Wuhan Coronavirus - COVID-19 Analysis & Summary - This is not just fucking pneumonia. It is everything but the kitchen sink. Lungs, heart, kidneys, liver, brain, blood vessels, testes. It affects them all.

[mr.moon1488]

Wait so what's the difference between namefag and tripfag?

A tripcode is unique, anyone can use any name. Basically, if you started posting a bunch of shit under just some name you put in, someone else could larp as you.

Edit:
Tripcodes are only really useful if let's say you're leaking some information, and plan to leak additional information later down the road. If you leak the info under a tripcode, people know whether it's you posting again, or some faggot trying to get attention/shill/etc.

 

[Sped Xing]

So why is he bragging about using a tripcode while denying that he uses tripcodes?

 

[Adamska]

Jesus Christ, I go to sleep and you decide to go on a super-sperg bender you absolute waste of oxygen.

ME NO WANT TO SEE @AltisticRight INFO CUZ IT BREAK BREAK ME AM POINT THAT WE ALL DIE NOW AND ME AM BIGBRAIN NOT SMOOTHBRAIN. MUST CLOP CLOP TO COCK COCK NOW OR CRASH INTO SLUMBER.

I love how you keep ignoring people who actually bother to look at the shit you post and refute it because you know on some level they're right and you can't accept that. That's why I mock your utter relevance at anything, because you can't be fucked to defend your point to a real people critique, and then chimp when shitheads like me just mock you for having no value and treat you as the joke you are.

Just lick your doorknobs dude.

 

[derpherp2]

A tripcode is unique, anyone can use any name. Basically, if you started posting a bunch of shit under just some name you put in, someone else could larp as you.

Edit:
Tripcodes are only really useful if let's say you're leaking some information, and plan to leak additional information later down the road. If you leak the info under a tripcode, people know whether it's you posting again, or some faggot trying to get attention/shill/etc.

So it's worse than a namefag.

@Drain Todger Fucks sake dude, nobody's going to ever take you seriously. You're an autistic tranny, you keep trying your hardest to fit in in areas where it's painfully obvious your input isn't wanted, and now you think all your failed attempts at standing out while fitting in in multiple forums is going to work here?

 

[mr.moon1488]

So why is he bragging about using a tripcode while denying that he uses tripcodes?

Lol, you'll need to consult a psychologist specializing in ASD for that answer.

 

[Spedestrian]

LOL. Reading comprehension fail. No wonder you guys always resort to ridicule instead of argumentation. You can’t even vaguely grasp the terminology. Vasculitis = blood vessel inflammation. I didn’t say anything about pulmonary signs.

No you exceptional individual, we're ridiculing you because you're acting like a pompous jackass while making statements that reveal your profound ignorance of the subject matter. For example:

So, basically, to sum up, COVID-19 causes cytokine storms and severe inflammation and tissue damage in many of major organs, hypoxemia, and diffuse clotting.

You did all that research and wrote that gigantic post just to show that SARS-CoV2 has largely the same effects as the original SARS-CoV:

https://www.atsjournals.org/doi/full/10.1164/ajrccm.182.3.436

Into the Eye of the Cytokine Storm

Where are the reports of vasculitis in COVID-19 patients? Is anyone even looking?

The fact that you think this is an important question is laughable. You might as well be asking for reports of people being wet in the rain. Vasculitis is an inflammatory disease of the blood vessels that is caused by a faulty immune system response. We already know COVID-19 provokes an immune response that can damage and inflame organs, and based on its similarity to SARS there's no reason to believe it wouldn't also do the same thing to the blood vessels.

What really fucking ruins my sides, though, is that you've already posted a report of vasculitis in a COVID-19 patient. You just didn't recognize it due to your cargo cult understanding of medicine. It's in this study:

Clinical pathology of critical patient with novel coronavirus pneumonia (COVID-19) (2020-02-26) [https://www.preprints.org/manuscript/202002.0407/v3/download]

Small vessels hyperplasia, vessel wall thickening, lumen stenosis, occlusion and
microthrombosis formation.

