1) SARS-CoV-2 AND MICROVASCULAR DESTRUCTION: IS THE SPIKE PROTEIN SIMPLY CAUSING THE “REMOVAL” (DESTRUCTION) OF THE MICROVASCULATURE? THE RELATION TO SYNDROME X
SYNDROME X was a disease that resembled coronary artery disease but the patients had clear coronary arteries. It was Image
2) dismissed as PSYCHOLOGICAL! It was discovered that the symptoms were of MICROVASCULAR CORONARY ARTERY DISEASE and a VERY REAL disease. Just like Long COVID. And, I believe, caused by the same pathologies – except they are for EVERY organ and system in the body in the case of
3) Long COVID. Please watch the referenced video. THE VESSELS ARE TOO SMALL TO REGISTER ON CONVENTIONAL TESTS.
A very interesting paper published in Nature Neuroscience 21 October 21 describes structural changes in cerebral small vessels of patients with COVID-19 and elucidate
4) potential mechanisms underlying the vascular pathology. In brains of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-infected individuals and animal models, they found an increased number of empty basement membrane tubes, so-called string vessels representing
5) REMNANTS OF LOST CAPILLARIES.
The authors of the paper attributed this loss to the main protease of SARS-CoV-2 “MPRO” and its ability to cleave NEMO.
The authors noted that the ablation of NEMO in brain endothelial cells induced microvascular pathology in mice that was
6) REMINISCENT (emphasis mine) of what we observed in brains of patients with COVID-19.
I offer another explanation REMINISCENT of the virus’ involvement with other organs.
There is a protein. A fascinating protein called FOG2. Friend of GATA (not Kamsky) 2. If you remove this
7) protein in the developing fetus, it simply dies. It does not develop a functional heart, among other things. If you block this protein in adults, it causes the cardiac microvasculature to erode – “disappear.”
I hypothesize this protein may be involved.
Let us look at a test
8) used for, among other things, diagnosis Systemic Sclerosis. The nailfold videocapillaroscopy test. In COVID patients there was one very interesting finding. COVID-19 doesn’t seem to significantly induce, in short-term, specific alterations in peripheral microvascular array as
9) evaluated by NVC, despite the severity of the disease, except for a SIGNIFICANT REDUCTION OF THE ABSOLUTE NUMBER OF NAILFOLD CAPILLARIES.
NOTE! The brain scans of COVID patients revealed REMNANTS OF LOST CAPILLARIES.
The same is true for the heart. A paper presented a
10) state-of-the-art review of CMD pathophysiology in COVID-19 from five aspects. As SARS-CoV-2-like virus particles were detected in a coronary endothelial cells, and massive coronary small vascular microthrombi were found in deceased COVID-19 patients.
A similar finding was
11) observed in the lungs. Microvascular endothelium is a main site of PAI-1 production, and the marked incorporation of PAI-1 in abnormal or persistent clots supports a plausible mechanism that may explain poor clot resolution in COVID-19.
The spike protein has many ways to
12) destroy the microvasculature.
In conclusion, the findings of a paper published 22 Nov 21 in Clinical Science suggest that the S protein may prompt PC dysfunction, potentially contributing to microvascular injury. This mechanism may have clinical and therapeutic implications.
CLINICIANS: Would tirofiban/Aggrastat be a potent therapeutic?

