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Latest frum my daughter:

Picture of her Covid Team of Resident Drs who have been tasked at her hospital with fighting this virus:

View attachment 840777

My daughter is lower right. (Picture is frum a conference about 7weeks ago. She was the principle speaker)
Her:
Our part of the hospital that houses the Covid pnts (patients) is being called "Covid Town" and we're being called the "Covid Cops"

Me: Whats the load like ?

Her: I don't even know the exact count but we have 19 on ventilators and have had more fatalities

Me: what r u seeing thats typical?

Her:Typical would be a lady who was diagnosed with covid last week
Came in to er respiratory failure , intubated and had cardiac arrest peri intubation
She is overweight, obese & now in [covid] icu

ME: any prior?

Her: We did cooling to 33C for brain preservation post cardiac arrest was down for 2 minutes so hopefully will be alright
Other than being obese she had no prior & no meds
All of our icu have history of either prior issues, smoking etc or and are obese. Virus is really mean to any1 that smokes or is overweight or old.
Have to go tyl
Hats off to our most valiant on the frontlines, especially with cases as desperate of these. I'd love to hear how arrests are conducted since they're the Covid Cops.
 

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CDC dashboards for US cases
https://www.cdc.gov/coronavirus/2019-ncov/cases-updates/cases-in-us.html

WHO dashboard for world wide cases including the curves
https://experience.arcgis.com/experience/685d0ace521648f8a5beeeee1b9125cd

China is the only curve that has leveled for new cases but has not decreased in reporting of new cases to the WHO.

Stuff that you can find readily but:
After exposure: 2-14 days to show symptoms with an average of 5 days
Common symptoms - shortness of breath, loss of smell or taste, fever, dry cough or sore throat
After the first symptom : 2 to 6 weeks to recover
Virus affects people's ability to breath by causing swelling at the back of the throat, then travels into the lungs. It is probable that shortness of breath indicates the virus has made it to the lungs. Body's immune response to the virus in the lungs creates thickening of the lung walls which reduces the transmission of oxygen between the blood and the lungs. You may also get fluid as part of the body's normal immune response, also called a viral pneumonia. The CDC lists viral pneumonia as the 8th leading cause of death in the United States before COVID-19. The thickening is effectively scar tissue and will not go away after you recover. I.e. permanent lung damage. Respirators are needed to increase the volume, and possibly quality, of the air to keep a persons' blood normally oxygenated or you suffocate. Thus an underlying condition that affects the body's abilities to process oxygen, quickly increases the possibility of it being fatal. The fluids from pneumonia will go away but you may not return to your previous lung capacity. How bad it is or isn't can't be determined until many more people recover and lots of testing and report writing is done.

Just don't get it if you can help it.

In areas of lower income, the percentage of 25-40 years old who die from COVID-19 is closer to 30%. In richer areas, or places with strong nationalized health care, 95% of those who die are over 70.

Don't trust me, get out to the CDC and WHO sites.
 
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Discussion Starter #24
A discussion with my daughter on HCQ (the malaria drug) therapy for treating Covid patients.

This is a summary with citings found after we spoke:

I'm tired of all the circular arguments regarding COVID-19 mostly by people with no medical background so I'm trying to understand the workings behind the mechanism by which the virus infects cells and how it operates utilizing primary sources. We know President Trump (whom anyone with a brain of science knows is an idiot) has been touting HCQ therapy for about a minute now, but the only literature I can find that promotes this therapy outside of anecdotal evidence and suspect blogs is from here:

https://chemrxiv.org/articles/COVID-19_Disease_ORF8_and_Surface_Glycoprotein_Inhibit_Heme_Metabolism_by_Binding_to_Porphyrin/11938173
Chinese caveats apply, but the gist of the study states that in conjunction to the already known mechanism of entry into cells via ACE2r respiratory epithelium, novel coronavirus may bind to membrane porphyrins leading to inhibition of heme metabolism w/ regards to RBCs. Drugs like HCQ and Avigan may reduce that binding all while preventing lysosomal release of proteases leading to decreased viral load
My first problem with this is that it's a model that just seems to be trying to explain a correlation with regards to acute phase reactants (ESR, ferritin) and decreasing Hgb in a small select group of patients. From what I know there does not seem to be any significant drop in Hgb in pts as a whole and labs would easily pick up massive degradation of RBCs. On top of that, I don't see how the virus would even infect RBCs considering they lack all the essential organelles needed for proper replication. Coronavirus isn't a protozoa like Malaria, thus how would HCQ's lysosomal effects even be relevant in this case?
UPenn is currently conducting a trial to see if this makes sense. Will be curious to see if this angle has actual merit.
Circulation has recently published an article on how ACE2r's downstream effects might be the actual culprit in these cases:
https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.120.047049
ACE2r converts Angiotensin I and II into Angiotensin 1,7 and 1,9 both of which are cardio-protective factors. Proteases like ADAM17 are upregulated when ACE2r is KO'd leading to expansion of pro-inflammatory markers such as TNF, IL4 and IFN. These things also lead to further coagulation issues (as reported from ICUs around the globe), vascular permeability problems (pulmonary edema, PNA) and myocardial issues (uncontrolled hypertension and MI).
We know pts with cardiac hx have higher expression of ACE2r and are thus at most risk and have the highest mortality associated with COVID-19. I'm more inclined to believe this angle rather than the hemoglobin one.
The curious case here is whether we continue drugs like ACEi/ARBs in these pts. Would depriving pts of substrates that can be converted into protective Angiotensin 1,7 and 1,9 be worthwhile? Or is that promoting a more harmful cascade in allowing for RAAS to function unmitigated?
NEJM has another good article regarding this:
https://www.nejm.org/doi/full/10.1056/NEJMsr2005760?query=featured_home
 
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Discussion Starter #25

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A discussion with my daughter on HCQ (the malaria drug) therapy for treating Covid patients.

This is a summary with citings found after we spoke:

I'm tired of all the circular arguments regarding COVID-19 mostly by people with no medical background so I'm trying to understand the workings behind the mechanism by which the virus infects cells and how it operates utilizing primary sources. We know President Trump (whom anyone with a brain of science knows is an idiot) has been touting HCQ therapy for about a minute now, but the only literature I can find that promotes this therapy outside of anecdotal evidence and suspect blogs is from here:

https://chemrxiv.org/articles/COVID-19_Disease_ORF8_and_Surface_Glycoprotein_Inhibit_Heme_Metabolism_by_Binding_to_Porphyrin/11938173
Chinese caveats apply, but the gist of the study states that in conjunction to the already known mechanism of entry into cells via ACE2r respiratory epithelium, novel coronavirus may bind to membrane porphyrins leading to inhibition of heme metabolism w/ regards to RBCs. Drugs like HCQ and Avigan may reduce that binding all while preventing lysosomal release of proteases leading to decreased viral load
My first problem with this is that it's a model that just seems to be trying to explain a correlation with regards to acute phase reactants (ESR, ferritin) and decreasing Hgb in a small select group of patients. From what I know there does not seem to be any significant drop in Hgb in pts as a whole and labs would easily pick up massive degradation of RBCs. On top of that, I don't see how the virus would even infect RBCs considering they lack all the essential organelles needed for proper replication. Coronavirus isn't a protozoa like Malaria, thus how would HCQ's lysosomal effects even be relevant in this case?
UPenn is currently conducting a trial to see if this makes sense. Will be curious to see if this angle has actual merit.
Circulation has recently published an article on how ACE2r's downstream effects might be the actual culprit in these cases:
https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.120.047049
ACE2r converts Angiotensin I and II into Angiotensin 1,7 and 1,9 both of which are cardio-protective factors. Proteases like ADAM17 are upregulated when ACE2r is KO'd leading to expansion of pro-inflammatory markers such as TNF, IL4 and IFN. These things also lead to further coagulation issues (as reported from ICUs around the globe), vascular permeability problems (pulmonary edema, PNA) and myocardial issues (uncontrolled hypertension and MI).
We know pts with cardiac hx have higher expression of ACE2r and are thus at most risk and have the highest mortality associated with COVID-19. I'm more inclined to believe this angle rather than the hemoglobin one.
The curious case here is whether we continue drugs like ACEi/ARBs in these pts. Would depriving pts of substrates that can be converted into protective Angiotensin 1,7 and 1,9 be worthwhile? Or is that promoting a more harmful cascade in allowing for RAAS to function unmitigated?
NEJM has another good article regarding this:
https://www.nejm.org/doi/full/10.1056/NEJMsr2005760?query=featured_home
This guy (at the start) is reporting an unusually high number of cardiac arrests in NYC.