That's clearly a description of vasculitis. Here's another reference for comparison:

https://www.ncbi.nlm.nih.gov/books/NBK459470/

And doctors can't figure out why patients on ventilators are dying.

No, they can figure it out, it's just that most of them are too busy saving people's lives to explain how medicine works to autistic simpletons. Here you go:

Ventilators Are No Panacea For Critically Ill COVID-19 Patients

Ventilators can be lifesaving for some critically ill patients, but they're no panacea. The experience so far with COVID-19 is that the majority of patients put on ventilators don't survive.

www.npr.org

Patients need a ventilator when their lungs can no longer deliver enough oxygen to keep the body going. And it's an extreme measure, Osborn says.

. . . .

Unfortunately, Osborn says, "the ventilator itself can do damage to the lung tissue based on how much pressure is required to help oxygen get processed by the lungs."

And coronavirus patients often need dangerously high levels of both pressure and oxygen because their lungs have so much inflammation.

. . . .

Also, the coronavirus often does a lot more damage to a person's lungs than pneumonia associated with the flu. "There is fluid and other toxic chemicals, cytokines we call them, raging throughout the lung tissue," she says.

In some patients, the damage is so bad that even ventilation won't help. So doctors have sometimes tried an even more extreme measure called extracorporeal membrane oxygenation, or ECMO, which delivers oxygen directly to a patient's bloodstream.

But this is still a stopgap measure. "Remember, ECMO too is a life-supporting treatment," Hajizadeh says. "So it's a bridge while we are allowing the lung to heal itself from a pneumonia."

But lungs don't always heal, no matter how much help they get from a machine, Osborn says. So people need to be diligent about social distancing to keep the virus from spreading.

Basically patients are dying on ventilators because by the time their condition is bad enough to warrant a ventilator their lungs are already damaged and inflamed. Doctors aren't putting people on ventilators because they think ventilators are magic, they're doing it to ensure that the functioning portions of their patient's lungs are getting as much oxygen as they can possibly process. Sometimes there's enough functioning lung remaining to keep ventilated patients alive while the rest of the lung heals, sometimes there isn't. It's as simple as that.

Hint, it's because their capillaries can no longer exchange oxygen with their alveoli.

No shit you mongoloid, COVID-19 causes diffuse alveolar damage. It's pretty hard for alveoli to do their job of exchanging oxygen with capillaries when they're fucking damaged:

https://www.thelancet.com/journals/lancet/article/PIIS2213-2600(20)30076-X/fulltext

This is, again, exactly like the original SARS:

Pathology and Pathogenesis of Severe Acute Respiratory Syndrome

It's not a "lung disease".

COVID-19 is a blood and vascular disease that ninja-attacks all your major fucking organs while also giving you insane inflammatory damage.

Yes it is a lung disease. Respiratory symptoms are the most notable part of its initial presentation and the primary cause of death is respiratory failure. Like SARS it can also cause severe systemic symptoms including damage to multiple organs and inflammatory responses affecting the blood vessels. This doesn't mean it's not a lung disease. Topographic classifications of disease don't necessarily mean that the disease only impacts that organ or system.

Jesus, what is it with the magical thinking? Do people think COVID-19 has a consciousness and it will somehow get angry if we unravel the truth about it? No. It’s quite the opposite.

The more we know about it, the less dangerous it is.

How the fuck can you know the term "magical thinking" without recognizing that's exactly what you're doing right now?

In psychiatry, magical thinking is a disorder of thought content; here it denotes the false belief that one's thoughts, actions, or words will cause or prevent a specific consequence in some way that defies commonly understood laws of causality.

Cobbling together a rudimentary understanding of COVID-19 will not make the virus less dangerous to you or anyone else, because there's no causal link between your knowledge and the doctors who are actually going to solve this shit. Those doctors already have professional research assistants to do what you're doing, and they're far too busy to be responding to your shit. The only doctors you're informing are those who have times to read hot takes from random laypeople, i.e. doctors who aren't busy actually fixing the issue.

