further studies if there is a different hypertrophy response in a single muscle fibers in masticatory muscle.
The present finding expands the current knowledge about load dependent muscle response. Beside the fact that contraction may regulate Akt1/PKBα in an intensity-, time-, and fiber type-specific manner [39, 40], it can be suggested that the response to a mechanical stimuli is inhomogeneous along a single muscle fiber at the activation and expression level. It is known that the loss of teeth and absent physiological masticatory contractile activities lead to a dramatic decrease in muscle cell masses and results especially in a strong atrophy of the alveolar bone [41]. Furthermore, it leads to an alteration of force transmission in the masticatory process [41]. Under consideration that mastication forces and mechanical loading of muscle cells are required for tissue integrity and extracellular matrix metabolism inducing phosphorylation of Akt1/PKBα in muscle cells located near to the MTJ within muscle-tendon-bone unit, it must be considered that the response is possibly not uniform along the fibres.
5. Conclusion
In the muscle-tendon-bone unit, tendons connect masticatory muscle cells to the alveolar bone and transmit masticatory forces generated by muscle cells to the alveolar bone cells. The transmission of this mechanical signal induces a full activation of Akt1/PKBα by simultaneous phosphorylation of the enzyme at Ser473 and at Thr308 in muscle fibers located near to the MTJ but not at the periphery of the muscle fibers. Therefore, we postulate that inhomogeneous physiological contractile load-dependent activation of the Akt1/PKBα phosphorylation at Thr308 and at Ser473 in masticatory muscle cells along the muscle fibers could play a role for the biological response, which can influence the development of muscle dystrophy.
Acknowledgment
This work contains part of the doctoral thesis of Mehrnoush Moghbeli.
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Melbourne Surgery
HOME About Us
SPECIALTIES General Surgery Dr LP Cheah Patient Feedback Plastic Surgery Neurosurgery Vascular Surgery Orthopaedics Urology Dental Surgery
PROBLEMS Gallstones Hernia Lipoma Sebaceous Cyst Ingrown Toenail Rectal Bleeding Abdominal Pain Bowel Cancer Breast cancer Skin Cancer Melanoma Dupuytren's contracture
OPERATIONS Excision of Skin Lesion Gastroscopy Colonoscopy Inguinal Hernia Repair Hernia Repair - Anterior abdominal wall Keyhole Gallbladder Surgery Pilonidal Sinus Excision Carpal Tunnel Release Vasectomy Thyroid Surgery Haemorrhoids Ganglion Excision
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HOSPITAL FORMS
Contact us
LIPOMA
This is a benign tumour of the fatty tissue under the skin and is very common. It can occur anywhere under the skin in the body. Typically one notices a lump under the skin. Often it is hard to define exactly where the lump ends as the lipoma is irregularly shaped.
Multiple lipomatosis (Decrum's disease) - some people develop multiple lipomas all over the body. There is a genetic predisposition for this.
Angiolipoma - this is usually a lipoma with a prominent vascular component. It is usually painful as well.
Atypical lipoma / well-differentiated liposarcoma - Any deep lipoma or lipoma >5cm should raise one's suspicion. Often occuring in the extemities. MRI findings include thickened/fibrous septa(>2mm) , associated non-fatty masses, prominent foci of high T2 signal, prominent areas of enhancement. Surgery is by wide local excision and long term follow-up is required.
Other variants:
Fibrolipoma
Chondroid lipoma - has cartilaginous elements as well
Osteolipoma - has bony elements within it
Lipoleiomyoma - has smooth muscle elements within it as well
Hibernoma - Lipoma arising from brown fat(morphogically similar to the fat of hibernating animals)(uncommon)
Surgery
Generally most lipomas under 5cm can be excised under local anaesthesia. Larger lipomas may require excision under general anaesthesia.
Local anaesthetic is used to provide analgesia, reduce the risk of bleeding and dissect a plane around the capsule of the lipoma.
An incision is made over the lipoma (I try to make that as short as possible and squeeze out the lipoma through the incision)
The lipoma often has arms extending outwards like a ginger(pseudopodia). It is important to excise all the pseudopodia of the lipoma to reduce the risk of recurrence.
The skin is closed with sutures.
Dressings should be kept on for a week.
Nondissolvable sutures are removed in 7-10 days. (in some situations, dissovable sutures can be used)
Risks of Surgery
1. Recurrence - the lipoma may come back in future
2. Wound problems - infection, breakdown, scarring
3. Scar, keloid formation
4. Pain, numbness, nerve damage(especially if the lipoma is close/attached to the nerve)
5. Bleeding - especially for large or intramuscular lipomas
6. Other risks - anaesthetic risks, fluid collection in space previously filled by lipoma(blood-stained fluid can be squeezed out from wound when lying on the wound)
Note: Mr LP Cheah is an expert in excising sebaceous cysts and lipomas. He sees a large number of such cases in his rooms. He also lectures on excision of sebaceous cysts and lipomas at the Minor Surgical Skills courses at the Royal Australasian College of Surgeons.
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Two Elements Individuals Do Definitely Not Understand With Regards To LASIK Eye Surgical Operation
The eye can be taken a look at with relative ease as to both its function and its structure. A practical evaluation consists of the ability to move in the orbit and the reaction of the pupil to light and lodging.
The function of the eye may be tested in several methods. The client may be asked to recognize illuminated letter or objects of differing sizes on exactly what is called the Snellen chart.
Conversely, the examination of the structural part of the eye might be made in a number of ways. Stress within the eyeball is determined by a "tonometer." In specific diseases, especially in glaucoma, the stress in the eyeball is increased noticeably.
Nevertheless, it ought to be well remembered that a patient with an eye issue may have other problems as well. Frequently other physical conditions are main and affect the eye as a effect. The appearance of the eye can signal the client and the physician to troubles in some disturbances of other parts of the body even prior to other signs provide themselves.
Consequently, one's dependence on sight is highlighted when one deals with a momentary or possible permanent loss of this crucial sense. When corrective steps are looked for, particular kinds of vision correction such as contact lenses or spectacles are recommended.
On the other hand, some individuals are bothered with the truth that they have some framed lenses or contact lenses in front of their eyes.
For this factor, advanced surgical operations were developed to motivate decreased utilization of contact lenses or glasses. Among which is the now popular LASIK eye surgical treatment.
Generally, LASIK eye surgical treatment is the short-term for "Laser-Assisted In Situ Keratomileusis." Like its concrete equivalent, LASIK eye surgical treatment is another form of vision correction. The only difference is that with this kind of surgical treatment, one's vision is fixed completely.
With LASIK eye surgery, the refractive errors in the cornea are completely changed. This can be done utilizing an "excimer laser."
The main purpose of this surgical treatment is to develop a threadlike, rounded "flap" in the cornea using a blade called "microkeratome." In a series of unfolding and laser processing, the cornea is lastly reformed, enabling better the eye to direct more light into the retina.
Appeal vs. Disadvantages
Amidst the growing appeal of LASIK eye surgery, there are still disadvantages that people need to understand. Probably, the primary reason that this type of eye surgical treatment has ended up being well accepted is since the majority of its cases had actually achieved success.
However, in spite of its success, there are still some drawbacks. Here is the list:
1. It is an operation applied to the most sensitive part of the eye
Since LASIK eye surgical treatment involves the operation of the retina, which is among the most sensitive portions of the eye, many people say that the operation can be really risky.
In other words, a easy mistake could practically trigger an individual's life time loss of sight. Hence, it is necessary to think about lots of factors before choosing whether LASIK eye surgical treatment is the best restorative measure one has to undergo.
2. It is not a best treatment
LASIK eye surgery might correct your vision but it does not necessarily indicate that it can offer you a best vision. Even if statistical reports show that 70% of the patients might have 20/20 vision, this does not always suggest they have ideal vision as well.
Provided all these things, it can be deduced that, in spite of the popularity of the operation, LASIK might not constantly be the ideal eye surgery the way the majority of people see it
Conversely, the evaluation of the structural part of the eye might be made in numerous ways. It ought to be well kept in mind that a client with an eye issue may have other issues. Often other this post physical conditions are primary and affect the eye as a consequence. The appearance of the eye can inform the doctor and the patient to problems in some disruptions of other parts of the body even prior to other symptoms present themselves.
Like its tangible counterpart, LASIK eye surgery is another type of vision correction.
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Knee Replacement in Young Patients
Knee Replacement in Young Patients | Bharath Orthopaedics
Table of Contents
knee replacement in young patients, knee replacement surgery is typically associated with older adults, but a growing number of young patients are undergoing this procedure to regain their mobility and quality of life. Knee issues can affect people of all ages, and for young adults facing debilitating knee problems, knee replacement surgery can be a life-changing solution. In this blog post, we will explore knee replacement for young patients, discussing its reasons, challenges, benefits, and what to expect during the recovery process.
Knee Replacement in Young Patients | Bharath Orthopaedics
Why young age arthritis is increasing?
The rising prevalence of arthritis in young individuals is attributed to factors like sedentary lifestyles, obesity, and increased sports-related injuries. Modern dietary habits and genetic factors also contribute. Sedentary behavior and excessive weight strain joints, while injuries may accelerate arthritis onset. These lifestyle shifts, coupled with genetic predispositions, collectively contribute to the increasing incidence of arthritis among the younger population.
Reasons for Knee Replacement in Young Patients
While knee replacement surgery is often associated with age-related wear and tear, young adults may require this procedure for various reasons:
1. Trauma and Injuries: Sports injuries, accidents, and trauma to the knee joint can result in severe damage that may require surgical intervention.
2. Genetic Factors: Some individuals may have a genetic predisposition to knee conditions such as osteoarthritis, leading to the need for a knee replacement at a younger age.
3. Rheumatoid Arthritis: Young adults with autoimmune conditions like rheumatoid arthritis may experience severe joint damage necessitating a knee replacement in young adults.
4. Congenital Conditions: Rare congenital conditions or developmental abnormalities can affect the knee joint’s structure and function, leading to early joint degeneration.
Challenges of Knee Replacement in Young Patients
Knee replacement surgery in young adults presents unique challenges:
1. Longevity of Implants: Young patients may outlive their artificial knee joint, and multiple replacements over a lifetime are a concern.
2. Activity Level: Young adults often have higher activity levels, which can put additional stress on the artificial joint, potentially leading to quicker wear and tear.
3. Future Revisions: The need for future revisions and additional surgeries can become a significant concern due to the patient’s longer life expectancy.
4. Expectations: Young patients may have higher expectations for their post-surgery quality of life and may need to manage these expectations realistically.
Knee Replacement in Patients: Benefits and Recovery
• Benefits of Knee Replacement in Young Patients: Knee replacement surgery in young adults offers numerous benefits, especially when considering the unique challenges faced by this demographic.
• Pain Relief: The foremost benefit is the effective relief of chronic knee pain. Young patients often experience pain due to various factors such as trauma, congenital joint issues, or autoimmune diseases. Knee replacement can significantly alleviate this pain, providing a new lease on life.
• Restored Mobility: Young adults aspire to maintain an active lifestyle. Knee replacement in young adults surgery can restore their mobility, enabling them to perform daily activities, participate in sports, and engage in recreational activities they enjoy.
• Preventing Further Damage: In cases of advanced osteoarthritis or rheumatoid arthritis, knee replacement can prevent further joint damage. By replacing the deteriorated joint with an artificial one, the surgery halts the progression of the disease, helping to preserve joint function.
• Improved Quality of Life: Ultimately, the goal of knee replacement in young patients is to enhance their overall quality of life. Pain-free, functional knees can lead to increased independence and a more fulfilling life.
• Recovery and Rehabilitation for Young Patients: Recovery from knee replacement surgery in young patients is a comprehensive process designed to address their specific needs.
• Hospital Stay: Typically, young patients may spend several days in the hospital after the surgery. During this time, they are closely monitored by the medical team to ensure a safe and smooth recovery.
• Physical Therapy: Rehabilitation is a critical component of the recovery process. Young patients work with physical therapists to rebuild strength, improve range of motion, and learn to walk with their new joint. Customized exercise programs are tailored to their age, fitness level, and goals.
• Pain Management: Post-operative pain and discomfort are managed through medication. The medical team prescribes pain relief medications to ensure that young patients remain comfortable as they progress through the rehabilitation process.
• Gradual Resumption of Activities: It’s important for young patients to gradually resume their activities. While they can expect a significant improvement in mobility, high-impact sports and activities that place excessive strain on the knee should be avoided. Consultation with the medical team regarding the timing of return to specific activities is crucial.
Risks of Knee Replacement Surgery
Knee replacement surgery, like any major procedure, carries potential risks. These include infection, blood clots, and anesthesia-related complications. There’s also a chance of implant issues, such as loosening or wear over time. Nerve or blood vessel damage and persistent pain are rare but possible. It’s crucial to discuss individual risks with the surgeon, considering factors like age, health, and overall condition before deciding on knee replacement.
Conclusion
Knee replacement for young patients is a viable solution for those facing debilitating knee issues. While the procedure presents its challenges, it offers significant benefits, including pain relief, restored mobility, and improved quality of life. With careful consideration, realistic expectations, and proper post-surgery care, young adults can experience a positive and active future after knee replacement in young patients.
Frequently Asked Questions
Yes, young patients can have knee replacement surgery if they have severe knee joint damage or pain due to conditions like osteoarthritis or injury. However, it’s typically considered a last resort when conservative treatments have failed. The choice to proceed depends on individual circumstances, health, and consultation with a specialist.
For young patients, knee replacement can provide pain relief, improve mobility, and enhance the quality of life. It can help them return to active lifestyles, regain their independence, and participate in activities they enjoy.
While the lifespan of an artificial knee varies, modern implants can last 15-20 years or more. Younger patients may require revision surgeries in the future, but advancements in materials and techniques aim to extend the durability of knee replacements. Maintaining a healthy lifestyle, following post-operative instructions, and regular check-ups can also help prolong the implant’s life.
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How to boost your immune system
How to boost your immune system
It’s one of your body’s most important systems, keeping you fit, healthy and free from illness - but what actually is your immune system? And how do you boost it?
We delve into what your immune system actually is and how you can boost it through simple lifestyle changes and supplementation.
What is your immune system?
Like a protective suit, or mask (which thanks to the current global pandemic we’re all pretty well acquainted with) the immune system is the part of your body that protects you against outside attackers (known as pathogens).
It’s made up of a number of different systems, organs, cells and chemicals that work together to help you to fend off bacteria and virus, fight infection and combat illness. Simply put, it’s the system that stops you from getting sick.
The main parts of the immune system are made up of:
• Innate system Adaptive system
• Complement system
• Lymphatic system
• Spleen Bone Marrow
• Thymus
Like lots of our bodies internal systems, it’s pretty complex.
How does it work?
The innate part of the immune system is the bit that starts to work as soon as nasties such as pathogens (toxins) start to attack the body. It’s the part that we all associate with immunity, as it keeps out viruses, bacteria, toxins and stops them from spreading around the body.
The adaptive part of the immune system kicks in once we have been exposed to the toxins. It cleverly uses antigens to memorise the threat and enhance your immune system’s response, shortening your recovery time once you’ve caught a cold or flu. It’s particularly clever, as It keeps an internal record of every germ (or microbe) that it has ever tackled so it can quickly recognise and defeat it should it enter the body again.
These are known as ‘memory cells’ and they work hard to detect illness-causing microbes before they have a chance to multiply and make you sick.
Pretty clever, right? But if that’s the case, why can I catch a cold more than once?
Common infections like flu and colds have to be fought many times, this is because they contain so many different viruses or strains of the same type of microbe that your immune system is required to fight them each time. Hence why if you want to try and avoid illness altogether, you should try to maintain a strong immune system.
What foods help to boost the immune system?
There are lots of myths and mis-conceptions online about how you can’t boost your immune system through diet and supplement. This couldn’t be more incorrect.
Strengthening your body’s natural defence system is possible with the right diet, supplementation and lifestyle changes.
As cliche as it sounds, the best thing you can do for your immune system is to eat a diet based on ‘live’ foods such as plants and stay clear of processed foods that are packaged on supermarket shelves. That being said, there are certain foods that can give your body the upper hand when trying to fight those pesky pathogens. Increasing your intake of whole plant foods like vegetables, fruits, nuts and seeds can help increase your immune boosting power.
Why do these types of foods boost your immune system?
Well firstly, they’re packed with antioxidants. Antioxidants are masters at decreasing inflammation in the cells of the body as they neutralise free radicals.
Free radicals continuously form in the body as you breathe and help convert food into energy. They are the things that make you age and without antioxidants, they would cause harm very quickly.
However, free radicals are also essential for staying healthy as they help keep your immune system in good working order. The key is managing the free radical and antioxidant balance.
If you lose this balance and end up with more free radicals than antioxidants, this is when oxidative stress, disease, illness and ageing is caused.
Plant foods are great for boosting your immune system as they feed the healthy bacteria within your gut, where 70% of your immunity resides. Maintaining a healthy gut microbiome can boost your immune system as it helps to keep harmful pathogens and free radicals from entering your body through the digestive tract.
Vegetables and fruits are packed with Vitamin C which is a key antioxidant and has been proven to strengthen your body’s natural defences.
Oranges are often hailed as a Vitamin C hero, and they are, but it can be found in abundance in lots of other foods such as:
• Broccoli
• Spinach
• Kale
• Green, yellow and red peppers
• Herbs; thyme and parsley
• Acerola
• Cherries
• Guavas
• Blackcurrents
If you want to experience the illness-fighting benefits of Vitamin C, the key is to consume it every day and not just when you think you’re getting sick.
LEARN MORE: DOES VITAMIN C HELP THE IMMUNE SYSTEM? >
What vitamins are good for the immune system?
It can often be challenging to get all of the vitamins that we need through diet alone. This is because, generally speaking, our diets are full of processed foods, meaning that they lack the vitamins and minerals designed to give us a strong immune system.
Whilst it’s known that a diet low in nutrients and high in sugar isn’t great on the waistline, what’s less well-known is that if you add salt, pesticides and colourants into the mix, you’ve created a cocktail for internal inflammation - your immune system’s worst nightmare.
The good news is that research has shown that supplementing your diet with certain vitamins can help boost your immune system and protect your body against illness.
Matt gives us the lowdown on his favourite immune boosting vitamins.
Vitamin C
A powerful antioxidant, Vitamin C is one of the best vitamins for building a strong immune system. It strengthens your body's natural defences by protecting healthy cells against free radicals, which like we said earlier, if left to accumulate, can cause a state of oxidative stress - which has been known to be linked to many chronic diseases and ageing.
LEARN MORE: HOW DOES VITAMIN C HELP THE IMMUNE SYSTEM? >
Elderberries
It’s an often told old wives’ tale but elderberries have long been used to treat infections, particularly those which affect the upper respiratory tract - so colds and flus. They contain a high level of antibacterial and antiviral qualities, meaning that they enhance your immune system response. They’ve also been shown to help shorten the duration and ease the symptoms of colds.
LEARN MORE: WHY ELDERBERRIES BOOST YOUR IMMUNE SYSTEM >
Zinc
Zinc is one of my favourite supplements for helping to boost the immune system. It helps both the innate and adaptive immune system to defend against oxidative stress. Like all minerals, our bodies can’t make Zinc, which means it must come from our food and supplements.
Zinc helps prevent illness by stimulating the activation of the cells responsible for fighting infection.
Vitamin B6
B6 plays a key part in supporting biochemical reactions within the immune system. This means that it increases the production of antibodies, therefore helping to boost your body’s illness-fighting responses.
Vitamin B12
B12 is well-known for boosting mood, energy and immunity. It works by supporting the normal function of red blood cells.
Further, it helps your metabolism to convert food into energy helping your body to meet the challenges that it goes through throughout the day.
Stress and the immune system
Stress and a weakened immune system go hand in hand. Cortisol is a hormone that is released into our blood when we are stressed, putting us into a fight-or-flight state.
Whilst an increase in cortisol is okay for short periods of time, when it is prolonged we are at a greater risk of inflammation and a weakened immune system.
This is because when we’re stressed the immune system’s ability to fight off pathogens (toxins) is affected, making us more prone to infections and illness. It’s a fact that those who live busy lives (and life is busy nowadays, right?) are more prone to stress.
So, if you’ve ever wondered why you come down with a cough, runny nose or stinking cold when you’ve got a big meeting, endless deadlines or when you’re trying to spin endless plates at home? It’s because your immune system’s ability to fight off infection is compromised by the stress that you’ve put your body under.
We are what we eat and more importantly, what we absorb. Eating nutritious foods, sleeping well and getting exercise can actually be a fantastic way to manage stress because it improves brain function, immune function, lowers blood pressure and helps to reduce toxins from the body.
Boost your health with better sleep
Most of us know that getting the right amount of shut eye is good for us, but who knew that it actually plays a crucial role in keeping our immune system fighting fit too.
Getting more sleep doesn't necessarily stop you from getting sick altogether, but getting less than 8 hours per day can have a detrimental effect on your immune system - which could cause you to pick up a nasty cold or flu.
Without sufficient sleep, your body makes fewer cytokines - the protein that targets infection and inflammation - which creates your immune response.
The body produces and releases cytokines when you’re asleep also, meaning that skimping on it can cause your immune system to weaken.
If you want to live a healthy life it’s crucial that you make sleep a priority. Make sure you get 8 hours every night and if it becomes interrupted try to make up for the lost rest with naps.”
Exercise and the immune system
It’s no secret that having a fitter body is going to give you a better chance of fighting off infection.
But did you know that physical activity can actually boost your immune system? Well, you know those nasty pathogens that we keep harping on about? Exercise helps to flush bacteria out of the lungs and the airways meaning that you’re less likely to get sick.
When you exercise, the white blood cells - the cells that help you fight disease - move around the body more quickly, meaning that they’re more likely to detect pathogens or illness causing toxins much sooner than someone who lives a sedentary lifestyle. Exercising helps lower stress thereby boosting your immune system also.
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bronchitis drugs - Bronchitis Treatment - List Of Excellent Drugs
Bronchitis remedy Natural Bronchitis treatment Bronchitis Bronchitis cure
Bronchitis Treatment - List Of Excellent Drugs
Modern society suffers mostly from various kinds of respiratory disorders, some contagious and some noncontagious. The markets are flooded with a variety of drugs to treat bronchitis and other disorders. All of us need to have adequate knowledge about how to maintain good health. We need to know the best drugs to treat bronchitis, in case we are stricken with it.
There are many things you can do to prevent the onset of bronchitis in any form. The most important thing to do is to stop smoking and avoid secondhand smoke. Avoid pollution by staying indoors during smog alerts and refrain from using sprays for cleaning, insect repelling, or deodorizing. These contain a large number of potentially harmful ingredients that can weaken your lung tissues if used too often. If you are sensitive to dairy products, avoid them because they can increase mucus formation. When you notice the beginning of a cough, get plenty of rest and apply mild heat on your chest and back before going to bed. Drink at least eight to 10 glasses of clear water every day and eat foods that are high in vitamin A, C, E and zinc. Foods that are high in these nutrients including eggs, chicken, pecans, citrus fruits, sunflower seeds, broccoli, sardines and avocados.
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Bronchitis Remedy
Bronchitis, a respiratory disorder that can affect anybody at anytime, is one among the most widespread ailments. However, people residing in polluted areas, cigarette smokers, infants, young children, old people, and people already suffering from lung disorders are more susceptible to bronchitis.
If you are diagnosed by the doctor with bronchitis the best thing to do is to get the best treatment for bronchitis, in order to avoid any complications. There are many treatments available for bronchitis. The main concern when suffering from bronchitis is the problems you have breathing. This disease, bronchitis is a respiratory system condition, so coughing and shortness of breath are a big problem when having bronchitis.
Michael Russell
Your Independent guide to Health
Treatment of Chronic Bronchitis On the other hand, chronic bronchitis, a long-term disorder, requires long-term care. If you are suffering from chronic bronchitis, you need to take a variety of drugs to obtain relief from the symptoms of the disorders along with drugs that might help cure the condition.
Abhishek is an ex-bronchitis sufferer and he has got some great tips for Bronchitis Treatment! Download his FREE 100 Pages Ebook, "How To Win Your War Against Bronchitis" from his website http://www.Health-Whiz.com/797/index.htm. Only limited Free Copies available.
Some doctors may recommend the consumption of antibiotics. But this is suited only for infections which recur. Also, the usage of steroids like Corticosteroids may sometimes be prescribed to those who may not act according to the recommended treatments. There are few doctors who might not prescribe this kind of medication as it may lead to many side effects. Corticosteroid is used only when its needed.
Before taking any sort of drug to treat bronchitis, consult your doctor. Your doctor will determine, on the basis of your medical history, whether or not a particular drug will be beneficial for you. Doctors are the most qualified to determine the best combination of drugs to treat bronchitis. They also give you the correct instruction about the usage of these drugs.
If the chronic bronchitis is to be considered very severe then you'll have to do "oxygen therapy." This is a kind of therapy which administers oxygen as its therapeutic modality where the oxygen supply would be heightened. With the use of a nasal cannula or a mask, oxygen would be supplied to us.
If it can't be prevented, there are suggested and prescribed medications like the following: 1. betaz- agonists [inhaled] - this kind of medication will be usually prescribed if chronic cough is present. You or a caretaker must be very cautious of the side effects like trembling and tenseness.
Bronchitis might be cured if you learn the ways for making yourself better. These information might also be very helpful for your caretaker. Relieve the cough.
For more resources about bronchitis or especially about bronchitis symptoms please visit http://www.bronchitis-guide.com/bronchitis-symptoms.htm About the Author:
There is no need to take any drugs to treat bronchitis that is caused by viruses. You simply need a lot of rest, water and fruit juices in abundance, and a humidifier. In addition, you have to avoid dust and polluted environments. The only drugs required in this conditions are those that alleviate the symptoms of bronchitis--anti-inflammatory drugs, pain killers, expectorants, and nasal decongestants.
If you're a smoker, it'll be recommended to you to discontinue smoking. Substances inside a cigarette have irritants which may contribute for the severity of the cough.
However, some patients take expectorants to facilitate easier breathing. Anti-inflammatory drugs will help you obtain relief from the various symptoms of bronchitis. In certain cases, bronchitis can lead to very painful sinusitis. Decongestants will help you alleviate this symptom. You might also require pain killers to ease the muscle pain that always comes with bronchitis.
Abhishek is an ex-bronchitis sufferer and he has got some great tips for Bronchitis Treatment! Download his FREE 100 Pages Ebook, "How To Win Your War Against Bronchitis" from his website http://www.Health-Whiz.com/797/index.htm. Only limited Free Copies available.
Bronchitis is a disease that can be tenacious as a stubborn dog. It is caused by a severe inflammation or the blocking of the air tubes in the lungs. Bronchitis generally occurs in two forms: acute or chronic. Acute bronchitis is the lesser condition of the two but it can still last for several weeks and may result in pneumonia if it is not taken care of right away. Chronic bronchitis, on the other hand, can eventually lead to more serious heart problems.
Chances for complete recovery from chronic bronchitis are slim. You need to identify the disease in its earliest stages and arrest its further progress immediately. You can do so by making major lifestyle changes such as moving to a cleaner area, quitting smoking, and giving up alcohol altogether.
2. Antibiotics - there are some antibiotics which would be prescribed by doctors for treating individuals who're in danger to develop various other complicated matters.
Use drugs which don't need a prescription. There are many recommended such medicines if you possess acute bronchitis. These drugs are given to decrease fever and any other discomfort pulled in by these kinds of symptoms.
Chronic bronchitis does entail long-term treatment when compared to acute one. Medical findings reveal that there's no cure for this chronic bronchitis. The prime objective for us to treat this kind of illness is by relieving you from these symptoms and by keeping off the complications.
In order to make your breathing a lot easier when you have bronchitis, here are some tricks for you to follow. First of all, when suffering from bronchitis, you must drink a lot of fluids. Try drinking at least nine galsses of water every day. This is very beneficial if you have bronchitis, because it helps to keep the mucus produced thin. Another thing to remember is to avoid any dairy products or sugar if you have bronchitis. They only weaken your immune system. Furthermore, the production of mucus will be increased by the use of these products, if you have bronchitis.
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Bronchitis treatment
Bronchitis can be recognized by the following symptoms: frequent and painful cough with phlegm, high fever, sore throat, chest pain, harsh sounds when breathing and chills. Acute bronchitis is the common result of an infection like the flu or an untreated cold. Chronic bronchitis is usually caused by a lung irritant like cigarette smoke, allergies, dust and all other forms of air pollution.
bronchitis, there is a big chance your airways will dry and the mucus will become thicker, which is very bad if you have bronchitis. The third thing to do in case of bronchitis is to use humidifiers or vaporizers. In cases of bronchitis, it will be a relief for you to have your airways moist. This two do just that. A hot bath of shower is also another great way to relief some of the bronchitis symptoms. Because when you have bronchitis, your airways are the ones that must be taken care of, be sure to avoid any irritants. Dust, chemicals or paint may irritate you airways even more and make your bronchitis worse. If you use aerosols or insecticides, try to stop that as long as you have bronchitis. They will only make the bronchitis worse.
3. Aspirin - a drug which is usually used like an "analgesic" for reducing minor pains, body aches etc. However, aspirins aren't recommended being used by children unless they're advised by their doctor.
Some of the medicines typically taken by patients suffering from chronic bronchitis are bronchodilators to dilate the bronchi and to enable easier breathing, antibiotics to destroy any bacteria that might be infecting your respiratory tract, and steroids. In certain cases, people suffering from chronic bronchitis require supplemental oxygen to help them deal with the low levels of oxygen in their body.
Treatment of Acute Bronchitis Acute bronchitis is the milder of the two types of bronchitis. There is no need to take any drugs to treat bronchitis of this type, which is a short-term disorder. Acute bronchitis lasts only for a couple of weeks or lesser if treated with care. The duration of the illness also depends on the type of microbe causing it.
1. Acetaminophen - a drug which is commonly used for relieving soreness of our body and fever as well. 2. Ibuprofen - this drug is given for individuals for giving aid to the fever which they possess.
It is a common mistake to take antihistamines, antibiotics, or decongestants for bronchitis. These drugs do not relieve inflamed windpipes and can even dry the mucus linings of the lungs. They can also make the mucus so thick that coughing can be very difficult and painful. Antibiotics don't usually help because most bronchitis is not caused by bacterial infections. Antibiotics hurt your chances of getting better by killing off friendly micro-organisms and making certain bacteria strains more antibiotic-resistant. A common herbal antidote for bronchitis is to try drinking half a cup of horehound tea three times a day. This can help to thin and release mucus that accumulates in the lungs of bronchitis patients.
Get optimum rest. The very best way for fighting these symptoms of bronchitis is to take ample amount of rest possible. By doing this, you'll be able to possess more energy which you need for fighting the infections.
A writer once said that every time medical science demonstrates that with proper resources and with proper treatment, diseases might be treated if they aren't cured.
The second useful trick when having bronchitis is not to take any cough suppressants. It is the first impulse that somebody has when suffering from bronchitis. This is not good, because when you cough, your body eliminates the mucus that is produced when you have bronchitis. If you take any drugs that are meant to suppress cough, the mucus may buildup. This can lead to serious complications of bronchitis, like pneumonia. Other drugs you should avoid in case of bronchitis are decongestants and antihistamines. Instead of helping you with your bronchitis, these drugs can make things worse. If you take them when you have
Be well-informed about the disorder most especially its handling would give a lot of benefits. Read more about how bronchitis is treated. Most importantly, speak with your doctor and don't fear to ask your queries if there are some vague terms which you couldn't understand.
Since cough might be very annoying, you must find ways to stop coughing. The very effective action is drinking plenty of fluids [non-caffeinated] like water and juices. Studies reveal that water is a best expectorant for easing your cough and it's thin like mucus.
Try getting enough sleep. If you don't sleep due to the inability to breathe normally, try increasing your bed's head. When you do this, the nasal passages and sinuses would have better amount of drainage and it won't induce a "tickle" inside the throat.
You have to take antibiotics or antibacterial drugs to treat bronchitis that is caused by bacteria; the drugs destroy the bacteria that are infecting your bronchi. In rare cases, the bronchitis might be caused by a fungus, and you will have to take antifungal drugs in addition to the other medicines that tackle the symptoms of bronchitis.
You can take a number of vitamins to promote healing of bronchitis as well as preventing it. Vitamin A in large doses taken daily for up to 30 days can promote faster healing of irritated mucus membranes and strengthens the whole immune system. Vitamin C taken along with it can boost your immunity also and helps build up better collagen and mucus linings in the lungs. Vitamin E is a powerful antioxidant that protects your lungs from air pollution. Zinc works with vitamin A to heal lung membranes and other tissues. An herb called astragalus taken daily in small doses can also help reduce symptoms associated with chronic bronchitis.
Along with the medication and the rest of the treatment plan, it is essential that you stop smoking. The earlier you quit smoking, the sooner you can undo the damage done to your lungs.
For more resources about bronchitis or especially about bronchitis symptoms please visit http://www.bronchitis-guide.com/bronchitis-symptoms.htm
Learn More about Natural Bronchitis Remedy
A Chinese proverb says: The person who says it cannot be done should not interrupt the person doing it. This protocol must be started with a good mood, a happy one because no matter what there is always a solution! This protocol contains fully detail explanations regarding natural and traditional therapies, healthy diet and exercises, body cleansing. It is important to understand...
Diagnosing chronic bronchitis can be very difficult, because chronic bronchitis shares several symptoms with other diseases including pneumonia and emphysema. During the examination the doctor will ask you for a full medical history, and then run a full physical check up. Your doctor will ask you about any symptoms you are experiencing, and probably inquire about your smoking habits, because...
One of the manifestations of chronic bronchitis is a productive cough accompanied by phlegm, which obstructs the free flow of air in the bronchial tubes. Chronic bronchitis is a long-term disorder that can last as long as two years. It is the fourth largest killer in the United States of America, and around ten million people fall victim to this disorder every year. About 40,000 deaths due to...
Bronchitis is a respiratory disease very commonly found now a days. In this condition the air passages in our lungs are inflamed. This disease can either be chronic, acute, or asthmatic. Acute bronchitis is short term. Caused by the viral infection beginning in the sinuses and/or the nose spreading in to the air passages, it is believed to be cured generally in 10-12 days. The chronic...
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Reference Guide To Aerobic Exercise
Over the past four a long time, numerous scientific reports have examined the relationships between bodily activity, physical fitness, and cardiovascular well being. After a baseline treadmill test to assess Vo2max, contributors of the Aerobic Center Longitudinal Study had their bodily exercise ranges assessed over a 12-month period ( sixteen ). Increased risk of musculoskeletal damage was related to will increase in cardiorespiratory health (as measured by a treadmill check), as well as increases in the amount of reported weekly physical activity.
In a study performed amongst US veterans, subjects had been categorised into 5 classes in response to health stage. The goals of the current study were to establish and perceive the relationship between health standing and the chance of harm in a 5-year occupational cohort of career hearth service members. Aerobic exercise ought to happen all through the week, with every session lasting at the very least 10 minutes. Age, physique composition, cardio health and health condition as threat components for musculoskeletal accidents in conscripts.
Quantitative methods, notably time-to-event regression fashions, were used to evaluate the connection between aerobic fitness and harm. Since then, most hearth departments have adopted minimal health standards, usually emphasizing aerobic capability as a definitive measure of overall health. Note: The recommendations are based mostly on American College of Sports Medicine/American Heart Association tips. Regular cardio exercise has even been shown to have the potential to extend your lifespan.
Table 6 presents the crude hazard ratios for the all-injury mannequin and the sprain and strain model in relation to age (<30 and="" ≥30="" years="" of="" age)="" and="" general,="" stratified="" by="" cardio="" fitness="" stage.="" when="" you="" observe="" a="" program="" of="" regular="" aerobic="" exercise,="" your="" cardiovascular="" system="" grows="" stronger="" and="" might="" meet="" the="" muscle="" tissue'="" calls="" for="" with="" out="" as="" a="" lot="" effort.="" even="" if="" in="" case="" you="" have="" a="" busy="" schedule,="" yow="" will="" discover="" time="" for="" several="" 10-minute="" durations="" of="" moderate-depth="" aerobic="">
Other fitness enhancements happen in the exercising muscle tissues, and are particular to those muscles being used within the mode of train (e.g. strolling, working, biking, or swimming). Gradually add time to the cardio coaching portion, working as much as a minimum of 20 minutes of aerobic exercise in each session.
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How Electric Toothbrushes Prevent Tooth Loss?
Four common causes of tooth loss
• Physical injury or traumaTooth loss can also be caused by incidents such as falls and vehicle accidents. You may, however, be cautious to avoid some common causes of tooth loss or damage as a result of accidents. Use your teeth to loosen knots, take off tags, and cut thread, not to remove caps, tops, or lids.
• Some diseases: Diabetes, hypertension, arthritis, smoking, poor nutrition.
• CavitiesCavities are holes in the teeth that develop as a result of a bacterial infection that leads to tooth decay. If left untreated, a cavity can kill the pulp in the middle of the tooth, necessitating a root canal or even tooth extraction.
• Gum disease is a condition that affects the gumsPeriodontal disease, often known as gum disease, is the leading cause of tooth loss in adults, accounting for 70% of all missing teeth. It all starts with bacteria and gum inflammation. As the disease advances, it damages the gum tissues and may even destroy the jawbone behind the gums, leaving the teeth without support.
Brushing twice a day and flossing at least once a day might help keep your smile healthy, but it's not always enough. Switching to an electric toothbrush not only improves your chances of keeping more of your natural teeth over time, but it also keeps your gum line healthy.
How electric toothbrushes help maintain oral health?
How electric toothbrushes help maintain oral health? - usmile
Avoiding Excessive Brushing
Did you know that brushing your teeth too hard can destroy enamel from the surface and cause sensitivity? One of the advantages of using an electric toothbrush is that it prevents you from brushing too aggressively. All you have to do is place your toothbrush on your teeth and let it do the rest. Your teeth will be cleaned thoroughly without causing any harm or abrasion.
Ensure that you brush for the appropriate amount of time
Did you know that brushing your teeth for at least two minutes, with at least 30 seconds in each quadrant of your mouth (upper and lower right and left sides) is recommended? Your electric toothbrush can be of assistance. Most have built-in timers, ensuring that you wash your teeth for the proper amount of time.
More thorough cleaning
Electric toothbrushes have vibrating or rotating bristles that help clean any troublesome or difficult-to-reach regions. Plaque accumulation on the teeth and gums is thoroughly removed, which helps to prevent cavities and gum disease. An electric toothbrush does the majority of the work for you, allowing you to brush your teeth evenly and thoroughly.
Brushing with usmile electric toothbrush promotes a healthier gum line and hence stronger teeth. Long-term use of an electric toothbrush helps users preserve roughly 20% more teeth than cleaning with a manual toothbrush alone. When you use an electric toothbrush in conjunction with a gum care toothpaste, you may help keep your gum line strong and avoid tooth loss.
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hypopiesis
Also found in: Dictionary, Thesaurus, Encyclopedia.
hy·po·ten·sion
(hī'pō-ten'shŭn),
1. Subnormal arterial blood pressure. Synonym(s): hypopiesis
2. Reduced pressure or tension of any kind.
[hypo- + L. tensio, a stretching]
hy·po·ten·sion
(hī'pō-ten'shŭn)
1. Subnormal arterial blood pressure.
Synonym(s): hypopiesis.
2. Reduced pressure or tension of any kind.
[hypo- + L. tensio, a stretching]
hypopiesis
abnormally low pressure, in particular, low blood pressure.
Patient discussion about hypopiesis
Q. how can u lower your bp naturally
A. a change in lifestyle- Reducing Salt and Sodium in Your Diet, change to a healthier diet,Maintaining a Healthy Weight, Being Physically Active, Limiting Alcohol Intake, Quitting Smoking. i don't think it can take you off meds , but it can lower the amount of the considerably.
More discussions about hypopiesis
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Advertisement
Acid reflux, in most cases, is caused by a confluence of stomach content and stomach acids going in reverse from the stomach into the esophagus and sometimes into the mouth. There is nothing good about this sudden shift to reverse when the contents of your stomach are returning with corrosive stomach acid. While not usually dangerous, it's certainly not a pleasant experience for most.
The cause of Acid reflux can be no more than an upset stomach or a particularly spicy or acidic meal. It can be considerably more severe if a regular occurrence. This seriousness is often rooted in the types of symptoms you're experiencing and more importantly their frequency. Acid reflux affects as many as one in five Americans regularly, but that paints a picture with too small of a brush. If you're taking antacids each day or your reflux is frequently returning, there is a potential for a more serious issue.
Gastroesophageal reflux disease (GERD) has inherent consequences if untreated and can even be fatal in the evening while you're sleeping by allowing stomach contents and stomach acid to block the esophagus. Heartburn by itself rarely represents something serious. It does, however, range from an annoyance, to downright painful. Dyspepsia is a bit more serious; it's a type of heartburn that can cause you to become panicky and cause considerable pain for many it affects.
Acid reflux is responsible for nearly 60% of emergency room visits when chest pain presents and heart attacks are suspects. Those that experience frequent and persistent heartburn and acid reflux should see a doctor. Those sleeping with acid reflux should make sure they are sleeping on their stomachs.
Common Symptoms
• Heartburn
• Bad Taste In The Mouth (Sour)
• Regurgitation
• Issues Swallowing
• Dyspepsia
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This site offers information designed for educational purposes only. You should not rely on any information on this site as a substitute for professional medical advice, diagnosis, treatment, or as a substitute for, professional counseling care, advice, diagnosis, or treatment. If you have any concerns or questions about your health, you should always consult with a physician or other healthcare professional.
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Is my Sore throat COVID 19 or a symptom of a non Coronavirus Health condition ?
Posted by Callie Torres
May 27, 2021
Although a sore throat is a relatively common symptom, during the COVID era, it can no longer be dismissed or ignored. Having a sore throat by itself doesn’t necessarily indicate you do or don’t have COVID. However, other symptoms in addition to the sore throat may help distinguish between a sore throat COVID 19 related and other etiologies including:
• Strep throat
• Allergies
• Influenza (the flu)
• Tonsillitis
• The common cold
How would I know if my Sore throat is caused by COVID disease?
A Sore throat is very common and not necessarily indicative of COVID or a medical infection or disease. For most people, a Sore throat by itself is not something to worry about affecting your health. However, if a Sore throat is paired with other symptoms then it is important that one see a medical doctor. The easiest and most accurate way to tell if a Sore throat is caused by a coronavirus such as COVID 19 is by getting an urgent coronavirus test. However, based on the combination of symptoms, it may be possible to have some insight into the underlying cause of a Sore throat before getting a medical test. Symptoms that point to sore throat COVID and are less likely in other infections include:
• Loss of smell (Anosmia)
• Loss of taste (Ageusia)
• Difficulty breathing or Shortness of breath (Dyspnea)
• Diarrhea
What common medical conditions besides Covid can cause a Sore throat?
A Sore throat, medically known as Pharyngitis, can be caused by a number of underlying medical or non-medical conditions besides COVID. Sore throat is a symptom and not an actual medical diagnosis. Some common medical conditions that cause Sore throat other than COVID 19 are:
covid 19 test
woman with influenza
Other non Covid medical causes of a Sore throat: Strep throat
Strep throat is an infection caused by the bacterium Streptococcus pyogenes, also known by the name group A Strep. Although strep throat and COVID may share some health symptoms such as fever, headache, and Sore throat, there are also several symptoms that may help to separate the strep throat from COVID sore throat. Treatment and care of strep throat may require an antibiotic prescription from an urgent care medical group, community hospital, and/or pharmacy services. Coronavirus is more likely to cause loss of smell/taste, diarrhea, and body aches. These health symptoms are uncommonly associated with strep throat. On the other hand, the following symptoms are more associated with strep throat than COVID-19:
• Painful Swallowing (Odynophagia)
• Small Pinpoint Red Spots in the Throat and Roof of the Mouth (Petechiae)
• Swollen Lymph Nodes Present in the Neck
• A Rash
• Swollen Red Tonsils
Other non Coronavirus medical causes of a Sore throat: Allergies
Allergies are caused by the body's immune response from a foreign substance known as irritants or allergens. Prevalent allergens include pollen, dander, and certain foods such as peanuts. The immune system normally works by fighting off harmful pathogens that are detrimental to one's health. However, it can go awry and find and fight off prevalent harmless environmental substances and cause symptoms like Sore throat. Although many allergy symptoms could be similar to those experienced in COVID coronavirus infection, individuals with allergies usually do not get loss of smell or taste, fever, body aches, or nausea. The most common allergy health symptoms include:
• Watery, Itchy, and Puffy Eyes
• Sneezing
• Runny and or Congested Nose
• Cough
• Headache
• Sore throat
Other non Covid medical causes of a Sore throat: The Flu
The flu (Influenza) and COVID are both contagious viruses, although they are caused by different organisms. The flu is caused by influenza viruses while COVID-19 coronavirus is caused by a new strain of coronavirus. SARS-CoV-2 is the scientific name for the new coronavirus strain. When comparing the two it is important note that COVID spreads more easily than the flu and causes more serious health infections in some individuals. Additionally, COVID may remain latent for longer than the flu, meaning individuals get infected and are contagious, but sometimes not yet showing symptoms. Individuals with the flu virus commonly show symptoms 1-4 days after infection, while individuals with coronavirus usually develop symptoms 2-14 days after initial infection. If you are unaware if your symptoms are caused by COVID or the flu, it is important that one take urgent care to quarantine away from people and get tested to reduce the risk of spread. Other prevalent health symptoms of the flu include:
• Body aches and muscle pain
• Chills
• Cough
• Fatigue
• Fever
• Headache
• Loss of appetite
• Sore throat
• Congested or runny nose
Other medical causes of a Sore throat: The Common cold
The common cold can be caused by several different viruses although the class of rhinoviruses are most common. Health symptoms of a cold commonly occur 2 - 3 days after an individual comes into contact with the virus. A cold is usually relatively harmless and the body's immune system can fight the virus on its own although sometimes symptoms like Sore throat may last a couple of days. Children are particularly prone to spreading colds. As colds are caused by viruses, antibiotics from an urgent care medical group and pharmacy services do not aid in fighting the infection. A cold commonly only lasts a few days and does not have many unique symptoms of COVID and coronavirus such as shortness of breath and loss of smell or taste. The most prevalent health symptoms of the common cold are:
• Runny nose
• Sore throat
• Sneezing
• Cough
• Nasal and sinus congestion
Other medical causes of a Sore throat: Tonsillitis
Tonsillitis is caused by inflammation of the pharyngeal tonsils. Tonsils are located bilaterally in the back of the throat. Tonsillitis can be caused by both bacterial and viral infections although viral infections are more common. Tonsillitis can be self-limited, meaning treatment by a medical professional is not necessary. However, infections can also be severe and require medical treatment, such as the use of antibiotics for the treatment of bacterial Tonsillitis. If tonsils are repeatedly infected and cause difficulty swallowing a surgery in which the tonsils are removed, Tonsillectomy, may be necessary. Tonsillitis commonly resolves in a few weeks and does not have many unique symptoms of COVID such as shortness of breath and loss of smell or taste. The most common symptoms include:
• Sore throat
• Painful swallowing
• Scratchy voice
• Pain with speaking
• Pain with eating
testing with a throat swab
Tonsillitis examination
If I have Sore throat symptoms when should I see my Doctor or visit an Urgent care?
Prior to COVID, little care was given to a simple Sore throat. However, with the COVID medical pandemic, a Sore throat may be indicative of an infection with Coronavirus and it is important to note and take care by finding the correct diagnosis. If you develop symptoms of COVID coronavirus the most important first step is to quarantine away from people and make sure not infect other individuals with the virus which is detrimental to their health. In order to be diagnosed with COVID, you may have to see your medical care doctor, a local urgent care, the hospital or your local health department to find an area that is conducting testing. Even if the medical test is negative, take care and quarantine away from people for at least 10 days as this reduces the risk of spread.
If you do get Coronavirus, try to take care and manage symptoms at home. If symptoms persist or cannot be managed, reach out to your medical doctor or visit a local community urgent care. Medications like steroids could help take care of symptoms like shortness of breath in some patients. Please note that if you get any of the following urgent health symptoms, dial 911 or proceed to the hospital emergency room:
• Difficulty breathing
• Chest pain or pressure
• Sudden dizziness or weakness
• Fainting
• Changes in vision and view
• Difficulty breathing
• Changes in mental status or confusion
• Persistent vomiting or diarrhea
• Coughing or vomiting blood
• Difficulty speaking
If I have a Sore throat symptoms and it is COVID disease related then when was I exposed to the viral spread?
Although a very small percent of individuals infected with COVID will present with ONLY a Sore throat, it is a possibility. If this is the case, according to the CDC services, exposure most likely occurred between 2-14 days prior to symptom onset. If you suspect infection due to COVID, it is important to take care and immediately quarantine away from people and get an urgent medical coronavirus test. If you have COVID and are infected it is urgent and important to reach out and notify individuals you were in contact with and remain at home for ten days time to reduce the spread of the disease.
What medical professionals specialize in treating Sore throats caused by Covid 19, Strep throat, Tonsillitis, the Flu or other infections ?
The majority of Sore throat presentation is to an outpatient clinic, and prompt/acute care also called urgent care. The medical professionals that one may see in these scenarios include internal medicine or family medicine trained health physicians, as well as nurse practitioners (NPs) and Physician assistants (PAs) that work in a group. However, if the Sore throat symptom lingers or has an abnormal health presentation a more specialized physician may be required to care for the patient or provide another point of view and other services. Otolaryngologists are the primary physicians that specialize in the management of diseases and disorders of the throat in patients including children.
An Otolaryngologist is a Physician with an Osteopathic medicine (D.O.) or Allopathy (M.D.) degree that has successfully completed a five year residency in the field of Otorhinolaryngology. The field of Otorhinolaryngology is more commonly known as Otolaryngology. These board-certified doctors are also known as ENTs because they work with diseases and conditions that affect the ears, nose, and throat of patients as well as the head and neck areas. As throat specialists, ENTs are the definitive experts on the causes and treatments for Sore throats. They are also the most experienced Physicians to diagnose and treat other symptoms of Covid 19 including Anosmia (loss of smell) and Ageusia (loss of taste) which are not usually encountered in non-covid related sore throats.
**Medical Advice Disclaimer ** This website does not offer medical advice. See details here
Posted by Callie Torres
Callie Torres is a Captain in the United States Air Force and a resident at Wash U/Barnes Jewish Hospital in St Louis. She is a freelance writer with many published medical articles as well as multiple peer-reviewed medical publications
Topics: Feature Medical Practice
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When Do Pregnancy Food Aversions Stop?
Aversions to some foods are very common and utterly uncomfortable during pregnancy. It’s common for them to appear in the early stages of pregnancy and pass by the time the second trimester rolls around, but it’s also conceivable that your appetite won’t return to normal until after the baby is delivered.
During the first trimester of pregnancy, aversions and morning sickness typically begin around the same time, generally within a week of each other.Food aversions and cravings are likely to be at their worst during the first half of pregnancy, but they may continue throughout the full nine months of pregnancy and even after delivery.They also have the option to leave and return at a later time.
When do food aversions start and end during pregnancy?
In most pregnancies, cravings for food begin to appear at the end of the first trimester, reach its height and become more intense during the second trimester, and then normally begin to lessen as the pregnancy draws to a close.At about the same time, many women who are pregnant report having at least one aversion to certain foods.Aversions to certain types of food are a common symptom of morning sickness and nausea.
What are pregnancy aversions and aversions?
Any meal might cause you to develop a hunger or an aversion to certain foods when you are pregnant.Even if you have a strong aversion to a certain meal at one time in your pregnancy, you could find that you start craving that dish later on in your pregnancy.On the other hand, aversions to foods are most frequently triggered by their pungent odors.Aversions that are common during pregnancy include:
You might be interested: When Does Your Stomach Start To Get Hard During Pregnancy?
When are you most likely to experience food aversions?
During the first trimester of your pregnancy, you may find that you have a strong aversion to some foods. On the other hand, you could develop aversions to certain foods at any time throughout your pregnancy. During your pregnancy, you may also find that you have a sudden aversion to certain foods at any moment.
Is it safe to eat what you aversion during pregnancy?
During pregnancy, it is important to remember that it is in your best interest to pay attention to your body.This indicates that it is OK to indulge one’s appetites while avoiding one’s aversions, provided that one does so in moderation.If, on the other hand, your aversions include meals that should not be skipped during pregnancy, you will need to find other ways to receive the nutrients your body needs.
How can I overcome food aversion during pregnancy?
The following are some suggestions that might assist you in overcoming food aversions and keeping a balanced diet while you are pregnant.
1. Don’t Wait Until You’re Hungry Before Eating
2. Substitute.
3. Find anything that can help ease the discomfort in your stomach.
4. Options.
5. Talk to Your Husband or Wife
6. Relax and take it easy on yourself
What Week Do food aversions end?
A lack of appetite as a result of generalized nausea can take hold at any time of day (it is not always ″morning sickness″), although it often reaches its height between weeks 6 and 14 of pregnancy. Aversions to certain foods are more likely to come and go throughout pregnancy, although in most cases they subside as the pregnancy continues.
You might be interested: What Dental Treatment Is Free During Pregnancy?
Why do I have food aversions during pregnancy?
During pregnancy, your body will go through a number of hormonal transitions.During the first few months of pregnancy, the level of the hormone human chorionic gonadotropin, often known as hCG, normally reaches its highest point around week 11 of the pregnancy.In addition to being linked to morning sickness, elevated levels of hCG may also play a role in the development of dietary aversions.
Is it normal to lose your appetite at 23 weeks pregnant?
There are a variety of reasons why you could have a loss of appetite during the second trimester of pregnancy.Even though this is completely normal, you need to make sure that both you and your kid are getting enough to eat.Loss of appetite and food aversions are common pregnancy symptoms that can linger far into the second trimester for some women.This is similar to how some women feel during the first trimester.
Is the 2nd trimester easier?
Even though the majority of pregnant women report that the second trimester is a great deal less stressful than the first, it is still very vital to educate yourself about your pregnancy at this stage. Learning about each week of your pregnancy will help you make more well-informed decisions and better prepare you for the major life changes that lie ahead.
Are food aversions boy or girl?
In spite of the fact that this hypothesis has not been supported by any research to yet, an increasing number of women report experiencing an aversion to chicken after giving birth to a daughter. In the meanwhile, aversions to red meat have been found to be connected with the delivery of a male child in a number of online forums pertaining to pregnancy.
Is it normal to feel nauseous all day while pregnant?
Morning sickness is the popular name given to the nausea and vomiting that many pregnant women experience in the early stages of their pregnancies. It is possible for you to become ill at any moment of the day or night, or you may feel ill during the whole day. Morning sickness is a distressing condition that can have a big negative impact on your day-to-day life.
You might be interested: What Is Group B Strep Test During Pregnancy?
What happens if you go a day without eating while pregnant?
Long stretches of time during pregnancy in which there is no consumption of food are linked to increased levels of corticotropin-releasing hormone in the mother as well as premature birth.
What happens if you ignore pregnancy cravings?
Although it’s true that many pregnant women experience distinct or odd food cravings, it’s totally common for pregnant women to not have any cravings at all. There is no cause for alarm just because you do not have any urges. In point of fact, if you don’t have a need for foods high in fat or sugar, you’ll have a better chance of selecting healthier options.
How long do smell aversions last in pregnancy?
However, we are all aware that this cannot occur. The encouraging news is that after the first trimester, the majority of pregnant women, although continuing to experience a heightened level of scent, do not continue to feel as repulsed by everything. 4 And it’s possible that you won’t have any nasal problems at all, or that you’ll just have a couple.
What happens if you don’t eat while pregnant?
There is a risk of difficulties if a woman does not get enough to eat when pregnant. A lack of proper nutrition during pregnancy can result in a number of issues, including stunted fetal growth, a low birth weight, and a loss of weight in the mother. Additionally, there is a correlation between it and impaired brain performance as well as behavioral issues in youngsters ( 29, 30, 31 ).
What does morning sickness feel like without vomiting?
When pregnant, a woman may have nausea or morning sickness that feels like: The overarching and persistent sensation that one has to throw up, yet without the pressing desire to actually do so. A sudden, intense need to vomit. A sensation that you are hungry, yet you are unable to consume anything due to lack of stomach capacity.
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• What does cbd oil do to you
Cbd oil drug interactions – the cyp450 pathway. research has begun to demonstrate that cannabidiol ( cbd) has the potential to effectively help a large number of people. cbd oil interacts with the endocannabinoid system in a way that produces very few unintended side- effects. learn what cbd oil is side effects, what it does, more. jerry klein gives the need- to- know information about using cbd oil to treat what does cbd oil do to you dogs. what does cbd oil do to you learn what cbd oil is what it does side effects. can i make my own cbd oil? it’ s not difficult to make your own cbd oil, what does cbd oil do to you nor does it require a lot of ingredients. click here for a simple recipe.
how do i know what dose of cbd i should take? every person is unique and your sensitivity to cbd will be different from someone else’ s. the research on cbd products and pain management has been promising. cbd can offer an alternative for people who have chronic pain rely on medications, such as opioids that can be habit. it’ s a question that seems to be on everyone’ s mind these days: does cbd oil get you high? it’ s an important question to ask— and answer— because cbd offers some rather profound medical benefits that can’ t be found anywhere else. but until fairly recently, those benefits could only be had by consuming the whole plant. if you live in a restricted state it’ s vital to make sure you’ re buying cbd hemp oil, , not a product derived from the cannabis plant if you want to stay on the right side of the law. what does cannabis oil what does cbd oil do to you do?
cbd oil is not cannabis: you will not get high, but you will experience positive health benefits. after passing an id check skin patches, drink powders, salves, candies, i was introduced to a “ budtender” who pointed me to an impressive array of cbd products — tinctures massage oil. with all the discussion of cbd oil in the media these days, you may be asking yourself if you need a prescription to buy cbd oil. cbd oil is certainly becoming a hot topic with even mainstream news media outlets discussing this viable option for the treatment of a wide variety of health issues [. what is cbd oil how does it make you feel? gather ' round, it' s time to talk about cbd' s effects on the body. any cannabis connoisseur worth their weed card knows that tetrahydrocannabinol . what does cbd oil do to you cbd hemp oil is extracted from the hemp plant. the hemp plant has buds that produce that oil. the hemp plant is commonly grown industrially to be used in research and as a raw material for varied products.
where can you find high- quality cbd oil? how long does cbd take to work? cbd can generally take from a few minutes to a couple of hours to work properly , the method of consumption, depending on the serving size the symptom you want to alleviate. by vaping sublingually ingesting cbd you can start feeling effects within minutes. additionally you might find it useful to record your daily experiences in a notebook so you can accurately narrow in on what works feels best for you. with that understanding in place it is now time to learn more about cbd oil how to find the right cbd oil dosage for you. how much cbd oil should i take? cbd oil may offer a range of benefits including reducing pain inflammation. evidence shows that the oil does not contain psychoactive properties and what so does not have the same effects as. cbd is also known to interact with several medications.
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cbd oil is slowly becoming an internationally accepted form of treatment for a wide range of conditions. still its neuroprotective anti- inflammatory properties are the real reason it’ s popular. instead cbd oil provides immense scientifically proven medicinal benefits with minimal no adverse effects. how does cbd oil taste? beginners to cbd oil are often reluctant to experience the taste of viscous oil. the nutty earthy grassy taste of cbd oil comes from the unfiltered organic hemp plant. the fda does not allow us to make any claims about what cbd hemp oil can do or may do for you. what but fibromyalgia, migraines , chronic pain, epilepsy, insomnia, we can pass along that we have numerous customers using our products regularly for things such as: cancer, anxiety, arthritis so much more. so i have to wonder: with its many accolades, how does cbd oil make you feel? cbd is the major, non- psychoactive cannabinoid complex from the cannabis plant that offers significant health benefits.
i have developed a new trick to decide as to how much cbd oil should i take. mostly we see that people start from a very what does cbd oil do to you low dose and then increase gradually. i started from a not too low , not too high dose then decreased it just a bit. that way i think i reached to my optimum level faster than it would have been otherwise. let me start by saying i am not a doctor i’ m a patient i use cbd. i am not affiliated with any cbd producers vendors, nor do i sell any cbd hemp products. does cbd make you high? experts do not recommend cbd oil for use in children, as there is little research on the effects of cbd oil on a child' s developing brain. however, people may use. how much kratom powder to use. cbd vape oil is simply cbd oil meant for use in a vaporizer.
Cbd oil and thyroid medicine. • the oil is available in cartridges refill bottles depending on the equipment you use. • vaporizers are tools that use heat to convert the content of oils other materials into vapor allowing the user to inhale them. though it might not sound like a problem for most people, there are many instances wherein you do not want to be unnecessarily tired. let’ s take a look at the science behind cbd oil to figure out whether in fact, not cbd oil does make you sleepy. first off, what is cbd oil? vaping pure cbd oil has helped me with my anxiety and i' ve noticeably felt calmer. here' s what you need to know about using cbd oil the potential side effects, , including whether it' s legal . however many people take cbd oil for other investigational non- proven uses. the main medical use of cbd oil is indeed not to improve epilepsy but to relieve chronic pain. among the various painful conditions people use cbd oil for inflammatory joint disorders such as rheumatoid arthritis osteoarthritis rank first. what is cbd oil good for?
