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Anonymous ID: facd12 July 31, 2021, 11:08 a.m. No.14238403   🗄️.is 🔗kun   >>8432 >>8522

SC2 is a vascular disease, it is not a respiratory disease! Down pointing backhand index

 

Rightwards arrow Spike protein is a highly pathogenic toxin and is the main infectious and virulent factor of SC2.

 

Rightwards arrowThis membrane glycoprotein has the S1 subunit that attacks the host target cells at surface receptors 2 (ACE2) that convert angiotensin.

 

Rightwards arrowThis is followed by viral entry and infection, caused by a change in the S1 subunit that is triggered by the spike / ACE2 binding.

 

Rightwards arrowThe Spike peak exists as homotrimers, protruding from the viral surface and contains an N-terminal (NTD) domain outside the membrane, a Right pointing backhand indextransmembrane domain, and an intracellular Right pointing backhand indexC-terminal domain (CTD).

 

Rightwards arrowBlood exposed to the Spike protein shows a spontaneously formed fibrin formation with abnormal amyloid deposits with or without thrombin.

 

Mechanism:

 

When the blood is exposed to the Spike protein the erythrocytes showed agglutination, hyperactivated platelets were observed, with membrane diffusion and formation of platelet-derived microparticles.

 

In all samples, spontaneous amyloid deposits formed after exposure to the Spike protein.

 

Amyloid is caused by deposits of abnormal (misfolded) proteins called amyloids, in tissues and organs throughout the body.

 

Rightwards arrow Proteins originate from a series of amino acids that fold into an anomalous three-dimensional shape, called a "sheet", There is also cerebral amyloid angiopathy (also called congophilic angiopathy), it is a form of angiopathy in which deposits of amyloid material are formed on the walls of the blood vessels of the central nervous system.

 

Rightwards arrowIn this pathological form, amyloid (Beta-amyloid) is found only in the brain.

 

Rightwards arrowThis explains the thrombin reactions in the brain area caused by SC2.

 

https://www.news-medical.net/amp/news/20210310/SARS-CoV-2-spike-S1-subunit-induces-hypercoagulability.aspx?__twitter_impression=true

 

https://twitter.com/BidoliNicola/status/1421517508654338050

Anonymous ID: facd12 July 31, 2021, 11:36 a.m. No.14238561   🗄️.is 🔗kun

The mean age of the patients (n = 93) was 52 ± 22 years and the male‐to‐female ratio was 50/43. The ACE2 staining pattern was consistent in the same types of tissue regardless of the pathological condition of the organ and disease status of the patient.

 

The first remarkable finding was that ACE2 was present in endothelial cells from small and large arteries and veins in all the tissues studied. Moreover, arterial smooth muscle cells were consistently positive for ACE2. Positive staining for ACE2 was also noted in myofibroblasts and the membrane of fat cells in various organs. Furthermore, ACE2 was found at specific sites in each organ as described below.

 

Marked ACE2 immunostaining was found in type I and type II alveolar epithelial cells in normal lungs (Figures ​(Figures1A1A and ​and1B).1B). This finding was confirmed by ACE2 expression in the lung type II alveolar epithelial cell line A549 (Figure ​(Figure1E)1E) and in lungs with fibrotic changes which revealed abundant staining of type II epithelial cells (Figures ​(Figures1C1C and ​and1D).1D). The cytoplasm of bronchial epithelial cells also showed weak positive ACE2 staining.

 

In nasal and oral mucosa and the nasopharynx, we found ACE2 expression in the basal layer of the non‐keratinizing squamous epithelium (Figure ​(Figure22A).

 

In addition to ACE2 localization in the smooth muscle cells and endothelium of vessels from the stomach, small intestine, and colon, we found ACE2 in smooth muscle cells of the muscularis mucosae and the muscularis propria (Figures ​(Figures2B,2B, ​B,2C,2C, and ​and2E).2E). Remarkably, ACE2 was abundantly present in the enterocytes of all parts of the small intestine including the duodenum, jejunum, and ileum, but not in enterocytes of the colon. The staining in enterocytes was confined to the brush border (Figures ​(Figures2B2B and ​and22D).

 

In the skin, ACE2 was present in the basal cell layer of the epidermis extending to the basal cell layer of hair follicles (Figures ​(Figures3A,3A, ​A,3C,3C, and ​and3D).3D). Smooth muscle cells surrounding the sebaceous glands were also positive for ACE2. Weak cytoplasmic staining was observed in sebaceous gland cells. A strong granular staining pattern for ACE2 was seen in cells of the eccrine glands (Figure ​(Figure33B).

 

Consistent with findings in other organs, the brain only revealed endothelial and smooth muscle cell staining (Figure ​(Figure44A).

 

Despite the clear endothelial staining of many small vessels, the endothelial lining of the sinusoids in the liver was negative for ACE2. Surface staining in bile ducts was occasionally observed. Kupffer cells and hepatocytes were negative (Figure ​(Figure44B).

 

In the spleen, thymus, lymph nodes, and bone marrow, cells of the immune system such as B and T lymphocytes, and macrophages were consistently negative for ACE2 (Figure ​(Figure4C).4C). In some lymph nodes, we noted positive staining in sinus endothelial cells in a granular staining pattern.

 

In the kidney, weak glomerular visceral ACE2 staining was observed, whereas the parietal epithelial cells were moderately positive. Despite the clear endothelial staining of vessels, the mesangium and glomerular endothelium were negative for ACE2. Abundant staining was seen in the brush border of the proximal tubular cells, whereas the cytoplasm of these cells was weakly positive. Epithelial cells from the distal tubules and collecting ducts showed weak cytoplasmic staining (Figure ​(Figure44D).

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7167720/