1) IMPORTANT EVIDENCE SUPPORTING THE HYPOTHESIS THAT SARS-CoV-2 IS PRIMARILY A DISEASE OF THE SPIKE PROTEIN’S INTERACTION WITH THE MICROVASCULATURE
A large study was posted today, which I believe greatly supports the hypothesis that COVID-19 is not only a Vascular Disease, but,
2) specifically, a disease of the MICROVASCULATURE. This is due, mainly, to the Spike Protein’s injury to the endothelium.
If we look at the mortality rates from the Trends and associated factors for Covid-19 hospitalisation and fatality risk in 2.3 million adults in England
3) study, we find that OBESITY IS ACTUALLY A VERY, VERY SLIGHT RISK FOR MORTALITY. HOWEVER, UNDERWEIGHT IS A VERY, VERY SIGNIFICANT RISK FOR MORTALITY.
If we look at the other major mortality risks, we observe that they are CHRONIC KIDNEY DISEASE, SEVERE MENTAL ILLNESS
4) (i.e. Schizophrenia) and LEARNING DISABILITIES.
These seeming disparate conditions do have ONE hallmark in common. THEY ARE ALL INTRINSICALLY RELATED TO MICROVASCULAR DYSFUNCTION.
SCHIZOPHRENIA
Vascular involvement in the pathophysiology of SZ (Bleuler, 1911) has gained some
5) salience in recent years to explain and unify physiologic abnormalities seen in SZ (Hanson and Gottesman, 2005; Moises et al., 2015; Schmidt-Kastner et al., 2012). These hypotheses place IMPARIMENR OF THE BRAIN MICROVASCULAR SYSTEM AS THE CENTRAL MECHANISM IN THE PATHOLOGY OF
6) SCHIZOPHRENIA.
LEARNING DISABILITIES
The Hypothesis: It has been identified that the visual impairment in T2D is related to microvascular complications, which may cause low blood and fluid flow to the eyes that may lead blurred vision, dry eyes or retinopathy according to the
7) severity of the condition. Due blurred vision that is caused by microvascular complications, reading difficulties can be developed which may trigger Dyslexia, however, it requires further research within the dyslexic patients and their microvascular system.
8) UNDERWEIGHT
Findings in a study from 2018 indicate Nailfold Capillaroscopic Pattern abnormalities are more frequently observed in UNDERWEIGHT INDIVIDUALS, indicating that MICROVASCULAR CHANGES may occur independently of an underlying connective tissue disease.
9) CHRONIC KIDNEY DISEASE
By setting the stage for the development of tissue fibrosis and end organ failure, microvascular rarefaction is a principal pathogenic factor in the development of severe organ dysfunction in CKD patients, especially CVD, cerebrovascular dysfunction,
10) muscular atrophy, cachexia, and progression of kidney disease. Treatment strategies for microvascular disease are urgently needed.
Full attention should be given to understanding the pathogenesis and progression of COVID-19 as a disease of the microvasculature.

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More from @Parsifaler

3 Dec
1) TODAY: A mathematical model supporting my hypothesis that it is the debris of damaged cells that does not undergo EFFEROCYTOSIS by the body which is causing the fatal cytokine storms.