– cbd oil for pain pain relief is probably the most common use of cbd or hemp oil. there’ s no shortage of anecdotal evidence that cbd oil is good for quick and sustainable pain relief without the risk of addiction common to traditional pharmaceutical options. does cbd oil really work? a doctor weighs in cbd oil has been touted as a cure- all for everything from anxiety to depression, but experts say more human research is needed to back up the claims. if you are trying to get rid of a prolonged illness, chances are the effects will take longer to work but if you are only taking cbd oil to enhance your overall health – the cbd oil is likely to start working almost instantly. other factors that what should be kept in account include mode of consumption and the actual dosage that is used. cbd oil dosage: 300mg 600mg, what 1000mg options. like we said once you start using cbd oil more frequently , are able to gauge how much you need you can jump up to the more high- potency products as needed. for reference, doses typically range anywhere from 5 mg to 100+ mg in a single day.
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generally plantar fasciitis patients report about pain aches beneath the heel though some may feel pain within the midfoot bottom region. normally only one foot gets affected, but in severe cases both the feet get impacted. some of the symptoms of plantar fasciitis include:. before going ahead talk about how does turmeric can help let us discuss a bit about the disease itself. cbd oil for anxiety dose. the plantar fascia is a thick tissue band that is found along the length of the underside of our feet. it connects our toes to our heel bone. plantar fasciitis ( heel spurs) is a medical condition. green borneo kratom has been reported to give mood boosts as well as a significant analgesic power that is noticeably superior to that of other commonly available strains of kratom; this is one of the most powerful , significant relaxation benefits effective strains of kratom leaf. ezkratom review – best kratom vendor or just a scam( ). authentic plant ap uncategorized.
save saved removed 0. that is before making a purchase of kratom it is important to read online kratom vendor reviews like their quality comparative prices on. best verified kratom vendors. table of contents. super speciosa; the kratom syndicate. asks for reviews on what does cbd oil do to you each order and in case of any inconvenience refunds all the money. 70hm kratom vendor was one of the most reputable companies in the kratom industry no wonder we used the platform as a. red thai kratom is one of the most extensively used kratom strains in the entire world. the extremely relaxing effects of this fantastic strain have increased its popularity over the years. top best brands cbd oil. red thai kratom gets its name from its red- veined leaves that what does cbd oil do to you grow mainly in areas of thailand. rising phoenix kratom provides five extract count in each container.
our extracts are 20: 1 ratio offering a super concentrated green maeng da kratom. our finely milled powder get you the most kratom. we use no filters ensuring only our 100% all- natural kratom in every extract. kratom for sale in phoenix. kratom mitragyna speciosa, which is also frequently referred to by its scientific name hails from the rainforests of southeast asia. kratom the gardenia, is commonly made from the dried leaves of the kratom tree, which has smooth, grey bark , which is related to coffee grows up to 82 feet tall. red vein indo kratom is sometimes difficult to find. entourage cbd oil 30 mg. part of the reason is that the naming system is not always consistent from one manufacturer to another. try red vein borneo kratom for an identical experience to the one described above. another interesting comparison can be had by trying red vein kratom products from other parts of southeast.
you can does look here to know health benefits of hemp oil, especially what are the health benefits of hemp oil for weight loss? there are several ways to lose weight such as health benefits of elaichi for weight loss, one of them is by using hemp oil. hemp oil contains omega- 3 fatty acids that are good and needed by your body. a tincture or oil generally refers to the same product derived from hemp. phenibut and kratom combination. if you want to make certain, you can ask for an ingredient list from the manufacturer of your supplement. how does cbd oil work for weight loss? one reason why cbd oil is helpful for weight loss is the way in which it affects your appetite. cbd interacts with the endocannabinoid system in your body.
how taking cbd oil for weight loss works involves this system. cbd stimulates different components in your body to help your body break down more fat , decreases lipid production, suppresses appetite, it helps burn more calories all the way down to the cellular level increases your. the bottom line is that cbd oil doesn’ t have the same effect as traditional cannabis. rather it is a non- psychoactive cannabinoid that is found in the cannabis plant is becoming popular for its various health benefits. the association between cbd oil weight loss is confusing since certain cannabis strains are known for increasing.
What does cbd oil do to you
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What does cbd oil do to you
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Two Exercises You Can Do Today for Stronger Bones
Low angle of group of athletic senior people stretching in fitness studioMaintaining livelihood and mobility takes work. Strong, healthy bones play an essential role in keeping you moving.
You might not believe it, but you have to work hard for healthy bones. Time is not on your side. Bones weaken with age, and this can lead to serious conditions like osteopenia and osteoporosis.
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It may seem strange, but your body is naturally inclined to lose bone as you get older. It’s your job to make sure you do what you can to keep it hanging around. If you don’t, you’re at an increased risk for bone breaks.
Getting adequate vitamin D and calcium is essential to maintaining strong, healthy bone and limiting bone loss. But they can only take you so far.
You see, calcium and vitamin D can stop bone loss by helping bone to rebuild. However, you need to give your body a reason—let’s call it encouragement—to build bone.
Think of it like muscle: if you don’t use it, you lose it.
Exercise gives your body encouragement to build bone. It puts stress on the bone so it becomes stronger.
Walking, jogging, hiking, resistance training, and more all make your body work against gravity to retain bone or make it stronger. These weight-bearing movements can stimulate bone production and potentially reduce the risk of osteopenia and osteoporosis.
Stronger muscles are an added benefit to your bones. They can help improve balance and make bones more resilient to bumps.
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Core strength is another essential component of bone health. Abdominal exercises, lower back exercises, yoga, Pilates, and tai-chi can be useful in strengthening the spine, which is prone to fractures and encouraging better balance.
If you can, get 30 minutes of weight-bearing exercise five times per week. You can switch it up, perhaps going for a walk on three days and doing tai chi, or another exercise, the remaining two days.
Maintaining bone strength can help you hold onto your livelihood and ultimately make life a little safer. Use these exercise ideas to bolster bone-healthy nutrition.
Author Bio
Devon Andre has been involved in the health and dietary supplement industry for a number of years. Devon has written extensively for Bel Marra Health. He has a Bachelor of Forensic Science from the University of Windsor, and went on to complete a Juris Doctor from the University of Pittsburgh. Devon is keenly aware of trends and new developments in the area of health and wellness. He embraces an active lifestyle combining diet, exercise and healthy choices. By working to inform readers of the options available to them, he hopes to improve their health and quality of life.
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6323511/
https://www.bones.nih.gov/health-info/bone/bone-health/exercise/exercise-your-bone-health#:~:text=Weight%2Dbearing%20and%20resistance%20exercises,weights%20%E2%80%93%20can%20also%20strengthen%20bones.
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Overhydration
Robert A. Star
University of Texas, Southwestern Medical Center, Dallas, Texas 75235-8856
Diuretics, especially thiazide diuretics, are a frequent cause of hyponatremia. Paradoxically, loop diuretics can be important adjuncts in the treatment of acute symptomatic hyponatremia, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), and diabetes insipidus.
HYPONATREMIA
Hyponatremia is caused by water retention due to a continued water intake more than the ability of the kidneys to excrete electrolyte-free water. The resulting hypo tonicity causes water movement into cells, with cell swelling. Swelling of brain cells causes cerebral edema, which results in the neurologic symptoms of hyponatremia. Since brain cells regulate their volume, patients are symptomatic only if the hyponatremia is acute or very severe.
What is the cause of the water retention? Normally, hyponatremia should suppress the secretion of antidiuretic hormone (arginine vasopressin or AVP), decreasing the water permeability of the collecting duct system, allowing the excess water to be excreted. However, AVP release is controlled by both osmotic and nonosmotic stimuli. In the latter case, AVP is released in response to non-osmotic stimuli such as reductions in effective arterial volume, irrespective
Diuretic Agents: Clinical Physiology and Pharmacology
Copyright © 1997 by Academic Press. All rights of reproduction in any form reserved.
TABLE 1 Etiology of Hyponatremia
Volume depletion
GI losses
Vomiting, diarrhea
Renal losses Diuretics, hypoaldosteronism, salt-wasting
Skin losses burns, cystic fibrosis
Abdominal sequestration; peritonitis; arsenic or mercury poisoning; pancreatitis, etc.
Potassium depletion
Normal
Primary polydipsia Hypothyroidism Glucocorticoid deficiency Drugs (see Table 2) Nausea, pain SIADH
Beer potomania
Volume excess
Congestive heart failure
Hepatic cirrhosis with ascites
Nephrotic syndrome with severe hypoalbuminemia
Renal failure of whether total extracellular volume (ECF) is reduced as in vomiting or expanded as in heart failure or cirrhosis with ascites, or normal as in pain, nausea or drugs. Indeed, except for patients with psychogenic polydipsia, all patients with sustained hyponatremia have elevated AVP levels. Therefore, it is helpful to categorize the conditions associated with hyponatremia by the volume status of the patients (decreased, normal, or increased; see Table 1). Hyponatremia occurs in beer potomania because the ability to excrete free water is decreased because of poor dietary intake [ 10]. Beer drinkers may ingest only 250 mOsmol/day or less of sodium, potassium, or protein. Hyponatremia will occur if they ingest more than 5 liters of water a day (since the minimum achievable urine osmolality is 50 mOsm).
Mild hyponatremia is a relatively common complication of diuretic therapy [ 16]. However, if patients drink large volumes of water, as occurs for unknown reasons in elderly women [6], severe hyponatremia may result. Three mechanisms contribute to the hyponatremia: (i) volume depletion causes increased AVP as discussed above, (ii) potassium depletion causes an intracellular shift of sodium for potassium, and (iii) impaired renal free water formation as a result of diminished delivery of filtrate (increased proximal reabsorption) or inhibition of sodium reabsorption in the diluting segments (loop of Henle and distal tubule). As described in Chapter VC1, most cases of hyponatremia are caused by thiazides, not loop diuretics. This occurs because they act at different sites along the nephron. Thiazides act primarily in the distal convoluted tubule and initial collecting duct to promote hypertonic salt loss. The loss of salt causes volume retention, and AVP induced water retention. The urine sodium + po tassium concentrations average about 150 mM, while plasma levels were below 110 mM. In contrast, loop diuretics act at the medullary thick ascending limb, causing hypotonic or isotonic fluid loss, in part, because they decrease medullary hypertonicity. Thus, hyponatremia is distinctly uncommon.
Hyponatremia generally occurs within the first 2 or 3 weeks of diuretic therapy. After this time, a new steady state is established in which water and solute intake is balanced by excretion. However, hyponatremia can become worse if vomiting, diarrhea, increased water intake, or a new drug is added.
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Research Article
VSIG4, a B7 family–related protein, is a negative regulator of T cell activation
Lorenz Vogt1, Nicole Schmitz1, Michael O. Kurrer2, Monika Bauer1, Heather I. Hinton1, Silvia Behnke2, Dominique Gatto1, Peter Sebbel1, Roger R. Beerli1, Ivo Sonderegger3, Manfred Kopf3, Philippe Saudan1 and Martin F. Bachmann1
1Cytos Biotechnology AG, Zurich-Schlieren, Switzerland. 2Department of Pathology, University Hospital, Zurich, Switzerland. 3Molecular Biomedicine, Swiss Federal Institute of Technology, Zurich, Switzerland.
Address correspondence to: Martin F. Bachmann, Cytos Biotechnology AG, Wagistrasse 25, 8952 Zürich-Schlieren, Switzerland. Phone: 41-1-733-47-07; Fax: 41-1-733-47-57; E-mail: [email protected].
Published October 2, 2006
Submitted: May 18, 2005; Accepted: July 18, 2006.
T cell activation by APCs is positively and negatively regulated by members of the B7 family. We have identified a previously unknown function for B7 family–related protein V-set and Ig domain–containing 4 (VSIG4). In vitro experiments using VSIG4-Ig fusion molecules showed that VSIG4 is a strong negative regulator of murine and human T cell proliferation and IL-2 production. Administration to mice of soluble VSIG4-Ig fusion molecules reduced the induction of T cell responses in vivo and inhibited the production of Th cell–dependent IgG responses. Unlike that of B7 family members, surface expression of VSIG4 was restricted to resting tissue macrophages and absent upon activation by LPS or in autoimmune inflammatory foci. The specific expression of VSIG4 on resting macrophages in tissue suggests that this inhibitory ligand may be important for the maintenance of T cell unresponsiveness in healthy tissues.
See the related Commentary beginning on page 2590.
Introduction
T cell responses are regulated by a complex network of activating and inhibitory signals. Recognition of peptides presented by MHC molecules is usually not sufficient for full T cell activation, but additional signals from costimulatory molecules are required (14). The most prominent costimulatory molecule expressed on T cells is CD28, interacting with the B7 family members CD80 and CD86 (5, 6). Engagement of CD28 facilitates T cell activation by enhancing TCR-mediated signaling and reducing the number of TCRs that need to be engaged for activation (7, 8). CTLA-4, a close homolog of CD28, also engages CD80 and CD86 (5, 6). Yet it serves a completely different function, since it reduces rather than enhances T cell responses.
Novel members of the CD28/B7 families have been identified recently. ICOS, engaging ICOSL (9, 10), has a function homologous to that of CD28 and generally enhances T cell responses; under some conditions, ICOS stimulation appears to selectively favor induction of Th2 cells (11, 12). Moreover, ICOS has been shown to mediate CD28-independent antiviral responses (13, 14) and to enhance antibody responses and germinal center formation (15, 16). Another new member of the family is the inhibitory receptor programmed death 1 (PD-1), which interacts with PD-ligand 1 (PD-L1) (B7-H1) and PD-L2 (B7-DC) (1721). PD-1 has a function similar to that of CTLA-4 and downmodulates T cell responses (18, 19). The same is true for BTLA, a CD28 homolog interacting with herpesvirus entry mediator on APCs (22, 23). There are 2 more B7 homologs with unknown receptors on T cells, called B7-H3 (24) and B7-H4 (B7x, B7S1) (22, 25, 26). Their function is less well established. B7-H3 is upregulated upon inflammation and has been suggested to function as both a positive and negative regulator of T cell responses (27, 28). B7-H4 is also expressed on DCs upon activation and is thought to function as a negative regulator (25).
Here we report the identification of a novel function of V-set and Ig domain–containing 4 (VSIG4). In vitro experiments showed that VSIG4 is at least as potent at inhibiting T cell responses as PD-L1. Furthermore, VSIG4 inhibited proliferation of mouse as well as human T cells. In vivo, administration of VSIG4-Ig fusion molecules was able to inhibit the induction of CTL responses as well as the development of Th cell–dependent IgG responses. Hence, VSIG4 is a potent negative regulator of T cell responses.
Results
VSIG4, a B7 family–related protein. Considering the importance of B7 family members as regulators of immune responses, we set out to screen for members of this protein family. To do so, a search using HMMR software was performed in silico on a translated expressed sequence tag (EST) database using a hidden Markov model (HMM) profile of the ectodomain of all known B7 family members. Obtained hits were further narrowed using different filters as outlined in Methods. Two of the remaining hits turned out to be the mouse clones BC025105 and NM_177789, which were almost identical and obviously derived from the same mRNA encoding the protein VSIG4. The protein sequence encoded by these cDNAs displayed about 20% identity and shared conserved amino acids with known B7 family members (Figure 1). Based on this homology, we concluded that VSIG4 was a B7 family–related protein 3. In contrast to the B7 family members, which contain 2 IgG domains, VSIG4 contains 1 complete IgV-type domain and a truncated IgC-type domain.
Sequence and homology of VSIG4.Figure 1
Sequence and homology of VSIG4. (A) Amino acid sequence alignment of murine VSIG4 with the putative human ortholog Z39Ig. The N-terminal signal sequences determined according to von Heijne (53) are underlined. The 2 Ig domains are in italics, and identical amino acids are indicated with dots. The gaps are indicated with dashes. Bold letters correspond to the predicted transmembrane domain. Overall, the 2 proteins show 44% identity, and within the common extracellular domain (aa 1–139), 78% identity was found between VSIG4 and Z39Ig. (B) Percentage of identity between the extracellular domains of known B7 superfamily members.
Further screening with the mouse sequence led to the identification of the putative human ortholog named Ig superfamily protein 39 (Z39Ig; GeneBank accession number NM_007268). The amino acid sequence of Z39Ig shows 44% identity with mouse VSIG4 (Figure 1A). Although identities in a similar range are observed between human and mouse sequences for B7 family members (Figure 1B), this degree of identity is relatively low. However, the moderate homology may be explained by the different length of the mouse (280 aa) and the human (399 aa) open reading frames. The putative human ortholog contains 2 complete extracellular IgG domains, like the members of the B7 family. Detailed analysis of the common sequence within the extracellular domain (aa 1–139) reveals 78% identity between the mouse and the human protein (Figure 1A). Moreover, Vsig4 and Z39Ig are found in corresponding gene clusters on the mouse and human X chromosome, respectively (data not shown). Although Z39Ig has been described previously by others, little about its biological function is currently known (2931). Recently, monocytes isolated from PBMCs and mature DCs derived from umbilical cord hematopoietic progenitor cells were shown to express Z39Ig, and Z39Ig has been proposed to be involved in the regulation of immune responses mediated by phagocytosis and/or antigen presentation (32).
In summary, VSIG4 contains typical features of B7 family members, suggesting that it is a B7 family–related protein. The degree of sequence identity and the chromosomal location identify Z39Ig as the human ortholog of VSIG4.
VSIG4 is specifically expressed on resting tissue macrophages. To characterize the expression pattern of Vsig4, the expression of Vsig4 in various tissues and cell types was evaluated by quantitative PCR. Vsig4 was found to be expressed at high levels in the liver, DCs, neutrophils, and macrophages. Low expression was found in various other tissues, including lung, heart, spleen, and lymph nodes, while no Vsig4 expression was found in T and B cells (Figure 2A). Hence, Vsig4 expression appears to be present in macrophages, neutrophils, and DCs and in a variety of peripheral tissues.
VSIG4 is expressed on resting peritoneal macrophages and downregulated uponFigure 2
VSIG4 is expressed on resting peritoneal macrophages and downregulated upon activation. (A) VSIG4 copies normalized to GAPDH in the respective tissues or cell types are shown. Sm muscle, smooth muscle. (B) Characterization of anti-VSIG4 rabbit serum. Left: EL4 (filled histogram) or EL4-VSIG4 cells (black lines) were stained with anti-VSIG4. Right: Western blot analysis of lysates from 293 and 293-VSIG4 cells with anti-VSIG4. (C) Peritoneal macrophages (Mϕ), monocytes, and neutrophils from blood and spleen and activated and naive DCs were stained with anti-VSIG4 (black lines) and preimmune serum (filled histograms). Gating markers are indicated above the histograms. Half of the CD11b+/Gr1 cells from the peritoneum (resident macrophages) showed VSIG4 expression. (D) Resting peritoneal macrophages and macrophages activated in vivo by thioglycolate (Thio) or LPS for 3 days were isolated, stained for the expression of VSIG4, and analyzed by FACS as described for C. Histograms of the gated CD11b+/Gr1 cell population are shown. (E) Resting peritoneal macrophages and macrophages activated in vivo by thioglycolate and PBMCs from the same animals were isolated and analyzed for VSIG4 expression by Western blotting using polyclonal anti-VSIG4 antibodies. PerC, peritoneal cells. (F) Dot plots of cells isolated from the peritoneum and stained with the indicated cell-surface marker and VSIG4 rabbit serum. (G) Freshly isolated peritoneal macrophages were either stained directly or cultivated in the presence or absence of 10 μg/ml LPS for 3 days and stained with anti-VSIG4 (black lines) or preimmune serum (filled histogram). Histograms of the gated CD11b+/Gr1low cell population are shown. Representative stainings of at least 2 independent experiments are shown.
To determine cell-surface expression of VSIG4, we generated a polyclonal rabbit serum against the extracellular domain of VSIG4. We first tested the specificity of the rabbit serum in cell lines ectopically expressing VSIG4. To this end, EL4 cells transduced with a recombinant retrovirus expressing VSIG4 were generated (EL4-VSIG4). As shown in Figure 2B, VSIG4 surface expression was detected with anti-VSIG4 rabbit serum on EL4-VSIG4 cells, whereas no staining was observed on EL4 cells transduced with empty expression vector. No staining was observed with preimmune serum on either cell population (data not shown). To test whether the serum also recognizes VSIG4 in cell lysates, 293 cells were transiently transfected with a VSIG4 expression vector, and cells were lysed and analyzed by Western blot. A distinct band of 46 kDa was detected in cell lysates of 293 cells transfected with the VSIG4 expression vector, and no signal was observed in nontransfected 293 cells (Figure 2B). Taken together, these data demonstrate that the anti-VSIG4 rabbit serum specifically recognizes surface VSIG4 as well as VSIG4 protein in cell lysates.
Having established that anti-VSIG4 serum was specific, we set out to analyze VSIG4 surface expression in various cell types. Several bone marrow–derived cell types were analyzed for VSIG4 cell-surface expression. In accordance with the expression data shown in Figure 2A, naive and activated T and B cells did not show VSIG4 surface expression (data not shown). Moreover, naive and activated DCs, blood and splenic neutrophils, and granulocytes did not show VSIG4 surface expression (Figure 2C), although some of these cell types were positive for Vsig4 mRNA expression. In contrast, a subpopulation of resting peritoneal macrophages expressed high levels of VSIG4 (Figure 2C). In the next step, we analyzed VSIG4 expression on resting and activated macrophage populations. To this end, VSIG4 expression in resting peritoneal macrophages and peritoneal macrophages obtained after in vivo activation by LPS or thioglycolate for 3 days was assessed. In contrast to resting macrophages, inflammatory macrophages activated in vivo did not show VSIG4 expression (Figure 2D). These results were confirmed by Western blotting, since VSIG4 protein could only be detected in cell lysates of naive peritoneal macrophages, whereas no VSIG4 could be detected in cell lysates of thioglycolate-treated macrophages. PBMCs from control and thioglycolate-injected mice also did not express VSIG4 (Figure 2E). The slightly faster migration of VSIG4 observed in lysates of peritoneal macrophages compared with the one observed in 293 cells (Figure 2B) could be explained by different glycosylation of the protein in the different cell types. Taken together, these results suggest that VSIG4 expression is restricted to resting macrophages and that the expression is lost upon activation. Since VSIG4 was only observed in a subpopulation of resting peritoneal macrophages, we wondered whether the VSIG4-positive population differed from the VSIG4-negative cells in the expression of different surface markers. To this end, cells from the peritoneum were isolated and stained with anti-VSIG4 and anti-CD11b, -GR1, -F480, and –MHC class II antibodies and analyzed by FACS. As shown in Figure 2F, the VSIG4-positive population was CD11bhigh, GR1low, and F480high, demonstrating that only resident macrophages of the peritoneal lavage are positive for VSIG4 expression. However the VSIG4-positive population did not differ in the expression of either CD86 or MHC class II from the VSIG4-negative population of resident peritoneal macrophages (Figure 2F).
Taken together, these results suggest that VSIG4 expression is restricted to resting macrophages and is lost upon activation. To test this further, resting peritoneal macrophages were isolated from naive mice and either stained directly or cultivated for 3 days in the presence or absence 10 μg/ml LPS. As shown in Figure 2G, VSIG4 expression was reduced upon activation with LPS. Hence, VSIG4 is downregulated in vitro upon activation of the cells. The slightly reduced expression of VSIG4 observed in the cells that had not been activated compared with freshly isolated peritoneal macrophages may be explained by partial activation during cultivation of the cells in tissue culture plates. In summary, these results demonstrate that VSIG4 is expressed on naive resting macrophages and that the expression is lost upon activation of these cells. Moreover, infiltrating activated macrophages did not display detectable VSIG4 expression. The more restricted expression of VSIG4 assessed by antibody staining compared with that assessed by RT-PCR is not without precedent, since mRNA for B7-H1 is found in many tissues, while protein expression is largely restricted to professional APCs (1721). In addition, most tissues, in particular the liver, contain resting macrophages as a potential source of VSIG4 expression. Indeed, histological analysis showed expression of VSIG4 macrophages in many tissues, including liver, thymus medulla, adipose tissue, and the heart (Figure 3; see also Figure 4 for costaining with CD68 and CD11b). In myocardium, a slightly uneven, at times patchy distribution of VSIG4-positive macrophages was seen. VSIG4 was not detected in intestines, kidney, skeletal muscle, salivary gland, lymph node, splenic white pulp, lung, and brain (data not shown).
VSIG4 is expressed on resting tissue macrophages.Figure 3
VSIG4 is expressed on resting tissue macrophages. Organs of untreated mice were assessed for VSIG4 expression by histology. (A and E) Kupffer cells lining the sinusoids of the liver were evenly positive for VSIG4. (B and F) Occasional macrophages of the red pulp of the spleen were positive, while macrophages of the white pulp were negative for VSIG4 (B). Within the red pulp (F), iron-laden macrophages (a weak granular signal was derived from the iron) were negative (small arrow), while other macrophages were weakly positive for VSIG4 (large arrowheads). (C and G) The myocardium showed an uneven distribution of VSIG4-positive macrophages. VSIG4 was also detected in tissue-resident macrophages of adipose tissue (D). VSIG4 was absent in thymic cortex and detected in rare macrophages of the thymic medulla (H). Representative stainings of at least 2 independent experiments are shown. Original magnification, ×60 (AD); ×150 (EH).
Macrophages in autoimmune infiltrates of the heart do not express VSIG4.Figure 4
Macrophages in autoimmune infiltrates of the heart do not express VSIG4. Myocarditis was induced by immunization with α–myosin heavy chain–derived peptide in CFA (CFA/Myhca), and as a control, untreated mice were used. Heart sections from inflamed hearts and control hearts were stained with VSIG4 (green) together with CD68, MHC class II (MHC II), or CD11b (red) as indicated. In untreated mice, a fraction of CD68- or CD11b-positive tissue-resident macrophages coexpressed VSIG4. (Note that all VSIG4-positive cells coexpressed Cd11b; in some cases, Cd11b expression was low, precluding visualization of the expression in an overlay image). In contrast, MHC class II–positive DCs showed no coexpression of VSIG4. In CFA/Myhca-immunized mice, inflammatory foci included numerous CD68-positive macrophages that showed no coexpression of VSIG4. Occasional VSIG4-positive macrophages were detected in the myocardium surrounding the inflammatory focus. On a consecutive histological section, abundant MHC class II expression was detected within the inflammatory infiltrate, probably mostly on activated macrophages. Representative stainings of at least 2 independent experiments are shown. Original magnification, ×150.
VSIG4 is downregulated in autoimmune tissue. Since VSIG4 was downregulated on macrophages activated by LPS or thioglycolate, we wanted to assess whether VSIG4 may also be absent on macrophages in autoimmune tissue. Thus, female BALB/c mice were immunized and boosted with myosin-derived peptides, leading to autoimmune inflammation of the heart (33). Three weeks later, VSIG4 expression was assessed on control heart and diseased heart. In the healthy tissue, VSIG4 expression was found on a fraction of CD68+ and CD11b+ macrophages but not on MHC class IIhigh DCs (Figure 4). In contrast, VSIG4 expression was not found in the confluent inflammatory infiltrates of hearts with myocarditis (Figure 4). Very rarely, a single VSIG4-positive macrophage could be detected within an inflammatory focus, and macrophages outside inflammatory foci expressed VSIG4 in normal numbers and unremarkable distribution (data not shown). This indicates that absence of VSIG4 expression was restricted to actual sites of inflammation. These histological data further support the notion that VSIG4 is downregulated upon the activation of the cells.
VSIG4 is a negative regulator of T cell proliferation. To study the function of the putative member of the B7 family, the extracellular domain of VSIG4 (aa 1–186) was fused to the human IgG1 constant region and expressed in 293-EBNA cells. The soluble fusion molecule was named VSIG4-Ig. Bearing in mind the importance of costimulatory molecules in positive and negative regulation of T cell activation, we first tested the role of VSIG4 in vitro in T cell proliferation assays. Briefly, increasing concentrations of anti-CD3 antibody (0, 0.25, 5, and 1 μg/ml) were coated in the presence of 5 μg/ml VSIG4-Ig or control IgG1. Purified CD4+ T cells were added, and proliferation was assessed after 48 hours by [3H]thymidine incorporation. As shown in Figure 5A, dose-dependent proliferation of T cells was observed with increasing concentrations of anti-CD3 antibody. Inclusion of immobilized VSIG4-Ig led to a strong reduction in T cell proliferation as compared with IgG1 at all 3 anti-CD3 concentrations used. IL-2 levels were also strongly reduced in culture supernatants of CD4+ T cells incubated in the presence of VSIG4 (Figure 5B). The inhibitory activity of VSIG4 on CD8+ T cells was analyzed next (Figure 5D). Proliferation assays as described above were performed with a fixed concentration of anti-CD3 (0.5 μg/ml) in the presence of 5 or 10 μg/ml VSIG4-Ig or control IgG1. As shown in Figure 5B, the inclusion of immobilized VSIG4-Ig fusion protein strongly inhibited proliferation of CD8+ T cells at both concentrations of VSIG4-Ig.
VSIG4 inhibits T cell proliferation and IL-2 production in vitro.Figure 5
VSIG4 inhibits T cell proliferation and IL-2 production in vitro. (A) Plates were coated with anti-CD3 at the indicated concentrations in the presence of 5 μg/ml VSIG4-Ig or control IgG1. Proliferation of purified CD4+ T cells was monitored after 2 days by [3H]thymidine incorporation. (B) Plates were coated with anti-CD3 at 0.5 μg/ml in the presence of 5 or 10 μg/ml VSIG4-Ig or IgG1 at the indicated concentrations. CD8+ T cell proliferation was monitored after 2 days by [3H]thymidine incorporation. (C) Costimulation assays were performed with purified CD4+ T cells with a fixed concentration of anti-CD3 (0.5 μg/ml) in the presence or absence of anti-CD28 (2 μg/ml) with either 5 μg/ml VSIG4-Ig or control IgG1. (D) IL-2 production of CD4+ T cells stimulated with 0.5 μg/ml anti-CD3 in the presence of 5 μg/ml VSIG4-Ig or control IgG1. (E) Proliferation assays were performed in the presence of 0.5 μg/ml anti-CD3 and VSIG4-Ig, PD-L1–Ig, PD-L2–Ig, or control IgG1 at a concentration of 10 μg/ml. (F) Proliferation assays were performed in the presence of 0.5 μg/ml anti-CD3 and VSIG4-Ig or control IgG1 at a concentration of 5 or 10 μg/ml in the absence or presence of 10 ng/ml IL-2. Error bars represent standard deviations for data from experiments performed in triplicate. Representative data from least 2 independent experiments are shown. The difference between VSIG4-Ig– and IgG1-treated cells was significant in all panels shown (P < 0.05). In F, the difference between VSIG4-Ig– and IgG1-treated cells in the presence of IL-2 was not significant (P > 0.05).
Having established that VSIG4-Ig is a strong inhibitor of T cell proliferation induced by anti-CD3, we wondered whether VSIG4-Ig could also inhibit T cell proliferation induced by anti-CD3 and anti-CD28. For this purpose, costimulation assays were performed with a fixed concentration of anti-CD3 (0.5 μg/ml) in the presence or absence of anti-CD28 (2 μg/ml) with either 5 μg/ml VSIG4-Ig or control IgG1. Purified CD4+ T cells were added, and proliferation was assessed by [3H]thymidine incorporation. VSIG4-Ig strongly inhibited proliferation of anti-CD3 as well as anti-CD3/anti-CD28–stimulated T cells (Figure 5C).
To benchmark the potency of VSIG4 as a negative regulator of T cell activation, we compared its inhibitory properties with those of PD-L1 and PD-L2, two well-known inhibitors of T cell activation. To this end, costimulation assays were performed with a fixed concentration of anti-CD3 (1.0 μg/ml) in the presence of 10 μg/ml VSIG4-Ig, PD-L1–Ig, or PD-L2–Ig. VSIG4 inhibited T cell proliferation at least as potently as PD-L1 and PD-L2 (Figure 5E).
Since incubation of T cells with VSIG4-Ig led to the inhibition of T cell proliferation with a concomitant reduction in IL-2 secretion, we wondered whether T cell proliferation could be rescued by the addition of IL-2. To this end, costimulation assays were performed with a fixed concentration of anti-CD3 with either 5 or 10 μg/ml VSIG4-Ig or, as a control, human IgG1 in the presence or absence of 10 ng/ml IL-2. Purified T cells were added, and proliferation was assessed by [3H]thymidine incorporation. The inhibitory activity of VSIG4-Ig could be abolished by the addition of IL-2 (Figure 5F). These results confirm the specific inhibitory activity of VSIG4-Ig and rule out unspecific toxic effects of the protein preparation.
As outlined earlier, based on the high degree of conservation as well as the genomic locus, we postulated that Z39Ig is the human ortholog of VSIG4. To test whether Z39Ig also negatively regulates T cell proliferation, the extracellular domain of Z39Ig (aa 1–280) was fused to the human IgG1 constant region and expressed in 293-EBNA cells. Costimulation assays as described above were performed with a fixed concentration of anti-CD3 (0.5 μg/ml) in the presence or absence of anti-CD28 (2 μg/ml) with either 5 μg/ml Z39Ig-Ig or control IgG1. Purified murine CD4+ T cells were added, and proliferation was assessed by [3H]thymidine incorporation. As shown in Figure 6A, Z39Ig-Ig strongly inhibited proliferation of anti-CD3– as well as anti-CD3/anti-CD28–stimulated murine T cells, documenting that the inhibitory function of VSIG4 is conserved across the species barrier. Furthermore, simulation of human CD4+ T cells with anti-CD3 resulted in reduced proliferation in the presence of plastic-bound Z39Ig-Ig (Figure 6B). These results demonstrate that VSIG4 functions as a negative regulator of mouse as well as human T cells.
Z39Ig, the human homolog of VSIG4, inhibits T cell proliferation.Figure 6
Z39Ig, the human homolog of VSIG4, inhibits T cell proliferation. (A) Proliferation assays were performed with purified mouse CD4+ T cells with 0.5 μg/ml anti-CD3 in the presence or absence of 2 μg/ml anti-CD28 with Z39Ig-Ig (human VSIG4) or control IgG1 at a concentration of 5 μg/ml. (B) Proliferation assays were performed with CD4+ T cells purified from human PBMCs in the presence of the indicated amounts of anti-CD3 together with Z39Ig-Ig (human VSIG4) or control IgG1 at a concentration of 20 μg/ml. Error bars represent standard deviations for data from experiments performed in triplicate. Representative data from at least 2 independent similar experiments are shown. The differences between Z39Ig-Ig– treated cells compared with control IgG1–treated cells were significant (P < 0.05) in both A and B.
In conclusion, these data demonstrate that VSIG4 is a strong negative regulator of T cell activation, providing further evidence that VSIG4 is indeed a B7 family–related protein.
VSIG4 negatively regulates CD8+ T cell responses and Th cell–dependent IgG responses in vivo. Having established the function of VSIG4 in vitro, we further explored the function of VSIG4 in vivo. We have previously shown that immunization of mice with peptide p33 derived from lymphocytic CMV glycoprotein coupled to virus-like particles (VLPs) derived from the bacteriophage Qβ induce strong primary CTL responses in mice (34, 35). To evaluate the in vivo effect of VSIG4 on the induction of CTLs, mice were treated with soluble VSIG4 (VSIG4-Ig) or a control protein (human IgG1 antibody) during vaccination with VLPs (Figure 7A). Accordingly, mice were injected i.p. on days –1, 1, and 3 with either mVSIG4-Ig or control IgG1. On day 0 mice were immunized with 50 μg of p33-Qβ mixed with CpGs as an adjuvant. To analyze specific cellular immune responses, p33-specific CD8+ T cells were measured in the 2 experimental groups by p33-specific tetramer staining 7 days after immunization. As shown in Figure 7B, immunized mice treated with VSIG4-Ig had a roughly 2.3-fold reduction in the number of p33-specific T cells in the blood. To further assess cellular T cell responses, intracellular IFN-γ production by splenic CD8+ T cells was measured by intracellular staining followed by FACS. As shown in Figure 7C, a 3.5-fold reduction in frequencies of IFN-γ–producing cells was observed in mice treated with VSIG4-Ig. Hence, similar to what was observed in vitro, VSIG4 inhibits CD8+ T cell activation in vivo.
Soluble VSIG4 inhibits induction of CTL responses and Th cell–dependent humFigure 7
Soluble VSIG4 inhibits induction of CTL responses and Th cell–dependent humoral immune responses in vivo. (A) Experimental diagram. Mice were injected with VSIG4-Ig or control IgG i.p. on days –1, 1, and 3 and immunized with Qβ-p33 VLPs with CpGs on day 0. Qβ-specific IgM and IgG responses were measured after 4 and 10 days. p33-specific CD8+ T cells were determined in the blood by tetramer staining on day 7. Mice were sacrificed on day 10, and levels of Qβ-specific B cells, AFCs, and p33-specific IFN-γ–expressing CD8+ T cells were determined from spleens. (BG) Averages of 2 independent experiments ± SEM are shown (n = 8). Differences between VSIG4-Ig– and IgG1-treated mice were significant in B, C, and the right panel of D, as well as F and G. P values obtained by Student’s t test are shown. (B) Percentage p33-specific CD8+ T cells. (C) Percentage p33-specific CD8+ T cells after in vitro stimulation with p33-pulsed DCs 10 days after immunization. (D) ELISA titers of the Qβ-specific IgM and IgG responses. (E) Staining and gating strategy for the detection of isotype-switched B cells by FACS. Activated, isotype-switched B cells were found in the indicated gate. A representative example of Qβ-binding B cells in the indicated gate is shown in the right panel. (F) Percentage of Qβ-specific B cells within the indicated gate in E in mice 10 days after immunization. (G) Number of Qβ-specific AFCs per 106 splenocytes as determined by ELISPOT are shown.
Humoral immune responses in the same mice were studied next. We have previously shown that Qβ VLPs induce an early, Th cell–independent IgM response followed by a Th cell–dependent IgG response (34, 36). To evaluate the in vivo effect of VSIG4 on the induction of humoral responses, IgG antibody titers, the number of antibody-forming cells (AFCs), and the number of Qβ-specific B cells were determined 10 days after immunization. Moreover, Qβ-specific IgM antibody titers were measured on day 4. The Th cell–independent IgM response was only marginally affected by treatment with VSIG4-Ig. In contrast, the Th cell–dependent IgG response against Qβ was reduced about 2-fold in mice treated with VSIG4-Ig (Figure 7D).
To further characterize B cell responses, Qβ-specific B cells were enumerated by FACS (36). Activated and isotype-switched B cells downregulate surface expression of IgM and IgD. Thus, in order to specifically stain Qβ-specific, isotype-switched B cells, a population of CD19+ B cells expressing low levels of IgM and IgD was assessed for its ability to bind Qβ (Figure 7E). As shown in Figure 7F, the percentage of Qβ-specific, isotype-switched B cells was reduced by a factor of about 2 in the VSIG4-treated animals. Numbers of Qβ-specific AFCs were assessed by ELISPOT and found to be decreased by a factor of about 3 (Figure 7G).
In summary, treatment of immunized mice with VSIG4-Ig inhibited Th cell–dependent IgG responses, as documented by reduced specific IgG titers and reduced frequencies of Qβ-specific B cells and AFCs. In contrast, the Th cell–independent Qβ-specific IgM response was only marginally affected by VSIG4. Thus, VSIG4-Ig appears to inhibit B cell responses by blocking T help.
Discussion
The induction of specific T cell responses is a tightly regulated process. While research initially focused on costimulatory molecules enhancing T cell activation, the list of inhibiting receptor-ligand pairs is growing (23, 37, 38).The present study describes the identification of VSIG4 as potent inhibitor of T cell activation.
All B7 homologs described so far share a characteristic expression pattern: they are expressed at relatively low levels on resting cells and are upregulated in response to inflammatory signals. Some of the B7 family members, such as B7-1 and B7-2 as well as B7-H4, are largely restricted to professional APCs, such as DCs and macrophages, while others, e.g., B7-H1, are expressed rather in nonimmunological tissues, especially upon stimulation with inflammatory cytokines. It is thought that most of the B7 family members have the ability to engage both activating and inhibitory receptors on T cells; whether or not T cells become activated appears to depend on the timing of the interaction, since inhibitory receptors are preferentially expressed on activated cells (6). Interestingly, VSIG4 has a different expression pattern; it is highly expressed on resting, peripheral tissue macrophages and is downregulated or lost upon activation. In addition, little expression is found on macrophages in lymphoid organs. Hence, the main function of VSIG4 may not be the downregulation of an ongoing T cell response but rather the prevention of T cell activation in the intact tissue. Only upon inflammatory insult is VSIG4 downregulated or superseded by de novo infiltrating VSIG4-negative macrophages, which subsequently allow for proper T cell responses in peripheral tissues. It is tempting to speculate that VSIG4 may therefore be involved in the maintenance of peripheral T cell tolerance and/or nonresponsiveness. Indeed, VSIG4 was not present in the inflammatory infiltrates in tissue affected by autoimmune disease. This concept is supported by the finding that resting DCs induce T cell tolerance rather than T cell activation (39, 40). Additionally, and not mutually exclusively, it is possible that VSIG4 induces the differentiation of regulatory T cells. However, in preliminary in vitro experiments, we did not observe an increased production of antiinflammatory cytokines by T cells upon stimulation with VSIG4 (data not shown).
The mechanism of VSIG4-mediated inhibition of T cell activation remains to be established. Although our data show that VSIG4 is able to directly inhibit T cell proliferation in vitro, it remains possible that VSIG4 may influence T cell activation indirectly in a manner similar to that described for CTLA-4. CTLA-4 is able to inhibit T cell activation through recruitment of the phosphatase shp-2, which reduces TCR-dependent signal transduction by dephosphorylation of signaling molecules (41, 42). Yet T cell responses mounted by CTLA-4–deficient, TCR-transgenic T cells are remarkably normal (43, 44). The more important function of CTLA-4 may therefore be to maintain peripheral tolerance. Indirect and direct mechanism(s) may account for this function, since CTLA-4 has been shown to be involved in the generation of regulatory T cells as well as inducing T cell anergy (4549).
While we were revising the current manuscript, a study was published describing VSIG4 as a novel complement-binding protein, CRIg (binding C3b and iC3b), specifically expressed by tissue macrophages, in particular Kupffer cells. This is an intriguing finding demonstrating that the complement system has not only receptors for fine-tuning of B cell responses (CD21) but also links the innate immune system with the regulation of T cell activation. Interestingly, binding of C3b or iC3b to VSIG4/CRIg triggers internalization of the receptor (50), suggesting that activation of the complement cascade removes the inhibitory properties of tissue macrophages, promoting inflammation. Hence, VSIG4/CRIg may be a new pathway of adaptive immune regulation by the innate immune system.
In conclusion, VSIG4 was shown to be a strong inhibitor of T cell proliferation in vitro and in vivo. The restricted expression of VSIG4 on resting tissue macrophages suggests that VSIG4 plays an important role in the maintenance of T cell unresponsiveness in healthy tissue.
Methods
Cloning of full-length VSIG4, VSIG4 protein expression, and production of polyclonal antibodies. Protein sequences of both human and mouse B7 family members including CD80, CD86, B7-H1, B7-H2, and B7-H3 were used to generate an HMM. Translated EST sequences were subjected to an HMM search using HMMR software (51). Known proteins such as B7 family members, butyrophilins, and myelin oligodendrocyte glycoproteins were eliminated, and redundant sequences were grouped. Remaining sequences were further analyzed for the occurrence of a catalog of different features such as particular domains and specified intrinsic features (N-terminal signal sequence, transmembrane domain, and at least 1 IgG domain), which are included in the SMART (Simple Modular Architecture Research Tool) program (52).
The full-length mouse VSIG4 cDNA was generated by RT-PCR from mouse macrophage total RNA. The PCR was performed on mouse macrophage–derived cDNA as template using the High Fidelity PCR System (Roche Diagnostics) composed of a unique enzyme mix containing thermostable Taq DNA polymerase, a proofreading polymerase (catalog 1732650; Roche Diagnostics), and the primers LV80-mC18f (5′-GTAGCTTCAAATAGGATGGAG-3′) and LV81-mC18b (5′-AAACTGTGTTCAGCAGGCAG-3′). The resulting PCR product (867 bp) of mVSIG4 was cloned into the pGEM-T plasmid. The nucleic acid sequence of VSIG4 was then verified by DNA sequencing of several independent clones. Z39Ig was cloned as described above from spleen cDNA using the following primers: 5′-aggaggctggaagaaaggac-3′ and 5′-cccccggcagagatacta-3′. VSIG4-Ig was prepared by fusing the coding region of the extracellular domain (aa 1–186) of VSIG4 to the constant region of human IgG1. Similarly, the extracellular domain of Z39Ig (aa 1–280) was fused to the constant region of human IgG1. The expression construct were transfected into EBNA cells (Invitrogen) using Lipofectamine Plus (Invitrogen) and the protein produced under serum-free conditions. VSIG4-Ig and Z39Ig fusion proteins were purified using a Protein A Sepharose column according to the manufacturer’s recommendations (Pharmacia).
For the generation of polyclonal anti-VSIG4 serum, rabbits were immunized with VSIG4-Ig fusion protein. Ig-specific antibodies were quantitatively removed from VSIG4 rabbit serum on a Sepharose column coupled with IgG1.
Macrophage preparation and stainings. Macrophages were collected from the peritoneal cavity of BALB/c mice by washing the peritoneum with 5 ml of PBS/1% BSA. To generate activated macrophages, BALB/c mice were either injected i.p. with thioglycolate (500 μl, 4% solution) or LPS (50 μg in 100 μl), and inflammatory macrophages were obtained from the peritoneum after 3 days, as described above. For the in vitro stimulation experiment, resident peritoneal macrophages were cultured for 3 days in 6-well plates in Iscove’s modified Dulbecco’s medium and completed with glutamine, antibiotics, and 10% FCS and the indicated amount of LPS (Sigma-Aldrich). Surface stainings were performed in the presence of Fc block (anti-CD16/CD32) on ice in PBS/0.1% FCS. All antibodies were from BD Biosciences — Pharmingen, with the exception of F480 (AbD Serotec) and CD68 (Acris Antibodies).
T cell proliferation assay. Purified T cells were stimulated by immobilized anti-CD3 antibody in the presence of immobilized mVSIG4-Ig fusion protein. The splenic T cells were purified from naive mice using CD4- and CD8-specific MACS beads (Miltenyi Biotec). For costimulation and inhibition assays, purified T cells (2 × 105 cells/well) were cultured in 96-well flat-bottom plates that were precoated at 4°C overnight with 75 μl/well of a solution containing the indicated concentrations of mouse anti–CD3e chain antibody NA/LE (145-2C11; BD Biosciences — Pharmingen), as well as the indicated concentrations of mVSIG4-Ig fusion protein or control proteins, such as antibody against mouse CD28 NA/LE (37.51; BD Biosciences – Pharmingen), recombinant mouse B7-H1–Ig chimera (catalog 1019-B7; R&D Systems), recombinant mouse PD-L2–Ig chimera (catalog 1022-PL; R&D Systems), and mouse gamma globulin (catalog 015-000-002; Jackson ImmunoResearch Laboratories Inc.). For measurement of T cell proliferation, the plates were cultured for 48–60 hours, and [3H]thymidine (1 μCi/well) was added 10–16 hours prior to harvesting of the cultures. [3H]thymidine incorporation was measured with a Wallac MicroBeta TriLux Liquid Scintillation counter (PerkinElmer).
In vivo assessment of T and B cell responses. Animal experiments were conducted according to guidelines set by the Swiss Federal Veterinary Office (BVET) and were approved by the Kantonale Veterinäramt of Zürich. For the animal studies, 6- to 18-week-old female C57BL/6 mice were used and kept in a specific pathogen–free facility at Cytos Biotechnology AG. Mice were injected i.p. with 500 μg of mVSIG4-Ig fusion protein or, alternatively, human IgG1κ (catalog I-5154; Sigma-Aldrich) on days –1, 1, and 3. Mice were immunized s.c. with 50 μg VLPs derived from the bacteriophage Qβ coupled with peptide p33 derived from lymphocytic choriomeningitis virus (Qβp33) in the presence of the CpG 1585 (5′-GGGGTCAACGTTGAGGGGGG-3′ stabilized by phosphothioester bonds. Qβ-specific antibody responses were measured at the indicated time points as described previously (36). Peptide p33–specific T cell responses were measured by tetramer staining at the indicated time points, and intracellular cytokine staining was performed as described previously using peptide p33–loaded DCs for stimulation (35). Qβ-specific B cells were enumerated by flow cytometry as described previously (36). Qβ-specific AFCs were measured by ELISPOT as described previously (36).
Induction of myocarditis and histological analysis. Wild-type BALB/c female mice at age 8–10 weeks were immunized on days 0 and 7 with 100 μg of a murine-specific α–myosin heavy chain–derived peptide (myhc-α 614–629 [Ac-SLKLMATLFSTYASAD-OH]) in a 1:1 emulsion with CFA (1 mg/ml; H37Ra; Difco; BD Diagnostics). All experiments were in accordance with Swiss federal legislation were approved by the Kantonale Veterinäramt of Zürich. Twenty-one days after the immunization, hearts were removed, OTC embedded, and frozen. Seven-micrometer cryostat sections were fixed in acetone and then processed for antibody staining according to standard protocols. The following antibodies were used: anti–MHC class II (MCA46B; Serotec), anti-CD68 (MCA1957; Serotec), anti-CD11b (BD Biosciences — Pharmingen), and polyclonal anti-VSIG4 antibodies. For secondary incubation, HRP- or alkaline-phosphatase–labeled goat anti-rat Ig antisera were used. For 2-color immunofluorescence studies, Cy3-labeled anti-rat Ig and Alexa 488–labeled anti-rabbit Ig sera were used. DAPI-containing cover medium was used for counterstaining.
Statistics. Two-sided Student’s t tests were performed using Excel Software. P ≤ 0.05 was considered significant.
Acknowledgments
We would like to thank Annette Oxenius for helpful discussions.
Footnotes
Nonstandard abbreviations used: AFC, antibody-forming cell; HMM, hidden Markov model; PD-1, inhibitory receptor programmed death 1; PD-L1, PD-ligand 1; VLP, virus-like particle; VSIG4, V-set and Ig domain–containing 4; Z39Ig, Ig superfamily protein 39.
Conflict of interest: L. Vogt, N. Schmitz, M. Bauer, H.I. Hilton, D. Gatto, P. Sebbel, R.R. Beerli, P. Saudan, and M.F. Bachmann are employed by Cytos Biotechnology AG and own stock or stock options in the company.
Citation for this article:J. Clin. Invest.116:2817–2826 (2006). doi:10.1172/JCI25673
See the related Commentary beginning on page 2590.
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Health Shared Logo whiteHealth Shared Logo dark
Medicines to prevent kidney damage in Diabetes
blood glucose controlcalcium channel blockersweight lossdialysisquality of lifeblood pressure controlkidney healthheart healthavoiding dialysis
Medicines to prevent kidney damage in Diabetes
Dr Mushtaqur Rahman, Consultant Endocrinologist and Diabetologist talks about various types of medicines which can be used to reduce the risk of Kidney failure in people with Diabetes. He talks about medicines to control blood glucose as well as medicines to reduce blood pressure including ACE inhibitors and ARB type drugs. He explains how medicines are best adjusted for Black and African heritage people as the benefits of certain other drugs are better.
More from this author:
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Women’s Wellness: UTI Treatment Without Antibiotics
About UTIs
A urinary tract infection (UTI) can knock you off your feet.
UTIs occur when bacteria enter the urinary tract and multiply. They affect one or more areas within the urinary tract. This can include the:
• urethra
• bladder
• ureters
• kidneys
They can cause:
• painful and frequent urination
• lower abdominal pain
• bloody urine
These infections are responsible for roughly 8 million doctor visits each year.
UTIs are the second most common type of infection to occur in the human body. They occur more often in women, but can affect men, too.
Women have a shorter urethra, so it’s easier for bacteria to enter their bladder. The National Institute of Diabetes and Digestive and Kidney Diseases estimates 40 to 60 percent of women will have at least one UTI in their lifetime.
Urinary tract infections in men are often related to an enlarged prostate (benign prostatic hypertrophy) blocking the flow of urine. This allows bacteria to have an easier time occupying the urinary tract.
In almost 90 percent of cases, the bacterium Escherichia coli is the cause of the UTI. E. coli is normally found inside the intestines. When confined to the intestines, it’s harmless. But sometimes this bacterium gets into the urinary tract and causes an infection.
Sex may trigger a UTI in women. This is because intercourse can move bacteria from the anal area to near the opening of the urethra. Women can lower their risk of infection by cleaning the genital area before any sexual activity and by urinating afterward.
Using spermicides, diaphragms, and condoms also raises the risk of a UTI. The risk is higher in people with a weakened immune system as well.
UTI stats
• UTIs are the second most common type of infection.
• E. coli is the cause of most UTIs, but viruses and other germs can also cause them.
• There are 8 million UTI-related doctor visits per year in the United States.
Why antibiotics sometimes don’t work
Most UTIs aren’t serious. But if left untreated, the infection can spread up to the kidneys and bloodstream and become life-threatening. Kidney infections can lead to kidney damage and kidney scarring.
Symptoms of a UTI usually improve within two to three days after starting antibiotic therapy. Many doctors prescribe an antibiotic for at least three days.
While this type of medication is the standard treatment, researchers are noticing that antibiotic-resistant bacteria are reducing the effectiveness of some antibiotics in treating UTIs.
Some UTIs don’t clear up after antibiotic therapy. When an antibiotic medication doesn’t stop the bacteria causing an infection, the bacteria continue to multiply.
The overuse or misuse of antibiotics is often the reason for antibiotic resistance. This can happen when the same antibiotic is prescribed over and over again for recurrent UTIs. Because of this risk, experts have been looking for ways to treat UTIs without antibiotics.
Antibiotic resistance 101
• When certain antibiotics are prescribed repeatedly, the bacteria they target can grow resistant to them.
• At least 2 million people per year in the United States contract antibiotic-resistant bacteria.
Are antibiotics going out of style?
So far, preliminary studies have been promising. Some research has shown that UTIs can be treated without traditional antibiotics by targeting E. coli’s surface component for adhesion, FimH.
Typically, the urinary tract flushes away bacteria when you urinate. But according to researchers, FimH can cause E. coli to firmly attach to the cells in the urinary tract. And because of this tight grip, it’s hard for the body to naturally flush the bacteria from the urinary tract.
If researchers can uncover a way to target this protein with other types of therapies, treating or preventing UTIs with antibiotics might become a thing of the past.
D-mannose is a sugar that sticks to E. coli. Recently, researchers have studied the possibility of using D-mannose and other mannose-containing substances to block the binding of FimH to the lining of the urinary tract. One small, limited study from 2014 showed positive results when attempting to prevent recurrent UTIs.
More research is needed, but potentially, a medication that utilizes a mannose-containing substance that opposes FimH from attaching to the lining of the urinary tract in one way or another could show promise for the treatment of UTIs caused by E. coli.
Researchers are also currently testing immune-boosting drugs. These could help urinary tract cells become more resistant to infections.
The American Urological Association (AUA) recommends vaginal estrogen as a non-antibiotic option for perimenopausal or postmenopausal women seeking to prevent recurrent infections.
Home remedies for UTIs
While treating UTIs without antibiotics may be a future possibility, for now, they remain the most effective standard treatment. However, a prescription medication doesn’t have to be the only line of defense.
Along with standard therapy, you can incorporate home remedies to feel better sooner and reduce the likelihood of recurrent infections.
1. Try cranberries
Cranberries may contain an ingredient that stops bacteria from attaching to the walls of the urinary tract. Research is inconclusive and more studies are needed, but you might be able to reduce your risk of UTIs with unsweetened cranberry juice, cranberry supplements, or dried cranberries.
2. Drink plenty of water
Although urinating can be painful when you have a UTI, it’s important to drink as many fluids as possible, particularly water. The more you drink, the more you’ll urinate. Urinating helps flush harmful bacteria from the urinary tract.
3. Pee when you need to
Holding your urine or ignoring the urge to urinate can allow bacteria to multiply in your urinary tract. As a rule of thumb, always use the bathroom when you feel the urge.
4. Take probiotics
Probiotics promote healthy digestion and immunity. They also may be effective in treating and preventing UTIs.
With a UTI, bad bacteria replace good bacteria in the vagina, especially those of one group called Lactobacillus. Probiotics can restore good bacteria and might reduce recurrence of a UTI.
5. Get more vitamin C
Increasing your intake of vitamin C may help prevent a UTI. Vitamin C strengthens the immune system and may help acidify the urineTrusted Source to prevent infection.
The takeaway
UTIs are painful, but with treatment, you can overcome an infection and prevent recurrent infections. Talk to your doctor if you have symptoms of a UTI. With proper treatment, you should begin to feel better in a few days.
Take your antibiotics as instructed — even after your symptoms improve — to prevent complications or a secondary infection.
If the UTI doesn’t resolve after antibiotic treatment or you end up with multiple episodes of a UTI, your doctor will likely do further testing.
This could be in the form of:
You may be referred to a urologist, depending on the severity of your UTI or if you have chronic infections.
Certain strains of bacteria can cause UTIs. They can range from mild to severe. The degree of severity depends on multiple factors, including:
• one’s immune system status
• the bacterium causing the UTI
• where in your urinary tract the UTI is happening
It’s also possible to have bacterial colonization in the urinary tract that’s not causing you to have a UTI. Your doctor will be able to provide you with an evaluation tailored to your needs in order to make the right diagnosis and determine the proper therapy.
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Advertisement
Is hospice care just for cancer patients?
Juliet Wilkinson
Oncology Nursing
Unequivocally, no. Hospice care is not just for cancer patients. Hospice and palliative care organizations provide care for anyone who qualifies with a life-limiting illness. According to the Medicare hospice explanation of benefits, this includes anyone suffering an illness curbing their life expectancy to six months or less. Patients in hospice do frequently suffer cancer, but they also include those suffering chronic lung disorders, cognitive disorders such as dementia and amyotrophic lateral sclerosis, or Lou Gehrig's disease.
Dr. Robin Miller, MD
Internal Medicine
Hospice care is end of life care. There are many conditions that may require hospice when patients reach the terminal stage. In addition to cancer, these may include illnesses such as congestive heart failure, amyotrophic lateral sclerosis, chronic obstructive pulmonary disease, AIDS and dementia.
Once the patient and doctors determine that a patient has reached the end of life, hospice can provide care to help alleviate symptoms such as pain, shortness of breath, and anxiety with the help of medications. Many programs offer alternative treatments such as acupuncture and massage.
Katie Ortlip
Hospice Nursing
Hospice care is end-of-life care for all people, not just those with cancer. I am currently caring for people with end stage heart disease, emphysema, and old age. About half of our patients have non-cancer diagnoses. As long as you are not seeking aggressive, curative treatment, and the doctor feels you have approximately six months or less to live, you are appropriate for hospice. Hospice focuses on comfort and quality of life, and supports the patient and family.
Continue Learning about Hospice Care
What Is Hospice Care?
What Is Hospice Care?
The end of life can be an emotionally and physically difficult time. Most adults say they’d prefer to die at home, pain free and surrounded by friends...
Read More
How is hospice care tailored to a person's needs?
LIVESTRONGLIVESTRONG
Hospice care is flexible and can be molded to fit the different needs and lifestyles of patients and...
More Answers
Does hospice provide 24-hour care?
Stacie KarczmiarzStacie Karczmiarz
It can depend on which hospice... just in my area alone there are three separate and independent, in...
More Answers
What is hospice care?
Sharine ForbesSharine Forbes
It was in 1967 that the term “hospice” was first utilized by Dame Saunders in London to describe the...
More Answers
Important: This content reflects information from various individuals and organizations and may offer alternative or opposing points of view. It should not be used for medical advice, diagnosis or treatment. As always, you should consult with your healthcare provider about your specific health needs.