In short, people are berating you without engaging your points because you've spewed so much bullshit that your claims no longer seem credible. I haven't been reading your posts that closely until now, but the shit I read in the last few pages is more than enough for me to write off your opinions on COVID-19 as the ramblings of a madman. And no, that's not a logical fallacy, it's an efficiency heuristic. Some of your claims may be valid, but nobody wants to dig through your shit looking for corn.

 

[derpherp2]

Anyone betting that his discord academics actually don't read his shit or are also as hysterical as he is?
Like attracts like after all, so I'm going to assume avoidant behavior attracts avoidant behavior and/or autism.

Also to add to the dude above me's point, it takes time to refute cited points, whether to judge the citation, or to provide counterstudies.

At this point the effort doesn't warrant the reward, also your autism is infectious. Maybe you're trying to distract from airborne Autism by dooming about airborne AIDs.

 

[Spooky Bones]

PIC RELATED, IT'S ME AND MY BITCH

 

[AltisticRight]

David Clop's response...
First obfuscate, then post walls of autistic drivel, much which are shit that happened over a month ago, then walls of links feeding into his confirmation bias.
Still, my data is near complete. Will do the modelling later. Wish I still had access to SAS, minitab is fucking annoying.

One month to go. Found some weird problems with WHO's data already. The 17th of March and 18th of March reports seem to be identical. I'm sure I didn't fuck up.
15th and 16th data are identical for murica as well, wtf WHO, learn how to proof-read. Oh wait, your leader is some kebab that doesn't even have a medical related degree.

As far as feelings go, the data doesn't seem routine and likely isn't "generated by a formula".
CPC sometimes are very dumb (especially their media figures, such as People's Daily sharing a stock photo to pass off as their death camps, end product did look similar so maybe it was built by that exact company but fucking hell, stop making fake news) but not that fucking stupid, stupid to a point that a brony clopper gets to throw terms he doesn't know around.

I think David Clop went to Academia Destiny. Scatterbomb with walls of links, such as economists and historians trying to do numbers, then claim the win!

When someone bothers to respond, he ignores half of them and doubles the amount of autistic barricades.

Works every time.

 

[1Tonka_Truck]

Uhh, wrong.

Does being this dumb cause you physical pain?

From the article you linked:

The island off the shore of The Bronx was mentioned by Mayor Bill de Blasio as a possible site for temporary burials of people killed by COVID-19.

Meanwhile, in the land of actually happening:

The city's Office of the Chief Medical Examiner quietly posted a significant policy change to its website on Tuesday: Instead of holding some bodies in refrigerated city storage for 30 days until they are claimed by families, the city will now hold them for less than a week.

Starting Tuesday, decedents who are not claimed by a funeral home within that short window will be sent to the Bronx's Hart Island, where a mass graveyard called City Cemetery contains more than 1 million unclaimed bodies — the largest such site in the US.

New York City will bury bodies on a remote island if they're unclaimed after 6 days because coronavirus deaths are overwhelming morgues

The city typically waits 30 days before interring bodies in mass graves on Hart Island, but the coronavirus' death toll is overwhelming the system.

www.businessinsider.com

(I'll add an archive when archive today stops shitting itself)

As a fun aside, imagine having a journalism or even creative writing degree and not knowing it's en masse.

A drone captured video of what appears to be inmates burying coffins in a mass Hart Island grave as the new coronavirus spreads across New York City.

 

[Fareal]

I make an argument. I advance a premise, and I provide sound evidence for the premise. Then, I come to a conclusion.

So, for instance, I argue that COVID-19 is a neurotropic disease. This conclusion is supported by the premises. Namely, that several papers on COVID-19 describe neurological manifestations, there is leaked footage showing collapses and seizures, and there are multiple experts coming out and expressing concern over the neurotropism of the virus.

I have satisfied the burden of proof. If you wish to attack this argument, you must demonstrate why the evidence doesn't actually mean what I think it means.

You can't just declare, by mere fiat, that my reasoning is faulty. This is a very common and juvenile mistake in online debates.

