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.

[Assman]

So, do you think I should work on personal fitness, study up, go to community college, and pursue biology seriously? I had some academics on Discord tell me the same.

If I wanted to get serious about any real scientific topic, I'd need quite a bit of remedial math to have enough of a foundation to work towards it.

I seriously need to go over pre-algebra, because my understanding of algebra, calculus, linear equations, and trig is virtually nil.

I had nothing else to do. No schooling. No friends. No one to fuck. Just play video games all day, troll people online, and jack off. That was it. That was my teenage years, that was my twenties, and it's now.

Holy shit. This reads almost exactly like an alternate reality where Zinnia Jones became self aware.

 

[Sped Xing]

Imagine being his age and realizing you'd completely wasted your life and could never hope to catch up.

 

[AltisticRight]

TBF backpacking anywhere at clop's level of greasy obesity is quite the accomplishment

Well, he was visiting various farms for sure.
Of course, Kiwifarms he expected kiwis, not bullies.
And he didn't know that there's no petting zoo here.

 

[Sped Xing]

Well, not for him is there a petting zoo.

 

[derpherp2]

why would we let him near the petting zoo? Tranny might think it's a buffet/orgy.

 

[Instant_Pot_User]

why would we let him near the petting zoo? Tranny might think it's a buffet/orgy.

Hey now, there's no evidence of him being a zoosadist (yet)
God help me why do I know what that is

 

[Drain Todger]

Sorry to be pedantic, but it's "QT interval". There is no medical term "QTC interval".

QTc means "Corrected QT Interval".

https://litfl.com/qt-interval-ecg-library/

QT Interval • LITFL Medical Blog • ECG Library Basics

archived 13 Apr 2020 23:12:48 UTC

archive.is

Corrected QT interval (QTc)

• The corrected QT interval (QTc) estimates the QT interval at a standard heart rate of 60 bpm.
• This allows comparison of QT values over time at different heart rates and improves detection of patients at increased risk of arrhythmias.

There are multiple formulas used to estimate QTc (see below). It is not clear which formula is the most useful.

• Bazett formula: QTC = QT / √ RR
• Fridericia formula: QTC = QT / RR 1/3
• Framingham formula: QTC = QT + 0.154 (1 – RR)
• Hodges formula: QTC = QT + 1.75 (heart rate – 60)

Note: The RR interval is given in seconds (RR interval = 60 / heart rate).

• Bazett and Fridericia are logarithmic corrections whereas Hodges and Framingham are linear correction formulae.
• Henry Cuthbert Bazett derived his formula in 1920. Bazett formula is the most commonly used due to its simplicity. It over-corrects at heart rates > 100 bpm and under-corrects at heart rates < 60 bpm, but provides an adequate correction for heart rates ranging from 60 – 100 bpm.
• Louis Sigurd Fridericia derived his formula in 1920 from 50 health individuals aged between 3 and 81 years old. Fredericia formula is the observed QT interval divided by cube root of RR interval, in seconds.
• Charbit B et al in a study of 108 patients found that automatic QT correction using Bazett formula had a sensitivity for detection of QT prolongation of 54% while automatic QT correction using Fridericia formula had 100% sensitivity.
• At heart rates outside of the 60 – 100 bpm range, the Fredericia or Framingham corrections are more accurate and should be used instead.
• If an ECG is fortuitously captured while the patient’s heart rate is 60 bpm, the absolute QT interval should be used instead!

Fortunately, there are now multiple i-phone apps that will calculate QTc for you (e.g. MedCalc), and the website MDCalc.com has a quick and easy QTc calculator that is free to use.

It makes it easier to compare the interval at different heart rates if you adjust it so that all your measurements use the same heart rate.

Someone with a pulse of 120 is going to produce a very different looking EKG from someone with a pulse of 80, unless you adjust both so you're looking at them as though their heart rates were both 60, which is what QTc does.

 

[AbraCadaver]

Drain’s gonna be so sad when a vaccine gets developed. What will he sperg about then? Back to fucking pastel cartoon horses I guess.

 

[Salad Dodger]

Fark. This tard would have to have a username that resembles mine.

 

[Shick]

Drain’s gonna be so sad when a vaccine gets developed. What will he sperg about then? Back to fucking pastel cartoon horses I guess.

How the vaccine is actually poison/fake/a way for Bill Gates to track and control the populace.

 

[Tookie]

How the fuck is this guy still going?

 

[Bridge to Nowhere]

How the fuck is this guy still going?

