Corona Virus Updates Part 6

a reply to: Serdgiam

The technologists are highly trained and a degree or certification was required to do them, plus training. I was almost activated for ELISA testing, luckily got to stay with my civilian job. Contamination is common with mass testing, that’s why they’re moving toward rapid testing. Swab and seal and send to the lab.

Incentivizing everything would be interesting, I would love more stimulus checks but this pandemic has boosted my income significantly, it would get rid of my student loans. My motivations are for my family and my future, I know others are the same way and they could abuse it. I personally believe putting out funds to increase reporting or accuracy of reporting has backfired and healthcare organizations are abusing it for money rather than the patient.

Most times in pandemics underreporting occurs, now I think we have overreporting and overuse of respirators, potentially dangerous aspects, just to get additional funding.

People are usually selfish, it’s only natural.

originally posted by: CatandtheHatchet
a reply to: McGinty
...the data is too fragmented from my perspective to come to any conclusions.

Ain't that the truth!

I think the UK made a point of resisting all cooperation and teamwork/sharing of data with China as well as S Korea and Europe (opting out of test and ventilator procurement schemes).

I too was at a loss as to why the UK was not learning lessons from these countries' devastation and locking down immediately (like New Zealand). I think the clue is in the slip Vallance made at a press conference revealing a herd immunity policy.

I totally respect that your assessment thus far of Boris' decisions differs from my own, but can i take the liberty of pointing you towards an excellent and easily digested timeline of the events and UK reactions since the start of the year. I posted it earlier, but in case you missed it:

appeasement.org...

Imo it leaves no room for doubt that the Tories mishandling and cover up has led to many thousands of deaths and will lead to many more if they remain unchallenged by the msm.

Just in case you wondered how busy our paramedics are here in the UK

twitter.com...

They really need to stop doing these videos, people quite rightly question the virus when the NHS staff have time to do these ridiculous videos. Disrespectful to anyone who is going through tough times at the moment.

a reply to: McGinty

When you think about it, a Government will never get anything perfectly right, all they can produce is an average Doo Doo and spread it about within their reach. We are on our own with this one, or with Darwin, where Nature favors the most intelligent personal response. The Tories track record is what we can expect, no more no less.

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A couple of days old, but a very readable article from Nature : Coronavirus Blood Clot Mystery Intensifies

This is like a storm of blood clots,” says Behnood Bikdeli, a fourth-year cardiology fellow at Columbia University in New York City. Anyone with a severe illness is at risk of developing clots, but hospitalized patients with COVID-19 appear to be more susceptible.

Studies from the Netherlands and France suggest that clots appear in 20% to 30% of critically ill COVID-19 patients1,2. Scientists have a few plausible hypotheses to explain the phenomenon, and they are just beginning to launch studies aimed at gaining mechanistic insights. But with the death toll rising, they are also scrambling to test clot-curbing medications.

...and that's the mystery right there: the anti-coagulants aren't totally effective -- this is where you have incidents of young people having strokes (and dying). It is believed that tiny clots are also clogging up the air sacs (alveoli) of the lungs, making it harder to get oxygen into the body.

At Columbia University in New York City, researchers are launching a clinical trial to compare the standard clot-preventing doses of blood thinners with a higher dose in people who are critically ill with COVID-19. Similar trials are planned for Canada and Switzerland. And scientists at Beth Israel Deaconess Medical Center have begun enrolment for a clinical trial to evaluate an even more powerful clot-busting medication called tissue plasminogen activator, or tPA. This drug is more potent, but carries higher risks of serious bleeding than do blood thinners.

With Remdesivir and seven other drugs in clinical trials and the first dose of a possible vaccine given to test (human) subjects, we may see more research showing up on the blood clot problem in the next month or so.

A grim (but not surprising) finding: People with coronavirus are dying 10 years earlier than they would have naturally: Study

And it's not "ten years chopped off the lives of people who were literally on their last legs."

Link to the scientific paper that the article is based on

The study, which is still awaiting peer review to ensure accuracy and validity, confirms what should seem obvious, but is nevertheless sobering: COVID-19 is not killing people who are already near death, rather it's claiming the lives of many people more than a decade before their time.

For men, it's actually taking 13 years off their lives.

What's interesting is that they did NOT set out to prove this... they were investigating data to show that it was really only affecting retirees in a significant way.

According to Dr. David McAllister, senior clinical lecturer and honorary consultant at the University of Glasgow Institute of Health and Wellbeing, he and his colleagues embarked on the study to test the assumption that the impact of COVID-19 may have been overstated, perhaps because the people who are dying would have died soon regardless of their infection.

a reply to: Byrd

This issue really interests me, especially in kids and the development of other complications like Kawasaki and petechiae.

Sepsis and clotting go hand in hand and sometimes the patient just bleeds depending on the inflammatory signaling. I don’t like how they mentioned d-dimer. That test is garbage to begin with and they are trying to find a replacement to effectively prevent DVT/PE or AFib and cardiac complications with clotting. D-dimer would be a mess in any critically ill patient with a war waging in the blood and other tissues. It’s also not reliable in this or any situation and needs other diagnostic criteria with it.

I’ll ask about the issues the next time I see a few people at work though. They know far more than I do but I haven’t seen any proposals about researching it yet. It would be easy in a mouse model.

a reply to: Byrd

I went through the papers and saw no mention of anything related to cytokine storms, which is quite disappointing. They did use the word "storm" though.. and seem to point in the general direction. Admittedly, I only took about an hour skimming through it all though.