Let’s clarify what the burden of proof means. I think you use it a lot without understanding the concept fully. That’s okay. I think maybe you don’t have much or any practice or training in formal debate, and I’m not clear if you understand why advancing a theory in medical science involves a different burden of proof than a straight formal debate of a philosophical or policy position.

I would really like you to read this link. I think you will be able to understand it, the classifications it uses, and the examples pretty easily. I feel like this will definitely help you understand why people question your sources and your interpretation of them so often. You are focusing a lot of energy into becoming frustrated as to why you are being questioned, rather than refining your research.

Burden of proof - Logical and Critical Thinking

The allocation of the burden of proof-- who has it and what weight it has-- has implications for what we have to do as logical and critical thinkers.

www.futurelearn.com

 

[Drain Todger]

Jesus Christ, I go to sleep and you decide to go on a super-sperg bender you absolute waste of oxygen.

I love how you keep ignoring people who actually bother to look at the shit you post and refute it because you know on some level they're right and you can't accept that. That's why I mock your utter relevance at anything, because you can't be fucked to defend your point to a real people critique, and then chimp when shitheads like me just mock you for having no value and treat you as the joke you are.

Just lick your doorknobs dude.

I addressed what @AltisticRight said. In fact, I dragged up the rest of the graphs that supported the argument that the data was fabricated to fit a curve.

I was going to let his last post slide unchallenged, but since you sassed me up, now I have to go back.

1. I'm in the middle of getting the data ready. Going to ignore all the babble coming from economists.
2. Of course it's not believable that no one is dying from the virus in China, because:
View attachment 1220844
Notice how China's numbers are very similar to Korea's?
Oh and yeah, people are still dropping dead from Coronachan.

I like how you pretend that these data sets are in any way equivalent.

South Korea and Singapore have comprehensive screening programs in place, while the authorities in China have basically stopped counting cases.

What this means is that South Korea and Singapore will be counting a much, much larger number of asymptomatic and mild cases than anywhere else.

South Korea Is Beating Covid-19. Here’s How.

South Korean has had success managing the coronavirus undefinedoutbreak. New cases diagnosed Monday dropped to 47undefined, the lowest level in weeks.

www.barrons.com

http://archive.is/Qwilg

Not only does this mean that they'll be better off at preventing the spread of the virus, it also means that their ratio of total cases to total deaths will look better than in other places. I find it amusing that the 1 in 55 death rate in Korea matches the presumed IFR of the disease almost exactly, about 1.8%, squarely in the middle of the 1 to 3% figure I've been hearing. This means that South Korea is detecting a very, very large number of the infections.

Only 6% Of Actual Coronavirus Cases Detected Worldwide, Researchers Estimate

The actual number of cases may actually be in the tens of millions, according to the report.

www.ibtimes.com

http://archive.is/1pkoG

Even hard-hit countries have only been detecting small percentages of the infected individuals, with Italy detecting only 3.5% of infections and the U.S. detecting only 1.59% of infections as of March 31. By comparison, Germany's detection rate is at 15.58% while South Korea's is at 49.47% and Japan's is at 25.16%.

So, here's a little experiment for you. Try adjusting your presumed RCFR ratios based on the actual detection rate, and then see where China lands.

Don't feel too bad. The US is doing the worst of all. The CDC demonstrated extreme incompetence bordering on criminal negligence.

CDC Tested Just 77 People For Coronavirus This Week

States are testing fewer than 100 people a day and the CDC tested even fewer in an entire week.

www.huffpost.com

http://archive.is/8pepb

No you exceptional individual, we're ridiculing you because you're acting like a pompous jackass while making statements that reveal your profound ignorance of the subject matter. For example:

You did all that research and wrote that gigantic post just to show that SARS-CoV2 has largely the same effects as the original SARS-CoV:

https://www.atsjournals.org/doi/full/10.1164/ajrccm.182.3.436

Into the Eye of the Cytokine Storm

Yes, exactly. It has largely the same effects as SARS-CoV. That's exactly what I've been saying this entire time. What makes this particularly infuriating is how the medical literature on COVID-19 almost refuses to acknowledge the multi-faceted features of SARS-CoV's pathology, including the vascular and neurological complications.