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Ovarian transitional cell carcinoma represents a poorly differentiated form of high-grade serous or endometrioid adenocarcinoma
Tadahisa Takeuchi, Yoshihiro Ohishi, Hiroko Imamura, Murasaki Aman, Kaai Shida, Hiroaki Kobayashi, Kiyoko Kato, Yoshinao Oda
研究成果: ジャーナルへの寄稿学術誌査読
23 被引用数 (Scopus)
抄録
Ovarian transitional cell tumors include Brenner tumors (BTs) and transitional cell carcinoma (TCC; non-BTs) according to the most recent World Health Organization classification. However, it remains a matter of debate whether TCC represents a distinct entity or a morphologic variant of highgrade serous adenocarcinoma (HG-SC). The purpose of this study was to resolve the above question by clarifying the morphologic, immunohistochemical, and molecular features of TCC. We reviewed 488 cases of epithelial ovarian carcinomas and reclassified them on the basis of the most recent World Health Organization classification with the modifications proposed by Ko bel and colleagues, and 35 cases of TCC were identified; 25 and 6 TCCs were admixed with HG-SC and endometrioid adenocarcinoma (EC), respectively, and the remaining 4 cases were pure TCC. TCC components were not observed in any clear cell carcinomas or mucinous adenocarcinomas. Only 2 cases of malignant BT were identified. In addition to TCCs, malignant BTs, and related adenocarcinomas, benign and borderline BTs were included in the following immunohistochemical and molecular analyses. Immunohistochemically, pure TCCs, TCCs admixed with HG-SC, and pure HG-SCs were characterized by frequent aberrant p53 expression (diffuse or null pattern) and WT1+/ ER+/PR+/IMP2+ immunophenotype, whereas BTs, including benign, borderline, and malignant BTs, were characterized by lack of aberrant p53 expression and WT1/ER/PR/IMP2 immunophenotype. In contrast to the BTs, pure ECs and TCCs admixed with EC showed an ER+/PR+ immunophenotype. Nearly all the tumors with a TP53 gene mutation by molecular analysis showed aberrant p53 staining patterns. In conclusion, TCC is not a distinct entity but a poorly differentiated form of serous or EC, as (1) most TCCs coexist with HG-SC (mostly) or EC (occasionally), and (2) the immunophenotype and molecular features are similar to those of HG-SC or EC but different from those of BTs.
本文言語英語
ページ（範囲）1091-1099
ページ数9
ジャーナルAmerican Journal of Surgical Pathology
37
7
DOI
出版ステータス出版済み - 7月 2013
!!!All Science Journal Classification (ASJC) codes
• 解剖学
• 外科
• 病理学および法医学
フィンガープリント
「Ovarian transitional cell carcinoma represents a poorly differentiated form of high-grade serous or endometrioid adenocarcinoma」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。
引用スタイル
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How to Help Someone With Depression
How to Help Someone With Depression thumbnail
How to Help Someone With Depression
how to help someone with depression
There are some actions you can take to assist your loved one regardless of whether they’re suffering from depression or just feeling sad. The first step is to listen to them. Don’t appear shocked or judgmental when they talk. It could cause them to stop talking or even shut down. Be attentive and ask questions with a gentle tone. Your loved one might be more open if you focus on them.
What Are The Signs Of Depression
Depression is a fairly common mental illness, but many people are unaware of the signs and symptoms. People who suffer from depression are depressed, sad and incapable of functioning properly. They may even lose interest in activities that they used to enjoy. These symptoms may last for weeks or even months, and can cause problems at social or work life. Because these symptoms often appear slowly, it could require a family member or friend to be the first member to recognize them.
If you continue to experience these symptoms and persist, you should visit your physician. Depression is an extremely serious mental illness, but it is treatable. A visit to your general practitioner (GP) can assist you in getting on the right track to feel better. A physician will examine you and inquire about your lifestyle and the things you do every day. The examination may include detailed questions regarding your mood and behavior, which is why it is essential to be honest and thorough.
What are the symptoms of Depression?
The symptoms of depression could vary for every person. They can include fatigue, social withdrawal, loss of enthusiasm for daily activities, and even loss. They can also cause changes in appetite or sleep patterns. People suffering from depression could also have difficulties with concentration and memory. In some instances, severe depression can lead to suicide attempts.
There are a variety of treatments for depression. Early intervention is key. It will allow you to overcome the symptoms before they become worse. Talking with a specialist in mental health can help you find the best treatment. There are many antidepressants you can take to help you manage your depression and get back to living your life. Also, therapy can aid you in learning to avoid future episodes of depression.
Depression is a chronic illness that can affect you for years. Although medication can relieve certain symptoms of depression, it will not address the main cause of the disorder. The majority of those who suffer from depression do not get the diagnosis. Although there is no diagnostic test for depression, a physician will ask about your past symptoms and recommend an appropriate treatment plan.
How to Help Someone who is Depression
It can be difficult for a loved one to understand how to support them if they suffer from depression. It is crucial to learn about the condition and share your knowledge with others. Discuss depression in general terms, the symptoms and the treatment options. It might be beneficial to seek professional help when someone you care for suffers from depression.
You can aid the person suffering from depression by being understanding and compassionate. Depression can cause people to self-medicate. This will make it difficult for the person to get the proper care they require. Most people with depression are embarrassed or shy of seeking help. If you have the time you can suggest to the person they seek help and give them space to talk about it.
How do you talk about depression with someone
If you’re concerned about someone you know who is suffering from depression, talking with them may help them feel less isolated and help bring a new perspective. It can also help you create a plan or strategy to help them cope with their feelings. If you’re a family member or a professional, you could offer advice and help.
Remember that everyone has bad days and sometimes is down. But, depression can make someone feel ashamed or alone. It can be triggered either by life events or triggers. It could also be a long-standing feeling. It is therefore essential to be patient and sensitive, and not be judgmental.
You can also call the local mental health services or a doctor if are concerned about someone’s mental condition. Be sure to get permission from the person in question first, as you may need to go against the person’s wishes. You can also contact the Depression Helpline for free and get specialist guidance on how to help.
Encouragement of the person to seek help for their depression
The first step to helping someone suffering from depression to seek help is to acknowledge that it is a medical issue. Although the person might feel uncomfortable about their depression, it is not something to be ashamed of. Depression can often be treated with the appropriate treatment. It is crucial to inform the person that they’re not crazy and that it is normal to feel this way.
A structured routine can be a great way to encourage those suffering from depression to seek assistance. A schedule for sleeping, taking medications, and physical activities can help the person feel more in control. It is also possible to assist people suffering from depression with chores around the house. Many organizations offer help for depression, including the National Alliance on Mental Illness. Many workplaces also provide mental health resources to help employees. Spiritual practices can also aid in a recovery of a person.
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ALPHA PSYCHIATRY
Original Articles
Metabolic syndrome and features in children and adolescents diagnosed with mood disorders and psychotic disorders
1.
Manisa Ruh Sagligi ve Hastaliklari Hastanesi Cocuk Ergen Psikiyatrisi Klinigi, Manisa
2.
Aksaray Egitim Arastirma Hastanesi, Cocuk Ergen Psikiyatrisi Birimi, Aksaray,
3.
Celal Bayar Universitesi Tip Fakultesi Cocuk Psikiyatri ABD, Manisa
4.
Aksaray Egitim Arastirma Hastanesi, Dermatoloji Birimi, Aksaray Uzm. Dr.
5.
Kepez Devlet Hastanesi, Cocuk Ergen Psikiyatrisi Birimi, Antalya
Alpha Psychiatry 2019; 20: 76-83
DOI: 10.5455/apd.299468
Read: 581 Downloads: 329 Published: 01 February 2019
Objective: Metabolic syndrome (METS) is described as cluster of risk factors including central obesity, hyperten-sion, low high-density lipoprotein (HDL), hypertriglyceridemia and hyperglycemia. The prevalence of METs has been associated with increased symptom severity and antidepressants utilization in many psychopathologies among adult population. We aimed to evaluate the effect of psychopathologies and antipsychotics in METs devel- opment, additionally to determine METs characteristics in children and adolescents diagnosed with bipolar and psychotic disorders. Methods: Thirty children and adolescents aged between 13-20 years old of whom were diag-nosed with bipolar mood disorders, schizophrenia, schizoaffective disorder and schizophreniform according to Diag-nostic and Statistical Manual of Mental Disorders, Fourth Edition Text Revision (DSM-IV-TR) criteria were compared with a 30 healthy children and adolescents in present study. The anthropometric measurements including body weight, height, body mass index (BMI), waist circumference (WC) as well as blood pressure measurements were documented. In addition, total cholesterol, triglyceride (TG), HDL, low-density lipoprotein (LDL) and fasting blood glucose (FBG) levels were measured and METs assessed according to the IDF (International Diabetes Foundation) criteria in participants. Results: Overall the prevalence of METs was 20% (n=12) in our study. Among the METs patients, nine were (27%) in the case group, three were (10%) were in control group. The mean BMI, body weight, WC, serum TG and FBG values of the METs group were found to be statistically higher than the healthy control group. Moreover it was also found that utilization of mood-stabilizing drugs has a statistically significant effect on the development of METs. Conclusion: Psychopathologies and antipsychotic utilization have associated with an increased risk for the development of metabolic disorders and METs in the children and adolescents population. In this respect our findings may provide a new approach with the management of treatment strategies particularly in children and adolescents with high risk of METs. [Anadolu Psikiyatri Derg 2019; 20(1.000): 76-83]
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What Are The Symptoms Of Heel Spur
Inferior Calcaneal Spur
Overview
A heel spur is caused by the displacement of calcium on the bone that forms on the underside of the heel, it may be one small bony protrusion or a collection of tiny, irregularly shaped growths on the bone of the heel, which is called the calcaneum. Heel spurs are sometimes painful, described as a knife digging into the heel and other times, a heel spur goes unnoticed and is only detected by an X-ray.
Causes
Over-pronation (flat feet) is a common cause of heel spurs, but people with unusually high arches (pes cavus) can also develop heel spurs. Women have a significantly higher incidence of heel spurs due to the types of footwear often worn on a regular basis.
Inferior Calcaneal Spur
Symptoms
If your body has created calcium build-ups in an effort to support your plantar fascia ligament, each time you step down with your foot, the heel spur is being driven into the soft, fatty tissue which lines the bottom of your heel. Heel spur sufferers experience stabbing sensations because the hard protrusion is literally being jabbed into the heel pad. If left untreated, Plantar Fasciitis and heel spurs can erode the fatty pad of the heel and cause permanent damage to the foot. Fortunately, most cases can be resolved without medications or surgeries.
Diagnosis
A Diagnosis of Heel Spur Syndrome is a very common reason for having heel pain. Heel pain may be due to other types of conditions such as tendonitis, Haglund’s Deformity, Stress Fracture, Tarsal Tunnel Syndrome, or low back problems. A more common condition in children is Sever’s Disease. The diagnosis is usually made with a combination of x-ray examination and symptoms.
Non Surgical Treatment
Heel spurs can be treated by wearing orthotic insoles inside the shoe. Orthotics are designed to correct incorrect gait, in particular over-pronation (rolling in of the foot and collapsing of the arches). Over-pronation is a very common foot condition, affecting at least half of the population. It is a major contributing cause of heel spurs. Orthotics are very effective in that the device corrects the foot to its natural position. By supporting the arches properly and preventing excess rolling in of the foot, the plantar fascia is placed under much less strain and stress compared to an unsupported foot. Less strain on the ligament means less pulling away from the heel bone, allowing the inflammation to heal faster. In addition to orthotic treatment, most podiatrists and physiotherapists recommend a series of exercises to help make the ligaments in the feet and legs longer and more flexible. In turn this will help reduce strain on the plantar fascia.
Surgical Treatment
Surgery involves releasing a part of the plantar fascia from its insertion in the heel bone, as well as removing the spur. Many times during the procedure, pinched nerves (neuromas), adding to the pain, are found and removed. Often, an inflamed sac of fluid call an accessory or adventitious bursa is found under the heel spur, and it is removed as well. Postoperative recovery is usually a slipper cast and minimal weight bearing for a period of 3-4 weeks. On some occasions, a removable short-leg walking boot is used or a below knee cast applied.
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Will A Heel Spur Cause Pain?
Calcaneal Spur
Overview
A heel spur is a buildup of calcium or a bone hook on the heel bone. This is typically the source of most heel pain. It usually takes an X-ray to see the heel spur protruding from the heel. Without proper heel spur treatment, a heel spur cause inflammation and lead to other ailments like plantar fasciitis and Achilles tendonitis. It is important to be examined by an orthopedic specialist.
Causes
A major cause of heel spur pain comes from the development of new fibrous tissue around the bony spur, which acts as a cushion over the area of stress. As this tissue grows, a callus forms and takes up even more space than the heel spur, leading to less space for the thick surrounding network of tendons, nerves, ligaments and supporting tissue. These important structures in the foot have limited space because of calcium or tissue buildup, which leads to swelling and redness of the foot, and a deep throbbing pain worsened with exercise.
Posterior Calcaneal Spur
Symptoms
Most bone spurs cause no signs or symptoms. You might not realize you have bone spurs until an X-ray for another condition reveals the growths. In some cases, though, bone spurs can cause pain and loss of motion in your joints.
Diagnosis
Most patients who are suffering with heel spurs can see them with an X-ray scan. They are normally hooked and extend into the heel. Some people who have heel spur may not even have noticeable symptoms, although could still be able to see a spur in an X-ray scan.
Non Surgical Treatment
Ice and use arch support . If you can localize the spur, cut a hole in a pad of felt and lay the hole over the spur. This supports the area around the spur and reduces pressure on it. Massage the spur. Start gently with your thumb and gradually increase the pressure until you?re pushing hard directly on the spur with your knuckle or another firm object. Even it if hurts, it should help. Arch support. Build up an arch support system in your shoes. Try to equalize the pressure of your body weight throughout your arch and away from the plantar area. Use a ?cobra pad? or other device that supports the arch but releases pressure on the painful area. If homemade supports do not work, see a podiatrist about custom orthotics.
Surgical Treatment
Surgery, which is a more radical treatment, can be a permanent correction to remove the spur itself. If your doctor believes that surgery is indicated, he will recommend an operation – but only after establishing that less drastic methods of treatment are not successful.
Prevention
o help prevent heel and bone spurs, wear properly designed and fitted shoes or boots that provide sufficient room in the toe box so as not to compress the toes. They should also provide cushioning in appropriate areas to minimize the possibility of the irritation and inflammation that can lead to bone spurs in the feet. If needed, use inserts that provide arch support and a slight heel lift to help ensure that not too much stress is placed on the plantar fascia. This helps to reduce the possibility of inflammation and overstress. Wearing padded socks can also help by reducing trauma. Peer-reviewed, published studies have shown that wearing clinically-tested padded socks can help protect against injuries to the skin/soft tissue of the foot due to the effects of impact, pressure and shear forces. Also consider getting your gait analyzed by a foot health professional for appropriate orthotics. If you have heel pain, toe pain or top-of-the-foot pain, see your doctor or foot specialist to ensure that a spur has not developed.
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5eff3d1f6f98e57329caed0ceb9053d3
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4,027,175,368,403,522,000
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Cholesterol: its regulation and role in central nervous system disorders
Cholesterol. 2012:2012:292598. doi: 10.1155/2012/292598. Epub 2012 Oct 17.
Abstract
Cholesterol is a major constituent of the human brain, and the brain is the most cholesterol-rich organ. Numerous lipoprotein receptors and apolipoproteins are expressed in the brain. Cholesterol is tightly regulated between the major brain cells and is essential for normal brain development. The metabolism of brain cholesterol differs markedly from that of other tissues. Brain cholesterol is primarily derived by de novo synthesis and the blood brain barrier prevents the uptake of lipoprotein cholesterol from the circulation. Defects in cholesterol metabolism lead to structural and functional central nervous system diseases such as Smith-Lemli-Opitz syndrome, Niemann-Pick type C disease, and Alzheimer's disease. These diseases affect different metabolic pathways (cholesterol biosynthesis, lipid transport and lipoprotein assembly, apolipoproteins, lipoprotein receptors, and signaling molecules). We review the metabolic pathways of cholesterol in the CNS and its cell-specific and microdomain-specific interaction with other pathways such as the amyloid precursor protein and discuss potential treatment strategies as well as the effects of the widespread use of LDL cholesterol-lowering drugs on brain functions.
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turmeric for high blood sugar
Turmeric For High Blood Sugar [Official] | Golfcar Turkey
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Your doctor will provide a listening with your doctor or any correct diagnosis and Type 2 diabetes.
diabetic treatment and management include turmeric for high blood sugar the following quizlete of the recovery.
These findings have proven to improve the risk of prediabetes and type 2 diabetes can be a treated with a serious risk for diabetes in patients with type 2 turmeric for high blood sugar diabetes.
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Co2 Extracted CBD Oil: Extraction Process Benefits
Content
CBD oil has been used to safely treat insomnia and anxiety in children with post-traumatic stress disorder , a type of anxiety disorder . In a Brazilian study, 57 men received either oral CBD or a placebo 90 minutes before they underwent a simulated public speaking test. The researchers found that a 300-mg dose of CBD was the most effective at significantly reducing anxiety during the test . Anxiety disorders and other mental health disorders can have devastating impacts on overall health and well-being. Several human studies have found that a combination of CBD and THC is effective in treating pain related to multiple sclerosis and arthritis. If you are interested in trying a CBD product, it’s best to seek one through a dispensary, which is an establishment legally licensed to sell marijuana, if they are available in your state.
• The only difference is in the atom’s arrangement, and that arrangement it’s the sole reason why each affects you differently.
• Reduced blood flow to several parts of the body, including the optic nerve, which can increase damage.
• Medial temporal structures and memory functions in adolescents with heavy cannabis use.
• Although there isn’t enough evidence to confirm that CBD can be used to help people with schizophrenia, the research is promising.
Viagra, Cialis, and Levitra, all help to expand blood vessels and relax muscles in the penis. This helps to improve blood flow into the penis, which can help to sustain an erection. PDE5 inhibitors are effective for the majority of men who try them. It may also reduce stress and anxiety, which could help to improve sexual performance. Schedule 1 drug, and is therefore a controlled substance and illegal at the federal level. Many U.S. states have or are consider changing the way they regulate THC, however, with some making marijuana medically accessible and others making it accessible recreationally.
People are often infected by kissing or eating from the same plates. Besides, if there is a person with herpes nearby who is coughing or sneezing, there is a high risk of airborne infection. Fortunately, most people infected with the herpes virus have an inactive form of infection and manage to bypass this unpleasant disease.
Want To Be Healthier?
There’s no evidence to suggest that CBD could worsen anxiety or related symptoms, as the above-mentioned review emphasizes. But if you feel like your anxiety increases when you use CBD, it’s important to speak with your doctor. When you use a CBD topical, little to no CBD will actually absorb into your bloodstream, which means that it’s not a suitable method for an internal issue like anxiety.
• This therapist put level 5 rub on my knees but think the menthol and camphor is what I felt, a little help at best I think but not sure CBD did anything.
• Cognition refers to the mechanism garnering knowledge and understanding via thoughts and everyday experiences which is mediated by the senses.
• A 2016 study found that CBD oil applied to the skin effectively treated anxiety and sleeping problems in a child with PTSD.
• This will help you track what works and what doesn’t for your condition.
And once again, we are in an early stage of both research and personal experimentation. While some studies and many users have suggested that CBD may even improve overall cognition, there is very little evidence for CBD as a memory-enhancer in a healthy brain (assuming a “healthy brain” actually does exist). A study on cannabis’ effects on memory confirmed that long-term THC use could actually impact memories, but what about CBD? Well, studies are currently testing it in models of memory impairment and memory function. Studies show that these memory affecting traits may begin to wear off over time.
There are two big brain messengers for memory that we’ll focus on. To focus on memory, we need to travel a specific part of the brain…the hippocampus. The majority of CBD supplements are sold this way, so you get access to a wider range of products.
4 CBD Market Trends All Entrepreneurs Should Be Aware Of
There is also plenty of evidence in scientific literature proving CBD’s anti-inflammatory and vasodilative properties, both relieving the effects of damage or constriction in vital blood vessels. CBD is even shown to maintain circadian rhythms, regulating and promoting healthy sleep cycles in patients showing signs of dementia. Currently, there is no evidence of any known benefit to the introduction of psychoactive compounds to patients can cbd oil help you sleep uk suffering from Alzheimer’s and other forms of dementia. On the other hand, studies show isolated pharmaceutical-grade CBD can considerably improve their quality of life by treating symptoms related to their disorders. Motivation is a critical factor in whether or not many people reach their fitness goals, which is why supplementing with CBD might give you the boost you need to actually do your workout and stick to your fitness plan.
If CBD oil can be used to treat pain like this, I think it will find a host of new users very soon. Humans most likely always knew about marijuana and it’s psychoactive properties, but THC use has skyrocketed over the last 100 years, or so. Emma Stone is a journalist based in New Zealand specializing in cannabis, health, and well-being.
While Alzheimer’s is still impossible to diagnose with full certainty, a series of tests and magnetic resonance imaging can determine the likelihood of the disease to a reasonable degree. Cannabidiol or CBD is one of two primary compounds found in the cannabis plant, the other being tetrahydrocannabinol . On the other hand, Epidiolex is dosed at 5mg per kilogram (2.2lbs) of body weight. However, you do need to be aware of possible drug interactions before introducing CBD into your diet. For example, if you’re taking blood thinners, then CBD may change the way these drugs work in your system, in a similar way that eating a grapefruit would.
• On the other hand, studies show isolated pharmaceutical-grade CBD can considerably improve their quality of life by treating symptoms related to their disorders.
• Because of the federal prohibitions on prescribing Schedule 1 substances, there is no Medicare coverage for the purchase of medical marijuana or CBD derivatives.
• Recent studies suggest that treatment with a combination of CBD and THC may help extend the life of some people with an aggressive form of cancer called glioblastoma, yet research is limited .
A benefit of taking CBD products is that they supplement and aid the body’s natural endocannabinoids. Most medical research suggests that CBD does not intoxicate you the same way THC does, but taking types of medical marijuana marketed as “high CBD” might mean there are traces of THC included in the substance. THC is addictive because it can change brain chemistry to make you feel relaxed, less anxious, sleepy, or even happy.
Marijuana-derived CBD products, on the other hand, are illegal federally but legal under some state laws. Also, keep in mind that the Food and Drug Administration has not approved nonprescription CBD products, which may be inaccurately labeled. Now, many people are turning to CBD for focus rather than relying on pharmaceuticals and other concentration methods. There are even specially curated strains dedicated to helping with mental acuity. A member of our medical expert team provides a final review of the content and sources cited for every guide, article, and product review concerning medical- and health-related topics. Inaccurate or unverifiable information will be removed prior to publication.
CBD For Pets: A Whole New World Of Supplements
Possible approaches include improved sleep hygiene, prescription sleep aids, and natural sleep aids. A good night’s sleep is essential to your overall health and wellbeing. Proper sleep ensures you feel well-rested and have energy for the next day. A good night’s rest also contributes to memory formation, helps grow and repair muscle and tissue, and prevents sickness. Being fatigued is more than just being tired, it is the point at which your whole body including your mind is completely exhausted.
• It may also interact with certain medications, so always check with your doctor before use.
• A 2010 study looked at the effects of CBD on 10 people with social anxiety disorder and participants were either given 400 milligrams of CBD or a placebo.
• The agency is just starting the process of hashing out some rules regarding CBD sales.
• It most often appears on the lips, although it can affect other parts of the body, including the genitals.
Reportedly, the pain experienced through our nerves can be dulled from CBD use, too. I am now going to answer several of the different manners in which CBD can help people. How to use CBD effectively depends on which receptors you want to target, among other things. The preliminary research being done with CBD is showing promising results.
Because of this, CBD products such as oils, concentrates, isolates and tinctures are legal throughout the United States. An inability to focus can arise from stress, lack of sleep, full-on disorders, or simple distractions that pull at our finicky attention spans. While CBD can’t prevent loud thunder cracking your eyes open at three in the morning or constant pings irradiating from your cell phone, its ability to help people focus has produced some exceptional results. CBD is touted for many maladies—chronic pain, anxiety, inflammation, depression—but an especially compelling outcome of taking CBD is its effect on cognition. Many companies are choosing to wield CBD’s benefits—and for good reason.
What Is Microdosing CBD? How To Microdose CBD & Tips On Finding An Optimal Dosage
It is important to note that THC, however, may be detected via drug tests. For those who want to avoid these risks, using broad-spectrum CBD is more recommended. CBD’s antipsychotic and neuroprotective properties may help alleviate the various symptoms of dementia. Reports state that a standard preparation of the What is a CBD oil tincture? herb improves neurocognition and enhances the everyday activities of Alzheimer’s and vascular dementia patients. The researchers concluded that acupuncture had mixed efficacy in treating cognitive impairments and dementia. Tetrahydrocannabinol is probably the best-known cannabinoid found in the cannabis plant.
• The brain’s immune system has long been involved as a significant factor in the development of Alzheimer’s disease, particularly a specialized type of immune cell called microglia.
• CBD might fix gloom and uneasiness by changing serotonin levels, as per scientists.
• Cannabidiol oil’s anti-inflammatory properties make it a great candidate for treating headaches and other types of chronic pain.
• One of the most well-known uses of CBD oil is as an analgesic, AKA a pain reliever.
Instead of focusing on your tasks, your mind is on your problems. By relaxing your mind, you’re able to concentrate on what’s in front of you. Anxiety disorders are caused by a unique combination of genetics, your environment, important life events, and learned coping patterns.
Could Cannabis Hold The Answer To Alzheimer’s Disease?
Since THC and CBD are being increasingly paired together in different formulations, a greater understanding of their interactions will eventually come to light. At present, it is unclear whether at specific concentrations CBD might counteract the effects of THC on memory and cognition. We are a Colorado-based CBD Oil Products company focused on quality, consistency and purity. Browse our wide selection of products to find a CBD solution that works for you. If you have any questions, don’t hesitate to reach out to us for help or answers. You also won’t forget significant facts or information, like your date of birth or your name or something along those lines.
• Researchers have investigated that CBD plays an important role in protecting our brain and also helps in reducing brain damage which is caused by various traumas.
• One of the most popular ways to help anxiety and sleep issues as well as other health conditions is by ingesting CBD either through CBD oil, edibles, tinctures, and more.
• There are very few medical studies on the effectiveness of CBD or medical marijuana, although the United States Food and Drug Administration has information on potentially beneficial uses for this approach to treatment.
• It’s good that you’re asking these things so that you can ensure you are on top of things when it comes to your wellness.
The United States Food and Drug Administration has approved CBD for some very limited medical uses, and several states have legalized both medical and recreational use of marijuana, both THC and CBD. NVISION® content is medically reviewed by a licensed Ophthalmologist, Optometrist, Surgeon or Doctor. These vision experts ensure the content is fact-based and up-to-date. I bought it for my mom, she has dementia and Lyme disease, she has been on CBD full spectrum for four weeks, better thinking, less depressed, much better. CBD being an antioxidant helps in slowing down this process as well as reducing oxidative stress in the brain. CBD may be able to reduce fatigue and stress and promote a relaxing sleep.
A Pronounced Working Memory Deficit Was Associated With Exposure To Stress Https:
The following is the list of natural ingredients added by the creators of Altai Balance. Most labs test CBD products for the presence of pesticides, residual solvents, mycotoxins, heavy metals, and microbial contaminants. A board certified oncology pharmacist with 25 years experience at the James Graham Brown Cancer Center in Louisville, Kentucky, Dr. Leslie Mudd now serves as the Cornbread Hemp resident pharmacist and medical expert. Dedicated to providing high quality CBD oil made from Kentucky-grown USDA organic hemp flowers. This is different from many companies who don’t choose organic or source their hemp from overseas, and from companies who use stems and leaves in their extract.
• If you don’t have much time for searching for a specialist you can trust or just want to get professional help right away — you can always get tips from Dr.Weedy online.
• People turn to it because it offers many of the same effects and benefits as marijuana, but it will not get you high.
• Dementia can lead to problems such as mood issues, concentration problems, and sometimes depression as well.
However, researchers are using this idea to better understand the relationship between CBD as a treatment and dementia, and there is still much that needs to be uncovered and understood. This means that there have Puis-je les acheter légalement ? been no concrete conclusions linking CBD as a way to prevent or help stop the progression of dementia. So far, there haven’t been large clinical trials among humans to study whether CBD can help with dementia.
Studies show, other than decreasing pain and inflammation, the oil also has neuroprotective effects and can be used to improve the quality of one’s skin. If you are looking for a whole body improvement, you should go with the oral tincture used daily. To enhance skin quality best bet would be topical BoutiqueToYou cream or skin serum which will also help with pain. CBD has been demonstrated to reduce anxiety or have no impact on anxiety even at large dosages, whereas THC lowers anxiety and raises it at larger levels. It’s theoretically feasible that CBD if it contains a high dose of THC, can make you uneasy.
Although levodopa is the most commonly used treatment for PD, which helps replenish the level of dopamine in the brain. But it does little in tackling the nonmotor symptoms of Parkinson’s disease. One of the most popular ways to help anxiety and sleep issues as well as other health conditions is by ingesting CBD either through CBD oil, edibles, tinctures, and more. If you are suffering from any of these signs or symptoms, it’s possible that you may have insomnia or another similar sleep condition.
It’s important to note that bitter melon has insulin-like qualities that can speed up the breakdown and utilization of unhealthy sugars and carbs. Regular consumption of bitter melon can increase glucose metabolism. It improves the body’s ability to absorb glucose, so you won’t need as much insulin to move glucose from the blood to body tissues.
Cannabis-derived CBD products are illegal on the federal level but are legal under some state laws. Hemp-derived CBD products (with less than 0.3% THC) are legal on the federal level but are still illegal under some state laws. Better known as CBD, it is one of more than 100 chemical compounds called cannabinoids that are found in the cannabis plant, Cannabis sativa . In some states marijuana is legal for both recreational use and medical use.
A dependency on cannabis is usually different than the extremes people imagine when it comes to an addiction to drugs. But there are differences in what is affected and how—cognitive processes, for example, are more affected than are the effects on the cardiovascular system and psychological tolerance is variable2. Welcome to the number one reason why many heavy marijuana consumers choose to take a tolerance break. More recent does cbd help woth anxiety studies have indicated that the question is not so simple. As a heavy consumer’s body adapts to these changes in the endocannabinoid system, they won’t continue to feel the same results of cannabis. Six different groups of the lab animals were given either CBD, THC, synthetic cannabinoids, or a placebo, where changes in behavioral responses were then compared with changes of density in six various areas of the brain.
It was discovered that the body adapts to the ingestion of large amounts of THC by reducing the number of cannabinoid receptors available in the body. This reduces does cbd oil help with seizures the effects of the psychoactive cannabinoids overtime on these receptors. However, there are more than one hundred different cannabinoids in cannabis.
They are responsible for many of the benefits of using cannabis. For example, CBD interacts with the receptors in the brain and can help with various conditions, such as sleep problems. It contains some beneficial components that are able to stop viruses from flaring up and causing more damage to your health.
Moreover, The CBD market is expected to see an exponential growth of 700 percent by 2020. The most important characteristic of CBD is it is non-psychoactive which means it will not get you “high” that one experiences by consuming marijuana. Adult hippocampal neurogenesis is abundant in neurologically healthy subjects and drops sharply in patients with Alzheimer’s disease. Further studies need to be conducted, especially on the proper dosage of CBD to achieve maximum efficacy in treating dementia. Patients and their family members are turning to alternative treatments like CBD. High-quality CBD products give consumers access to batch testing reports and lab analyses.
Fresh Tom Collins-Inspired CBD Cocktails To Kick Off Summer
Sublingual application allows for results to be experienced within 30 to 60 minutes after its use, and the effects can be felt for 4 to 6 hours. Depending on one’s metabolism, the effects can last between 6 and 12 hours. However, the effects of the CBD oil could take at least 20 minutes to an hour to appear.
• Cannabis users who consume high levels of cannabis over prolonged periods may experience an adverse effect on long term memory.
• While much is to be explored about the ECS and CB2 receptors, this suggests that CBD usage might play a significant role in boosting our metabolism.
• Additionally, according to preliminary research, THC is considerably more effective than the approved drugs for Alzheimer’s disease in mice, a disease characterized by worsening memory loss.
• As of August 2019, CBD products in Canada could only be sold by authorized retailers or federally licensed medical companies, limiting their access to the general public.
In contrast to the acute effects, less consistency exists regarding the long-term effects of cannabis use on neurocognitive functioning. A major difficulty that appears when interpreting studies that compared cannabis users with control subjects regarding their memory performance is the heterogeneity of the selected samples. Based on the methodological approaches in the literature, Table 3 summarizes the studies in terms of the subject selection criteria employed and the confounding factors that have been considered. Cannabis contains varying amounts of the potentially therapeutic compound cannabidiol , which may help quell anxiety. However, there’s no question that marijuana can produce short-term problems with thinking, working memory, executive function, and psychomotor function . This is because marijuana’s main psychoactive chemical, THC, causes its effect by attaching to receptors in brain regions that are vital for memory formation, including the hippocampus, amygdala, and cerebral cortex.
Some neurotransmitters in the brain provide instructions for the body’s immune system and signal it when to activate its line of defense, where to engage it, and how strongly to involve it. The ECS also acts as an immuno-cannabinoid modulator as it gathers and interprets signals from cannabinoids. CBD oil vapes are one of the accelerated ways to get CBD into the body since it enters the bloodstream through the lungs, without going through the digestive system.
CBD has several properties that can help address some of the root causes of poor attention and focus. But if you don’t do anything to clear your brain fog, it can soon build up and affect how long does it take cbd oil to help depression your day-to-day life. Your productivity at work or school can suffer, and the stress from these problems could also begin to affect your relationship with the people around you. https://www.youtube.com/embed/zHAhDfnIECY
The neurons are involved in the allocation of memories and therefore, any form of damage to them might result in loss of memory or amnesia. Each neuron may be connected to up to other nerve cells and transmit signals to each other via as many as a substantial 1000 trillion synaptic connections. On an average, humans have around 100 billion neurons and many neighbouring cells known as neuroglia which is involved in nourishing and protecting the nerve cells. Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids.
Some studies suggest that even chronic low doses of THC can help to improve cognitive function — at least in animal models . As far as humans are concerned, there is growing data suggesting its positive effects on memory . We have all experienced temporary memory glitches, but if memory loss becomes chronic and compromises your daily functioning, it may be time to seek out treatment. The statements made regarding these products have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease. Please consult your health care professional about potential interactions or other possible complications before using any product.
does cbd help memory
And in a growing number of states, marijuana is legal for recreational use. For that reason, it has been difficult for researchers in the United States to obtain federal research funding to study marijuana, limiting the amount of high-quality evidence available. Also known as Huntington’s chorea, this disease is an inherited disorder that leads to degeneration of brain cells — which often results in symptoms of dementia. A digestive imbalance may also be a significant factor in the progression of Parkinson’s and the seriousness of its symptoms. Cannabinoids such as CBD have been shown to produce neuroprotective and antioxidant effects on the brain which, along with its anti-inflammatory properties, can be effective in managing Parkinson’s disease-induceddementia.
• If you buy through links on this page, we may earn a small commission.
• For those suffering from memory loss, CBD oil may be an all-natural alternative to traditional medications or increasing concerns about impaired functioning.
• So if the product is appropriate it can cause harm and can make my anxiety worse.
• While CBD at higher doses does not appear to have serious negative consequences, these products may also contain higher levels of THC than reported on the label.
• The authors claim that CBD’s activity is independent of dopamine receptor antagonism, which makes it a promising treatment for the condition .
• White Mulberry is known to be one of the most potent herbal medicines in the world, and research shows it can help with various diseases including hypertension and diabetes.
In 2020, the FDA conducted a study of 147 CBD products and found that half contained THC. In 2017, the government made changes to the regulations so that restrictions would be removed, which meant a doctor was able to prescribe cannabidiol to patients. Several industrial hemp varieties can be legally cultivated in Western Europe. A variety such as “Fedora 17” has a cannabinoid profile consistently around 1%, with THC less than 0.3%. Efforts to isolate the active ingredients in cannabis were made in the 19th century. Cannabidiol was studied in 1940 from Minnesota wild hemp and Egyptian Cannabis indica resin.
• Decades ago, scientists did not know that our bodies can produce cannabinoids all on our own.
• It can be said that CBD helps in improving cognition and thereby, boosts memory function which is one of the major cognitive abilities.
• Exercise and mindful meditation both boost BDNF and neurogenesis so that’s three things we can do to support mental health.
• Multiple studies have used different forms of CBD when investigating whether CBD is an effective treatment for PTSD.
• Most CBD products do not have FDA approval, which also means they have not undergone thorough tests.
Since CBD products are becoming more prevalent in mainstream wellness supplements, some companies have implemented CBD Drug Test guidelines. These suggest a cutoff amount where THC content can be admissible how much delta 8 thc is in hemp in negligible quantities. However, these products are considered to have inferior efficacy when compared to full spectrum CBD products, according to anecdotal reports and preliminary research.
Healthline has strict sourcing guidelines and relies on peer-reviewed studies, academic research institutions, and medical associations. CBD gummies are one does cbd oil help with joint pain of the most common and popular ways to take CBD. Each gummy contains the same amount of CBD per package, making it easier to know what dose you’re taking.
In addition to this, CBD might interact with some other drugs resulting in liver toxicity. So when you consume this compound with other medications, you have to ask a doctor for knowing whether it results in any drug interactions. Diseases such as Parkinson’s, dementia, Alzheimer’s usually involve inflammation of the neural tissues in the brain. CBD being a powerful anti-inflammatory agent can help in fighting such inflammation thus slowing down the progression of the disease. In a study done in 2015, mice showing symptoms of Alzheimer’s were given a combination of THC and CBD. It was discovered that the mice showed an improvement in learning skills and there was also a change in the amyloid-beta clumps was seen in the brain.
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You are using an unsupported browser. Please upgrade your browser to a newer version to get the best experience on DrugBank.
Identification
NameEthotoin
Accession NumberDB00754 (APRD00962)
TypeSmall Molecule
GroupsApproved
DescriptionEthotoin is a hydantoin derivative and anticonvulsant. Ethotoin exerts an antiepileptic effect without causing general central nervous system depression. The mechanism of action is probably very similar to that of phenytoin. The latter drug appears to stabilize rather than to raise the normal seizure threshold, and to prevent the spread of seizure activity rather than to abolish the primary focus of seizure discharges. Ethotoin is no longer commonly used.
Structure
Thumb
Synonyms
(+-)-3-Ethyl-5-phenylhydantoin
1-Ethyl-2,5-dioxo-4-phenylimidazolidine
3-Ethyl-5-phenyl-2,4-imidazolidinedione
3-Ethyl-5-phenyl-imidazolidine-2,4-dione
3-Ethyl-5-phenylhydantoin
3-Ethyl-5-phenylimidazolidin-2,4-dione
Ethotoin
Ethotoïne
Ethotoinum
Etotoina
External Identifiers Not Available
Approved Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
PeganoneTablet250 mg/1OralRecordati Rare Diseases Inc1957-04-22Not applicableUs
Approved Generic Prescription ProductsNot Available
Approved Over the Counter ProductsNot Available
Unapproved/Other Products Not Available
International Brands
NameCompany
AccenonDainippon Sumitomo
PegoanoneNot Available
Brand mixturesNot Available
SaltsNot Available
Categories
UNII46QG38NC4U
CAS number86-35-1
WeightAverage: 204.2252
Monoisotopic: 204.089877638
Chemical FormulaC11H12N2O2
InChI KeySZQIFWWUIBRPBZ-UHFFFAOYSA-N
InChI
InChI=1S/C11H12N2O2/c1-2-13-10(14)9(12-11(13)15)8-6-4-3-5-7-8/h3-7,9H,2H2,1H3,(H,12,15)
IUPAC Name
3-ethyl-5-phenylimidazolidine-2,4-dione
SMILES
CCN1C(=O)NC(C1=O)C1=CC=CC=C1
Pharmacology
IndicationFor the control of tonic-clonic (grand mal) and complex partial (psychomotor) seizures.
Structured Indications
Clinical Trials Not Available
PharmacodynamicsEthotoin is a hydantoin derivative and anticonvulsant. Ethotoin exerts an antiepileptic effect without causing general central nervous system depression. The mechanism of action is probably very similar to that of phenytoin. The latter drug appears to stabilize rather than to raise the normal seizure threshold, and to prevent the spread of seizure activity rather than to abolish the primary focus of seizure discharges.
Mechanism of actionThe mechanism of action is probably very similar to that of phenytoin. The latter drug appears to stabilize rather than to raise the normal seizure threshold, and to prevent the spread of seizure activity rather than to abolish the primary focus of seizure discharges. Ethotoin inhibits nerve impulses in the motor cortex by lowering sodium ion influx, limiting tetanic stimulation.
TargetKindPharmacological actionActionsOrganismUniProt ID
Sodium channel protein type 5 subunit alphaProteinyes
inhibitor
HumanQ14524 details
Related Articles
AbsorptionFairly rapidly absorbed, however, the extent of oral absorption is not known.
Volume of distributionNot Available
Protein bindingNot Available
Metabolism
Hepatic. The drug exhibits saturable metabolism with respect to the formation of N-deethyl and p-hydroxyl-ethotoin, the major metabolites.
SubstrateEnzymesProduct
Ethotoin
Not Available
p-Hydroxyl-ethotoinDetails
Route of eliminationNot Available
Half life3 to 9 hours
ClearanceNot Available
ToxicitySymptoms of overdose include drowsiness, loss of or impaired muscle coordination, nausea, visual disturbance, and, at very high doses, coma.
Affected organisms
• Humans and other mammals
PathwaysNot Available
SNP Mediated EffectsNot Available
SNP Mediated Adverse Drug ReactionsNot Available
Interactions
Drug Interactions
DrugInteractionDrug group
1,1,1,2 TetrafluoroethaneThe risk or severity of adverse effects can be increased when Ethotoin is combined with 1,1,1,2 Tetrafluoroethane.Investigational
7-NitroindazoleThe risk or severity of adverse effects can be increased when 7-Nitroindazole is combined with Ethotoin.Experimental
AcenocoumarolEthotoin may increase the anticoagulant activities of Acenocoumarol.Approved
AcepromazineThe risk or severity of adverse effects can be increased when Acepromazine is combined with Ethotoin.Approved, Vet Approved
AceprometazineThe risk or severity of adverse effects can be increased when Aceprometazine is combined with Ethotoin.Approved
adipiplonThe risk or severity of adverse effects can be increased when adipiplon is combined with Ethotoin.Investigational
AgomelatineThe risk or severity of adverse effects can be increased when Agomelatine is combined with Ethotoin.Approved, Investigational
AlfaxaloneThe risk or severity of adverse effects can be increased when Alfaxalone is combined with Ethotoin.Vet Approved
AlfentanilThe risk or severity of adverse effects can be increased when Alfentanil is combined with Ethotoin.Approved, Illicit
AlphacetylmethadolThe risk or severity of adverse effects can be increased when Alphacetylmethadol is combined with Ethotoin.Experimental, Illicit
AlprazolamThe risk or severity of adverse effects can be increased when Alprazolam is combined with Ethotoin.Approved, Illicit, Investigational
AmisulprideThe risk or severity of adverse effects can be increased when Amisulpride is combined with Ethotoin.Approved, Investigational
AmitriptylineThe risk or severity of adverse effects can be increased when Amitriptyline is combined with Ethotoin.Approved
AmobarbitalThe risk or severity of adverse effects can be increased when Amobarbital is combined with Ethotoin.Approved, Illicit
AmoxapineThe risk or severity of adverse effects can be increased when Amoxapine is combined with Ethotoin.Approved
AmperozideThe risk or severity of adverse effects can be increased when Amperozide is combined with Ethotoin.Experimental
AripiprazoleThe risk or severity of adverse effects can be increased when Aripiprazole is combined with Ethotoin.Approved, Investigational
ArticaineThe risk or severity of adverse effects can be increased when Articaine is combined with Ethotoin.Approved
AsenapineThe risk or severity of adverse effects can be increased when Asenapine is combined with Ethotoin.Approved
AzaperoneThe risk or severity of adverse effects can be increased when Azaperone is combined with Ethotoin.Vet Approved
AzelastineEthotoin may increase the central nervous system depressant (CNS depressant) activities of Azelastine.Approved
AzelastineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Azelastine.Approved
BaclofenThe risk or severity of adverse effects can be increased when Baclofen is combined with Ethotoin.Approved
BarbitalThe risk or severity of adverse effects can be increased when Barbital is combined with Ethotoin.Illicit
BenperidolThe risk or severity of adverse effects can be increased when Ethotoin is combined with Benperidol.Investigational
BenzocaineThe risk or severity of adverse effects can be increased when Benzocaine is combined with Ethotoin.Approved
Benzyl alcoholThe risk or severity of adverse effects can be increased when Benzyl alcohol is combined with Ethotoin.Approved
BrexpiprazoleThe risk or severity of adverse effects can be increased when Ethotoin is combined with Brexpiprazole.Approved
BrimonidineThe risk or severity of adverse effects can be increased when Brimonidine is combined with Ethotoin.Approved
BrimonidineBrimonidine may increase the central nervous system depressant (CNS depressant) activities of Ethotoin.Approved
BromazepamThe risk or severity of adverse effects can be increased when Bromazepam is combined with Ethotoin.Approved, Illicit
BrompheniramineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Brompheniramine.Approved
BrotizolamThe risk or severity of adverse effects can be increased when Brotizolam is combined with Ethotoin.Approved, Withdrawn
BupivacaineThe risk or severity of adverse effects can be increased when Bupivacaine is combined with Ethotoin.Approved, Investigational
BuprenorphineEthotoin may increase the central nervous system depressant (CNS depressant) activities of Buprenorphine.Approved, Illicit, Investigational, Vet Approved
BuspironeThe risk or severity of adverse effects can be increased when Buspirone is combined with Ethotoin.Approved, Investigational
ButabarbitalThe risk or severity of adverse effects can be increased when Butabarbital is combined with Ethotoin.Approved, Illicit
ButacaineThe risk or severity of adverse effects can be increased when Butacaine is combined with Ethotoin.Vet Approved
ButalbitalThe risk or severity of adverse effects can be increased when Butalbital is combined with Ethotoin.Approved, Illicit
ButambenThe risk or severity of adverse effects can be increased when Butamben is combined with Ethotoin.Approved
ButethalThe risk or severity of adverse effects can be increased when Butethal is combined with Ethotoin.Approved, Illicit
ButorphanolThe risk or severity of adverse effects can be increased when Butorphanol is combined with Ethotoin.Approved, Illicit, Vet Approved
CarbamazepineThe risk or severity of adverse effects can be increased when Carbamazepine is combined with Ethotoin.Approved, Investigational
CarbinoxamineThe risk or severity of adverse effects can be increased when Carbinoxamine is combined with Ethotoin.Approved
CarfentanilThe risk or severity of adverse effects can be increased when Carfentanil is combined with Ethotoin.Illicit, Vet Approved
CarisoprodolThe risk or severity of adverse effects can be increased when Carisoprodol is combined with Ethotoin.Approved
CetirizineThe risk or severity of adverse effects can be increased when Cetirizine is combined with Ethotoin.Approved
Chloral hydrateThe risk or severity of adverse effects can be increased when Chloral hydrate is combined with Ethotoin.Approved, Illicit, Vet Approved
ChlordiazepoxideThe risk or severity of adverse effects can be increased when Chlordiazepoxide is combined with Ethotoin.Approved, Illicit
ChlormezanoneThe risk or severity of adverse effects can be increased when Chlormezanone is combined with Ethotoin.Approved, Withdrawn
ChloroprocaineThe risk or severity of adverse effects can be increased when Chloroprocaine is combined with Ethotoin.Approved
ChlorphenamineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Chlorphenamine.Approved
ChlorpromazineThe risk or severity of adverse effects can be increased when Chlorpromazine is combined with Ethotoin.Approved, Vet Approved
ChlorprothixeneThe risk or severity of adverse effects can be increased when Chlorprothixene is combined with Ethotoin.Approved, Withdrawn
ChlorzoxazoneThe risk or severity of adverse effects can be increased when Chlorzoxazone is combined with Ethotoin.Approved
CilostazolThe serum concentration of Cilostazol can be increased when it is combined with Ethotoin.Approved
CinchocaineThe risk or severity of adverse effects can be increased when Cinchocaine is combined with Ethotoin.Approved, Vet Approved
CitalopramThe risk or severity of adverse effects can be increased when Ethotoin is combined with Citalopram.Approved
ClemastineThe risk or severity of adverse effects can be increased when Clemastine is combined with Ethotoin.Approved
ClidiniumThe risk or severity of adverse effects can be increased when Ethotoin is combined with Clidinium.Approved
ClobazamThe risk or severity of adverse effects can be increased when Clobazam is combined with Ethotoin.Approved, Illicit
clomethiazoleThe risk or severity of adverse effects can be increased when clomethiazole is combined with Ethotoin.Investigational
ClomipramineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Clomipramine.Approved, Vet Approved
ClonazepamThe risk or severity of adverse effects can be increased when Ethotoin is combined with Clonazepam.Approved, Illicit
ClonidineThe risk or severity of adverse effects can be increased when Clonidine is combined with Ethotoin.Approved
ClorazepateThe risk or severity of adverse effects can be increased when Clorazepate is combined with Ethotoin.Approved, Illicit
ClozapineThe risk or severity of adverse effects can be increased when Clozapine is combined with Ethotoin.Approved
CocaineThe risk or severity of adverse effects can be increased when Cocaine is combined with Ethotoin.Approved, Illicit
CodeineThe risk or severity of adverse effects can be increased when Codeine is combined with Ethotoin.Approved, Illicit
CyclizineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Cyclizine.Approved
CyclobenzaprineThe risk or severity of adverse effects can be increased when Cyclobenzaprine is combined with Ethotoin.Approved
CyproheptadineThe risk or severity of adverse effects can be increased when Cyproheptadine is combined with Ethotoin.Approved
DantroleneThe risk or severity of adverse effects can be increased when Ethotoin is combined with Dantrolene.Approved
DapiprazoleThe risk or severity of adverse effects can be increased when Dapiprazole is combined with Ethotoin.Approved
DapoxetineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Dapoxetine.Investigational
deramciclaneThe risk or severity of adverse effects can be increased when deramciclane is combined with Ethotoin.Investigational
DesfluraneThe risk or severity of adverse effects can be increased when Desflurane is combined with Ethotoin.Approved
DesipramineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Desipramine.Approved
DesloratadineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Desloratadine.Approved, Investigational
DesvenlafaxineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Desvenlafaxine.Approved
DetomidineThe risk or severity of adverse effects can be increased when Detomidine is combined with Ethotoin.Vet Approved
DexbrompheniramineThe risk or severity of adverse effects can be increased when Dexbrompheniramine is combined with Ethotoin.Approved
DexmedetomidineThe risk or severity of adverse effects can be increased when Dexmedetomidine is combined with Ethotoin.Approved, Vet Approved
DextromoramideThe risk or severity of adverse effects can be increased when Dextromoramide is combined with Ethotoin.Experimental, Illicit
DextropropoxypheneThe risk or severity of adverse effects can be increased when Dextropropoxyphene is combined with Ethotoin.Approved, Illicit, Withdrawn
DezocineThe risk or severity of adverse effects can be increased when Dezocine is combined with Ethotoin.Approved
DiazepamThe risk or severity of adverse effects can be increased when Diazepam is combined with Ethotoin.Approved, Illicit, Vet Approved
DicoumarolEthotoin may increase the anticoagulant activities of Dicoumarol.Approved
DifenoxinThe risk or severity of adverse effects can be increased when Ethotoin is combined with Difenoxin.Approved, Illicit
DihydrocodeineThe risk or severity of adverse effects can be increased when Dihydrocodeine is combined with Ethotoin.Approved, Illicit
DihydroetorphineThe risk or severity of adverse effects can be increased when Dihydroetorphine is combined with Ethotoin.Experimental, Illicit
DihydromorphineThe risk or severity of adverse effects can be increased when Dihydromorphine is combined with Ethotoin.Experimental, Illicit
DimenhydrinateThe risk or severity of adverse effects can be increased when Ethotoin is combined with Dimenhydrinate.Approved
DiphenhydramineThe risk or severity of adverse effects can be increased when Diphenhydramine is combined with Ethotoin.Approved
DiphenoxylateThe risk or severity of adverse effects can be increased when Diphenoxylate is combined with Ethotoin.Approved, Illicit
DoramectinThe risk or severity of adverse effects can be increased when Doramectin is combined with Ethotoin.Vet Approved
DoxepinThe risk or severity of adverse effects can be increased when Ethotoin is combined with Doxepin.Approved
DoxylamineDoxylamine may increase the central nervous system depressant (CNS depressant) activities of Ethotoin.Approved, Vet Approved
DPDPEThe risk or severity of adverse effects can be increased when DPDPE is combined with Ethotoin.Investigational
DronabinolDronabinol may increase the central nervous system depressant (CNS depressant) activities of Ethotoin.Approved, Illicit
DroperidolDroperidol may increase the central nervous system depressant (CNS depressant) activities of Ethotoin.Approved, Vet Approved
DrotebanolThe risk or severity of adverse effects can be increased when Drotebanol is combined with Ethotoin.Experimental, Illicit
DuloxetineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Duloxetine.Approved
DyclonineThe risk or severity of adverse effects can be increased when Dyclonine is combined with Ethotoin.Approved
EcgonineThe risk or severity of adverse effects can be increased when Ecgonine is combined with Ethotoin.Experimental, Illicit
ECGONINE METHYL ESTERThe risk or severity of adverse effects can be increased when ECGONINE METHYL ESTER is combined with Ethotoin.Experimental
EcopipamThe risk or severity of adverse effects can be increased when Ethotoin is combined with Ecopipam.Investigational
EfavirenzThe risk or severity of adverse effects can be increased when Efavirenz is combined with Ethotoin.Approved, Investigational
EnfluraneThe risk or severity of adverse effects can be increased when Enflurane is combined with Ethotoin.Approved, Vet Approved
EntacaponeThe risk or severity of adverse effects can be increased when Entacapone is combined with Ethotoin.Approved, Investigational
EscitalopramThe risk or severity of adverse effects can be increased when Ethotoin is combined with Escitalopram.Approved, Investigational
EstazolamThe risk or severity of adverse effects can be increased when Estazolam is combined with Ethotoin.Approved, Illicit
EszopicloneThe risk or severity of adverse effects can be increased when Eszopiclone is combined with Ethotoin.Approved
EthanolEthotoin may increase the central nervous system depressant (CNS depressant) activities of Ethanol.Approved
EthchlorvynolThe risk or severity of adverse effects can be increased when Ethchlorvynol is combined with Ethotoin.Approved, Illicit, Withdrawn
EthosuximideThe risk or severity of adverse effects can be increased when Ethosuximide is combined with Ethotoin.Approved
Ethyl biscoumacetateEthotoin may increase the anticoagulant activities of Ethyl biscoumacetate.Withdrawn
Ethyl carbamateThe risk or severity of adverse effects can be increased when Ethyl carbamate is combined with Ethotoin.Withdrawn
Ethyl loflazepateThe risk or severity of adverse effects can be increased when Ethyl loflazepate is combined with Ethotoin.Approved, Illicit
EthylmorphineThe risk or severity of adverse effects can be increased when Ethylmorphine is combined with Ethotoin.Approved, Illicit
EtidocaineThe risk or severity of adverse effects can be increased when Etidocaine is combined with Ethotoin.Approved
EtifoxineThe risk or severity of adverse effects can be increased when Etifoxine is combined with Ethotoin.Withdrawn
EtizolamThe risk or severity of adverse effects can be increased when Etizolam is combined with Ethotoin.Approved
EtomidateThe risk or severity of adverse effects can be increased when Etomidate is combined with Ethotoin.Approved
EtoperidoneThe risk or severity of adverse effects can be increased when Ethotoin is combined with Etoperidone.Approved
EtorphineThe risk or severity of adverse effects can be increased when Etorphine is combined with Ethotoin.Illicit, Vet Approved
EzogabineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Ezogabine.Approved
FelbamateThe risk or severity of adverse effects can be increased when Ethotoin is combined with Felbamate.Approved
FencamfamineThe risk or severity of adverse effects can be increased when Fencamfamine is combined with Ethotoin.Approved, Illicit, Withdrawn
FentanylThe risk or severity of adverse effects can be increased when Fentanyl is combined with Ethotoin.Approved, Illicit, Investigational, Vet Approved
FexofenadineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Fexofenadine.Approved
FlibanserinThe risk or severity of adverse effects can be increased when Ethotoin is combined with Flibanserin.Approved
FludiazepamThe risk or severity of adverse effects can be increased when Fludiazepam is combined with Ethotoin.Approved, Illicit
FluindioneEthotoin may increase the anticoagulant activities of Fluindione.Investigational
FlunarizineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Flunarizine.Approved
FlunitrazepamThe risk or severity of adverse effects can be increased when Flunitrazepam is combined with Ethotoin.Approved, Illicit
FluoxetineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Fluoxetine.Approved, Vet Approved
FlupentixolThe risk or severity of adverse effects can be increased when Flupentixol is combined with Ethotoin.Approved, Withdrawn
FluphenazineThe risk or severity of adverse effects can be increased when Fluphenazine is combined with Ethotoin.Approved
FlurazepamThe risk or severity of adverse effects can be increased when Flurazepam is combined with Ethotoin.Approved, Illicit
FluspirileneThe risk or severity of adverse effects can be increased when Fluspirilene is combined with Ethotoin.Approved
Fluticasone PropionateThe risk or severity of adverse effects can be increased when Fluticasone Propionate is combined with Ethotoin.Approved
FluvoxamineThe risk or severity of adverse effects can be increased when Fluvoxamine is combined with Ethotoin.Approved, Investigational
FosphenytoinThe risk or severity of adverse effects can be increased when Ethotoin is combined with Fosphenytoin.Approved
FospropofolThe risk or severity of adverse effects can be increased when Fospropofol is combined with Ethotoin.Approved, Illicit
GabapentinThe risk or severity of adverse effects can be increased when Gabapentin is combined with Ethotoin.Approved, Investigational
gabapentin enacarbilThe risk or severity of adverse effects can be increased when Ethotoin is combined with gabapentin enacarbil.Approved
Gamma Hydroxybutyric AcidThe risk or severity of adverse effects can be increased when Gamma Hydroxybutyric Acid is combined with Ethotoin.Approved, Illicit
GepironeThe risk or severity of adverse effects can be increased when Ethotoin is combined with Gepirone.Investigational
GlutethimideThe risk or severity of adverse effects can be increased when Glutethimide is combined with Ethotoin.Approved, Illicit
GuanfacineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Guanfacine.Approved, Investigational
HalazepamThe risk or severity of adverse effects can be increased when Halazepam is combined with Ethotoin.Approved, Illicit, Withdrawn
HaloperidolThe risk or severity of adverse effects can be increased when Haloperidol is combined with Ethotoin.Approved
HalothaneThe risk or severity of adverse effects can be increased when Halothane is combined with Ethotoin.Approved, Vet Approved
HeroinThe risk or severity of adverse effects can be increased when Heroin is combined with Ethotoin.Approved, Illicit
HexobarbitalThe risk or severity of adverse effects can be increased when Hexobarbital is combined with Ethotoin.Approved
HydrocodoneEthotoin may increase the central nervous system depressant (CNS depressant) activities of Hydrocodone.Approved, Illicit
HydromorphoneThe risk or severity of adverse effects can be increased when Hydromorphone is combined with Ethotoin.Approved, Illicit
HydroxyzineHydroxyzine may increase the central nervous system depressant (CNS depressant) activities of Ethotoin.Approved
IloperidoneThe risk or severity of adverse effects can be increased when Ethotoin is combined with Iloperidone.Approved
ImipramineThe risk or severity of adverse effects can be increased when Imipramine is combined with Ethotoin.Approved
IndalpineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Indalpine.Investigational, Withdrawn
IsofluraneThe risk or severity of adverse effects can be increased when Isoflurane is combined with Ethotoin.Approved, Vet Approved
KetamineThe risk or severity of adverse effects can be increased when Ketamine is combined with Ethotoin.Approved, Vet Approved
KetazolamThe risk or severity of adverse effects can be increased when Ketazolam is combined with Ethotoin.Approved
KetobemidoneThe risk or severity of adverse effects can be increased when Ketobemidone is combined with Ethotoin.Approved
LamotrigineThe risk or severity of adverse effects can be increased when Lamotrigine is combined with Ethotoin.Approved, Investigational
LevetiracetamThe risk or severity of adverse effects can be increased when Ethotoin is combined with Levetiracetam.Approved, Investigational
LevobupivacaineThe risk or severity of adverse effects can be increased when Levobupivacaine is combined with Ethotoin.Approved
LevocabastineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Levocabastine.Approved
LevocetirizineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Levocetirizine.Approved
LevodopaThe risk or severity of adverse effects can be increased when Ethotoin is combined with Levodopa.Approved
Levomethadyl AcetateThe risk or severity of adverse effects can be increased when Levomethadyl Acetate is combined with Ethotoin.Approved
LevomilnacipranThe risk or severity of adverse effects can be increased when Ethotoin is combined with Levomilnacipran.Approved
LevorphanolThe risk or severity of adverse effects can be increased when Levorphanol is combined with Ethotoin.Approved
LidocaineThe risk or severity of adverse effects can be increased when Lidocaine is combined with Ethotoin.Approved, Vet Approved
LithiumThe risk or severity of adverse effects can be increased when Lithium is combined with Ethotoin.Approved
LofentanilThe risk or severity of adverse effects can be increased when Lofentanil is combined with Ethotoin.Illicit
LoratadineThe risk or severity of adverse effects can be increased when Loratadine is combined with Ethotoin.Approved
LorazepamThe risk or severity of adverse effects can be increased when Lorazepam is combined with Ethotoin.Approved
LoxapineThe risk or severity of adverse effects can be increased when Loxapine is combined with Ethotoin.Approved
Lu AA21004The risk or severity of adverse effects can be increased when Lu AA21004 is combined with Ethotoin.Investigational
LurasidoneThe risk or severity of adverse effects can be increased when Lurasidone is combined with Ethotoin.Approved
Magnesium SulfateMagnesium Sulfate may increase the central nervous system depressant (CNS depressant) activities of Ethotoin.Approved, Vet Approved
MaprotilineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Maprotiline.Approved
MeclizineThe risk or severity of adverse effects can be increased when Meclizine is combined with Ethotoin.Approved
MedetomidineThe risk or severity of adverse effects can be increased when Medetomidine is combined with Ethotoin.Vet Approved
MefloquineThe therapeutic efficacy of Ethotoin can be decreased when used in combination with Mefloquine.Approved
MelatoninThe risk or severity of adverse effects can be increased when Melatonin is combined with Ethotoin.Approved, Nutraceutical, Vet Approved
MelperoneThe risk or severity of adverse effects can be increased when Melperone is combined with Ethotoin.Approved
MepivacaineThe risk or severity of adverse effects can be increased when Mepivacaine is combined with Ethotoin.Approved, Vet Approved
MeprobamateThe risk or severity of adverse effects can be increased when Meprobamate is combined with Ethotoin.Approved, Illicit
MesoridazineThe risk or severity of adverse effects can be increased when Mesoridazine is combined with Ethotoin.Approved
MetaxaloneThe risk or severity of adverse effects can be increased when Metaxalone is combined with Ethotoin.Approved
MethadoneThe risk or severity of adverse effects can be increased when Methadone is combined with Ethotoin.Approved
Methadyl AcetateThe risk or severity of adverse effects can be increased when Methadyl Acetate is combined with Ethotoin.Approved, Illicit
MethapyrileneThe risk or severity of adverse effects can be increased when Methapyrilene is combined with Ethotoin.Withdrawn
MethaqualoneThe risk or severity of adverse effects can be increased when Methaqualone is combined with Ethotoin.Illicit, Withdrawn
MethocarbamolThe risk or severity of adverse effects can be increased when Methocarbamol is combined with Ethotoin.Approved, Vet Approved
MethohexitalThe risk or severity of adverse effects can be increased when Methohexital is combined with Ethotoin.Approved
MethotrimeprazineEthotoin may increase the central nervous system depressant (CNS depressant) activities of Methotrimeprazine.Approved
MethoxyfluraneThe risk or severity of adverse effects can be increased when Methoxyflurane is combined with Ethotoin.Approved, Vet Approved
MethsuximideThe risk or severity of adverse effects can be increased when Ethotoin is combined with Methsuximide.Approved
MethylphenobarbitalThe risk or severity of adverse effects can be increased when Methylphenobarbital is combined with Ethotoin.Approved
MetyrosineEthotoin may increase the sedative activities of Metyrosine.Approved
MianserinThe therapeutic efficacy of Ethotoin can be decreased when used in combination with Mianserin.Approved
MidazolamThe risk or severity of adverse effects can be increased when Midazolam is combined with Ethotoin.Approved, Illicit
MilnacipranThe risk or severity of adverse effects can be increased when Ethotoin is combined with Milnacipran.Approved
MinocyclineMinocycline may increase the central nervous system depressant (CNS depressant) activities of Ethotoin.Approved, Investigational
MirtazapineEthotoin may increase the central nervous system depressant (CNS depressant) activities of Mirtazapine.Approved
MolindoneThe risk or severity of adverse effects can be increased when Molindone is combined with Ethotoin.Approved
MorphineThe risk or severity of adverse effects can be increased when Morphine is combined with Ethotoin.Approved, Investigational
NabiloneNabilone may increase the central nervous system depressant (CNS depressant) activities of Ethotoin.Approved, Investigational
NalbuphineThe risk or severity of adverse effects can be increased when Nalbuphine is combined with Ethotoin.Approved
NefazodoneThe risk or severity of adverse effects can be increased when Ethotoin is combined with Nefazodone.Approved, Withdrawn
NitrazepamThe risk or severity of adverse effects can be increased when Nitrazepam is combined with Ethotoin.Approved
Nitrous oxideThe risk or severity of adverse effects can be increased when Nitrous oxide is combined with Ethotoin.Approved, Vet Approved
NormethadoneThe risk or severity of adverse effects can be increased when Normethadone is combined with Ethotoin.Approved, Illicit
NortriptylineThe risk or severity of adverse effects can be increased when Nortriptyline is combined with Ethotoin.Approved
OlanzapineThe risk or severity of adverse effects can be increased when Olanzapine is combined with Ethotoin.Approved, Investigational
OlopatadineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Olopatadine.Approved
OndansetronThe risk or severity of adverse effects can be increased when Ondansetron is combined with Ethotoin.Approved
OpiumThe risk or severity of adverse effects can be increased when Opium is combined with Ethotoin.Approved, Illicit
OrlistatThe serum concentration of Ethotoin can be decreased when it is combined with Orlistat.Approved, Investigational
OrphenadrineEthotoin may increase the central nervous system depressant (CNS depressant) activities of Orphenadrine.Approved
OsanetantThe risk or severity of adverse effects can be increased when Osanetant is combined with Ethotoin.Investigational
OxazepamThe risk or severity of adverse effects can be increased when Oxazepam is combined with Ethotoin.Approved
OxetacaineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Oxetacaine.Investigational
OxprenololThe risk or severity of adverse effects can be increased when Oxprenolol is combined with Ethotoin.Approved
OxybuprocaineThe risk or severity of adverse effects can be increased when Oxybuprocaine is combined with Ethotoin.Approved
OxycodoneThe risk or severity of adverse effects can be increased when Oxycodone is combined with Ethotoin.Approved, Illicit, Investigational
OxymorphoneThe risk or severity of adverse effects can be increased when Oxymorphone is combined with Ethotoin.Approved, Investigational, Vet Approved
PaliperidoneThe risk or severity of adverse effects can be increased when Paliperidone is combined with Ethotoin.Approved
ParaldehydeEthotoin may increase the central nervous system depressant (CNS depressant) activities of Paraldehyde.Approved
ParoxetineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Paroxetine.Approved, Investigational
PentazocineThe risk or severity of adverse effects can be increased when Pentazocine is combined with Ethotoin.Approved, Vet Approved
PentobarbitalThe risk or severity of adverse effects can be increased when Pentobarbital is combined with Ethotoin.Approved, Vet Approved
PerampanelPerampanel may increase the central nervous system depressant (CNS depressant) activities of Ethotoin.Approved
PerazineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Perazine.Investigational
PerospironeThe risk or severity of adverse effects can be increased when Perospirone is combined with Ethotoin.Approved
PerphenazineThe risk or severity of adverse effects can be increased when Perphenazine is combined with Ethotoin.Approved
PethidineThe risk or severity of adverse effects can be increased when Pethidine is combined with Ethotoin.Approved
PhenindioneEthotoin may increase the anticoagulant activities of Phenindione.Approved
PhenobarbitalThe risk or severity of adverse effects can be increased when Phenobarbital is combined with Ethotoin.Approved
PhenoxyethanolThe risk or severity of adverse effects can be increased when Phenoxyethanol is combined with Ethotoin.Approved
PhenprocoumonEthotoin may increase the anticoagulant activities of Phenprocoumon.Approved
PhenytoinThe risk or severity of adverse effects can be increased when Phenytoin is combined with Ethotoin.Approved, Vet Approved
PimozideThe risk or severity of adverse effects can be increased when Pimozide is combined with Ethotoin.Approved
PipamperoneThe risk or severity of adverse effects can be increased when Pipamperone is combined with Ethotoin.Approved
PipotiazineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Pipotiazine.Approved
PiritramideThe risk or severity of adverse effects can be increased when Ethotoin is combined with Piritramide.Investigational
PizotifenThe risk or severity of adverse effects can be increased when Ethotoin is combined with Pizotifen.Approved
PomalidomideThe risk or severity of adverse effects can be increased when Ethotoin is combined with Pomalidomide.Approved
PramipexoleEthotoin may increase the sedative activities of Pramipexole.Approved, Investigational
PramocaineThe risk or severity of adverse effects can be increased when Pramocaine is combined with Ethotoin.Approved
PrazepamThe risk or severity of adverse effects can be increased when Prazepam is combined with Ethotoin.Approved, Illicit
PregabalinThe risk or severity of adverse effects can be increased when Pregabalin is combined with Ethotoin.Approved, Illicit, Investigational
PregnanoloneThe risk or severity of adverse effects can be increased when Ethotoin is combined with Pregnanolone.Investigational
PrilocaineThe risk or severity of adverse effects can be increased when Prilocaine is combined with Ethotoin.Approved
PrimidoneThe risk or severity of adverse effects can be increased when Ethotoin is combined with Primidone.Approved, Vet Approved
ProcaineThe risk or severity of adverse effects can be increased when Procaine is combined with Ethotoin.Approved, Investigational, Vet Approved
ProchlorperazineThe risk or severity of adverse effects can be increased when Prochlorperazine is combined with Ethotoin.Approved, Vet Approved
PromazineThe risk or severity of adverse effects can be increased when Promazine is combined with Ethotoin.Approved, Vet Approved
PromethazineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Promethazine.Approved
ProparacaineThe risk or severity of adverse effects can be increased when Proparacaine is combined with Ethotoin.Approved, Vet Approved
PropofolThe risk or severity of adverse effects can be increased when Propofol is combined with Ethotoin.Approved, Investigational, Vet Approved
PropoxycaineThe risk or severity of adverse effects can be increased when Propoxycaine is combined with Ethotoin.Approved
ProtriptylineThe risk or severity of adverse effects can be increased when Protriptyline is combined with Ethotoin.Approved
PSD502The risk or severity of adverse effects can be increased when PSD502 is combined with Ethotoin.Investigational
QuazepamThe risk or severity of adverse effects can be increased when Quazepam is combined with Ethotoin.Approved, Illicit
QuetiapineThe risk or severity of adverse effects can be increased when Quetiapine is combined with Ethotoin.Approved
RacloprideThe risk or severity of adverse effects can be increased when Ethotoin is combined with Raclopride.Investigational
RamelteonThe risk or severity of adverse effects can be increased when Ethotoin is combined with Ramelteon.Approved, Investigational
RemifentanilThe risk or severity of adverse effects can be increased when Remifentanil is combined with Ethotoin.Approved
RemoxiprideThe risk or severity of adverse effects can be increased when Remoxipride is combined with Ethotoin.Approved, Withdrawn
ReserpineThe risk or severity of adverse effects can be increased when Reserpine is combined with Ethotoin.Approved
RisperidoneThe risk or severity of adverse effects can be increased when Risperidone is combined with Ethotoin.Approved, Investigational
RitanserinThe risk or severity of adverse effects can be increased when Ethotoin is combined with Ritanserin.Investigational
RomifidineThe risk or severity of adverse effects can be increased when Romifidine is combined with Ethotoin.Vet Approved
RopiniroleEthotoin may increase the sedative activities of Ropinirole.Approved, Investigational
RopivacaineThe risk or severity of adverse effects can be increased when Ropivacaine is combined with Ethotoin.Approved
RotigotineEthotoin may increase the sedative activities of Rotigotine.Approved
RufinamideThe risk or severity of adverse effects can be increased when Rufinamide is combined with Ethotoin.Approved
S-EthylisothioureaThe risk or severity of adverse effects can be increased when S-Ethylisothiourea is combined with Ethotoin.Experimental
Sage 547The risk or severity of adverse effects can be increased when Ethotoin is combined with Sage 547.Investigational
ScopolamineThe risk or severity of adverse effects can be increased when Scopolamine is combined with Ethotoin.Approved
SecobarbitalThe risk or severity of adverse effects can be increased when Secobarbital is combined with Ethotoin.Approved, Vet Approved
SertindoleThe risk or severity of adverse effects can be increased when Sertindole is combined with Ethotoin.Approved, Withdrawn
SertralineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Sertraline.Approved
SevofluraneThe risk or severity of adverse effects can be increased when Sevoflurane is combined with Ethotoin.Approved, Vet Approved
Sodium oxybateSodium oxybate may increase the central nervous system depressant (CNS depressant) activities of Ethotoin.Approved
StiripentolThe risk or severity of adverse effects can be increased when Ethotoin is combined with Stiripentol.Approved
SufentanilThe risk or severity of adverse effects can be increased when Sufentanil is combined with Ethotoin.Approved, Investigational
SulpirideThe risk or severity of adverse effects can be increased when Sulpiride is combined with Ethotoin.Approved
SuvorexantEthotoin may increase the central nervous system depressant (CNS depressant) activities of Suvorexant.Approved
TandospironeThe risk or severity of adverse effects can be increased when Ethotoin is combined with Tandospirone.Investigational
TapentadolTapentadol may increase the central nervous system depressant (CNS depressant) activities of Ethotoin.Approved
TasimelteonThe risk or severity of adverse effects can be increased when Ethotoin is combined with Tasimelteon.Approved
TemazepamThe risk or severity of adverse effects can be increased when Temazepam is combined with Ethotoin.Approved
TetrabenazineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Tetrabenazine.Approved
TetracaineThe risk or severity of adverse effects can be increased when Tetracaine is combined with Ethotoin.Approved, Vet Approved
TetrodotoxinThe risk or severity of adverse effects can be increased when Tetrodotoxin is combined with Ethotoin.Investigational
ThalidomideEthotoin may increase the central nervous system depressant (CNS depressant) activities of Thalidomide.Approved, Investigational, Withdrawn
ThiamylalThe risk or severity of adverse effects can be increased when Thiamylal is combined with Ethotoin.Approved, Vet Approved
ThiopentalThe risk or severity of adverse effects can be increased when Thiopental is combined with Ethotoin.Approved, Vet Approved
ThioridazineThe risk or severity of adverse effects can be increased when Thioridazine is combined with Ethotoin.Approved
ThiothixeneThe risk or severity of adverse effects can be increased when Thiothixene is combined with Ethotoin.Approved
TiagabineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Tiagabine.Approved
TiaprideThe risk or severity of adverse effects can be increased when Ethotoin is combined with Tiapride.Investigational
TiletamineThe risk or severity of adverse effects can be increased when Tiletamine is combined with Ethotoin.Vet Approved
TizanidineThe risk or severity of adverse effects can be increased when Tizanidine is combined with Ethotoin.Approved
TolcaponeThe risk or severity of adverse effects can be increased when Tolcapone is combined with Ethotoin.Approved, Withdrawn
TopiramateThe risk or severity of adverse effects can be increased when Topiramate is combined with Ethotoin.Approved
TramadolThe risk or severity of adverse effects can be increased when Tramadol is combined with Ethotoin.Approved, Investigational
Trans-2-PhenylcyclopropylamineThe risk or severity of adverse effects can be increased when Trans-2-Phenylcyclopropylamine is combined with Ethotoin.Experimental
TranylcypromineThe risk or severity of adverse effects can be increased when Tranylcypromine is combined with Ethotoin.Approved
TrazodoneThe risk or severity of adverse effects can be increased when Trazodone is combined with Ethotoin.Approved, Investigational
TriazolamThe risk or severity of adverse effects can be increased when Triazolam is combined with Ethotoin.Approved
TrifluoperazineThe risk or severity of adverse effects can be increased when Trifluoperazine is combined with Ethotoin.Approved
TriflupromazineThe risk or severity of adverse effects can be increased when Triflupromazine is combined with Ethotoin.Approved, Vet Approved
TrimipramineThe risk or severity of adverse effects can be increased when Trimipramine is combined with Ethotoin.Approved
TriprolidineThe risk or severity of adverse effects can be increased when Triprolidine is combined with Ethotoin.Approved
Uc1010The risk or severity of adverse effects can be increased when Ethotoin is combined with Uc1010.Investigational
Valproic AcidThe risk or severity of adverse effects can be increased when Valproic Acid is combined with Ethotoin.Approved, Investigational
VenlafaxineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Venlafaxine.Approved
VigabatrinThe risk or severity of adverse effects can be increased when Ethotoin is combined with Vigabatrin.Approved
VortioxetineThe risk or severity of adverse effects can be increased when Vortioxetine is combined with Ethotoin.Approved
WarfarinEthotoin may increase the anticoagulant activities of Warfarin.Approved
XylazineThe risk or severity of adverse effects can be increased when Xylazine is combined with Ethotoin.Vet Approved
ZaleplonThe risk or severity of adverse effects can be increased when Zaleplon is combined with Ethotoin.Approved, Illicit, Investigational
ZiconotideThe risk or severity of adverse effects can be increased when Ethotoin is combined with Ziconotide.Approved
ZimelidineThe risk or severity of adverse effects can be increased when Ethotoin is combined with Zimelidine.Withdrawn
ZiprasidoneThe risk or severity of adverse effects can be increased when Ziprasidone is combined with Ethotoin.Approved
ZolazepamThe risk or severity of adverse effects can be increased when Zolazepam is combined with Ethotoin.Vet Approved
ZolpidemEthotoin may increase the central nervous system depressant (CNS depressant) activities of Zolpidem.Approved
ZonisamideThe risk or severity of adverse effects can be increased when Ethotoin is combined with Zonisamide.Approved, Investigational
ZopicloneThe risk or severity of adverse effects can be increased when Zopiclone is combined with Ethotoin.Approved
ZotepineThe risk or severity of adverse effects can be increased when Zotepine is combined with Ethotoin.Approved
ZuclopenthixolThe risk or severity of adverse effects can be increased when Zuclopenthixol is combined with Ethotoin.Approved, Investigational
Food InteractionsNot Available
References
Synthesis Reference
Close, W.J.; U.S. Patent 2,793,157; May 21, 1957; assigned to Abbott Laboratories.
