Eh, [expletive] it. Let's just let it burn its way through and see what happens, I guess. We can be the control along with Sweden.
On that note, looking at Sweden, I see they're at and have been stuck at 560ish deaths / million population which would put USA at 185K deaths before this whole things blows over.
We're almost there. *Nervous laughter*
Knock Knock. USA at 560ish deaths / million while Sweden has increased to 576. America will probably overtake, deaths per capita wise, a country that never locked down here in the next week.
Sweden at least has managed to kind of level off (about 200-250 new cases per day in a country of 10M) and is averaging about 1 death per day leading Tegnell to openly ponder raising the gathering size limit from 50 to 500. Of course, America is planning on packing football stadiums with fans here in a month so Sweden ain't got nothing on us there.
As always, we'll wait and see. I guess this would be as good of a time as any to point out the Stanford Professor Michael Levitt's theory that covid will only kill about one months worth of people +/- in a community (a number that happens to be about 550-600 deaths per million people). That number is +/- 200-230K for America, I think, though the amount of people lost in nursing homes early on will raise that number somewhat.
I really don't know where this information comes from. SD has had a high day of 623, which wasn't really 623. It was a day that several prior days were reported incorrectly, and was corrected on this day. The other high is 423. Hard to find how to average 475 when you never have an actual day over 450.Just saying that these people need to look at what they are commenting on before firing off a tweet.
Maybe take a look at North Dakota also. The numbers here are a lot higher than they have been in the past also. And there wasn't a bike rally here. Maybe also take a look at which towns are spiking and compare it to towns that have recently opened up colleges. Obviously people from North and South Dakota are too dumb to go to college, so it must be out of staters.
I could also tell you a little about Sturgis. First, if the city council voted to cancel the event, how in the world would they stop these bikers? They were going to come anyway. And yes, it is a town of about 7,000 but most of those people take the week off and get the hell out of town during the rally. Every year. These things I know as my unit was backup military police every year I was in the National Guard. And I think IMA said it, everyone should stay away unless it is something you are in to. It is kind of a crap show. But there are plenty of outdoor things going on so you don't have to sit in a crowded bar all day. If you do though, getting COVID is kinda on you.
And while I detest Smashmouth, the guy said bleep-covid. So what? Does that mean he doesn't believe it, or says just get it and whatever? Not in my eyes. I've said bleep-cancer before. That hardly means I think it is a hoax. I think it is a terrible thing, so bleep-it.
The bradykinin hypothesis provides a model that “contributes to a better understanding of Covid-19” and “adds novelty to the existing literature,” according to scientists Frank van de Veerdonk, Jos WM van der Meer, and Roger Little, who peer-reviewed the team’s paper. It predicts nearly all the disease’s symptoms, even ones (like bruises on the toes) that at first appear random, and further suggests new treatments for the disease.
As Jacobson and team point out, several drugs target aspects of the RAS and are already FDA approved to treat other conditions. They could arguably be applied to treating Covid-19 as well. Several, like danazol, stanozolol, and ecallantide, reduce bradykinin production and could potentially stop a deadly bradykinin storm. Others, like icatibant, reduce bradykinin signaling and could blunt its effects once it’s already in the body.
Interestingly, Jacobson’s team also suggests vitamin D as a potentially useful Covid-19 drug. The vitamin is involved in the RAS system and could prove helpful by reducing levels of another compound, known as REN. Again, this could stop potentially deadly bradykinin storms from forming. The researchers note that vitamin D has already been shown to help those with Covid-19. The vitamin is readily available over the counter, and around 20% of the population is deficient. If indeed the vitamin proves effective at reducing the severity of bradykinin storms, it could be an easy, relatively safe way to reduce the severity of the virus.
Other compounds could treat symptoms associated with bradykinin storms. Hymecromone, for example, could reduce hyaluronic acid levels, potentially stopping deadly hydrogels from forming in the lungs. And timbetasin could mimic the mechanism that the researchers believe protects women from more severe Covid-19 infections. All of these potential treatments are speculative, of course, and would need to be studied in a rigorous, controlled environment before their effectiveness could be determined and they could be used more broadly.
Covid-19 stands out for both the scale of its global impact and the apparent randomness of its many symptoms. Physicians have struggled to understand the disease and come up with a unified theory for how it works. Though as of yet unproven, the bradykinin hypothesis provides such a theory. And like all good hypotheses, it also provides specific, testable predictions — in this case, actual drugs that could provide relief to real patients.
The researchers are quick to point out that “the testing of any of these pharmaceutical interventions should be done in well-designed clinical trials.” As to the next step in the process, Jacobson is clear: “We have to get this message out.” His team’s finding won’t cure Covid-19. But if the treatments it points to pan out in the clinic, interventions guided by the bradykinin hypothesis could greatly reduce patients’ suffering — and potentially save lives.
