1) ARE THE SIDE EFFECTS OF THE SPIKE PROTEIN THERAPIES ACTUALLY VASCULITIS AND NOT THE "IMMUNE SYSTEM WORKING?"

Given the recent and abundant evidence that the S1 subunit of the SARS-CoV-2 spike protein damages blood vessels, is it perhaps more than likely that the spike is
2) being cleaved and the cleaved S1 unit is attacking blood vessels?

If one notes the "side effects" of the spike protein therapies, they are PRECISELY the same as VASCULITIS:

Hay fever
Fever
Loss of appetite and weight loss
Joint and muscle pain
Fatigue
Cough
3) Abdominal pain and gastrointestinal bleeding
Weakness, fatigue or a general feeling of being unwell
Rash or skin sores
Pain, numbness and tingling in your hands and feet
Severe abdominal pain
Shortness of breath

If the blood vessels in the heart are being attacked by the
4) spike, this would cause Acute Coronary Syndrome. This chorus now sounds all too familiar:

Chest pain (angina) or discomfort, often described as aching, pressure, tightness or burning
Pain spreading from the chest to the shoulders, arms, upper abdomen, back, neck or jaw
5) Nausea or vomiting
Indigestion
Shortness of breath (dyspnea)
Sudden, heavy sweating (diaphoresis)
Lightheadedness, dizziness or fainting
Unusual or unexplained fatigue
Feeling restless or apprehensive

Investigation into biomarkers for vasculitis in recipients of spike protein
6) therapies must be done immediately. All spike protein therapies must be paused while this possibility is investigated.

mayoclinic.org/diseases-condi…

mayoclinic.org/diseases-condi…

ncbi.nlm.nih.gov/pmc/articles/P…

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More from @Parsifaler

9 Jul
1) URGENT! Has the spike protein been created to hijack dendritic cells to cross the blood brain barrier and invade the CNS? Literally commandeering the DCs like a cavalry?

The spike has even HIGHER binding affinity for DC-SIGN than ACE2. DC-SIGN is a recepton on dendritic
2) cells that allows for their manipulation. They INVADE the central nervous system during periods of SEVERE INFLAMMATION.

Besides endothelial cells of the BBB, another endothelial cell type that has been extensively studied in leukocyte migration is the high endothelial venules
3) (HEVs). These specialized postcapillary venules allow exit of blood cells into secondary lymphoid organs. The role of HEVs with respect to leukocyte trafficking into the CNS has not been well studied. HEV differentiation markers, however, have been shown to be expressed in
Read 5 tweets
6 Jul
1) PLATELET FACTOR 4 AUTOANTIBODIES: THE MOST IMPORTANT RISK FACTOR

I believe I have found the most important risk factor for COVID-19. The frequency of preexisting PF4 antibodies is estimated at 1.4% in normal, 4.5% in elderly, 4.8% in pregnant and 8.6% in diabetic subjects!
2) THE DAMAGE DONE BY THE SPIKE PROTEIN TO THE ENDOTHELIUM MIMICS ACUTE CORONARY SYNDROME. THIS ACTIVATES THE IMMUNE RESPONSE TO PF4 AND EXPLAINS WHY HEPARIN MAKES THE CONDITION WORSE!

To explain the preexistence of HIT antibodies, it was proposed that heparin-like molecules
3) (glycosaminoglycans) on injured endothelium bind
with PF4 to form complexes with which the antibodies
react. Neoantigens appeared to cause conformational
change of PF4 to induce the production of heterogenetic antibodies in the Ig subclass in the presence of heparin like
Read 6 tweets
6 Jul
1) There appears to be an intimate associate between the spike protein and clotting. Especially microclotting, which has been obeserved in the alveoli of severe covid. There have been strokes and heart attacks even in asymptomatic cases.

However, what are the mechanisms
2) of this connection? One very important clue is the role of Interstitial Lung Disease. The spike protein has been proven to cause synctia in the lung. Patients showed extensive blood clotting of the lung arteries and veins (thrombosis). Second, several lung cells were
3) abnormally large and had many nuclei, resulting from the fusion of different cells into single large cells. This formation of fused cells (syncytia) is due to the viral spike protein, which the virus uses to enter the cell. When the protein is present on the surface of cells
Read 8 tweets
5 Jul
1) MOLECULAR MIMICRY AND THE MICROBIOME APPROACH (NOT JUST GUT MICROBIOME, BACTERIA ARE UBIQUITOUS IN THE BODY), SARS-CoV-2 IS A BACTERIOPHAGE:

It appears to be increasingly apparent that metabolism and transcription dysregulation are front and center in COVID-19. It could be
2) that there is a "CO-CONSPIRATOR" in the body of those who suffer from severe disease and death. For example, cross-reactions with H. Pylori alone can trigger idiopathic thrombocytopenic purpura. There may be unidentified bacteria that SARS-CoV-2 is infecting in the body,
causing much of this dysregulation. Please watch the referenced video. It is extremely important.

journals.lww.com/co-rheumatolog…

pubmed.ncbi.nlm.nih.gov/32358202/

ncbi.nlm.nih.gov/pmc/articles/P…

Read 7 tweets
4 Jul
1) COVID-19: A DISEASE OF TRANSCRIPTIONAL ERROR - EPIGENETICS

COVID-19 is without question a multi-systemic syndrome like no other with vast variance and involvement. I believe we are viewing the disease incorrectly. COVID-19 is unique. Instead of the DISEASE causing PATHOLOGY,
2) the DISEASE dysregulates TRANSCRIPTION causing the HOST to cause PATHOLOGY.

It is the only logical conclusion I can arrive at given the unprecedented panoply of systemic involvement and symptoms, and how UNIQUE it ultimately is, to each host.

Many different diseases and
3) syndromes, including cancer, autoimmunity, neurological disorders, diabetes, cardiovascular disease, and obesity, can be caused by mutations in regulatory sequences and in the transcription factors, cofactors, chromatin regulators, and noncoding RNAs that interact with these
Read 6 tweets
2 Jul
1) LKB1, MASTER COVID SPECTRE: FROM CARCINOGENESIS TO METABOLISM, AM DYSFUNCTION AND SKELETAL MUSCLE HOMEOSTASIS

I believe without question the spike protein is downregulating/"turning off" expression of LKB1. At first glance, the most immediate danger is carcinogenesis
2) as it was found that loss of Lkb1 was sufficient to drive the initial steps of carcinogenesis ex vivo.

Lkb1 plays an important role in regulating glucose homeostasis and energy metabolism. In addition, there is also evidence that has highlighted a prominent role for Lkb1 in
3) the function of macrophages. Lkb1 inhibits the activation and inflammatory function of innate macrophages. It was found that disruption of Lkb1 impaired the self-renewal of AMs, contributing to the reduction of AMs, which led to aggravated symptoms and EXCESSIVE accumulation
Read 9 tweets

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