Updated Boris Johnson is CURED. He was in the ICU - but did not have pneumonia, was not on a ventilator, and was given oxygen.
https://www.thetimes.co.uk/article/boris-johnson-leaves-intensive-care-597w3p5fv
Updated Boris Johnson is CURED. He was in the ICU - but did not have pneumonia, was not on a ventilator, and was given oxygen.
https://www.thetimes.co.uk/article/boris-johnson-leaves-intensive-care-597w3p5fv
Purell Frank wrote:
I am getting on board with this hemoglobin idea.
They didn't know why the sickle cell trait protected people from malaria until 2011. Malaria attack hemoglobin and sickle cell creates a different kind of hemoglobin.
They didn't know that lungs produce about half of your blood cells until recently.
They don't knowexactly how HCQ works against malaria, but it does. It seems to protect agaist covid-19, but maybe not for the reasons they are looking for.
The areas hardest hit by by deaths seem to be inhabited by ethnicities that have this trait more prevalent. African Americans, Latinos, and Mediterraneans have a higher percentage of it and a higher death rate. Whites have lower rates and Asians have the lowest.
Also, it doesn't seem to affect young people. The deaths in men are higher than women. Guess how hemoglobin levels are related to there factors?
If it is somehow related to their hemoglobin levels, I’m wondering since Sickle Cell Anemia is predominately found in African Americans then is there a correlation? Or the carriers? And as for males vs females, maybe menstrual cycle plays a part? Or what about people living in high altitude places vs sea level?
yes.
They are putting people on ventilators too late due to the shortage, and inexperience. In Italy they are starting to put people on ventilators are not far gone enough to still survive.
Legion wrote:
That paper is interesting but it used computational methods only (conserved domain analysis, homology modeling, and molecular docking). The authors acknowledge this is not experimental proof and that their paper is academic in nature.
Here's an intelligent response. The authors of the article have no evidence that the virus actually attacks haemoglobin. They just used a computer to see what proteins fit onto it. This kind of screening by computer is a cottage industry now with all the protein structures on line and easy to use software to calculate the fit.
You guys are all missing the key pieces for understanding the pathophysiology of serious illness with SARSCoV2 (aka Wuhan Biosafety L4 virus).
#1. This disease does not cause viral pneumonia as much as it does lung damage due to pulmonary hypertension/edema. That's right. It's much like high altitude mountain sickness or HACE. As a matter of fact, the hallmark ground glass opacities seen in the lung with COVID are a characteristic finding of ppl starved for oxygen in high altitudes. No doubt the hemoglobin phenomenon is key to understanding how all of this works. Viral infection of RBE and epithelial cells lining vasculature cause hemoglobin to be stripped of Fe thereby rendering it unable to deliver O2 to your tissues and remove CO2 therefrom. Further complicating matters, the hypoxia causes your vessels to constrict esp the aterioles (supplying blood to the aveoli at the base of the lung). The pulmonary hypoxic hypertension is essentially vascular remodeling in the lung - attempting to divert blood to areas of the lung with more oxygen. The problem is that there is no area of the lung with more oxygen because the hemoglobin is the problem. The heart is put under tremendous stress trying to move blood through highly pressurized lungs. The chronic hypoxia triggers inflammation and damage to blood vessels, causing scarring and narrowing of blood vessels. Symptomatically (at least at the beginning of the illness), this process causes the feeling of fatigue, dizziness, chest pain, breathlessness, irregular heart beat, hypoxia and O2 depletion. Some people report feelings of heat and pain in their extremities, doctors are reporting pseudo frost-bite. This is due to vasoconstriction of peripheral blood vessels and the beginning stages of gangrene due to lack of blood to the extremities. Over time, the blood vessels begin to get leaky from cellular apoptosis (programmed cell death) and break down leading to widespread organ damage. Notice how the first organs to be damaged are those that are highly vascularized? Like heart (muscle), lungs, liver (see high ALT/AST enzymes indicative of liver damage in many pts) and kidney. Yes, the retina is highly vascularized but it is protected by the blood-brain-barrier (at least initially with this disease).
