Covid-19 News

  • Subcellular fractionation analyses indicated that RIPK1 increased VDR retention in the cytoplasm, which may account for its inhibition of VDR transcriptional activity. Consistent with the reporter analyses, 1,25D3-induced growth suppression was more pronounced in RIPK1-null MEFs and RIPK1-knockdown ovarian cancer cells than in control cells. Our studies have defined RIPK1 as a VDR repressor, projecting RIPK1 depletion as a potential strategy to increase the potency of 1,25D3 and its analogs for cancer intervention.


    Sounds like Darwinism is at work. Virus usually eliminate people with less fit gens. CoV-19 seems just to remind us that we are still a part of nature.

  • there has to be a physical effect that causes the imbalance. The effects of a gene (or disease) can be measured directly by measuring food intake, digestion waste products, and the energy output

    Yes, there are physiological items that effect the burning efficiencies, the desires, the conversion of material into fat and other items. However, the bottom line is that weight gain will not occur unless there is more calories taken in than are released into the environment. Likewise there cannot be weight loss unless somehow more calories are released into the environment than taken in. If you do not believe it try to go without any calories taken in for a few years and see if you do not loose weight.


    Of course the question is why do some take in more, or use (or expel) less.

  • Surely Trump is taking hydroxychloroquine after advocating it so strongly? And why hasn't Zelenko offered his services?

    Trump is receiving a two-antibody combo drug that's currently in late-stage studies from Regeneron Pharmaceuticals Inc.


    Trump also was taking zinc, vitamin D, an antacid called famotidine, melatonin and aspirin.


    as a precautionary measure he received a single 8 gram dose of Regeneron's polyclonal antibody cocktail. He completed the infusion without incident. In addition to the polyclonal antibodies, the President has been taking zinc, vitamin D, famotidine, melatonin, and a daily aspirin.


    https://wxow.com/2020/10/02/to…sitive-for-coronavirus-2/


    PS- famotidine = Pepsid AC

  • Trump's anti-BAT:


    We know: Remdesivir, and 8g experimental antibody cocktail.


    We also know:

    Mr Trump was also taking zinc, vitamin D, famotidine, melatonin and aspirin, Dr Conley said.


    This is great news, it means that we have now decoupled Hydroxychloroquine good or bad from any political left/right Trump / anti-Trump considerations. It can now be considered only on its merits (which Trump appears not to believe in any more). That, personally, has no effect on my judgement of it. people here might be interested in famotidine and melatonine, but also note that this did not prevent him from getting COVID.


    THH


    PS - I wish Trump and all those other Republican administration high-ups a full recovery with no nasty long-Covid after-effects. It is a horrible disease when not asymptomatic and you would not wish it on your worst enemy. I also hope that they will decide (or be pushed to decide by the remaining white house insiders who have not caught COVID) to obey the CDC best practice social distancing regulations in future rather than use breaking them as a part of a political campaign.

  • but also note that this did not prevent him from getting COVID.


    Just as a reminder: Even after a vaccination you can get CoV-19 if you inhale a large amount of aerosols in deep lung. It's all a matter of how many symptoms you will see afterwards.


    And also: All humans are different: You will face your own personal trial to heal you again. There are many signs that some gens, also some that are linked to obesity, will increase your risk. Just take care an watch your body.

  • That's quite enough Trump. He is just one person with Covid, along with possibly a million others, giving him special status demeans the others, many of them suffering without recourse to adequate care.


    You will notice Alan I was no more than drawing valid inferences:


    (1) Trump not taking HCQ himself removes part of the politics in that debate. Welcome.

    (2) What Trump does take under medical advice is interesting: his status is such that his doctors will do their absolute best regardless of rules.


    I can't see that noting this demeans anyone else.

  • For all you and I know his Doctors are putting out spin about his meds while feeding him a diet of fried spleen.


    For the fans of rarely tested experimental drugs: Just google : ' remdesivir "kidney damage" '


    According NYT: “The president’s vitals over the last 24 hours were very concerning and the next 48 hours will be critical in terms of his care,”

  • Remdesivir was shown to be almost equally effective in vitro to HCQ in the original Wang et al paper back in February wasn't it, and later on it was confirmed in the massive Gordon et al molecular biology Nature paper testing a very large number of potential antivirals. HCQ still stands as being a cheap remedy along with ivermectin (although the dose-response relations suggest you need more like 100 mg doses rather than just 15 mg). Its just ridiculous that further research on refining HCQ was stamped on by the political situation, presumably all research funding for exploring whether the S-enantiomer was more effective than the mixture of isomers was cut. Or maybe the Chinese have already purified this and are distributing it widely to their own citizens (the upper classes presumably) without letting on the the rest of the World? With all Trump's recent blame gaming at the Chinese Emperor and his communist dynasty they are probably thinking why should we help this potential enemy?:)

  • Drbeen Medical Lectures: Regneron Antibody Cocktail (Trump COVID-19)

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    Drbeen Medical Lectures: Bromhexine Protocol Talk with Dr. Harrison

    (Bromhexine available over the counter everywhere outside U.S. and online)

    (Also says nutraceuticals (curcumin, luteolin, ursolic acid) block viral entry.