Without stalling the cytokine storm, what I suspect is precipitating the issue in the first place (among many other symptoms), its going to be an uphill battle to ameliorate the clotting issues.

At least they are looking at proteases, but it seems quite a jump to recombinant stuff. Some interesting funding in some of those references though..

In applicable patients, something like nattokinase administered alongside treatments that directly address immune modulation issues might just meet with significant success as long as it is started before things run completely out of control.

Many of the treatments that can operate as viral inhibitors also appear to either operate as effective immune suppressants or modulators. Id suspect the former to be a preference in later progressions, with the latter being preferred before a full blown storm occurs.

a reply to: TheAMEDDDoc

Thanks for the info

Agreed on mass testing.. Do something enough times and there will be some mistakes, but it seems like the actual administration of the tests has some solid training.

I still have serious doubts about the nature of the tests, and would really like to be able to see amplification cycles published. Its a longstanding issue with tests of this nature, and it seems information gets more obscure about them as time goes on rather than more clear.

I think that an "incentive" program might have worked to start with, but am less sure how it would play out now. I doubt Ill be receiving anything myself either way.

Its been an interesting thing to watch play out though, not necessarily in a good way. I think that a lot of things were overlooked in order to shift business to large corporations as well.. But in the case of things like ventilators, it seems that they might not be the best choice for SOP anyway.

a reply to: TheAMEDDDoc

My thread here explains the cause of the irregular clotting. The anticoagulants will not function as expected.

Liver distress - iron overload - oxidative stress and ferroptosis cell death cascade - cytokine storm and coagulation

I believe there are blood anomalies created by a number of potential factors.
High IL-6》high hepcidin levels drive ferritin into the cells where it is degraded in the lysosomes 》this results in free iron loading to higher and higher intracellular levels, simultaneously lower iron available for blood oxygen transport》Sars-Cov2 can bind to CD147 gylcoprotien on cell surfaces》 red blood cells express CD147 protein and may become ineffective or even release hemoglobin into the plasma.》

Iron loaded cells eventually are triggered to initiate Ferraptosis cell death either through external stress (oxidarive stress, immune response, or inflammation) or internal stress (viral intrusion), the lysosome releases all the free Iron into the cells cytoplasm》 this creates reactive oxygen species and destroys the cell, releasing free iron and oxidative radicals into the extracellular space. 》 this causes more oxidative stress, more immune signaling, more inflammation, and triggers more Ferroptosis cell death.》

Vicious cascading cycle begins and free iron begins to accumulate in the blood stream》 trivalent iron ion (FeIII) generates in aqueous solutions powerful hydroxyl radicals that subsequently modify fibrinogen molecules converting them to insoluble fibrin-like polymer.
It should be emphasized that such a polymer is not only resistant to fibrinolytic dissolution, but also to proteolytic digestion, i.e. with chymotrypsin, that normally degrades fibrin(ogen) into smaller polypeptide fragments.》

This parafibrin can cause irregular clotting throughout the body and fatal blockage in various vital organs.
this whole process is initiated by liver distress and continued liver dysfunction drives much of the excess iron and hemoglobin to the lungs where it is taken up by the alveolar macrophages. 》 the combination of all these factors make the lungs the primary failure point once the cascading ferroptosis cell death and corresponding cytokine storm begins.


Soul

a reply to: SoulReaper

Thanks for that! I’ve no idea what it means, but really looking forward to the reactions possibly getting an idiots guide from the more learned folk here.

Wuhan have new cases of the virus... looks like

Wuhan reports first coronavirus cluster since restrictions were lifted after another Chinese city goes into lockdown amid fears of a COVID-19 rebound

www.dailymail.co.uk...

Wuhan, the epicentre of the novel coronavirus outbreak in China, reported on Monday its first cluster of infections since a lockdown on the central Chinese city was lifted a month ago, stoking concerns of a wider resurgence of the disease. The news comes after Shulan, a city in north-eastern China, imposed lockdown measures on its 600,000 residents, also due to a cluster of cases. The new infections in both cities sounded a note of caution amid efforts to ease coronavirus-related restrictions across China as businesses restart and individuals go back to work.

Like Arnie said:

I'll be back.

Wuhan reported five new confirmed cases, all of whom live in the same residential compound. One of them was the wife of an 89-year-old male patient reported a day earlier in the first confirmed case in the city in more than a month.

a reply to: SoulReaper

Thank you, saves me time. I’ll ask our people if they’ve seen this possibility and if they’ve noticed any genes that cause these issues in the virus.

Wonderful, ACE2, CD147 like blood borne parasites, GRP78 and furin. Free iron from it binding to blood cells would just increase viral replication and then the patient is in deep. Maybe T-cell suppression or exhaustion too. I also wonder if this thing can cause up regulation in some of these receptors, not causing a beneficial response but signaling one happened and inducing a host response to increase stress and other signaling to further compromise host defenses.

Might also explain some of these other issues going on with secondary diseases and why some of these random meds are working on these additional binding sites.

Looking at some of the KO strains being prepped for our studies, they are wondering why the ACE2 mice are surviving, this helps explain why. I still can’t believe how similar the spike is to SARS.

Thanks for the article.