The model focuses on cells that trigger inflammation
2) through molecular patterns: infected cells carrying pathogen-associated molecular patterns (PAMPs) and damaged cells producing damage-associated molecular patterns (DAMPs). The former signals the presence of pathogens while the latter signals danger such as hypoxia or the lack
3) of nutrients. Analyses show that SARS-CoV-2 infections can lead to a self-perpetuating feedback loop between DAMP expressing cells and inflammation. It identifies the inability to quickly clear PAMPs and DAMPs as the main contributor to hyperinflammation.
Read 4 tweets
3 Dec
1) THE SPIKE PROTEIN, MICROVASCULAR DESTRUCTION/DYSFUNCTION/VIT D
YOU CANNOT FIND WHAT YOU ARE NOT LOOKING FOR!
There is no easy way to measure MICROVASCULAR DISEASE. IT HAS NOT BEEN LOOKED FOR! We have missed the forest for the trees. PLEASE READ WHY VITAMIN D IS SO IMPORTANT! ImageImage
2) Vitamin D is known to elicit a vasoprotective effect, while vitamin D deficiency is a risk factor for endothelial dysfunction (ED). ED is characterized by reduced bioavailability of a potent endothelium-dependent vasodilator, nitric oxide (NO), and is an early event in the
3) development of atherosclerosis. In endothelial cells, vitamin D regulates NO synthesis by mediating the activity of the endothelial NO synthase (eNOS). Under pathogenic conditions, the oxidative stress caused by excessive production of reactive oxygen species (ROS) facilitates
Read 7 tweets
30 Nov
1) MY MOST IMPORTANT FINDING TO DATE
MORE FOCUS > WHY COVID-19 LOOKS LIKE RADIATION POISONING
COVID-19: NOT JUST A VASCULAR DISEASE BUT A DISEASE OF SYSTEMIC MICROANGIOPATHY FOLLOWED BY SYSTEMIC FIBROSIS, ALMOST CERTAINLY INDUCED BY THE TISSUE-DAMAGING EFFECTS OF THE SPIKE
2) PROTEIN
Please review the first image. It is the most important image about the pathogenesis of COVID-19 we will ever see. Please note that SUPEROXIDE PRODUCTION CORRESPONDS DIRECTLY WITH SPIKE PROTEIN LEVELS. SARS-CoV-2 Spike protein (S protein) induced an excessive ROS
3) production in a dose dependent manner in endothelial cells.
Next, please replace Ionizing Radiation in the second image with Spike Protein. Now we understand why pathologists are observing that COVID-19 patients appear to be dying of “Radiation Poisoning.” The Spike Protein
Read 16 tweets
26 Nov
1) SONATA ALLEGRO FORM: DEVELOPMENT – SKEWED T CELL RECEPTOR REPERTOIRE AND THE SPIKE PROTEIN – SEVERE HYPERINLAMMATORY REACTION AND AUTOIMMUNE DISEASE/SEVERE COMBINED IMMUNODEFICIENCY
Continuing with our study of the Graft vs Host Disease (GVHD) “response” to the SARS-CoV-2
2) Spike Protein.
Upon further investigation, I believe the GVHD-like response being observed in those exposed to the Spike Protein of SARS-CoV-2 is due to the Spike’s ability to SKEW TCR (T Cell Receptor) repertoire. This appears to occur via a variety of mechanisms.
First, and
3) ironically, there is a massive T-Cell activation and proliferation due to a super-antigenic portion of the Spike Protein. Using in silico modeling and analysis, it was found that SARS-CoV-2 encodes a superantigen motif near its S1/S2 cleavage site. This region is highly
Read 11 tweets
23 Nov
1) This is a long one. Please bear with it and read to the end of the thread.
SEVERE COVID, MIS-C, MIS-A, MIS-V, LONG COVID AND AUTOIMMUNITY
MOLECULAR MIMICRY OF THE SARS-CoV-2 SPIKE PROTEIN AS “GRAFT,” ITS ACTIONS IN COVID-19 AND GRAFT VS HOST DISEASE: DISEASES OF TARGET TISSUE
2) DESTRUCTION
In my studies, I keep finding a disease which, like an ostinato, is omnipresent in my research results. Interestingly, a parallel with a game I play to unwind led me to a breakthrough.
I play Hearthstone. It is my “mindless” activity to unwind while being able to
3) use my mind, but not in a mind-bending way. I consider myself to be pretty good at the game. I usually make Legend these days. Another Legend player told me that when you are crafting an original deck, and it is not working, look at the cards that are left in your hand when
Read 17 tweets
20 Nov
What I have been saying all along.

I take back my self-questioning in a previous post. I am one of the greatest medical geniuses to ever live. I want to help HUMANITY!

Everything I have said: GIT2 was originally identified as a keystone protein in aging through latent semantic
Indexing (LSI) in the hypothalamus of aging rats. This involvement of GIT2 in the aging process was further demonstrated by the upregulation in both human and primate hypothalamic tissue and in the presence of hydrogen peroxide. Additionally, it was found that GIT2 was strongly
involved in DNA damage repair, through recruitment of ATM to the sites of damage to start the DNA damage repair process. In this age-controlling paradigm it was demonstrated that GIT2 possessed a NEAR IRREVERSIBLE ASSOCIATION with the senescence regulator p53.
Read 4 tweets

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