OtherGround Forums OG doc. AMA on COVID-19

4/29/20 1:43 PM
2/4/09
Posts: 11148
Job Security -
NoNeed4aScreenName -
MattyECB -
NoNeed4aScreenName -
MattyECB -
prof - For the medical professionals:

One worry has been that if there is a second wave of COVID-19
it could coincide or overlap with the flu season, hence putting far more pressure on the health care system and hospitals than we are even seeing now.

On the other hand, it seems there may be some factors mitigating that scenario:

1. We will in all likelihood still have in place the type of physical distancing practices we've become accustomed to, and other practices, that have "lowered the curve" infection rate for COVID. It would seem other contagious disease infection rates like The Flu would also be much lower due to this as well. (Of course if COVID rates in a second wave are maintained just below hospital capacity, even reduced flu infection could push hospitalizations above the threshold).

2. Hopefully we will be better prepared in a second wave, having ramped up production of PPE and other necessary equipment, having established better emergency care plans for overflow, etc.

So one thing I haven't seen info on yet:

Are infection rates for any other diseases down at this time, due to physical distancing etc - colds, flu, whatever?
 

When I checked a week or two ago, flu deaths were in line with historical expectations if you adjusted for the lag in reporting that we tend to see.

 

Comparing non-COVID deaths after the fact will definitely help us suss out the accuracy of our diagnoses in absence of real testing and arguably help us understand which pre-existing conditions get fucked by COVID. Everyone jokes about inflated numbers for pre-existing conditions, but you can have a great prognosis and life expectancy with diabetes but get mouth fucked by COVID.

 

The research on obesity, diabetes, and smoking as COVID risk factors is still nascent but already pretty damning.

The diabetes tie in could be the fact that now they have started to explore ARBs and ACEi in diabetes. 

 

In patients with type 2 diabetes, hypertension, and microalbuminuria, ACE inhibitors and ARBs have been shown to delay the progression to macroalbuminuria. (A) In those with type 2 diabetes, hypertension, macroalbuminuria (>300 mg/day), and renal insufficiency, an ARB should be strongly considered.

 

https://www.google.com/search?q=arbs+ace+diabetes&oq=arbs+ace+diabetes&aqs=chrome..69i57j0l2.5042j0j7&client=ms-android-rogers-ca&sourceid=chrome-mobile&ie=UTF-8

 

 

IMO if they want to really tackle this. Target ACE2 and find a workaround for the Mas pathway to alleviate ARDS

That's fascinating. Besides learning it in undergrad a decade ago, I haven't touched diabetes material at all. Didn't know the Ace2 receptor was involved in its pathogenesis, and I've only read statistical studies linking it to COVID.

 

Thanks for giving me something fun to look up!

we can take this information we are learning from Covid and probably make some important new discoveries in lung treatment. 

 

I feel like we can for one thing revolutionize ARDS treatment 

Don’t know if this is relevant to this discussion, but some of my colleagues ran a regression model on about 700 patients admitted to hospitals here for COVID-19 to look for risk factors of death or ICU-treatment. About 30% of them were on ACE-inhibitors.

They found age, male sex and beta-blocker treatment to be risk factors - but not ACE- or ARB-inhibitors.

IMO, the Beta-blockers are probably showing up due to residual confounding from not being able to properly adjust for cardiovascular comorbidity. Still, it seems like ACE-inhibitors at least do no harm - at least until we have the results from the ongoing RCTs.

Sorry I misread. So it is in fact only one of the 2 that puts patients more at risk. 

4/29/20 1:45 PM
2/4/09
Posts: 11149

Makes sense that that would be the case. Since ACE inhibitors would prevent he substrate for ACE2 to be formed. 

 

ARBS Target further down the pathway!!

 

This is why I was asking earlier if Mataleo noticed any differences in the meds! This is a pretty good find if I'm thinking correctly now

4/29/20 1:45 PM
11/23/10
Posts: 240
jcblass - I saw a hysterical post on social media, citing 135 new CV cases in Texas along with 10 deaths, the worst ever on record for the state.

Of course everyone is blaming the increase on the recent re-opening and suggesting the Governor has blood on his hands (expected).

