MATHS MATHS MATHS MATHS MATHS
FUCK I LOVE MATPLOTLIB AND MATLAB
Huh. You know, that's interesting.
I don't disagree with you. I actually see your point. If he just kept adjusting his function to account for changes in the variance in the data, then wasn't he basically trying to mislead everyone?
And, for that matter, if that shit Barron's dragged up is just bullshit, then why did they publish it? Don't they care about their reputation? What the hell is up with that? Is it all just propaganda? Was I completely misled?
Dude, I think you're onto something, here. I think you better call Melody Goodman and figure out what she was smoking when she came up with that R-squared of 0.99. Come on, let's get this cage match going. I'd pay good money to see that:
Dr. Melody Goodman researches social risk factors that contribute to health disparities among underserved communities in urban areas and develops culturally competent and evidence-based solutions.
publichealth.nyu.edu
God. Half of these news articles about this thing are just pure clickbait bullshit.
Anyway, what I'm trying to do here is far more of a workload than one person can reasonably handle on their own. You'd need a whole
team to unravel this thing.
I was discussing all this with my own doctor this morning, and he said I needed a break, that I'd already taken on too much work, that I'd been losing sleep, that my cortisol levels were too high, et cetera, et cetera.
However, I didn't want to just wallow in defeat. I wanted to keep going. See where I ended up. Hopefully not in a nut ward.
This.... is like teaching Chinese postgrads, and whoever handles induction for freshmen at your college should be assblasted for failing to insist on a mandatory course on citations and academic writing. That’s their fault, not yours. I will lead you through the basics and then you can Google-fu yourself a few basic guides from other colleges to keep as a reference.
It is setting students up to fail to assume that they all know how to write an academic paper, and it annoys me when institutions take your money and don’t give you the skills you need to succeed.
The first thing every academic paper has is a thesis. Yes, even your first year essays. If you approach your work from the beginning of your academic career correctly, the skills will quickly become second nature. All a thesis is, really, is a sentence or two outlining the proposition that your paper intends to prove (or disprove, but the negative thesis is best avoided in humanities if you can).
You then arrange about three to five main strands of argument that will support your thesis. You will discuss each of these in a seperate sub heading, or chapter. It isnt that important how you divide them, but as your reader I should be able to easily distinguish one argument from another. As you discuss each one, you should also pick up the major arguments against it, the major known issues with the analysis, and any areas of doubt/lack of info, and deal with each one. You aim to rebut any material that says “your argument is wrong”, and you aim to illustrate what information is missing and how it may be gathered in response to material that says “you just don’t have enough evidence to support this argument”.
If there seems to be a shitload of material that says you are wrong or that there’s no information to support your argument and you are just pulling it out of your ass, this is a strong signal to sit down, go back carefully through all the material you have, and reconsider your assumptions and the conclusions you’ve drawn from those. It’s absolutely fine to be wrong. But if you submit wrong stuff to me, I have to mark you accordingly. It’s fine to take a couple of hours to recheck your thinking.
Now, in order to support each of your arguments, you need academic work. (In medical sciences, you will need data unless you’re doing a Cochrane review. I haven’t written a science paper since high school, so I will leave it to the better educated than me in this thread to talk you through data handling skills.) You need what a much missed professor of mine used to call in fruity tones “ssscholarly aaaaarticles”. Some sources, as we all remember from our first ever history lesson at school, are better than others. This is because they are written by people who are more authoritative in the field; they were published in a leading journal that has stricter peer review standards; the authors don’t have obvious or declared notable conflicts of interest; the paper emits from academics appointed to a prestigious institution. These on their own are not infallible and none on their own will be enough. It is however true to say that the better ‘score’ an article gets by these metrics, the less complete bullshit it is likely to be compared to the work of I.M. Clown self published on his Wordpress site.
More and more journals are going open source or digitising. This is marvellous because it’s a real pain in the ass to go to the library, and your friends will distract you if they show up there too. But I will check your sources when I mark your work. I will without fail check any source I am not already academically familiar with, and if it smells like shit, I will feed back that the source was not compelling enough to support your argument. This is not “academik boolying“, this is my actual job. Not all sources are equally good. Quite a lot of shit gets vanity published, and a thing you need to know is which journals are the vanity journals in your field, and avoid ever relying on them. (Also don‘t submit your work to them for publication, it makes you look like a spastic who couldn‘t get published anywhere else).
You should refer to specific parts of the sources that support your argument. Don’t just throw a footnote in or say “As Chandler argues, blah blah blah”. Because then I will go and read Chandler like a Pharisee to see if they supoort your argument, and if they don’t I will be pissed at your laziness and your attempt to smokescreen me with a source that doesn’t support your argument, and I will take my feelings out on your grade. In fact I am required to ding you for that shit.