General References
1. SCHWADE ED, RICHARDS RK, EVERETT GM: Peganone, a new antiepileptic drug. Dis Nerv Syst. 1956 May;17(5):155-8. [PubMed:13317788 ]
External Links
ATC CodesN03AB01
AHFS CodesNot Available
PDB EntriesNot Available
FDA labelNot Available
MSDSNot Available
ADMET
Predicted ADMET features
PropertyValueProbability
Human Intestinal Absorption+1.0
Blood Brain Barrier+0.9936
Caco-2 permeable+0.5629
P-glycoprotein substrateNon-substrate0.592
P-glycoprotein inhibitor INon-inhibitor0.8358
P-glycoprotein inhibitor IINon-inhibitor0.9401
Renal organic cation transporterNon-inhibitor0.8532
CYP450 2C9 substrateNon-substrate0.7507
CYP450 2D6 substrateNon-substrate0.9115
CYP450 3A4 substrateNon-substrate0.7383
CYP450 1A2 substrateNon-inhibitor0.9045
CYP450 2C9 inhibitorNon-inhibitor0.914
CYP450 2D6 inhibitorNon-inhibitor0.9619
CYP450 2C19 inhibitorNon-inhibitor0.9025
CYP450 3A4 inhibitorNon-inhibitor0.8591
CYP450 inhibitory promiscuityLow CYP Inhibitory Promiscuity0.8483
Ames testNon AMES toxic0.7056
CarcinogenicityNon-carcinogens0.8655
BiodegradationNot ready biodegradable0.8423
Rat acute toxicity2.1653 LD50, mol/kg Not applicable
hERG inhibition (predictor I)Weak inhibitor0.886
hERG inhibition (predictor II)Non-inhibitor0.8724
ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397 )
Pharmacoeconomics
Manufacturers
• Lundbeck inc
Packagers
Dosage forms
FormRouteStrength
TabletOral250 mg/1
Prices
Unit descriptionCostUnit
Peganone 250 mg tablet1.33USD tablet
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
PatentsNot Available
Properties
StateSolid
Experimental Properties
PropertyValueSource
melting point94 °CPhysProp
water solubility5280 mg/LNot Available
logP1.05SANGSTER (1994)
Predicted Properties
PropertyValueSource
Water Solubility2.38 mg/mLALOGPS
logP1.11ALOGPS
logP1.07ChemAxon
logS-1.9ALOGPS
pKa (Strongest Acidic)11.29ChemAxon
pKa (Strongest Basic)-8.4ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count2ChemAxon
Hydrogen Donor Count1ChemAxon
Polar Surface Area49.41 Å2ChemAxon
Rotatable Bond Count2ChemAxon
Refractivity55.05 m3·mol-1ChemAxon
Polarizability20.68 Å3ChemAxon
Number of Rings2ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
Mass Spec (NIST)Download (8.5 KB)
Spectra
Spectrum TypeDescriptionSplash Key
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, PositiveNot Available
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, PositiveNot Available
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, PositiveNot Available
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, NegativeNot Available
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, NegativeNot Available
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, NegativeNot Available
MSMass Spectrum (Electron Ionization)splash10-0udi-6920000000-01714c9dcd6c4cf02362View in MoNA
Taxonomy
DescriptionThis compound belongs to the class of chemical entities known as phenylhydantoins. These are heterocyclic aromatic compounds containing an imiazolidinedione moiety substituted by a phenyl group.
KingdomChemical entities
Super ClassOrganic compounds
ClassOrganoheterocyclic compounds
Sub ClassAzolidines
Direct ParentPhenylhydantoins
Alternative Parents
Substituents
• 5-phenylhydantoin
• Phenylimidazolidine
• Alpha-amino acid or derivatives
• Ureide
• Monocyclic benzene moiety
• Benzenoid
• Dicarboximide
• Urea
• Carboxylic acid derivative
• Azacycle
• Organic oxide
• Organooxygen compound
• Organonitrogen compound
• Organopnictogen compound
• Organic nitrogen compound
• Carbonyl group
• Organic oxygen compound
• Hydrocarbon derivative
• Aromatic heteromonocyclic compound
Molecular FrameworkAromatic heteromonocyclic compounds
External Descriptors
Targets
Kind
Protein
Organism
Human
Pharmacological action
yes
Actions
inhibitor
General Function:
Voltage-gated sodium channel activity involved in sa node cell action potential
Specific Function:
This protein mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient. It is a tetrodotoxin-resistant Na(+) channel isoform. This channel is respon...
Gene Name:
SCN5A
Uniprot ID:
Q14524
Molecular Weight:
226937.475 Da
References
1. Overington JP, Al-Lazikani B, Hopkins AL: How many drug targets are there? Nat Rev Drug Discov. 2006 Dec;5(12):993-6. [PubMed:17139284 ]
2. Imming P, Sinning C, Meyer A: Drugs, their targets and the nature and number of drug targets. Nat Rev Drug Discov. 2006 Oct;5(10):821-34. [PubMed:17016423 ]
3. Lenkowski PW, Ko SH, Anderson JD, Brown ML, Patel MK: Block of human NaV1.5 sodium channels by novel alpha-hydroxyphenylamide analogues of phenytoin. Eur J Pharm Sci. 2004 Apr;21(5):635-44. [PubMed:15066664 ]
4. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [PubMed:11752352 ]
Enzymes
Kind
Protein
Organism
Human
Pharmacological action
unknown
Actions
inhibitor
General Function:
Steroid hydroxylase activity
Specific Function:
Responsible for the metabolism of a number of therapeutic agents such as the anticonvulsant drug S-mephenytoin, omeprazole, proguanil, certain barbiturates, diazepam, propranolol, citalopram and imipramine.
Gene Name:
CYP2C19
Uniprot ID:
P33261
Molecular Weight:
55930.545 Da
References
1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. doi: 10.1093/nar/gkp970. Epub 2009 Nov 24. [PubMed:19934256 ]
Comments
comments powered by Disqus
Drug created on June 13, 2005 07:24 / Updated on August 17, 2016 12:23
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Stop In Hate Yourself For Smoking
Most those that smoke want to quit, and there are plenty of people who use the e-cig. Smoking is a deadly habit that catches upto everyone that will it definitely. So read through this article and visit what that can be done to truly get gone your smoking habit for really. And enhance your sex life.
Add exercise to your weekly routine to replace smoking. Smoking wreaks havoc on the body, and if you rid yourself of these ill effects, you will notice an in energy and better lung convenience of your physical exercises. As your body becomes stronger and more fit, may never be often unwilling to undo each one of that extended labor by using tobacco.
Hypnosis may appear far more than simply stage caliburn vape show, more than a parlor trick. Hypnotism is practiced by many professional Hypnotherapists, and smoking has been utilized to help millions men and women to overcome fears, conquer difficult problems, and to relax and reduce stress.
When are generally feeling a minute of weakness, call someone in your support web 2 . 0. It could be loved ones member, friend or colleague, anyone that you can make use of to for you to how you will feel. Not only does cell phone act like a good diversion until your craving has ended, it is always good to understand that you are not alone when dealing with this associated with issue.
Save money – smoking is not merely the an expensive habit to maintain due to the high price the product, but may longer term costs consider too. Insurance policy will be more expensive and you may potentially have more health problems too. Health conditions such as stroke, diabetes, erectile dysfunction, and heart attack in smokers are common.
Try recording all motives and positive outcomes that will happen on your part quitting burning. If you find yourself grasping for reasons to persevere, you can refer for you to this list for better.
Create signifies spot as well as aside the funds would certainly have that would purchase tobacco smoking. When you’ve made it to a year smoke-free, take the money and buying yourself something you need to have. The cost of cigarettes is really at high level that you could be even get a micro-vacation!
So it seems that the trick to stopping smoking cigarettes successfully is find your motivation (do you wish to live for enough time to start to see grandkids betrothed?) and keep that image in front of you at year ’round. Take nicotine substitutes if you have to and steer clear of environments where individuals smoke more, like pubs.Join a sports club instead, something like tennis, table tennis, swimming or even chess.
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5eff3d1f6f98e57329caed0ceb9053d3
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-8,420,166,578,721,233,000
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Skip to main content
Leukocyte trafficking in alveoli and airway passages
Abstract
Many pulmonary diseases preferentially affect the large airways or the alveoli. Although the mechanisms are often particular to each disease process, site-specific differences in leukocyte trafficking and the regulation of inflammation also occur. Differences in the process of margination, sequestration, adhesion, and migration occur that can be attributed to differences in anatomy, hemodynamics, and the expression of proteins. The large airways are nourished by the bronchial circulation, whereas the pulmonary circulation feeds the distal lung parenchyma. The presence of different cell types in large airways from those in alveoli might contribute to site-specific differences in the molecular regulation of the inflammatory process.
Introduction
Many of the diseases that affect the lungs involve inflammation. Some diseases, such as asthma, bronchiectasis, and infection with common environmental pathogens, affect primarily the airways, whereas others affect the distal bronchi, bronchioles, and alveoli, including bacterial pneumonia and the acute respiratory distress syndrome. Although many aspects of host defense and the inflammatory response are common to these two sites, there are differences in the mechanisms through which the inflammatory response occurs (Table 1). Many of these differences are related to the particular disease, for example the immune response in asthma compared with innate immunity in bacterial pneumonia, but some of the differences are due to the differences in the circulations and in the structural cell types that form the proximal airways compared with the distal air spaces. For example, the airways are fed largely by the bronchial circulation, whereas the distal air spaces are supplied by the pulmonary circulation. In addition, the airway epithelial cells seem to be important in the regulation of the inflammatory response, whereas in the more distal airways the alveolar macrophages and dendritic cells seem important. The purpose of this review is to compare the mechanisms underlying the response of leukocytes to stimuli that affect primarily one of these two lung regions.
Table 1 Differences between the alveoli and the airways
Alveoli and distal airways
Leukocyte margination
The distal bronchioles and alveolar spaces are lined by cuboidal epithelium and type I and II alveolar epithelium, respectively, and are fed by the pulmonary circulation. The pulmonary capillary bed comprises many short interconnecting segments, and a capillary pathway from an arteriole to a venule contains approximately 40–100 capillary segments (reviewed in [1,2]). In normal lungs, this bed contains a large pool of marginated neutrophils, monocytes, and lymphocytes, which are thought to be important in host defense. The concentration of neutrophils in the capillary blood measures 20–60 times the concentration in the large systemic vessels. The transit time of neutrophils through this capillary bed is longer, measuring on average 26–40 s, compared with the transit times of plasma or red blood cells of 1.5-4.0 s [1,2,3,4]. This longer transit time is thought to be due to the time required for neutrophils to deform to an oblong shape to pass through the 40-60% pulmonary capillary segments that are narrower than spherical neutrophils [5]. Measurements of neutrophil shape showed that neutrophils in arterioles were nearly spherical (shape factor of 1.1) whereas neutrophils in the capillary bed had shape factors of 1.5 ± 0.3, suggesting that most neutrophils must deform and elongate to travel through the capillary bed [5,6]. These studies indicate that the ability to deform is critical in the traffic of neutrophils through normal pulmonary capillaries.
Leukocyte sequestration
During the acute inflammatory response within regions of the distal lung tissue, neutrophils sequester within the capillary bed. Studies examining the role of known adhesion molecules, including L-selectin, P-selectin, and CD11/CD18, have demonstrated no role for these molecules in the initial stages of sequestration, when neutrophils are stopping and accumulating [7,8]. Once neutrophils have stopped, then L-selectin and CD11/CD18 are required to keep the sequestered neutrophils within the capillaries, at least in response to some stimuli.
In many organs fed by the systemic vasculature, neutrophil emigration occurs through the post-capillary venules. Hemodynamic patterns and selectin-mediated rolling of leukocytes are the major mechanisms through which leukocytes sequester at these sites. However, because rolling does not occur within the pulmonary capillary bed and adhesion molecules seem not to be required [68], we and others developed alternative hypotheses that focused on the role of the mechanical properties of neutrophils and other leukocytes, particularly on their ability to deform. Observations from many laboratories demonstrated that inflammatory stimuli, particularly those which bind to the seven transmembrane-spanning G protein linked receptors, induce changes in the cytoskeleton of neutrophils that result in a decreased ability to deform [9,10,11]. These studies led to the hypothesis that stimulus-induced increases in F-actin at the cell periphery led to a decreased deformability, preventing neutrophils from trafficking through the capillary bed and therefore increasing their sequestration at sites of inflammation. The role of these changes in vivo was suggested by observations demonstrating that neutrophils sequestered in the pulmonary capillaries of rabbits after the infusion of complement protein 5 fragments were rounder than neutrophils in the capillaries of control rabbits [9]. Although the hypothesis that this increased stiffness and decreased ability to deform mediates the initial sequestration of neutrophils within the pulmonary capillary bed at sites of inflammation has been difficult to prove directly, a considerable number of circumstantial data have accumulated that support this concept. Current studies are focused on understanding the mechanisms through which inflammatory mediators induce this rearrangement of the cytoskeleton.
The cytoskeletal changes that mediate the decreased deformability seem transient, and adherence between the neutrophils and the endothelial cells occurs within 5–30 min. The mechanical properties of these adherent and crawling neutrophils become very complex. Yanai et al [12] have demonstrated, with the use of optical tweezers, that granules within the cytoplasm of the leading edge are easier to oscillate than granules in the body or the trailing region of neutrophils. Schmid-Schoenbein et al [13] have suggested that pseudopods have more rigid viscoelastic properties than the remainder of the leukocyte. A full understanding of the biochemical and mechanical events that occur during adhesion and crawling has not yet emerged but is an important topic of investigation; the events might be modulated in part through signaling by ligated adhesion molecules. Neutrophil adhesion to endothelial cells induces changes in both neutrophils and endothelial cells that result in cytoskeletal and other intra-cellular alterations that are probably required for the subsequent steps in the response of neutrophils. For example, when neutrophils bind to pulmonary microvascular endothelial cells through intercellular cell-adhesion molecule-1 (ICAM-1), ICAM-1-dependent intracellular signaling responses are initiated [14]. This signaling response seems to require reactive oxygen species generated by xanthine oxidase, and results in the remodeling of the cytoskeleton through signaling pathways that are only now being explained.
Leukocyte emigration
Following sequestration and initial adhesion, neutrophils migrate along the capillary endothelium and into the interstitium and alveoli. There are at least two pathways through which this emigration occurs, one that uses the leukocyte adhesion molecule CD11/CD18 and one that does not. Which adhesion pathway is selected appears to depend upon the stimulus (reviewed in [11]). Stimuli that induce CD18-dependent emigration include Escherichia coli, E. coli lipopolysaccharide, Pseudomonas aeruginosa, IgG immune complexes, interleukin-1, and phorbol myristate acetate. These stimuli seem to act by inducing the translocation of nuclear factor-κB, resulting in the production of inflammatory cytokines (including tumor necrosis factor-α) and ICAM-1 on the pulmonary capillary endothelial cells [11,15]. Stimuli that induce CD11/CD18-independent neutrophil emigration include Streptococcus pneumoniae, group B Streptococcus, Staphylococcus aureus, hydrochloric acid, hyperoxia, and C5a. Although the mechanisms through which the CD11/CD18-independent mechanisms occur are less clearly described, neutrophil emigration occurs in the absence of enhanced ICAM-1 expression on the pulmonary capillary endothelium, and interferon-γ might be an important regulator of this response. This pathway of neutrophil emigration seems not to require known adhesion molecules, because numerous studies blocking the function of these adhesion molecules, either singly or in combination with blocking antibodies, small molecules, or genetic depletion, have demonstrated no defect in CD11/CD18-independent neutrophil migration. Current studies are focused on identifying new genes by using differential display and gene microarrays to compare transcripts made during CD18-dependent and CD18-independent neutrophil emigration.
Neutrophils migrate into the alveolar spaces through a well-defined pathway. The site of sequestration and migration is, as demonstrated by many investigators, the pulmonary capillary bed rather than the post-capillary venules. Neutrophils migrate between endothelial cells through junctions located between the thick and the thin walls of the capillary loops [16]. This junctional site overlies discontinuities in the basal laminae and is the site of interactions with interstitial fibroblasts within the alveolo-capillary walls. The neutrophils then crawl into the interstitium, where they are often in contact with the fibroblasts and may be crawling along them [17]. They then crawl to sites where type I cells are adjacent to type II cells and preferentially migrate between these two cell types to enter the alveolar space. The process of migration is accompanied by an increase in neutrophil volume, from approximately 128 ± 9 μm3 to 266 ± 9 μm3 [18]. Although this increase in volume seems to be mediated through the sodium/proton antiport, the function of the volume change is not yet clear.
Airways and the bronchial circulation
Leukocyte trafficking in response to stimuli within the more proximal bronchi occurs through the bronchial circulation. This circulation consists of a capillary network in the subepithelial region of the bronchi and a deeper system of arterioles, capillaries, and venules. The diameter of these capillaries has not been definitively determined under physiological conditions, but they are likely to be wider than pulmonary capillaries. The bronchial circulation displays many attributes of the systemic circulation in general but has an unusual drainage system. More than 85% of the systemic blood flow to the bronchial circulation returns to the left ventricle, indicating the presence of anastomoses between the bronchial and the pulmonary circulations [19]. These anastomoses have been identified at the pre-capillary, capillary, and post-capillary levels within the pulmonary circulation.
It has been difficult to establish whether the bronchial vessels contain a marginated pool of neutrophils or other leukocytes. Baile et al [19] demonstrated that the fraction of neutrophils requiring a longer time than red blood cells to pass through the bronchial circulation was lower (50–60%) than the percentage in trafficking through the pulmonary circulation (80%). This smaller margination within the bronchial circulation might be due to differences in the anatomy or the hydrodynamic dispersive forces between these two vascular beds. This study might in fact overestimate margination within the bronchial circulation, because a portion of neutrophils could be delayed within the pulmonary microvasculature while traversing the anastomotic pathways. However, these studies do suggest that margination within the bronchial circulation is less than that observed in the pulmonary circulation.
Aspects of the inflammatory response in airways compared with alveoli
The expression of adhesion molecules in normal lungs and in response to inflammatory stimuli is different in these two circulations. Normally, the pulmonary arterioles and venules express P-selectin, ICAM-1, and vascular cell adhesion molecule-1 (VCAM-1), but not E-selectin, whereas the pulmonary capillaries express only low levels of ICAM-1 and none of the other adhesion molecules [15,20]. During the inflammatory response induced by a variety of mediators (including bacteria), the expression of E-selectin, P-selectin, and ICAM-1 is often increased on pulmonary arterioles and venules. However, in the pulmonary capillaries, where neutrophil migration primarily occurs, only ICAM-1 expression is enhanced, and so far only in response to stimuli that elicit CD18-independent neutrophil migration. In contrast, in the bronchial microvasculature, P-selectin is expressed on nearly all vessels, and E-selectin, VCAM-1, and ICAM-1 are expressed on many [20]. Inflammatory stimuli induce the upregulation of these molecules. For example, the bronchial microvasculature of asthmatic lungs showed increased expression of selectins, VCAM-1, and ICAM-1, in comparison with non-asthmatic lungs [21,22].
Another difference in the inflammatory response within the large airways from that in the distal lung parenchyma is in the cells that regulate the response. In alveoli, alveolar macrophages and dendritic cells seem to be important modulators of the inflammatory response. The role of type I epithelial cells seems small, although definitive studies have not been performed. Type II cells might provide an important source of mediators regulating the inflammatory response, particularly in the production of surfactant proteins that modulate the inflammatory response and in the production of ICAM-1 on their surface, whose function is still unclear [15,23]. In contrast, the many types of epithelial cell lining the airways seem to regulate the response within the bronchi, as well as the lymphocytes, macrophages, fibroblasts, smooth-muscle cells, and other cells within the interstitium, which is much wider than that within the alveolo-capillary walls. Although some chemokines and other mediators might be uniquely produced at only one site, many of the mediators produced in the distal and proximal lung regions are similar. It remains to be determined whether this difference in structural components is important in the regulation of the inflammatory response.
There are considerably fewer studies examining the function of adhesion molecules in bronchial inflammation. During ozone-induced neutrophil emigration, CD11/ CD18, as well as members of the selectin family, seem important in neutrophil emigration [24]. In patients with asthma and animals with airways hyper-reactivity after sensitization and challenge with ovalbumin, the major cell types are lymphocytes and eosinophils. The adhesion molecules in this animal model that seem to be required for the egress of these cells into the interstitium and air spaces include VLA-4/VCAM-1, CD11/CD18-ICAM-1, P-selectin, and E-selectin [22,25,26]. To my knowledge, CD11/CD18 is crucial in the emigration of leukocytes through the bronchial circulation, and no CD18-independent pathways have been described.
Conclusion
There are striking differences in leukocyte trafficking between the alveoli and the proximal airways of the lungs. These differences appear to have multiple etiologies, including differences in anatomy such as the diameter of the vessels and the cell types that regulate the response, differences in both the expression and the function of adhesion molecules by endothelial cells, and differences in the stimuli which induce the inflammatory response at these sites. Although much has been learned about the regulation of inflammation in the past decade, enormous amounts remain to be uncovered, and our current knowledge clearly touches only the tip of the complexities that underlie host defense and inflammation in the lungs.
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Acknowledgements
I thank James C. Hogg, Joseph P. Mizgerd, and Qin Wang for numerous invaluable discussions over many years, and Virginia Ehrbar for help with preparing the manuscript. I apologize to the many scientists whose work I was unable to cite because of limitations on citation numbers. This work was supported by NIH HL 48160, HL 52466 and HL 33009, and a Clinical Scientist Award in Translational Research from the Burroughs Wellcome Fund.
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Doerschuk, C.M. Leukocyte trafficking in alveoli and airway passages. Respir Res 1, 4 (2000). https://doi.org/10.1186/rr24
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• DOI: https://doi.org/10.1186/rr24
• adhesion molecules
• margination
• neutrophils
• pulmonary inflammation
• sequestration
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Best seller
Which one is better for contraceptive pills
Nowadays, people do everything in accordance with the plan. If there is no child planning and planning, when the husband and wife are in the same room, there must be certain contraceptive measures. Although there are many methods of contraception, not every one is easy It is relatively simple and effective to adopt a condom, but men’s friends generally do not like it. The way of bringing a confession ring belongs to a once -and -for example. Will choose to take contraceptives for contraception. These female friends want to know which one is better for contraceptives?
Under normal circumstances, contraceptives are roughly divided into three types, one is long -acting contraceptives, and the other is short -term contraceptives. The third is emergency contraceptive pill. The effect of long -acting contraceptives is very good, and it is not It needs to be eaten frequently and has a small impact on physical health, so female friends who want long -term contraception can take long -term contraceptives.
Temporarily contraceptive after marriage. In order to condition the body, you can take short -acting contraceptives. The effect of short -acting contraceptives is also very good, but the time that can work after each medicine is not very long. Mocile contraceptives and short -acting contraceptives contain both progesterone and estrogen. Estrogen has the effects of protecting and nutritional ovarian and uterus. Therefore, eating these two types of contraceptives generally does not affect physical health, and side effects are relatively small.
The emergency contraceptive pills are different from the short -acting contraceptive, because the emergency contraceptive pills only contain the components of progesterone and the component of no estrogen. It is relatively large, and progesterone can cause human gastrointestinal dysfunction, so after taking emergency contraceptives, most of them will cause symptoms such as dizziness, nausea, vomiting, and irregular menstruation. , But if you take too often, it will cause endocrine disorders.
After reading the introduction above, I believe everyone understands, which one is better for contraceptives? I hope that all female friends can do their own body care, take contraceptive measures when they do not want their children, and try not to let accidental pregnancy and artificial abortion happen to themselves.
We will be happy to hear your thoughts
Leave a reply
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Male Enhancement – Can Korean Red Ginseng Help?
January 26, 2019 by zitavass0
There are a lot of popular male enhancement products out there nowadays. However, if you want to ensure that your choice is actually effective, you will need to look for certain ingredients, such as Korean red ginseng.
In a nutshell, ginseng refers to a kind of plant that is used in various health and wellness supplements due to its many benefits. There are 11 natural forms of ginseng and Korean red ginseng is just one of them. However, this form is the one that is most commonly used in male enhancement products because it is known to be highly beneficial in improving sexual performance. Find out more about this herb here.
For starters, studies show that Korean red ginseng is potentially effective at lowering a person’s risk for cancer (specifically gastric cancer), though more research may be needed to actually confirm this. It is also known to counteract any side effects that may come with chemotherapy. Other studies also show that this her b has various anti-carcinogenic compounds that can fight other kinds of cancer, such as lung cancer.
That aside, this herb is also being used in Asia to battle viral infections and to boost immunity, in general. It is also known to be beneficial against HIV and can even heighten the overall effectiveness of various treatments used for HIV. Red ginseng is also beneficial when used with HAART when battling HIV.
In terms of male enhancement and sexual function, Korean red ginseng is beneficial for both men and women. In fact, is has been used since ancient times as a sexual cure of sorts. Studies show that it can effectively battle erectile dysfunction. It is also known to be a great natural alternative to chemical drugs when wanting to treat sexual dysfunction.
Naturally, some things will need to be followed in order to ensure that Korean red ginseng works the way it is meant to for male enhancement, though.
Generally speaking, the FDA in the USA considers Korean red ginseng safe since most people are able to tolerate it well. However, there are some forms of it that may come with mild side effects like insomnia, anxiety, restlessness and headaches. Most of the time, these side effects occur in diabetics because it may lower one’s blood sugar levels and bring about hypoglycemia in the process.
As with other nutrients and herbs used for therapy, it would therefore be highly advisable to talk to your doctor before taking any male enhancement products with Korean red ginseng in them. This would hold especially true if you have certain conditions and are taking certain medications at the moment. It goes without saying that you should make it a point to do proper research beforehand and only turn to male enhancement products that have top quality and reliable formulations.
If you suffer from premature ejaculation, then you should also know that there are two kinds of this condition out there: the acquired kind and the lifelong kind. The former usually occurs in adults and is mostly caused by relationship problems, stress and medical conditions like high blood pressure or hypertension. Conversely, the latter usually occurs during a man’s teenage years, specifically during their first sexual experiences. This mostly occurs because of deep psychological problems, like early masturbation and quick masturbation.
If you want to delay your ejaculation, then male enhancement products may be able to help you out a lot. Fortunately, there are various pills and supplements out there that can help you do so. Some of them even come with added benefits like stronger and longer lasting erections. You just need to make sure you find the right ones.
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Gluten probably won’t kill you and a gluten-free diet probably won’t either
Gluten-free diets are all the rage. I mean, if your yogurt label says ‘gluten-free’ then gluten must be bad right? But wait, what about those recent headlines claiming there’s arsenic in gluten-free foods? Is it safe to eat literally anything?
If you feel this way trying to navigate nutrition advice, you’re not alone. According to headlines practically anything can either kill you or cure you. This might leave you feeling like science is wishy washy, and maybe you should turn to your pastor or yoga instructor for nutrition advice instead. The truth is, food science is nuanced and headlines are not. In this post, we’ll guide you through the gluten gamut and share some general tips for navigating nutrition science news.
First, unless you’re one of the less than 2% of people with Celiacs disease or a wheat allergy, you probably don’t need to worry about gluten. Gluten is a protein found in wheat that helps to give bread that nice gooey texture. Contrary to some claims that gluten is a byproduct of modern “genetic tinkering”, we’ve been eating gluten since the dawn of wheat domestication about 10,000 years ago. We’ve only been digesting gluten-related news hysteria for about the last 6 years thanks to a book called “Wheat Belly”.
“Wheat Belly” was written by Dr. William Davis after he noticed that the health and weight of many of his patients improved when they stopped eating wheat. He attributes this difference to gluten and inflammation. In the science world, we call this kind of evidence “anecdotal” because it comes from casual observations not carefully controlled studies. Scientists have tested Davis’s theory by administering controlled tests where (for example) people with self-reported gluten sensitivities consumed either wheat or whey proteins. So far, the evidence doesn’t match the anecdote.
But reports of celiac disease and other wheat-related allergies ARE on the rise. There are several possible explanations for this. Our attention to the diagnosis of these conditions and the sensitivity of the tests required to confirm them has increased. Additionally allergies and autoimmune diseases like celiac are on the rise in general. We don’t yet know why this is, but one intriguing possibility is the hygiene hypothesis–basically, in our increasingly urbanized and sterile environment, children are exposed to less immune challenges, causing their immune system to mistake friend for foe. There is some evidence to support this hypothesis. For example, children who grow up on dairies or in close contact with pets are less likely to develop asthma and allergies.
That still doesn’t explain why some people feel better when they cut wheat out of their diets. Wheat has changed over the ages with breeding, so it’s possible that modern wheat could cause irritation, but it is difficult to say, because cutting wheat out of your diet means cutting a whole lot of other stuff too. Obviously if you give up beer, pizza, and cookies your health will improve. By eliminating wheat, you’d probably eat less processed foods which tend to be high in sugars, calories, salts, etc.
The promise of a gluten-free diet has lead 1 in 3 Americans to consider the switch, expanding a niche market into an advertiser’s dream. You can now buy gluten-free chicken nuggets, brownies, and even beer. What luck! Now we can go gluten-free and still have all the junk that typically hides in wheat-based processed foods. But headlines are now claiming that these foods may come with a side of heavy metals and arsenic.
In a study published recently by the University of Illinois, scientists found 50% more arsenic and 60% more lead in the urine of people on a self-reported gluten-free diet. Before you set fire to your pantry, food toxicologist Dr. Carl Winter noted that these “estimates are all below levels of concern identified by the US EPA,” but by less of a margin of safety than is typically allowed for compounds such as pesticides which are carefully monitored and highly scrutinized.
To put these amounts into perspective, Arsenic has an LD50 of 15mg/kg. That means if you fed a bunch of 1kg rats 15mg of straight arsenic, half of them would die. But rats are pretty small. It would take 900 mg of Arsenic in one serving to kill a Gwyneth Paltrow-sized rat. That’s about 5000 times more arsenic that you’d find in a typical 1 pound bag of rice. In urine, the limit considered safe for arsenic is 100ug/L which is still way more than the 12ug/L found from those on a Gluten-free diet (for comparison, those who eat gluten still peed 8ug/L of arsenic).
What’s more, the specific source of the arsenic in gluten-free diets is important. Although they didn’t directly test for it, the researchers speculate that these elevated levels of arsenic come from an increased consumption of rice. Many gluten-free products contain rice flour as a substitute for wheat flour, and according to UC Davis rice extension specialist Dr. Bruce Linquist, “arsenic is higher in rice than many other cereal crops due to the anaerobic soil conditions rice is grown under”. Other studies have found arsenic in rice-based gluten-free foods but not in gluten-free foods lacking rice. This doesn’t mean you should throw away all the rice in your cabinet either. As toxicologists like to say, the dose makes the poison. One study indicated that Asian households living in the US are only exposed to about 2.8 ug of arsenic per day from eating rice. There’s more arsenic than that in our tap water.
So what’s the takeaway? Gluten probably won’t kill you and a gluten-free diet probably won’t either. Neither will rice or tap water. On the other hand, too much of absolutely anything can kill you. A small number of celiac patients have faced arsenic poisoning because they were unknowingly eating rice-based products 3 meals a day. For anyone, especially children, the FDA recommends a varied diet to decrease the risk of exposure to arsenic. The same strategy can be applied to many dietary concerns. Variety is good, homogeneity is bad. So although it’s cliche, a good rule of thumb is everything in moderation–even arsenic.
About the Authors
Jenna E Gallegos, Lynn Ly, and Eric Walters are graduate students at the University of California in Davis. This post was written as part of a project called “Science REALLY says” which seeks to ensure scientific data is accurately represented by the media. It originally appeared on the Science Says blog. For more content from the UC Davis science communication group “Science Says“, follow us on twitter @SciSays and like us on facebook.
Acknowledgements
We thank Dr. Carl Winter (food toxicology extension specialist, UC Davis) and Dr. Bruce Linquist (sustainable management of rice systems extension specialist, UC Davis) for helpful comments.
References
Bulka, C. M., Davis, M. A., Karagas, M. R., Ahsan, H., & Argos, M. (2017). The Unintended Consequences of a Gluten-Free Diet. Epidemiology (Cambridge, Mass.), 1–7. https://doi.org/10.1097/EDE.0000000000000640
Kim, H., Patel, K. G., Orosz, E., Kothari, N., Demyen, M. F., Pyrsopoulos, N., … C, C. (2016). Time Trends in the Prevalence of Celiac Disease and Gluten-Free Diet in the US Population: Results From the National Health and Nutrition Examination Surveys 2009-2014. JAMA Internal Medicine, 108(5), 818–824. https://doi.org/10.1001/JAMAINTERNMED.2016.5254
Mantha, M., Yeary, E., Trent, J., Creed, P. A., Kubachka, K., Hanley, T., … Creed, J. T. (2016). Estimating Inorganic Arsenic Exposure from U.S. Rice and Total Water Intakes. Environmental Health Perspectives, (August). https://doi.org/10.1289/EHP418
Pietzak, M. (2012). Celiac disease, wheat allergy, and gluten sensitivity: when gluten free is not a fad. JPEN. Journal of Parenteral and Enteral Nutrition, 36(1 Suppl), 68S–75S. https://doi.org/10.1177/0148607111426276
Jara, E. a, & Winter, C. K. (2014). Dietary exposure to total and inorganic arsenic in the United States, 2006–2008. International Journal of Food Contamination, 1(1), 3. https://doi.org/10.1186/s40550-014-0003-x
Vierk, K. A., Koehler, K. M., Fein, S. B., & Street, D. A. (2007). Prevalence of self-reported food allergy in American adults and use of food labels. Journal of Allergy and Clinical Immunology, 119(6), 1504–1510. https://doi.org/10.1016/j.jaci.2007.03.011
Munera-Picazo, S., Burló, F., & Carbonell-Barrachina, A. A. (2014). Arsenic speciation in rice-based food for adults with celiac disease. Food Additives & Contaminants. Part A, Chemistry, Analysis, Control, Exposure & Risk Assessment, 31(8), 1358–66. https://doi.org/10.1080/19440049.2014.933491
Agency for Toxic Substances and Disease Registry (ATSDR). 2007. Toxicological Profile for Arsenic. Atlanta, GA: U.S. Department of Health and Human Services, Public Health Services. https://www.atsdr.cdc.gov/toxguides/toxguide-2.pdf
US Food and Drug Administration. (2016) Arsenic in Rice and Rice Products. https://www.fda.gov/Food/FoodborneIllnessContaminants/Metals/ucm319948.htm
Darren Seifer. (2012) Is Gluten-Free Eating a Trend Worth Noting? Report from The NPD Group. https://www.npd.com/perspectives/food-for-thought/gluten-free-2012.html
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Data monitoring committees (DMCs) for clinical trials have been used for many years and are vital tools for ensuring that patient safety is carefully reviewed in an unbiased manner. Historically, these committees were most often utilized for larger and relatively long-term Phase III trials with mortality or serious morbidity primary endpoints. There is broad consensus that independent DMC review by experts with no bias or conflict of interest with the sponsor company is critical to ensure patient safety during the conduct of these pivotal trials. More recently, despite the increased complexity of adding DMC oversight to trials, there has been an increase in their use. This expansion has primarily occurred into earlier stage trials that may be supportive of a registration. These non-pivotal trials may include adaptive design elements or protocol defined interim analyses allowing flexibility in the data gathering process.
Monitoring committees for these types of trials usually consist of either expert researchers completely independent from the company, or internal sponsor employees who are not in communication with study investigators and are separated from the clinical study team conducting the trial. Often the purview of committees for these types of trials is not only safety monitoring but also an evaluation of efficacy. Modifications to trial design as allowed by the protocol, such as adding dosage groups, adding patients to an existing dosage group, changing dose duration, and modifying inclusion/exclusion criteria may be included in the committee’s charter. The committee may recommend or decide to stop the trial based on the data review. Even in this new paradigm not all trials should have a DMC, many are too short in duration or enroll too few patients to allow efficient use of an independent review committee. Once the decision to have a DMC has been made, however, should there be more consideration in using a committee composed of both internal and external experts? In circumstances where the DMC is being put in place to only monitor safety independent of the study team it is probably more expedient to decide between a committee of internal experts, or form an external committee before establishing the appropriate oversight process. In adaptive trials, however, where the DMC is charged with making decisions or recommendations on future trial conduct then consideration of a mixed committee is reasonable.
Internal experts for DMCs are often selected because they are independent from the study team and bring deep drug development and global regulatory experience to the committee as well as therapeutic expertise. Since these experts are internal they possess a detailed knowledge of the company’s decision-making criteria. They have full access to data on the development candidate from prior or current work that is being conducted outside of the trial being monitored, and an ability to communicate with internal departments to prioritize rapid data analyses that maybeneeded for decision-making. Independent non-sponsor associated experts are often chosen because of their knowledge of the disease state, experience in treating the targeted patients, and their ability to act as patient advocates. Many of these experts also have extensive experience with regulatory agencies in connection with the disease under study. This blend of different perspectives and abilities may be highly valuable in adaptive trial situations where speed and efficiency are essential for making rapid decisions. This is especially the case in earlier stage trials where incorrect decisions can have severe consequences on the development program.
During the conduct of an adaptive trial it is critical that decisions are made after a rigorous discussion of the data and its impact on the future course of the study. This type of discussion is most productive when as many different perspectives as possible are included. By utilizing a mixed committee the blinded data can be reviewed with many of the consequences for future development being considered from a patient, treating physician, regulatory, and sponsor perspective. This type of just-in-time discussion is not possible when only internal or external experts are able to review blinded data and the course of the trial is decided. When this type of review during a trial does not occur, changes in the direction of the clinical development program for future studies can be made later after the trial is completed but this may cause a loss of valuable time and effort. Confidence that the committee has fully evaluated the severity of adverse events, the extent of efficacy, and the contribution of various inclusion/exclusion criteria can be increased when a mixed committee is reviewing the data. These considerations become even more important when the patient population being studied is relatively small, or is poorly studied, as in the case of many orphan diseases. In these instances, data from every patient is extremely valuable and decisions on the future conduct of the study require expertise that can only be provided when internal and external experts are both participating in the data review.
Once the decision has been made to utilize a mixed committee, there are several logistical considerations crucial for success. The charter for the committee must be very explicit in determining the decision-making process. Is the committee making the final decision on the trial’s conduct or does it make a recommendation to the sponsor? Does the committee decide by consensus or by vote? If it is by vote, do all members have full voting rights? The composition of the committee and the selection of the committee chair are always carefully considered for a DMC but this decision is even more critical when the committee is mixed in composition. In many circumstances, if the effort to include outside expertise is desired it is reasonable to have one of the external members chair the committee. The size of the committee should remain reasonably small, but is probably best served when there is a balance of internal and external experts.
There are many different strategies for designing clinical development programs, but the ultimate goal in early stage trials should always be to determine as quickly as possible whether or not a program should be continued or halted. If the program is to be continued, what can be done to learn as much about the new potential therapy in the most efficient manner? Given the tremendous effort and cost of bringing a development candidate into the clinic, it is crucial decisions are made rapidly but with the best information available, and with as many perspectives included as possible. An adaptive trial design allows us to learn from the data as it is being collected, but it also leads to the potential of making mistakes due to insufficient analysis. Given the criticality of making rapid and correct decisions during the conduct of a trial, as well as the need to maintain the trial’s integrity, a mixed DMC is a tool that can be utilized to maximize the probability of success.
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Chronic female pelvic pain
Chronic female pelvic pain is pain in a woman's lower abdomen that lasts for 6 months or more and is not related to pregnancy. It may be constant or come and go and range from mild to severe.
Many things can cause chronic pelvic pain, including pelvic infections. But sometimes the cause is a mystery.
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Discussion: Normal vs. Abnormal ECG
A wave as a deviation from the baseline must be seen as an important measure. Specifically, the EGC under analysis shows that a P-wave does not exceed 2.4 squares, and the T-wave is upright in leads I and II (Jones, 2019). The specified characteristics indicate the presence of a normal heartbeat. Another essential characteristic of an ECG is a QRS complex. Representing the depolarization of the right and the left ventricles of the patient’s heart, the specified element of the cardiogram allows for assessing the extent of the large ventricular muscle contraction. The normal duration of the QRS complex is typically 80-100 ms, the one under analysis being 95, which is why any deviations from the specified norm must be seen as a reason for concern (Jones, 2019). Remarkably, apart from being the most noticeable part of the waveform, the QRS complex is also the most critical element thereof, which is why it needs to be the center of attention when analyzing the information presented in the ECG. The multitude of the QRS complexes represents the sinus rhythm, which is, in essence, the heart rhythm. In the case under analysis, the sinus rhythm is 80 beats per minute (bpm), which is within the normal (50-100 bmp) range.
The T-wave, namely, a curve after the QRS complex, must be upright and curved. The ST segment, which connects the QRS complex to the rest of the elements, should be flat. The analyzed one has a minor curve, yet slight elevation or lowering is possible as long as it remains within a 1 mm range. Finally, the QT and PR intervals, which are represented by the lines on the right and on the left sides of the QRS complex correspondingly, must be within 0.4-0.44s (QT) and 0.12-0.20 ms (RS) (Jones, 2019). In this case, they are at a 0.41 me and a 0.18 ms rate, which aligns with the set standard. Thus, overall, the ECG results observed in the specified case are those of a healthy patient.
Reference
Jones, S. A. (2019). ECG mastery: Improving your ECG interpretation skills. F.A. Davis.
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AssignZen. "Discussion: Normal vs. Abnormal ECG." August 22, 2023. https://assignzen.com/discussion-normal-vs-abnormal-ecg/.
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AssignZen. 2023. "Discussion: Normal vs. Abnormal ECG." August 22, 2023. https://assignzen.com/discussion-normal-vs-abnormal-ecg/.
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Go to page content
Heather Hanks
Written by Heather Hanks
Reviewed by Dr Jessica Gunawan
Quiz: Find Out What’s Causing Your Excessive Sweating
Published | 5 min read
Staying cool is easier said than done. Excessive sweating can be triggered by several things. Find out what is the root cause and how you can stay dry and breezy.
Excessive sweating min scaled
Excessive sweating is bound to happen if you live in the south or someplace warm. It’s also common during the warm summer months or when you get nervous.
But if you notice that you sweat more than those around you, it could be due to a condition characterized by excessive, unprovoked sweating called hyperhidrosis.
Take our quiz below to find out if you suffer from excessive sweating and what you can do about it.
What is Hyperhidrosis?
Hyperhyrosis is defined as excessive sweating for no apparent reason. It occurs when the sweat glands overreact, causing you to sweat more than you need to.
There are two types of hyperhidrosis. Primary focal hyperhidrosis is a chronic skin disorder that develops before age 25. It’s not associated with any health conditions and mostly affects the under arms, hands, feet, and head.
Meanwhile, secondary generalized hyperhidrosis is due to underlying medical conditions, such as type 2 diabetes and Parkinson’s disease. It mostly occurs in adults and can be exaggerated by certain medications, such as zinc supplements and anti-inflammatory drugs such as naproxen (Aleve).
What Causes Excessive Sweating?
Sweat is necessary to keep the body cool, but excessive amounts can be embarrassing and should be treated by a doctor.
A normal amount of sweat is normal for the body to keep itself cool, such as when you’re sick, nervous, or exercising. It occurs when messages are sent to your sweat glands, telling them to produce sweat.