Do you need prescription to buy HCQ?

 

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Discussion Starter #27
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That's good. Unless it's for cleaning a fish tank I suppose.

On the other hand, a producer (of the medicine) in the Netherlands has gotten police protection, since 'obscure men' visited his office to buy a huge amount, not long after Trump started promoting it.

Vague types said:
A drug manufacturer from Zeewolde*was placed under 24-hour police security on Saturday. Jan Willem Popma's company Ace makes chloroquine, an old malaria medicine that had a positive effect on a number of Covid-19 patients. Now Popma is getting increasing visits from "vague types", not only at work but also at his home, he said to EenVandaag.

"Last week several expensive cars came up my street that you normally never see here, with striking young drivers who knocked on my door. They offered large amounts for the pills, but I have already distributed my entire supply across the country. All the pills we produced are distributed the same day," Popma said to EenVandaag.
https://nltimes.nl/2020/03/23/chloroquine-maker-24-hour-security-drug-used-treat-covid-19-patients
 

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Discussion Starter #29
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Hydroxycholorquine and Chloroquine are NOT the same thing..............

https://www.medicinenet.com/chloroquine_aralen_vs_hydroxychloroquine_plaquenil/article.htm



<<<<<<<-----------------------take it frum a koon!

They're both used to treat malaria but they are not the same drug. And the CDC link in my previous post warns against using foreign (non USA) made drugs that may only impersonate HCQ.
Thanks, but I was not considering anything myself.

According to Trump "some people would add 'hydroxy'.

 

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Discussion Starter #31
Thanks, but I was not considering anything myself.

According to Trump "some people would add 'hydroxy'.

President Trump has zero credibility with me and I pay no attention what so ever to any of his self congratulatory shows. I've tried to only listen to those who are trying to assemble medical data based on science; Dr's directly involved, etc. and thats why I started this thread.
 

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President Trump has zero credibility with me and I pay no attention what so ever to any of his self congratulatory shows. I've tried to only listen to those who are trying to assemble medical data based on science; Dr's directly involved, etc. and thats why I started this thread.
My point was more that in my country apparently many drugdealers were interested in the substance (in this case chloroquine). Not necessarily to send to the US, rather that the same thing may be going on in the US, esp targetted to people who don't have healthcare. People who can't afford to involve a dr. but might end up in an ambulance with a cardiac arrest. (or end up under treatment by people like your daughter)

I hope that's not the case, obviously

I think the opioid crisis has shown that kind of a shadow (black) market of prescription drugs is not unrealistic.
 

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Discussion Starter #33
New USA covid deaths projection is now down to 60,000ish.........
https://www.cnn.com/2020/04/08/politics/what-matters-april-8/index.html

Just a couple days ago it dropped from over 100,000 to 82,000 now to 60,000.


<<<<<<<<--------------------take it frum a koon!

Before they're done the projections will be lower than the total number of actual deaths......... (Insert sarcasm gif)
 

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Re: Transmission from bats to humans, apparently people sold bats at the "wet market" in China, probably as ingredients for traditional medicine.
 