Question: Isn't the incubation period for this virus 7-10 days. If so, wouldn't that mean anyone getting sick today or dying today contracted the virus well before re-opening. Not to mention nearly 50% of all Texas deaths are in nursing homes, so the people dying are not getting it from Waffle House on their day out of the house.



I don’t know the specifics, but you’re right about the incubation period. And the statistics may reflect retroactively included cases from back in time (like the UK added >4000 deaths to their total today, but the deaths didn’t happen today, they just happened in peoples’ homes).

The deaths you see today are an indicator of the degree of spreading 2-5 weeks ago. If they go up the day you lift quarantine measures, it’s not because of the lift - it’s because the measures were inadequate 2-5 weeks ago. So it’s a sign that you need/needed more social distancing, not less. From a heathcare perspective at least.

The nursing homes get their infections from staff and visitors.  If those can go to waffle house, it’s almost the same as the old folks going there (with how infectious COVID-19 is, and the lack of PPE in waffle houses and in many nursing homes)

4/29/20 1:45 PM
4/20/20
Posts: 278
Easters -

Another one for the professionals - can someone explain (bro science is best) exactly why testing is so important compared to hospitalizations?  I keep hearing "test, test, test" but why is testing so important when hospitalizations are so low?  Is it just the ability to isolate and track?  

 

I guess I just dont see how testing is going to change much.  Right now it seems like there's enough tests in my region to test anybody who meets the criteria, but they're still saying they need to double testing capacity.  Is the plan to start testing asymptomatic citizens too?  Isnt the protocal going to be the same, quarantine for two weeks if you have symptoms, positive test or not?  

Not a pro, but here's my take.

 

Lots of people have mild symptoms, or none at all, but still carry the virus and can spread it to others who may have much more severe reactions. 

 

If you can't get tested, you'll never know if you're spreading it around.

4/29/20 2:31 PM
1/1/01
Posts: 65686
jcblass - I saw a hysterical post on social media, citing 135 new CV cases in Texas along with 10 deaths, the worst ever on record for the state.

Of course everyone is blaming the increase on the recent re-opening and suggesting the Governor has blood on his hands (expected).

Question: Isn't the incubation period for this virus 7-10 days. If so, wouldn't that mean anyone getting sick today or dying today contracted the virus well before re-opening. Not to mention nearly 50% of all Texas deaths are in nursing homes, so the people dying are not getting it from Waffle House on their day out of the house.




Incubation is between 1-14 days. I've seen 5 days cited as the average.

But are you sure Texas already reopened? I thought that was happening May 1st.
4/29/20 2:36 PM
2/4/09
Posts: 11152
NoNeed4aScreenName -

Makes sense that that would be the case. Since ACE inhibitors would prevent he substrate for ACE2 to be formed. 

 

ARBS Target further down the pathway!!

 

This is why I was asking earlier if Mataleo noticed any differences in the meds! This is a pretty good find if I'm thinking correctly now

This would also coincide with the pilot study where they measured different levels and the angiotensin intermediates and saw that buildup of angiotensin I leads to poor prognosis in ARDS. 

 

The pathway for the protective features of ACE2 Get blocked upstream because of ACEi

4/29/20 2:48 PM
11/23/10
Posts: 241
madmartigan -
Easters -

Another one for the professionals - can someone explain (bro science is best) exactly why testing is so important compared to hospitalizations?  I keep hearing "test, test, test" but why is testing so important when hospitalizations are so low?  Is it just the ability to isolate and track?  

 

I guess I just dont see how testing is going to change much.  Right now it seems like there's enough tests in my region to test anybody who meets the criteria, but they're still saying they need to double testing capacity.  Is the plan to start testing asymptomatic citizens too?  Isnt the protocal going to be the same, quarantine for two weeks if you have symptoms, positive test or not?  

Not a pro, but here's my take.

 

Lots of people have mild symptoms, or none at all, but still carry the virus and can spread it to others who may have much more severe reactions. 

 

If you can't get tested, you'll never know if you're spreading it around.

