Post by the Scribe on Apr 30, 2020 18:38:32 GMT
Disturbing if true so I found a youtube that speaks to maintaining a healthy endothelium which I am sure most people have no clue existed. Sometimes the best information in an article comes from the comments sections below it. Be the smart one; avoid crowds, practice social distancing, wear masks, avoid conservatives (whom are not practicing safety because they hate the government and think this is a plot to take down Trump) and use common sense. If you can find a high quality monolaurin once supplies replenish BUY SOME and keep it in your arsenal.
news.yahoo.com/top-coronavirus-model-predicts-100000-dead-by-the-end-of-the-pandemics-first-wave-this-summer-232144312.html
Anonymouse
11 hours ago
We may have been looking at this from the wrong perspective from the start, that this is not a virus which infects the lung. This is a virus which does infect the lung as a way of entry. But it seems to do its most damage in the endothelium of the body. And this would explain why we are seeing such amounts of hypoxemia without the concomitant or accompanying drop in compliance of the lung. It's because it's not the lungs that are causing the hypoxia necessarily. In every case. But in many of the cases, it's possible that this is being mitigated by angiotensin 2 by out of control thrombosis, by hyper coagulation and by endothelial inflammation. This would also explain why patients might be getting signs in their feet. These could represent embolic phenomenon, which are going to the distal extremities.
Yes, it attacks the lungs most; but it also can do severe damage to the heart, blood vessels, kidneys, gut, skin and brain.
Cardiologist Harlan Krumholz of Yale University says it "can attack almost anything in the body with devastating consequences. It's ferocity is breathtaking and humbling".
We also now know it has two pathways for infection, the ACE2 receptor (which is found in organs throughout the body) and the CD147 receptor on T-cells (found in the immune system). And the more I read about this, the more I start to see that angiotensin converting enzyme 2. Yes, the very target of the Coronavirus is an extremely important enzyme in the balance of that oxidative stress. And when ACE 2 is lost, that balance is pushed in favor of oxidative stress. And so to really understand how to protect yourself from COVID 19 or how to treat a patient with Koven 19, what that requires is a complete understanding of what is oxidative stress. And what are the strategies that the body uses to mitigate oxidative stress.
So why is all of this happening? It may be happening because the virus is taking out ACE2 because it is binding to ACE2 and as it binds it's now rendering that enzyme inactive. When ACE2 is down regulated, it can no longer mitigate the effects of angiotensin2 and specifically oxidative stress on the endothilium.ACE2-based treatment approaches may be a novel approach to limit aberrant vascular responses and atherothrombosis.
Sources:https://www.thelancet.com/journals/lancet/article/PIIS0140-67362030937-5/fulltext 2nd source www.ncbi.nlm.nih.gov/pmc/articles/PMC7156948/pdf/main.pdf
There is some stuff coming out from hematologists that is saying.. the virus is acting as if its primary target is the endothelium. Read the reports from Hooman Poor, Adam Cuker and pathologist Sharon Fox. Maybe the secret is not to fight this disease like a respiratory illness, but treat it as a blood/endothelial disorder and immune system gone haywire. Clot busting drugs and anti rejection drugs to modify the cytokine response? Pathologist Fox says when you look at these bodies you see they are riddled with blood clots in the small vessels of the body, the lungs being hit the hardest with clots.
What happens when you breathe the virus in, it's going to go first into your lungs specifically to the ACE 2 receptor in your lungs. And what we all thought and imagined was that we were going to get ARDS, and that is why we started treating patients with hypoxia. Secondary to ARDS. Because this is what we all have been expecting for months and months.But the virus gets worse and spreads and then it starts to go into the blood vessels. And the blood vessels inside of them also have ACE 2 receptors. What happens now when it goes into ACE 2, we get thrombosis, AT-11. These things happen so quickly even before the ARDS gets bad enough to cause the H type of lung problem, we have thrombosis which is causing the ground glass opacification, and we get the L type lung problem.