The fact that you think this is an important question is laughable. You might as well be asking for reports of people being wet in the rain. Vasculitis is an inflammatory disease of the blood vessels that is caused by a faulty immune system response. We already know COVID-19 provokes an immune response that can damage and inflame organs, and based on its similarity to SARS there's no reason to believe it wouldn't also do the same thing to the blood vessels.

What really fucking ruins my sides, though, is that you've already posted a report of vasculitis in a COVID-19 patient. You just didn't recognize it due to your cargo cult understanding of medicine. It's in this study:

That's clearly a description of vasculitis. Here's another reference for comparison:

https://www.ncbi.nlm.nih.gov/books/NBK459470/

Reports are scant. Don't pretend that one single blurb in one single paper is enough to get the attention of every doctor treating every patient.

No, they can figure it out, it's just that most of them are too busy saving people's lives to explain how medicine works to autistic simpletons. Here you go:

Ventilators Are No Panacea For Critically Ill COVID-19 Patients

Ventilators can be lifesaving for some critically ill patients, but they're no panacea. The experience so far with COVID-19 is that the majority of patients put on ventilators don't survive.

www.npr.org

I have been tracking that information, yes. I am aware that 70 to 80% of the patients being intubated have died, yes.

Basically patients are dying on ventilators because by the time their condition is bad enough to warrant a ventilator their lungs are already damaged and inflamed. Doctors aren't putting people on ventilators because they think ventilators are magic, they're doing it to ensure that the functioning portions of their patient's lungs are getting as much oxygen as they can possibly process. Sometimes there's enough functioning lung remaining to keep ventilated patients alive while the rest of the lung heals, sometimes there isn't. It's as simple as that.

No shit you mongoloid, COVID-19 causes diffuse alveolar damage. It's pretty hard for alveoli to do their job of exchanging oxygen with capillaries when they're fucking damaged:

https://www.thelancet.com/journals/lancet/article/PIIS2213-2600(20)30076-X/fulltext

This is, again, exactly like the original SARS:

Pathology and Pathogenesis of Severe Acute Respiratory Syndrome

Yes it is a lung disease. Respiratory symptoms are the most notable part of its initial presentation and the primary cause of death is respiratory failure. Like SARS it can also cause severe systemic symptoms including damage to multiple organs and inflammatory responses affecting the blood vessels. This doesn't mean it's not a lung disease. Topographic classifications of disease don't necessarily mean that the disease only impacts that organ or system.

Hah. Finally. Someone with actual knowledge.

There are numerous mechanisms at work here that have nothing to do with the interior of each alveolus and everything to do with the physiology of the vascular system, and the way the virus affects it.

First of all, this virus inhibits the entry receptor, ACE2, and causes Angiotensin II to back up. Has anyone considered that pulmonary hypertension in the capillaries of the alveoli may be a problem, because of the excess Ang II?

Dr. Nick Mark, on Twitter, describes a capillary shunt mechanism by which hypoxic pulmonary vasoconstriction may close off blood supply to the capillaries and harm oxygen exchange with the alveoli:

Thread by @nickmmark: Lots of talk about funny hemoglobin and ‘happy hypoxic’ people with #COVID19. I think we can explain everything using plain old pulmonary ph…

Thread by @nickmmark: Lots of talk about funny hemoglobin and ‘happy hypoxic’ people with #COVID19. I think we can explain everything using p pulmonary physiology. Let’s dive into hypoxic pulmonary vasoconstriction (HPV) and hypoxic ventilatory drive (HV…

threadreaderapp.com

http://archive.is/dALZy

This is all fine and good, but did he take into account that the virus imbalances the RAAS and causes an over-abundance of a vasoconstrictive hormone that could do the same thing as hypoxic pulmonary vasoconstriction?