#2 The other key piece to understanding this monster virus is that it seems to selectively cause more serious disease in certain ppl due to G6PD deficiency. G6PD is an enzyme that regulates the neutralization of destructive free radical, highly reactive O2 species in the body. Certain cells like white blood cells generate reactive oxygen to destroy lipid membranes of pathogens (like viruses, plasmodium [parasitic protozoans], bacteria, etc). But, with widespread generation of reactive oxygen due to viremia, damage of red blood cells, lymphocytes (CD8 and CD4 killer T-cells and macrophages), microvascular tissue results. This is further compounded in some people who have a deficient ability to sop up and neutralize reactive O2 (i.e., specifically people who are lacking in the G6PD enzyme). So, which demographics have lesser amounts of this enzyme you ask? Well, men first of all because the gene is found on the X-chromosome and thus they only have 1 working gene instead of 2 like women do. Certain demographics have mutations in this enzyme: African Americans, West Africans, Middle Easterners, Italians, Spaniards, ppl of Mediterranean descent (thought to confer resistance to malaria). And certain ppl with pro-inflammatory states such as those with diabetes, insulin resistance, obesity, metabolic syndrome, hypertension, hypercoagulation disorders, cardiovascular disease tend to have lower G6PD levels.
So, what can be done to treat the cascade of tissue damage inflicted by the China virus? Use of anticoagulants to minimize blood clots. Diuretics to reduce swelling. Treatments for relaxing blood vessels and opening them like inhaled nitrous oxide, viagra (yeah, guys get them Rx filled!), calcium channel blockers and prostacyclins. Boost the production of hemoglobin, supplement with iron, provide Oxygen supplementation, use of hyperbaric chambers, altitude tents. I think therapies used in pts with cystic fibrosis to move out mucus deep in the lungs might help (e.g., vest therapy, back clapping, nebulizer therapy with various active agents). Lung transplant if things get bad enough (why do you think China has been perfecting their live harvesting organ donation and lung transplant programs)?
What shouldn't be used? Ventilators when the source of your issue is hypoxia due to vessel construction/pulmonary hypertension. People aren't having a problem using the muscles for inflating their lungs. They're having problems WITH THEIR LUNGS! High pressure ventilators are just doing more damage by forcing delicate vessels open (which could be opened other ways like via inhaled nitrous oxide, pressurized chambers) and damaging the alveoli which seem to be functioning okay (note: The damage in the lung seems to be primarily in the bronchiole tubes (ciliated columnar cells selectively damages hence why there is a dry cough these cells die and can't clear out the debris; interesting connection with cystic fibrosis here since these cells are thought to at least in part express the CFTR gene and be involved in CF pathogenesis).
Whew. I have to take a break now. It's exhausting educating y'all.
Bye
I find this theory very interesting. I have no medical background whatsoever, but I can provide a story that may or may not relate to this theory. Near the end of March, I had a week of very unusual symptoms which I can either chalk off to stress or possibly to COVID19.
At the beginning, I felt a small amount of pain/tightness in my chest, especially when trying to take in a full volume of air (i.e. fill my lungs). As the week progressed, in addition to that I acquired a perpetual headache, general achiness, and heart palpitations even during moderate stress (like going up the stairs). I wasn't necessarily out of breath, but I'm a runner, and I know that my heart rate shouldn't be shooting up when I'm walking up the stairs.
After a week of this, I started to get nervous, so I went to the urgent care to make sure I wasn't about to die. The doctor saw a suspicious spot on my chest x-ray and gave me a shot of some strong antibiotic (can't remember the name...started with an R, I think?) and a prescription for azithromycin. She sent the x-ray away for analysis.
The morning after, I felt considerably better, literally overnight. I thought that seemed unlikely. The x-ray analysis came back a few days later, and the report came back negative for anything. The doctor called me and seemed almost embarrassed to admit that nothing came back, like she made a mistake. It made me wonder if I was just under stress for that week (it was the week we were all put on "lock down") or if I really had some sort of illness.
However, I know exactly what my symptoms felt like because I have felt them before: in Peru at 13000+ feet. My heart was working noticeably harder than it normally does, and I had a headache. Not really "out of breath" because I'm in fantastic LRC shape. The only thing was in this case the headache didn't go away after the first day, like it did in Peru. It felt exactly like a long period of acclimitization to altitude.
All I can say is that I felt much, much better very quickly after the medication, and I certainly wasn't under less stress. If I had to make a guess, I think I really did have something. If it turns out that COVID19 attacks the blood rather than the lungs, it might explain this strange experience.
flying finn wrote:
yes.
They are putting people on ventilators too late due to the shortage, and inexperience. In Italy they are starting to put people on ventilators are not far gone enough to still survive.
Could be, but Italy has not been putting only the sickest patients with the least chance of survival on ventilators. They have started prioritising the younger, fitter patients with a better chance of survival overall and more life to live. However the ventilators are still not really saving lives.