Yeah. It’s for tracing and isolating those with too little symptoms or wits to self-isolate on their own accord. Especially those who interact with vulnerable groups.

I think a lot of countries want to be able to do what e.g. South Korea has been able to do. That is, keeping the epidemic contained in a sustainable way (lockdown is only viable for a few weeks) through wide-spread, free-for-all testing and aggresively tracing and testing contacts of positive cases. Too bad it’s only really feasible if the number of actively infected isn’t too high, and if you have the gear and infrastructure (test kits, PPE or secure sampling facilities, and spacious sampling sites).

I’m certain that is what we’re going to in my country, perhaps starting as early as next week. Both virus and antibody testing with very few limitations it seems. They’ve set up sampling site tents around the country, and the authorities have leaked some stuff about the long-term strategy, but the details haven’t come out yet.

There’s no guarantee as to how effective it will be though. It may only work in South Korea because of their particular habits/culture of social interaction lessens spread enough for this approach to keep up. If people stop being mindful of social distancing and hygiene, it will fail for sure. So many unknowns with this. 

4/29/20 3:17 PM
4/26/13
Posts: 4748
Job Security -
madmartigan -
Easters -

Another one for the professionals - can someone explain (bro science is best) exactly why testing is so important compared to hospitalizations?  I keep hearing "test, test, test" but why is testing so important when hospitalizations are so low?  Is it just the ability to isolate and track?  

 

I guess I just dont see how testing is going to change much.  Right now it seems like there's enough tests in my region to test anybody who meets the criteria, but they're still saying they need to double testing capacity.  Is the plan to start testing asymptomatic citizens too?  Isnt the protocal going to be the same, quarantine for two weeks if you have symptoms, positive test or not?  

Not a pro, but here's my take.

 

Lots of people have mild symptoms, or none at all, but still carry the virus and can spread it to others who may have much more severe reactions. 

 

If you can't get tested, you'll never know if you're spreading it around.

Yeah. It’s for tracing and isolating those with too little symptoms or wits to self-isolate on their own accord. Especially those who interact with vulnerable groups.

I think a lot of countries want to be able to do what e.g. South Korea has been able to do. That is, keeping the epidemic contained in a sustainable way (lockdown is only viable for a few weeks) through wide-spread, free-for-all testing and aggresively tracing and testing contacts of positive cases. Too bad it’s only really feasible if the number of actively infected isn’t too high, and if you have the gear and infrastructure (test kits, PPE or secure sampling facilities, and spacious sampling sites).

I’m certain that is what we’re going to in my country, perhaps starting as early as next week. Both virus and antibody testing with very few limitations it seems. They’ve set up sampling site tents around the country, and the authorities have leaked some stuff about the long-term strategy, but the details haven’t come out yet.

There’s no guarantee as to how effective it will be though. It may only work in South Korea because of their particular habits/culture of social interaction lessens spread enough for this approach to keep up. If people stop being mindful of social distancing and hygiene, it will fail for sure. So many unknowns with this. 

So right now if you have a fever or dry cough you call your doctor and they either say come in for a test or stay home and quarantine as if you’re positive.  What changes with more tests? You get symptoms, call your doctor, and everybody goes in for a test?  Right now we’re all supposed to act as if we’re positive, especially if we hAve symptoms.  I guess I just don’t see how having more tests helps so much that we can impoement slow opening until we have them 

4/29/20 3:21 PM
12/1/12
Posts: 2443
Caladan -
used2wrestle -

Randomized remdesivir data just came out positive. Let the markets rip! What a roller coaster.

Looks like they just tested a 5 day treatment vs a 10 day treatment and found the 5 day was just as effective. Good news that IF it works, they would be able to get to more people sooner.

 

I don't think we have data yet regarding its efficacy. Theoretically its possible that the 5 day treatment and 10 day treatment had the same results because the treatment doesn't work. Someone can correct me if I'm wrong.

There were 2 trials with news today. One was a placebo controlled trial. Accelerated approval coming.

 

4/29/20 3:33 PM
4/20/20
Posts: 289
Easters -
Job Security -
madmartigan -
Easters -

Another one for the professionals - can someone explain (bro science is best) exactly why testing is so important compared to hospitalizations?  I keep hearing "test, test, test" but why is testing so important when hospitalizations are so low?  Is it just the ability to isolate and track?  