Angiotensin II

Angiotensin II | C50H71N13O12 | CID 172198 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.

pubchem.ncbi.nlm.nih.gov

It could be hypoxia closing off those capillaries. It could also be that the tissues are saturated in Ang II commanding them to constrict. How would you be able to tell the difference without biopsying the tissue?

http://archive.is/5GGLZ

Next, you have Dr. Farid Jalali's hypothesis of micro-thromboembolism blocking off capillaries because of diffuse clotting:

http://farid.jalali.one/covid19emailpdf.pdf

Do we know if the blockage of the alveolar capillaries is due to vasoconstriction, or is it due to a proliferation of many tiny blood clots?

Last, but not least, there's this:

COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism

The novel coronavirus pneumonia (COVID-19) is an infectious acute respiratory infection caused by the novel coronavirus. The virus is a positive-strand RNA virus with high homology to bat coronavirus. In this study, conserved domain analysis, homology modeling, and molecular docking were used to...

chemrxiv.org

http://archive.is/wj71U

The novel coronavirus pneumonia (COVID-19) is an infectious acute respiratory infection caused by the novel coronavirus. The virus is a positive-strand RNA virus with high homology to bat coronavirus. In this study, conserved domain analysis, homology modeling, and molecular docking were used to compare the biological roles of certain proteins of the novel coronavirus. The results showed the ORF8 and surface glycoprotein could bind to the porphyrin, respectively. At the same time, orf1ab, ORF10, and ORF3a proteins could coordinate attack the heme on the 1-beta chain of hemoglobin to dissociate the iron to form the porphyrin. The attack will cause less and less hemoglobin that can carry oxygen and carbon dioxide. The lung cells have extremely intense poisoning and inflammatory due to the inability to exchange carbon dioxide and oxygen frequently, which eventually results in ground-glass-like lung images. The mechanism also interfered with the normal heme anabolic pathway of the human body, is expected to result in human disease. According to the validation analysis of these finds, chloroquine could prevent orf1ab, ORF3a, and ORF10 to attack the heme to form the porphyrin, and inhibit the binding of ORF8 and surface glycoproteins to porphyrins to a certain extent, effectively relieve the symptoms of respiratory distress. Favipiravir could inhibit the envelope protein and ORF7a protein bind to porphyrin, prevent the virus from entering host cells, and catching free porphyrins. Because the novel coronavirus is dependent on porphyrins, it may originate from an ancient virus. Therefore, this research is of high value to contemporary biological experiments, disease prevention, and clinical treatment.

COVID-19 can apparently interrupt heme metabolism, resulting in a whole lot of free heme floating around and perhaps even progressing to hemolytic anemia. This seems to be supported by the high ferritin findings and the clotting. This is what excess free heme can do:

Excess of heme induces tissue factor-dependent activation of coagulation in mice

http://archive.is/aq1un

However, the diffuse clotting could also potentially be caused by viral sepsis, regardless. Therefore, the heme metabolism interruption hypothesis does not rule out coagulation by other causes.

In summary, COVID-19 is a vascular disease with lung signs secondary to the vascular manifestations. It attacks the blood and blood vessels first, and then your lungs get fucked.

That's why people are sitting around jawing looking fine, and then suddenly, they're hypoxic and blue in the face.

A few competing hypotheses, here. Which is it, genius?

• Does the virus close off alveolar capillaries with hypoxic pulmonary vasoconstriction, or does Angiotensin II cause them to constrict by activating AT1R?
• Are the capillaries being blocked by huge numbers of tiny blood clots due to vasculitis and/or viremia?
• Is the virus attacking heme metabolism and causing large amounts of free heme to float about, causing lowered hemoglobin, hypoxemia, elevated ferritin, and clotting?

 

[XYZpdq]

and really even if that digging footage is everything it claims to be and is anomalous amounts of digging that's still only proof of preparation not proof of events
"everybody is panicking that something might happen so we'd better panic too" is exactly what started this mess

 

[Spooky Bones]

Hah. Finally. Someone with actual knowledge

 

[SIGSEGV]

Did you guys know that @Drain Todger has been researching a cure for COVID-19 without telling us? I thought he cared about us.

 

[Sped Xing]

David, we trusted you.

