Posted on 05/04/2020 3:29:25 AM PDT by RaceBannon
The states are all over the place right now, and will stay that way for a while.
Some have severe lockdowns, some have moderate lockdowns, some have lockdown-lite etc.
States will be slowly releasing folks through May and June.
Since there is a several week delay between gathering of crowds and CV deaths it will probably take until mid-summer for everything to hit the fan....
I’d argue workplaces with poor ventilation, crowded work stations and shared bathrooms will probably spread this quite efficiently.
so it seems to me you need to continue to look at how various diseases were studied prior to covid to determine how to deal with oxidative stress. take whatever disease you have...like hypertension...and start chugging away at the buzzwords used by Medcram..angiotensin II, 1,7 etc.
I suspect you will see a lot of NAC used in articles
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30937-5/fulltext
Our findings show the presence of viral elements within endothelial cells and an accumulation of inflammatory cells, with evidence of endothelial and inflammatory cell death. These findings suggest that SARS-CoV-2 infection facilitates the induction of endotheliitis in several organs as a direct consequence of viral involvement (as noted with presence of viral bodies) and of the host inflammatory response. In addition, induction of apoptosis and pyroptosis might have an important role in endothelial cell injury in patients with COVID-19. COVID-19-endotheliitis could explain the systemic impaired microcirculatory function in different vascular beds and their clinical sequelae in patients with COVID-19. This hypothesis provides a rationale for therapies to stabilise the endothelium while tackling viral replication, particularly with anti-inflammatory anti-cytokine drugs, ACE inhibitors, and statins.7, 8, 9, 10, 11 This strategy could be particularly relevant for vulnerable patients with pre-existing endothelial dysfunction, which is associated with male sex, smoking, hypertension, diabetes, obesity, and established cardiovascular disease, all of which are associated with adverse outcomes in COVID-19.
btw my relative who succumbed to the cytokine storm had no known underlying issues and did not have thalessemia.
So who knows why the flu wrecked the body in that case
Young, Fit, Athlete but not Super Athlete. Dead in about 4 days from pneumonia/sepsis
more from that yahoo commentor
2nd source https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156948/pdf/main.pdf
There is some stuff coming out from hematologists that is saying.. the virus is acting as if its primary target is the endothelium. Read the reports from Hooman Poor, Adam Cuker and pathologist Sharon Fox. Maybe the secret is not to fight this disease like a respiratory illness, but treat it as a blood/endothelial disorder and immune system gone haywire. Clot busting drugs and anti rejection drugs to modify the cytokine response? Pathologist Fox says when you look at these bodies you see they are riddled with blood clots in the small vessels of the body, the lungs being hit the hardest with clots.
What happens when you breathe the virus in, it’s going to go first into your lungs specifically to the ACE 2 receptor in your lungs. And what we all thought and imagined was that we were going to get ARDS, and that is why we started treating patients with hypoxia. Secondary to ARDS. Because this is what we all have been expecting for months and months.
But the virus gets worse and spreads and then it starts to go into the blood vessels. And the blood vessels inside of them also have ACE 2 receptors. What happens now when it goes into ACE 2, we get thrombosis, AT-11. These things happen so quickly even before the ARDS gets bad enough to cause the H type of lung problem, we have thrombosis which is causing the ground glass opacification, and we get the L type lung problem.
The final common denominator which take most of the patients into ICU is a process known as oxidative stress. The people with the worst oxidative stress from a baseline standpoint are those people with cardiovasular diseases, diabetes and over weight. Happy hypoxics. Cardiovasular collapse, blood clots in their vessels. These are the ones put on ventiators but to little avail.
An understanding of oxidative stress and how it might be involved in COVID-19 may give an avenue for therapeutics.” Have a pulse/O2 oxygen saturation monitor http://blauoximeter.pg-blog.com/ on hand. A pulse oximeter can provide early warning of the kinds of breathing problems associated with Covid-19 pneumonia. Take your readings now, when you are well, so you have a baseline to compare with. And do this lying down (as you would be if sick), so your baseline is a true baseline. Heart rate increases just by sitting up. Knowing these numbers will be very helpful in deciding if you need to seek medical attention.
if anyone wants to listen to this and give us the 3 plants that this herbalist recommends...I cant sit through it.
https://www.lostbookofremedies.com/vsl/index.php?split=310
you cant fast forward so that means she is trying to sell something most likely
but she does have a pedigree.