 

I guess I just dont see how testing is going to change much.  Right now it seems like there's enough tests in my region to test anybody who meets the criteria, but they're still saying they need to double testing capacity.  Is the plan to start testing asymptomatic citizens too?  Isnt the protocal going to be the same, quarantine for two weeks if you have symptoms, positive test or not?  

Not a pro, but here's my take.

 

Lots of people have mild symptoms, or none at all, but still carry the virus and can spread it to others who may have much more severe reactions. 

 

If you can't get tested, you'll never know if you're spreading it around.

Yeah. It’s for tracing and isolating those with too little symptoms or wits to self-isolate on their own accord. Especially those who interact with vulnerable groups.

I think a lot of countries want to be able to do what e.g. South Korea has been able to do. That is, keeping the epidemic contained in a sustainable way (lockdown is only viable for a few weeks) through wide-spread, free-for-all testing and aggresively tracing and testing contacts of positive cases. Too bad it’s only really feasible if the number of actively infected isn’t too high, and if you have the gear and infrastructure (test kits, PPE or secure sampling facilities, and spacious sampling sites).

I’m certain that is what we’re going to in my country, perhaps starting as early as next week. Both virus and antibody testing with very few limitations it seems. They’ve set up sampling site tents around the country, and the authorities have leaked some stuff about the long-term strategy, but the details haven’t come out yet.

There’s no guarantee as to how effective it will be though. It may only work in South Korea because of their particular habits/culture of social interaction lessens spread enough for this approach to keep up. If people stop being mindful of social distancing and hygiene, it will fail for sure. So many unknowns with this. 

So right now if you have a fever or dry cough you call your doctor and they either say come in for a test or stay home and quarantine as if you’re positive.  What changes with more tests? You get symptoms, call your doctor, and everybody goes in for a test?  Right now we’re all supposed to act as if we’re positive, especially if we hAve symptoms.  I guess I just don’t see how having more tests helps so much that we can impoement slow opening until we have them 

But if you don't have symptoms you don't call. You don't get tested .

 

So more tests means you can go , ideally, to somw testing kiosk, get a clean bill of health, and you and eveyone else can feel confident you're not spreading the virus .

 

 

4/29/20 4:01 PM
12/1/12
Posts: 2444

NIAID just pressed released more details on the pos. trial now. Trial was stopped early by IDSMC and patients were switched to treatment. 31% reduction in recovery time (stat sig.) 8% mortality vs. 11.6% on placebo. Emergency use authorization coming possibly this afternoon.

4/29/20 4:04 PM
2/4/09
Posts: 11154
used2wrestle -

NIAID just pressed released more details on the pos. trial now. Trial was stopped early by IDSMC and patients were switched to treatment. 31% reduction in recovery time (stat sig.) 8% mortality vs. 11.6% on placebo. Emergency use authorization coming possibly this afternoon.

14 days discharge doesnt seem to spectacular. Anyone have any links to the study?

4/29/20 4:24 PM
2/4/09
Posts: 11155

Does anyone have access to the data? There were 2 trials for Gilead and Redemsivir right? Anyone with access to the Lancet article wanna post it? I'm paywalled. 

 

If anyone has the other trial data could you post it? 

 

No need for the intro or filler. Just the methods and results please. 

4/29/20 4:31 PM
9/8/02
Posts: 26004
Tomato Can - 
jcblass - I saw a hysterical post on social media, citing 135 new CV cases in Texas along with 10 deaths, the worst ever on record for the state.

Of course everyone is blaming the increase on the recent re-opening and suggesting the Governor has blood on his hands (expected).

Question: Isn't the incubation period for this virus 7-10 days. If so, wouldn't that mean anyone getting sick today or dying today contracted the virus well before re-opening. Not to mention nearly 50% of all Texas deaths are in nursing homes, so the people dying are not getting it from Waffle House on their day out of the house.




Incubation is between 1-14 days. I've seen 5 days cited as the average.