 

[derpherp2]

Let’s clarify what the burden of proof means. I think you use it a lot without understanding the concept fully. That’s okay. I think maybe you don’t have much or any practice or training in formal debate, and I’m not clear if you understand why advancing a theory in medical science involves a different burden of proof than a straight formal debate of a philosophical or policy position.

I would really like you to read this link. I think you will be able to understand it, the classifications it uses, and the examples pretty easily. I feel like this will definitely help you understand why people question your sources and your interpretation of them so often. You are focusing a lot of energy into becoming frustrated as to why you are being questioned, rather than refining your research.

Burden of proof - Logical and Critical Thinking

The allocation of the burden of proof-- who has it and what weight it has-- has implications for what we have to do as logical and critical thinkers.

www.futurelearn.com

@Drain Todger
If you're too autistic to read it I'll explain.

The burden of proof lies on the claimant - the one making the claim, the proof usually requires actual proof and not the appearance of proof by jerry-rigging multiple irrelevant news articles (a problem inofitself and a massive hit on your credibility) together in some vain attempt at making your claim more official looking and pretending a discord room is some sort of academic backing to your nonexistent clout.

There are probably different intricacies depending on whatever specific shit is involved but the end result is the same.

Aside from that there's also your general behavior. And also the general academic dishonesty.

To put it even simpler, every single claim you've ignored without actually providing a counterpoint is assumed true until you go back and rectify it. This includes the hilarious ones. Pedophile.

To put it EVEN SIMPLER: What you're doing is the equivalent of a retard wiping his nose on a picture of a picture of a picture of a summary of a critic review of a summary of a picture of something actually meaningful and turning it in as OC donut steal. Then tardraging when nobody wants to even touch it.
Repeatedly
For the past... month?
On multiple schools.

 

[Vince McMahon]

I addressed what @AltisticRight said. In fact, I dragged up the rest of the graphs that supported the argument that the data was fabricated to fit a curve.

I was going to let his last post slide unchallenged, but since you sassed me up, now I have to go back.



I like how you pretend that these data sets are in any way equivalent.

South Korea and Singapore have comprehensive screening programs in place, while the authorities in China have basically stopped counting cases.

What this means is that South Korea and Singapore will be counting a much, much larger number of asymptomatic and mild cases than anywhere else.

South Korea Is Beating Covid-19. Here’s How.

South Korean has had success managing the coronavirus undefinedoutbreak. New cases diagnosed Monday dropped to 47undefined, the lowest level in weeks.

www.barrons.com

http://archive.li/Qwilg

Not only does this mean that they'll be better off at preventing the spread of the virus, it also means that their ratio of total cases to total deaths will look better than in other places. I find it amusing that the 1 in 55 death rate in Korea matches the presumed IFR of the disease almost exactly, about 1.8%, squarely in the middle of the 1 to 3% figure I've been hearing. This means that South Korea is detecting a very, very large number of the infections.

Only 6% Of Actual Coronavirus Cases Detected Worldwide, Researchers Estimate

The actual number of cases may actually be in the tens of millions, according to the report.

www.ibtimes.com

http://archive.li/1pkoG

So, here's a little experiment for you. Try adjusting your presumed RCFR ratios based on the actual detection rate, and then see where China lands.

Don't feel too bad. The US is doing the worst of all. The CDC demonstrated extreme incompetence bordering on criminal negligence.

CDC Tested Just 77 People For Coronavirus This Week

States are testing fewer than 100 people a day and the CDC tested even fewer in an entire week.

www.huffpost.com

http://archive.li/8pepb

Yes, exactly. It has largely the same effects as SARS-CoV. That's exactly what I've been saying this entire time. What makes this particularly infuriating is how the medical literature on COVID-19 almost refuses to acknowledge the multi-faceted features of SARS-CoV's pathology, including the vascular and neurological complications.



Reports are scant. Don't pretend that one single blurb in one single paper is enough to get the attention of every doctor treating every patient.



I have been tracking that information, yes. I am aware that 70 to 80% of the patients being intubated have died, yes.



Hah. Finally. Someone with actual knowledge.