"Researchers in Wuhan, for instance, reported that, of 37 critically ill Covid-19 patients who were put on mechanical ventilators, 30 died within a month. In a U.S. study of patients in Seattle, only one of the seven patients older than 70 who were put on a ventilator survived; just 36% of those younger than 70 did."
New York is estimating 80% of Covid patients die on ventilators. UK early estimates are 65%.
The American Journal of Respiratory and Critical Care Medicine, researchers in Germany and Italy said their Covid-19 patients were unlike any others with acute respiratory distress. Their lungs are relatively elastic (“compliant”), a sign of health “in sharp contrast to expectations for severe ARDS.” Their low blood oxygen might result from things that ventilators don’t fix.
https://www.statnews.com/2020/04/08/doctors-say-ventilators-overused-for-covid-19/Problem with this paper is that it is only a computer simulated molecular docking. It's highly unreliable and not peer-reviewed. Strongest argument against this hypothesis is that if it were true we would not see rapid improvement in those who are treated successfully with antivirals like Remdesivir as the damaged red blood cells would take weeks to rebuild as RBC life time is around 120 days. Also we would see huge increase in erythropoietin but as far as I know that is not the case. Currently the most plausible theory is that bilateral ground glass opacity which is closely resembles altitude sickness is caused by pulmonary embolism due to endothelial dysfunction that results in thrombotic microvasculopathy. The mechanism is as follows: - SARS-CoV-2 spike S1 protein binds to ACE2 enzymatic domain on the surface of cells - ACE2 binding results in endocytosis and translocation of both the virus and the enzyme into endosomes - ACE2 loss leads to increase in Angiotensin II via renin-angiotensin system upregulation - Angiotensin II is known to promote endothelial dysfunction - endothelial dysfunction results in thrombotic vasculopathy thus also in pulmonary embolism
A Hungry, Violent Mob wrote:
Read this a few days ago and it sounded promising, then was deleted from medium...
http://web.archive.org/web/20200405061401/https://medium.com/@agaiziunas/covid-19-had-us-all-fooled-but-now-we-might-have-finally-found-its-secret-91182386efcbThis paper seems to back it up.
https://chemrxiv.org/articles/COVID-19_Disease_ORF8_and_Surface_Glycoprotein_Inhibit_Heme_Metabolism_by_Binding_to_Porphyrin/11938173I think doctors are figuring out this is a blood disease and not a respiratory one. Oh, and hydroxychloroquine works.......
Just read Real news and real medical journals, not online nonsense. Ignore emergency docs who get thrown out of icus and then talk to clueless reporters about how ventilators are harming people. Yes, infections increase the risk of thrombosis and decrease the ability of blood to carry oxygen (though in a round about way). This is well known, not unique to coronavirus, and is always a problem in critically ill patients. And btw, the covid 19 virus infects cells through binding the ACE2 receptor which is prevalent everywhere but especially the lungs. The article in question is from a computer scientist in China and published online. It’s meaningless as published.
And yes ventilators are able to cause damage to the lungs, particularly when the lungs are stiff, which can occur in a condition called ards. ARDS is a result of severe covid 19 pneumonia, but ARDS is not specific to coronavirus but is the physiologic result of many conditions. Fortunately there is a body of physicians and researchers who have studied this problem for decades. The result is the ARDS network which provides quidelines on how to best ventilate and care for patients with the condition. The guidelines are continuously updated. Mortality rates among elderly patients with severe sepsis (such as those requiring a ventilator) in the icu are very high regardless of the infection but the icu mortality rates with covid are higher than expected. Deviation from guidelines and unproven (and highly questionable) therapies like chloroquine will lead to an even higher rate of mortality, that much is certain.
Disinformation is deadly and science will save lives. Be safe y’all
Thanks for the clarification and education. Makes sense. Appreciate it.
Interesting news today showing a novel mutation in the RNA polymerase of certain viral strains of SARS-CoV2 carried by Europeans and pts in North America . This shows the virus is quickly evolving and different strains of this virus may co-exist. The possible biological significance of this finding is not known at this time; however, clearly more research is needed as these findings may have profound diagnostic, therapeutic and prognostic implications.
rundoc wrote:
Just read Real news and real medical journals, not online nonsense. Ignore emergency docs who get thrown out of icus and then talk to clueless reporters about how ventilators are harming people. Yes, infections increase the risk of thrombosis and decrease the ability of blood to carry oxygen (though in a round about way). This is well known, not unique to coronavirus, and is always a problem in critically ill patients. And btw, the covid 19 virus infects cells through binding the ACE2 receptor which is prevalent everywhere but especially the lungs. The article in question is from a computer scientist in China and published online. It’s meaningless as published.