If you have hyperhidrosis, your sweat glands start to overproduce sweat for no apparent reason or singling from other parts of your body.
The causes of hyperhidrosis may vary depending on what type you have. Focal hyperhidrosis may be due to heat, anxiety, emotional stress, and hot foods.
Secondary generalized hyperhidrosis may be due to medical conditions such as infections, menopause, thyroid problems, metabolic disorders, gout, certain cancers, and more.
Take our quiz to find out what’s causing your excessive sweating and how to treat it
If you answered mostly “A:” Normal sweating
You seem to be sweating normally, like when you’re overheated, exercising, or getting anxious about something.
Make sure you use deodorant! Take a small towel with you when you’re exercising outdoors.
If you’re about to face a situation that you know will make you nervous (like a job interview or a date), maybe you could bring along a lightweight jacket or a cardigan to hide the sweat stains on your clothes.
If you answered mostly “B:” You may have primary focal hyperhidrosis
There’s a chance that you’re suffering from primary focal hyperhidrosis. This suggests that your excessive sweating is not caused by another illness, and you most likely inherited it from a family member.
The symptoms of primary focal hyperhidrosis are:
1. You are sweating on specific parts of the body, also known as focal areas: hands, feet, underarms, and face or head. The sweating is symmetrical, which means they’re occurring both on the left and right sides at the same time.
2. You have at least one episode of excessive sweating every week.
3. Sweating occurs when you wake up, but not when you sleep.
4. You have been sweating excessively since childhood or teenage.
If you answered mostly “C:” You may have secondary generalized hyperhidrosis
What you’re experiencing is most likely secondary generalized hyperhidrosis. The word “secondary” here means another medical condition causes excessive sweating or is a side effect of a medication you take for another sickness.
The symptoms are:
1. Sweating occurs all over or on larger areas of the body (generalized areas).
2. Night sweats.
3. Symptoms appear only after a person becomes adult.
If you have this type of hyperhidrosis, it’s best to consult a doctor to find if you have other underlying health issues, such as diabetes, gout, accident-induced injury, menopause, obesity, hyperthyroidism, or a tumor. Your doctor will also ask you if you have been taking any medicines.
How to Treat Excessive Sweating
Several treatments for excessive sweating are available, ranging from home remedies to medication and even botox,
According to Zhou Bin Rong, Senior Traditional Chinese Medicine (TCM) physician at Eu Yan Sang, these excessive sweating symptoms are likely due to the imbalance of body functions.
For example, if someone perspires often in the morning and feels fatigued all the time, then he or she may be suffering from weak qi (yang deficiency). If someone is experiencing sweaty palms or feet, then the problem could lie in the spleen, heart, stomach and kidney.
“If the sweat has a yellowish tint, or you find a lot of sweat stains on your clothes, then your body may have a lot of damp heat,” she explains.
There are some treatment options you can try to treat excessive sweating.
Proven treatments for excessive sweating
Doctors would usually suggest treatments that will work such as, antiperspirants, deodorants, botox injections, and iontophoresis treatment.
Botox injections and iontophoresis should be done under the supervision of a medical practitioner. However, many natural remedies can also be considered.
Herbal remedies
Lok Mei Pa Pills contain a blend of herbs, such as astragalus, ginseng, and cordyceps, that may help control excessive sweating by treating yang-deficiency, invigorating the kidneys, and increasing vitality.
Oral medications
Anticholinergics are oral medications prescribed to patients with secondary generalized hyperhidrosis.
Talk to your doctor to make sure anticholinergics won’t clash with other medications you take.
Acupuncture
Physician Zhou Bin Rong says acupuncture can potentially be an effective treatment to hyperhidrosis, along with TCM and healthy diet
It bears remembering that a treatment that works for one person might not work for another.
Sometimes, a person must undergo a combination of treatments before they can finally find the solution to their condition.
The point remains that hyperhidrosis is treatable and, therefore, not something you should be ashamed of.
Consult your doctor or a TCM physician for a proper diagnosis and personalized treatment. In the end, remember that everyone sweats!
References
1. International Hyperhidrosis Society. N.d. Diagnosing Hyperhidrosis. [Accessed on 24 January 2022]
2. International Hyperhidrosis Society. N.d. Two Types of Hyperhidrosis. [Accessed on 24 January 2022]
3. International Hyperhidrosis Society. Natural Remedies. [Accessed on 24 January 2022]
4. International Hyperhidrosis Society. Oral Medications. [Accessed on 24 January 2022]
5. American Academy of Dermatology Association. N.d. Hyperhidrosis: Signs and Symptoms. [Accessed on 24 January 2022]
6. Shen-Nong. N.d. Chinese Medicine Treatment for Excessive Daytime Sweating. [Accessed on 28 January 2022]
7. Cleveland Clinic. 2020. Hyperhidrosis. [Accessed on 24 January 2022]
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Warning: openlog() has been disabled for security reasons in /home/nhakhoav/public_html/fareastdental.com/modules/syslog/syslog.module on line 103
Gum recession: Skip to content Skip to navigation
Gum recession
Mon, 15/07/2019 - 16:54
Gum recession: Causes
When your gum recede or pull away from your teeth, it is called gum recession. Gum recession can happen to people of all ages. Sometimes it happens even if a person takes good care of his or her teeth.
Gum recession can cause problems for your dental health. If you have gum recession, your dentist can help you understand the causes and recommend a treatment.
When teeth are healthy, gum tissue fits around each tooth like a cuff. In a tooth with gum recession, the gum tissue has pulled away from the tooth. This can leave the tooth root exposed. Since the root surface does not have a hard enamel covering like the crown (top) of the tooth, the root may become sensitive to hot and cold. Also, the exposed root is more at risk for decay.
Causes:
Gum recession can be caused by:
• Periodontal (gum) disease
• Brushing your teeth too hard or using a hard-bristled toothbrush
• Trauma to gum tissues, such as a sport injury
• Partial that don’t fit right
• Genetics – some people are born with gums that are thin or weak
• Prominent tooth roots or attachment mussles that can push gums out of place
• Smoking and using any kind of tobacco
Ref : http://www.ada.org/en/~/media/ADA/Publications/Files/ADA_PatientSmart_Gum_Recession
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Health
Dermatologist checks a mole on a patient's back
Dermatologist checks a mole on a patient's back
Dermatologist checks a mole on a patient's back
Other Benign Skin Growths
What are other benign skin growths?
As a person grows older and is exposed to sunlight, the skin changes in response to this exposure. Most people have some skin marks, such as freckles and moles, which may multiply or darken over time. Benign means they are not cancer.
What are the different types of skin growths?
Skin growth
Characteristics
Treatment
Dermatofibromas
Small, firm, red or brown bumps caused by an accumulation of fibroblasts (soft tissue cells under the skin). They often occur on the legs and may itch. They are more common in women.
Dermatofibromas can be surgically removed if they become painful or itchy.
Dermoid cyst
A benign tumor which is made up of hairs, sweat glands, and sebaceous glands. Some internal dermoid tumors may even contain cartilage, bone fragments, and teeth.
Dermoid cysts may be removed surgically for cosmetic reasons.
Freckles
Darkened, flat spots that typically appear only on sun-exposed areas of the skin. Freckles are common in people with blond or red hair.
No treatment is needed for freckles.
Keloids
Smooth, firm, raised, fibrous growths on the skin that form in wound sites. Keloids are more common in people with dark skin.
Keloids respond poorly to most treatment approaches. Injections of corticosteroid drugs may help to flatten the keloids. Other treatment approaches may include surgery, laser, or silicone patches to further flatten the keloids.
Keratoacanthomas
Round, flesh-colored growths that have a crater that contains a pasty material. These growths tend to appear on the face, forearm, or back of the hand. They usually disappear after a couple of months, but may leave scars. Many feel they are a form of squamous cell carcinoma.
Treatment usually includes a skin biopsy to rule out skin cancer. Other treatment may include surgical removal or injections of corticosteroids or fluorouracil.
Lipomas
Round or oval, easily movable lumps under the skin caused by fatty deposits. Lipomas are more common in women and tend to appear on the forearms, torso, and back of the neck.
Lipomas are generally harmless. But if the lipoma changes shape or you have symptoms, your healthcare provider may do a biopsy. Treatment may include surgical removal.
Moles (nevi)
Small skin marks caused by pigment-producing cells in the skin. Moles can be flat or raised, smooth or rough, and some contain hair. Most moles are dark brown or black, but some are skin-colored or yellowish. Moles can change over time and often respond to hormonal changes.
Most moles are benign and no treatment is necessary. Some benign moles may develop into skin cancer (melanoma). See below for signs.
Atypical moles (dysplastic nevi)
Larger than normal moles (more than a half inch across), atypical moles are not always round. Atypical moles can be tan to dark brown, on a pink background. These types of moles may occur anywhere on the body.
Treatment may include removal of any atypical mole that changes in color, shape or diameter. In addition, people with atypical moles should avoid sun exposure, since sunlight may accelerate changes in atypical moles. People with atypical moles should see a doctor for any changes that may indicate skin cancer.
Pyogenic granulomas
Red, brown, or bluish-black, raised marks caused by excessive growth of capillaries (small blood vessels) and swelling. Pyogenic granulomas usually form after an injury to the skin and bleed easily.
Some pyogenic granulomas disappear without treatment. Sometimes, a biopsy is needed to rule out cancer. Treatment may include surgical removal and electrodessication of the base.
Seborrheic keratoses
Flesh-colored, brown, or black wart-like spots. More common in middle-aged and older people, seborrheic keratoses may be round or oval and look like they are stuck on the skin.
Usually, no treatment is needed. If the spots are irritated, or the person wants them removed for cosmetic reasons, treatment may include freezing the area with liquid nitrogen or surgery.
Skin tags
Soft, small, flesh-colored skin flaps on the neck, armpits, or groin. They are very common. They may be linked to metabolic syndrome and increased risk of heart disease.
If the skin tags are irritated, or the person wants them removed for cosmetic reasons, treatment may include freezing the tags with liquid nitrogen, electrodesiccation, or surgery by cutting them off.
Normal mole
Normal Mole
Distinguishing benign moles from melanoma
Certain moles are at higher risk for changing into cancerous growths such as malignant melanoma, a form of skin cancer. Moles that are present at birth and atypical moles have a greater chance of becoming cancerous. Finding cancerous skin growths early is important because that’s when treatment is most likely to be effective. Use this ABCDE chart below to help you see changes in your moles at the earliest stages. The warning signs include:
Melanoma
Sign
Characteristic
Skin cancer showing asymmetry.
Asymmetry
When half of the mole does not match the other half
Skin cancer showing irregular border.
Border
When the border (edges) of the mole are ragged or irregular
Skin cancer showing more than one color.
Color
When the color of the mole varies throughout
Skin cancer with dotted-line circle and arrow showing diameter.
Diameter
If the mole's diameter is larger than a pencil's eraser
Skin lesions showing evolution of skin cancer.
Evolving
Changes in the way the mole looks over time
jhm-calendar
Request an Appointment
Find a Doctor
Find a Doctor
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5eff3d1f6f98e57329caed0ceb9053d3
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-336,286,217,065,478,100
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Difficulty of visual search modulates neuronal interactions and response variability in the frontal eye field
Jeremiah Y. Cohen, Pierre Pouget, Geoffrey F. Woodman, Chenchal R. Subraveti, Jeffrey D. Schall, Andrew F. Rossi
Research output: Contribution to journalArticlepeer-review
Abstract
The frontal eye field (FEF) is involved in selecting visual targets for eye movements. To understand how populations of FEF neurons interact during target selection, we recorded activity from multiple neurons simultaneously while macaques performed two versions of a visual search task. We used a multivariate analysis in a point process statistical framework to estimate the instantaneous firing rate and compare interactions among neurons between tasks. We found that FEF neurons were engaged in more interactions during easier visual search tasks compared with harder search tasks. In particular, eye movement-related neurons were involved in more interactions than visual-related neurons. In addition, our analysis revealed a decrease in the variability of spiking activity in the FEF beginning ∼100 ms before saccade onset. The minimum in response variability occurred ∼20 ms earlier for the easier search task compared with the harder one. This difference is positively correlated with the difference in saccade reaction times for the two tasks. These findings show that a multivariate analysis can provide a measure of neuronal interactions and characterize the spiking activity of FEF neurons in the context of a population of neurons.
Original languageEnglish (US)
Pages (from-to)2580-2587
Number of pages8
JournalJournal of neurophysiology
Volume98
Issue number5
DOIs
StatePublished - Nov 2007
Externally publishedYes
ASJC Scopus subject areas
• Neuroscience(all)
• Physiology
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Dive into the research topics of 'Difficulty of visual search modulates neuronal interactions and response variability in the frontal eye field'. Together they form a unique fingerprint.
Cite this
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5eff3d1f6f98e57329caed0ceb9053d3
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6,629,132,491,002,394,000
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Chemotherapy
The info in these pages is for adults having chemotherapy, although some of it will matter for children. Talk to your doctor for particular info about chemotherapy for children.
What Is It?
Chemotherapy is making use of drugs to kill or slow the development of cancer cells. Chemotherapy drugs are also called cytotoxics, which implies poisonous (poisonous) to cells (cyto). A few of these drugs are obtained from natural sources such as plants, while others are totally developed in the lab. There are many types of chemotherapy drugs, which are typically used in various combinations and at various strengths.
How Does Chemotherapy Work?
Many chemotherapy drugs get in the blood stream and travel throughout the body to reach cancer cells in various organs and tissues.
Chemotherapy drugs target and injure rapidly dividing cells, but since the drugs are not cancer specific, both cancer cells and some regular cells are affected. When typical cells are harmed, this can cause side effects.
By the time your next treatment begins, your body’s normal cells have actually normally recuperated but the cancer cells have not. This is due to the fact that cancer cells do not repair quickly, so they recover more slowly than regular cells. This implies that more cancer cells are destroyed with every treatment.
Chemotherapy (chemo)
Chemotherapy (chemo) generally describes using medicines or drugs to treat cancer. The thought of having chemotherapy frightens lots of people. However understanding what chemotherapy is, how it works, and what to expect can typically help calm your fears. It can likewise give you a better sense of control over your cancer treatment.
Some types of chemotherapy can be provided straight at the tumour site rather than travelling through the bloodstream. Examples are chemotherapy wafers for brain cancer and chemoembolisation for liver cancer. As the treatment is localised, side effects are less typical.
Why Have Chemotherapy?
Chemotherapy can be used for various reasons:
To help other treatments: Chemotherapy can be provided either before or after other treatments. Used in advance(neo-adjuvant therapy), its purpose is to make the cancer smaller so your primary treatment is more reliable. If chemotherapy is given after your main treatment (adjuvant therapy), its objective is to obtain rid of any remaining cancer cells that may not be seen on scans.
Cure: Some cancers can be cured by chemotherapy on its own or in mix with other treatments, such as surgery or radiotherapy.
To manage the cancer: If the cancer is too large and can’t be cured, chemotherapy can be used to control the cancer’s development for a prolonged time period.
Symptom relief: When the cancer cannot be cured but causes symptoms such as pain, treatment– such as chemotherapy – can supply relief. This is called palliative treatment.
How Is Chemotherapy Offered?
Chemotherapy can be given in a variety of ways. Most people have chemotherapy through a vein (intravenously). It can also be prescribed orally (tablets or capsules), as a cream, or as injections into various parts of the body.
Does Chemotherapy Harm?
• Having intravenous chemotherapy may seem like having your blood taken.
• If you have a temporary tube (cannula) in your hand or arm, only the preliminary injection might hurt.
• If you have a central venous gain access to device, it ought to not be painful.
• Some treatments will cause side effects. Nevertheless, chemotherapy drugs are continuously being enhanced to give you the best possible outcomes and to minimize side effects.
If you feel burning, coolness, pain or other uncommon sensation where a cannula or central venous gain access to device enters your body, or if you have inflammation or inflammation over the injection site, inform your doctor or nurse immediately.
Procedure
How is chemotherapy used to treat cancer? Chemotherapy is the use of any drug to treat any disease. However to many people, the word chemotherapy suggests substance abuse for cancer treatment. It’s often reduced to “chemo.”.
Surgery and radiation therapy eliminate, kill, or damage cancer cells in a certain area, but chemo can work throughout the whole body. This implies chemo can eliminate cancer cells that have actually spread (metastasized) to parts of the body far from the initial (main) tumor.
Where Will I Have Treatment?
Many people have chemotherapy on an outpatient basis during day visits to a medical facility or center. Sometimes an over night hospital stay might be needed. Some individuals can have chemotherapy at home if they use a portable pump or have oral chemotherapy.
How Long Does Treatment Last?
How frequently and how long you have chemotherapy depends upon the kind of cancer you have and the drugs that are used. You may have treatment daily, weekly or regular monthly for a number of months to a year.
Chemotherapy is commonly given up courses (cycles), with rest periods between. This enables regular cells to recuperate and your body to restore its strength. If your body needs more time to recuperate, i.e. for the blood count to return to regular, your next cycle might be postponed.
Your doctor will discuss your treatment strategy with you. Sometimes people have chemotherapy over 6-12 months, but it’s possible to have it for a shorter or longer period.
Some individuals who have chemotherapy to manage the cancer or to relieve symptoms (palliative treatment) might have routine treatment for many months or years.
How Much Does Treatment Cost?
Chemotherapy drugs are costly, however the majority of people just pay a fraction of the cost as lots of drugs are greatly subsidised by the Pharmaceutical Benefits Scheme (PBS). However, there are some drugs that are not covered by the PBS.
Your nurse, expert or clinic will tell you what you will have to pay. You will generally have to cover the cost of medications taken at home to relieve the side effects of chemotherapy (such as anti-nausea drugs).
Can Chemotherapy Be Offered During Pregnancy?
Being identified with cancer during pregnancy is uncommon – about one in 1000 women are affected.
It is possible for some pregnant women to have chemotherapy. Your medical team will go over all the available treatment options with you. Their suggestions will be based upon the kind of cancer you have, its stage, the other treatment options, and how to avoid damaging your establishing baby. Often chemotherapy or other treatment can be delayed till after the baby’s birth.
The majority of pregnant women with cancer feel nervous about the possible impact of treatment on their coming child. Being well-informed about possible treatments and side effects can make it much easier to make decisions and handle what happens.
If you have chemotherapy during pregnancy, your doctor will probably encourage you to stop having it at least 3– 4 weeks prior to your delivery date. This is due to the fact that chemotherapy increases your risk of bleeding or getting an infection during the birth. Stopping chemotherapy allows your body time to recuperate from the side effects.
Scientists are presently doing long-lasting research studies on women and children to explore this problem even more. It is known that providing chemotherapy in the first trimester (12 weeks) increases the risk of abnormality. However, some studies on children who were exposed to chemotherapy in the womb during the 2nd and third trimesters show that chemotherapy did not impact their advancement.
Various chemotherapy drugs may impact a developing baby in various ways. For instance, chemotherapy may cause premature delivery. Pre-term infants frequently have other health problems, such as respiratory problems and delayed development.
Your doctor can talk in information about your specific situation and what is best for your health and your unborn baby.
If you buy something through a link on this page, we may earn a small commission.
Health Recovery Tips
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Why is mental health treated differently than physical health?
Most physical illnesses, like most mental illnesses, cannot be seen by the naked and untrained eye. Indeed, brain chemistry is just as physically rooted as the chemistry of the rest of the body. Some mental disorders are more understood and treatable than some physical disorders.
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Quick Answer: What Is It Called When You Dont Like Textures?
Is SPD a mental illness?
Diagnosis.
Sensory processing disorder is accepted in the Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood (DC:0-3R).
It is not recognized as a mental disorder in medical manuals such as the ICD-10 or the DSM-5..
Is SPD considered special needs?
While SPD may affect the child’s auditory, visual, and motor skills, and the ability to process and sequence information, it is not, at present, specifically identified as a qualifying disability, making a child eligible for special education and related services.
Is hypersensitivity a disorder?
What Is Hypersensitivity? Hypersensitivity — also known as being a “highly sensitive person” (HSP) — is not a disorder. It is an attribute common in people with ADHD.
How do I overcome tactile sensitivity?
Try gradually to incorporate a variety of tactile experiences in play, eating, bath time, etc. It will usually be easier for the child to initiate play himself rather than having new or potentially threatening sensations imposed upon him. Demonstrate on yourself and make it fun.
What is tactile sensitivity?
The word “tactile” refers to the sense of touch, and tactile dysfunction (also known as tactile sensitivity) is a form of sensory dysfunction that causes that sense to be heightened to the point of discomfort or even pain. Children with tactile dysfunction feel certain sensations more strongly than most people do.
What are the 3 patterns of sensory processing disorders?
Summary of Sensory Processing Disorder Subtypes.Pattern 1: Sensory Modulation Disorder.Sensory Over-Responsivity.Sensory Under-Responsivity.Sensory Craving.Pattern 2: Sensory-Based Motor Disorder.Postural Disorder.Dyspraxia/Motor Planning Problems.More items…
What is sensory anxiety?
Sensory Overload and Anxiety Some may be oversensitive to sounds, sights, textures, flavors, smells and other sensory input. Others may be undersensitive to things like temperature and noise. Some kids are both oversensitive and undersensitive. Anxiety is most common in kids who are oversensitive.
Is food aversion a sign of autism?
Autism often comes with hypersensitivity to textures. So remember that it may be how a food feels in the mouth, rather than its flavor, that produces a food aversion.
What is the difference between autism and SPD?
Children with autism have disruptions in brain connectivity along social and emotional pathways, whereas those pathways are intact in children with SPD alone. Children with SPD tend to have more problems with touch than do those with autism, whereas children with autism struggle more with sound processing.
What does sensory overload feel like?
Share on Pinterest Common symptoms of sensory overload include a sense of discomfort, loss of focus, and an inability to ignore loud sounds. Sensory overload happens when one or more of the body’s five senses become overwhelmed.
What is it called when you dont like textures?
If you are hypersensitive to the point that it interferes with your functioning, you may have SPD. Many adults describe the feeling as being assaulted, attacked, or invaded by everyday experiences. They are bothered by sounds or textures that most people don’t hear or feel.
Why do certain textures make me uncomfortable?
It’s enhancing some senses in your body (be it sound, touches, smell etc) that make you “extra” aware of the texture you are experiencing, which therefore can cause discomfort.
Is Picky Eating a sign of autism?
Even though picky eating is a common problem, research suggests that it’s usually a temporary and normal part of development. However, children with autism often have more chronic feeding problems that go beyond picky eating. This may mean the child won’t eat an entire category of food such as proteins or vegetables.
What is tactile defensiveness?
1 Tactile defensiveness. Tactile defensiveness is a severe sensitivity to being touched and usually involves an adverse reaction to initiating touch with non-noxious tactile stimulation.
Is being tactile a good thing?
Tactile stimulation can trigger oxytocin, the love hormone. It also lowers cortisol levels, reducing anxiety and stress,” she says. Touch can have huge health benefits, Akhtar adds.
What is food texture aversion?
Food texture aversion is very common amongst picky eaters, particularly those with autism spectrum disorder. this can make introducing new foods very challenging for parents. Food aversions relating to textures can cause fussy eaters to reject foods, instigate gagging and reduce their nutrient intake.
Is SPD on the autism spectrum?
Sensory processing problems are commonly seen in developmental conditions like autism spectrum disorder. Sensory processing disorder is not recognized as a stand-alone disorder.
What is Brumotactillophobia?
Brumotactillophobia is the impressive technical term for fear of different foods touching each other.
Can anxiety cause sensory issues?
This can contribute to symptoms of sensory overload. Mental health conditions such as generalized anxiety disorder and PTSD can also trigger sensory overload. Anticipation, fatigue, and stress can all contribute to a sensory overload experience, making senses feel heightened during panic attacks and PTSD episodes.
What are signs of sensory issues?
If your child has a hard time gathering and interpreting those sensory inputs, they may show signs of sensory issues. These may include difficulty with balance and coordination, screaming, or being aggressive when wanting attention, and jumping up and down frequently.
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Urinary tract infections, UTIs for those painfully familiar, create a cycle of discomfort by encouraging an increased urine output while simultaneously making urination a painful experience that can make it feel like the urinary system is on fire. Several things can cause UTIs, but is a deficiency in fluid intake one of those causes?
The Relationship Between Water Intake and UTIs
When asked how to prevent a UTI, it’s more accurate to answer drinking enough water—drinking less water doesn’t bring an increased risk as much as drinking more water can be a prevention factor for a common UTI among women called recurrent cystitis.
Cystitis is the medical term for bladder infections and women are more likely to experience these due to their anatomy. This kind of UTI is usually treated with antibiotics taken for 3-to-5 days after prescription, but a 2018 study showed that women who drank plenty of water stopped needing antibiotics before women who didn’t.
The recommended amount of fluid for people who have biological traits considered to be female is 9 cups daily. That fluid doesn’t need to come directly from water. Anything with water in it, from tea and coffee to fruits and vegetables, will hydrate the body. Water is the best, simplest form of hydration, though.
That same study showed that women who experience recurrent infections of the bladder but stay hydrated cut their returning bouts of cystitis by 50%.
Causes of UTIs
Constipation
One uncomfortable, possibly painful bathroom issue causing another may seem impossibly unfair, but we’re talking about waste here—you should expect it to play dirty. Constipation becomes a risk factor for UTIs thanks to the amount of time waste is spending in your body. It gives bacteria a larger window to breed and makes it harder to completely expel waste from the bladder, making you more susceptible to UTIs.
Intercourse
Sexual intercourse brings bacteria close to the urethra opening, increasing the risk of infection if bacteria enter the body. Cut this risk down by urinating after intercourse.
Certain contraceptives, specifically spermicides and diaphragms, can also increase the risk of UTIs.
Holding It In
Constipation is a risk factor for UTIs due to the amount of time bacteria gets to spend hanging out in your body, and the same holds true for holding in urine.
Try to expel your liquid waste at least every 6 hours. This shouldn’t be difficult if you have normal bathroom habits—just listen to your body and go when you need to go. This will expel bacteria before it can multiply in your bladder and cause an infection.
If you’re taking medications for allergies or cold/flu, be mindful of your bathroom schedule and drink more water if you think you should be visiting the bathroom more. These sorts of medicines are antihistamines, which can make you pee less.
Tight Clothing
Wearing tight clothing, especially during workout sessions, can create a hostile environment for bodies with vaginas. They’ll hold in bacteria that breed well in these sorts of conditions.
Wearing cotton underwear may also help reduce the risk of UTIs.
Symptoms of UTIs
Prevalent Peeing
You shouldn’t ignore any urge to urinate, but if you’re experiencing a persistent, strong urge to go to the bathroom that feels like it’s beginning to interfere with your concentration or quality of life, your body may be trying to tell you about its UTI. This urge is often joined by a burning sensation when urine leaves the body. To further compound matters, a smaller amount of urine than usual may be passed when you’re experiencing a UTI, meaning that visits to the bathroom will become more frequent. These three symptoms can combine to become a very bad time.
Speaking of pee, urine expelled during a UTI may appear cloudy or give off a strong smell. It may also appear pink, red or syrupy. This is a sign that blood is in the urine.
Pelvic Pain
In women, UTIs can cause pain in the pelvic area, especially in its center and around the pubic bone.
Irregularities in Blood Sugar
Not providing the body with a steady (and healthy) amount of sugar can make it more susceptible to infection, particularly UTIs. These changes in blood sugar can cause UTIs, but they can also make UTIs into a symptom of something else. If your UTI is accompanied by high cholesterol, tingling, numbness or increased hunger, it’s a good idea to see a doctor. These are all indicators of undiagnosed diabetes.
How to Prevent UTIs
As the aforementioned study states, getting the recommended amount of water daily goes a long way when attempting to prevent recurrent UTIs. Many sources will cite cranberry juice as another prevention method. While it doesn’t hurt to drink it, there’s also no scientifically proven link between cranberry juice and UTI prevention.
In order to avoid introducing bacteria into the urinary tract, wipe from back to front to keep waste away from the urethra and vagina. Also, as mentioned before, pee after intercourse and avoid potentially troublesome contraceptives. Other feminine products that may cause irritation, like douches, deodorants and some powders, should also be kept away from the urethra.
It’s just as important to treat a UTI. If they’re allowed to persist in women, they can lead to kidney infections. If they’re left untreated in men, they can narrow the urethra.
Maintain Optimal Hydration with DripDrop and Save 25%
Keeping your body supplied with the right levels of hydration can be difficult during a normal day, let alone a day when a UTI has you running back and forth from the bathroom, painfully expelling urine only to repeat the process soon after. Drinking a lot of water will help the body combat the waste that made you unwell while that hydration will have other positive effects, like lowering blood pressure and improving mood (something you may be having trouble with considering the circumstances).
Supplementing that hydration with a DripDrop packet adds three times the number of electrolytes than a sports drink. Electrolytes are substances that assist the body with everything from communication and oxidation to immune functions, so they may give you the boost you need to kick a UTI to the curb.
Subscribe with DripDrop to save 25%, or sample various flavors with a multi-flavor pouch.
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|
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Heilpflanzen-Welt - Die Welt der Heilpflanzen!
Heilpflanzen-Welt - Natürlich natürlich!
December 2019
Med Sci Sports Exerc. 1992 Nov; 24(11): 1290-7.
Serum sex hormones and endurance performance after a lacto-ovo vegetarian and a mixed diet.
Raben A, Kiens B, Richter EA, Rasmussen LB, Svenstrup B, Micic S, Bennett P.
August Krogh Institute, University of Copenhagen, Denmark.
Serum sex hormones and endurance performance after a lacto-ovo vegetarian and a mixed diet. Med. Sci. Sports Exerc., Vol. 24, No. 11, pp. 1290-1297, 1992. The effect of a lacto-ovo vegetarian (V) and a mixed, meat-rich (M) diet on the level of serum sex hormones, gonadotropins, and endurance performance of eight male endurance athletes was investigated in a 2 x 6 wk cross-over study. The energy contribution from carbohydrate, fat, and protein was 58%, 27%, and 15% on the V diet and 58%, 28%, and 14 E% on the M diet. For total fasting serum testosterone (T) there was a significant interaction between diet and time (P < 0.01). Thus, the V diet resulted in a lower total T level (13.7, 9.8-32.4 nmol.l-1) (median and range) compared with the M diet (17.4, 11.8-33.5 nmol.l-1). During exercise after 6 wk on the diets total T was also significantly lower on the V than on the M diet (P < 0.05). Serum free testosterone, however, did not differ significantly during the 6 wk dietary intervention periods and neither did serum concentrations of sex hormone binding globulin, dihydrotestosterone, dehydroepiandrosterone sulphate, 4-androstenedione, estrone, estradiol, estrone sulphate, or gonadotropins. Endurance performance time was higher for six and lower for two after the mixed diet compared with the vegetarian diet. This was not significant, however. In conclusion, 6 wk on a lacto-ovo vegetarian diet caused a minor decrease in total testosterone and no significant changes in physical performance in male endurance athletes compared with 6 wk on a mixed, meatrich diet.
Search only the database:
© Top Fit Gesund, 1992-2019. Alle Rechte vorbehalten – ImpressumDatenschutzerklärung
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Schedule an appointment today:
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What is Obesity Hypoventilation Syndrome? (Diagnosis and Treatment)
Very obese children and adults who have daytime fatigue and difficulty concentrating may be suffering from obstructive sleep apnea but in up to 20% of cases, the diagnosis may be even more serious. Obesity Hypoventilation Syndrome, or OHS, is a sleep-related respiratory problem that can cause serious and in some cases irreversible damage to the body, greatly increasing mortality risk over a fairly short period of time.
The key to managing this condition is knowing how to spot it early.
What Is Obesity Hypoventilation Syndrome (OHS)?
OHS, sometimes referred to as hypercapnic sleep apnea or Pickwickian Syndrome , is form of sleep-disordered breathing. Its characterized by the following:
1. Patients are seriously overweight ( obese ), with a BMI greater than 30.
2. They have a higher-than-normal amount of carbon dioxide, or CO2, in the bloodstream (a condition called hypercapnia ). This hypercapnia is present during the daytime but gets worse during sleep, sometimes leading to severe oxygen deprivation in the arterial blood supply.
3. This hypercapnia is caused by hypoventilation , or respiratory depression: episodes of shallow breathing or slower-than-normal breathing that are not caused by a lung disease, a neurologic disorder, or muscle weakness. People with OHS tend to hypoventilate more during REM sleep than in non-REM sleep. Sometimes their breath ceases altogether (similar to an apnea event).
This disease is associated exclusively with obesity. About 90% of patients diagnosed with OHS also have Obstructive Sleep Apnea (OSA).
OHS is dangerous because the high CO2 levels, combined with a lack of sufficient oxygen in the blood, can be a precursor to hypoxia or hypoxemia chronic, severe oxygen deprivation that causes tissue to deteriorate.
Over time, this deterioration leads to serious and even deadly emergencies like cardiopulmonary arrest (failure of the heart muscle) or respiratory failure.
How OHS Is Different from OSA
Although the two conditions are often closely related, they’re not the same, and they’re not always linked.
Some basic facts about OHS and OSA:
• About 8090% of the time, people with obesity hypoventilation syndrome (OHS) also have obstructive sleep apnea (OSA). However, researchers believe only about 1020% of people with obstructive sleep apnea also have OHS.
• While both OSA and OHS involve respiratory disruptions, these disruptions differ. If you have OSA, an obstruction of your upper airway will cause you to cease breathing many times per night (or even many times per hour). Typically, these apnea occurrences last a few seconds to a few minutes and wake you up with a gasp or choking sensation. After you return to sleep, you resume breathing normally until the next apnea occurs. During the day when you’re awake, however, you typically don’t experience such breathing irregularities.
• With OHS, you would experience long, continuous episodes of hypoventilation (shallow or slow breathing) while you sleep. These worsen in REM sleep. Unlike OSA, which affects you when you’re asleep, hypoventilation also occurs during the day when you’re awake. Whereas someone with OSA alone may have normal blood oxygen levels during the daytime, someone with OHS (or OHS and OSA) will have low blood oxygen levels and high CO2 levels both day and night.
OHS Symptoms
What does it feel like to have OHS? You may not notice any disruption to your sleep quality, particularly if you are not experiencing obstructive sleep apnea in addition to OHS.
However, you will likely experience some of the following:
• Concentration problems
• Difficulty exercising
• Excessive daytime sleepiness or fatigue
• Hyperactivity (in children)
• Prolonged nighttime sleep (though you are still tired after waking)
• Morning headaches
• Moodiness
• Memory problems
• Mouth breathing
• Nightmares
• Snoring
How OHS Is Diagnosed
OHS can be tricky to diagnose because its symptoms overlap with so many other conditions.
For example, its not uncommon for someone who’s very obese to feel tired, short of breath, or moody. People with OHS also frequently have other conditions like asthma or diabetes, which can present with some of the same problems.
If you have the known risk factors for OHS, in combination with the above symptoms, your physician may order lab tests to confirm a diagnosis.
Known OHS risk factors include:
• Clinical obesity
• Visible fat deposits around the chin and abdomen
• Swelling in the legs
• Thoracic kyphosis (forward curvature of the upper spine a hump)
• Facial or palate irregularities that might obstruct the upper airway
• Polyps, cysts, or other irregularities in the nasal passages
• Signs of right-sided heart failure
• A concavity of the chest a possible sign that the respiratory muscles have been overused while trying to overcome an obstruction
• The excessive use of drugs or alcohol, depressants, and certain medications like antihistamines
If your physician suspects OHS based on your medical history and the above risk factors, she may order the following tests to confirm a diagnosis.
• An arterial blood gas test to confirm daytime hypercapnia. You may have OHS if your carbon dioxide level is higher than 45 mm Hg.
• Echocardiogram to check for arrhythmias or damage to the ventricles of the heart (possible side effects of undetected OHS).
• Pulmonary function tests to show if you have an upper airway obstruction or a reduction in lung capacity or breathing efficiency.
• Chest radiograph (CXR) to look for deformities of the chest wall or signs of heart failure.
Your doctor may also check for an accumulation of blood or fluid in your tissue, higher-than-normal red blood cell count, high blood pressure in the lungs ( pulmonary artery hypertension ), and any signs of heart strain, enlargement, dysfunction, or right-sided heart failure.
In addition to these tests, your doctor may order an overnight polysomnography (sleep study) to check for hypoventilation, hypoxia and hypercapnia during sleep.
During the sleep study, sleep lab technicians can also conduct a nocturnal pulse oximetry to measure your heart rate and oxygen levels. Pulse oximetry can show whether you also have obstructive sleep apnea in addition to (or in lieu of) OHS.
Treatment of OHS
Currently, the treatment approach for OHS entails two steps:
1. Losing weight. Obesity appears to be the main cause of OHS. To reverse or improve symptoms, you should try to return to a normal body weight with a healthy BMI. Some patients cannot achieve this goal with diet and exercise alone, especially if respiratory symptoms are too severe to allow for cardiovascular exercise. In those cases, bariatric surgery may be recommended.
2. Complying with non-invasive ventilation (NIV), CPAP, or Bi-level PAP therapy . OHS patients without OSA may be given an NIV mask that provides assisted ventilation supplemented with oxygen. This treatment can help to normalize blood oxygen levels and prevent hypoxemia. In the case of OHS with OSA, CPAP or Bi-level PAP therapy may be more effective because the forced air pressure overcomes the soft tissue obstruction in the upper airway.
The bad news is, untreated OHS is very serious. In most cases, by the time it’s diagnosed, it’s already done enough damage to the heart and lungs to put you at a 23% risk of death over 18 months. That risk grows to 46% over 50 months.
The good news is, diagnosing and treating OHS with PAP therapy can improve or even normalize blood CO2 levels, bringing the mortality risk down to less than 10%.
Further Reading
News & Updates
Telehealth Patient
Telehealth for sleep evaluations
Telehealth is a hot topic. Although its recent rise is partially linked with the decline in in-person visits during the coronavirus pandemic, telehealth has in fact been heralded as the ‘next big thing’ in healthcare for more than a decade. The American Academy of Sleep Medicine (AASM) has announced its commitment to advancing the use…
Read more
sleep apnea and insomnia patient
Will Sleep Apnea Cause Insomnia?
Everyone has trouble sleeping at some point in their life. A late-afternoon latte, an overly indulgent dinner or nerves about an upcoming work milestone can keep you up into the wee hours of the night. The next day may not be one of your best –- you might be irritable, exhausted and unfocused — but…
Read more
Sleep Apnea Raises Your Risk of Sudden Cardiac Death: Get the Facts
You may have heard of sleep apnea, but do you really know what it is? Far from a harmless sleep disorder that keeps you from a sound night’s rest, sleep apnea can lead to serious health complications, including sudden cardiac death. According to the American Sleep Apnea Association, 22 million Americans suffer from sleep apnea.…
Read more
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Treatment for a hyperextended knee
Hyperextended knee is a condition where the knee is stretched or twisted in a way that the ligaments are torn and result to severe pain and discomfort while walking. Even gentle bending causes severe pain. [youtube url=”https://www.youtube.com/watch?v=VfVgWgw3NdU”] Hyperextension of the knee happens when the knee joint extends beyond the normal range of motion and severely …
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Related JoVE Video
Pubmed Article
Lhx2 regulates a cortex-specific mechanism for barrel formation.
Proc. Natl. Acad. Sci. U.S.A.
PUBLISHED: 11-21-2013
LIM homeodomain transcription factors are critical regulators of early development in multiple systems but have yet to be examined for a role in circuit formation. The LIM homeobox gene Lhx2 is expressed in cortical progenitors during development and also in the superficial layers of the neocortex in maturity. However, analysis of Lhx2 function at later stages of cortical development has been hampered by severe phenotypes associated with early loss of function. We identified a particular Cre-recombinase line that acts in the cortical primordium after its specification is complete, permitting an analysis of Lhx2 function in neocortical lamination, regionalization, and circuit formation by selective elimination of Lhx2 in the dorsal telencephalon. We report a profound disruption of cortical neuroanatomical and molecular features upon loss of Lhx2 in the cortex from embryonic day 11.5. A unique feature of cortical circuitry, the somatosensory barrels, is undetectable, and molecular patterning of cortical regions appears disrupted. Surprisingly, thalamocortical afferents innervate the mutant cortex with apparently normal regional specificity. Electrophysiological recordings reveal a loss of responses evoked by stimulation of individual whiskers, but responses to simultaneous stimulation of multiple whiskers were present, suggesting that thalamic afferents are unable to organize the neurocircuitry for barrel formation because of a cortex-specific requirement of Lhx2. We report that Lhx2 is required for the expression of transcription factor paired box gene 6, axon guidance molecule Ephrin A5, and the receptor NMDA receptor 1. These genes may mediate Lhx2 function in the formation of specialized neurocircuitry necessary for neocortical function.
Authors: Anna J. Nichols, Ryan S. O'Dell, Teresa A. Powrozek, Eric C. Olson.
Published: 04-03-2013
ABSTRACT
Cortical development involves complex interactions between neurons and non-neuronal elements including precursor cells, blood vessels, meninges and associated extracellular matrix. Because they provide a suitable organotypic environment, cortical slice explants are often used to investigate those interactions that control neuronal differentiation and development. Although beneficial, the slice explant model can suffer from drawbacks including aberrant cellular lamination and migration. Here we report a whole cerebral hemisphere explant system for studies of early cortical development that is easier to prepare than cortical slices and shows consistent organotypic migration and lamination. In this model system, early lamination and migration patterns proceed normally for a period of two days in vitro, including the period of preplate splitting, during which prospective cortical layer six forms. We then developed an ex utero electroporation (EUEP) approach that achieves ~80% success in targeting GFP expression to neurons developing in the dorsal medial cortex. The whole hemisphere explant model makes early cortical development accessible for electroporation, pharmacological intervention and live imaging approaches. This method avoids the survival surgery required of in utero electroporation (IUEP) approaches while improving both transfection and areal targeting consistency. This method will facilitate experimental studies of neuronal proliferation, migration and differentiation.
25 Related JoVE Articles!
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Whole Cell Recording from an Organotypic Slice Preparation of Neocortex
Authors: Robert C. Foehring, Dongxu Guan, Tara Toleman, Angela R. Cantrell.
Institutions: University of Tennessee Health Science Center.
We have been studying the expression and functional roles of voltage-gated potassium channels in pyramidal neurons from rat neocortex. Because of the lack of specific pharmacological agents for these channels, we have taken a genetic approach to manipulating channel expression. We use an organotypic culture preparation (16) in order to maintain cell morphology and the laminar pattern of cortex. We typically isolate acute neocortical slices at postnatal days 8-10 and maintain the slices in culture for 3-7 days. This allows us to study neurons at a similar age to those in our work with acute slices and minimizes the development of exuberant excitatory connections in the slice. We record from visually-identified pyramidal neurons in layers II/III or V using infrared illumination (IR-) and differential interference contrast microscopy (DIC) with whole cell patch clamp in current- or voltage-clamp. We use biolistic (Gene gun) transfection of wild type or mutant potassium channel DNA to manipulate expression of the channels to study their function. The transfected cells are easily identified by epifluorescence microscopy after co-transfection with cDNA for green fluorescent protein (GFP). We compare recordings of transfected cells to adjacent, untransfected neurons in the same layer from the same slice.
Neuroscience, Issue 52, Organotypic, neocortex, somatosensory, pyramidal cell, slice preparation, biolistic transfection
2600
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Preparing Undercut Model of Posttraumatic Epileptogenesis in Rodents
Authors: Wenhui Xiong, Xingjie Ping, Jianhua Gao, Xiaoming Jin.
Institutions: Indiana University School of Medicine.
Partially isolated cortex ("undercut") is an animal model of posttraumatic epileptogenesis. The surgical procedure involves cutting through the sensorimotor cortex and the underneath white matter (undercut) so that a specific region of the cerebral cortex is largely isolated from the neighboring cortex and subcortical regions1-3. After a latency of two or more weeks following the surgery, epileptiform discharges can be recorded in brain slices from rodents1; and electrical or behavior seizures can be observed in vivo from other species such as cat and monkey4-6. This well established animal model is efficient to generate and mimics several important characteristics of traumatic brain injury. However, it is technically challenging attempting to make precise cortical lesions in the small rodent brain with a free hand. Based on the procedure initially established in Dr. David Prince's lab at the Stanford University1, here we present an improved technique to perform a surgery for the preparation of this model in mice and rats. We demonstrate how to make a simple surgical device and use it to gain a better control of cutting depth and angle to generate more precise and consistent results. The device is easy to make, and the procedure is quick to learn. The generation of this animal model provides an efficient system for study on the mechanisms of posttraumatic epileptogenesis.
Neuroscience, Issue 55, epilepsy, traumatic brain injury, brain, mouse, rat, surgery
2840
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TMS: Using the Theta-Burst Protocol to Explore Mechanism of Plasticity in Individuals with Fragile X Syndrome and Autism
Authors: Lindsay M. Oberman, Jared C. Horvath, Alvaro Pascual-Leone.
Institutions: Beth Israel Deaconess Medical Center.
Fragile X Syndrome (FXS), also known as Martin-Bell Syndrome, is a genetic abnormality found on the X chromosome.1,2 Individuals suffering from FXS display abnormalities in the expression of FMR1 - a protein required for typical, healthy neural development.3 Recent data has suggested that the loss of this protein can cause the cortex to be hyperexcitable thereby affecting overall patterns of neural plasticity.4,5 In addition, Fragile X shows a strong comorbidity with autism: in fact, 30% of children with FXS are diagnosed with autism, and 2 - 5% of autistic children suffer from FXS.6 Transcranial Magnetic Stimulation (a non-invasive neurostimulatory and neuromodulatory technique that can transiently or lastingly modulate cortical excitability via the application of localized magnetic field pulses 7,8) represents a unique method of exploring plasticity and the manifestations of FXS within affected individuals. More specifically, Theta-Burst Stimulation (TBS), a specific stimulatory protocol shown to modulate cortical plasticity for a duration up to 30 minutes after stimulation cessation in healthy populations, has already proven an efficacious tool in the exploration of abnormal plasticity.9,10 Recent studies have shown the effects of TBS last considerably longer in individuals on the autistic spectrum - up to 90 minutes.11 This extended effect-duration suggests an underlying abnormality in the brain's natural plasticity state in autistic individuals - similar to the hyperexcitability induced by Fragile X Syndrome. In this experiment, utilizing single-pulse motor-evoked potentials (MEPs) as our benchmark, we will explore the effects of both intermittent and continuous TBS on cortical plasticity in individuals suffering from FXS and individuals on the Autistic Spectrum.
Neuroscience, Issue 46, Transcranial Magnetic Stimulation, Theta-Burst Stimulation, Neural Plasticity, Fragile X, Autism
2272
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A Proboscis Extension Response Protocol for Investigating Behavioral Plasticity in Insects: Application to Basic, Biomedical, and Agricultural Research
Authors: Brian H. Smith, Christina M. Burden.
Institutions: Arizona State University.
Insects modify their responses to stimuli through experience of associating those stimuli with events important for survival (e.g., food, mates, threats). There are several behavioral mechanisms through which an insect learns salient associations and relates them to these events. It is important to understand this behavioral plasticity for programs aimed toward assisting insects that are beneficial for agriculture. This understanding can also be used for discovering solutions to biomedical and agricultural problems created by insects that act as disease vectors and pests. The Proboscis Extension Response (PER) conditioning protocol was developed for honey bees (Apis mellifera) over 50 years ago to study how they perceive and learn about floral odors, which signal the nectar and pollen resources a colony needs for survival. The PER procedure provides a robust and easy-to-employ framework for studying several different ecologically relevant mechanisms of behavioral plasticity. It is easily adaptable for use with several other insect species and other behavioral reflexes. These protocols can be readily employed in conjunction with various means for monitoring neural activity in the CNS via electrophysiology or bioimaging, or for manipulating targeted neuromodulatory pathways. It is a robust assay for rapidly detecting sub-lethal effects on behavior caused by environmental stressors, toxins or pesticides. We show how the PER protocol is straightforward to implement using two procedures. One is suitable as a laboratory exercise for students or for quick assays of the effect of an experimental treatment. The other provides more thorough control of variables, which is important for studies of behavioral conditioning. We show how several measures for the behavioral response ranging from binary yes/no to more continuous variable like latency and duration of proboscis extension can be used to test hypotheses. And, we discuss some pitfalls that researchers commonly encounter when they use the procedure for the first time.
Neuroscience, Issue 91, PER, conditioning, honey bee, olfaction, olfactory processing, learning, memory, toxin assay
51057
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Regioselective Biolistic Targeting in Organotypic Brain Slices Using a Modified Gene Gun
Authors: Jason Arsenault, Andras Nagy, Jeffrey T. Henderson, John A. O'Brien.
Institutions: University of Toronto, MRC-Laboratory of Molecular Biology, Cambridge, UK.
Transfection of DNA has been invaluable for biological sciences and with recent advances to organotypic brain slice preparations, the effect of various heterologous genes could thus be investigated easily while maintaining many aspects of in vivo biology. There has been increasing interest to transfect terminally differentiated neurons for which conventional transfection methods have been fraught with difficulties such as low yields and significant losses in viability. Biolistic transfection can circumvent many of these difficulties yet only recently has this technique been modified so that it is amenable for use in mammalian tissues. New modifications to the accelerator chamber have enhanced the gene gun's firing accuracy and increased its depths of penetration while also allowing the use of lower gas pressure (50 psi) without loss of transfection efficiency as well as permitting a focused regioselective spread of the particles to within 3 mm. In addition, this technique is straight forward and faster to perform than tedious microinjections. Both transient and stable expression are possible with nanoparticle bombardment where episomal expression can be detected within 24 hr and the cell survival was shown to be better than, or at least equal to, conventional methods. This technique has however one crucial advantage: it permits the transfection to be localized within a single restrained radius thus enabling the user to anatomically isolate the heterologous gene's effects. Here we present an in-depth protocol to prepare viable adult organotypic slices and submit them to regioselective transfection using an improved gene gun.
Neuroscience, Issue 92, Biolistics, gene gun, organotypic brain slices, Diolistic, gene delivery, staining
52148
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Functional Neuroimaging Using Ultrasonic Blood-brain Barrier Disruption and Manganese-enhanced MRI
Authors: Gabriel P. Howles, Yi Qi, Stephen J. Rosenzweig, Kathryn R. Nightingale, G. Allan Johnson.
Institutions: Stanford University , Duke University Medical Center, Duke University .
Although mice are the dominant model system for studying the genetic and molecular underpinnings of neuroscience, functional neuroimaging in mice remains technically challenging. One approach, Activation-Induced Manganese-enhanced MRI (AIM MRI), has been used successfully to map neuronal activity in rodents 1-5. In AIM MRI, Mn2+ acts a calcium analog and accumulates in depolarized neurons 6,7. Because Mn2+ shortens the T1 tissue property, regions of elevated neuronal activity will enhance in MRI. Furthermore, Mn2+ clears slowly from the activated regions; therefore, stimulation can be performed outside the magnet prior to imaging, enabling greater experimental flexibility. However, because Mn2+ does not readily cross the blood-brain barrier (BBB), the need to open the BBB has limited the use of AIM MRI, especially in mice. One tool for opening the BBB is ultrasound. Though potentially damaging, if ultrasound is administered in combination with gas-filled microbubbles (i.e., ultrasound contrast agents), the acoustic pressure required for BBB opening is considerably lower. This combination of ultrasound and microbubbles can be used to reliably open the BBB without causing tissue damage 8-11. Here, a method is presented for performing AIM MRI by using microbubbles and ultrasound to open the BBB. After an intravenous injection of perflutren microbubbles, an unfocused pulsed ultrasound beam is applied to the shaved mouse head for 3 minutes. For simplicity, we refer to this technique of BBB Opening with Microbubbles and UltraSound as BOMUS 12. Using BOMUS to open the BBB throughout both cerebral hemispheres, manganese is administered to the whole mouse brain. After experimental stimulation of the lightly sedated mice, AIM MRI is used to map the neuronal response. To demonstrate this approach, herein BOMUS and AIM MRI are used to map unilateral mechanical stimulation of the vibrissae in lightly sedated mice 13. Because BOMUS can open the BBB throughout both hemispheres, the unstimulated side of the brain is used to control for nonspecific background stimulation. The resultant 3D activation map agrees well with published representations of the vibrissae regions of the barrel field cortex 14. The ultrasonic opening of the BBB is fast, noninvasive, and reversible; and thus this approach is suitable for high-throughput and/or longitudinal studies in awake mice.
Neuroscience, Issue 65, Molecular Biology, Biomedical Engineering, mouse, ultrasound, blood-brain barrier, functional MRI, fMRI, manganese-enhanced MRI, MEMRI
4055
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Setting-up an In Vitro Model of Rat Blood-brain Barrier (BBB): A Focus on BBB Impermeability and Receptor-mediated Transport
Authors: Yves Molino, Françoise Jabès, Emmanuelle Lacassagne, Nicolas Gaudin, Michel Khrestchatisky.
Institutions: VECT-HORUS SAS, CNRS, NICN UMR 7259.
The blood brain barrier (BBB) specifically regulates molecular and cellular flux between the blood and the nervous tissue. Our aim was to develop and characterize a highly reproducible rat syngeneic in vitro model of the BBB using co-cultures of primary rat brain endothelial cells (RBEC) and astrocytes to study receptors involved in transcytosis across the endothelial cell monolayer. Astrocytes were isolated by mechanical dissection following trypsin digestion and were frozen for later co-culture. RBEC were isolated from 5-week-old rat cortices. The brains were cleaned of meninges and white matter, and mechanically dissociated following enzymatic digestion. Thereafter, the tissue homogenate was centrifuged in bovine serum albumin to separate vessel fragments from nervous tissue. The vessel fragments underwent a second enzymatic digestion to free endothelial cells from their extracellular matrix. The remaining contaminating cells such as pericytes were further eliminated by plating the microvessel fragments in puromycin-containing medium. They were then passaged onto filters for co-culture with astrocytes grown on the bottom of the wells. RBEC expressed high levels of tight junction (TJ) proteins such as occludin, claudin-5 and ZO-1 with a typical localization at the cell borders. The transendothelial electrical resistance (TEER) of brain endothelial monolayers, indicating the tightness of TJs reached 300 ohm·cm2 on average. The endothelial permeability coefficients (Pe) for lucifer yellow (LY) was highly reproducible with an average of 0.26 ± 0.11 x 10-3 cm/min. Brain endothelial cells organized in monolayers expressed the efflux transporter P-glycoprotein (P-gp), showed a polarized transport of rhodamine 123, a ligand for P-gp, and showed specific transport of transferrin-Cy3 and DiILDL across the endothelial cell monolayer. In conclusion, we provide a protocol for setting up an in vitro BBB model that is highly reproducible due to the quality assurance methods, and that is suitable for research on BBB transporters and receptors.
Medicine, Issue 88, rat brain endothelial cells (RBEC), mouse, spinal cord, tight junction (TJ), receptor-mediated transport (RMT), low density lipoprotein (LDL), LDLR, transferrin, TfR, P-glycoprotein (P-gp), transendothelial electrical resistance (TEER),
51278
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The Use of Magnetic Resonance Spectroscopy as a Tool for the Measurement of Bi-hemispheric Transcranial Electric Stimulation Effects on Primary Motor Cortex Metabolism
Authors: Sara Tremblay, Vincent Beaulé, Sébastien Proulx, Louis-Philippe Lafleur, Julien Doyon, Małgorzata Marjańska, Hugo Théoret.
Institutions: University of Montréal, McGill University, University of Minnesota.
Transcranial direct current stimulation (tDCS) is a neuromodulation technique that has been increasingly used over the past decade in the treatment of neurological and psychiatric disorders such as stroke and depression. Yet, the mechanisms underlying its ability to modulate brain excitability to improve clinical symptoms remains poorly understood 33. To help improve this understanding, proton magnetic resonance spectroscopy (1H-MRS) can be used as it allows the in vivo quantification of brain metabolites such as γ-aminobutyric acid (GABA) and glutamate in a region-specific manner 41. In fact, a recent study demonstrated that 1H-MRS is indeed a powerful means to better understand the effects of tDCS on neurotransmitter concentration 34. This article aims to describe the complete protocol for combining tDCS (NeuroConn MR compatible stimulator) with 1H-MRS at 3 T using a MEGA-PRESS sequence. We will describe the impact of a protocol that has shown great promise for the treatment of motor dysfunctions after stroke, which consists of bilateral stimulation of primary motor cortices 27,30,31. Methodological factors to consider and possible modifications to the protocol are also discussed.
Neuroscience, Issue 93, proton magnetic resonance spectroscopy, transcranial direct current stimulation, primary motor cortex, GABA, glutamate, stroke
51631
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Manufacturing and Using Piggy-back Multibarrel Electrodes for In vivo Pharmacological Manipulations of Neural Responses
Authors: Anna Dondzillo, Jennifer L. Thornton, Daniel J. Tollin, Achim Klug.
Institutions: University of Colorado Medical Campus.
In vivo recordings from single neurons allow an investigator to examine the firing properties of neurons, for example in response to sensory stimuli. Neurons typically receive multiple excitatory and inhibitory afferent and/or efferent inputs that integrate with each other, and the ultimate measured response properties of the neuron are driven by the neural integrations of these inputs. To study information processing in neural systems, it is necessary to understand the various inputs to a neuron or neural system, and the specific properties of these inputs. A powerful and technically relatively simple method to assess the functional role of certain inputs that a given neuron is receiving is to dynamically and reversibly suppress or eliminate these inputs, and measure the changes in the neuron's output caused by this manipulation. This can be accomplished by pharmacologically altering the neuron's immediate environment with piggy-back multibarrel electrodes. These electrodes consist of a single barrel recording electrode and a multibarrel drug electrode that can carry up to 4 different synaptic agonists or antagonists. The pharmacological agents can be applied iontophoretically at desired times during the experiment, allowing for time-controlled delivery and reversible reconfiguration of synaptic inputs. As such, pharmacological manipulation of the microenvironment represents a powerful and unparalleled method to test specific hypotheses about neural circuit function. Here we describe how piggy-back electrodes are manufactured, and how they are used during in vivo experiments. The piggy-back system allows an investigator to combine a single barrel recording electrode of any arbitrary property (resistance, tip size, shape etc) with a multibarrel drug electrode. This is a major advantage over standard multi-electrodes, where all barrels have more or less similar shapes and properties. Multibarrel electrodes were first introduced over 40 years ago 1-3, and have undergone a number of design improvements 2,3 until the piggy-back type was introduced in the 1980s 4,5. Here we present a set of important improvements in the laboratory production of piggy-back electrodes that allow for deep brain penetration in intact in vivo animal preparations due to a relatively thin electrode shaft that causes minimal damage. Furthermore these electrodes are characterized by low noise recordings, and have low resistance drug barrels for very effective iontophoresis of the desired pharmacological agents.
Neuroscience, Issue 71, Biophysics, Physiology, Neurobiology, Medicine, Pharmacology, Mechanical Engineering, Electrical Engineering, Piggyback electrode, iontophoresis, iontophoresis pump, single cell recording, neural excitation, neural inhibition, in vivo electrophysiology
4358
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Mapping Inhibitory Neuronal Circuits by Laser Scanning Photostimulation
Authors: Taruna Ikrar, Nicholas D. Olivas, Yulin Shi, Xiangmin Xu.
Institutions: University of California, Irvine, University of California, Irvine.
Inhibitory neurons are crucial to cortical function. They comprise about 20% of the entire cortical neuronal population and can be further subdivided into diverse subtypes based on their immunochemical, morphological, and physiological properties1-4. Although previous research has revealed much about intrinsic properties of individual types of inhibitory neurons, knowledge about their local circuit connections is still relatively limited3,5,6. Given that each individual neuron's function is shaped by its excitatory and inhibitory synaptic input within cortical circuits, we have been using laser scanning photostimulation (LSPS) to map local circuit connections to specific inhibitory cell types. Compared to conventional electrical stimulation or glutamate puff stimulation, LSPS has unique advantages allowing for extensive mapping and quantitative analysis of local functional inputs to individually recorded neurons3,7-9. Laser photostimulation via glutamate uncaging selectively activates neurons perisomatically, without activating axons of passage or distal dendrites, which ensures a sub-laminar mapping resolution. The sensitivity and efficiency of LSPS for mapping inputs from many stimulation sites over a large region are well suited for cortical circuit analysis. Here we introduce the technique of LSPS combined with whole-cell patch clamping for local inhibitory circuit mapping. Targeted recordings of specific inhibitory cell types are facilitated by use of transgenic mice expressing green fluorescent proteins (GFP) in limited inhibitory neuron populations in the cortex3,10, which enables consistent sampling of the targeted cell types and unambiguous identification of the cell types recorded. As for LSPS mapping, we outline the system instrumentation, describe the experimental procedure and data acquisition, and present examples of circuit mapping in mouse primary somatosensory cortex. As illustrated in our experiments, caged glutamate is activated in a spatially restricted region of the brain slice by UV laser photolysis; simultaneous voltage-clamp recordings allow detection of photostimulation-evoked synaptic responses. Maps of either excitatory or inhibitory synaptic input to the targeted neuron are generated by scanning the laser beam to stimulate hundreds of potential presynaptic sites. Thus, LSPS enables the construction of detailed maps of synaptic inputs impinging onto specific types of inhibitory neurons through repeated experiments. Taken together, the photostimulation-based technique offers neuroscientists a powerful tool for determining the functional organization of local cortical circuits.