But are you sure Texas already reopened? I thought that was happening May 1st.

You could be right, which would make the post even more hysterical. LOL, some are already blaming the governor for re-opening deaths, and the state is still closed, fml.
4/29/20 5:10 PM
1/1/01
Posts: 98915
EFM - 
the_shrike -
Trust -

Today's MedCram update - COVID-19 is really a lot worse than a flu, it's destroying blood vessel walls

Just watched that.  Frightening

Also mind boggling that there are people out there who are looking at this disease at this level.  Almost hard to believe.


Well prepare to have your mind boggled even more.  

This is still hypothetical level, stuff, but here he shows what could potentially be going on at a very low (detailed) level.  Basically the SAR-CoV-2 virus blocks angiotensin 1,7 from regulating the production of superoxides, which would be wreaking havoc on vessels.  

He starts off plainly saying COVID-19 is an endothelial disease.  

Edited: 4/29/20 5:13 PM
2/4/09
Posts: 11157
Trust -
EFM - 
the_shrike -
Trust -

Today's MedCram update - COVID-19 is really a lot worse than a flu, it's destroying blood vessel walls

Just watched that.  Frightening

Also mind boggling that there are people out there who are looking at this disease at this level.  Almost hard to believe.

 

Well prepare to have your mind boggled even more.  

This is still hypothetical level, stuff, but here he shows what could potentially be going on at a very low (detailed) level.  Basically the SAR-CoV-2 virus blocks angiotensin 1,7 from regulating the production of superoxides, which would be wreaking havoc on vessels.  

He starts off plainly saying COVID-19 is an endothelial disease.  

Son of a bitch. I could have hit this one on the head of the nail. THis is the shit I've been talking about. Seems like other researchers are taking the same stance 

 

 

A hypothesis for pathobiology and treatment of COVID?19: the centrality of ACE1/ACE2 imbalance

 

SARS viruses and Angiotensin action/signaling

Infection of cells by SARS viruses that bind ACE2 results in two effects: inhibition of ACE2 activity and

decrease of ACE2 expression in infected cells (Kuba et al., 2005; Haga et al., 2008; Glowacka et al.,

2010; Zhang et al., 2020). Indirect evidence for the latter response in COVID-19 is data showing

elevation in circulating ANG II with viral infection and increased circulating ANG II peptide with higher

viral loads (Liu et al., 2020b).

Our hypothesis is founded on the following ideas that derive from data in reports cited in ensuing

sections:

1. SARS viruses decrease ACE2 activity and expression.

2. The decrease in ACE activity creates an imbalance in signaling by ACE1 and ACE2 products

3. This imbalance increases ANG II/AGTR1 signaling and is superimposed on concurrent

pathology (e.g., chronic lung disease, cardiac remodeling in the lung and heart, respectively).

ANG II is a pivotal mediator of injury in both tissues; enhancement of its effects together with

signaling from comorbidities can increase severity of COVID-19.

4. In patients more susceptible to the damaging effects of ANG II, the decrease in ACE2 activity

by SARS viruses can unleash a cascade of injurious effects through a heightened imbalance in

the actions of the products of ACE1 versus ACE2.

5. The proposed imbalance in the signaling and actions of products of ACE1/ACE2 implies the

potential of pharmacological approaches that redress this imbalance via: a) decrease in ACE1

activity, b) blockade of AGTR1, and/or c) increase in ACE2-mediated signaling by affinity-

trapping the SARs virus, enhancement of ACE2 expression/activity, or d) by agonists for

receptors of ACE2-derived peptides

 

https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1111/bph.15082

4/29/20 5:16 PM
1/1/01
Posts: 98916
NoNeed4aScreenName - 
Trust -
EFM - 
the_shrike -
Trust -

Today's MedCram update - COVID-19 is really a lot worse than a flu, it's destroying blood vessel walls

Just watched that.  Frightening

Also mind boggling that there are people out there who are looking at this disease at this level.  Almost hard to believe.

 

Well prepare to have your mind boggled even more.  

This is still hypothetical level, stuff, but here he shows what could potentially be going on at a very low (detailed) level.  Basically the SAR-CoV-2 virus blocks angiotensin 1,7 from regulating the production of superoxides, which would be wreaking havoc on vessels.  