    Full regimen is shown at video time 20:00)

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    COVID-19 ACUTE: TREATMENT WITH HIGH DOSES OF IVERMECTIN IN MODERATE,

    SEVERE AND CRITICAL CASES. Table: DOSE OF IVERMECTINE ACCORDING TO

    SEVERITY, VIRAL LOAD AND RESPONSE TO TREATMENT

    https://www.researchgate.net/p…AND_RESPONSE_TO_TREATMENT


    Taming the cytokine storm: repurposing montelukast for the attenuation and

    prophylaxis of severe COVID-19 symptoms (montelukast = Singulair)

    https://www.sciencedirect.com/…cle/pii/S1359644620303718

  • This says that Wilson was "never the same" after recovering from the flu. I have read that about several other people. They recovered, but they were weak, and seemed much older. The same may be true of COVID-19.


    Flu, AFAIK, develops into pneumonia and consequent possible scarring of lung tissue.


    COVID does that too - but it has an extra effect that certainly Flu does not so easily replicate, which is that blood vessels everywhere start leaking and blood clotting and this shows in long-term heart, kidney, brain problems as well as typical lung scarring.


    Since these problems are caused by a cytokine storm (bradykinin induced most likely) that is directly induced locally by virus proteins, rather being just the bodies normal immune response, things are a lot worse typically than Flu in terms of long-term aftereffects.


    That much is known, though the exact mechanism is still under investigation - similarly how to stop it.


    For example (comment on the link above):


    This is my first post here but I have to say that I’m struggling that anyone is taking bradykinin seriously. The amount of ACE2 in the lungs is negligible. Anyone can go to the human protein atlas to see for themselves the tissues where ACE2 is strongly expressed.

    https://www.proteinatlas.org/ENSG00000130234-ACE2/tissue

    And read the following publications

    https://pubmed.ncbi.nlm.nih.gov/32715618/

    https://pubmed.ncbi.nlm.nih.gov/32675206/

    https://pubmed.ncbi.nlm.nih.gov/32170560/

    And compare and contrast these 2020 publications to the 2004 publication which shows abundant ACE2 in lungs

    https://pubmed.ncbi.nlm.nih.gov/15141377/

    And then go to this Nottingham COVID Research Group website to see that ACE2 does NOT get up-regulated in severely ill patients

    https://www.nottinghamcrg.info/results

    To recap, ACE2 is not responsible for severe COVID-19 lung disease. It cannot be because there is not enough of it to sustain a serious infection in that organ.

    Whereas Neuropilin-1, which is abundant in the lungs, has been shown to be a SARS-CoV-2 receptor

    https://www.biorxiv.org/content/10.1101/2020.07.29.227462v1

    We (https://arxiv.org/abs/2004.10274) and others (PMID:32130973) think that integrins will join Neuropilin-1 as receptors in the lungs. The best evidence so far to be made publicly available for the role of integrins as SARS-CoV-2 receptors can be found on the Nottingham website linked above.



    Taming the cytokine storm: repurposing montelukast for the attenuation and

    prophylaxis of severe COVID-19 symptoms (montelukast = Singulair)

    https://www.sciencedirect.com/…cle/pii/S1359644620303718


    On that topic, it is welcome people are thinking about that like this paper proposing montelukast. The real progress treating COVID will come from inhibiting that storm and all of the consequent short and long term problems. Once we have done that COVID really does become something like Flu, very nasty, and will kill some, but no worse than many other things.


    The trouble is that the cytokine (or bradykinin, or hyaleurin) storm is incredibly complex (as you can see from the above argument with the bradykinin hypothesis) and while we know all these things correlate we don't really know cause and effect well, and hence don't know which interventions, blocking or promoting a particular interaction, will work. Most likely we already have drugs that in a suitable cocktail, carefully dosed, will be remarkably effective. Finding them is the problem because in vitro experiments and simulations can't study the whole system, and trials on people don't give you much information each trial so it can take a long time to work out all the candidate helpful drugs and then how they combine.


    I guess we can hope eventually we get a really good understanding of all the cytokine system interactions and then work out theoretically what would be a good bet. It will be a big deal for medicine understanding this, and we are in a much better place to do this now than we were even 10 years ago.


    Coming back to montelukast. The theoretical justification for that does not mention bradykinin, nor these other new ideas that studying COVID has provoked, and therefore is a bit incomplete. Does not mean it is wrong, just all these "it might work" justifications are uncertain, only a few will actually pan out.


    THH


    On the subject of monoclonal antibodies as treatment - since this is topical - obviously anything that reduced viral replication will reduce the cytokine storm effects. I guess the question is how well this works - normal wisdom is that anti-virals - including monoclonal antibodies, and not that much help once the infection has taken hold. COVID might be different not least because a high viral presence in the body seems associated with all this cytokine storm nastiness.

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