Neuroscience, Issue 56, glutamate uncaging, whole cell recording, GFP, transgenic, interneurons
3109
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Whole-cell Patch-clamp Recordings from Morphologically- and Neurochemically-identified Hippocampal Interneurons
Authors: Sam A. Booker, Jie Song, Imre Vida.
Institutions: Charité Universitätmedizin.
GABAergic inhibitory interneurons play a central role within neuronal circuits of the brain. Interneurons comprise a small subset of the neuronal population (10-20%), but show a high level of physiological, morphological, and neurochemical heterogeneity, reflecting their diverse functions. Therefore, investigation of interneurons provides important insights into the organization principles and function of neuronal circuits. This, however, requires an integrated physiological and neuroanatomical approach for the selection and identification of individual interneuron types. Whole-cell patch-clamp recording from acute brain slices of transgenic animals, expressing fluorescent proteins under the promoters of interneuron-specific markers, provides an efficient method to target and electrophysiologically characterize intrinsic and synaptic properties of specific interneuron types. Combined with intracellular dye labeling, this approach can be extended with post-hoc morphological and immunocytochemical analysis, enabling systematic identification of recorded neurons. These methods can be tailored to suit a broad range of scientific questions regarding functional properties of diverse types of cortical neurons.
Neuroscience, Issue 91, electrophysiology, acute slice, whole-cell patch-clamp recording, neuronal morphology, immunocytochemistry, parvalbumin, hippocampus, inhibition, GABAergic interneurons, synaptic transmission, IPSC, GABA-B receptor
51706
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Utilizing Transcranial Magnetic Stimulation to Study the Human Neuromuscular System
Authors: David A. Goss, Richard L. Hoffman, Brian C. Clark.
Institutions: Ohio University.
Transcranial magnetic stimulation (TMS) has been in use for more than 20 years 1, and has grown exponentially in popularity over the past decade. While the use of TMS has expanded to the study of many systems and processes during this time, the original application and perhaps one of the most common uses of TMS involves studying the physiology, plasticity and function of the human neuromuscular system. Single pulse TMS applied to the motor cortex excites pyramidal neurons transsynaptically 2 (Figure 1) and results in a measurable electromyographic response that can be used to study and evaluate the integrity and excitability of the corticospinal tract in humans 3. Additionally, recent advances in magnetic stimulation now allows for partitioning of cortical versus spinal excitability 4,5. For example, paired-pulse TMS can be used to assess intracortical facilitatory and inhibitory properties by combining a conditioning stimulus and a test stimulus at different interstimulus intervals 3,4,6-8. In this video article we will demonstrate the methodological and technical aspects of these techniques. Specifically, we will demonstrate single-pulse and paired-pulse TMS techniques as applied to the flexor carpi radialis (FCR) muscle as well as the erector spinae (ES) musculature. Our laboratory studies the FCR muscle as it is of interest to our research on the effects of wrist-hand cast immobilization on reduced muscle performance6,9, and we study the ES muscles due to these muscles clinical relevance as it relates to low back pain8. With this stated, we should note that TMS has been used to study many muscles of the hand, arm and legs, and should iterate that our demonstrations in the FCR and ES muscle groups are only selected examples of TMS being used to study the human neuromuscular system.
Medicine, Issue 59, neuroscience, muscle, electromyography, physiology, TMS, strength, motor control. sarcopenia, dynapenia, lumbar
3387
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Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABAA Receptors
Authors: Laura E. Brown, Celine Fuchs, Martin W. Nicholson, F. Anne Stephenson, Alex M. Thomson, Jasmina N. Jovanovic.
Institutions: University College London.
Inhibitory neurons act in the central nervous system to regulate the dynamics and spatio-temporal co-ordination of neuronal networks. GABA (γ-aminobutyric acid) is the predominant inhibitory neurotransmitter in the brain. It is released from the presynaptic terminals of inhibitory neurons within highly specialized intercellular junctions known as synapses, where it binds to GABAA receptors (GABAARs) present at the plasma membrane of the synapse-receiving, postsynaptic neurons. Activation of these GABA-gated ion channels leads to influx of chloride resulting in postsynaptic potential changes that decrease the probability that these neurons will generate action potentials. During development, diverse types of inhibitory neurons with distinct morphological, electrophysiological and neurochemical characteristics have the ability to recognize their target neurons and form synapses which incorporate specific GABAARs subtypes. This principle of selective innervation of neuronal targets raises the question as to how the appropriate synaptic partners identify each other. To elucidate the underlying molecular mechanisms, a novel in vitro co-culture model system was established, in which medium spiny GABAergic neurons, a highly homogenous population of neurons isolated from the embryonic striatum, were cultured with stably transfected HEK293 cell lines that express different GABAAR subtypes. Synapses form rapidly, efficiently and selectively in this system, and are easily accessible for quantification. Our results indicate that various GABAAR subtypes differ in their ability to promote synapse formation, suggesting that this reduced in vitro model system can be used to reproduce, at least in part, the in vivo conditions required for the recognition of the appropriate synaptic partners and formation of specific synapses. Here the protocols for culturing the medium spiny neurons and generating HEK293 cells lines expressing GABAARs are first described, followed by detailed instructions on how to combine these two cell types in co-culture and analyze the formation of synaptic contacts.
Neuroscience, Issue 93, Developmental neuroscience, synaptogenesis, synaptic inhibition, co-culture, stable cell lines, GABAergic, medium spiny neurons, HEK 293 cell line
52115
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Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates
Authors: Alison X. Xie, Kelli Lauderdale, Thomas Murphy, Timothy L. Myers, Todd A. Fiacco.
Institutions: University of California Riverside, University of California Riverside, University of California Riverside.
Close to two decades of research has established that astrocytes in situ and in vivo express numerous G protein-coupled receptors (GPCRs) that can be stimulated by neuronally-released transmitter. However, the ability of astrocytic receptors to exhibit plasticity in response to changes in neuronal activity has received little attention. Here we describe a model system that can be used to globally scale up or down astrocytic group I metabotropic glutamate receptors (mGluRs) in acute brain slices. Included are methods on how to prepare parasagittal hippocampal slices, construct chambers suitable for long-term slice incubation, bidirectionally manipulate neuronal action potential frequency, load astrocytes and astrocyte processes with fluorescent Ca2+ indicator, and measure changes in astrocytic Gq GPCR activity by recording spontaneous and evoked astrocyte Ca2+ events using confocal microscopy. In essence, a “calcium roadmap” is provided for how to measure plasticity of astrocytic Gq GPCRs. Applications of the technique for study of astrocytes are discussed. Having an understanding of how astrocytic receptor signaling is affected by changes in neuronal activity has important implications for both normal synaptic function as well as processes underlying neurological disorders and neurodegenerative disease.
Neuroscience, Issue 85, astrocyte, plasticity, mGluRs, neuronal Firing, electrophysiology, Gq GPCRs, Bolus-loading, calcium, microdomains, acute slices, Hippocampus, mouse
51458
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Viability Assays for Cells in Culture
Authors: Jessica M. Posimo, Ajay S. Unnithan, Amanda M. Gleixner, Hailey J. Choi, Yiran Jiang, Sree H. Pulugulla, Rehana K. Leak.
Institutions: Duquesne University.
Manual cell counts on a microscope are a sensitive means of assessing cellular viability but are time-consuming and therefore expensive. Computerized viability assays are expensive in terms of equipment but can be faster and more objective than manual cell counts. The present report describes the use of three such viability assays. Two of these assays are infrared and one is luminescent. Both infrared assays rely on a 16 bit Odyssey Imager. One infrared assay uses the DRAQ5 stain for nuclei combined with the Sapphire stain for cytosol and is visualized in the 700 nm channel. The other infrared assay, an In-Cell Western, uses antibodies against cytoskeletal proteins (α-tubulin or microtubule associated protein 2) and labels them in the 800 nm channel. The third viability assay is a commonly used luminescent assay for ATP, but we use a quarter of the recommended volume to save on cost. These measurements are all linear and correlate with the number of cells plated, but vary in sensitivity. All three assays circumvent time-consuming microscopy and sample the entire well, thereby reducing sampling error. Finally, all of the assays can easily be completed within one day of the end of the experiment, allowing greater numbers of experiments to be performed within short timeframes. However, they all rely on the assumption that cell numbers remain in proportion to signal strength after treatments, an assumption that is sometimes not met, especially for cellular ATP. Furthermore, if cells increase or decrease in size after treatment, this might affect signal strength without affecting cell number. We conclude that all viability assays, including manual counts, suffer from a number of caveats, but that computerized viability assays are well worth the initial investment. Using all three assays together yields a comprehensive view of cellular structure and function.
Cellular Biology, Issue 83, In-cell Western, DRAQ5, Sapphire, Cell Titer Glo, ATP, primary cortical neurons, toxicity, protection, N-acetyl cysteine, hormesis
50645
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Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice
Authors: Robert S. McNeill, Ralf S. Schmid, Ryan E. Bash, Mark Vitucci, Kristen K. White, Andrea M. Werneke, Brian H. Constance, Byron Huff, C. Ryan Miller.
Institutions: University of North Carolina School of Medicine, University of North Carolina School of Medicine, University of North Carolina School of Medicine, University of North Carolina School of Medicine, University of North Carolina School of Medicine, Emory University School of Medicine, University of North Carolina School of Medicine.
Current astrocytoma models are limited in their ability to define the roles of oncogenic mutations in specific brain cell types during disease pathogenesis and their utility for preclinical drug development. In order to design a better model system for these applications, phenotypically wild-type cortical astrocytes and neural stem cells (NSC) from conditional, genetically engineered mice (GEM) that harbor various combinations of floxed oncogenic alleles were harvested and grown in culture. Genetic recombination was induced in vitro using adenoviral Cre-mediated recombination, resulting in expression of mutated oncogenes and deletion of tumor suppressor genes. The phenotypic consequences of these mutations were defined by measuring proliferation, transformation, and drug response in vitro. Orthotopic allograft models, whereby transformed cells are stereotactically injected into the brains of immune-competent, syngeneic littermates, were developed to define the role of oncogenic mutations and cell type on tumorigenesis in vivo. Unlike most established human glioblastoma cell line xenografts, injection of transformed GEM-derived cortical astrocytes into the brains of immune-competent littermates produced astrocytomas, including the most aggressive subtype, glioblastoma, that recapitulated the histopathological hallmarks of human astrocytomas, including diffuse invasion of normal brain parenchyma. Bioluminescence imaging of orthotopic allografts from transformed astrocytes engineered to express luciferase was utilized to monitor in vivo tumor growth over time. Thus, astrocytoma models using astrocytes and NSC harvested from GEM with conditional oncogenic alleles provide an integrated system to study the genetics and cell biology of astrocytoma pathogenesis in vitro and in vivo and may be useful in preclinical drug development for these devastating diseases.
Neuroscience, Issue 90, astrocytoma, cortical astrocytes, genetically engineered mice, glioblastoma, neural stem cells, orthotopic allograft
51763
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Juxtasomal Biocytin Labeling to Study the Structure-function Relationship of Individual Cortical Neurons
Authors: Rajeevan T. Narayanan, Hemanth Mohan, Robin Broersen, Roel de Haan, Anton W. Pieneman, Christiaan P.J. de Kock.
Institutions: VU University Amsterdam.
The cerebral cortex is characterized by multiple layers and many distinct cell-types that together as a network are responsible for many higher cognitive functions including decision making, sensory-guided behavior or memory. To understand how such intricate neuronal networks perform such tasks, a crucial step is to determine the function (or electrical activity) of individual cell types within the network, preferentially when the animal is performing a relevant cognitive task. Additionally, it is equally important to determine the anatomical structure of the network and the morphological architecture of the individual neurons to allow reverse engineering the cortical network. Technical breakthroughs available today allow recording cellular activity in awake, behaving animals with the valuable option of post hoc identifying the recorded neurons. Here, we demonstrate the juxtasomal biocytin labeling technique, which involves recording action potential spiking in the extracellular (or loose-patch) configuration using conventional patch pipettes. The juxtasomal recording configuration is relatively stable and applicable across behavioral conditions, including anesthetized, sedated, awake head-fixed, and even in the freely moving animal. Thus, this method allows linking cell-type specific action potential spiking during animal behavior to reconstruction of the individual neurons and ultimately, the entire cortical microcircuit. In this video manuscript, we show how individual neurons in the juxtasomal configuration can be labeled with biocytin in the urethane-anaesthetized rat for post hoc identification and morphological reconstruction.
Bioengineering, Issue 84, biocytin, juxtasomal, morphology, physiology, action potential, structure-function, histology, reconstruction, neurons, electrophysiological recordings
51359
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Modeling Neural Immune Signaling of Episodic and Chronic Migraine Using Spreading Depression In Vitro
Authors: Aya D. Pusic, Yelena Y. Grinberg, Heidi M. Mitchell, Richard P. Kraig.
Institutions: The University of Chicago Medical Center, The University of Chicago Medical Center.
Migraine and its transformation to chronic migraine are healthcare burdens in need of improved treatment options. We seek to define how neural immune signaling modulates the susceptibility to migraine, modeled in vitro using spreading depression (SD), as a means to develop novel therapeutic targets for episodic and chronic migraine. SD is the likely cause of migraine aura and migraine pain. It is a paroxysmal loss of neuronal function triggered by initially increased neuronal activity, which slowly propagates within susceptible brain regions. Normal brain function is exquisitely sensitive to, and relies on, coincident low-level immune signaling. Thus, neural immune signaling likely affects electrical activity of SD, and therefore migraine. Pain perception studies of SD in whole animals are fraught with difficulties, but whole animals are well suited to examine systems biology aspects of migraine since SD activates trigeminal nociceptive pathways. However, whole animal studies alone cannot be used to decipher the cellular and neural circuit mechanisms of SD. Instead, in vitro preparations where environmental conditions can be controlled are necessary. Here, it is important to recognize limitations of acute slices and distinct advantages of hippocampal slice cultures. Acute brain slices cannot reveal subtle changes in immune signaling since preparing the slices alone triggers: pro-inflammatory changes that last days, epileptiform behavior due to high levels of oxygen tension needed to vitalize the slices, and irreversible cell injury at anoxic slice centers. In contrast, we examine immune signaling in mature hippocampal slice cultures since the cultures closely parallel their in vivo counterpart with mature trisynaptic function; show quiescent astrocytes, microglia, and cytokine levels; and SD is easily induced in an unanesthetized preparation. Furthermore, the slices are long-lived and SD can be induced on consecutive days without injury, making this preparation the sole means to-date capable of modeling the neuroimmune consequences of chronic SD, and thus perhaps chronic migraine. We use electrophysiological techniques and non-invasive imaging to measure neuronal cell and circuit functions coincident with SD. Neural immune gene expression variables are measured with qPCR screening, qPCR arrays, and, importantly, use of cDNA preamplification for detection of ultra-low level targets such as interferon-gamma using whole, regional, or specific cell enhanced (via laser dissection microscopy) sampling. Cytokine cascade signaling is further assessed with multiplexed phosphoprotein related targets with gene expression and phosphoprotein changes confirmed via cell-specific immunostaining. Pharmacological and siRNA strategies are used to mimic and modulate SD immune signaling.
Neuroscience, Issue 52, innate immunity, hormesis, microglia, T-cells, hippocampus, slice culture, gene expression, laser dissection microscopy, real-time qPCR, interferon-gamma
2910
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Flat-floored Air-lifted Platform: A New Method for Combining Behavior with Microscopy or Electrophysiology on Awake Freely Moving Rodents
Authors: Mikhail Kislin, Ekaterina Mugantseva, Dmitry Molotkov, Natalia Kulesskaya, Stanislav Khirug, Ilya Kirilkin, Evgeny Pryazhnikov, Julia Kolikova, Dmytro Toptunov, Mikhail Yuryev, Rashid Giniatullin, Vootele Voikar, Claudio Rivera, Heikki Rauvala, Leonard Khiroug.
Institutions: University of Helsinki, Neurotar LTD, University of Eastern Finland, University of Helsinki.
It is widely acknowledged that the use of general anesthetics can undermine the relevance of electrophysiological or microscopical data obtained from a living animal’s brain. Moreover, the lengthy recovery from anesthesia limits the frequency of repeated recording/imaging episodes in longitudinal studies. Hence, new methods that would allow stable recordings from non-anesthetized behaving mice are expected to advance the fields of cellular and cognitive neurosciences. Existing solutions range from mere physical restraint to more sophisticated approaches, such as linear and spherical treadmills used in combination with computer-generated virtual reality. Here, a novel method is described where a head-fixed mouse can move around an air-lifted mobile homecage and explore its environment under stress-free conditions. This method allows researchers to perform behavioral tests (e.g., learning, habituation or novel object recognition) simultaneously with two-photon microscopic imaging and/or patch-clamp recordings, all combined in a single experiment. This video-article describes the use of the awake animal head fixation device (mobile homecage), demonstrates the procedures of animal habituation, and exemplifies a number of possible applications of the method.
Empty Value, Issue 88, awake, in vivo two-photon microscopy, blood vessels, dendrites, dendritic spines, Ca2+ imaging, intrinsic optical imaging, patch-clamp
51869
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Mouse in Utero Electroporation: Controlled Spatiotemporal Gene Transfection
Authors: Asuka Matsui, Aya C. Yoshida, Mayumi Kubota, Masaharu Ogawa, Tomomi Shimogori.
Institutions: RIKEN Brain Science Institute.
In order to understand the function of genes expressed in specific region of the developing brain, including signaling molecules and axon guidance molecules, local gene transfer or knock- out is required. Gene targeting knock-in or knock-out into local regions is possible to perform with combination with a specific CRE line, which is laborious, costly, and time consuming. Therefore, a simple transfection method, an in utero electroporation technique, which can be performed with short time, will be handy to test the possible function of candidate genes prior to the generation of transgenic animals 1,2. In addition to this, in utero electroporation targets areas of the brain where no specific CRE line exists, and will limit embryonic lethality 3,4. Here, we present a method of in utero electroporation combining two different types of electrodes for simple and convenient gene transfer into target areas of the developing brain. First, a unique holding method of embryos using an optic fiber optic light cable will make small embryos (from E9.5) visible for targeted DNA solution injection into ventricles and needle type electrodes insertion to the targeted brain area 5,6. The patterning of the brain such as cortical area occur at early embryonic stage, therefore, these early electroporation from E9.5 make a big contribution to understand entire area patterning event. Second, the precise shape of a capillary prevents uterine damage by making holes by insertion of the capillary. Furthermore, the precise shape of the needle electrodes are created with tungsten and platinum wire and sharpened using sand paper and insulated with nail polish 7, a method which is described in great detail in this protocol. This unique technique allows transfection of plasmid DNA into restricted areas of the brain and will enable small embryos to be electroporated. This will help to, open a new window for many scientists who are working on cell differentiation, cell migration, axon guidance in very early embryonic stage. Moreover, this technique will allow scientists to transfect plasmid DNA into deep parts of the developing brain such as thalamus and hypothalamus, where not many region-specific CRE lines exist for gain of function (GOF) or loss of function (LOF) analyses.
Neuroscience, Issue 54, In utero, electroporation, transfection, CNS, gene expression, gain of function, loss of function, neuron, axon
3024
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A Method for 2-Photon Imaging of Blood Flow in the Neocortex through a Cranial Window
Authors: Ricardo Mostany, Carlos Portera-Cailliau.
Institutions: University of California, Los Angeles.
The ability to image the cerebral vasculature (from large vessels to capillaries) and record blood flow dynamics in the intact brain of living rodents is a powerful technique. Using in vivo 2-photon microscopy through a cranial window it is possible to image fluorescent dyes injected intravenously. This permits one to image the cortical vasculature and also to obtain measurements of blood flow. This technique was originally developed by David Kleinfeld and Winfried Denk. The method can be used to study blood flow dynamics during or after cerebral ischemia, in neurodegenerative disorders, in brain tumors, or in normal brain physiology. For example, it has been used to study how stroke causes shifts in blood flow direction and changes in red blood cell velocity or flux in and around the infarct. Here we demonstrate how to use 2-photon microscopy to image blood flow dynamics in the neocortex of living mice using fluorescent dyes injected into the tail vein.
Neuroscience, Issue 12, red blood cell, cortex, fluorescein, rhodamine, dextran, two-photon, 2-photon, capillary
678
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In vivo Imaging of Deep Cortical Layers using a Microprism
Authors: Thomas H. Chia, Michael J. Levene.
Institutions: Yale University.
We present a protocol for in vivo imaging of cortical tissue using a deep-brain imaging probe in the shape of a microprism. Microprisms are 1-mm in size and have a reflective coating on the hypotenuse to allow internal reflection of excitation and emission light. The microprism probe simultaneously images multiple cortical layers with a perspective typically seen only in slice preparations. Images are collected with a large field-of-view (~900 μm). In addition, we provide details on the non-survival surgical procedure and microscope setup. Representative results include images of layer V pyramidal neurons from Thy-1 YFP-H mice showing their apical dendrites extending through the superficial cortical layer and extending into tufts. Resolution was sufficient to image dendritic spines near the soma of layer V neurons. A tail-vein injection of fluorescent dye reveals the intricate network of blood vessels in the cortex. Line-scanning of red blood cells (RBCs) flowing through the capillaries reveals RBC velocity and flux rates can be obtained. This novel microprism probe is an elegant, yet powerful new method of visualizing deep cellular structures and cortical function in vivo.
Neuroscience, Issue 30, Cortex, Layer V, Multiphoton Microscopy, Brain, Mouse, Fluorescence, Microprism, Imaging, Neurovasculature, In vivo
1509
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Functional Mapping with Simultaneous MEG and EEG
Authors: Hesheng Liu, Naoaki Tanaka, Steven Stufflebeam, Seppo Ahlfors, Matti Hämäläinen.
Institutions: MGH - Massachusetts General Hospital.
We use magnetoencephalography (MEG) and electroencephalography (EEG) to locate and determine the temporal evolution in brain areas involved in the processing of simple sensory stimuli. We will use somatosensory stimuli to locate the hand somatosensory areas, auditory stimuli to locate the auditory cortices, visual stimuli in four quadrants of the visual field to locate the early visual areas. These type of experiments are used for functional mapping in epileptic and brain tumor patients to locate eloquent cortices. In basic neuroscience similar experimental protocols are used to study the orchestration of cortical activity. The acquisition protocol includes quality assurance procedures, subject preparation for the combined MEG/EEG study, and acquisition of evoked-response data with somatosensory, auditory, and visual stimuli. We also demonstrate analysis of the data using the equivalent current dipole model and cortically-constrained minimum-norm estimates. Anatomical MRI data are employed in the analysis for visualization and for deriving boundaries of tissue boundaries for forward modeling and cortical location and orientation constraints for the minimum-norm estimates.
JoVE neuroscience, Issue 40, neuroscience, brain, MEG, EEG, functional imaging
1668
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Principles of Site-Specific Recombinase (SSR) Technology
Authors: Frank Bucholtz.
Institutions: Max Plank Institute for Molecular Cell Biology and Genetics, Dresden.
Site-specific recombinase (SSR) technology allows the manipulation of gene structure to explore gene function and has become an integral tool of molecular biology. Site-specific recombinases are proteins that bind to distinct DNA target sequences. The Cre/lox system was first described in bacteriophages during the 1980's. Cre recombinase is a Type I topoisomerase that catalyzes site-specific recombination of DNA between two loxP (locus of X-over P1) sites. The Cre/lox system does not require any cofactors. LoxP sequences contain distinct binding sites for Cre recombinases that surround a directional core sequence where recombination and rearrangement takes place. When cells contain loxP sites and express the Cre recombinase, a recombination event occurs. Double-stranded DNA is cut at both loxP sites by the Cre recombinase, rearranged, and ligated ("scissors and glue"). Products of the recombination event depend on the relative orientation of the asymmetric sequences. SSR technology is frequently used as a tool to explore gene function. Here the gene of interest is flanked with Cre target sites loxP ("floxed"). Animals are then crossed with animals expressing the Cre recombinase under the control of a tissue-specific promoter. In tissues that express the Cre recombinase it binds to target sequences and excises the floxed gene. Controlled gene deletion allows the investigation of gene function in specific tissues and at distinct time points. Analysis of gene function employing SSR technology --- conditional mutagenesis -- has significant advantages over traditional knock-outs where gene deletion is frequently lethal.
Cellular Biology, Issue 15, Molecular Biology, Site-Specific Recombinase, Cre recombinase, Cre/lox system, transgenic animals, transgenic technology
718
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Cortical Neurogenesis: Transitioning from Advances in the Laboratory to Cell-Based Therapies
Authors: Arnold R. Kriegstein.
Institutions: University of California, San Francisco - UCSF.
Neuroscience, Issue 6, neurogenesis, cortex, electroporation, injection, stem cells, brain, Translational Research
241
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What is Visualize?
JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.
How does it work?
We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.
Video X seems to be unrelated to Abstract Y...
In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.
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Options View topic - Gout Symptoms and Gout Home Remedies- Why Curing Gout
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Gout Symptoms and Gout Home Remedies- Why Curing Gout
Gout Symptoms and Gout Home Remedies- Why Curing Gout
by charles » Sat Oct 01, 2016 6:13 pm
Gout Symptoms - Gout Home Remedies- Why Curing Gout Naturally is Safe, Simple and Effective
"What are the most some efficient natural gout remedies?" a customer once asked me? I immediately told him that there are many remedies for gout that have received positive feedback from my customers.
2. Your weight- Do you know what your BMI is? Checking your body mass index can allow you to see what your ideal weight is. You should always try to be within 30 lbs. of your ideal weight. Obesity increases the risk of uric acid.
4. Vitamin Therapy- Research studies have shown that a deficiency in vitamins such as A, B5 and E are serious factors that can lead to the formation and advancement of gout symptoms. You should get a quality multi-vitamin and also supplement individual vitamins if needed. We had at first written a rough assignment on Decrease Uric Acid. Then after a few improvisions and enhancements here and there, we have ended up with this end product.
5. Fruity Therapy- Water soluble fiber is very beneficial to your health. There are at least 20 reasons to be eating fruits and veggies. A couple reasons are that some fruits actually neutralize uric acid and flush uric acid. Fiber is notorious for flushing the body and uric acid is excluded from the flush. Opportunity knocks once. So when we got the opportunity to write on Purines, we did not let the opportunity slip from our hands, and got down to writing on Purines.
However, by curing gout naturally, you can say good bye to the pain and the high uric acid levels which cause gout.
3. Flush Uric Acid- You can naturally flush uric acid with water. Go and buy a Nalgene water bottle and begin measuring how much water you drink per day. You should be drinking half your body weight in ounces per day. Coordinating matter regarding to Gout took a lot of time. However, with the progress of time, we not only gathered more matter, we also learnt more about Gout.
Under normal circumstances, the purines you find in many foods are broken down into uric acid, and the body gets rid of it without any problems. However, for someone with gout, getting rid of this uric acid is problematic, and the result is painful crystals forming in the joints - leading to gout pain. When this happens, there are medications that can help with the pain, but one of the best things a person can do it to is to find low purine foods and make them a major part of their diet. This can offer much-needed relief for most.
When looking for low purine foods for your diet, you can find a great variety of things you can have that won't cause any issues with your gout. If you love thick soups, you can have them as long as they are made with low fat milk. Cheese and milk are fine, but again, they should be low in fat. You can also enjoy things like gelatin and a great variety of fruits and fruit juices. Gout bulletin board just fine, but remember to watch the calories if you are attempting to get your weight down. You can also enjoy things like pasta, and peanut butter is okay for a treat.
Image
People from this Condition. the Acute Attack this Fluid is the
You may have a hard time finding new foods to eat at first, but after a while you will get used to reading labels and figuring out what works for you and what does not. Any special diet requires a little thought and work, and the low purine foods diet is no exception. After a while though, reading and deciphering items in the store by reading through the ingredients list will become second nature, and you will become accustomed to knowing how to build your own menu with little thought. Feeling better should be all the motivation you need.
When choosing your low purine foods, you can have some medium purine rated foods with them about once a day if it does not bother you. Those would include some meats like beef, pork, and possibly chicken. Some seafood choices are relatively safe as well. You should experiment to find what bothers you and what works out well. As long as you work at limiting the purines, you are going to feel much better each day. You might want to have lobster bisque on occasion, as long as you limit your portions, and don't have any other medium purine foods for the rest of the day.
There are some general directions for a low purine diet, but always listen to your doctor's advice in addition to this information. A low purine diet is going to contain almost fifty percent carbohydrates each day, and no more than thirty percent of the diet each day should be made up of fats. The rest should be healthy and lower purine protein sources. Drinks that are normally not allowed on many special diets are actually encouraged. These include soda and coffee. The reason being as that they act as directics, helping your body to flush out the excess uric acid. It's important to drink plenty of water as well to keep your body well hydrated. Alcohol, however, in most forms is not something you should be drinking.
Gout (Metabolic Arthritis) is a Type of Arthritis Caused by Too Much Uric Acid in the Body
Uric acid is normally flushed out by the kidneys. Gout often affects the big toe but can also affect the ankle, knee, foot, hand, wrist or elbow. A disabling form of arthritis found most often in the feet - specifically the big toe - and occasionally in other joints. Symptoms include intense episodes of joint pain and swelling, which often happen at night, followed by pain-free periods. high uric acid blood level will sometimes allow formation of uric acid crystals in the joints, especially at the base of the large toe. Fortunately, gout almost always can be completely controlled with medication and changes in diet. this condition monosodium urate crystals are deposited on the articular cartilage of joints and in the particular tissue like tendons. Urate crystals may form in joints, resulting in inflammation and pain. Urate crystals may also form in the kidney and urinary tract, resulting in kidney stones.
Always seek a medical opinion before starting any low purine diet or taking any herb or medicine. Check your medicines for side effects as there are many for any gout pills supplied by a doctor or health practitioner After reading what was written here, don't you get the impression that you had actually heard about these points sometime back. Think back and think deeply about Gout Indomethacin.
Tart Cherries or Cherry Juice
A daily dose will help to prevent it and a few doses when he has a bout will help as well. It can reduce uric acid within an hour or less. You can also buy tart cherry in a dried capsule form though the fruit or juice is still better. It also helps with other muscle pain and can actually help the body heal faster from workouts. It's a natural anti-inflammatory agent.
Apple Cider Vinegar : 1 x tablespoon mixed with a table spoon of filtered water, make sure it is organic with "Mother" still in it , add honey to taste and take about an hour after a meal 3 times a day..this will regulate your pH levels and reduce them...clean your teeth also after using this as it stains..then after an attack reduce this to once a day. It is of no use thinking that you know everything, when in reality, you don't know anything! It is only because we knew so much about Acute Gout that we got down to writing about it!
There is a great deal of debate in the medical world about the effects of overall diet on arthritis and using diet toward alleviating the condition. Doctors have known for a long time that diet affects gout, a specific type of arthritic condition, however the jury remained out for a long time on other common types of arthritis such as rheumatoid and osteoarthritis. However, overall dietary health is important and does come into play. Being overweight can affect certain arthritic conditions, forcing some joints to carry more of a load. This added weight stresses the joints, causing overuse or more wear to components, and pain, especially in the knees. So making sure arthritic sufferers eat god foods and get help from healthcare providers to create and follow a well-balanced dietary plan is advised. To begin, here is a look at some vitamins, minerals, nutrients / foods and some herbal applications to consider. VITAMINS Vitamin B5 - When grouped and tanked together, B vitamins work at their peak. They, and B5 specifically, are good for reducing swelling. Vitamin B3 - This vitamin reduces tissue swelling and dilates small arteries, increasing blood flow. Note that Vitamin B3 is NOT advised for persons with high blood pressure, gout or sliver disorders. Vitamin B6 - Another B that reduces tissue swelling. Vitamin B12 - This vitamin aids in multiple functions. It helps with cell formation, digestion, myelin production, nerve protection. Vitamin C - This vitamin acts as an anti-inflammatory, relieving pain, and rids the body of free radicals. Vitamin E - This is a strong antioxidant that protects joints from free radicals while increases joint flexibility. Vitamin K - This vitamin assists with mineral deposit into the bone matrix.
MINERALS Boron
This trace mineral aids in bone health. Calcium - This is a much-needed mineral for bone health. Magnesium - Magnesium helps keep calcium in balance within the system. Zinc - This mineral is necessary for bone growth, but is often lacking in arthritic patients. Manganese - Manganese is also necessary for bone growth. However, do not ingest manganese with calcium because they can work against each other. Copper - Copper helps to strengthen connective tissue. Germanium - This antioxidant helps with pain relief. Sulfur - A lack of sulfur can result in deterioration of ligaments, cartilage, collagen and tendons. NUTRIENT COMBOS Chondroitin Sulfate - This lubrication in joints, joint fluid and connective tissue, can be found in the sea cucumber. Gelatin - Help with raw cartilage replenishing with this cheap source. Glucosamine Sulfate - This combo is necessary for tendon, ligament, bone, cartilage, and synovial (joint) fluid formation. Quercetin - This helps with inflammation reduction. Type II Collagen - Use this for growth and repair of joints, articular cartilage and connective tissue.
OTHER FACTORS
There are many factors to consider with regards to arthritic diets and nutritional healing, and each factor may not apply to each individual. For example, certain people are allergic to specific foods, and these allergies can indeed worsen arthritic conditions. Ingesting foods that contain sodium nitrate or tartrazine can inflame rheumatoid arthritis, while ingesting foods containing a substance called hydrazine can contribute to systemic lupus erythematosus, an arthritic condition connected to lupus. There is a rare type of arthritis called Behcet's Disease, and eating black walnuts can cause flare-ups in people with this rare condition. So as you see, there is a variety of arthritic conditions and along with them a variety of foods that may trigger them. The best way to approach the situation is to examine each arthritic condition and tailor one's approach based upon the specifics.
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Advertisement
Abstract
We have developed an efficient and rapid method for detection of Epstein-Barr virus (EBV)-specific CD8+ T-cell frequencies both in freshly isolated peripheral blood mononuclear cells (PBMCs) and in vitro established cytotoxic T lymphocyte (CTL) lines. Responder cells are thereby stimulated with an autologous lymphoblastoid cell line for 5 hours and intracellular accumulation of interferon γ (IFNγ) is detected by multiparameter flow cytometric analysis. EBV-specific CD8+ T-cell frequencies ranged between 0.63% and 1.29% in PBMCs of 5 healthy long-term EBV carriers. Using EBV-specific T-cell lines, it was shown that flow cytometric analysis is more sensitive than limiting dilution analysis for CTL precursors and enzyme-linked immunospot assay detecting IFNγ-producing T cells. The class I restriction of IFNγ production was confirmed using an anti-class I monoclonal antibody (MoAb). Information on other cytokine production of EBV-specific CTLs could be obtained using combinations of anti-cytokine MoAbs. The sensitive and rapid nature of the flow cytometric assay for EBV-specific CD8+ T-cell frequency has significant advantages for evaluation of EBV-specific CD8+ T-cell responses in PBMCs of patients with EBV-related diseases.
EPSTEIN-BARR VIRUS (EBV) is well known to be associated with several malignant diseases. These include a proportion of Hodgkin’s lymphomas, nasopharyngeal carcinomas, Burkitt’s lymphomas, and immunoblastic lymphomas seen in immunocompromised hosts.1
Primary infection with EBV is usually asymptomatic, although some may suffer from acute infectious mononucleosis.1 After primary infection, a strong HLA class I–restricted, virus-specific CD8+ cytotoxic T lymphocyte (CTL) response is elicited in healthy individuals.2 This response is believed to play an important role in controlling the virus both during primary infection and in the long-term carrier state whereby EBV persists for life in a subset of B cells.
An increased understanding of the mechanisms by which T lymphocytes recognize virus-specific antigens has stimulated much interest in the use of CTLs as adoptive immunotherapy for EBV-associated disease. An early candidate for such treatment was EBV-associated lymphoproliferative disease (LPD), which is seen in patients receiving allogeneic bone marrow transplantation from mismatched family members or unrelated donors.3 4 The incidence is between 5% and 30%, particularly if marrow was depleted of T cells to prevent graft-versus-host disease.5
Unfractionated populations of lymphocytes from the peripheral blood of donors6 7 or EBV-specific CTL lines from donor lymphocytes have been used for treatment and/or prophylaxis of posttransplant EBV-associated LPD.8 9 However, the utility of unfractionated lymphocyte infusion is limited by potentially fatal communications that arise from alloreactive T cells also present in the infusion. To overcome this problem, infusions of EBV-specific CTL lines from donor lymphocytes have been successfully used, especially as prophylaxis against EBV-associated LPD in transplant recipients considered at high risk.10 Recently, adoptive immunotherapy (using unfractionated lymphocytes or EBV-specific CTLs) has been applied for treatment or prophylaxis of EBV-associated LPD in patients with solid organ transplants,7 11 severe chronic active EBV infection,12 or EBV-positive Hodgkin’s disease.13
In any cases of immunotherapy for EBV-associated diseases, to confirm the effects of the treatment, demonstration of elevation of EBV-specific cellular immunity in the patients is necessary. For this purpose, bulk CTL activities in peripheral blood mononuclear cells (PBMCs) stimulated in vitro with an autologous EBV-infected lymphoblastoid cell line (LCL) or limiting dilution analysis (LDA) for CTL precursors that lysed the LCL have been frequently used.7-13 The disadvantage is that it takes at least approximately 10 days to raise bulk CTL, and the assay is not very quantitative. LDA is one of the established methods for quantitative detection of CTL precursor frequencies in PBMCs of healthy seropositive individuals14 and of patients receiving allogeneic bone marrow transplants.15 However, it again takes 2 to 4 weeks to obtain the results, and the procedures are particularly laborious. In addition, both experiments need γ-irradiating radioisotopes, which are potentially hazardous for the examiners.
Recently, Waldrop et al16 reported that human cytomegalovirus-specific CD4+ T-cell frequencies can be detected by flow cytometry. Kern et al17 showed that CD8+ peptide-specific T-cell frequencies can be measured in samples whose HLA is known. Both methods are based on multiparameter flow cytometric assays that detect rapid intracellular accumulation of cytokines after in vitro antigen stimulation in the presence of intracellular transport blockers such as Brefeldin A.
We report here a highly efficient method to detect whole EBV-specific CD8+ T-cell frequencies irrespective of HLA typing. PBMCs are thereby incubated with an autologous LCL in the presence of Brefeldin A for a short period (5 hours), and the rapid intracellular accumulation of interferon γ (IFNγ) is detected by multiparameter flow cytometric analysis. Using these methods, we found approximately 1% of peripheral CD8+ T cells of seropositive individuals to be EBV-specific. The method is more sensitive and takes less time than LDA for CTL precursors and enzyme-linked immunospot (ELISPOT) assays. In addition, it can provide more information on cytokine production of EBV-specific CD8+ T cells upon natural stimulation when combinations of anticytokine monoclonal antibodies (MoAbs) are used.
MATERIALS AND METHODS
Blood donors.
The blood donors consisted of (1) long-term healthy carriers of EBV defined as having both EBV-viral capsid antigen (VCA)-IgG and EBV nuclear antigen (EBNA) antibodies and (2) EBV-seronegative individuals defined as having no EBV-VCA-IgG antibodies.1 Some donors were tested for their HLA class I typing of PBMCs with classical serological methods. Study design and purpose were fully explained to all donors. Peripheral blood was obtained after informed consent was confirmed.
Preparation of PBMCs, LCLs, and CD8+ EBV-specific CTL lines.
PBMCs were obtained by centrifuging heparinized blood over Ficoll/Hypaque (Pharmacia Biotech AB, Uppsala, Sweden). LCLs were prepared by transforming PBMCs with B95-8 cell culture supernatant as previously described.12 LCLs were cultured in Iscove’s modified Dulbecco’s medium (GIBCO, Grand Island, NY) supplemented with 2 mmol/L L-glutamine, 50 U/mL penicillin, 50 μg/mL streptomycin, 5 × 10−5 mol/L β-mercaptoethanol, and 10% heat-inactivated fetal calf serum (FCS; Hyclone, Logan, UT; referred to as culture medium). EBV-specific T-cell lines were initiated by culturing 2 × 106 PBMCs and 2 × 105autologous irradiated LCLs in 2 mL of culture medium in each well of 24-well plates. Ten days after the stimulation, CD8+ cells were isolated using immunomagnetic beads (Dynabeads M-450 CD8; Dynal, Oslo, Norway) following the manufacturer’s instructions. Detachment of immunomagnetic beads from isolated cells was achieved using Detachabeads (Dynal). Isolated cells were greater than 95% CD8+ according to flow cytometric analysis. These CD8+ T cells were further stimulated with autologous irradiated LCLs weekly in the presence of 50 U/mL recombinant interleukin-2 (IL-2).
CTL assay.
CTL assays were performed using 51Cr-release as previously described.12 Briefly, CTLs were suspended in fresh culture medium at the desired cell concentration and seeded in wells of V-bottomed 96-well plates (Costar, Cambridge, MA) containing51Cr-labeled LCLs (2,500 cells/well). Each assay was performed in triplicate. After 5 hours of incubation, the supernatants were harvested and radioactivity was counted with a γ-counter. The percentage of specific lysis was calculated as follows: percentage of specific lysis = (experimental lysis − minimum lysis) × 100/(maximum lysis − minimum lysis). Minimum lysis was obtained by incubating the target cells with the culture medium alone. Maximum lysis was obtained by exposing the target cells to 1% Nonidet-P40.
Detection of CTL precursor frequency by LDA.
LDA for cytotoxicity was performed essentially as previously reported.14 15 Isolated CD8+ cells were diluted in 96-well U-bottom plates (24 replicates/dilution). Irradiated autologous LCLs (2 × 104), PBMCs (103), and IL-2 (40 U/mL) were added to each well. On day 7, IL-2 was added to 40 U/mL. CTL assays were performed on day 12. To assay CTL precursor frequency, 100 μL of cell suspension from each well was transferred into a well of 96-well V-bottom plates containing51Cr-labeled 2,500 LCLs. After 5 hours of incubation in a humidified 5% CO2 incubator at 37°C, the supernatant was harvested and radioactivity was counted with a γ-counter. Wells were scored as positive for CTL recognition if the level of specific lysis exceeded 3 standard deviations above the mean spontaneous release from the target cells. The frequency of CTL precursors was estimated at which 37% of the wells were negative from the slope of a regression plot of the log percentage of negative versus input cell numbers.
Detection of IFNγ producing CD8+ T cells in response to LCLs by flow cytometry.
For determination of CD8+ antigen-specific T lymphocyte frequency, intracellular cytokine assessment using flow cytometry was performed as previously described, with slight modifications.16 17 Briefly, PBMCs or EBV-specific CTLs were resuspended at a concentration of 1 × 106/mL in culture medium. Autologous or HLA-disparate LCLs were resuspended at a concentration of 1 × 106/mL in the culture medium. Aliquots of the responder cells (1 mL) and LCL (1 mL) were mixed in 16 × 125 mm culture tubes in the presence of 10 μg/mL Brefeldin A (Sigma Chemical Co, St Louis, MO) and incubated in a humidified 5% CO2 incubator at 37°C for 5 hours. As a control, the same numbers of responder cells and LCLs were separately incubated in the presence of the Brefeldin A and mixed before staining with MoAbs. For blocking experiments, an anti-class I MoAb (clone W6/32; Cedarlane, Hornby, Ontario, Canada) or isotype-matched monoclonal mouse IgG antibodies were used at a final concentration of 47 μg/mL. After the incubation, the cell suspensions were fixed with 4% paraformaldehyde in phosphate-buffered saline (PBS) for 10 minutes at room temperature. After washing with PBS, cells were permeabilized with IC Perm (BioSource International, Camarillo, CA) and stained with PC5-labeled anti-CD8 (Coulter, Miami, FL), phycoerythrin (PE)-labeled anti-CD69 (Coulter), and fluorescein isothiocyanate (FITC)-labeled antihuman IFNγ (Becton Dickinson, San Jose, CA) MoAbs. In some experiments, T cells were stimulated with 50 ng/mL of phorbol myristate acetate (Sigma) and 500 ng/mL of ionomycin (Sigma) and stained with PE-labeled anti–IL-4 or anti–IL-13 MoAbs (Becton Dickinson). Stained cells were analyzed by FACScan (Becton Dickinson) using the LYSIS II software. Live-gating of CD8high lymphocytes was performed, and up to 20,000 events were acquired for each analysis.
ELISPOT assay.
An ELISPOT assay was performed as previously described, with slight modifications,18 19 using 96-well MultiScreen-HA plates with a nitrocellulose base (Millipore, Bedford, MA), coated with 10 μg/mL of anti-IFNγ MoAb (Genzyme, Cambridge, MA). Isolated CD8+ T cells were added in graded numbers of 500, 250, and 125 per well containing autologous irradiated LCLs (1 × 105) and IL-2 (50 U/mL). Each dilution was seeded in triplicate. The plates were incubated in 5% CO2 incubator at 37°C for 28 hours and extensively washed with PBS containing 0.05% Tween-20. A polyclonal rabbit anti-IFNγ antibody (Genzyme) was added to individual wells and left for 90 minutes at room temperature, followed by peroxidase-conjugated goat antirabbit IgG (Genzyme) for an additional 90 minutes. For visualization of IFNγ-specific spots, 100 μL of 0.1 mol/L sodium acetate buffer (pH 5.0) containing 3-amino-9-ethylcarbasole (Sigma) and 0.015% H2O2 was added to each well. After 30 minutes, the reaction was stopped by washing with water and the plates were dried. The bottom membranes were photographed and spots were counted. Only diffuse large spots were considered specific, because wells containing only LCLs gave tiny spots. The percentage frequency of antigen-specific CD8+ T cells was calculated as follows: percentage frequency = numbers of spots × 100/input cell numbers.
RESULTS
We applied a strategy using tricolor analysis for detection of EBV-specific IFNγ-producing T cells. First, the PC5-labeled anti-CD8 MoAb was used for gating the population. Second, the PE-labeled anti-CD69 MoAb was used for enhancement of precise detection of responding T cells. CD69 is upregulated on activated T cells before cytokine production and thus allows more definitive clustering of the true responding fraction.20 As an unstimulated control, we used responder cells and LCLs that had been separately incubated in the same medium with Brefeldin A and mixed and stained after fixing.
Frequency of EBV-specific CD8+ T cells in PBMCs of EBV-seropositive and -seronegative individuals.
We first tested PBMCs of long-term healthy EBV carriers for the frequency of EBV-reactive IFNγ-producing CD8+ T cells. When PBMCs from seropositive individuals were used, 0.87% and 1.32% of total CD8+ cells produced IFNγ in response to autologous LCLs (Fig 1B and D). We defined the specific frequency (SF) as follows: percentage of a sample stimulated with LCLs − percentage of the same sample unstimulated (note that the unstimulated samples were also incubated with Brefeldin A and mixed with LCLs after fixation for comparable staining conditions). The SFs of donors 1 and 2 were 0.85% (Fig 1A and B) and 1.29% (Fig 1C and D), respectively. Those of the 2 other healthy EBV-carriers were 0.63% and 1.08% (graphic data not shown). In contrast, the SF of antigen-specific T cells in PBMCs of an EBV-seronegative donor was 0.03% (Fig 1E and F), showing the specificity of the assay. Those of the 2 other EBV-seronegative donors were 0.02% and 0.00%, respectively (graphic data not shown). Thus, clustering of IFNγ-producing CD8+ T cells was never found using PBMCs of EBV-seronegative donors. When stimulated with completely HLA class I-mismatched LCLs, IFNγ-producing CD8+ T cells from either seropositive or seronegative individuals ranged between 0.21% and 0.55% (graphic data not shown). Thus, such alloreactive frequency was lower than EBV-specific frequency in PBMCs of seropositive individuals and higher than that of seronegative individuals as far as we tested.
Fig. 1.
EBV-specific IFNγ-producing CD8+ T cells in PBMCs of EBV-seropositive (A through D) and EBV-seronegative (E and F) individuals. PBMCs were stimulated with autologous LCLs (B, D, and F) at a responder stimulator ratio of 1. After fixation and permeabilization, the cells were stained for CD8, CD69, and IFNγ. CD8+ cells were gated and analyzed by flow cytometry. Unstimulated PBMCs were also incubated, fixed, and then mixed with autologous LCLs before staining (A, C, and E). The frequency of CD8+/CD69high T cells that produced IFNγ is shown as a percentage of the total number of CD8 cells.
Comparison of 4 different assays for quantification of EBV-specific CD8+ T-cell frequencies.
Next, we compared the sensitivities of 4 different assays, namely the standard CTL assay, intracellular IFNγ production assay, ELISPOT assay, and standard LDA for CTL precursors, using 2 CD8+EBV-specific CTL lines.
CTL activities of the lines are shown in Fig 2. The effector target ratio that yielded the same percentage of target lysis was 1.5 to 2 times higher for CTLs from donor YI than for those from donor KK. Flow cytometric analysis of EBV-specific T cells for SFs of CTL lines from donors KK and YI were 39.2% and 25.2%, respectively (Fig 3). With the ELISPOT assay, the frequency of CTLs from donor KK was approximately 2 times higher than that from donor YI (Fig 4A and B). The mean (and standard deviation) frequencies of all the wells tested were 11.2% (3.5%) and 5.7% (1.7%), respectively (Table 1). LDA analysis gave values of 2.3% and 0.23% for CTL precursor frequencies (Fig 5A and B). Thus, the values with the 4 assays roughly correlated, except for LDA, which gave a 10-fold difference between the 2 samples (Table 1). The CTL line from donor YI was growing more slowly than that from donor KK, and this might reflect the discrepancy of the data of LDA. Flow cytometric analysis of EBV-specific T-cell frequencies using intracellular IFNγ production gave the highest values.
Fig. 2.
CTL activities of the EBV-specific CD8+T-cell lines from donors KK (•) and YI (▪).
Fig. 3.
Flow cytometric analysis of IFNγ production in 2 CD8+ EBV-specific CTL lines from donor KK (A and B) and YI (C and D). (A and C) Unstimulated CTLs; (B and D) CTLs stimulated with autologous LCLs at a responder stimulator ratio of 1. After fixation and permeabilization, the cells were stained for CD8, CD69, and IFNγ. CD8+ cells were gated and analyzed by flow cytometry. The frequency of CD8+/CD69high T cells that produced IFNγ is shown as a percentage of the total number of CD8 cells.
Fig. 4.
ELISPOT assay for detecting IFNγ-producing cells in 2 CD8+ EBV-specific T-cell lines from donors KK (A) and YI (B). The mean and standard deviation are shown for each dilution.
Table 1.
Summary of Data for Frequencies of CD8+ EBV-Specific T Cells
Fig. 5.
LDA analysis of the 2 CTL lines from donors KK (A) and YI (B).
Class I–restricted production of IFNγ from EBV-specific CD8+ CTLs.
We further examined the class I restriction of the response. EBV-specific CTLs were stimulated by autologous (HLA-A24/A26, B52/B62, and C3) and various allogeneic LCLs (Fig6). Approximately 27% of CTLs produced IFNγ upon stimulation of autologous LCLs (Fig 6A and B). When LCLs sharing HLA-A26, B62, and C3 class I molecules were used as stimulators, 8.8% of CD8+ T cells produced IFNγ (Fig 6C). LCLs sharing A24 and B62 with the CTL stimulated 2.8% of the CD8+ T-cell population (Fig 6D). LCLs sharing only A24 or C3 the CTL stimulated 1.2% and 0.3% of the CD8+ T-cell population (Fig 6E and F). These data indicated that HLA-A24, A26, and B62 are presenting EBV antigens. To confirm that the IFNγ production is class I-restricted, the same CTLs were stimulated by autologous LCLs in the presence of anti-class I MoAb (Fig6G) or isotype-matched mouse MoAb (Fig 6H) as a control. The IFNγ-producing CD8+ T-cell population was drastically reduced (0.36%) with anti-class I MoAb, but not with control MoAb (31%). These results indicate that the IFNγ in the CD8+T cells was produced through authentic recognition of antigens presented by class I molecules.
Fig. 6.
Class I restriction of the IFNγ production in an EBV-specific CD8+ CTL line. EBV-specific CTLs were stimulated by autologous ([B] HLA-A24/A26, B52/B62, and C3) and various allogeneic LCLs ([C] HLA-A11/A26, B62, and C3/C4; [D] A11/A24, B61/B62, and C4; [E] A2/A24, B7/B61, and C7; [F] A2, B35/B46, and C1/C3). The underlined alleles were shared by CTLs and each LCL line. Unstimulated CTLs were also incubated, fixed, and then mixed with autologous LCLs before staining (A). The same CTLs were also stimulated by autologous LCLs in the presence of an anti-class I MoAb (G) or an isotype-matched MoAb (H). The frequency of CD8+/CD69high T cells that produced IFNγ is shown as a percentage of the total number of CD8 cells.
Dual staining for IFNγ/IL-4 or IL-13 in EBV-specific CD8+ CTLs.
Recently, Nazaruk et al21 reported that EBV-specific CD8+ T cells can be subdivided into 2 subsets: the first of which expresses high levels of IFNγ, but little or no IL-4, whereas the second subset is IFNγ/IL-4 or IL-13 double-positive, paralleling the classically described Th1 and Th2 subsets of CD4+ T cells. They used phorbol myristate acetate and ionomycin for activation of CTLs. This artificial stimulation may give a different outcome compared with physiological T-cell receptor engagements, because a different signal transduction pathway is used.22 Thus, we examined production of the 3 cytokines by EBV-specific CTLs using LCLs as natural ligand stimulators. The results are shown in Fig 7. When an EBV-specific CTL line was stimulated with autologous LCLs, the 2 subsets mentioned above were observed in both combinations of IFNγ/IL-4 (Fig 7B) and IFNγ/IL-13 (Fig 7E). The cell distribution pattern roughly resembled those after stimulation with phorbol myristate acetate and ionomycin (Fig 7C and F), but the proportions were different.
Fig. 7.
Examination of production of 3 different cytokines by EBV-specific CTLs using LCLs as natural ligand stimulators or phorbol myristate acetate and ionomycin as chemical stimulators. (A and D) Unstimulated CTLs; (B and E) CTLs stimulated with autologous LCL at a responder stimulator ratio of 1; and (C and F) CTLs stimulated with phorbol myristate acetate and ionomycin. After fixation and permeabilization, the cells were stained for CD8, IFNγ, and IL-4 (A through C) or IL-13 (D through F). CD8+ cells were gated and analyzed using flow cytometry.
DISCUSSION
We introduce here an efficient and rapid method for detection of EBV-specific CD8+ T-cell frequencies both in freshly isolated PBMCs and in vitro established CTL lines. So far, LDA has been used for the detection of CTL precursor frequencies in healthy individuals. The frequency of EBV-specific memory CTL precursors in long-time carriers is thereby usually in the 0.0005% to 0.2% range.14 23 24 We found, although in limited numbers of samples, approximately 1% of peripheral CD8+ T cells in long-term carriers to be EBV-specific. As Waldrop et al16claimed, the increased sensitivity of flow cytometric assays is likely due to a combination of factors, such as (1) the very efficient capture of produced cytokine within the cytoplasm of the secretion-inhibited responding cells; (2) the relatively short-term period (5 hours) that largely precedes the onset of activation-induced apoptosis; and (3) the higher sensitivity of fluorescence detection of cytokines by flow cytometry than by ELISPOT assay. Alternatively, the discrepancy in frequencies between IFNγ-producing CD8+ T-cell and CTL precursors may reflect the existence of noncytolytic CD8+EBV-specific T cells.21 25 Indeed, subpopulations with such a phenotype may increase the sensitivity of assays based on IFNγ production. Practically, however, the flow cytometric assay appears to be useful, if not in all situations, for rough estimation of CTL populations because our results demonstrated that gain of CTL activity of EBV-specific memory T cells with in vitro stimulation by autologous LCLs paralleled the massive increase of antigen-specific IFNγ-producing CD8+ T cells.
Recently, Tan et al26 reported the frequencies of CD8+ T cells specific for EBV antigens in long-term virus carriers, using LDA, ELISPOT assay, and tetrameric major histocompatibility complex-peptide complexes, focusing some CTL epitopes. They demonstrated that values obtained from MHC-peptide tetramer staining were 4.4-fold higher than those obtained from ELISPOT assays, which were, in turn, 5.3-fold higher than those obtained from LDA on the average. In our report, values obtained from IFNγ production using flow cytometry were approximately 4-fold higher than those obtained from ELISPOT assays, which were higher than those obtained from LDA (Table 1). Thus, IFNγ production assay using flow cytometry may have sensitivity comparable with that of MHC-peptide tetramer staining.
EBV has 2 types of replication cycles, namely lytic infection, in which infectious virions are produced, and latent infection, which is represented by LCLs. Some of both cycle proteins are well recognized by CD8+ T cells in PBMCs of patients suffering infectious mononucleosis27 and also in long-term healthy carriers.26 Because the majority of LCLs constitutively express EBV latent cycle antigens, our system may preferentially detect T cells specific to EBV latent cycle proteins, which are therapeutically important to control over posttransplant EBV-associated LPD.
Another advantage of the cytokine production assay using flow cytometry is that it is possible to assess multiple cytokines on an EBV-specific, single-cell basis. Nazaruk et al21 demonstrated that a subset of EBV-specific CD8+ T-cell lines produced IL-4 or IL-13 in addition to IFNγ upon stimulation with phorbol myristate acetate and ionomycin. They claimed that the subset has the ability to activate B cells and promote EBV-associated LPD and lymphoma development in immunocompromised individuals with impaired EBV-specific CTL responses.21 We observed here such a subset of EBV-specific CD8+ T cells upon stimulation with autologous LCLs. Although the cell distribution pattern resembled those stimulated with the drugs, the proportions were slightly different, giving more physiological information because of the natural ligand stimulation used.
Altogether, the method presented here saves time, gives more information, and probably is more accurate than LDA for detecting antigen-specific T cells, as is the case for human cytomegalovirus-specific CD4+ T cells.16 The rapid determination of EBV-specific CD8+ T-cell frequency could have significant advantages in clinical settings in which EBV infection is concerned. For example, the immunological effects of adoptive immunotherapy for EBV-related disease can be monitored easily and rapidly. In some patients with EBV-associated LPD after allogeneic bone marrow transplantation, regression occurs in accordance with elevation of EBV-specific cellular immunity, spontaneously,28 or as a result of reduction of immunosuppression.29 The flow cytometric assay as a tool for realtime monitoring of EBV-specific cellular immunity may be useful in decision making for performing donor leukocyte transfusion, a treatment potentially associated with fatal graft-versus-host disease.30
ACKNOWLEDGMENT
The authors thank T. Yoshida and M. Hirata for technical assistance.
Footnotes
• Address reprint requests to Kiyotaka Kuzushima, MD, Laboratory of Viral Oncology, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya 464-0021 Japan.
• Supported by grants-in-aid for Scientific Research from the Ministry of Education, Science and Culture of Japan (11138268 to T.T. and 11877055 to K.K.) and partly by JSPS-RFTF 97L00703.
• The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. section 1734 solely to indicate this fact.
• Submitted February 22, 1999.
• Accepted July 1, 1999.
REFERENCES
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Effective Training Techniques
for Weight Management
See also: The Importance of Exercise
In this busy day and age we often get caught up in a whirlwind and put things of importance to one side, and exercise is often one of these things.
Here are some effective training techniques to reduce the time needed for weight management by making the time you spend in the gym (or kitchen) more effective.
Training Techniques
Intervals
Intervals are a common technique used to reduce fat and improve cardiovascular health and endurance. Intervals are essentially “High intensity exercises for short periods of time (10 - 40 seconds) followed by a low intensity period; then repeating several rounds of this”. This approach to exercise is far more effective than the very common “steady pace” fitness training where, for example, people walk on a treadmill for an hour or jog at a steady pace until they get tired. The steady pace concept comes from the angle of “You have to put in the hours” when, in reality, “You have to put in the effort”.
For example, if you complete a 20 second sprint on a bike, followed by 40 seconds of steady pace cycling, and repeat this 10 times, this will only take 10 minutes, and you will burn far more calories compared to if you just cycled at a steady pace for 20 minutes. You can burn more calories in a shorter period of time. This is the basic concept of intervals: effort over time.
Strength Training Compound Exercises
Strength training is an effective way to burn calories and strengthen your major muscle groups to help reduce the risk of injury, ensuring your normal daily tasks are easier. Also, the more muscle mass you have, the more calories your body burns each day, making it easier to burn fat and more likely that your body will keep the fat off. Strength training should be a part of your programme even if your goal is not to build too much muscle. Strength training will still provide many benefits to your health and fitness, as well as burn a lot of calories.
The Top 5 Exercises I Would Recommend
1. Deadlift (this sounds quite intimidating but it's simply a squat whilst picking up weight from the floor.)
2. Squat
3. Chest Press
4. Seated Row
5. Overhead Press
These five exercises will help you strengthen most of the main muscles in the body:
• Legs, which will reduce the risk of knee injuries.