There are numerous mechanisms at work here that have nothing to do with the interior of each alveolus and everything to do with the physiology of the vascular system, and the way the virus affects it.

First of all, this virus inhibits the entry receptor, ACE2, and causes Angiotensin II to back up. Has anyone considered that pulmonary hypertension in the capillaries of the alveoli may be a problem, because of the excess Ang II?

Dr. Nick Mark, on Twitter, describes a capillary shunt mechanism by which hypoxic pulmonary vasoconstriction may close off blood supply to the capillaries and harm oxygen exchange with the alveoli:

Thread by @nickmmark: Lots of talk about funny hemoglobin and ‘happy hypoxic’ people with #COVID19. I think we can explain everything using plain old pulmonary ph…

Thread by @nickmmark: Lots of talk about funny hemoglobin and ‘happy hypoxic’ people with #COVID19. I think we can explain everything using p pulmonary physiology. Let’s dive into hypoxic pulmonary vasoconstriction (HPV) and hypoxic ventilatory drive (HV…

threadreaderapp.com

http://archive.li/dALZy

This is all fine and good, but did he take into account that the virus imbalances the RAAS and causes an over-abundance of a vasoconstrictive hormone that could do the same thing as hypoxic pulmonary vasoconstriction?

Angiotensin II

Angiotensin II | C50H71N13O12 | CID 172198 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.

pubchem.ncbi.nlm.nih.gov

It could be hypoxia closing off those capillaries. It could also be that the tissues are saturated in Ang II commanding them to constrict. How would you be able to tell the difference without biopsying the tissue?

http://archive.li/5GGLZ

Next, you have Dr. Farid Jalali's hypothesis of micro-thromboembolism blocking off capillaries because of diffuse clotting:

http://farid.jalali.one/covid19emailpdf.pdf

Do we know if the blockage of the alveolar capillaries is due to vasoconstriction, or is it due to a proliferation of many tiny blood clots?

Last, but not least, there's this:

COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism

The novel coronavirus pneumonia (COVID-19) is an infectious acute respiratory infection caused by the novel coronavirus. The virus is a positive-strand RNA virus with high homology to bat coronavirus. In this study, conserved domain analysis, homology modeling, and molecular docking were used to...

chemrxiv.org

http://archive.li/wj71U

COVID-19 can apparently interrupt heme metabolism, resulting in a whole lot of free heme floating around and perhaps even progressing to hemolytic anemia. This seems to be supported by the high ferritin findings and the clotting. This is what excess free heme can do:

Excess of heme induces tissue factor-dependent activation of coagulation in mice

http://archive.li/aq1un

However, the diffuse clotting could also potentially be caused by viral sepsis, regardless. Therefore, the heme metabolism interruption hypothesis does not rule out coagulation by other causes.

In summary, COVID-19 is a vascular disease with lung signs secondary to the vascular manifestations. It attacks the blood and blood vessels first, and then your lungs get fucked.

That's why people are sitting around jawing looking fine, and then suddenly, they're hypoxic and blue in the face.

A few competing hypotheses, here. Which is it, genius?

• Does the virus close off alveolar capillaries with hypoxic pulmonary vasoconstriction, or does Angiotensin II cause them to constrict by activating AT1R?
• Are the capillaries being blocked by huge numbers of tiny blood clots due to vasculitis and/or viremia?
• Is the virus attacking heme metabolism and causing large amounts of free heme to float about, causing lowered hemoglobin, hypoxemia, elevated ferritin, and clotting?

David, bitte.

 

[AnOminous]

That’s my whole point. You habitually indulge in ridicule because rhetoric simply escapes you.

No, we indulge in ridicule because THAT IS WHAT THE FUCKING SITE IS FOR YOU DUMB HORSE FUCKING MORON.

 

[derpherp2]

No, we indulge in ridicule because THAT IS WHAT THE FUCKING SITE IS FOR YOU DUMB HORSE FUCKING MORON.

And even if it wasn't dude has the credibility of a hysterical tranny cosplaying as a scientist.
One could even say he is a hysterical tranny cosplaying as a scientist, but the world will never truly know.