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
4) produces likely as much ROS as Ionizing Radiation! I am certain this is its “dirty little secret.” This also explains all the aging effects observed.
However, for now let’s stay focused on the Systemic Microangiopathy which I believe we are observing. What happens once the ROS
5) damage occurs is that, just as in Radiation Damage, A number of biological processes contribute to the pathogenesis of radiation-induced organ fibrosis. Simply describing fibrosis as a scar related to overproduction of collagen—a preprogrammed terminal event—fails to capture
6) the complexity of the processes involved. Ionizing radiation injury, as many other physical, chemical, or biologic insults, may result in ROS generation and inflammation, with subsequent induction of TF-mediated thrombin generation, platelet activation, LTGF-b1 activation, and
7) macrophage polarization.
Feed-forward loops, as TGF-b1 promotes ROS formation, amplify these profibrotic signals in the promotion of myofibroblast accumulation and the production of ECM to cause fibrosis.
The molecular processes driving fibrosis are wide-ranging and complex.
8) The TGF-β cascade, which plays a major role in fibrosis, involves the binding of a ligand to a serine–threonine kinase type II receptor that recruits and phosphorylates a type I receptor.
TGF-β is a potent stimulator of the synthesis of extracellular matrix proteins in most
9) fibrogenic cells. TGF-β is synthesized and secreted by inflammatory cells and by effector cells, thereby functioning in both an autocrine and paracrine fashion. The complexity of the TGF-β system is illustrated by its interactions with other cell-signaling pathways.
10) For example, TGF-β stimulates sonic hedgehog signaling in lung fibroblasts, and sonic hedgehog signaling, in turn, regulates fibroblast function.
It has been determined that there is a MASSIVE, SUDDEN AND UNCONTROLLED INCREASE IN TGF-B. As a result, the sudden and
11) uncontrolled increases in active TGF-β (possibly with the help of some proinflammatory cytokines such as TNFα, IL-6, and IL-1β) inevitably result in rapid and massive edema and fibrosis that remodels and ultimately blocks the airways. This leads to the functional failure of
12) the lungs and death of the patients.
The microvasculature is being lacerated and scarred. It is being so injured that is repairing repairs. Layer upon layer of non-functioning fibrous tissue. This, unfortunately hearkens back to my hypothesis that the Spike Protein of
13) SARS-CoV-2 is turning us into masses of living cartilage.
In addition, inflammation in COVID-19 disease increases crescentically towards the small vessels (microangiopathy) suggesting that COVID-19-induced endotheliitis is a small vessel vasculitis not involving the main
14) coronaries. The inflammatory neuropathy of epicardial nerves in COVID-19 disease provides further evidence of an angio- and neurotrophic affinity of SARS-COV2 and might potentially contribute to the understanding of the high prevalence of cardiac complications such as
15) myocardial injury and arrhythmias in COVID-19. Another recent study by Ko et al. demonstrated protein spikes fragments in endothelial cells of cutaneous lesions lacking RNA evidence in ISH suggesting that endothelial incorporated spikes elements rather than the presence of

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More from @Parsifaler

2 Dec
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, Image
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 Image
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 Image
Read 11 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
17 Nov
1) COVID-19, ACE2 DEPLETION AND RAMPANT ANG II OVEREXPRESSION: A DISEASE OF LOCAL AND SYSTEMIC RAS
The great puzzle of COVID-19 may finally be solved. The immense number of systems involved, and the vast number of symptoms presented can be explained by the implication of Systemic
2) and Local Renin-Angiotensin Aldosterone (RAS) systems.
The RAS systems (both local (non-Renin dependent) and systemic (Renin-dependent) are primarily responsible for fluid homeostasis, most notably blood pressure regulation. However, the RAS system has evolved over time to
3) be responsible for far, far more than just fluid homeostasis. Everything we are seeing in COVID-19, both acute and in its sequelae, can be explained by the overexpression of a single peptide: Angiotensin II. This peptide, necessary to maintain a healthy blood pressure, is kept
Read 20 tweets
17 Nov
1) LESSONS FROM THE PAST INTENTIONALLY SUPPRESSED: PRE SARS-CoV-2 KNOWLEDGE OF ACE2, ITS FUNCTIONS AND THE SARS-CoV SPIKE PROTEIN
To begin with, please read the following paragraph:
To further clarify whether the intraperitoneally injected Spike-Fc protein directly affected lung
2) pathology in mice, we examined the localization of the injected Spike-Fc protein in lung. Spike-Fc was detected in lung homogenates by western blot using human Fc–specific antibody, whereas injected control-Fc was not detected. In addition, using immunohistochemistry, we found
3) that Spike-Fc protein localized to bronchial epithelial cells, inflammatory exudates and alveolar pneumocytes. Notably, Spike-Fc primarily localized to severe lesions. This localization of Spike-Fc protein is similar to Spike antigen staining in SARS-CoV–infected mice.
Read 17 tweets

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