A lot of it is beyond my understanding, but what I find really noteworthy is how similar the bradykinin hypothesis is to what is starting to be accepted as fact. For starters, this explains the vascular nature of the disease. At the beginning, I think covid was treated more as a respiratory disease than vascular. But, with the blood clots/thrombi found in autopsies due to the blood cells being ravaged, as well as the strokes and heart attacks caused by those blood clots, the vascular nature of the disease became better known over time.
Also, the cytokine storm was proposed as a hypothesis early on and it appears that bradykinin and cytokine would act very similar in a lot of ways wrt inflammation and damage to the organs. Only bradykinin seems to explain even more symptoms than cytokine does. And, helps further explain the vascular damage in the paragraph above.
In the end, I'm not smart enough to fully understand all the things the paper/study is saying and I haven't had time to look into it all that deeply, but I do find it very interesting that this hypothesis is able to so closely match what has been observed.
ETA: also similar to what is believed/possibly proven at this point is that summit recognizes that sars cov 2 attaches to the ace2 receptor.
Geddy, you got me going back down the rabbit hole here trying to remember stuff I'd seen before but have since forgotten. And, then try to understand bradykinin's function more in depth which....there's not a lot on that I can understand.
As I mentioned earlier, it's interesting how the computer model mirrors many different beliefs that I've heard.
The most in depth biochemical explanation I've seen, not that it is correct just that it was a doctors attempt to explain his hypothesis, was essentially Sars-Cov-2 attached to the ACE2 receptor. ACE2 converts Angiotensin 2 (ATII) to Angiotensin 1,7 (AT1,7) but as ACE2 decreases due to Sars-Cov-2 binding to it, ATII increases and AT1,7 decreases.
O2 is converted to H2O in the body by accepting like 4 electrons and obviously combining with hydrogens. Water is obviously not harmful, O2 is obviously not harmful.
But ATII prevents O2-->H20, Sars-Cov-2 prevents O2-->H20, AT 1,7 helps O2--> H2O, and ACE2 helps O2-->H2O. In essence Sars-Cov-2 inhibits ACE2 and AT 1,7 while increasing ATII. As such, the O2-->H2O reaction is disrupted and the body is left with an abundance of O2 that has received an electron (superoxide, very bad) or two electrons (H2O2 - hydrogen peroxide, also not good). So instead of O2 and H2O, you end up with superoxides and hydrogen peroxide (oxidative stress). This in turn damages the blood cell and it releases these little hair like particles (vwf) whose job is to help the blood coagulate because typically they're released when the cell is damaged. And, this forms clots in the body....which is bad. Further, the broken chemical/chain reaction disrupts the ADP <--> ATP conversion and makes it difficult for the body to recharge ADP to ATP (which is the body's main source of energy).
This is why NAC was recommended because it cut those vwf hair strands while also helping to produce an antioxidant (glutathione) that could help convert superoxides and H2O2 to water thus restoring the chemical reaction.
The full explanation can be seen in Medcram episodes 63, 66, and 69 iirc on youtube if you want to go down the rabbit hole with me and spend a couple hours doing so. And, just a reminder, this is not the results of some scientific paper, it's just the hypothesis of the medcram team. So, it's not a fully vetted or even partially vetted hypothesis. It's 3 guys. But, it does make sense. So, I just assume this is true in some form.
Anyway, how this all relates to bradykinin (BK). It kind of doesn't, but it kind of does in that we're talking about some of the same enzymes.
Looking at the study....and.....I'm not 100% sure I understand this correctly. The model after analyzing everything shows:
1. ACE is downregulated. ACE2 is therefore upregulated giving Sars-Cov-2 more receptors.
2. ACE inactivates BK and by being downregulated leads to an increase in BK.
3. A C1 inhibitor was downregulated leading to an increase in kallkarin plasma (KP). Kallikarin plasma is the precursor to BK. Less C1 leads to increased KP leads to increased BK. (KP is inactivated by zinc, fwiw, again if zinc is in the cell).
4. BK leads to AT 1,9 which leads to permeable blood vessels, inflammation, and pain.
So, it's like a perfect storm allowing BK to be produced in excess which is causing a [expletive] load of bad. In the process its creating more receptors for the virus to enter the cells and replicate. And, the permeable blood vessels can more/less explain a ton if not all the symptoms.
*Shrugs* I think that's what it says at least.
Also, its noteworthy that BK would negate any oxidative stress as suggested by medcram as it aids in converting O2-->H2O, however the permeable cells would also possibly spill vwf into the blood causing thrombi/clots though I don't think the model ever gets into it. Though, it's a long paper and I didn't get through it all. I still tend to believe some form of medcrams theory is correct because it so neatly and perfectly describes the fatigue due to the loss of ADP to ATP, but that may me being a homer. And apparently that fatigue can just as easily be caused by the permeable cells? IDK.
tl;dr: I don't know what I'm talking about, but the model provides an extremely plausible biochemical explanation to the mechanics of the virus from what little I understand.