And yes ventilators are able to cause damage to the lungs, particularly when the lungs are stiff, which can occur in a condition called ards. ARDS is a result of severe covid 19 pneumonia, but ARDS is not specific to coronavirus but is the physiologic result of many conditions. Fortunately there is a body of physicians and researchers who have studied this problem for decades. The result is the ARDS network which provides quidelines on how to best ventilate and care for patients with the condition. The guidelines are continuously updated. Mortality rates among elderly patients with severe sepsis (such as those requiring a ventilator) in the icu are very high regardless of the infection but the icu mortality rates with covid are higher than expected. Deviation from guidelines and unproven (and highly questionable) therapies like chloroquine will lead to an even higher rate of mortality, that much is certain.
Disinformation is deadly and science will save lives. Be safe y’all
The virus no doubt infects many cells via host cell ACE2 protein-protein docking mechanisms and allows direct uptake in to cells during activated endocytosis (and delivery to acidified endosomes where the virus is able to fuse directly with endosomal membrane and release contents into cytoplasm). There is another host cell protein that interacts with the virus called TMPRSS2 which cleaves the 2 subunits of the virus (at the unique furin cleavage site - thanks master mind Chinese scientists!) and enables direct host cell- virus membrane-membrane fusion. This enables the virus to deliver it's contents directly into the cytoplasm without the need for uptake into the cell. Then there is indirect uptake of the virus via passive endocytosis. I think this third mechanism occurs because the virus is able to bind oligosaccharides/glycan residues on the surface of many cells. The passive mechanism is like the receptor-mediated ACE2 entry involving delivery to endosomes and release of viral contents into the cytoplasm due to the acidification of these organelles
Very interesting ideas and discussions. Let's assume that this is all correct. What can presumably healthy, uninfected people do to protect themselves and prepare themselves in the event of infection? Are there supplements to the diet (antioxidant foods?) or vitamins (vit C or iron?) that could be taken to help?
He's not a doctor. He's a cryptocurrency promoter who read a single medical article and thinks that makes him an expert on an incredibly complicated novel viral pathogen that the collective medical community worldwide is struggling to understand.
I'm just gonna leave these here:
Help me to understand wrote:
I heard another U.S. doctor saying that ventilators were not working for the majority, I believe he was citing it was more of an oxygen issue. I guess this is why they call then Practicing Physicians...
I pointed this out from the start. In fact, I have personally witnessed people killed by ventilators in hospitals long before this current fiasco. Yes, it is exactly an oxygen exchange issue! Many healthy people would die from being forced onto ventilators the way they have been brutally used in most hospitals. More people would live if they weren't used at all.
So basically this is all bunk, and I'm crazy? At least I know now!
Any alternative theories from the medical types regarding my experience? Stress?
I'm certain that the symptoms were real, but not certain of the cause. I've experienced stress before and not experienced symptoms like this...very strange.
sick of COVID wrote:
You guys are all missing the key pieces for understanding the pathophysiology of serious illness with SARSCoV2 (aka Wuhan Biosafety L4 virus).
#1. This disease does not cause viral pneumonia as much as it does lung damage due to pulmonary hypertension/edema. That's right. It's much like high altitude mountain sickness or HACE. As a matter of fact, the hallmark ground glass opacities seen in the lung with COVID are a characteristic finding of ppl starved for oxygen in high altitudes. No doubt the hemoglobin phenomenon is key to understanding how all of this works. Viral infection of RBE and epithelial cells lining vasculature cause hemoglobin to be stripped of Fe thereby rendering it unable to deliver O2 to your tissues and remove CO2 therefrom. Further complicating matters, the hypoxia causes your vessels to constrict esp the aterioles (supplying blood to the aveoli at the base of the lung). The pulmonary hypoxic hypertension is essentially vascular remodeling in the lung - attempting to divert blood to areas of the lung with more oxygen. The problem is that there is no area of the lung with more oxygen because the hemoglobin is the problem. The heart is put under tremendous stress trying to move blood through highly pressurized lungs. The chronic hypoxia triggers inflammation and damage to blood vessels, causing scarring and narrowing of blood vessels. Symptomatically (at least at the beginning of the illness), this process causes the feeling of fatigue, dizziness, chest pain, breathlessness, irregular heart beat, hypoxia and O2 depletion. Some people report feelings of heat and pain in their extremities, doctors are reporting pseudo frost-bite. This is due to vasoconstriction of peripheral blood vessels and the beginning stages of gangrene due to lack of blood to the extremities. Over time, the blood vessels begin to get leaky from cellular apoptosis (programmed cell death) and break down leading to widespread organ damage. Notice how the first organs to be damaged are those that are highly vascularized? Like heart (muscle), lungs, liver (see high ALT/AST enzymes indicative of liver damage in many pts) and kidney. Yes, the retina is highly vascularized but it is protected by the blood-brain-barrier (at least initially with this disease).