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More from @Parsifaler

Jan 16,
1) AN ENERGY-BASED MITOCHONDRIAL EXPLANATION OF SPIKE PROTEIN PATHOGENESIS: SLOWLY TURNING THE POWER OFF
As we have not yet determined the primary pathogenesis of COVID-19, I propose that the disease is one of progressive Mitochondrial Dysfunction from a pathogen (therapeutic?)
2) delivered via the Endothelium and distributed throughout the body to all organs and tissues.
PREMISE: S1 and Trimer both induced mitochondrial damage including functional deficits in mitochondrial respiration.
For example: It is well established that the brain uses more energy
3) than any other human organ, accounting for up to 20 percent of the body's total haul. Therefore, it would only be logical that one of the first signs of mitochondrial dysfunction would be brain fog. Indeed, brain fog has been theorized as being an energy, or mitochondrial
Read 5 tweets
Jan 15,
1) A CERTAIN PATHWAY TO SPIKE PROTEIN MEDIATED AUTOIMMUNE/FIBROTIC DISEASE
TGF-β DRIVEN IMMUNITY, SEVERE COVID-19 OR PROLONGED SPIKE PROTEIN EXPOSURE RESULTS IN AUTOIMMUNE/FIBROTIC DISEASE (VASCULITIS)
A very interesting paper from March of 2021 made a startling observation which
2) was concluded with the foreboding statement: Whether or not the antibodies generated in the continued immune reactions of COVID-19 patients in the ICU are harmless, or whether they may even cause detrimental immunopathology remains to be shown.
Why is this of interest now?
3) We have been searching for a satisfactory explanation for the observed myocarditis, autoimmune issues and vasculitis which are appearing ever increasingly.
What the paper demonstrated was that they analyzed samples from six patients within the first week after ICU admission,
Read 13 tweets
Jan 11,
1) AN ONCOGENIC “FLASH DRIVE”: THE SPIKE PROTEIN OF SARS-CoV-2 AND CANCER
When I first began studying the SARS-CoV-2 virus I was initially concerned about its Spike Protein’s potential ability to induce prion disease, as the spike has homology with our Prion protein and it
2) induces a strong Unfolded Protein response.
However, almost two years after I reached that conclusion, I believe it is only part of the story. Yes, I am still concerned that it may induce Prion Disease. But, what concerns me more is that its interactions and mimicking of the
3) human Prion Protein may be more “effective” having a role in tumorigenesis and metastasis.
In fact, the more I look at the Spike Protein now, and with the now common knowledge that the Spike Protein mimics Trousseau Syndrome, I now believe that the Spike Protein may be a
Read 15 tweets
Jan 10,
1) COVID-19 COAGULATION ABNORMALITIES AS TROUSSEAU SYNDROME
IS THE SPIKE PROTEIN INDUCING GENERALIZED CANCER AND COULD THOSE IMMEDIATELY EXPERIENCING COAGULATION ABNORMALITIES HAVE OCCULT CANCERS?
Malignancy affects the hemostatic system and the hemostatic system affects
2) malignancy.
Cancer's "purpose" is to invade organs and disrupt their normal functioning by rendering cells dysfunctional. These dysfunctional cells then spread, disrupting further cells, and so on until the victim dies.
The way cancer accomplishes this is to spread through
3) vessels. If it spreads through blood vessels, it must cross the barrier of the blood vessels to enter organs, including blood vessels themselves. Therefore disrupting (activating) the endothelium is essential to "breaking through" that barrier.
The close relationship between
Read 11 tweets
Jan 9,
1) Guild Navigator:
You are transparent. I see many things. I see plans within plans. (DUNE)
VASCULAR DISEASE AS CAMOUFLAGE: THE SPIKE PROTEIN OF SARS-CoV-2 AS MICROTUMOR
Respiratory disease held the world in a false awe at the beginning of the COVID-19 pandemic. Health
2) authorities the world over reiterated the same narrative: We have a new Respiratory Virus. Those of us who looked closely at the disease from the beginning knew that wasn’t the true picture – or at least not the full picture.
Then, slowly, over the course of the first year of
3) the pandemic, everyone else began to realize this, too. Finally, towards the end of 2020, COVID-19 was universally recognized as a Vascular Disease. However, I have realized the virus’ deception does not stop there.
IT IS ONLY A VASCULAR DISEASE INSOMUCH AS THE SPIKE PROTEIN
Read 17 tweets
Jan 8,
1) AN EXPLANATION FOR THE SUDDEN CARDIAC DEATHS:
I believe the endocytosis of the Spike Protein is interfering with Ryanodine Receptors causing a calcium channelopathy resulting in Catecholaminergic Polymorphic Ventricular Tachycardia. This is a potentially fatal arrhythmia Image
2) which is induced when the heart rate exceeds 120 bpm.
The intracellular actions of the Spike Protein with Cathepsin L, a protease on the plasma membrane of host cells, increases Ca2+ release from the endoplasmic reticulum (ER) via the ryanodine receptors (RyRs). The associated ImageImage
3) elevation of cytosolic Ca2+ concentration, in turn, increases cathepsin L activity. Cathepsin L promotes virus fusion with host cells by cleaving and activating the spike (S) protein. High levels of extracellular and cytosolic Ca2+ concentrations are also necessary for virus
Read 6 tweets

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