They've made doom and gloom their lifestyle, they don't have much else to do in their life.

 

[derpherp2]

How the fuck is this guy still going?

You know attentionwhores, they have to do extreme mental gymnastics so they can look themselves in the mirror.

Totally don't care tho bro, we seriously didn't notice you hiding some of your account shit. Your gay ops DFE plan went off without a hitch.

@Drain Todger
Did you seriously think doing everything BUT privatizing your account would be subtle? lol.

 

[Drain Todger]

@Drain Todger
Did you seriously think doing everything BUT privatizing your account would be subtle? lol.

I was tired of people commenting on my profile activity, so I disabled it.

"Oh, you're looking at this, oh, you're looking at that, oh wow look at this self-absorbed, imbecilic twat."

Seriously, who gives a fuck what thread I'm reading and for how long?

 

[1Tonka_Truck]

I was tired of people commenting on my profile activity, so I disabled it.

What would you say if I told you accomplished nothing by doing so?

 

[Troonos]

God, I'm so sad that I didn't join this thread two weeks ago. What a masterpiece of a train wreck.

This retard is about as informed about coronavirus as Karen is about the dangers of vaccines and benefits of essential oil. Sitting on a gaming PC and doing Google searches isn't actual research. He isn't producing any new information or analyzing existing information from an expert perspective. He lacks the background to be informing the public. That's dangerous, bro.

 

[Instant_Pot_User]

I was tired of people commenting on my profile activity, so I disabled it.

oh wow look at this self-absorbed, imbecilic twat

 

[Drain Todger]

Drain’s gonna be so sad when a vaccine gets developed. What will he sperg about then? Back to fucking pastel cartoon horses I guess.

God, I'm so sad that I didn't join this thread two weeks ago. What a masterpiece of a train wreck.

This exceptional individual is about as informed about coronavirus as Karen is about the dangers of vaccines and benefits of essential oil. Sitting on a gaming PC and doing Google searches isn't actual research. He isn't producing any new information or analyzing existing information from an expert perspective. He lacks the background to be informing the public. That's dangerous, bro.

A vaccine for SARS-CoV-2 may be very, very difficult to develop. Here, let me translate a few papers into layman-speak.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3335060/

Immunization with SARS Coronavirus Vaccines Leads to Pulmonary Immuno…

archived 23 Mar 2020 20:12:04 UTC

archive.is

All vaccines induced serum neutralizing antibody with increasing dosages and/or alum significantly increasing responses. Significant reductions of SARS-CoV two days after challenge was seen for all vaccines and prior live SARS-CoV. All mice exhibited histopathologic changes in lungs two days after challenge including all animals vaccinated (Balb/C and C57BL/6) or given live virus, influenza vaccine, or PBS suggesting infection occurred in all. Histopathology seen in animals given one of the SARS-CoV vaccines was uniformly a Th2-type immunopathology with prominent eosinophil infiltration, confirmed with special eosinophil stains. The pathologic changes seen in all control groups lacked the eosinophil prominence.

Translation: When they tried coming up with a vaccine for SARS-CoV, back in the day, the mice successfully produced antibodies that stopped the virus, but they also had immune reactions in their lungs that damaged their lung tissue anyway.

https://www.nature.com/articles/s41577-020-0308-3

COVID-19: immunopathology and its implications for therapy | Nature R…

archived 10 Apr 2020 22:34:30 UTC

archive.is

The detection of SARS-CoV-2-specific IgM and IgG in patients provided the basis for disease diagnosis, in conjunction with RT-PCR-based tests. However, two studies, based on the analysis of 222 and 173 patients with COVID-19, respectively, reported that patients with severe disease frequently had an increased IgG response and a higher titre of total antibodies, which was associated with worse outcome5,9. This was suggestive of possible antibody-dependent enhancement (ADE) of SARS-CoV-2 infection. The immunopathological effects of ADE have been observed in various viral infections, characterized as antibody-mediated enhancement of viral entry and induction of a severe inflammatory response. Worryingly, it was shown that a neutralizing monoclonal antibody targeting the receptor-binding domain of the spike protein of the related Middle East respiratory syndrome (MERS) virus can enhance viral entry. A potential pathogenic effect of antibodies targeted at SARS-CoV-2 would be of major concern for vaccine development and antibody-based therapies. Additional independent large-cohort studies are needed to substantiate or dismiss this possibility.

Translation: SARS-CoV-2 may have something called antibody-dependent enhancement, where an incorrect antibody response actually helps a virus infect your cells. This is very similar to what happens when someone gets one strain of Dengue, and then contracts a different strain of Dengue. They get ADE and they get very, very sick.