The final common denominator which take most of the patients into ICU is a process known as oxidative stress. The people with the worst oxidative stress from a baseline standpoint are those people with cardiovasular diseases, diabetes and over weight. Happy hypoxics. Cardiovasular collapse, blood clots in their vessels. These are the ones put on ventiators but to little avail. If you have high risk factors for severe disease, like heart or lung problems, diabetes, or those age 60 and over, consider getting a pulse oximeter. Here is one recommended on blauoximeter.pg-blog.com/ A pulse oximeter can provide early warning of the kinds of breathing problems associated with Covid-19 pneumonia. Take your readings now, when you are well, so you have a baseline to compare with. And do this lying down (as you would be if sick), so your baseline is a true baseline.
news.yahoo.com/top-coronavirus-model-predicts-100000-dead-by-the-end-of-the-pandemics-first-wave-this-summer-232144312.html
Anonymouse
11 hours ago
We may have been looking at this from the wrong perspective from the start, that this is not a virus which infects the lung. This is a virus which does infect the lung as a way of entry. But it seems to do its most damage in the endothelium of the body. And this would explain why we are seeing such amounts of hypoxemia without the concomitant or accompanying drop in compliance of the lung. It's because it's not the lungs that are causing the hypoxia necessarily. In every case. But in many of the cases, it's possible that this is being mitigated by angiotensin 2 by out of control thrombosis, by hyper coagulation and by endothelial inflammation. This would also explain why patients might be getting signs in their feet. These could represent embolic phenomenon, which are going to the distal extremities.
Yes, it attacks the lungs most; but it also can do severe damage to the heart, blood vessels, kidneys, gut, skin and brain.
Cardiologist Harlan Krumholz of Yale University says it "can attack almost anything in the body with devastating consequences. It's ferocity is breathtaking and humbling".
We also now know it has two pathways for infection, the ACE2 receptor (which is found in organs throughout the body) and the CD147 receptor on T-cells (found in the immune system). And the more I read about this, the more I start to see that angiotensin converting enzyme 2. Yes, the very target of the Coronavirus is an extremely important enzyme in the balance of that oxidative stress. And when ACE 2 is lost, that balance is pushed in favor of oxidative stress. And so to really understand how to protect yourself from COVID 19 or how to treat a patient with Koven 19, what that requires is a complete understanding of what is oxidative stress. And what are the strategies that the body uses to mitigate oxidative stress.
So why is all of this happening? It may be happening because the virus is taking out ACE2 because it is binding to ACE2 and as it binds it's now rendering that enzyme inactive. When ACE2 is down regulated, it can no longer mitigate the effects of angiotensin2 and specifically oxidative stress on the endothilium.ACE2-based treatment approaches may be a novel approach to limit aberrant vascular responses and atherothrombosis.
Sources:https://www.thelancet.com/journals/lancet/article/PIIS0140-67362030937-5/fulltext 2nd source www.ncbi.nlm.nih.gov/pmc/articles/PMC7156948/pdf/main.pdf
There is some stuff coming out from hematologists that is saying.. the virus is acting as if its primary target is the endothelium. Read the reports from Hooman Poor, Adam Cuker and pathologist Sharon Fox. Maybe the secret is not to fight this disease like a respiratory illness, but treat it as a blood/endothelial disorder and immune system gone haywire. Clot busting drugs and anti rejection drugs to modify the cytokine response? Pathologist Fox says when you look at these bodies you see they are riddled with blood clots in the small vessels of the body, the lungs being hit the hardest with clots.
What happens when you breathe the virus in, it's going to go first into your lungs specifically to the ACE 2 receptor in your lungs. And what we all thought and imagined was that we were going to get ARDS, and that is why we started treating patients with hypoxia. Secondary to ARDS. Because this is what we all have been expecting for months and months.But the virus gets worse and spreads and then it starts to go into the blood vessels. And the blood vessels inside of them also have ACE 2 receptors. What happens now when it goes into ACE 2, we get thrombosis, AT-11. These things happen so quickly even before the ARDS gets bad enough to cause the H type of lung problem, we have thrombosis which is causing the ground glass opacification, and we get the L type lung problem.
The final common denominator which take most of the patients into ICU is a process known as oxidative stress. The people with the worst oxidative stress from a baseline standpoint are those people with cardiovasular diseases, diabetes and over weight. Happy hypoxics. Cardiovasular collapse, blood clots in their vessels. These are the ones put on ventiators but to little avail. If you have high risk factors for severe disease, like heart or lung problems, diabetes, or those age 60 and over, consider getting a pulse oximeter. Here is one recommended on blauoximeter.pg-blog.com/ A pulse oximeter can provide early warning of the kinds of breathing problems associated with Covid-19 pneumonia. Take your readings now, when you are well, so you have a baseline to compare with. And do this lying down (as you would be if sick), so your baseline is a true baseline.