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DrStool

Anditsgone 5/15/20

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Monoclonal antibody therapeutics has been around for 30 years. In fact everyone of us who was breast fed received antibodies from our mother's milk which protected us from pathogens until we developed our own functioning adaptive immune system. Giving plasma from recovered patients to infected patients has already be proven effective. It works because it transfers IgG from a recovered patient to a sick patient which binds the virus and leads to its removal. The problem there is plasma donations are few and you may not get enough of the type of antibody that will work best i.e. that has a high enough titer and specificity and can inactivate the virus.  Monoclonal antibody therapeutics solves this because we can test millions of antibodies and find the one that is 100% effective and produce in cheaply in unlimited amounts. There is a downside to every therapy and the major downside here is that immunity is not permanent because IgG antibodies don't last forever. So you would need to periodically get another dose. The other issue is once the disease is too advanced and you already have organ damage or a cytokine storm it isn't going to help.  So you either need to take it early in the coarse of disease or take it as a prophylactic. Antibodies are produced by B Cells and when a B Cell with an IgM surface antibody binds successfully to the virus (hopefully to the S Protein) it starts to multiply into many plasma B Cells that produce plasma IgG which have the same binding  domains. Once IgG binds to the S protein on the surface of the virus the virus is marked for destruction. IgG looks like the letter Y and is composed of two light chains and two heavy chains. Only the heavy chains differ between IgM and IgG. It is the light chains on the "arm" of the Y that bind specifically to the S protein.  

https://en.wikipedia.org/wiki/Antibody

https://en.wikipedia.org/wiki/Monoclonal_antibody_therapy

A paper regarding the research is being submitted to a peer reviewed journal:

https://investors.sorrentotherapeutics.com/news-releases/news-release-details/sti-1499-potent-anti-sars-cov-2-antibody-demonstrates-ability

There are several companies with candidate monoclonal antibodies. Which will be FDA approved first will be worth watching but with anything involving the FDA it will take time and involve several trials. 

https://www.biorxiv.org/content/10.1101/2020.03.11.987958v1.full.pdf

My sister has already produced antibodies against SARS-CoV-2 in cows. Why? because in the third world consumption of cow colostrum containing antibodies may cheaply offer some immunity to the virus without medical intervention. 

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9 minutes ago, sandy beach said:

GE back to 1991 levels.

Jack Welch is still smiling.........(passed away in March 2020)

in 2001.......severance payment of $417 million

>: He had a book called "Winning".......

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Bundesliga plays tomorrow.......

FOX sports is televising.........Some others are streaming......

I Hope This Turns Out Good!

 

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What's the story with beta blockers and COVID19?  I know there are those that believe it helps to block the virus from binding to the cells.  Any investigational studies? Or will this be a non starter because it's too easy, dirt cheap, and widely available?  

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1 hour ago, DrStool said:

What's the story with beta blockers and COVID19?  I know there are those that believe it helps to block the virus from binding to the cells.  Any investigational studies? Or will this be a non starter because it's too easy, dirt cheap, and widely available?  

I think the current hypothesis is that ARBs could enhance COVID-19 reactions:

 

"The connection between ARBs and COVID-19
Professor Murray Esler is the senior director of the Baker Heart and Diabetes Institute and consultant cardiologist at the Alfred Hospital Melbourne and Adjunct Professor of Medicine at Monash University.

 

Professor Esler told newsGP he first became concerned about ARBs and COVID-19 when talking to his daughter, a public health physician in the Northern Territory, a few weeks ago.
 
‘The first clue was really that severe COVID-19 infection was more common in hypertension, and hypertensive patients are really not predisposed to infection at all, so that was very odd,’ he said.

 

‘So that suggested perhaps this predisposition to severe COVID-19 infection in hypertension could possibly be a drug effect mediated by ARBs which upregulates ACE-2, and potentially predisposes to infectivity but also in particular, severe infection.’
 
Professor Esler has been in contact with colleagues in Lombardy, Italy, who are currently exploring it further."

 

https://www1.racgp.org.au/newsgp/clinical/ace-inhibitors-arbs-and-covid-19-what-gps-need-to

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That's old news. The latest is that there seems to be some benefit based on tracking of Wuhan patients. 

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Association of Inpatient Use of Angiotensin Converting Enzyme Inhibitors and Angiotensin II Receptor Blockers with Mortality Among Patients With Hypertension Hospitalized With COVID-19.

https://www.ncbi.nlm.nih.gov/pubmed/32302265

Retrospective, multicenter study of 1128 adult pts with HTN diagnosed with COVID19: Taking ACEI/ARB: 188 Not Taking ACEI/ARB: 940 Unadjusted 28d Mortality: No ACEI/ARB: 9.8% ACEI/ARB: 3.7% P = 0.01

ACEI/ARB also associated with decreased mortality compared to other antihypertensive drugs (aHR 0.30; 95% CI 0.12 to 0.70; p = 0.01 Bottom Line: Inpt use of ACEI/ARB was ASSOCIATED with lower risk of all-cause 28d mortality compared with ACEI/ARB non-users.

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Ok. Not sure what that said but sounded good. ARB is beta blockers?

 

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There'd be a lot of **BEEPS** as Doc cursed his way through the episode.

Powell would say something dishonest or stupid.

Doc would lose his mind and start hollering.

Stoolies would cheer their televisions.

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24 minutes ago, Jimi said:

There'd be a lot of **BEEPS** as Doc cursed his way through the episode.

Powell would say something dishonest or stupid.

Doc would lose his mind and start hollering.

Stoolies would cheer their televisions.

I am smiling just thinking about it......🤣

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