L-glutamine (a GABA precursor) was studied clinically for COVID-19, but the study was poorly designed and results were rather weak. I expect little benefit from glutamine in COVID-19.
How could you possibly justify refusing to treat *known, universally* elevated plasma 5-HT, in an often-lethal disease state that is *defined* in part by *frank, known symptoms of elevated plasma 5-HT*?
The things we are discussing about 5-HT2 antagonists and plasma serotonin, about attempting to halt progression in the early severe stage, are relevant *during* these events.
Rates of PTSD following survival from severe COVID-19 exceed 30%, ditto anxiety and depression.
The ventilator settings required to keep these patients alive tend to permit blood CO2 levels to rise somewhat, in avoiding excessive mechanical damage to the lungs.
This has been repeatedly demonstrated to cause severe anxiety and promote PTSD.
@HenkPoley This paper indicated that a single exposure to 70% ethanol largely preserved filtration efficacy, comparable to dry heat or UV sanitizing. However, further exposure events gradually worsened filtration efficacy.
Theoretical justification arises from the fact that endosomal entry is of only secondary importance for SARS-CoV-2 replication in the respiratory tract.
Both TMPRSS (proteases at the cell membrane) and cathepsins (proteases in endosomes) must be blocked.
Continuing to hear extremely favorable case reports informally for cyproheptadine even in severe COVID-19.
Publications forthcoming, but worth highlighting now given magnitude of improvement-- extubation within days, reversal of renal failure, stark decline in D-dimer, etc.
Try it for 48 hours and see. It's just an old allergy medication. Side effects are minor and it is already known to be effective in serotonin syndrome.
It blocks 5-HT2A (platelet activation) and 5-HT2B (cardiac remodeling, pulmonary fibrosis).
People want ironclad proof for everything. It doesn't exist. It never will. Even the best trials only apply to a certain stage of the disease in a certain set of the population at a certain dose with a certain baseline standard of care.
One must weigh evidence and combine signals in a safe way. That is all.
"First, the only certainty is that there is no certainty. Second, every decision, as a consequence, is a matter of weighing probabilities. Third, despite uncertainty we must decide and we must act."
More evidence inflammasome activation predicts severe COVID-19, and acts as a major driver of disease progression.
They release IL-1β, which summons neutrophils and promotes (highly pro-thrombotic) NETosis, plus IL-18, which prompts IFNγ secretion (very inflammatory, apoptotic).
Certain virally infected or antigen-swamped white blood cells smash their emergency self-destruct button, explode, and release huge amounts of signaling molecules that summon exploding neutrophils and tell other classes of WBCs to order nearby cells to die.
This strongly contributes to the severe lung clotting and often serious broader lung tissue damage that define the state we call "severe COVID-19."
@Deadly_Statins it's pretty nasty. the systemic inflammatory response is intense and can hit hard and fast. not a cold or flu at all. not like anything I've ever caught before. glad I was able to abort it.
@Deadly_Statins trying very hard not to catch it again. basically just hiding out in my residence as much as possible.
@Deadly_Statins the percentage of people with active infections out in public right now is obscene; it would be apocalyptic if IFR were higher.
unfortunately because there are so many of them, hospitals are turning people away and IFR *is* getting higher, slowly, inexorably.
The less aggressive usually draw the moderate/severe line based on need for oxygen support. However, this labels most hospital cases severe, losing granularity. Some add a 'critical' category to compensate, but this is an overloaded term.
In discussions here, I draw the moderate/severe line around onset of hypoxemia on high-flow oxygen, often onset of pulmonary microthrombosis and soon rising D-dimer, with a high risk of ARDS and DAD but not quite there yet. This matches my reading of the literature.
@poiThePoi@GephenS@youyanggu@mattparlmer No. But keep in mind 30% is the highest reported figure. Vast majority of counties are lower. So it could make sense roughly given that.
At this point they are just letting it rip. Not enough people cared soon enough with enough coordination.
@poiThePoi@GephenS@youyanggu@mattparlmer Although tbf the average visually at least does appear to be about 20% as you assumed. I agree with that reading of the map colors.
Either something is off, or... the delayed impact from positive test to hospitalization is going to go entirely unmanaged. They are full already.
@poiThePoi@GephenS@youyanggu@mattparlmer If this model is accurate, which it may indeed be, then Iowa CFR is likely to increase materially within the next 2 weeks as staffing ratios fall and admission refusals cut deeper into the scale of severity in spite of overflow capacity.
9 added to My Authors