• Arms
• Back, which can help prevent lower back issues later on in life.
• Chest and shoulders, shoulders being one of the most injured set of joints and muscles.
• The first 2 exercises also involve a lot of core muscle work.
If you are unsure how to do some of these exercises, I would recommend booking an induction at your gym and asking the fitness instructors, or booking a few personal training sessions.
When doing these exercises, aim to do 4 sets of 12 repetitions, with around 90 seconds rest between each set. This means each exercise will have a total of 48 repetitions.
These five exercises are recommended regardless of your gender. Strengthening these muscle groups will create a more well-rounded body.
Have a Plan or Routine
“Failing to plan is planning to fail.”
Having a goal without a plan is never advisable: you wouldn't start a business, build a house, or even drive somewhere you've never been to before without having a plan (or map!) When a building is constructed, a solid plan is created behind the scenes before the first material is ever touched, and there is good reason for this.
Having a plan will break down your journey into sizeable portions, small enough for you to follow yet not feel overwhelmed. Everyone needs a slightly different plan depending on their starting position, time constraints, motivation and knowledge of health and fitness.
Create a personalised programme for you to follow yourself, or hire a coach / online coach to do it for you. Generally speaking a plan should be replaced every 4 to 10 weeks to keep things fresh, make improvements and changes to the plan, and keep motivation levels high.
For general fat loss and fitness training, a typical hour long session could look something like this:
• 5 minutes of warming up
• 15 minutes of interval training
• 35 minutes of strength training
• 5 minutes of stretching
Find an Activity You Enjoy
Enjoying the process of training is one of the most important factors for long term weight management.
Nobody wants to do something they do not enjoy, so make sure you have an enjoyable routine. Maybe not every minute of it will be fun, but you don’t want to dread going to the gym every day, especially if it means that you end up skipping more days than you make, and you don’t put in as much effort when you are there.
The Skills You Need Guide to Life: Looking After Yourself
Further Reading from Skills You Need
The Skills You Need Guide to Life: Looking After Yourself
Based on some of our most popular content, this eBook will help you to live a happier, healthier and more productive life.
Learn how to look after your body and mind: the fundamental first steps to personal development.
This eBook, now in its second edition, with new and revised content, is designed to make life both easier and better.
Nutritional Notes
“A bad diet cannot be out-worked.”
Although this article is Effecting Training Techniques for Weight Management, I feel I must mention that what you eat is well over 60% of managing your weight, and to keep the eating advice simple I would recommend you just stick to the basics:
• Don’t try to follow any crazy diets: these aren’t maintainable and many of them completely cut out certain foods that are healthy for you. Furthermore, as soon as the extreme diet is finished and the person has lost some weight, people often put the weight back on because they revert to the same eating habits they had prior to starting the diet.
• Aim for 3 - 4 meals a day.
• Do not skip any meals in the hope you will lose weight faster, especially breakfast. Eating early will boost the metabolic process and 'kickstart' the body for the day.
• To manage your weight on the scales, everything has to be functioning perfectly inside of your body. Under-eating can cause hormone imbalances, which can alter the rate at which you burn fat and build muscle. Under-eating can also reduce muscle mass, which will weaken your body and put more pressure on the surrounding joints and make injuries more likely.
• On days you aren't as active, try to eat smaller portion sizes. On days you are quite active, increase portion sizes during your earlier meals of the day.
• Say goodbye to sugar.
• Load up on fruit in-between meals and vegetables during each meal to increase vitamin and mineral consumption as this will improve the efficiency of your body's mechanics.
Bringing It All Together
• Find an activity you enjoy and focus on high intensity exercise to burn more calories in a shorter time frame.
• Have a routine and change it every 4 – 10 weeks
• . Include strength training in your plan, especially the compound exercises such as Deadlifts and Squats.
• Training big muscle groups will burn more calories than training small muscle groups.
• The number on the scales ultimately comes down to your eating habits. Assess your eating habits, identify the biggest problem (sugar consumption, big meal portions, skipping breakfast, eating out too often, or alcohol consumption?) and tackle this issue first, then gradually move down the list.
About the Author
Zayd Cox is a health and fitness blogger and personal trainer based in London. He provides online coaching for people wanting guidance on how to improve their health, weight and fitness.
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How to Naturally Increase GABA for Better Sleep
How to Achieve Restful Sleep With GABA
Wouldn’t it be wonderful to have a natural, mental, and physical “off” switch to downshift your brain and body at the end of the day? In these stressful times, relaxation and restful sleep are more important than ever to well-being.
If you’re feeling stressed out or are unable to unwind, instead of turning to a glass of wine, refined carbohydrates – or worse, prescription medication – consider healthier ways to unlock your body’s natural ability to remain calm.
One healthy way to promote R&R is to get more of the amino acid gamma-aminobutyric acid (GABA) into your diet through foods or supplementation. Think of GABA as a calm balm for both the mind and body.
Here’s how it works.
GABA for Sleep and Relaxation
GABA is naturally produced within the body, where it functions as a neurotransmitter. Neurotransmitters are the brain’s messengers, which move from one neuron to another to relay information. Some neurotransmitters induce activity while others inhibit activity. GABA is the key inhibitory transmitter of the brain.
What does that mean?
GABA helps to slow down your brain’s neuron activity and decreases activity in the central nervous system. In other words, it helps to calm worrisome, ruminating thoughts, as well as balance mood, alleviate painful sensations and relax the body.
Supporting healthy sleep with GABA supplementation has gained traction in recent years.
What the Research Says
Though research on GABA supplementation and sleep is limited, some scientific studies indicate promising results. One study showed that subjects who took GABA fell asleep more quickly and enjoyed better sleep quality.
GABA has mild relaxation properties that support a balanced mood and restful sleep. Lower activity of this neurotransmitter in some brain regions has been linked to mood challenges, difficulties with self-control, and excessive worry.
How to Increase GABA
You can eat GABA-rich foods and/or take GABA supplements to help support your body’s ability to unwind.
GABA Foods
The best way to get GABA in your diet is to eat an abundance of the plant foods that contain GABA. What’s more, the foods that contain GABA are also highly nutritious. You’ll be supporting your overall health and your body’s relaxation mechanisms at the same time!
GABA-rich foods include cruciferous vegetables, beans, peas, tomatoes, spinach, mushrooms, sprouted grains, rice (particularly brown rice), and chestnuts. Also, enjoy fermented foods (kefir, yogurt, tempeh, kimchi, etc.) and oolong and white teas, which all naturally contain GABA.
GABA Supplements
A simple and easy way to ensure you get plenty of GABA is through supplementation. If you have difficulties entering a relaxed state before bedtime, you might consider taking GABA.
GABA Calming Support
Gaba Calming Support by BrainMD GABA Calming Support is a unique combination of clinically proven ingredients that can help you cope with restlessness, irritability, and other challenges associated with occasional anxiety. This formula can help calm your racing thoughts to help prepare you for sleep; it doesn’t cause drowsiness, so it’s safe to take during the day. It includes:
• GABA – by slowing the excessive firing of neurons, it supports the body’s natural mechanisms for quieting the mind and gradually falling asleep.
• L-Theanine – working mainly by way of GABA receptors on nerve cells, this unique amino acid can have calming and relaxing effects while preserving mental focus.
• Lemon balm (Melissa officinalis) – a member of the mint family that has been used as a medicinal herb for over 2000 years, lemon balm increases GABA activity in the brain as well as the activity of acetylcholine, a major neurotransmitter that promotes mental focus.
• Magnesium – sometimes called the relaxation mineral, magnesium plays important roles in mind and body relaxation, the calming of racing thoughts, and in promoting overall sleep quality.
• Vitamin B6 – also known as pyridoxine and pyridoxal-5-phosphate, vitamin B6 helps the brain produce the neurotransmitter serotonin, which helps promote relaxation and enhance mood.
This formula can help facilitate the production of calming brain waves, correct stress-causing nutritional deficiencies, and promote relaxation.
GABA Calming Support is a natural sleep aid that has helped countless people get quality sleep and can help you too!
At BrainMD, we’re dedicated to providing the highest purity nutrients to improve your physical health and overall well-being. For more information about GABA Calming Support and our full list of brain healthy supplements, please visit us at BrainMD.
Kim Henderson
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Advertisement
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The inability to selectively target undesirable T cell responses driving a myriad of immunopathologic conditions including autoimmunity, allergy, inborn disorders of immune regulation, and allogeneic rejection, is a fundamental clinical problem. While progress has been made with newer immunosuppressive drugs, the underlying strategy remains one of global suppression in order to inhibit a few detrimental effector T cells. This broad inhibitory approach is the equivalent of declaring martial law on the immune system;curtailing the normal and beneficial actions of most adaptive immune cells in order to stop the rare rogue T cell. Current strategies have three major drawbacks: (i) they lack specificity;(ii) they increase the risks of opportunistic infections and cancers;and (iii) they are associated with substantial agent-specific organ damage and toxicity. Thus, it is clear that we need to find novel and non-toxic means of controlling infrequent, yet injurious T cells, while maintaining beneficial memory and na?ve T cells to combat pathogens. We believe we have a novel approach to the specific targeting of unwanted T cells in vivo. As T cells transition between their developmental states - na?ve, activated effector, quiescent memory, and activated memory - we have found that they exhibit unique attributes that can be exploited to render their demise. First, we have observed that acutely-activated T cells display a strong DNA damage response (DDR) in vivo. Second, we found that etoposide, a chemotherapeutic agent in wide clinical use, ablates activated T cells while sparing na?ve and quiescent memory T cells. Mechanistically, we hypothesize that antigenic activation of T cells renders them uniquely susceptible toDDR-mediated apoptosis, which may be therapeutically triggered with either DNA- damaging and/or DDR-modulating agents, while affording survival of na?ve and pre-existing memory T cells. This hypothesis will be tested by (i) defining the parameters of successful in vivo targeting of effecto T cells using modulators of the DDR;(ii) defining downstream mechanisms of DDR-driven apoptosis in activated T cells;and (iii) determining the selectivity/efficacy of DDR manipulation for targeting human disease-associated T cells. Our long-term goal is to spare beneficial immunity, while purging undesirable T cells with minimal toxicity in a broad array of clinical contexts.
Public Health Relevance
White blood cells can be a double-edged sword. They are essential for protecting us from infectious diseases, but are also responsible for autoimmune diseases and are a major barrier for transplantation. Current therapies are immunosuppressive because they do not discriminate between protective and pathologic cells. We have developed a therapy that can target and kill acutely activated, pathologic T cells, whilst sparing beneficialT cells. Studies in this proposal will examine how this therapy can be improved, how it works, and if it can be translated to human cells.
Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
1R01AI109810-01A1
Application #
8780156
Study Section
Special Emphasis Panel (ZRG1)
Program Officer
Bourcier, Katarzyna
Project Start
2014-07-15
Project End
2018-03-31
Budget Start
2014-07-15
Budget End
2015-03-31
Support Year
1
Fiscal Year
2014
Total Cost
Indirect Cost
City
Cincinnati
State
OH
Country
United States
Zip Code
45229
Carroll, Kaitlin R; Elfers, Eileen E; Stevens, Joseph J et al. (2018) Extending Remission and Reversing New-Onset Type 1 Diabetes by Targeted Ablation of Autoreactive T Cells. Diabetes 67:2319-2328
Li, Kun-Po; Shanmuganad, Sharmila; Carroll, Kaitlin et al. (2017) Dying to protect: cell death and the control of T-cell homeostasis. Immunol Rev 277:21-43
McNally, Jonathan P; Millen, Scott H; Chaturvedi, Vandana et al. (2017) Manipulating DNA damage-response signaling for the treatment of immune-mediated diseases. Proc Natl Acad Sci U S A 114:E4782-E4791
Ladle, Brian H; Li, Kun-Po; Phillips, Maggie J et al. (2016) De novo DNA methylation by DNA methyltransferase 3a controls early effector CD8+ T-cell fate decisions following activation. Proc Natl Acad Sci U S A 113:10631-6
Kurtulus, S; Sholl, A; Toe, J et al. (2015) Bim controls IL-15 availability and limits engagement of multiple BH3-only proteins. Cell Death Differ 22:174-84
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increases
The best fitness club
Sports diet
Experts recommend to train on an empty stomach. 2 hours before classes need to be supported, providing the body’s energy supply.
Basic nutrition athlete – vegetable and animal food. It should include carbohydrates (55-60%), fats (30%), positively influencing the energy balance in the body, as well as the proteins (15 %) – essential muscle builders.
If the training is short and intense (bike riding, running, sports walking for 30-35 minutes), it makes sense to choose products with index from 65 to 130, if prolonged (endurance) average – with an index below 65.
Raises the question of the consumption of potatoes and white bread, the most advanced of attendees, sports complexes from them trying to refuse. Continue reading
Complex morning physical exercises
This topic is relevant because in modern adverse environmental conditions in combination with a sedentary lifestyle a person experiences a very negative impact on your body. Disrupts its normal functioning, weakens the immune system, provoking the development of various diseases.
In such conditions it is very important to apply the array of instruments that contribute to the preservation and strengthening of health of the body. A healthy person is a full-fledged member of society who has a high level of physical and mental health, good health, mental and spiritual comfort.
One of the activities that have a beneficial effect on the health of the body, is morning hygienic gymnastics. In addition to the specific effect of facilitating the transition from dormancy to a state of active wakefulness, exercise exercise increases the level of General physical activity. For the majority of the urban population morning exercise is often the only specialized medical exercise.
Like most effects on the body, exercise is only useful if it is correctly used, which takes into account the specifics of the functioning of the body after sleep, as well as the individual characteristics of a particular person. Continue reading
What to eat before and after workout
We all know about the importance of exercise, but are often faced with the question about what to eat before and after workout, and how long to wait after eating before you go to the gym? Does it matter? Yes, indeed, as the food is largely “responsible” for how effective your workout! Diet and exercise go hand in hand, and if you know that it is advisable to eat 5 times a day, moderate portions, you also need to know how much and what is before getting into the gym, so you can derive maximum benefit from your workout. Exercise on a full stomach will make you sluggish, and malnutrition will not give you enough power to complete
the workout. The same applies to food and after sports activities. So what kind of food you should choose as your main diet before training and after?
The foods that you eat before exercising, as well as their volume, give us a lot of questions. If you consume a lot of food just before going Continue reading
The Pressure in the team
Procedure Participants stand/sit in a circle with trainer. The trainer instructs participants and immediately shows an example of the movement (e.g., up-down, up-down). Then the coach starts the warm-up. If…
Continue reading →
Diet for fitness classes
So, you train 2 to 3 times a week and eat 3 to 4 times a day. Now, I hope you understand that what you eat is as important as…
Continue reading →
Methodological manual
INTRODUCTION The course "the Age peculiarities of man" is one of the important disciplines in the biomedical training of specialists in the field of physical culture and sports. This course…
Continue reading →
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Cupping Therapy
It seems like every time you read something or turn on the TV there is someone showing off their cupping marks or doing a demonstration. Cups are easily acquired and viewed by many to not be harmful. However, I would caution you to seek the advice of a licensed acupuncturist prior to using. The reason being that even though there are benefits of cupping therapy, contrary to popular belief, is NOT for everyone.
The benefits of cupping therapy
It can be very beneficial for pain. It can also help relieve toxins from the body and increase flood flow. However, in Chinese Medicine pain can be due to many different reasons. If the reason for your low back pain is due to deficiency then cupping is not for you, and in fact it can make you worse. Only a practitioner of Chinese Medicine can tell you if cupping would be beneficial for your situation. Secondly, cupping should ONLY be performed once the prior marks are gone or mostly gone. Constant cupping of the same spot before it has had a chance to heal could cause damage to the skin and muscle tissue. There is such a thing as too much cupping.
So what is cupping?
benefits of cupping therapy at Calandra Acupuncture Chicago
Cupping Therapy
Cupping is not something unique to just Chinese Medicine. Ever see the Godfather where Fredo is an infant and getting cupped because he has pneumonia? The truth is that cupping, in one form or another, appears in a number of societies.
There are many different types of cupping. All of them have the basic premise of causing a suction on the skin.
Fire cupping: use glass jars that look like mini fish bowls. A flame is used to remove the oxygen from in side of the jar prior to putting it on the skin which causes suction. Historically, a cup would be made out of bone or bamboo.
Plastic cupping: uses a small specially designed plastic cup with an apparatus that is used to remove the oxygen. For many practitioners this is the most preferred method. Primarily because it is easier to control the amount of suction being created, and is easier to use on sensitive areas like the face.
Rubber cupping: uses rubber cups. You commonly see professional athletes walking around with these. They are easily applied because the work much like a suction cup would.
Wet cupping: Uses the same concepts with fire cupping or with the plastic cups. However, prior to applying the cup a small incision is made in the skin. Once the cup is applied blood is pulled into the cup. Although a very powerful treatment very few practitioners still do this because of blood born pathogens.
Sliding cupping: Cups are applied over an oil or massage cream, and then moved up and down the major muscles. Most commonly used on the back.
What does cupping do and what about those marks?
Cupping is used primarily as a fascial release. It is used to remove “stasis” deep within the muscle tissue to help relieve pain and toxins. Cupping can also be used in facial rejuvenation treatments as a means to increasing blood flow. Once again.. do not try that at home unless you want a giant hickey on your forehead.
Depending on the amount of stasis present in the tissue you may have small marks varying from red to almost black. These marks last about a week or two. Arnica gel and a lot of water help them to dissipate a little faster. It is encouraged that, like with a massage, that you stay well hydrated so that the lactic acid from the muscle does not resettle.
Are you looking to try this therapy? If you would like to try the benefits of cupping therapy, please contact us at Calandra Center for Health and Wellness, located in Chicago’s South Loop and Arlington Heights. Cupping is offered at both locations.
Connect and Share:
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What is the Difference Between a Podiatrist and Orthopedic Doctor?
We often see the question floating around “what is the difference between a Podiatrist and an Orthopedic doctor?”. To your surprise, the answer is there are actually more similarities than differences, but the differences are important to note.
Podiatrist
As we’ve explained in our first article, a Podiatrist is a doctor of Podiatric Medicine, a Physician, and Surgeon who treats the ankle, foot, and other related structures of the leg. Not only do Podiatrists treat injuries, but they also treat ongoing complications related to health issues. Some common conditions they treat are corns, calluses, bunions, as well as various foot alignments such as tumors, ulcers, fractures, skin or nail diseases.
Podiatrists are doctors and they go through years of schooling and residency programs to become experts specifically on the foot and ankle. This is where they learn about a variety of fields like anesthesiology, internal medicine, infectious disease, surgery, ER, and pediatrics.
Orthopedic Doctor
Orthopedics is a medical specialty that focuses on the diagnosis, correction, prevention, and treatment of patients with skeletal deformities - disorders of the bones, joints, muscles, ligaments, tendons, nerves and skin. Orthopedic doctors treat people of all ages and conditions. Most orthopedic doctors practice general orthopedics, while some specialize in treating the foot, hand, shoulder, spine, hip, knee, and others in pediatrics, trauma or sports medicine.
Orthopedic doctors go through years of schooling and residency, just like all medical professionals, but their areas of expertise are broad unless they decide to further specialize their practice. About 50% of the orthopedist’s practice is non-surgical and the other 50% goes to necessary surgical management.
Similarities
As we stated before, these two doctors do indeed have similarities. For starters, they are both highly-qualified specialists. They both are required to attend years of rigorous schooling to ensure they are experts in their fields. They also both go through residencies, where they gain hands-on experience to further solidify their knowledge.
They also both have the knowledge required to diagnose conditions and injuries related to the foot and ankle.
Differences
Some of the key differences between a Podiatrist and Orthopedic doctor are the fact that a Podiatrist only specializes in the foot and doctor. Unless an Orthopedic doctor decides to further specialize in that area of the body, the extent of their knowledge on the feet and ankles is not as in-depth as a Podiatrist.
Podiatrists also expand their area of expertise to the bones, joints, soft tissues, dermatology, and biomechanics of the feet and ankle. An Orthopedic doctor will only focus on the bones, joints, soft tissues, and if the complication or injury related to other areas of the body. So, in a situation where someone is experiencing problems with walking, an Orthopedic doctor will be needed if these complications are related to the hip, back, spine, or any other part of the body.
Which Doctor Should You See?
Overall, a Podiatrist and Orthopedic doctor are similar in some ways, but they each serve their own unique purpose. If you are still not sure of which one to see for feet and ankle complications or injuries, your best bet is to visit a Podiatrist first so they can determine if it really is the foot or ankle creating the problem.
For more information, feel free to reach out to any of our offices or use our contact form to get in touch!
Contact Us Today
© 2015 by Total Foot Care & Wellness Clinic.
We Deliver Exceptional Foot Care With A Smile!
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national stem-cell therapy logo
Stem Cell Therapy for Stroke Patients
Help Spread The Word, Share Post:
Stem cell therapy is showing incredible potential for recovery of function after acute stroke. Stem cells are the body’s natural healing system, and when injected into muscle tissue can produce new cells to replace those destroyed by the stroke. These stem cells work by secreting enzymes that break down damaged cells and stimulate growth of healthy ones; they also help to protect against inflammation and reduce scarring.
A stroke is a lack of blood flow to the brain due to a blockage in one of the arteries. This can be caused by either a clot blocking off an artery or a burst blood vessel that blocks off the normal flow of blood and oxygen. A stroke is often fatal and can cause paralysis, speech difficulties, and various cognitive problems. However, the use of stem cell therapy has been shown to reduce the risk of death and improve overall function post-stroke.
Stroke patient in rehab with physical therapist.
Stroke is the 4th most common cause of death in the United States with over 795,000 strokes occurring every year. The two major forms of stroke are cerebral ischemia and hemorrhagic stroke. Hemorrhagic strokes account for about 10% of all strokes. Strokes can be devastating due to the damage to brain tissue, causing muscle paralysis, speech impairment, cognitive disabilities, and changes in mood and personality.
Stem cells are being used in medical treatment with the hope of being able to fix damaged tissue. There are many advantages of using stem cells for patients, but there are also some disadvantages to consider. One disadvantage is that some patients may not be good candidates for producing stem cells in the lab. Other disadvantages may include lack of access to good quality stem cells and the high cost that might not be covered by insurance.
What is the success rate of stem cell therapy?
Stem cells have been a hot topic in the medical industry. Originally only known for their potential to cure cancer, stem cells have now been used in a variety of other treatments. One of the most common being the treatment of stroke patients. In a study done by researchers from Hong Kong, they found that out of the twenty-three patients who had undergone stem cell therapy for their stroke, twelve showed significant improvement and were able to walk without assistance.
Can stem cells heal the brain?
Stem cell therapy for stroke patients has been one of the most promising advancements in the medical field. Scientists have found that stem cells can regenerate brain tissue, which may play an important role in healing strokes. Stem cells are able to do this because they are able to become any type of cell in the body, and brain tissue is no different.
In conclusion, stem cell therapy for stroke patients shows much promise for health improvement. Progress continues to be made in this field every day and in time stem cell therapy might be one of the leading forms of rehab for stroke patients.
The California Institute for Regenerative Medicine has awarded $31 million to three Stanford researchers to launch trials of treatments for common diseases, include stroke treatment.
*** All content on NationalStemCellTherapy.com is for informational purposes only. All medical questions and concerns should always be consulted with your licensed healthcare provider.
*** All content on NationalStemCellTherapy.com is for informational purposes only. All medical questions and concerns should always be consulted with your licensed healthcare provider.
*** Our website contains affiliate advertisements. We may receive a commission for purchases made through these ads at no additional cost to you.
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workup
Also found in: Dictionary, Wikipedia.
workup
(wûrk′ŭp′)
n.
A thorough medical examination for diagnostic purposes.
workup
(work'up?)
The process of obtaining all of the necessary data for diagnosing and treating a patient. It should be done in an orderly manner so that essential elements will not be overlooked. Included are retrieval of all previous medical and dental records, the patient's family and personal medical history, social and occupational history, physical examination, laboratory studies, x-ray examinations, and indicated diagnostic surgical procedures. The patient's workup is an ongoing process wherein all hospital personnel involved cooperate in attempting to determine the correct diagnosis and effective therapy. See: charting; problem-oriented medical record
sepsis workup
A colloquial term for the evaluation of a patient, esp. a neonate, with a fever, for laboratory evidence of severe infection. Common tests for febrile neonates include a complete blood count; blood cultures, cerebrospinal fluid, urine, and stool samples; and chest x-ray. Most neonates with a fever are given immediate treatment with broad-spectrum antibiotics pending the results of cultures.
Patient discussion about workup
Q. I have experienced alot of hair loss over the last few months, my doctor did a complete blood workup on me, And everything came back normal. My question is what could cause this and how can I get my thick hair back without rogain and other evasive actions. And could this be a symptom of something else? Womens hair loss does not run in my family, so I am really concened about this.
A. Hair loss can be caused by malnutrition, and lack in certain vitamins, however such malnutrition would have an impact on your blood work and if the results were normal I doubt that is the reason for your hair loss. Stress is another very important factor, which is known today to have a connection with hair loss. Are you in a stressful period in your life? Perhaps when things calm down for you the situation will improve.
More discussions about workup
References in periodicals archive ?
The diagnostic workup included history taking, physical examination and imaging of the urinary tract.
The use of AclarusDx could help speed up the full diagnostic workup.
However, none of these studies attempted to control for workup bias.
The cases involve amputations/fingertip injuries, anesthesia and pain management, arthritis, burns, compartment syndromes, congenital conditions, contractures, Dupuytren contracture, fractures/dislocations/nonunions/malunions, infections/bites, infections/extracasations, instability, osteonecrosis, peripheral nerve issues, soft tissue defects, tenosynovitis, traumatic injuries to the tendon, tumors, and vascular conditions, with each case including a description of the problem, key anatomy, workup, treatment, alternatives, principles and pearls, and pitfalls.
Subsequent workup revealed widespread metastatic disease, for which the patient was treated with chemoradiotherapy.
The appropriate workup of stress urinary incontinence (SUI) can vary substantially depending on the patient profile.
M2 EQUITYBITES-July 24, 2019-D2 Consulting Acquires WorkUp to Boost Operational Efficiencies Patient Engagement
Magnetic Resonance Imaging (MRI), metabolic workup and more recently genetic analysis may be required.12
In general chapters, they cover peri-operative workup; contrast, sedation, analgesia; drugs in interventional radiology; noninvasive imaging; devices (wires and catheters); and vascular access.
Reports generated after a multidisciplinary tumor board (MTB) review and subsequent workup were compared to radiology, pathology, and genetic testing results from outside institutions.
Among the examples she highlighted where comanagement can have a favorable impact were optimization of perioperative pain management pathways; how to handle the use of disease-modifying antirheumatic drugs (DMARDs) in patients undergoing THA/TKA; the latest thinking on the appropriateness of low-dose aspirin for deep vein thrombosis (DVT) prophylaxis; a simple way to predict postop delirium in older individuals without known dementia; how to decide which postoperative fevers warrant a costly infectious disease workup; and the optimal wait time from arrival at the hospital with a fractured hip to THA.
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Understanding Dementia: The psychological effects on older adults and their family members are evident as well.
Dementia is not only a problem that affects the quality of life and independence of millions of older people worldwide, but it also significantly affects their emotional health. Despite the clinical nature, the memory loss caused by dementia can have profound consequences on individuals, as it often results in frustration, sadness, and anxiety. One should definitely acknowledge the high emotional cost this condition has for both the victim and the family.
As it starts to progress, the memory loss becomes worse, creating difficulties in recognizing the surrounding things, disorientation and confusion about where they are. Picture yourself making efforts to remember important life events or a person who you usually associate with your better days. It leads an individual to the point of being sad and lonely, not being able to face these close to them and regard his own life.
This drastic loss of communication sometimes takes away the emotional connection with other individuals close to the patient, such as family members. To see someone whom you love in those difficulties to recall essential events and the names of relatives is not the easy thing that can emotionally laden. It is able to weaken the ties and make you unwell with the bitter feelings of hopelessness and unhappiness. The selective loss of memories and references to past activities is a big emotional challenge for the affected person and their family members.
Moreover, alongside speech and cognitive dysfunctions characteristically associated with dementia, the level of distress can be heightened and shifts in behaviour could take place. For the families, this process can create a difficult and sometimes hopeless situation as they are arranging to provide the necessary support and the needed understanding to their relative.
The emotional burden of dementia cannot be undervalued. A deep sense of loss and detachment prevails among the affected person, which can even traumatize the family as a whole. The society as a whole should be led to caring for the people with dementia and the families that are affected by this emotionally challenging condition, while providing support that they may need. Although there are no cures for dementia right now; there are medications/therapies that can help slow down its advancement and also enhance the quality of life for the ones affected by the disease, which is a source of hope and relief in these emotional areas.
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Struggling with a mid-afternoon energy slump? This hormone might be the culprit
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1/5
your healthy cortisol cycle
Graphic: Abby Maker
You’re Superwoman in the morning, you power through lunchtime meetings, and then you fade around 3 p.m.—just to feel wide awake when 9 p.m. rolls around.
Sound familiar? It’s not because of what you ate or the fact that you’ve been sitting too long (though those factors might make it worse). And it’s definitely not all in your head. There’s a hormone that’s responsible for this whole thing.
You’re Superwoman in the morning, you power through lunchtime meetings, and then you fade around 3 p.m.—just to feel wide awake when 9 p.m. rolls around.
Cortisol is the hormone that governs your blood sugar, blood pressure, digestion, hunger cravings, digestion, sleep/wake patterns, physical activity, and your capacity to cope with stress,” says gynecologist Sara Gottfried, MD, author of the New York Times bestseller The Hormone Reset Diet. In other words, it’s mission control for being a functional human being. “When you’re in fight-or-flight [mode], cortisol’s role is to raise blood pressure (so you can run) and blood sugar (to power your muscles), and to modulate your immune system.”
For example, when you’re getting a big energy spike just as you start thinking about winding down and going to sleep, it’s an indication that your cortisol levels are staying high at a time when, according to their natural 24-hour rhythm, they should be tapering off.
Other hints that the ebb-and-flow pattern is just…off: everything from brain fog to insomnia to weight gain and irregular periods.
What does a healthy cortisol cycle look like? And how can you get back to balance? Dr. Gottfried shares her science-backed methods for hormonal harmony.
Get Started
2/5
cortisol out of balance
Photo: StockSnap/Matthew Hamilton
So, what’s normal?
For most people, there’s a natural spike in the morning, which explains why we feel a burst of no-coffee-required energy in the a.m.—either right away or once we’ve moved around a bit and shaken off the cobwebs—and a lull in the afternoon. And for some people, it spikes again in the afternoon or evening (hello, night owls).
But generally, the highest levels are made in the morning, less is produced during the day, and very little in the evening. Only minimal amounts of cortisol are produced while you sleep. “When your cortisol levels are in balance, you feel calm, cool, and collected all the time,” says Dr. Gottfried. “You sleep well, and are able to manage stress without it overcoming you. Your blood pressure and blood sugar levels are normal.”
3/5
how to get better sleep
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What if your cortisol switch is always “on”?
The hormone’s levels should bottom out around midnight, while you’re asleep, explains Dr. Gottfried. That’s when your cells can perform their greatest repair. “If your cortisol levels are still high while you’re sleeping, your body can’t do the healing it needs. As a result, you wake up feeling fatigued, like you want coffee—which raises cortisol—and perhaps you have trouble recovering from exercise.”
Chronic stress is a likely culprit, as it almost constantly produces cortisol and makes it near impossible to wind down. “High evening cortisol makes you feel like you don’t need rest at the time when you actually need it most.”
The result: depleted adrenals, which in turn cause serotonin, dopamine, norepinephrine, and epinephrine (AKA all the mood-balancing hormones you want to be coursing through you) to plummet. Lack of sleep makes it harder to sleep because of stress and high cortisol, so it becomes an endless cycle. Dr. Gottfried sums it up bluntly: “It’s crucial to mind your cortisol.”
4/5
stress inflammation diet
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Is this the same as adrenal fatigue?
The two modern-day woes are in fact related. Cortisol is produced in the adrenal glands, which is controlled by the hypothalamic pituitary adrenal thyroid gonadal (HPATG) axis. In times of stress, the HPATG axis signals the adrenal glands to increase cortisol production. Once cortisol levels increase, they basically tell the HPATG, “Don‘t worry, we’ve got this,” and the HPATG axis stops inducing the adrenal glands to increase cortisol production.
Your body is designed to do this rarely—think four times a year—and then experience long periods of calm. The problem is that most of us run around stressed too much of the time. When stress is chronic, the HPATG axis keeps triggering the adrenals to produce more and more cortisol, leading to adrenal disregulation.
5/5
google reserve details
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How do you bring things back to balance?
Good news: Dr. Gottfried believes lifestyle and supplemental strategies are powerfully effective for most women. A lot of the advice boils down to the usual no-brainers: a whole-foods diet, appropriate exercise, and stress management via meditation, breathing exercises, and yoga.
Here are some specific places to begin:
Eat nutrient-dense food. Avoid refined carbs and sugar like the plague. (Which is tough when cravings can be a symptom of high cortisol. Don’t give in—it only spirals downward.) If you’re a low-cortisol person during the day, eat “slow carbs” such as sweet potatoes at night.
Exercise in the morning. And if your levels are high, remember that cardio can raise cortisol. Dr. Gottfried says switching from running to yoga and Pilates made all the difference for her weight.
Maintain a contemplative practice. This one is nonnegotiable—especially if you’re struggling with your weight. A study from the University of California at San Francisco showed that obese women who began a mindfulness program and stuck with it for four months lost belly fat. That makes sense because your belly fat contains four times (!) the cortisol receptors as fat elsewhere in the body.
Take omega-3 supplements. Men and women who took 4,000 milligrams of fish oil a day for six weeks lowered their morning cortisol to healthier levels and increased their lean body mass, according to a 2010 Gettysburg College study. Look for a supplement that has been third-party-tested and is free of mercury and other endocrine disruptors.
Take rhodiola. This adaptogenic herb, a form of ginseng, is the best botanical treatment for balancing stress hormones, says Dr. Gottfried. Aim for 200 milligrams once or twice a day.
Take vitamin C. It’s been shown to lower cortisol in surgical patients and students in stressful situations, and is a safe supplement to add to your regimen. Try 750 to 1,000 milligrams per day, maximum, since more may cause a loose stool (which, real talk, could stress you out enough to send your cortisol levels back through the roof).
Take vitamin B5. It appears to reduce excessive cortisol in people under high stress, Dr. Gottfried notes—plus, it’s a low-risk treatment. Aim for 500 milligrams per day.
Another way to lower your stress levels: believe it or not, self-hypnosis. Or, even better, make this calm-inducing dessert tonight
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Ray Ban Sunglasses 0Rb3025
Ray Ban Sunglasses 0Rb3025
There was no increase in falls in either exercise group compared to UC during the intervention period (resulting from increased exposure to risk). The FaME arm experienced a significant reduction in injurious falls compared to UC (incidence rate ratio (IRR) 0.55, 95% CI 0.31, 0.96; p = 0.04) and this continued during the 12 months after the end of the intervention (IRR 0.73, 95% CI 0.54, 0.99; p = 0.05). There was also a significant reduction in the incidence of all falls (injurious and non injurious) in the FaME arm compared with UC (IRR 0.74, 95% CI 0.55, 0.99; p = 0.04) in the 12 month period following the cessation of the intervention.
Until the 1920s, more than 10 measles cases per 100,000, or 0.01 percent, resulted in death. However, by 1955, with advances in medicine and huge progress in sanitation, nutrition, and living standards, those rates steadily declined from 1900 levels to 0.03 deaths per 100,000, a mere 0.00003 percent! By the time the measles vaccine was introduced in 1963, the disease had already lost its death grip on the developed world. Measles cases with no distinction of measles deaths since the inoculation was introduced, a decidedly deceptive omission of earlier years’ data..
Background and Objectives: People with dementia are vulnerable when in hospital, with serious risks to their physical and emotional wellbeing. Hospital staff are expected to understand and respond to the emotions of the patient; however, it is not known how this can be achieved. We provide a concise description of achievable emotion focused care for patients with dementia.Design and Methods: Exploratory qualitative interviews were conducted with a whole UK hospital ward providing dementia care, constituting 47 staff members.
This essay is devoted to an analysis of the semantic significance of a fashionable view of proper names, the Predicate Theory of names (PT), typically developed in the direction of the Metalinguistic Theory of names (MT). According to MT, syntactic evidence supports the conclusion that a name such as Kennedy TM is analyzable in terms of the predicate (general term) individual named Kennedy TM TM. This analysis is in turn alleged to support a descriptivist treatment of proper names in designative position, presumably in contrast with theories of names as directly referring rigid designators TM.
“Mauritius is a must see destination in the Indian Ocean and is one of the most strategic resort markets. These new management contracts are an important step for us to establish our presence and to further expand our upper upscale resort network in the region. Our ultimate objective is to add value to our owners and shareholders”, added Elie Younes, Executive Vice President Chief Development Officer of Rezidor..
Archives
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5eff3d1f6f98e57329caed0ceb9053d3
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1,304,985,168,847,137,300
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PMCCPMCCPMCC
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J Virol. 2004 May; 78(9): 4385–4388.
PMCID: PMC387720
Four Viruses, Two Bacteria, and One Receptor: Membrane Cofactor Protein (CD46) as Pathogens' Magnet
CD46 (also known as membrane cofactor protein or MCP) is a regulator of complement activation that is expressed in most or all human nucleated cell types. CD46 was initially identified as binding and inactivating C3b and C4b complement products, a process protecting human cells from lysis by autologous complement (18). It also serves as a receptor for several human pathogens: an enveloped RNA virus (measles virus [MV]), an enveloped DNA virus (human herpesvirus 6), a nonenveloped DNA virus (adenovirus of different serotypes), and two types of bacteria (Streptococcus pyogenes and pathogenic Neisseria) (13, 27). Moreover, bovine CD46 was recently shown to serve as a receptor for bovine viral diarrhea virus (BVDV), an enveloped RNA virus. That six different pathogens selected the same molecule as a port of cell entry is of interest not only for microbiologists and immunologists, who wonder what makes CD46 such a seductive molecule, but also for gene therapists, who are seeking opportunities for targeting disease sites.
BOVINE CD46 IS A CELLULAR RECEPTOR FOR A PESTIVIRUS
A recent study by Maurer et al. (22) identified bovine CD46 as the receptor for BVDV, a small, enveloped RNA virus that belongs to the genus Pestivirus within the family Flaviviridae. BVDV is an important pathogen of cattle and accounts for syndromes of the intestinal, respiratory, and reproductive tracts. The search for the BVDV receptor started with a monoclonal antibody that blocked infection. This antibody was shown to recognize a bovine protein with a significant sequence homology to porcine and human CD46 (22). Expression of bovine CD46 in porcine cells increased susceptibility of these cells to infection with one strain of BVDV, whereas expression of bovine CD46 in human cells enhanced virus binding but did not allow productive infection. Thus, BVDV tropism must be influenced by factors other than bovine CD46 availability: alternative receptors, coreceptors, or postentry events.
The identification of a ubiquitous molecule serving as the BVDV receptor also raised questions regarding its relevance for tropism and pathogenesis. BVDV replicates in essentially all organs and tissues, but initially this virus selectively infects the tonsils and then spreads to other lymphatic tissues before the occurrence of viremia (17). Even if CD46 is an ubiquitous protein, it was recently shown that certain interactions of this protein occur specifically in immune cells. In particular, coengagement of CD46 and CD3 in the presence of interleukin 2 induces the development of cells with a T-regulatory 1 phenotype (14). This observation raises the possibility that BVDV and other pathogens interfere with fundamental processes in the immune response by altering CD46 function (see last section). Thus, BVDV interactions with CD46 of immune cells may induce fundamentally different effects as with other cell types.
MV AND CD46: ATTENUATION THROUGH STRONGER BINDING?
There are interesting parallels between BVDV and MV: both pathogens initially spread in lymphatic cells and induce a strong immunosuppression. MV was the first pathogen shown to use CD46 as a receptor: the glycoproteins of the attenuated strain Edmonston were used to set up a screening system based on the inhibition of cell fusion. A library of 3,000 monoclonal antibodies raised against surface proteins expressed in MV-permissive cells yielded one clone whose supernatant interfered with MV glycoprotein-induced fusion (26). The protein recognized by this monoclonal antibody was characterized as being CD46 and was shown to support MV entry in rodent cells (7, 25). MV did replicate in rodent cells expressing human CD46 but not at the same levels reached in human cells.
The question of the relevance of an ubiquitous receptor for the pathogenesis of a lymphotropic virus was raised again when it was shown that the H protein of the attenuated Edmonston strain interacted more efficiently with CD46 than the proteins of certain wild-type MV strains (16). When it was then found that wild-type strains rely on SLAM (signaling lymphocyte activation molecule or CD150) for cell entry (34), the receptor-tropism question seemed solved to the advantage of SLAM: this molecule is expressed only in certain immune cells, a fact that better explains the immunosuppressive nature of MV infection. In addition, two other immunosuppressive MV relatives, the morbilliviruses canine distemper virus and rinderpest virus, use canine and bovine SLAM but not CD46 as their receptors, respectively (9, 35).
Nevertheless, it remains conceivable that MV interactions with CD46 contribute to tropism and immunosuppression. Certain wild-type MVs interact with CD46 (19, 31); the binding affinity of the respective attachment proteins and CD46 has not been determined, but it is lower than that of the attachment protein of the vaccine strain (120 nM) (4, 29). A scenario for MV attenuation considers that it is related to early efficient entry of the vaccine strain in nonimmune cells, dampening the effects of the timely attack of SLAM-expressing lymphocytes and macrophages strategically executed by wild-type strains.
CD46 MEDIATES ATTACHMENT AND ENTRY OF DIFFERENT ADENOVIRUSES
Adenoviruses are icosahedral, nonenveloped DNA viruses. Most of the 51 adenovirus serotypes are only mildly pathogenic; they are grouped in six species, A to F. Members of all species except B use the coxsackievirus-adenovirus receptor (CAR), as a port of cell entry (2, 28). Entry of a group D serotype (Ad37) appeared to be an exception because it requires sialic acid rather than the CAR protein (1). Four recent publications have identified human CD46 as a receptor for different adenovirus serotypes: Ad3 (33), Ad11 (28), Ad35 (8), and Ad37 (38). These data collectively indicate that CD46 is a receptor for several group B adenoviruses, including Ad3, Ad11, and Ad35, and for a group D adenovirus, Ad37.
The data presented are in each case compelling because receptor identification and characterization were based on different techniques. Initially Segerman et al. (32), based on gifted insight, postulated that CD46 is a cellular receptor for Ad11 and then showed this by rendering rodent cells permissive to Ad11 infection through CD46 expression and by blocking binding and infection with soluble fiber knob (the viral attachment protein) or anti-CD46 antibodies. Independently, Gaggar et al. (8) produced a recombinant Ad35 fiber knob protein and used it to purify potential receptors. The cellular proteins binding to the recombinant knob protein were analyzed by mass spectroscopy, and CD46 was identified. Gaggar et al. then went on to show that CD46 supports cell entry and productive Ad35 replication and that it also supports the attachment of the other species B adenoviruses, serotypes 11, 14, 16, and 50. In another independent approach, Wu et al. (38) characterized the receptor for Ad37 (group D), a serotype associated with epidemic keratoconjunctivitis. CD46 again was identified with other proteins as a candidate for binding to Ad37 in a virus overlay assay. It was then shown that nonpermissive cells promoted adenovirus replication upon CD46 expression and that an antibody specific for the most external domain of CD46 blocked Ad37 infection of two human cell lines. In a fourth study Sirena et al. (33) screened an expression library made from cDNAs of cells that efficiently bound Ad3. The rodent cells that gained the capacity of binding fluorescent Ad3 particles expressed either one of the major CD46 isoforms. These cells internalized Ad3 and developed cytopathic effects. These authors also showed that Ad3 binds with an affinity of 0.3 nM human cells and CD46-expressing rodent cells but not control rodent cells. Finally it was shown that the CD46 ectodomain binds the Ad3 fiber head.
RECEPTOR TISSUE DISTRIBUTION AND VECTOR TARGETING
The above data prove beyond reasonable doubt that human CD46 is a receptor for several adenoviruses. Again the issue of the relevance of CD46 for viral tropism has to be raised, and again the existence of alternative receptors, coreceptors, and postentry virulence determinants has to be invoked to explain the distinctive tropism and pathology of the different adenovirus-based serotypes. An interesting observation in this respect is that the CD46 C isoform, which is highly expressed in the eye (cornea/conjunctiva) and brain, is preferentially used by Ad37.
In the perspective of adenovirus vector applications, the fact that certain strains contact a ubiquitous protein rather than the much less readily available CAR is good news. Present gene therapy protocols rely on vectors derived from Ad2 and Ad5, two species C adenoviruses that use CAR as a receptor. However, CAR is expressed only in a few tissues, and efficient adenovirus-mediated transgene expression is associated with CAR availability (11). The question now becomes how successful gene transfer protocols can be, based on CD46 usage and, more in general, whether and how a ubiquitous molecule can be exploited for vector targeting.
The fact that certain viruses become attenuated when they bind tightly to ubiquitous receptors expressed at high levels (reference 20 and references therein) is a warning of the difficulties that have to be overcome. For example, tick-borne encephalitis virus adapts to negatively charged heparan sulfate: local patches of predominantly positively surface charges evolve in its attachment protein (20). The positively charged amino acids are selected in tissue culture, but when a tissue culture-adapted virus is passed into mice neuroinvasiveness is attenuated.
This does not mean that any level of heparan sulfate binding may preclude vector targeting. In contrast, low-affinity binding may concentrate viral particles in a given organ expressing high heparan sulfate levels and facilitate subsequent interactions with a high-affinity receptor or a coreceptor. Detailed knowledge of the organ distribution and concentration of receptor and coreceptor molecules is necessary to predict the efficiency of targeting approaches. Characterization of the interactions of the viral attachment proteins with their receptors is also required to plan the production of recombinant viruses with carefully balanced affinities to different receptors. Towards this it was shown that selectively receptor-blind viruses can be created through the introduction of point mutations in their attachment proteins (5, 36, 39).
The art of vector targeting is only beginning to develop into a science (6, 37). Ligand-directed targeting of viral vectors to disease sites is based on the present, incomplete framework of knowledge about receptor hierarchy and tissue distribution and proceeds slowly. Alternative approaches to targeting that rely on the characterization of the tropism of viruses collected from primates or other mammals are being pursued (10). Moreover, chimeras of different viral species are being produced in the perspective of generating vector libraries with novel receptor specificities from which individual vectors can be selected. These approaches will synergize with studies of viral structure and assembly to guide the development of vectors with incrementally higher tissue and cell specificity.
WHY CD46?
Is it a particular structure or structural pattern, a strategic location in a subcompartment of the cell surface, or another characteristic that predestines CD46 to be a port of entry for so many pathogens? CD46 is a type I membrane glycoprotein (Fig. (Fig.1).1). From its amino terminus there are four tandem complement control protein (CCP) modules followed by one or two heavily O-glycosylated serine/threonine/proline-rich (STP) domains, a transmembrane region, and two alternative cytoplasmic tails (15). As shown in Fig. Fig.1,1, pathogens recognize different structures in the CD46 ectodomain: MV binds to the two external CCP modules, human herpesvirus 6 binds to modules 2 and 3, and pathogenic Neisseria relies on the STP domains for cell attachment (3, 12, 24, 30). Preliminary data derived only from antibody competition experiments suggest that different adenovirus strains may contact different CCP modules (32, 38). Taken together, these data indicate that there is not a single structural target for pathogens on CD46.
FIG. 1.
CD46 structure, domains interacting with different pathogens, and postulated cytoplasmic tail-dependent signaling are shown. Large elongated ovals, CCP modules; small ovals, STP domains; thin lines originating in the STP domains, O-linked oligosaccharides; ...
The cellular mechanisms facilitating cell entry of the different CD46-dependent pathogens are also fundamentally different: no subcellular compartment is consistently implicated in the pathogens' interactions. MV and human herpesvirus 6 enter cells by pH-independent fusion of their membrane with the plasmalemma, adenovirus species C enters via clathrin-dependent endocytosis (23), and other adenovirus species are likely to use similar endocytotic mechanisms; Neisseria does not enter cells routinely but relies on CD46 for the initial attachment, facilitating subsequent adhesion. Table Table11 shows different pathogens' interactions with CD46.
TABLE 1.
Pathogen interactions with CD46
Thus, the question of what makes CD46 a pathogen's magnet remains, and the answer may have to be sought inside the cell. If different pathogens use the same CD46 function to create a favorable environment and elude detection and destruction, how do they elicit a signal? Probably through the CD46 intracellular domain. CD46 has two alternative cytoplasmic tails that result from alternative splicing. Since these tails are only 23 and 16 residues in length, it was initially assumed that their contribution to the conditioning of the cytoplasm may not be significant. However, two recent studies have shown that CD46 can drive T-cell differentiation (14) and that the CD46 cytoplasmic tails have a divergent role in T-cell-induced inflammation (21). Thus, CD46 not only regulates complement activation but fine-tunes the T-cell-mediated cellular response, thereby bridging innate and acquired immunity. It is conceivable that all the CD46-targeting pathogens interfere with cytoplasmic tail-elicited intracellular signaling pathways, thereby unbalancing the immune response. Once again, pathogens are trying to teach us cell biology and immunology. Microbiologists and gene therapists should pay attention.
Acknowledgments
I thank several colleagues for sharing their data and manuscripts prior to publication and thank Larry Pease for critical reading of the manuscript.
This research was supported by grants of the National Institutes of Health (CA90636 and AI57761) and by the Mayo, Siebens, and Eisenberg Foundations.
Notes
The views expressed in this Commentary do not necessarily reflect the views of the journal or of ASM.
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Articles from Journal of Virology are provided here courtesy of American Society for Microbiology (ASM)
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Exploring the Benefits of Antioxidants
Holistic Fitness/ Nutrition / Dec 31st, 1969 / 0 COMMENTS / A+ | a-
The following article was originally published in "Health Keepers," a magazine created by Trinity's founder, Dr. Wendell Whitman. Health Keepers is a publication of Trinity School of Natural Health Inc. This article appeared in Volume 1 • Issue 3 • Summer 1998, pg 9-10, 30. This article originally titled, "Antioxidants" was written by Max Sherman, R Ph.
Dr. Kenneth Cooper, the father of the worldwide aerobics movement and preventative medicine, has authored a book called The Antioxidant Revolution. In it, Cooper provides a program of diet and exercise which [may] delay the signs of aging and reduce the risk of cancer and heart disease. The diet consists of megadoses of beta carotene and vitamins C and E, the antioxidants Dr. Cooper claims to act as a personal defense system to provide a longer and healthier life.
Health store and pharmacy shelves are now stocked with an array of these vitamins in a number of dosage forms, plus a host of others, including coenzyme Q 10 (ubiquinol-10), pycnogenol, selenium, curcumin, bioflavonoids, grapeseed extract, lycopene, and lipoic acid. The latter is an approved supplement in Germany for the treatment of diabetic neuropathy and is effective against both water- and fat-soluble free radicals. Lipoic acid has recently been introduced in the United States. Lycopene is a fat-soluble antioxidant found in tomato sauce and is similar to beta carotene. According to the Tomato Research Council and the American Health Foundation, lycopene can [help to] ward off prostate, digestive tract, and other cancers.
Curcumin is the yellow pigment and primary active component of turmeric (Circuma longa). It is comparable to standard antioxidants like vitamins C and E, and a powerful inhibitor of lipid peroxide. Pycnogenol is the trade name of a potent antioxidant extracted from the bark of the French maritime pine in southern France and is a member of the bioflavonoid family. Bioflavonoids enhance the body’s utilization of vitamin C and prolong its healing activity.
The multiple choices and combinations of antioxidants are no doubt confusing to the layperson. The [nutrition expert] should be equipped to clarify any questions regarding the oxidative process, mechanism of action, definitions, indications for use, dosage and administration, and precautions. This article will provide some of that information and references for additional study.
Mechanism of Action. Before health professionals can advise clients on antioxidant [protocols], they should be aware of a number of terms and definitions.
These include:
Radical: A radical is an atom or molecule which contains one or more unpaired electrons.
Free Radical: A free radical is a radical which has moved out of the immediate molecular environment of its generation. Free radicals are often defined as reactive oxygen species occurring in tissues and cells. They have the ability to react with most normal cellular components, causing cell and tissue damage.
Oxidation: An increase in the positive valance state of a substance, such as by removal of one or more electrons from a molecule. (Conversely, reduction is the addition of one or more electrons to a molecule.) Thus, when one substance is oxidized, the other is reduced.
Peroxidation: The introduction of a peroxyl (0-0) moiety into a molecule. Lipid peroxy radicals are formed when oxygen attacks the fatty acids in cell membranes.
Reactive: Reactivity is a measure of the rate at which a substance is transformed chemically. It is not a property intrinsic to an individual substance but is dependent on the nature and concentrations of available reactants.
Oxidation. Cellular metabolism produces oxidant by-products which can cause extensive damage to DNA, proteins, and lipids. Oxidation also occurs when phagocytic cells combat bacteria, parasite and virus-laden cells with nitric oxide (NO), superoxide (O2), hydrogen peroxide (H2O2), and hypochlorite (OCl), a powerful oxidant mixture. These oxidants protect humans from immediate death from infection but cause oxidative damage to DNA and mutation, thereby contributing to the carcinogenic process. Cytochrome P-450 enzymes, one of the body’s defense mechanisms to prevent acute toxic effects from foreign chemicals, are another source of oxidant by-products that can damage DNA.
Metabolic processes, phagocytic reactions, and cytochrome P-450 enzymes are three endogenous sources for most of the oxidants produced by the cells. Exogenous sources include cigarette smoke, which contains the oxides of nitrogen; excessive intake of iron and copper salts, which can promote the generation of oxidizing radicals from peroxides; and diets that contain plant foods with large amounts of phenolic compounds. Oxidant damage occurring from any of these sources appears to be a major contributor to aging and degenerative diseases of aging, such as atherosclerosis and cardiovascular disease, cancer, cataracts, and brain dysfunction. Fortunately, the human body makes several important antioxidants. The most important include ubiquinol and glutathione. Enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase also destroy some free radicals.
Animals with longer life spans appear to have higher levels of SOD to detoxify the free radical superoxide. Superoxide dismutase has been touted as an anti-aging drug, but when ingested, it decomposes into basic amino acids, which do not recombine to form SOD.
The chemistry of free radicals is extremely complex and beyond the scope of this article. In addition, there are a number of continuous interactions between free radicals and biological molecules which result in inconclusive linking between free radicals and injury. The prevalence of oxygen in biological tissues and the rapid reaction of most organic radicals with oxygen (forming peroxyl radicals and hydroperoxides) further confound the issue.
Antioxidants may act at different levels in the oxidative process by:
1. scavenging initiating radicals
2. binding metal ions
3. scavenging peroxyl radicals
4. removing oxidatively damaged biomolecules
Some antioxidant molecules are synthesized in the body, for example, glutathione or ubiquinol, whereas others have to be provided as micronutrients, such as ascorbic acid, beta carotene, vitamin E, and trace metals like selenium.
Dosage. Dr. Cooper bases his dosage requirements for the antioxidants vitamin C, vitamin E, beta carotene, and selenium on age and activity level. While he mentions ubiquinol, he believes there is not sufficient data to recommend it at this time. From vitamin E, he recommends the natural form, which is designated as d-alpha-tocopherol. Although the dl- or synthetic form has antioxidant activity, it may actually inhibit the d-form from entering cell membranes. Cooper’s daily dosage recommendations include vitamin C—500 to 3000 mg, vitamin E—200 to 1200 IU, beta carotene—10,000 to 50,000 IU, and selenium, an optional 50 to 100 mcg. The dose is dependent upon activity level, gender, and body weight. Active people, particularly weight lifters and runners, require higher dosages, as do men and individuals who weigh more.
Antioxidants should be taken in divided doses and with food to enhance absorption. Vitamin E supplements are contraindicated in patients taking anticoagulants since vitamin E increases their effects. Because of possible liver toxicity, beta carotene should not be consumed with alcohol or used as a supplement for the client who drinks excessively. Large doses of vitamin C are contraindicated in diabetics, and doses greater than 4000 mg daily may cause gastric distress or kidney stones. Selenium may lower the risk of certain cancers, but this has yet to be confirmed.
Selenium doses greater than 200 mcg per day are not recommended.
Final Thoughts. In light of all the detrimental effects of free radicals and the possible benefits taking antioxidants, it appears prudent for the health professional to recommend vitamins C, E, and beta carotene to his or her clients.
References:
According to original article, "
References available upon request."
Note: This article was edited to adhere to current legal and practical standards.
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For the Health of Your Brain, Please Pay Attention to Daily Diet
• For the Health of Your Brain, Please Pay Attention to Daily Diet
• This passage will introduce some kinds of food that are beneficial and harmful to the health of brain, which you should pay special attention to. Foods that are beneficial to the health of brain are as follows:
1. Nuts
Nuts such as walnuts, almonds, pine nuts, etc, not only are rich in omega-3 unsaturated fatty acids, but also contain a large number of antioxidants like vitamin E and selenium. These antioxidants can protect the brain cells from the damage of free radicals. The researchers from United States Department of Agriculture have found out that, nuts also contain a kind of mineral called as "boron". It will affect the electrical activity in the brain, and make people's intelligent reaction become more sensitive. Experts point out that, parents can provide their children with some nuts at breakfast.
2. Berries
Berries (such as strawberry, blueberry, cranberry, etc.) contain a lot of antioxidants, which can help reduce the damage of free radicals, as well as delay ageing. Animal experiments have shown that, berries are closely related with the function of motor nerve, memory and cognitive ability. What's more, berries also contain a variety of vitamins. When the brain cells synthesize acetylcholine--the neurotransmitter of memory, vitamins play an indispensible role.
3. Milk
Milk not only can supplement great amounts of calcium to the body, but can also provide some important nutrients for brain--protein and vitamin B group. According to the statistics, nowadays most of the primary school students eat too much meat, and this may cause the deficiency of calcium. If parents are worried about the lactose intolerance of their children, they can choose non-sugar yogurt and add some fruits or nuts in it, which can improve the flavor.
4. Pumpkin
Pumpkin is the best source of beta-carotene. The Dutch study has found out that, beta-carotene can maintain the thinking ability sensitive. Beside pumpkin, dark green leafy vegetables, carrot, bell pepper, sweet potato, papaya and mango are also rich in beta-carotene. In addition, pumpkin seeds contain a large number of zinc, which can promote the development of brain. If the intake of zinc is insufficient, it will cause memory loss and inattention. Experts point out that, as long as you take in adequate zinc, the memory will be increased by 12%. Sunflower seeds, brown rice and whole grains are also good sources of zinc.
Then what kinds of food are harmful to our brain?
1. Food containing caffeine: such as coffee, strong tea, chocolate, soda, and so on. These kinds of food will reduce the blood flow in brain and in many human organs, cause dehydration in the brain, and thus affect the thinking ability. Experts remind parents, children under 12 years old should keep away from caffeine. This is because the metabolic function of children's kidneys has not yet fully developed, so the caffeine will not be easily expelled out of the body, thus it will make the children absent-minded and affect their study.
2. Fried food: fried food will easily produce a lot of free radicals in the body, and thus cause damages on the brain cells and brain tissue.
3. Refined sugar: sugar is a kind of carbohydrate, which can be easily decomposed by the body. This may make the level of blood sugar fluctuate, and affect the operation and function of the brain.
4. Artificial additives: it has been proved that artificial additives such as food colorants and sugar substitutes are very harmful to children's brain. They will affect children's learning ability, and lead to symptoms such as hyperactivity and inattention.
Besides what we have mentioned above, a nutritious and healthy breakfast also plays an important in the health of the brain. In a word, as long as you pay attention to the above suggestions that we have discussed, you can keep your brain healthy.