Once you have written all this shit up, you have to write a conclusion about whether or not the stuff you just wrote supports your thesis. If it doesn’t you better have a damn good reason why and be able to analyse why not.
The last thing you write is your introduction, because that tells me what you are you going to tell me in the rest of the paper, so it’s easiest to write this last because by then, you know what’s actually in the paper.
So, in recap, the first thing you need in your corona epic is a thesis. I think from all I have read of your train of thought, the thesis you are trying to prove is that coof is a neurotrophic virus. So focus on that and sources that prove that, and the individual strands of argument that will support that. Don’t fire hose links and tweets (you have to be ultra careful using fucking tweets as a source, okay?) without explaining how they supoort your thesis. Don’t get sidetracked.
You are familiar with popular science books. Try and aim for that informational but readily digestible tone in your writing.
Good luck with reworking your document. I’m interested to see the finished product.
I... dear god, you're right.
My "thesis" is junk. I didn't actually make an argument. I just firehosed papers with little to support it and without inline citations. I need to go back to the drawing board and cull it down to just the important bits.
I've never actually written a term paper or a research paper in my life. I've never been to college. I don't have access to any college portals or anything like that, so any research I
do gather would basically have to be from open journals (paywall removers, maybe?). I suppose I was trying to do something I'm not particularly qualified to do.
There is something dreadfully wrong with the picture I've assembled of this virus. It's a scattershot mess that relies on scant data. Lots of papers with positive hits, but the sample sizes aren't particularly large, and the data on the prevalence of each individual complication is lacking.
Many of the complications associated with COVID-19 can also occur with influenza, but they seem more common and more severe with this virus. Basically, what I'm trying to prove is that COVID-19 can cause a sort of widespread vascular syndrome that affects all the vital organs, in addition to a neurological syndrome that causes encephalitis and/or medullary dysfunction. The virus could be entering the bloodstream, causing systemic viremia, and then, from there, it may attempt to infiltrate many of the other highly-vascularized organs, such as the brain, lungs, kidneys, et cetera. It could even be attacking the blood-brain barrier directly, given the presence of ACE2 receptors in those tissues. Meanwhile, it also seems to be able to enter the nerves and infect them. There are a number of papers that point to this.
This conflicts with the mainstream account of the virus as, essentially, a respiratory disease first and foremost. Again, some doctors are very confused by the silent hypoxemia caused by this thing. It behaves less like a respiratory disease and more like a blood disease.
But there needs to be ample proof. "Seems" and "maybe" and "perhaps" aren't good enough. I'm in a disadvantaged position, here. I have no access to confidential information, nor do I have any direct access to any laboratories working with the pathogen or with tissue samples. Frankly, anyone who's handling that stuff has brass balls that clack together and shoot lightning out their ass. If someone offered me a vial of live SARS-CoV-2, it doesn't matter how much gear I'm wearing or if it's under a fume hood or whatever. I would run screaming in the opposite direction.
It was mostly desperation and germaphobia and a desire to protect people close to me that drove me to this point to begin with, otherwise, I wouldn't have given much of a damn.
However, at some point, I must confess that I developed a very real fascination with the topic. I mean, enough to buy $500 in biology and virology textbooks, anyway. I had very little knowledge of viruses about 2 months ago. All I knew was that, y'know, they went into your cells and did bad stuff and replicated a whole lot.
However, I started catching on quickly. Viruses use entry receptors for endocytosis. Those receptors are found on the outside of human and animal cells. They often perform normal biological functions like hormone regulation and chemical signaling. You know, just like the "fun" receptors, like dopamine receptors and opioid receptors and whatnot. The virus can block them in the process of using them, almost like a receptor-blocking drug. Once it gets inside a cell, it breaks down, releases its payload, and then, the process of transcription begins, essentially like sending a set of tool paths to a CNC mill, ordering the cell to produce more virions. The viral particles thus produced can undergo exocytosis and leave gently, or they can pull a chestburster and cause the cell to lyse violently like a Flood Carrier Form from Halo going poof and releasing a bunch of infection forms.
The thing about SARS-CoV-2 is that it has furin cleavage sites on the spike glycoproteins that SARS-CoV lacks, because of its slightly different genetics. Furin is a protein that reaches out and cuts other proteins to activate them. You can think of a cleavage site on a coronavirus spike protein as almost being like a perfect video game ledge for a grappling hook (the Furin) to latch onto. It tricks your own furin into cleaving it and activating it.