#2 The other key piece to understanding this monster virus is that it seems to selectively cause more serious disease in certain ppl due to G6PD deficiency. G6PD is an enzyme that regulates the neutralization of destructive free radical, highly reactive O2 species in the body. Certain cells like white blood cells generate reactive oxygen to destroy lipid membranes of pathogens (like viruses, plasmodium [parasitic protozoans], bacteria, etc). But, with widespread generation of reactive oxygen due to viremia, damage of red blood cells, lymphocytes (CD8 and CD4 killer T-cells and macrophages), microvascular tissue results. This is further compounded in some people who have a deficient ability to sop up and neutralize reactive O2 (i.e., specifically people who are lacking in the G6PD enzyme). So, which demographics have lesser amounts of this enzyme you ask? Well, men first of all because the gene is found on the X-chromosome and thus they only have 1 working gene instead of 2 like women do. Certain demographics have mutations in this enzyme: African Americans, West Africans, Middle Easterners, Italians, Spaniards, ppl of Mediterranean descent (thought to confer resistance to malaria). And certain ppl with pro-inflammatory states such as those with diabetes, insulin resistance, obesity, metabolic syndrome, hypertension, hypercoagulation disorders, cardiovascular disease tend to have lower G6PD levels.
So, what can be done to treat the cascade of tissue damage inflicted by the China virus? Use of anticoagulants to minimize blood clots. Diuretics to reduce swelling. Treatments for relaxing blood vessels and opening them like inhaled nitrous oxide, viagra (yeah, guys get them Rx filled!), calcium channel blockers and prostacyclins. Boost the production of hemoglobin, supplement with iron, provide Oxygen supplementation, use of hyperbaric chambers, altitude tents. I think therapies used in pts with cystic fibrosis to move out mucus deep in the lungs might help (e.g., vest therapy, back clapping, nebulizer therapy with various active agents). Lung transplant if things get bad enough (why do you think China has been perfecting their live harvesting organ donation and lung transplant programs)?
What shouldn't be used? Ventilators when the source of your issue is hypoxia due to vessel construction/pulmonary hypertension. People aren't having a problem using the muscles for inflating their lungs. They're having problems WITH THEIR LUNGS! High pressure ventilators are just doing more damage by forcing delicate vessels open (which could be opened other ways like via inhaled nitrous oxide, pressurized chambers) and damaging the alveoli which seem to be functioning okay (note: The damage in the lung seems to be primarily in the bronchiole tubes (ciliated columnar cells selectively damages hence why there is a dry cough these cells die and can't clear out the debris; interesting connection with cystic fibrosis here since these cells are thought to at least in part express the CFTR gene and be involved in CF pathogenesis).
Whew. I have to take a break now. It's exhausting educating y'all.
Bye
"Monster virus?" How can this be a monster virus if it has been throughout the world since as early as mid-2019 and it is proving to be less deadly than the seasonal flu, even though the social distancing also applies to the flu and there is a flu vaccine protecting about half the US population?
The CCD, WHO and US politicians have some man and lady-splainin' to do.
newredsun wrote:
sick of COVID wrote:
You guys are all missing the key pieces for understanding the pathophysiology of serious illness with SARSCoV2 (aka Wuhan Biosafety L4 virus).