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Discussion Starter #35
Re: Transmission from bats to humans, apparently people sold bats at the "wet market" in China, probably as ingredients for traditional medicine.



<<<<<<<<---------------------take it frum a koon!

Talks about the bat connection - link in post #19 of this thread. Maybe thats what you're referring to. If I recall its also about having & keeping the bats as pets.
 

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I just see the ones who most benefits from this bullshit are central banks and governments.
The WHO and other internationals organizations ( like the ONU AND IMF ) are just totally useless and clueless but they can steal your money and your great-grand son money using debt for whatever are their intentions ...

And let's be real... we are seeing the collapse of the dollar and nobody is gonna lost more than the americans people .
 

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According to the National Review from April 8th, another theory is that the virus jumped from bats to pangolins (which are more commonly sold than bats for traditional medicine).

"...pangolins, the anteater-like other animal species that is suspected to be a possible “transfer species” — i.e, the bat gives COVID-19 to the pangolin, some human being either eats or otherwise comes in contact with the pangolin, and contracts the virus. This doesn’t mean that those markets never sold bats or pangolins. But it does mean that they weren’t common enough to be easily witnessed and mentioned in news coverage."

Regardless of the purpose (food, medicine, or pets) or the source (bat or pangolin) the wet markets were probably the cause.

In his book from 1991, "What Kind of God," writer Zhou Quing uncovered serious safety food problems in China. I can only imagine that traditional medicine ingredients fare no better in terms of regulation or inspection.
 

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Discussion Starter #38
Spoke with my dawter yesterday. She really had nothing new to report. More cases , more deaths, everone trying to hang on and at this point riding the storm out..........



<<<<<<------------------take it frum a koon!

She told me she's pulling her turn as Nursing Home On Call - its for 2 weex and she's glad she doesn't need to do the Covid rounds for awhile.
HER: " I used to hate Nursing Home call. So boring but after what I've been thru the last 6 weex; its like being on a complete paid vacation. I sit home, mostly, work most of the time on my study & research projects, play with the cats and if/when a nursing home needs a Dr., I go....."
 

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Hey koon. Could you please forward this to your bright little girl and see what her thoughts? I am having trouble deciohering all of it. Already posted in other thread though.

=======

I just found this article from that same name, Zhi Shengli, dated 2007.

Received 20 May 2007.
Accepted 15 November 2007.

*Corresponding author. Mailing address for Z. Shi: State key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, Hubei 430071, China
https://jvi.asm.org/content/82/4/1899

Tldr; in the discussion (most bottom part) i found this :

Our previous results showed that the SL-CoVs identified in bats are similar to SARS-CoV in genome sequence and organization. The key difference between these two groups of closely related viruses lies in their S protein sequences, specifically, the RBM, in which there are two deletions in the bat SL-CoV S sequences (29). From previous published studies indicating the importance of the structural fit between the receptor ACE2 and the S protein of SARS-CoV variants and the sensitivity of S proteins to point mutations in the RBM region, it was speculated that SL-CoV S is unlikely to use ACE2 as a receptor for cell entry unless the bat ACE2 homolog is significantly different from those of other mammals


Then a big BUT.

To address these unanswered questions, we cloned and expressed the bat R. pearsonii ACE2 gene and examined the abilities of ACE2 proteins from human, palm civet, and R. pearsonii to support infection by HIV-based pseudoviruses containing different S protein constructs.

Our results indicated that the bat SL-CoV (Rp3) S protein is unable to use ACE2 for cell entry regardless of the origin of the ACE2 molecule.

We also demonstrated that the human SARS-CoV S cannot use bat RpACE2 as a functional receptor.

On the other hand, we demonstrated that after replacement of a small segment (aa 310 to 518) of Rp3-S by the cognate sequence of BJ01-S, the CS protein mimics the function of BJ01-S in regard to receptor usage in the HIV pseudovirus assay system.
And my mind went blank right after that. Poofs.






Sent sans PC
 
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