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Walter M Chesnut

@Parsifaler

Mar 18, 2022 • 11 tweets • 3 min read • Read on X

1) OMNIPOTENT TROPISM; OMNIPOTENT MOLECULAR MIMICRY: A Terrifying Monster To Blood Vessels – AND NEURONS! Most Likely More
I don’t quite know how to say this. But I am shaking as I write this. I was smoking a cigar and contemplating a DM an amazing (and famous) doctor sent me.

2) The DM was about Pericytes and the Spike Protein. And I just kept thinking about it. Slowly, it dawned on me. And now I am shaking as I write this.
Spike in Endothelium. Spike in Pericytes. Spike in Basement Membrane. Spike in Myelin Sheath. Spike in Axon. Spike distributed

3) through Blood Vessels. Spike distributed through Axons. Inducing Fibrosis. Inducing Autoimmunity.
Don’t you see? It is an omnipotent burrower! And why? Because of its massive TROPISM!
And then I remembered a paper I had read from 2005. It talked about how Coronaviruses cause

4) MS via molecular mimicry. Several mechanisms have been proposed to explain how a viral infection could lead to an autoimmune disease. Amongst these mechanisms is molecular mimicry. According to this model, a non-self agent first activates an immune cell. Then, the cell

5) recognizes a self-element that shares antigenic conformation with the pathogen and directs a response towards it. Individuals who are genetically predisposed to respond to this antigenic determinant of a pathogen having a similar conformation to a determinant on a self-antigen

6) could develop an autoimmune response following infection. Shared sequences or similar determinant conformations between coronavirus and myelin proteins such as myelin basic protein (MBP) and proteolipid protein (PLP) have been identified. Molecular mimicry provides a unifying

7) mechanism that could explain both the genetic and environmental aspects in the triggering of MS.
So, if an ORDINARY Coronavirus can induce MS. What about one whose Spike Protein has a SIXTY-FOLD increase in peptide sharing?
A massive heptapeptide sharing exists between

8) SARS-CoV-2 spike glycoprotein and human proteins. Such a peptide commonality is unexpected and highly improbable from a mathematical point of view, given that, as detailed under the “Methods” section, the probability of the occurrence in two proteins of just one heptapeptide

9) is equal to ~ 20−7 (or 1 out of 1,280,000,000). Likewise, the probability of the occurrence in two proteins of just one hexapeptide is close to zero by being equal to ~ 20−6 (or 1 out of 64,000,000).
That’s right.

10) The odds of TWO shared peptides occurring is 1 IN 1.28 BILLION.
It may be that everything the Spike Protein touches is either attacked by the body, turns to scar tissue, or both. My God. Stop this MADNESS!
Please read the referenced papers. They are extremely important.

11)
ncbi.nlm.nih.gov/labs/pmc/artic…
ncbi.nlm.nih.gov/labs/pmc/artic…
ncbi.nlm.nih.gov/labs/pmc/artic…

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Walter M Chesnut

@Parsifaler

Jan 23, 2023

1) Although decreased translation fidelity causes protein misfolding and aggregation in both cardiomyocytes and Purkinje cells, the downstream pathways that lead to cell death in the two cell types may be quite different. Interestingly, a point mutation in the editing domain of

2) human mitochondrial AlaRS (AARS2) has been associated with infantile mitochondrial cardiomyopathy, suggesting increased errors in either cytoplasmic or mitochondrial protein synthesis can lead to cell death in the heart. In summary, our data show that a global reduction in

3) translational fidelity, rather than disruption of a specific protein, can induce defects in proteostasis in numerous cell types in the mouse. It is thus possible that proteinopathy can occur in the brain, heart, or even other tissues as a combination of genetic and/or

Read 4 tweets

Walter M Chesnut

@Parsifaler

Jan 3, 2023

On Damar Hamlin and Dr. Sutterer's "diagnosis" of Commodio Cordis
I am shocked that Commodio Cordis (CC) is named as the cause. Please examine the images carefully. In CC Ventricular fibrillation can be triggered by chest wall IMPACT ONLY OVER THE HEART, and predominantly occurs

with impact over the center of the left ventricle. Although CC usually involves impact from a baseball, it has also been reported during hockey, softball, lacrosse, karate, and other sports activities in which a relatively hard and compact projectile or bodily contact caused

impact to the person's precordium. Are we to believe that with the padding that professional football players wear, the location of the heart and the location of the impact, that this was actually CC?