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{"entity": "publication", "iuid": "2bbe0fe4a34842559adbcfa051baa28a", "timestamp": "2019-12-15T14:20:40.281Z", "links": {"self": {"href": "https://publications.scilifelab.se/publication/2bbe0fe4a34842559adbcfa051baa28a.json"}, "display": {"href": "https://publications.scilifelab.se/publication/2bbe0fe4a34842559adbcfa051baa28a"}}, "title": "D-amino acid oxidase activator gene (DAOA) variation affects cerebrospinal fluid homovanillic acid concentrations in healthy Caucasians.", "authors": [{"family": "Andreou", "given": "Dimitrios", "initials": "D"}, {"family": "Saetre", "given": "Peter", "initials": "P"}, {"family": "Werge", "given": "Thomas", "initials": "T"}, {"family": "Andreassen", "given": "Ole A", "initials": "OA"}, {"family": "Agartz", "given": "Ingrid", "initials": "I"}, {"family": "Sedvall", "given": "G\u00f6ran C", "initials": "GC"}, {"family": "Hall", "given": "H\u00e5kan", "initials": "H"}, {"family": "Terenius", "given": "Lars", "initials": "L"}, {"family": "J\u00f6nsson", "given": "Erik G", "initials": "EG"}], "type": "journal article", "published": "2012-10-00", "journal": {"volume": "262", "issn": "1433-8491", "issue": "7", "pages": "549-556", "title": "Eur Arch Psychiatry Clin Neurosci"}, "abstract": "The D-amino acid oxidase activator (DAOA) protein regulates the function of D-amino oxidase (DAO), an enzyme that catalyzes the oxidative deamination of D-3,4-dihydroxyphenylalanine (D-DOPA) and D-serine. D-DOPA is converted to L-3,4-DOPA, a precursor of dopamine, whereas D-serine participates in glutamatergic transmission. We hypothesized that DAOA polymorphisms are associated with dopamine, serotonin and noradrenaline turnover in the human brain. Four single-nucleotide polymorphisms, previously reported to be associated with schizophrenia, were genotyped. Cerebrospinal fluid (CSF) samples were drawn by lumbar puncture, and the concentrations of the major dopamine metabolite homovanillic acid (HVA), the major serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) and the major noradrenaline metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) were measured. Two of the investigated polymorphisms, rs3918342 and rs1421292, were significantly associated with CSF HVA concentrations. Rs3918342 was found to be nominally associated with CSF 5-HIAA concentrations. None of the polymorphisms were significantly associated with MHPG concentrations. Our results indicate that DAOA gene variation affects dopamine turnover in healthy individuals, suggesting that disturbed dopamine turnover is a possible mechanism behind the observed associations between genetic variation in DAOA and behavioral phenotypes in humans.", "doi": "10.1007/s00406-012-0313-z", "pmid": "22454242", "labels": {"NGI Uppsala (SNP&SEQ Technology Platform)": null}, "xrefs": [{"db": "pmc", "key": "PMC3464385"}], "notes": null, "qc": null, "created": "2017-05-04T15:00:58.151Z", "modified": "2017-10-16T09:12:02.277Z"}
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Vitamin D2 vs. Vitamin D3. What’s the difference?
Vitamin D2 vs. Vitamin D3. What’s the difference?
There are 13 essential vitamins necessary for good health, and you can get enough of most of them through eating a wide variety of healthy foods. There is one exception to that rule. “A good diet will provide adequate amounts of all the vitamins except D.”1 Vitamin D is actually made by the human body when bare skin is exposed to sunlight. Ultraviolet rays from the sun interact with a specific type of cholesterol found in the skin and produce vitamin D.
Like other vitamins such as vitamin K and B, vitamin D is actually made up of several different forms of the nutrient. The two forms that are used by the human body are vitamins D2 and D3. Since the majority of people do not get enough sun exposure, it’s not uncommon to become deficient in vitamin D, in which case, it becomes necessary to take a supplement. So, should you be taking vitamin D2 or D3 supplements?
Which one is better for you?
To answer this question, you’ll need to understand the difference between the two forms of the essential vitamin. Vitamin D2 can be found in plants; vegetarians or vegans who live a healthy lifestyle and eat a diet high in vegetables are getting more D2.
Although you can get some D3 from consuming animal products such as whole eggs and oily fish, the main way humans get this essential vitamin is through being outdoors and allowing their skin to absorb sunshine. The issue with that concept is that dermatologists recommend using sunblock on exposed skin to prevent skin cancer.
Perhaps the more important distinguishing factor between the two forms of D is that vitamin D3 is more easily converted by the liver and kidneys into the bioactive form of vitamin D that the body needs. The National Institute of Health conducted a meta-analysis on research surrounding whether supplementing with D2 or D3 was more effective at raising the blood serum level of vitamin D. “In conclusion, our results suggest a favoring toward cholecalciferol (D3) rather than calciferol (D2) supplementation with respect to the more effective improvement of vitamin D status.”2
Which one could you use more of?
It’s difficult to get enough vitamin D through natural sources alone and deficiency in the population is rising. In a February, 2020 report, The National Center for Biotechnology Information concluded this: “About 1 billion people worldwide have vitamin D deficiency.”3 Taking vitamin D supplements can help increase your blood serum level of the nutrient. Because it is more easily converted into a useful form, vitamin D3 supplements may be preferred over D2.
Vitamin D deficiency can be more common among people who don’t eat animal products, including the few that contain vitamin D3. In fact, one of the risks of going vegan cold turkey is that there are certain vitamins and minerals that are difficult to get in a plant-sourced diet. Taking a gradual, thoughtful approach to this big lifestyle change allows time to figure out ways to ensure you replace these nutrients.
The vitamins for vegans that VLN offers are 100% plant-based and aimed at supplementing essential nutrients, like vitamin D3, that can be lacking in a diet that includes no meat or dairy.
References
On call: Vitamin D2 or D3?, Health.Harvard.edu.
Comparison of vitamin D2 and D3 supplementation, Ncbi.nlm.nih.gov.
Vitamin D Deficiency, Ncbi.nlm.nih.gov.
NOTE: Harvard Health Publishing, and The National Center of Biotechnology Information (NCBI) have not reviewed or approved the above article.
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Iron storage and detoxification in human ferritins
LEBRUN_U20DTP2
Iron is an essential micronutrient for life, but its reactivity also means that it is potentially extremely toxic, and uncontrolled reactions with O2 can generate reactive oxygen species, which cause cellular damage and death. Indeed, breakdown in cellular iron metabolism is linked, directly or indirectly, to many disease states. Thus, organisms/cells must carefully regulate the amount and form of iron. This is, in part, achieved through storage of iron as a ferric mineral solubilised within ferritin proteins, which are found in all types of cells.
Ferritins are composed of 24 subunits arranged in a highly symmetric fashion to form a football-shaped molecule, in which a rust-like iron mineral is formed. Animal ferritins are composed of a mixture of two types of subunits, H-chain and L-chain, and the H-chain type contains an active site that catalyses the formation of the mineral. The aim of the project is to understand how human ferritins store/detoxify iron, and what the consequences of variable H/L subunit proportions are for this mechanism. New fundamental insight gained through the project will impact on understanding of cellular iron metabolism and its importance for health.
This multi-disciplinary project will be based in the Le Brun lab at UEA, and will involve protein purification, biochemistry, spectroscopy, crystallography and rapid kinetic methods, offering excellent training potential for the appointed student within a supportive and stimulating environment.
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Keto for athletes
Keto for Athletes: Yes or No?
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In our first post, Keto Dieting: Understanding the Basics, we discussed variations of keto dieting and looked at how keto diets affect clinical and non-clinical populations. Overwhelmingly, data suggest that there are health benefits for both populations. However, perhaps the most convincing argument against carbohydrate restriction and keto diets concerns athletic performance due to the athlete’s reliance on carbohydrate for fuel. In this post, we will investigate the role of keto dieting in athletic performance. As a matter of course, instead of searching for the “why or why not use keto as an athlete,” I prefer to take what is an obviously (to me) healthier diet and explore questions such as, “how many carbs can I eat on a keto diet … as an active person or athlete? or “can I optimize my performance while sustaining ketosis?”
The Use and Purpose of Dietary Fuels
Ketogenic diets are severely devoid of carbohydrate. Well, at least that is what we tend to think. From the diet’s inception, it has been restricted to 20-50g total carbohydrate per day. Only recently have a few individuals begun to question if that limit is necessary and under which conditions ketogenesis, and a greater carbohydrate, intake may occur simultaneously.
Why would we do such a thing?! If carbohydrates are bad, then they are just bad, right? And if they are bad, then shouldn’t we want to avoid them all. Period. While still less egregious than making the same association about fat, such as with the last nutritional paradigm, it is not a dichotomous situation. Carbs have a role. Fat has a role. I would argue that fat has a much more important role, but we cannot forget about carbohydrate altogether.
We have essential fats. We have essential amino acids. We have no essential carbohydrates. Still, they are widely considered the “base of human nutrition.” Since you can’t hear my tone in your head, read “base of human nutrition” with a low, sarcastic, and pompous sarcastic tone. In biological terms, “essential” means something that we need to eat because our bodies require it to survive and they cannot manufacture it on their own.
Put differently, without eating fat and protein, we die. Without eating carbohydrate, we don’t die. Are our lives rich and fulfilled? Maybe – it depends who you ask, how long they’ve lived following a carbohydrate-unrestricted eating pattern, their activity/athletic levels, and other factors. Some of you are thinking, “Hey! Fiber!” Fiber is not essential either. It’s fine; it’s just not essential. Sugar is not essential. Starch is not essential. Whole wheat is not essential. Not essential. Not essential. Not essential. Understand?
The Physiological Role of Carbs
Just because they are not essential, does not mean they are useless. Carbohydrates are an energy source. They are used to make ATP, which our cells use to do all the cool things they do. Carbs are our “preferred” energy source because they don’t do anything else, and as a result of circumstance (eating high carb diets), they are observed as being metabolized at high rates – hence “preferred.”
Carbs make ATP now, or they are stored to make ATP for later. If muscle and liver cells are full of glycogen, carbs are converted to fat to be stored, but they are not as easily converted back. Luckily, our metabolisms are flexible, or at least, they are flexible as long as we don’t screw it up!).
Still, the creation of new glucose (gluconeogenesis) is possible, and this process can satisfy all of our carbohydrate needs. It is often said that our brain cells need more than can be supplied through this process. However, that is not entirely true. Humans can fast for hundreds of days and be just fine because any unmet carbohydrate needs are satisfied by ketones. That only leaves the blood cells which require carbs, and when we fast, all our blood does not dry up, so that theory doesn’t hold any water either.
An Evolutionary Aside
If we have essential fats and essential proteins, but we have no essential carbs, which do you think we evolved consuming? Which of the three were available in great enough quantity and frequency to support life such that we did not evolve the processes necessary to create them endogenously?
Bioenergetics, Briefly
Carbohydrates serve as an energy (calorie) source. Most of those living in the United States do not require any more energy than they are already getting. Over 70% of adults are overweight, and this number continues to increase. Calories in, calories out (CICO) is not a bioenergetic law, but it is still a rule that cannot be ignored. Eating too much still yields unpleasant consequences. However, we have to consider the calories out half of the equation.
We are only going to meaningfully increase calories expended (out) via exercise or other methods of physical activity. Certain types of exercise have specific dietary needs. One of the needs can be carbohydrate. There are levels to this.
At rest, we use a mix, about 50/50 to 65/35 of fat and carbohydrate, respectively, for our ATP needs (changes with training status, but even more with diet – up to 100% fat with carbohydrate restriction). As we start exercising, the rate of energy expenditure increases, but the mix stays the same. To a point.
As exercise intensity (speed, weight) increases, metabolic needs start to switch over to anaerobic glycolysis more exclusively. This means we burn more carbs. It’s not that we use less fat, fat burning increases until it “maxes out” then the extra energetic demand is made up from carbs. On a related note, the “fat burning zone” on cardio machines is not the most effective for losing body fat. It is simply an indicator of how fast as you can go before carbohydrate utilization goes up. Consider the recent popularity of HIIT style of exercise. This involves going way over the “fat-burning zone,” yet many feel it provides greater fat loss effects.
The point is that different exercise intensities utilize different fuel sources. At rest, we use about 50% fat 50% carbohydrate, and that changes to nearly 100% fat with keto-adaptation. During exercise, carbohydrates are still required when exercise intensity exceeds the “fat-burning zone.” In practical terms, if your exercise intensity makes you “feel the burn,” you’re using carbohydrates as fuel, and a lot of them. That is a great indicator that you are working hard. However, if the carbs are not available, you have a metabolic barrier to hard work – you can only perform the action if the fuel (carbs) are there to use.
Therefore when carbohydrates are in short supply, exercise performance suffers and higher intensity exercise performance, in particular, is impaired. However, with keto-adaptation, this does NOT appear to be the case. Nonetheless, most studies examining a ketogenic diet still find it detrimental to initial power output – the amount of force a muscle can create in an instant at the beginning of exercise. This adverse effect to power output is completely recovered once carbohydrate are added to a ketogenic diet. The trick is balancing.
A New Rule of Keto for Athletes
Referencing back to part 1 of this series, “a” ketogenic diet is not “the” ketogenic diet. Athletes, individuals with large calories (as carbohydrate) out, have a need for more carbohydrate, and they can maintain ketosis while meeting that need.
One of the first reports of this was indirect. Volek compared the metabolic characteristics of elite endurance athletes consuming a ketogenic diet or a typical high carbohydrate diet. The ketogenic athletes consumed over 80g per day of carbohydrate, equivalent to 10% of their total energy intake. Now consider variance. The exact data is 82 ± 62 grams per day. Thus, while some are keeping their diet strict – “the” keto diet – others are having success eating 140g per day (~2g/kg bodyweight) or more, as that’s only one standard deviation from the mean.
Keep in mind that these are ELITE endurance athletes. This is not for everyone. However, the study highlights a very important point. “The” diet has not been adapted for all populations, and it stresses that exercise, a healthy activity that we should all be doing(!), accommodates greater carbohydrate consumption.
As previously mentioned, my dissertation research included targeted carbohydrate intake as part of participants ketogenic diet. We tested escalating doses of carbohydrate in conjunction with exercise while participants were consuming a ketogenic diet as well. All participants maintained ketosis when consuming 20g pre-exercise, and some (about 10%) maintained ketosis consuming 60g. That is 10g over “the” diet’s limit in addition to the carbs consumed from the rest of their diet. They were eating about 1g/kg bodyweight or half as much as the athletes. As a percentage of calories, the carbohydrate-based controls ate about 50% carbs, 25% fat, 25% protein. The keto diets consumed between 5-15% carbs, 63-70% fat, and 22-25% protein. Ranges are provided to show the base keto diet as well as with the addition of 60g supplemental carbs. Most aspects of performance can be maintained with the base keto diet, but others, such as peak power output, needed at least the 20g added back in. Again, these data are in review.
Population sample is important. In the first example, we have elite athletes, and in the second example, recreationally trained college kids. Although I can personally guarantee that the participants in my study were trained hard, the workload does not compare to the best ultra-endurance athletes in the country. However, the information still helps us establish the pattern. Carbohydrates are activity dependent.
What Carbs Were Allowed?
Although a keto diet can be a carnivore diet, we generally still want to encourage sufficient vegetable consumption. Quick aside: you’re only allowed to be carnivore if you eat liver and other organ meats. In my work just described, all participants had a fiber goal, and in the keto groups, the fiber goal for the men was 18g and 15g for the women. While fiber is generally healthy, in research it is simply used as a marker to indicate diet quality, not so much for its own effects. Since fiber is fermented to fat anyway, I encourage the net carb calculation (total carbs minus fiber). Participants were instructed that the major contributors to their net carb counts should be nuts, seeds, avocado, coconut, olives, and low-carb vegetables, such as broccoli, celery, peppers, onions, salad greens, etc.
For those of you who already do that and want the “extra” carbs for performance, we used a pea starch called Carb10®, which is available as a supplement (disclaimer, I now sell one [as a result, not a cause, of the research] under Archetype Nutrition). I also recommend honey, rice, fruits, and even cookies as other options as long as you are responsible about it.
A Ketogenic Diet for the Healthy
In order to support different lifestyles, “the” diet needs to be adapted. We need to go beyond the rigid limits and let the diet be based on what it produces. A ketogenic diet can have all the characteristics and results of the ketogenic diet while permitting a more flexible and athletic lifestyle.
Encompassed within this, is metabolic flexibility in general. The standard American diet programs our metabolisms to use carbohydrate while “forgetting” how to use fat for ATP generation at high rates. Long term adherence to ketogenic diets can do the same in the other direction. A holistic approach to health involves diet AND exercise. The two are related.
Just as we would adapt a “normal” diet to support athletic activity by modifying carbohydrate consumption, we can modify a ketogenic diet. I would argue that we need to exercise as part of a ketogenic diet so that we can transition into a primarily anaerobic metabolism (that which is used to make ATP for high intensity exercise). We need it as part of any healthy lifestyle, but stick with me.
As previously stated, while keto-adapted we use fat for nearly all of our energy needs. The best way to maintain metabolic flexibility while keto-adapted is to periodically reintroduce carbs. The exercise creates the stimulus for those carbs to be used rather than stored. We train the metabolism to have duality, and we have no negative effects of carbs (such as fat storage, extended elevations in insulin/glucose, etc.).
For the athletes, or the physically active with performance goals, the inverse is true. The exercise isn’t necessary to manage the carbohydrates and metabolic flexibility, the carbs are necessary to support performance. They are the only fuel source that can be used to support high-intensity activity, and athletes need to train at high intensity.
What is the solution to this keto-carb dilemma? Eat enough, but not too much. It’s the same as everything else really. We’re just at a different point on the spectrum than we thought. The best time to eat more carbohydrate is near exercise, so they go in and get burned up without having time to be stored. They are just energy molecules after all. Use the energy, and it won’t be stored.
For the complete scoop on dosing carbs while keto, and for the other 4 new rules, read my e-book, The New Rules of Keto. It is totally free. It is free because these are the things I want you to know. I think it’s vital to the growth of the low-carb movement and our ability as a species to improve our quality and quantity of life! If athletes and other active individuals need not avoid ketogenic diets, is there anyone who should? Find out in part 3!
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Jordan M. Joy PhD, CSCS*D, CISSN is the Director of R&D at MuscleSport. He holds a PhD in Nutrition from Texas Woman’s University, a MS in Applied Sport Nutrition from Northeastern University, a BS in Exercise Science from the University of Tampa, and a 1635+ lbs powerlifting total in the 198 pound class. Jordan has worked as a scientist and coach in both academia and the fitness industry since 2011, publishing over 100 scientific papers, formulating dozens of dietary supplements, and working with over 1,000 clients. His work has primarily been investigating methods to optimize body composition and athletic performance through training, diet, and supplementation, and his athletes include collegiate and professional team sport athletes, elite bodybuilders, and actors.
1 Comment
1. A rather interesting article on keto for athletes with great information. I would like to add a few points, first as a scientist and then as an athlete myself and also working with several athletes who are in keto or carnivore.
From the perspective of science:
Carbohydrates are not the preferred fuel. It is very easy to assume that it is because the moment we eat carbohydrates, the body switches off ketone burning and burns glucose instead. This, most assume, means that glucose must have priority.
However, the truth is that the body must switch to glucose burning, because there is no way to store excess glucose in our blood without toxicity (hyperglycemia can lead to blood glucose toxicity if it is a chronic condition) so it is a literal emergency for the body to get glucose used immediately or if too much was consumed and cannot be used, store it as lactate or convert it to triglycerides. This is so important, that the body has a glucose switch that turns ketone production on when the blood glucose level drops to or below 80 mg/dL (4.44 mmol/L) and turn on the other fuel (ketones), while when the blood glucose exceeds 99 mg/dL (5.4 mmol/L), it immediately switches off ketone burning and moves to glucose burning.
While we certainly have a few organs that can only use glucose for fuel, red blood cells are among those because they lack mitochondria, there is no organ in our body that requires so much glucose that gluconeogenesis cannot produce enough glucose, and therefore we must eat carbs. We have 2 sources for glucose from not-carbohydrate diet: protein is what obviously everyone thinks of, but our stored fats are in triglycerides form. Each triglyceride has a glycerin cap, which is converted to glycerol via glyceroneogenesis, and glycerol converts to glucose. And while it is assumed that it is not easy for our body, it is exactly as hard as converting protein to glucose, and so it happens all day long.
While we certainly make ATP out of glucose—be it from carbs or from protein—we also make ATP out of fat. Our mitochondria cannot distinguish between the sources of Acetyl-CoA, which is what all of these macronutrients convert to before the mitochondria can generate ATP. So from the perspective of our energy-machines, it makes little difference which energy form is used—except that from fat/ketones much more ATP is generated than from carbs, and with less oxidative stress.
From the perspective of an athlete:
I weightlift and work with many endurance athletes—all of them migraineurs, since I specialize in migraines. My athletes—and me—are always in ketosis. I find the literature—Phinney and Volek—fascinating, because it doesn’t hold for any of us migraineurs. In fact, many of us sometimes must go out of our ways to get out of ketosis—like before a medical procedure—and are unable to. This summer I really wanted to come out of ketosis to see how I would manage migraines after years in ketosis and a ton of healing, and even eating 100 gr carbs a day didn’t get me out of ketosis. And some of the carbs I tried were not “keto friendly” carbs. I ate ice cream, sweet potatoes, cherries, watermelon, peaches, nectarines, and similar, very specifically to see if I would be kicked out of ketosis. We also don’t come out of ketosis from exercise.
I am not sure how people come out of ketosis since I have not been able to, nor have any of the migraineurs I talked to ever so far could. The only time it seems everyone comes out of ketosis for a short time is from very high stress (death in the family or similar) or medications—such as corticosteroids. In fact, I noticed that after a high-carbs meal (100 net carbs grams) my blood glucose may increase to 120-130 (at the beginning as I started to eat fruits, it jumped much higher), and my blood ketones will at first increase. This increase has not yet been reported anywhere else. It represents the backed-up ketones by the sudden switch off from using ketones as a result of increased glucose and insulin activity in the blood, while the liver is still making ketones for a few seconds longer. I found that after eating carbs like this, my blood ketones will land at 0.5-0.6 and won’t budge while I use up all excess blood glucose. Once the excess glucose is used up, my blood ketones start to be used again.
Of course, if one measures ketones in urine, that will likely show zero for those who use ketones efficiently. In urine only the ketone overflow—those produced but are not used—are released.
As an athlete, lifting weights, ketosis I am told is not ideal because it is an anaerobic activity. I found that to be false to some degree. While, indeed, I am sure that one uses glucose lifting very heavy weights all of a sudden, there is plenty of time for gluconeogenesis between sets—hence the need to wait for a minute or two between sets—and glucose is replenished via gluconeogenesis very quickly in that time.
Endurance athletes face the challenge of running out of stored glycogen—400 Calories (100 gr) in the liver and 1600 Calories (400 gr) in the muscles. It takes about 2 hours to run out of this fuel, depending on the athlete. In my keto migraine group several marathoners, ultramarathoners, triathletes, ironman, etc., have ran/swam/biked their races—some well over 2 hours and not one needed to supplement with carbohydrates. My recommended “gel pack” equivalent for them was made of soft cheese mixed with hardboiled eggs and salt in little packets to be able to squeeze into the mouth like gel, and to drink salted water all through, and drink milk (if they are milk drinkers, and most migraineurs are) or eat meat after the race. So far, every single athlete completed whatever race they entered with great success, without bonking, and, most importantly, without migraine.
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About Your Visit
Detect Eye Problems Before You Have Symptoms
Vision test
Eye exams aren’t only for people with poor vision. They’re an important way of detecting eye problems before you have symptoms. Eye doctors can also catch other health problems — like diabetes and glaucoma— early.
WHAT TO EXPECT
After filling out paperwork, you’ll go to the examining room to meet the doctor. Here are some things you can expect.
You will be asked about your general health, medicines you are taking and any family history of eye diseases.
You’ll read from charts of random letters. Your doctor may also test other aspects of your vision such as your peripheral (side) vision, and color perception.
You will be tested to check the pressure in your eye with a device called a tonometer. Tonometry tests for glaucoma.
The exam will closely evaluate different parts of your eye with a device similar to a microscope called a slit lamp.
You will probably get drops to dilate your eyes: to make the pupils open wide. This will help your doctor get a clear view of the inside of your eye most notably the retina and macula. Dilation makes your eyes sensitive to light for a few hours. You’ll need to bring sunglasses and wear them after the exam until the drops wear off. You may need someone to drive you home if you do not feel safe driving.
Depending on your eye condition, you may need other additional tests or exams.
Patient Forms
Many of our files require Adobe Acrobat.
Adobe Reader notification
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Subscribe to our Newsletter
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How much water should I drink
How much water should I drink?
HOW MUCH WATER SHOULD I DRINK EACH DAY? IS ONE OF THE MOST POPULAR GOOGLE SEARCH TERMS IN THE WORLD.
Unfortunately, there’s no hard and fast rule when it comes to hydration. Aside from helping digestion and absorption of food, water regulates body temperature, carries nutrients and oxygen to cells and removes toxins and other wastes. Water also cushions joints and protects tissues and organs, including the spinal cord, from shock and damage. Conversely, lack of water (dehydration) can be the cause of many ailments.
The human body is made up of 55% – 75% water, which means water is essential for all of our bodily processes. However, why is it that nearly two-thirds of us are chronically dehydrated?
You can become dehydrated by not drinking enough water, and you can also cancel out the water you have consumed by drinking a sugary soft drink, caffeinated drinks and other drinks which have a diuretic effect. These diuretics promote the loss of body fluids which can lead to dehydration.
You’ve probably heard the 8×8 rule (8 glasses, 8 ounces/250ml each) as the answer for how much water to drink, however, there’s no official source or specific evidence for this recommendation. Water requirements vary from person to person and even from day to day for the same person. Consider this: you’ll need to drink more water after running 10 miles than when you’re relaxing at home. If you take a vacation to a hotter climate and perspiring a lot, your body is losing bodily fluids more rapidly which means you’ll need to increase your water intake.
Learning to tell the more subtle signs could be the difference between satisfactory health and radiant health—many doctors even believe that dehydration is a leading cause of diseases.
It’s best to listen to your intuition, common sense and pay attention to the signs that your body gives you.
Three signs your body is telling you to drink more water:
1. You’re thirsty.
If you wait until you’re thirsty, you may already be dehydrated (especially after physical exertion, during which your body loses a lot of water through sweat). It’s better to drink a generous portion of pure water regularly throughout the day to take overthinking out of the process. If you’re going to do physical exertion in the next 24hrs increase your intake to pre-empt the dehydration process and also reduce that thirsty feeling.
2. Your urine is a dark yellow.
For optimal health, urine should always be a pale yellow colour. If it’s darker, it means that your kidneys are retaining fluids. In turn, this can mean a greater percentage of your urine is made up of toxins and other excretions. Because of this fluid retention, you’ll pee less often while still being dehydrated. Some people complain about having to urinate frequently when they drink a lot of water. The reality, though, is that a healthy, well-hydrated person will urinate at least 7 or 8 times a day—the inconvenience of which is far overshadowed by the dangers of dehydration.
3. You suffer from headaches, digestive problems, heartburn, fatigue, high cholesterol, confusion, anxiety, irritability, urinary tract infection or signs of premature ageing.
These can all signal chronic dehydration. If you suffer from any of these symptoms, make a conscious effort to up your water intake and see if they’re alleviated. And of course, consult a professional if they continue.
Make sure you’re drinking the right kind of water
Once you have your personal water needs figured out, you need to ensure that you’re drinking clean, nourishing water.
I wish that I could say that any water is good water (maybe that was the case a long time ago), but in reality, both tap water and bottled are often dangerous toxin sources. In some cases, bottled water is even worse than tap water.
It can be said that the body will not retain impure water as effectively. This means even if you think you’re drinking enough water but still feel dehydrated, you may need to upgrade your water source. Drinking nutrient-rich, alkaline water without fluoride such as AlkaWay water can be beneficial in your body getting the most benefit from the water that you’re drinking. It’s a very common response from the friends of people who have begun drinking AlkaWay water to comment “Oh, you look so… juicy!”.
Water: the most neglected nutrient in your diet but one of the most vital.
Learn to listen to your body. You’ll be able to make choices that are more aligned with your health needs. And the better shape you keep your body in the more equipped it will be to send you accurate signals about what it needs. It’s a virtuous cycle.
Hydration is a perfect context for practising this kind of self-listening because the signs are so easy to discern. Doing so with regularity will enable you to live consciously, brightly and vibrantly.
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Kidney & Heart, study & practice
Kidney & Heart, study & practice
Index
IMMUNOSUPPRESSION & TOLERANCE PARADIGM SHIFT PROTOCOLS
Immunosuppression in Kidney Transplant Programme and Paradigm shift to Tolerance
Contents
1. Cellular and humoral mechanism
2. Transplant tolerance
3. Complete tolerance - congenital, acquired
4. Prope tolerance
5. CAR-T therapy for tolerance
6. References
7. TK TRANSPLANT Protocols
____________
1. Cellular and humoral mechanism in physiology, rejection and tolerance
The figure explains basic immunological behavior of lymphoid tissue toward self and non-self antigens during embryogenesis and in adult life. It also shows the mechanism of graft rejection and strategies of graft tolerance.
Mechanism of rejection and strategies of tolerance.
Mechanism of rejection and strategies of tolerance.
_____________
2. Transplant tolerance
Transplant tolerance is defined as a state of donor-specific unresponsiveness to the allograft without a need for on going pharmacologic immunosuppression. These strategy could eliminate many of the adverse events associated with immunosuppressive medicines.
• In embryogenesis, mechanism of T-cell tolerance is the clonal deletion of auto-reactive T-cells in the thymus, haematopoietic and other lymphoid tissue, to the foetal antigens so that the organism is rendered self-tolerant to self-antigens. Therefore there is clonal expansion of T-cells, not exposed to exogenous antigens, and not reactive to the foetal antigens.
• In ex-utero life, the process of deletion is reversed to the state of proliferation on exposure to exogenous antigens whether organ or organism.
• Against organism, survival of the individual depends on antimicrobial agents and protection depends on vaccination.
• For grafted organs, we need immunosuppression unless state of tolerance is achieved.
• Since, the whole process of immune identification and rejection is carried out by haematological immune cells, the principle guide to tolerance, the suppression of this mechanism is the hall mark of graft maintenance and possible tolerance.
• In theory and practice, there are three strategies of achieving tolerance:
1. Complete tolerance: achieving a state of haemochimerism of recipients and donors lymphoid tissue.
2. More recent, prope or near tolerance where immune-reactive t-cells are eliminated or inhibited.
3. The most recent, CAR-T therapy using t-reg cells, engineered for ablating t-cell immune-reactivity through anergy.
Proposed Tolerance protocol for low immunogenic riskLRD
Proposed Tolerance protocol for low immunogenic riskLRD
_____________
3. Complete tolerance
• Congenital complete tolerance takes place in Transplant between monozygotic twins as there is no immune-reactivity between the twins because of genetic similarities (1).
• Acquired complete tolerance was achieved anecdotally in multiple myeloma cases where total bone marrow, and lymphoid ablation was obtained by whole body irradiation and chemotherapy, followed by donor specific bone marrow transfusion to repopulate the recipients marrow and lymphoid tissue before renal transplantation – a form of haematological chimerism (2). As the immunogenic t-cells belong to the renal donor, complete tolerance is achieved. Even though, not a reality in clinical transplantation yet, experimental animal transplantation is promising.
____________
4. Prope tolerance
Two types of prope or partial tolerance are currently known.
• i) Pioneered initially by Dr Calne with use of Campath 1H (Cambridge University Pathology) in clinical organ transplantation. It showed achieving a partial tolerance where allografts could be maintained with minimal immunosuppression. Campath 1H is a humanised chimeric rabbit monoclonal antibody against human CD52 lymphocyte receptor, where Fc segment of rabbit IgG monoclonal antibody is replaced by human Fc segment. CD52 antigen is present in all lymphocytes. Thus administration of campath causes lymphocyte depletion for long time. Later new lymphocytes, generated from lymphoid tissue, behave like niave lymphocytes to the grafted organ. As such, do not show marked rejection response to the foreign organ. Two IV administration of 20 mg at 3 months interval, achieves ablation of lymphocytes for long time, allowing the recipients lymphoid tissue to repopulate with lymphocytes, naïve to the allograft. Thus achieving immune tolerance. INTAC, 3C and similar studies showed promising results for minimising long-term immunosuppression (3).
• ii) More recently with newer unique mab against co-stimulatory signal inducing TCR (CTLA-4, CD28, B7, CD137), t-cell co-stimulation (signal-2) is blocked inducing t-cell anergy.
BENEFIT study used Belatacept, a selective co-stimulation blocker which is a human fusion protein combining extracellular portion of cytotoxic t-lymphocyte associated antigen 4 (CTLA-4) with Fc of human IgG1, showed prope tolerance in phase 3 trial (4).
_____________
5. CAR-T therapy
Principles of CAR-T therapy:
1)Anti cancer therapy: Immune cells (T-regulator cells) from patient’s blood (i.e. Acute lymphobkastic leukemia) is drawn and equipped with a Chimeric Antigen Receptor (CAR-T). The antigen receptor is a genetically engineered receptor (mostly a monoclonal antibody against the antigen. The antigen is the target cell surface protein i.e. lymphoblastic cell surface antigen). The mRNA producing the mab is synthesized in laboratory. It is incorporated in a harmless virus used as vector. The virus containing the genetic sequence is then transfected in patient's T-reg cell. Thus T-reg cell is converted into a CAR-T cells. These cells are multiplied to a million count, and then transfused back to the patients blood stream. The CAR-T cells containng the mab get attached to the surface antigen of i.e. ALL cells, and destroy the cancer cells. The receptor binds itself to a specific protein on the cancer cell and activates the CAR-T cells to kill the cancer cells.
2) CAR-T therapy in transplant tolerance using Chimeric Antigen Receptor for regulatory T-cells (T-reg): When you can block Signal-2, there is T-cells anergy, and fail to induce graft rejection.
Signal-2 is known as Co-stimulatory signal: APC surface antigen B7-1 & 7-2 get attached to TCR CD28 (homologous to CTLA-4), of T-cell receptor. Upon this signal-2 activation, the lymphocyte, which could be either T-4 or T-8 cell, is activated when CD3 of the T-cells is activated by corresponding antigen of APC. The T-cell proliferation occurs, to cause graft rejection. Therefore, blocking signal-2 either by monoclonal antibody against CTLA-4 antigen or APC B-7 antigen, T-cell activation can be blocked and you get tolerance by so called T-cells anergy.
BENEFIT study used Belatecept (mab against B-7) for this purpose.
This mab can be delivered by CAR-T cell to the target cell antigen CTLA-4 on the surface of T-cells to block attachments with B-7 antigen of APC instead of iv Monoclonal antibody (Belatecept). Thus produce same kind of T-cell anergy producing tolerance. This is explained below:
CAR-T (virus containing the genetically engineered mab forming mRNA against CTLA-4 antigen, is transfected to patients isolated T-reg cells), multiplied and transfused back to patient during transplantation. This CAR-T cells containing the mab against the CTLA-4, find the T-cells containing CTLA-4 antigen on their surface and blocks it. Thus APC containing the graft antigen with their B7-1 & 7-2 surface antigen can not bind to the CTLA-4 antigens as they are already occupied by mab from the CAR-T. Thus, co-stimulation as described above is blocked and T-cells activation and proliferation does not occur, resulting in tolerance.
Most recently, this research on CAR-T therapy targeting T-reg (regulatory T-cells) has been pioneered. The genetically engineered T-reg cells are aimed to block co-stimulatory signaling receptors as mentioned above. Thus blocks T-effector cell up-regulation. The readministered genetically engineered CAR-T-reg cells with receptor (mab) component for CTLA-4 antigen of T-cell as described above, blocks CTLA-4, making them unavailable for binding to B7 antigen of APC, resulting in absent co-stimulation, and thus induce T-cell anergy to CD-3, CD-4 and CD-8 lymphocytes. This is akin to induction of tolerance in organ transplant. This has been shown to be effective in skin, islet cell graft and has been speculated to be effective in inducing tolerance in renal and liver allograft (5).
_____________
6. References
1. Brown JB. Homografting of skin: with report of success in identical twins. Surgery. 1937. 102:558.
2. Bühler LH, Spitzer TR, Sykes M, et al. Induction of kidney allograft tolerance after transient lymphohematopoietic chimerism in patients with multiple myeloma and end-stage renal disease. Transplantation. 2002 Nov 27. 74(10):1405-9.
3. Michael J. Hanaway, M.D, E. Steve Woodle, M.D., Shamkant Mulgaonkar, et al. Alemtuzumab Induction in Renal Transplantation. For the INTAC Study Group. N Engl J Med 2011; 364:1909-1919, DOI: 10.1056/NEJMoa1009546.
4. F. Vincenti, B. Charpentier , Y. Vanrenterghem, et al. A Phase III Study of Belatacept‐based Immunosuppression Regimens versus Cyclosporine in Renal Transplant Recipients (BENEFIT Study). https://doi.org/10.1111/j.1600-6143.2009.03005.x (accessed on 13 January 2019)
5. Qunfang Zhang, Weihui Lu, Chun-Ling Liang, et al. Chimeric Antigen Receptor (CAR) Treg: A Promising Approach to Inducing Immunological Tolerance. Front. Immunol. 9:2359. doi: 10.3389/fimmu.2018.02359.
6. Suhail SM, Woo KT (2020) Paradigm Shift to Tolerance from Conventional Immunosuppression in Renal Transplant: A Basic Strategy through Lymphocyte Depletion. J Nephrol Ren Dis 4:121.
____________________________
Points for immunosuppresion for engraftment.
Points for immunosuppresion for engraftment.
7. TK IMMUNOSUPPRESSION PROTOCOL currently in vogue for different types of kidney transplantation
All protocols are summarized by the author of TK IMMUNOSUPPRESSIVE TRANSPLANT Protocols in the following images:
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Vegetable high in protein
Vegetable high in protein is contrary to a world hungry for increasingly more animal products. In the West there is a decline in the demand for pork and beef, but that for chicken and fish is rocketing.
These broad bean flowers are the promise of vegetable high in protein.
This page was last updated by Dr Barrie Lewis on 25th April, 2019.
Broad beans are the richest vegetable high in protein; they are also the best source of L dopamine. A couple tablespoons per day is enough to supply many Parkinson's patients with sufficient of this hormone. The bright white flowers with their black centres are beautiful.
How to plant broad beans is for all of us who want to live a long life free from the degenerative neurological diseases.
Cattle can get much of their protein from grass by ruminating, but chickens and pigs rely on legumes for their amino acids, and in particular soyabeans. For this reason, the demand for vegetables high in protein for animal feed has risen by fifty percent in the last ten years, and will continue to soar.
But this page is not about animal feed; it concerns those humans who like their meat, but want to get an increasing amount of protein from their veggies; and that means more legumes, and more specifically pulses.
The World Health Organisation has recently declared, after scientists scanned the best research, that processed meat like bacon is definitely a potential cause of metastatic disease, and all red meat "probably" is. (1)
And so the Western World is wisely slowly weaning itself off of burgers and turning to fish and fowl; a colorectal malignancy isn't pleasant.
Vegetable high in protein
Enjoy vegetable high in protein so you don't fall on your own sword; that's what having bacon and a frankfurter every morning for breakfast, ham for lunch, and a steak for dinner is.
How much red meat is healthy remains undefined; perhaps twice a week, but certainly not more than once a day.
Vegans won't be reading this page; they already know the answers. But if you like me enjoy red meat periodically but have a deep desire to reach old age without serious illness, then these are important matters to consider.
For the chiropractor those enjoying vegetable high in protein are also far less likely to be obese; that's important for the joints that we treat every day.
Pulses are those legumes that we humans can enjoy for our protein; they are found in pods like the bean and pea.
Our hens in the garden go crazy over pulses, but unlike us they can also get their protein from other legumes like alfalfa and clover.
2016 is officially the year of the pulses, but really this century should have been wholly dedicated.
Increasing world production of pulses at 50 percent every ten years, as has been happening, just to be fed to animals, isn't sustainable. Very soon, not because we choose to eat less red meat, but because we're forced to, those legumes are going to be mainly for human consumption.
And that's not a bad thing; they are a far healthier source of protein than cattle and pigs; and substantially cheaper too.
There are sound permaculture reasons for growing pulses for human consumption too; legume lovers require much less water from the environment than those demanding red meat every day; the cattle need a lot extra.
One big plus about growing pulses, and legumes in general, is that nitrogen producing bacteria attach to their roots, enriching the soil lessening the need for inorganic fertilizers.
Another reason for enjoying vegetables high in protein is their fibre; pulses are rich in both forms. The soluble type is especially important as it absorbs water giving the stool bulk; they also reduces the absorption of animal cholesterol in the gut, and stabilise blood sugar. That's vital for all of us and not just diabetics; surges in glucose provoke an insulin surge storing it as adipose tissue.
Pulses have a very low glycemic index; they have little effect on blood sugar when consumed.
That means that pulses can be enjoyed on the paleo diet, but banters still must avoid them if they are following the rules to the letter; they must aim for almost zero carbohydrate. People who get much of their protein from legumes are rarely if ever fat.
There's plenty of research showing that both forms of fibre, also found in 100 percent whole grains, reduce colorectal cancer and other bowel diseases. It's also important for those undergoing chiropractic help for a slipped disc; bearing down on the toilet is very painful.
100 percent whole grains have a substantial amount of protein too but typically half of that in most pulses. However most flour is refined and has much less.
Broad beans have the highest protein; about four times that of most other legumes.
Pulses are particularly rich in the B vitamins, and many important minerals including the anti oxidants magnesium and zinc. Women of child bearing age need to be enjoying them for the large amount of iron; a deficiency is the chief cause of tired all the time syndrome.
In short, vegetable high in protein like our pulses play a very important role in preventing cancer, obesity, type 2 diabetes and heart disease.
Probably my favourite green pulses are beans and peas, and dried chickpeas for making hummus.
We plant broad beans because they are so easy to grow in both spring and autumn, and are the highest in vegetable protein; reap them when they are still young and tender.
This authentic hummus recipe made with chickpeas is our favourite vegetable high in protein.
Tree nuts
Tree nuts too are rich in protein; what's more they are not contrary to popular belief particularly fattening, and are especially beneficial to those who are diabetic or suffering from metabolic syndrome; they help to stabilise the blood sugar.
Pecans nutrition is my favourite, though walnuts are especially high in omega-3 fatty acids; they help reduce inflammation in the body; obviously that's also favourable to those undergoing chiropractic treatment.
Hens
The consumption of chicken meat has risen by over 50% since the turn of the century. Much of the legumes grown are going to feed the hens; they are highly efficient converters of dietary protein thus the industry is demanding more vegetable high in protein for the fowls.
Food waste can be fed to worm farms which then make wonderful protein for chicken feed.
It's just another part of backyard permaculture; working with nature rather than against it.
A chicken farm is another source of protein.
Which of these chickens would you rather enjoy for dinner? Actually we're not eating those below; we just enjoy their bright orange yolked eggs. They are feasting on a couple of shovelfuls from the worm farm.
Even in a small garden you can entertain yourself with the wonder of worm farms; if you don't have fowls, toss them in the compost heap. They will devour all your kitchen waste.
Eggs from these free range chickens enjoying their breakfast from the worm farm provide excellent supplement to vegetable high in protein.
Chicken tractors
Egg laying hens demand a lot of greens; one way to make plentiful vegetable waste available to them are these chicken tractors. Make sure it's placed over clover periodically for vegetable high in protein.
Their chicken litter provides a fertilizer high in nitrogen for your plants.
Nitrogen fixation bacteria
Proteins are made up of a string of amino acids; they have an amine group which contains a nitrogen atom. Nitrogen fixation bacteria that attach to the roots of legume plants enable them to capture this vital element from the atmosphere, and become a vegetable high in protein.
Lightening contributes nitrogen to the soil to a lesser extent.
It is the work of these bacteria on legumes that enables them to become a vegetable high in protein.
It's not a subject we want to hear but there is now abundant evidence that processed meat is definitely cancer causing; it's in Group 1 along with tobacco and asbestos, though the risk is lower.
And ordinary red meat is in Group 2A and "probably" is. The WHO stresses that the evidence is not conclusive, as there could be confounding factors, but the suggestion is that a 100 gram portion eaten daily would increase the risk of colorectal tumours by 17%.
So we are faced with introducing vegetables high in protein to the dinner table, or getting metastatic disease; it's not comfortable for me either, a lover of red meat. So, to our mutton stew we add chickpeas, bacon is kept for high an holy days and we never eat polony and frankfurters. You plot your own course.
Chiropractic
Why all this about vegetable high in protein on a chiropractic website, you may be asking. Those on an inflammatory diet do not respond as well to our treatment; or to any other for that matter.
1. Chiropractic Help
2. Avocado Benefits
3. Vegetable high in protein
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Interesting challenges of the day
1. Mr S is a 76 year old man with neck pain of some 9 months duration. Luckily, most of the discomfort is upper cervical which is only rarely arthritic; his lower cervical spine is a degenerative mess that I've left alone. After seven treatments his pain and stiffness is 50 percent better, and he's happy in the circumstances. He can sleep through the night now and that makes a huge difference.
2. Mr P is 32 year old man with very severe lower back pain radiating to the big toe which is 30 percent numb. He had an episode three weeks ago, took anti inflammatories and was soon better as is typical of the medial disc herniation. But before it healed, after a trivia it came roaring back, much worse. The characteristic crossed sign was evident; sitting in a chair, straightening the right leg provoked severe left back pain and tingling in the leg. He's doing well.
3. Severe lower back pain is scary; just ask Mrs P. Just watching her get out of the car I she was in trouble; she had a slipped disc at L4 making her lean towards the opposite side; luckily she had no pain in the leg. Despite family pressure that this was far too severe for a chiropractor, she persevered. Within five days she was standing upright, and after two weeks almost painfree.
Despite a hectic job, she wisely took my advice and stayed home for what I call exercising bed rest.
4. Mr S has had lower back, groin and back of thigh and calf pain for fourth months.
He has a pincer deformity in the hip causing the stabs in the groin, and a degenerative facet causing the sciatica. Both are responding well to chiropractic and he's well pleased; sixty five percent better after three treatments.
5. Mr T is a wise man; he's taken a warning TIA seriously and has lost 15 pounds, and has at least as much again to lose. A change to a low starch diet and half hour daily walk has made the difference; but the walking is making his foot and back miserable. The expensive orthotic is hopeless; luckily his hips and back are fine, but he needs a simple heel lift.
6. I too have had serious lower back issues, luckily fixed by my own chiropractor; so I too have to do my exercises, take care when lifting supers full of honey, gardening and using the chainsaw. Regaining the function of your spine is just as important as the pain.
7. My own granddaughter, only 7 is hypermobile giving her pelvic, knee and ankle issues. Xrays show a mildly dysplastic hip. Years ago we would have called it growing pains. She too regularly needs chiropractic care and luckily responds well. Increased range of motion is more difficult than too stiff in my opinion. Our care is for kids too.
8. This 65 year old lady is a serious gardener; every day she is bending, lifting and digging for 2 to 3 hours a day. It regularly catches her in the sacroiliac joint, so she has a treatment once a month that sorts it out. She does her lower back exercises faithfully.
9. This 88 year old lady is an inspiration; every day she is busy in the community. With a nasty scoliosis she manages very well with a chiropractic adjustment every six weeks and exercises faithfully done.
10. Mr X is a 71 year old retired man who wants to continue with maintenance care every six to eight weeks; he had suffered from two years of lower back pain when he first came a year ago. He has no discomfort now after 8 chiropractic treatments, but is aware that danger lurks.
11. Mrs C has been having severe headaches, and taking a lot of analgesics. It's a non complicated upper cervical facet syndrome, and she's doing well.
12. Mr D is a 38 old year man with chronic shoulder pain after a rotator cuff tear playing cricket. It responded well to treatment, but he knows he must do his exercises every day; for two years he couldn't sleep on that shoulder.
13. Mr D, a 71 year old man, has a severe ache in the shoulder and midback since working above his head. Trapped nerve tests are negative but he has advanced degenerative joints of Luschka; after just two treatments he is 50 percent better. Can we reach 90?
And so the day goes; chiropractors shouldn't be treating the elderly most medical sites state but that's so much bunkum.
Have a problem that's not getting better? Looking for a different slant on your pain? Want to pose a question?
Interesting questions from visitors
CLS writes:
Greetings, Dr B.
You helped me quite some time back with a soothing and professional response which turned out to be exactly correct. I now consult a local chiropractor. You write a superb newsletter, too.
Your own unresolved problem. Pose a question
Knowing that up to 70% of the time the correct diagnosis is made with no examination, no special tests, no xrays, but just from the history, there's a fair chance I can add some insight to your unresolved problem. But at least 30% of the time, I may be quite wrong! Give plenty of detail if you want a sensible reply.
You visited this chiropractic help site no doubt because you have a problem that is not resolving and want to know more about what chiropractors do.
The quickest and most interesting way is to read one of my ebooks of anecdotes. Described by a reader as gems, both funny and healthful, from the life and work of a chiropractor, you'll love them. Priced right at $2.99, though Kindle fiddles the price without telling me.
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Home » Posts tagged 'Dental Care'
Tag Archives: Dental Care
Why Do People Need a Dentist?
Dentists are experts in the area of oral health. They help people to maintain their teeth and gums by cleaning and repairing them. Dentists also provide other services, such as filling cavities and extracting teeth.
The dental profession is growing rapidly, with more people seeking dental care every year. This is because dental problems can be painful and debilitating, and can lead to other health problems if left untreated.
Dentists at https://smilesofelgin.com/ recommend regular visits to keep your teeth and gums healthy. If you have any questions about your oral health or want to schedule an appointment, please contact your dentist's office.
There are many reasons why you might need to get dental implants for your teeth. Some of these include: If you have lost all of your natural teeth because of decay or injury, replacing them with dental implants may be an option that can restore a smile and improve your appearance.
Dental implants are made up of very high-quality titanium, which is stronger than gold and more durable than most other metals. They are created by placing a tiny rod into the jawbone and then inserting a screw into the rod.
The screw is attached to a small plate that fits perfectly over the tooth root, giving it stability and forming a bridge between the implant and the tooth root.
The implant will remain in place permanently when it is attached to your jawbone. The stability of the implant will allow you to smile with confidence. Once your implants are placed, they can be used for the rest of your life.
Basic Dental Care: Essential Information That You Should Know
The way to save on dental therapies in a time as it has grown into an expensive affair in the majority of the nations? Everyone may have asked this question a few days before going for remedies. There are a lot of means by which you can save on the remedies. Among the very best methods for affordable cheap dental remedies would be to visit states like Hungary and Poland, in which remedies are extremely low. You can find the best and affordable dental care at https://comfortdentalframingham.com/.
The therapy of the teeth is an expensive affair in several nations like the UK, France, Germany, the US, and Canada. But today, dental tourism has boomed considerably and you could get cheap dental remedies, far under the treatment price you need to incur in your country.
Dental Hygiene Birmingham - St. Pauls Square Dental Practice
Image Source: Google
An individual can save approximately 75 percent of the treatment price when picking affordable treatments overseas. Cosmetic cleansing, implants, root canal treatments, crowning, bonding, and bonding will cost you a lot less when picking affordable dental hygiene overseas, particularly in countries like Hungary.
When picking affordable treatments overseas, you don't need to be worried about the treatment and attention. The dentists are globally recognized and are easily accessible for any consultation. Equipped with the latest gear, the dental practices overseas will also be much reputed and preserve global standards. The team is quite cooperative and societal in every facet.
You could even save on therapies throughout the medical insurance policies. As dental tourism has thrived, the majority of the medical insurance providers have comprised cheap dental treatments overseas in their own policies. When you select a medical insurance plan, ensure the treatment in the dentist can be contained inside. Additionally, you can find private dental insurance policies that assist with saving on dental remedies.
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Get The Guinea Hen Weed and Sinusitis Answers you Need
Get the facts about Guinea Hen Weed and Sinusitis. As alternative medicines and holistic healing become more and more popular due to the medical community’s increased dedication to studying its ability to cure disorders thought to be incurable or curable with the use of expensive medicines.
With citizens around the world feeling the crunch of harsh economic times, the number of those seeking natural methods to heal themselves has risen. Patients no longer have the means or the access to high priced medical treatments with all of the bells and whistles. If you suffer with Sinusitis, prepare to be wowed by Guinea Hen Weed benefits – a natural herb considered by many, the Guinea Hen Weed Cancer Cure.
The Guinea Hen Weed and Sinusitis Connection
Guinea Hen Weed and Sinusitis have developed a symbiotic relationship based on this demand. For centuries now in the countries where it is indigenous, the tea has been thought to have the ability to cure many disorders that have confounded modern medicine. Caribs living in Guatemala have already linked the two, using the Guinea Hen Weed Plant to treat the affliction.
From diabetes to cancer to intense birthing pains, this tea is thought to aid those suffering. Sinusitis is often caused by infection, which increases the link between the herb and sinusitis because the herb is often used to treat infections in other areas of the body. Guinea hen weed has also been proven to reduce bacteria and fungi, which are also linked to sinusitis.
So, what is the correlation between the two? Guatemalan herbalists have been known to crush the plant’s roots and breathe it in through the nasal passages. This is thought to relieve the inflammation of the nasal cavities. The relief that is delivered to the patient by using this method of treatment is said to last a very long time.
There is a specific way to go about making the concoction. Those who wish to go this route are encouraged to pick several leaves and put them to dry. Once the leaves are dried, they are then ground up into the tiniest fractions possible and left in a glass bottle.
Once leaf particles are safely encased in glass bottle, add 2 or 3 droplets of shilling oil and a quarter of a teaspoon of white rum. After doing so, allow the mixture 24 hours to settle. Once it has settled, inhale through your nostrils. There’s also always the more popular form to take it internally through Guinea Hen Weed Tea.
Guinea Hen Weed and Sinusitis Conclusion
Herbalists and holistic healers have long made the connection between Guinea Hen Weed and Sinusitis relief. As doctors become more educated and pass their knowledge along to the people, the usage of guinea hen weed for sinusitis relief will certainly become more widespread. Countries where the herb is indigenous have already been implementing the herb for a variety of maladies for hundreds of years. Research is a never ending process and should be able to provide new treatments connecting Guinea Hen Weed and Sinusitis.
We’ve found top sources to buy Guinea Hen Weed.
Continue reading for further insight on Guinea Hen Weed Side Effects.
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Spinal Tap Test and Multiple Sclerosis Diagnosis
spinal tap (also known as lumbar puncture) is one of the tests used to diagnose multiple sclerosis (MS). The test is done in a hospital or clinic setting where a small sample of the cerebrospinal fluid (CSF) is collected, using a thin needle, from the lower lumber region (lower back). A sample that shows abnormal results in proteins and inflammatory cells may indicate MS.
Besides MS, this test is used to confirm conditions such as meningitis, Guillain-Barre syndrome, or brain and spinal cord cancers.
Getting a spinal tap
CSF is clear liquid that acts as a cushion, protecting the brain and the spinal cord. Usually, this fluid is colorless and has the same consistency as water. Nutrients, and substances as well as waste products from the brain, move through cerebrospinal fluid.
Before the test, your may be asked to take a computerized tomography (CT) or a magnetic resonance imaging (MRI) scan to make sure that this test is necessary. Tell your doctor if you’re taking blood-thinning medication (anticoagulants).
You will be asked to wear a hospital gown and likely will be told to lie on your side with your legs pulled up to the chest. The position flexes and spreads the vertebrae, so the doctor can more easily insert a needle between two lower lumbar-region vertebrate. (You will have already be given a local anesthetic to numb the area.) A thin, hollow needle is inserted, passing between vertebrate and through the spinal membrane into the spinal canal.
CSF pressure is measured, and a small fluid sample is collected for analysis, then another measure of fluid pressure is taken. While the needle is in, you may feel some pressure in your back. While the needle is being placed, you may also feel a sudden and brief, sharp pain in a leg, should the needle touch a nerve in the canal.
A bandage will be placed over the site, and you may be told to lie still for a while to reduce the change of post-procedure headaches.
The entire procedure lasts about 45 minutes, and it usually takes less than 2 days for your body to naturally replace lost fluid.
Possible side effects
Spinal tap tests are typically very low risk. However, some people may experience any of these side effects:
• Headache. This is the most common side effect, and it usually starts a day or two after the test. It can last from a few hours to a week or more. Headaches are usually worse while standing or sitting, and can be accompanied nausea, vomiting or dizziness. They are best treated with bed rest, drinking fluids, and simple painkillers.
• Back pain. Some people may have lower back pain after the test. Usually, the pain is confined to the area where the needle penetrated, but pain can also be felt in the legs.
• Bleeding. There is a risk of bleeding near the area where the needle was inserted. In rare situations, bleeding can occur in the epidural area in the spine itself.
Spinal tap and MS diagnosis
After the CSF sample is collected, the sample is sent to laboratory to test for immune cells, antibodies, and other proteins that indicate an abnormal immune system response within the central nervous system, a sign that the body is attacking itself.
Results indicating MS may include:
• Presence of oligoclonal bands, a group of proteins (called immunoglobulins) that show inflammation in the central nervous system.
• High levels of immunoglobulin G (IgG) antibodies. People with low levels of IgG are more prone to infections.
• Other proteins resulting from the breakdown of myelin (the fatty substance that surrounds and protects nerve cells) may also be present.
Although a spinal tap is used in diagnosing MS, it is not specific to this disease. Other tests need to be considered before a confirmed diagnosis of MS can be made.
Note: Multiple Sclerosis News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis, or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.
Questions to Ask Your Doctor If You’re Newly Diagnosed
Illustration of doctor an patient talked
We consulted some of our community contributors at MS News Today and came up with 12 questions people should consider asking their doctors after an MS diagnosis.
Check it out by clicking here.
Dancing Doodle
Did you know some of the news and columns on Multiple Sclerosis News Today are recorded and available for listening on SoundCloud? These audio news stories give our readers an alternative option for accessing information important for them.
Listen Here
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Readers ask: What The Hell Is Crossfit?
CrossFit is a competitive exercise program Functional exercises are ones that mimic real-life movements, and usually require little or no equipment, like burpees, push-ups, and sit-ups, as well as movements with barbells, dumbbells, kettlebells, jump ropes, pull-up bars, rings, and medicine balls.
What exactly is CrossFit?
A form of high intensity interval training, CrossFit is a strength and conditioning workout that is made up of functional movement performed at a high intensity level. These movements are actions that you perform in your day-to-day life, like squatting, pulling, pushing etc.
What is CrossFit and why is it bad?
Another study found that CrossFit workouts carried more risk than traditional weightlifting, likely because of the intensity of workouts where some participants may “push themselves beyond their own physical fatigue limit and may ultimately lead to technical form breakdown, loss of control, and injury.”
What’s the point of CrossFit?
CrossFit is a lifestyle characterized by safe, effective exercise and sound nutrition. CrossFit can be used to accomplish any goal, from improved health to weight loss to better performance. The program works for everyone — people who are just starting out and people who have trained for years.
You might be interested: Readers ask: How Much Is It To Register For The Crossfit Open 2018?
What is CrossFit in simple terms?
CrossFit, in its simplest definition, is a fitness routine that personal trainer Greg Glassman developed over several years in the mid- to late-1990s. CrossFit is designed to improve your overall physical abilities, including your endurance, strength, flexibility, speed, coordination, balance, and more.
What does a CrossFit workout consist of?
A typical CrossFit workout is 1 hour. It’s split up into 4 parts including the warm up (5-10 minutes), strength component (15 minutes), WOD (20-30 minutes) and cool down (5 minutes).
What is the difference between gym and CrossFit?
CrossFit workouts focus on performing more repetitions in exercises in order to get more of a workout in within a certain amount of time. Individuals that work out at a gym may or may not enlist the assistance of a personal trainer. CrossFit does add a personal trainer to the regimen. It focuses on tracking results.
Is CrossFit good or bad for your body?
The competitive nature of the sport might push you to perform better, but it also can be a recipe for disaster if you force yourself to do higher reps and higher weights than what your body is prepared for. The answer is, if done properly and correctly, CrossFit is not bad.
What are the risks of CrossFit?
CrossFit is a high-intensity form of exercise. Your risk for injuries increases anytime you increase the intensity of your workouts or the amount of weight you’re lifting. Some common CrossFit injuries include:
• low back pain.
• rotator cuff tendonitis.
• Achilles tendonitis.
• knee injuries.
• tennis elbow.
Why is CrossFit controversial?
The relationship between CrossFit and exertional rhabdomyolysis has been a subject of controversy for the company. Some medical professionals have asserted that both the CrossFit methodology and the environment created by CrossFit trainers put athletes at high risk for developing rhabdomyolysis.
You might be interested: Quick Answer: Who Are The Crossfit Workout Snamed After?
Is CrossFit really worth it?
If you are looking to get into great cardiovascular shape then yes, CrossFit will definitely help you with that. While there is weight training involved in many of their workouts they are all still great cardiovascular workouts that will definitely get you into great shape.
Why is CrossFit so popular?
One of the possible reasons Crossfit may be so popular is because of the uniqueness of the workouts. Crossfit also uses exercises without weights such as pull-ups, muscle-ups, and leg lifts. While Crossfit uses more unique workouts, it also incorporates basic exercises that people are familiar with, such as running.
What are the basic principles of CrossFit?
They are cardiovascular/respiratory endurance, stamina, strength, flexibility, power, coordination, agility, balance, and accuracy.
What is the theory of CrossFit?
All of CrossFit’s workouts are based on functional movements. These are the core movements of life, found everywhere, and built naturally into our DNA. They move the largest loads the longest distances so they are ideal for maximizing the amount of work done in the shortest time (intensity).
What makes CrossFit different?
CrossFit combines cardio and strength Rather than being all about endurance or all about strong, explosive movements, CrossFit taps both your aerobic and anaerobic energy systems, Casey says.
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