The spike glycoprotein of the newly emerged SARS-CoV-2 contains a potential cleavage site for furin proteases, an observation with implications for the zoonotic origin of the virus and its epidemic spread in China.
www.virology.ws
This makes it highly infectious because it allows for HIV-like high-efficiency cell-to-cell fusion, and it's why that one scientist in that one retracted paper said "Hey, this spike looks like HIV gp120". It's not actually gp120, by the way. Just a lookalike.
Spike proteins on coronaviruses are trimeric and look like a great big caveman club, or a cartoon chicken drumstick. The end that sticks into the lipid membrane is tiny. The exposed end is huge and studded with glycosylation sites.
Glycans are often overlooked because of their chemical complexity and limited throughput and sensitivity of existing analytical instruments. But understanding their complicated structures and function may hold the key to successful diagnosis, treatment, and prevention of COVID-19.
www.genengnews.com
Anyway, what I hypothesized is that this may make the virus more active and invasive in the human body than SARS-CoV was. As in, what I suspected was that the spike of SARS-CoV-2 is essentially more bioactive than the spike of SARS-CoV, resulting in deeper infiltration of the tissues of individual virions (one wonders at how this thing could be less lethal than SARS, if that were the case). In other words, rather than thinking of this solely as enhanced human-to-human transmission, we might also think of it as enhanced cell-to-cell transmission
inside the body, which might explain the possible neurotropism.
There are admittedly things about all this that I
don't understand. The finding of possible heme metabolism interruption is
bizarre. They didn't actually examine the virus doing this
in vitro or
in vivo or anything. They found the relationship with a computer model, it seems. This came completely out of left field for me.
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
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. Since the ability of chloroquine to inhibit structural proteins is not particularly obvious, the therapeutic effect on different people may be different. Favipiravir could inhibit the envelope protein and ORF7a protein bind to porphyrin, prevent the virus from entering host cells, and catching free porphyrins. This paper is only for academic discussion, the correctness needs to be confirmed by other laboratories. Due to the side effects and allergic reactions of drugs such as chloroquine, please consult a qualified doctor for treatment details, and do not take the medicine yourself.
What they're trying to say is that the ORF8 and the spike of the virus can potentially bind porphyrin, leaving it unavailable for hemoglobin production. Okay. That sounds to me like they're proposing this thing can cause a form of anemia.
Where are the blood labs showing anemia in COVID-19 patients? Where is the proof? So patients have been consistently found with elevated ferritin. So what? Did they look at the RBCs to see if they really were dysfunctional or not? Did they confirm it?
COVID-19 Research: Findings from a new study released by Chinese researchers , Dr Wenzhong Liu from Sichuan University and Dr Hualan Li from Yibin University has revealed that the Sars-CoV-2 coronavirus attacks hemoglobin in the the red blood cells through a series of cellular actions, that...
www.thailandmedical.news
I just found another very interesting preliminary document:
In it, they claim that splenic shrinkage in autopsies of COVID-19 victims indicates erythrocyte depletion. Okay. Where are the peer-reviewed papers showing this?
I can't just keep shadow-boxing with myself on this. I'm trying to make a point, and that point is that the mainstream focus on the respiratory manifestations of this disease is wrong. Dead wrong. I don't think the lungs are even the primary site of infection. I'm starting to think the blood vessels and bloodstream are.
If you're looking for some form of pneumonia with this thing, you're basically looking for pneumonia that is secondary to viremia, porphyria, vasculitis, and/or encephalitis
before the disease infiltrates the vital organs, like the heart, lungs, and kidneys. My new theory is that this virus causes sepsis in the blood and damage to blood vessels above all else, and from there, it enters the organs, causing inflammation and cytokine release syndrome while simultaneously promoting clot formation and infiltrating nervous tissue. The multi-organ manifestations are a simple consequence of the fact that this virus touches the blood and the nerves
first, and from there, it spreads to every corner of the body with ACE2 receptors and infects those tissues. The pneumonia, the renal tubular damage, and the cardiomyopathy are all because the viremia touches every one of those organs by entering them through the bloodstream, while also causing sepsis, bacterial co-infections, and cytokine release syndrome.
Recently, we've been hearing that this thing has killed a lot of African-Americans in Chicago. A proportionately huge number, actually. 30% of the population, but 70% of the deaths. Why is that? Well, black people have higher rates of hypertension. It's just a fact.
The American Heart Association helps explain why being African American raises your chances of having high blood pressure, also called hypertension.
www.heart.org
Hypertension primes the body for COVID-19 infection. The body undergoes polymorphic changes in genetic expression that result in higher populations of ACE2 receptors on the outside of cells. Why is this? Well, it's simple. ACE2 converts Ang II to Ang 1-7, and it balances out the high blood pressure by converting a vasopressor hormone to the opposite, a vasodilator.
