Or maybe, I just felt like people deserved the truth.
No. I already conceded that I was wrong about that part, and you were right.
That Barron's article was clickbait. Surprisingly well-disguised clickbait that most people won't recognize as clickbait, but clickbait nonetheless.
There are other articles claiming a very high R-squared where the authors fit a curve to the data:
You have the math skills to go out there and seriously debunk this claim. I'm not even kidding. If these fuckers are full of shit, you should set them straight. Get in touch with Dr. Melody Goodman and see how she came up with her statistical model.
I wanna know what the hell is actually going on here, and why this claim of fabricated data continues to be repeated by authoritative sources if it's false.
No. I live with mommy and daddy because my father is an emotionally manipulative, co-dependent jerk who guilt-trips me every time I make any suggestion of moving out.
"Ohh waaaaaah, are you gonna leave me with your mother? I'll just shrivel up and blow away in the wind."
"Hey, don't you know in Europe, families have dynastic wealth because children live with their parents more often? Moving out is a scam. They just want you to pay your own set of bills."
I have suggested moving out numerous times, and this is the response I consistently get. Guilt-tripping me to stay.
I'm like, "Whatever, I guess I'll just play another thousand hours of Skyrim, then".
Plum of a job? I'm exhausted all the fucking time. My door-to-door time is frequently from 0430 in the morning to 1945 at goddamn night, for a whole week, and then, the next workweek, it's 1630 in the afternoon to 0745 in the morning the following day. It's fucking
exhausting. Being under fluorescent lights all day and exposed to 105 decibel engine room noise fucking
destroys your mental health. Anyone who has been in this industry for more than 15 years is some manner of vegetable, because lack of sleep and stress have destroyed their minds.
I know a guy who's so exceptional, the first thing he does, every time he gets on watch, is to start scatting.
Like singing, off-key, "Doot-doo-doooooooo!"
He's down to his last brain cell.
Impossible. I know a guy here who threatened to shoot his boss in the face,
right to his boss's face. He wasn't fired.
Oh, and the reason why he threatened to shoot his boss in the face was because he was a Neo-Nazi and his boss wanted to bring some African-American kid down into the engine room for show and tell as part of Big Brothers Big Sisters of America, and he was all like, "If you bring that darkie down here I'm gonna get my .45 and I'm gonna blow your head off."
Right to his boss's face.
And
he still wasn't fired.
It's a union job. There's no interview or anything to get in. You just show up at job call, and they call a certain number of heads, and you're hired. I wasn't given preferential treatment. I just signed on the dotted line, and I got the job, same as everyone else in the group that was called. Simple as that.
By the way, if anyone wants to get on my ass for nepotism, gimme a fucking break. There are like several dozen people working here who are friends or family of an existing employee. Two other people in the group of 20 I got hired in were friends and family of existing employees.
Merchant Marine is rife with nepotism. It's just the way it is.
Oh, no, no. There is absolutely no need to apologize. I would be delighted to speak with someone who has actual biology expertise. That's what I'm here for.
Oh. I thought that they generally only put papers from fairly reputable journals in the NCBI database.
I was discussing all this with a couple immunologists, and the general consensus was that a Th2 vaccine would be difficult or even impossible to make for a SARS-like virus due to the immunopathological reaction it incites in the lung tissue. There are ways around this, technically.
They can try and induce immunogenicity by other means and avoid the negative host response, of course. However, it's tricky. I was worried that the challenges involved in all this would delay a vaccine.
A number of people infected with COVID-19 who recovered from it are showing very limited antibody responses:
Background The COVID-19 pandemic caused by SARS-CoV-2 coronavirus threatens global public health. Currently, neutralizing antibodies (NAbs) versus this virus are expected to correlate with recovery and protection of this disease. However, the characteristics of these antibodies have not been...
www.medrxiv.org
Analysis of blood samples from 175 coronavirus patients released from hospital showed nearly a third had low levels of antibodies and in some patients, they could not be detected at all.
www.newsweek.com
That's another problem. What if they give someone a vaccine, and they don't even have any antibody response at all?
There's more:
There's also this:
Antibody-dependent enhancement (ADE) of viral entry has been a major concern for epidemiology, vaccine development, and antibody-based drug therapy. However, the molecular mechanism behind ADE is still elusive. Coronavirus spike protein mediates viral entry into cells by first binding to a...
jvi.asm.org
Some have suspected that SARS-CoV-2 has ADE, like Dengue. So, if someone gets a different coronavirus, and then they get COVID-19, they might have an incorrect antibody response and the antibodies may actually aid the virus in infecting immune cells.