Dr Nicole Apelian
bkmk
“I’d argue workplaces with poor ventilation, crowded work stations and shared bathrooms will probably spread this quite efficiently.”
That is correct and ‘the experts’ have almost figured it out too. If it were only spread by people with obvious symptoms, then contact tracing would have been simple.
The smart thing would be to keep people who do not need to be in an office to work at home. I have zero interaction, really, all day. People who sit 15 feet from me still message me from TEAMs or Skype to communicate. There's no real reason I need to be in the office. I'd bet there are thousands like this.
so perhaps why Ace inhibitors MIGHT be a problem with covid 19 ..we have seen that theorized but havent really seen a definitive answer. the more I read the more I think this was an experiment for whatever reason that went wrong. why do malaria drugs if given early seem to work when malaria is from a parasite?
—
https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.116.309602
We propose the hypothesis that high levels of Ang II, which cause hypertension, protect against cerebral malaria.
Furthermore, it is important to consider that angiotensin receptor blockers, by shifting circulating Ang II to stimulate the AT2 receptor, may be protective against cerebral malaria, whereas ACE inhibitors would reduce the levels of Ang II, possibly increasing the likelihood of developing cerebral malaria on infection with Pfalciparum. In this context, it may be preferable to use angiotensin receptor blockers rather than ACE inhibitors for the treatment of hypertension in malaria endemic areas or at least in hypertensive patients with malaria.
“Cramer says Trump can’t raise tariffs on China with 30 million unemployed: ‘That is 1932’”
Yea, my simple question from the start was how do those tiny Coronavirus virons know if a person has high blood pressure, since hypertension itself doesn’t cause any chemical changes in the human body.
Answer: Since it’s not the hypertension alone, it must be the drugs being used to control the hypertension. Also, it would be interesting to know if hospitals are continuing to give ACE Inhibitors to people already taking them. after they’ve come down with Coronavirus. To me it seems logical to get them off of those drugs immediately - but then again, I’m not an ‘expert’, like those at the CDC. LOL.
Where are you finding county numbers, for TX?
interesting article for scientists..no help to just ole regular people
Human ACE2 receptor polymorphisms predict SARS-CoV-2 susceptibility
https://www.biorxiv.org/content/10.1101/2020.04.07.024752v1.full
In a letter to the editor in the journal Dermatologic Therapy, Dr. Carlos Wambier — an assistant professor of dermatology and clinician educator at Brown University’s Warren Alpert Medical School — and a team of researchers from New York University, Applied Biology, Inc., and universities in Spain, India and Italy lay the groundwork for a hypothesis: the same male hormones that cause hair loss are linked to the vulnerability of patients to SARS-CoV-2.
https://www.brown.edu/news/2020-04-07/androgen
Q: What might it mean for individuals who take anabolic-androgenic steroids, whether for approved uses or otherwise?
In the same way the U.S. Centers for Disease Control and Prevention recommended avoiding corticosteroids in COVID-19 patients, it might be important to avoid androgen hormones during the pandemic, particularly for police officers, health care workers and members of the military. There’s a link in that some corticosteroids also bind to androgen receptors. In addition, women who use progestogens for birth control that increase androgen activity (those that can cause acne or increased facial hair), might also consider contraceptive progestogens with anti-androgen activity.
Amazon VP quits his million dollar job ‘in dismay’ at firing of whistleblowers who raised unsafe warehouse working conditions - and he slams the tech giant’s actions as ‘chickens**t’
midlife crisis really screwed up Bezos.
https://coronavirus.jhu.edu/map.html
I’m not sure if this is what you’re looking for, but on this map you can select US, then Texas, then under the admin 1 tab you can see county by county death counts for Texas, and under the admin 2 tab you can see confirmed case counts for Texas counties.
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