He starts off plainly saying COVID-19 is an endothelial disease.  

Son of a bitch. I could have hit this one on the head of the nail. THis is the shit I've been talking about. Seems like other researchers are taking the same stance 

 

 

A hypothesis for pathobiology and treatment of COVID?19: the centrality of ACE1/ACE2 imbalance

 

SARS viruses and Angiotensin action/signaling

Infection of cells by SARS viruses that bind ACE2 results in two effects: inhibition of ACE2 activity and

decrease of ACE2 expression in infected cells (Kuba et al., 2005; Haga et al., 2008; Glowacka et al.,

2010; Zhang et al., 2020). Indirect evidence for the latter response in COVID-19 is data showing

elevation in circulating ANG II with viral infection and increased circulating ANG II peptide with higher

viral loads (Liu et al., 2020b).

Our hypothesis is founded on the following ideas that derive from data in reports cited in ensuing

sections:

1. SARS viruses decrease ACE2 activity and expression.

2. The decrease in ACE activity creates an imbalance in signaling by ACE1 and ACE2 products

3. This imbalance increases ANG II/AGTR1 signaling and is superimposed on concurrent

pathology (e.g., chronic lung disease, cardiac remodeling in the lung and heart, respectively).

ANG II is a pivotal mediator of injury in both tissues; enhancement of its effects together with

signaling from comorbidities can increase severity of COVID-19.

4. In patients more susceptible to the damaging effects of ANG II, the decrease in ACE2 activity

by SARS viruses can unleash a cascade of injurious effects through a heightened imbalance in

the actions of the products of ACE1 versus ACE2.

5. The proposed imbalance in the signaling and actions of products of ACE1/ACE2 implies the

potential of pharmacological approaches that redress this imbalance via: a) decrease in ACE1

activity, b) blockade of AGTR1, and/or c) increase in ACE2-mediated signaling by affinity-

trapping the SARs virus, enhancement of ACE2 expression/activity, or d) by agonists for

receptors of ACE2-derived peptides

 

https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1111/bph.15082


That all sounds lot like what he goes through in the video.  You would understand it a lot better than I do. 

Edited: 4/29/20 5:25 PM
2/4/09
Posts: 11158
Trust -
NoNeed4aScreenName - 
Trust -
EFM - 
the_shrike -
Trust -

Today's MedCram update - COVID-19 is really a lot worse than a flu, it's destroying blood vessel walls

Just watched that.  Frightening

Also mind boggling that there are people out there who are looking at this disease at this level.  Almost hard to believe.

 

Well prepare to have your mind boggled even more.  

This is still hypothetical level, stuff, but here he shows what could potentially be going on at a very low (detailed) level.  Basically the SAR-CoV-2 virus blocks angiotensin 1,7 from regulating the production of superoxides, which would be wreaking havoc on vessels.  

He starts off plainly saying COVID-19 is an endothelial disease.  

Son of a bitch. I could have hit this one on the head of the nail. THis is the shit I've been talking about. Seems like other researchers are taking the same stance 

 

 

A hypothesis for pathobiology and treatment of COVID?19: the centrality of ACE1/ACE2 imbalance

 

SARS viruses and Angiotensin action/signaling

Infection of cells by SARS viruses that bind ACE2 results in two effects: inhibition of ACE2 activity and

decrease of ACE2 expression in infected cells (Kuba et al., 2005; Haga et al., 2008; Glowacka et al.,

2010; Zhang et al., 2020). Indirect evidence for the latter response in COVID-19 is data showing

elevation in circulating ANG II with viral infection and increased circulating ANG II peptide with higher

viral loads (Liu et al., 2020b).

Our hypothesis is founded on the following ideas that derive from data in reports cited in ensuing

sections:

1. SARS viruses decrease ACE2 activity and expression.

2. The decrease in ACE activity creates an imbalance in signaling by ACE1 and ACE2 products

3. This imbalance increases ANG II/AGTR1 signaling and is superimposed on concurrent

pathology (e.g., chronic lung disease, cardiac remodeling in the lung and heart, respectively).