This is why people with comorbidities like obesity, diabetes, hypertension, and so forth, are dying in droves. It's not because their conditions have weakened their bodies. It's because their conditions have
primed their bodies for the virus with polymorphic changes.
The human body is very plastic and adaptable. See this Chubbyemu vid, for instance:
This guy drank 50 beers a day as his only "nutrition" and had chronically low sodium as a result. His brain tissue actually underwent polymorphic changes to compensate for the electrolytic imbalance, so when they treated it with sodium,
whoops, now he's fucked because his body's received a jolt of sodium it wasn't expecting.
High blood pressure and diabetes and all these other conditions do something similar with the RAAS. Over the long-term, they cause changes to the body. Namely, they promote more ACE2 proliferation.
ACE2, coronavirus, COVID19, SARS, hypertension
www.nephjc.com
There's something that ties this all together.
Something.
What am I
missing, here? What an infuriating puzzle.
This is an extremely complicated pathology. This ain't your grandma's flu. This is something completely different.
I'm going to do something I've never done in my life. I am going to attempt to write an actual paper. And I'm going to have Kiwi Farms review it.
Heh, the random.txts are writing themselves.
I need to go do some more research. And a whole lot more writing. This is going to take a while.
I see the truth, now. The shit I've put out so far is basically trash. Useless. Sure, a scientist might find it handy to have all those papers in one place, but no one else will be able to make use of it.
Let's see if I can come up with something that meets a more rigorous standard.
Honestly after the full on career ending demolition you got by
@AltisticRight and the fact you're silently fuming and reading this thread based on activity, you should just lick your doorknobs dude.
He pushed my shit in so hard, those doorknobs are actually looking pretty tasty right now, I must confess.
Bravo for the post on technical writing,
@Fareal! You pretty much nailed it, but I want to add a few things:
@Drain Todger has never gone to college, and has
at best a high-school education (depending on whether he actually learned anything useful from his
uneducated cultist parents when they were
half-assedly homeschooling him).
View attachment 1222900
Just to clarify, are these people preaching that they can fight/cure STD's using faith/prayer? Because if they are they need to be stopped. Like call the CDC or whatever the appropriate organization is and stop them from spreading misinformation.
forums.spacebattles.com
(
https://archive.li/08Uv2#selection-2411.0-2411.19)
Here's a pretty useful resource for everyone that doesn't have university access to journal subscriptions for research articles (i.e. present for you,
@Drain Todger!). Works pretty well for many articles that are otherwise paywalled, but of course some newer papers might not be immediately available if they haven't ripped them yet:
The first pirate website in the world to open mass and public access to tens of millions research papers
sci-hub.tw
I think I posted this one too earlier, but I'll post it again. Pretty much
everyone I knew at university used this, because fuck spending $200+ on a textbook.
Library Genesis is a scientific community targeting collection of books on natural science disciplines and engineering.
libgen.is
This will actually come in handy. Thank you.
...
View attachment 1224302
“@MLocker01 @MichaelCoudrey This is a very old version of this document. My latest version can be found at: https://t.co/3yx672YYfu I'm currently working on something of a thesis on this virus, using this pseudo-bibliography as a basis. This thing is extremely complex.”
twitter.com
(
https://archive.li/Yyj1H)
Yes, I'm writing a paper right now. It's at 995 words (including the 207-word abstract) and 22 citations so far.
One of the PhDs I was in touch with on Discord, an immunologist who uses the handle WesternBlotter, recommended I use Zotero to manage the papers and the cites, which makes everything a whole lot easier. I'm going to draft a rough outline, and then, I'm going to go back over it in detail a couple times to see if there was anything I missed. I also need to go around and basically just keep gathering papers, like as many of the relevant ones as I can, digging through the various publisher portals and stuff. Some publishers are making their COVID-19-related stuff free right now, which is nice.
Rather than just tossing crap out there, I'm going to be very careful with this thing. The goal is to show how COVID-19 relates both to SARS and autoimmune disorders, which organs it affects, and what mechanisms it uses. I'm probably going to have well over 100 papers cited by the time this thing is done.
Feb 18, 2020
Feb 16, 2020
Feb 15, 2020
Aug 29, 2017
Aug 19, 2016
Are you aware that some of us actually earned degrees in relevant or adjacent subjects and what you're saying here is pretty fuckin disrespectful in addition to being incredibly stupid? (I've deliberately not argued medical issues with you, and instead kicked the autistic, for the same reason that I kind of think that making medical articles available to deranged autistic meta-hypochondriacs such as yourselves was a big mistake. Plus, your shit is deadly to read.)
en.wikipedia.org
thefederalist.com
www.nationalreview.com
twitter.com