COVID-19 patients have T lymphocytopenia. A common finding in COVID-19 is that patients' tissues have every inflammatory cytokine in them, causing severe damage and fibrosis, and they have low CD4 and CD8 counts and high Th17. The CD4 and CD8 cells that are present are hyper-activated. In other words, there is a low population of them, and the ones that are present are working overtime.
Even though it can't quite replicate in them, apparently, the virus can lure the immune system into attacking and destroying T cells. This may create a blind spot in the immune response, in a sense. It may also be contributing to the bacterial secondary infections that have been witnessed. More study of this phenomenon is needed.
Yep, steroids. China has been giving patients huge doses of methylprednisolone to try and dampen the immune response. This has problems of its own. You need an immune response to get rid of the virus, and if you suppress the immune system too much, you may give the virus the upper hand. Personally, I think that for the critical cases, it may be better to give them something like CytoSorb instead of steroids. It's an extracorporeal filtration device that gets rid of sepsis by absorbing excess cytokines and other crap from the blood. It's made by a company in New Jersey.
This “cytokine storm” can trigger a viral sepsis in coronavirus infection where viral replication and excessive, uncontrolled systemic inflammation.
cytosorbents.com
CytoSorb® is the first specifically approved extracorporeal cytokine adsorber in the European Union, designed to reduce the “fuel to the fire” of deadly inflammation often seen in critically-ill patients in the intensive care unit (ICU) and those undergoing complex open heart surgery...
cytosorbents.com
Unfortunately, this is kind of a boutique therapy that would be difficult to administer to everyone. You need a dialysis machine or an ECMO, or something else that pumps the blood out of the body, through the filter, and back in. It would have to be triaged for the most critical of cases, of course.
The filter consists of a canister full of adsorbent polymer beads with micro-pores that pull in the cytokines and junk. It was designed specifically to deal with sepsis that would ordinarily be lethal, which is a thing that happens with cytokine storms:
They have more than just elevated IL-6. They have elevated IL-1β, IL-18, TNF-α, IL-6, IL-8
and IL-10, among other things. The cytokine storms this thing causes are so severe, it causes fibrosis and hemorrhagic necrosis of tissue. It can do this in the lungs, the brain, and who knows where else:
Clinical pathology of critical patient with novel coronavirus pneumonia (COVID-19) (2020-02-26) [https://www.preprints.org/manuscript/202002.0407/v3/download]
Pathological findings of COVID-19 associated with acute respiratory distress syndrome (2020-02-1
[https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30076-X/fulltext]
Wherever the virus sets up a site of infection, it lures this massive host response that destroys healthy tissue. ACE2 receptors, the entry receptor of the virus, are basically everywhere.
Evidence of the COVID-19 Virus Targeting the CNS: Tissue Distribution, Host–Virus Interaction, and Proposed Neurotropic Mechanisms (2020-03-13) [https://pubs.acs.org/doi/10.1021/acschemneuro.0c00122]
SARS-CoV-2 can get into the lungs, heart, kidneys, GI tract, brain, testes, and possibly even the blood vessels themselves, and cause massive and damaging inflammatory responses.
Vasculitis was a finding with SARS. Very serious vasculitis. Why is vasculitis absent from so much COVID-19 research? The two viruses use the same entry receptor, ACE2, and affect pretty much all of the same tissues.
ACE2 receptors are found in the endothelial lining of blood vessels and the blood-brain barrier. What if the hypoxemia that patients are suffering with this virus is simply because vasculitis is causing the immune system to attack the walls of blood vessels and capillaries, leading to sepsis, viremia, clotting, et cetera?
What if the alveoli in people's lungs aren't exchanging oxygen due to an inflammatory and vasoconstrictive response, and pumping air into their lungs with a ventilator is useless?
They're inflating people's lungs like balloons with this damn virus, with ridiculously high PEEP settings that injure their alveoli, and they still can't oxygenate these people.
Why? Because it's in the blood and blood vessels. It can cause viremia, vasculitis, and perhaps even focal vasoconstriction by preventing the degradation of Angiotensin II, a highly vasoconstrictive and inflammatory hormone.
Please, god. Please, tell me someone understands what I'm saying here.
@evrae please, please back me up on this. I feel like I'm going nuts.