#1. This disease does not cause viral pneumonia as much as it does lung damage due to pulmonary hypertension/edema. That's right. It's much like high altitude mountain sickness or HACE. As a matter of fact, the hallmark ground glass opacities seen in the lung with COVID are a characteristic finding of ppl starved for oxygen in high altitudes. No doubt the hemoglobin phenomenon is key to understanding how all of this works. Viral infection of RBE and epithelial cells lining vasculature cause hemoglobin to be stripped of Fe thereby rendering it unable to deliver O2 to your tissues and remove CO2 therefrom. Further complicating matters, the hypoxia causes your vessels to constrict esp the aterioles (supplying blood to the aveoli at the base of the lung). The pulmonary hypoxic hypertension is essentially vascular remodeling in the lung - attempting to divert blood to areas of the lung with more oxygen. The problem is that there is no area of the lung with more oxygen because the hemoglobin is the problem. The heart is put under tremendous stress trying to move blood through highly pressurized lungs. The chronic hypoxia triggers inflammation and damage to blood vessels, causing scarring and narrowing of blood vessels. Symptomatically (at least at the beginning of the illness), this process causes the feeling of fatigue, dizziness, chest pain, breathlessness, irregular heart beat, hypoxia and O2 depletion. Some people report feelings of heat and pain in their extremities, doctors are reporting pseudo frost-bite. This is due to vasoconstriction of peripheral blood vessels and the beginning stages of gangrene due to lack of blood to the extremities. Over time, the blood vessels begin to get leaky from cellular apoptosis (programmed cell death) and break down leading to widespread organ damage. Notice how the first organs to be damaged are those that are highly vascularized? Like heart (muscle), lungs, liver (see high ALT/AST enzymes indicative of liver damage in many pts) and kidney. Yes, the retina is highly vascularized but it is protected by the blood-brain-barrier (at least initially with this disease).
#2 The other key piece to understanding this monster virus is that it seems to selectively cause more serious disease in certain ppl due to G6PD deficiency. G6PD is an enzyme that regulates the neutralization of destructive free radical, highly reactive O2 species in the body. Certain cells like white blood cells generate reactive oxygen to destroy lipid membranes of pathogens (like viruses, plasmodium [parasitic protozoans], bacteria, etc). But, with widespread generation of reactive oxygen due to viremia, damage of red blood cells, lymphocytes (CD8 and CD4 killer T-cells and macrophages), microvascular tissue results. This is further compounded in some people who have a deficient ability to sop up and neutralize reactive O2 (i.e., specifically people who are lacking in the G6PD enzyme). So, which demographics have lesser amounts of this enzyme you ask? Well, men first of all because the gene is found on the X-chromosome and thus they only have 1 working gene instead of 2 like women do. Certain demographics have mutations in this enzyme: African Americans, West Africans, Middle Easterners, Italians, Spaniards, ppl of Mediterranean descent (thought to confer resistance to malaria). And certain ppl with pro-inflammatory states such as those with diabetes, insulin resistance, obesity, metabolic syndrome, hypertension, hypercoagulation disorders, cardiovascular disease tend to have lower G6PD levels.
So, what can be done to treat the cascade of tissue damage inflicted by the China virus? Use of anticoagulants to minimize blood clots. Diuretics to reduce swelling. Treatments for relaxing blood vessels and opening them like inhaled nitrous oxide, viagra (yeah, guys get them Rx filled!), calcium channel blockers and prostacyclins. Boost the production of hemoglobin, supplement with iron, provide Oxygen supplementation, use of hyperbaric chambers, altitude tents. I think therapies used in pts with cystic fibrosis to move out mucus deep in the lungs might help (e.g., vest therapy, back clapping, nebulizer therapy with various active agents). Lung transplant if things get bad enough (why do you think China has been perfecting their live harvesting organ donation and lung transplant programs)?
What shouldn't be used? Ventilators when the source of your issue is hypoxia due to vessel construction/pulmonary hypertension. People aren't having a problem using the muscles for inflating their lungs. They're having problems WITH THEIR LUNGS! High pressure ventilators are just doing more damage by forcing delicate vessels open (which could be opened other ways like via inhaled nitrous oxide, pressurized chambers) and damaging the alveoli which seem to be functioning okay (note: The damage in the lung seems to be primarily in the bronchiole tubes (ciliated columnar cells selectively damages hence why there is a dry cough these cells die and can't clear out the debris; interesting connection with cystic fibrosis here since these cells are thought to at least in part express the CFTR gene and be involved in CF pathogenesis).
Whew. I have to take a break now. It's exhausting educating y'all.
Bye
"Monster virus?" How can this be a monster virus if it has been throughout the world since as early as mid-2019 and it is proving to be less deadly than the seasonal flu, even though the social distancing also applies to the flu and there is a flu vaccine protecting about half the US population?
The CCD, WHO and US politicians have some man and lady-splainin' to do.
Um, because it has killed thousands upon thousands of Americans in under 2 months? And the virus kills ppl in a grueling, agonizing manner?
2,600 Bad Wigins
I am not that smart ,but if this is true and you ran with Covid19 it would be like running at altitude .