ANG II is a pivotal mediator of injury in both tissues; enhancement of its effects together with

signaling from comorbidities can increase severity of COVID-19.

4. In patients more susceptible to the damaging effects of ANG II, the decrease in ACE2 activity

by SARS viruses can unleash a cascade of injurious effects through a heightened imbalance in

the actions of the products of ACE1 versus ACE2.

5. The proposed imbalance in the signaling and actions of products of ACE1/ACE2 implies the

potential of pharmacological approaches that redress this imbalance via: a) decrease in ACE1

activity, b) blockade of AGTR1, and/or c) increase in ACE2-mediated signaling by affinity-

trapping the SARs virus, enhancement of ACE2 expression/activity, or d) by agonists for

receptors of ACE2-derived peptides

 

https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1111/bph.15082

 

That all sounds lot like what he goes through in the video.  You would understand it a lot better than I do. 

That's a review article that was just released on the 24th I believe. He's basically outlining what I have been saying is happening in the lungs. I think he's elaborating on the review.. I'm watching the med cram video now. I'm excited to see what he covers. I think that doctor is part of the journal team. THanks for the vid. 

 

It would be the same thing that is occuring the lungs but when ACE2 gets overwhelmed it no longer provides any type of protection to the lungs and then ARDS. 

 

I never bothered to bring in the free radical aspect of it (superoxide or any other ROS) but as free radicals increase you start to see lipid oxidation and protein carbynolation....

4/29/20 6:14 PM
2/27/11
Posts: 11279
NoNeed4aScreenName -

Does anyone have access to the data? There were 2 trials for Gilead and Redemsivir right? Anyone with access to the Lancet article wanna post it? I'm paywalled. 

 

If anyone has the other trial data could you post it? 

 

No need for the intro or filler. Just the methods and results please. 

This one?

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31022-9/fulltext

 

doesnt seem to be paywalled?

 

4/29/20 6:29 PM
2/4/09
Posts: 11159
pidgey -
NoNeed4aScreenName -

Does anyone have access to the data? There were 2 trials for Gilead and Redemsivir right? Anyone with access to the Lancet article wanna post it? I'm paywalled. 

 

If anyone has the other trial data could you post it? 

 

No need for the intro or filler. Just the methods and results please. 

This one?

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31022-9/fulltext

 

doesnt seem to be paywalled?

 

Yeah I seem to have gotten around it. I went to one link and it said to subscribe but searching google got me to it without subscribing.  

 

Thanks though

4/29/20 7:58 PM
2/4/09
Posts: 11162
Trust -
EFM - 
the_shrike -
Trust -

Today's MedCram update - COVID-19 is really a lot worse than a flu, it's destroying blood vessel walls

Just watched that.  Frightening

Also mind boggling that there are people out there who are looking at this disease at this level.  Almost hard to believe.


Well prepare to have your mind boggled even more.  

This is still hypothetical level, stuff, but here he shows what could potentially be going on at a very low (detailed) level.  Basically the SAR-CoV-2 virus blocks angiotensin 1,7 from regulating the production of superoxides, which would be wreaking havoc on vessels.  

He starts off plainly saying COVID-19 is an endothelial disease.  

Brings me back to my masters time. This is what I studied. Free radical biology. 

 

Essentially I was looking at oxidative metabolism in hypoxic/anaerobic environments. Studying free radicals as possible signaling molecules. 

 

Started as a way to try and determine the underlying mechanism for muscle fatigue to free radicals as signals for crosstalk between the mitochondria and the cell nucleus

Edited: 4/29/20 10:54 PM
1/1/01
Posts: 19483

not a doc but family members are.  They at major medical Center in major American city. We have cases, but nothing like NYC.

 

"flatten the curve" is given as the reason for the star at home orders. But stalling for time also brings other good things. The hospitals in this area are recycling masks by dosing then with hydrogen peroxide. Each mask can be used up to 20 times. This has pretty much solved the mask problem around here. You may wonder why it matters, but you won't get treated if all the docs are sick.