Antibody-dependent enhancement - Wikipedia

en.wikipedia.org

News Feature: Avoiding pitfalls in the pursuit of a COVID-19 vaccine

As they race to devise a vaccine, researchers are trying to ensure that their candidates don’t spur a counterproductive, even dangerous, immune system reaction known as immune enhancement. The teams of researchers scrambling to develop a coronavirus disease 2019 (COVID-19) vaccine clearly face...

www.pnas.org

News Feature: Avoiding pitfalls in the pursuit of a COVID-19 vaccine …

archived 14 Apr 2020 01:47:01 UTC

archive.is

Graham emphasizes alternative ways in which a vaccine could potentially induce more serious COVID-19 infections: Th2 immunopathology, in which a faulty T cell response triggers allergic inflammation, and poorly functional antibodies that form immune complexes, activating the complement system and potentially damaging the airways.
Both processes were at play as an unfortunate situation unfolded in the 1960s, according to Graham. Researchers at the time were pursuing a vaccine against RSV, the leading cause of severe respiratory illness in infants. In trials of one vaccine candidate, several children who received the vaccine developed a serious illness when infected with the natural virus (7). Two toddlers died. In this case, researchers noticed severe damage and the unexpected presence of lots of neutrophils and eosinophils, both immune cells, in the children's lung tissue. A similar inflammatory response was seen in animal models of RSV, in which cytokines, a type of immune cell, had invaded and damaged tissue.

Translation: Same as with the mouse study with SARS, researchers are worried that a vaccine may trigger severe inflammatory reactions in the lungs.

https://www.nature.com/articles/s41423-020-0424-9

SARS-CoV-2 infects T lymphocytes through its spike protein-mediated m…

archived 12 Apr 2020 01:39:17 UTC

archive.is

Based on the results of pseudovirus and live virus infection, here we proved that (1) SARS-CoV-2 could infect T cells, (2) SARS-CoV-2 infected T cells through receptor-dependent, S protein-mediated membrane fusion, and (3) infection could be inhibited by EK1 peptide. However, we observed a very low expression level of hACE2 in T cells; therefore, we further proposed that a novel receptor might mediate SARS-CoV-2 entry into T cells. Similar to MERS-CoV, SARS-CoV-2 infection of T cells is abortive. A recent study reported that viral reads barely displayed in PBMC samples from COVID-19 patients through transcriptome sequencing of RNAs. Thus, it was inferred that SARS-CoV-2 could not infect PBMCs. However, the transcriptomic characteristics of PBMCs were detected and analyzed from three patients. Two SARS-CoV-2 reads were detected in one patient’s PBMCs, and zero reads in another.3 This result could be attributed to nonproductive replication of SARS-CoV-2 in T lymphocytes, with little viral genome in PBMCs possibly degrading in the sample collection and RNA extraction process. Thus, the questions of SARS-CoV-2 infection and replication in primary T cells and whether the infection induces apoptosis in T cells still need further research, potentially evoking new ideas about pathogenic mechanisms and therapeutic interventions.

Translation: SARS-CoV-2 can actually infect, replicate inside, and destroy your immune cells.

COVID-19 is serious business. Anyone who isn't taking this virus seriously is out of their damn mind.

 

[Instant_Pot_User]

Here, let me translate a few papers into layman-speak.

oh wow look at this self-absorbed, imbecilic twat

Translation: SARS-CoV-2 can actually infect, replicate inside, and destroy your immune cells.
COVID-19 is serious business. Anyone who isn't taking this virus seriously is out of their damn mind.

I'm no virologist, but I'm pretty sure that's not that unique. Also, everyone's taking this shit seriously, faggot.

 

[Drain Todger]

I'm no virologist, but I'm pretty sure that's not that unique.

Yeah, it's not unique. It's also a property of HIV, Ebola, and Epstein-Barr.

https://www.scmp.com/news/china/society/article/3079443/coronavirus-could-target-immune-system-targeting-protective

Coronavirus could attack immune system like HIV by targeting protecti…

archived 16 Jan 2021 00:04:10 UTC

archive.is

To the surprise of the scientists, the T cell became a prey to the coronavirus in their experiment. They found a unique structure in the virus’ spike protein that apparently triggered the fusion of a viral envelope and cell membrane when they came into contact.

The virus’s genes then entered the T cell and took it hostage, disabling its function of protecting humans.

Not good. Not good at all.