Nonsense. Rapidly stated, narrative, ARRANT NONSENSE.

Read 6 tweets

Walter M Chesnut

@Parsifaler

Apr 11, 2022

1) UPDATED SYNTHESIS: EXTREMELY URGENT
IT’S COMPLICATED, BUT CLEAR – LOOKING ONE MOVE DEEPER
THE SPIKE PROTEIN PATHOGENIC ALGORITHM – DUAL PATHS TO TERMINAL SYSTEMIC FIBROSIS: IMMEDIATE FOR THOSE WITH SIGNIFICANT COMORBIDITIES, INDUCED FOR THOSE WITHOUT
The Spike Protein is

2) inducing terminal systemic fibrosis of all organs, including the blood, via two principal mechanisms.
The first is a direct, immediate path via binding to RGD-binding integrins, which includes several TGF-β -activating integrins. This this activates Myofibroblasts which

3) induces Fibrosis. Indeed, in autopsies of COVID-19 patients with advanced disease, 38% collagen deposition was found in their lungs.
This is a rapid and certainly fatal circumstance.
But, this is not limited to the lungs. In a series of cardiac autopsies conducted in

Read 12 tweets

Walter M Chesnut

@Parsifaler

Apr 8, 2022

1) MORE THAN AMYLOIDOSES. ALL HUMAN TISSUES ARE BEING TRANSFORMED INTO FIBROUS MASSES. INCLUDING. THE. BLOOD.
AMYLOIDOSIS. FIBROSIS. | AUTOPSIES. INCREASED ORGAN WEIGHT. | CLOTS. AMYLOIDS.
The tissues of the body, INCLUDING THE BLOOD, are being either DEPOSITED WITH FIRBILS OR

2) BEING TRANSFORMED INTO FIBRILS. Amyloidosis > Deposition of Fibrils. Fibrosis > Transformation into Fibrils.
The Spike Protein is transforming (at least) all human tissue (perhaps other species?) into non-functioning fibrous masses.
I was reading papers in the solarium after

3) dinner while having a cigar. And I kept thinking about Amyloidosis and Fibrosis. I have seen both. Is it one? Is it the other? After reading more papers – AND SOME AUTOPSY REPORTS - I came to a startling and incredibly disturbing conclusion. It is BOTH!
THE CLOTS WE ARE

Read 9 tweets

Walter M Chesnut

@Parsifaler

Apr 8, 2022

1) THE SPIKE PROTEIN IS THE “AMYLOID” BEING DEPOSITED AND INDUCING AMYLOIDOSES: A MAJOR FINDING MISSED
SEVERE COVID MAY BE DUE TO THE ADDED DEPOSITION OF COMPLEMENT WITH THE SPIKE
The paper “The histologic and molecular correlates of COVID-19 vaccine-induced changes in the skin”

2) made a case for the immune response to the Spike Protein causing self-limited hypersensitivity reactions to the vaccine. However, if you study the paper carefully, you notice that the authors have missed a far more important finding.
The biopsy specimens of normal skin post

3) vaccine and of skin affected by the post-vaccine eruption showed rare deep microvessels positive for spike glycoprotein with no complement deposition contrasting with greater vascular deposition of spike protein and complement in skin biopsies from patients experiencing severe

Read 6 tweets

Walter M Chesnut

@Parsifaler

Apr 4, 2022

1) PLEASE READ THIS ENTIRE THREAD. IT IS URGENT.
Building on all recent work. By far my most important synthesis:
A NEW KIND OF CANCER: THE MARRIAGE OF ONCOGENESIS AND PRIONOPATHY
THE PROGRESSIVE DESTRUCTION OF TISSUE AND ORGANS BY THE AMYLOIDOGENIC AND OLIGOMERIC PROPERTIES OF

2) THE SARS-CoV-2 SPIKE PROTEIN
It has been proposed that Alzheimer's disease might be a 'whole body' problem, as amyloid-beta can travel, cancer-like, to brain from other parts of body.
Normal mice that had been joined (via bloodstreams) to genetically modified partners for a

3) year "contracted" Alzheimer's disease. The researcher song says the amyloid-beta traveled from the genetically-modified mice to the brains of their normal partners, where it accumulated and began to inflict damage.
Not only did the normal mice develop plaques, but also a

Read 11 tweets

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