 

The other thing is that stalling allows trials for drugs. We had a remsidevir trial here (their opinion before the latest finding was that  it did work). But they're also finding good preliminary results with another drug used for something else that is tested in 50% of the population and is even OTC in some countries. I searched for this drug in Google and found nothing.   I'm guessing there are promising drug repurposing drug trials all over the country you haven't heard about yet.

 

After the whole chloroquinine disaster, you can't blame them for shutting up.. Point is that there are hopeful things that are not yet in the media and it's not all about a vaccine.

4/29/20 11:47 PM
1/7/09
Posts: 16216

 

Can a doctor comment on this video?  It's one of those things where someone with legit credentials is talking in a confident manner that sounds authoritative, but as a layman you have no idea if whether what is being said is accurate or not

4/30/20 1:24 AM
1/1/01
Posts: 11819
turducken - 

 

Can a doctor comment on this video?  It's one of those things where someone with legit credentials is talking in a confident manner that sounds authoritative, but as a layman you have no idea if whether what is being said is accurate or not




Jebus! That video and the comment section seem to be a conspiritard clusterfuck. Like bees to honey.
4/30/20 4:06 AM
11/23/10
Posts: 242
Easters -
Job Security -
madmartigan -
Easters -

Another one for the professionals - can someone explain (bro science is best) exactly why testing is so important compared to hospitalizations?  I keep hearing "test, test, test" but why is testing so important when hospitalizations are so low?  Is it just the ability to isolate and track?  

 

I guess I just dont see how testing is going to change much.  Right now it seems like there's enough tests in my region to test anybody who meets the criteria, but they're still saying they need to double testing capacity.  Is the plan to start testing asymptomatic citizens too?  Isnt the protocal going to be the same, quarantine for two weeks if you have symptoms, positive test or not?  

Not a pro, but here's my take.

 

Lots of people have mild symptoms, or none at all, but still carry the virus and can spread it to others who may have much more severe reactions. 

 

If you can't get tested, you'll never know if you're spreading it around.

Yeah. It’s for tracing and isolating those with too little symptoms or wits to self-isolate on their own accord. Especially those who interact with vulnerable groups.

I think a lot of countries want to be able to do what e.g. South Korea has been able to do. That is, keeping the epidemic contained in a sustainable way (lockdown is only viable for a few weeks) through wide-spread, free-for-all testing and aggresively tracing and testing contacts of positive cases. Too bad it’s only really feasible if the number of actively infected isn’t too high, and if you have the gear and infrastructure (test kits, PPE or secure sampling facilities, and spacious sampling sites).

I’m certain that is what we’re going to in my country, perhaps starting as early as next week. Both virus and antibody testing with very few limitations it seems. They’ve set up sampling site tents around the country, and the authorities have leaked some stuff about the long-term strategy, but the details haven’t come out yet.

There’s no guarantee as to how effective it will be though. It may only work in South Korea because of their particular habits/culture of social interaction lessens spread enough for this approach to keep up. If people stop being mindful of social distancing and hygiene, it will fail for sure. So many unknowns with this. 

So right now if you have a fever or dry cough you call your doctor and they either say come in for a test or stay home and quarantine as if you’re positive.  What changes with more tests? You get symptoms, call your doctor, and everybody goes in for a test?  Right now we’re all supposed to act as if we’re positive, especially if we hAve symptoms.  I guess I just don’t see how having more tests helps so much that we can impoement slow opening until we have them 

The idea that has been hinted at over here, is that if you have symptoms or suspect that you have been exposed, you self-isolate and get tested on day 4, 6 and 8 after symptom onset or exposure. If you test positive, you (the citizen) are obliged to tell all your contacts, whom you may have exposed to COVID-19, to go and get tested 3 times. And then the positives among them have to contact those they may have exposed etc etc.

It should help catch those with no brains or symptoms and limit their spreading of the disease. If everyone did what you describe and took care not to infect others, I agree that would be almost as good as this. Most studies estimate that most spreading occurs before/without symptoms, and there are too many careless people in the community, so I think it is worth s shot to try the strategy (even with all the issues and limitations it has; for example the low sensitivity of the tests is a problem, even when you test the same person 3 times).