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Text No, it's those horrible vaccines. He never would have had this if he had not taken that vaccine! Right? That's what your getting at?
originally posted by: CriticalStinker
We’re going to find out even more people have it too, not because more people have it than ever, but because of consumer electronics.
Newer smart watches have an ECG.
originally posted by: asabuvsobelow
Did I mention the Vaccine ? I simply saying it's not normal in Athletes .
According to the Department of Health and Human Services' fact sheet, the main stated goal of Operation Warp Speed was to "produce and deliver 300 million doses of safe and effective vaccines with the initial doses available by January 2021...
originally posted by: NorthOfStuff
a reply to: Oldcarpy2
It looks to me like the privacy of our personal medical details took a big hit about 36 month ago.
Where exactly is the line drawn between personal and private medical information post Covid?
originally posted by: GenerationGap
originally posted by: NorthOfStuff
a reply to: Oldcarpy2
It looks to me like the privacy of our personal medical details took a big hit about 36 month ago.
Where exactly is the line drawn between personal and private medical information post Covid?
This. Its personal medical information that should only be shared with your doctors, close family, and the hostess at Applebees to prove you are a medically viable specimen that can sit at the bar.
originally posted by: Salamandy
What’s wrong with mention that it was probably the clot shot?
Have you seen the news about that # or maybe witnesses people in real life taking that # and having problems?
originally posted by: thethinkingman
Do you understand why the vaccine is much more dangerous than the virus????
The virus cannot go into any cell in your body, it mainly will only get into the lungs, throat and nose, only with a very severe infection will you see any damage and further distribution of the virus. The nanoparticles have a far greater level of movement around the body and are far greater quantities than when compared with virion numbers.
these areas of the body would never be affected in all people infected by the virus.
originally posted by: Xtrozero
originally posted by: asabuvsobelow
Did I mention the Vaccine ? I simply saying it's not normal in Athletes .
Don't play coy, what forum are you in right now....
originally posted by: asabuvsobelow
Meaning this uptick of Heart related issues in Professional sports is not normal
Now there is another variable being ignored which is the use of PED's ' Performance Enhancing Drugs ' in particular the use of HGH ' Human Growth Hormone ' which is known to cause Cardiomegaly which leads to many Cardiovascular issues , This could be the clue that everyone is missing Athletes with Cardiomegaly who are also Vaccinated are at great risk of Cardiovascular issues .
Nonetheless, even relatively low ACE2 expression levels in endothelial cells (e.g., compared to levels in epithelial cells) , along with the high expression levels of ACE2 in other cell types of the vasculature (e.g., heart fibroblasts/pericytes) indicate that the vasculature can be sensitive to free-floating S protein or its subunits/peptide fragments .
These effect(s), especially in capillary beds, and the prolonged antigen presence in the circulation, along with the systemic excessive immune response to the antigen, can then trigger sustained inflammation (discussed later) which can injure the endothelium, disrupting its antithrombogenic properties in multiple vascular beds.
Reportedly, intravenous (i.v.) injection of the S1 subunit in mice results in its localization in endothelia of mice brain microvessels showing colocalization with ACE2, caspase-3, IL-6, tumor necrosis factor a (TNF-a), and C5b-9; it was thus suggested that endothelial damage is a central part of SARS-CoV-2 pathology which may be induced by the S protein alone .
Also, the S1 subunit (or recombinant S1 RBD) impaired endothelial function via downregulation of ACE2 and induced degradation of junctional proteins that maintain endothelial barrier integrity in a mouse model of brain microvascular endothelial cells or cerebral arteries; this latter effect was more enhanced in endothelial cells from diabetic versus normal mice .
In support of this, administration of the S protein promoted dysfunction of human endothelial cells as evidenced by, for example, increased expression of the von Willebrand factor .
Other reports indicate that S1 can directly induce coagulation by competitive binding to both soluble and cellular heparan sulfate/heparin (an anticoagulant), while cell-free hemoglobin, as a hypoxia counterbalance, cannot attenuate disruption of endothelial barrier function, oxidative stress, or inflammatory responses in human pulmonary arterial endothelial cells exposed to S1 .
Consistently, S protein binds fibrinogen (a blood coagulation factor), and S protein virions have been found to enhance fibrin-mediated microglia activation (data not yet peer-reviewed) and induce fibrinogen-dependent lung pathology in mice, while S1 binding to platelets' ACE2 triggers their aggregation.
Interestingly, both the ChAdOx1 (AstraZeneca) and BNT162b2 vaccines can elicit antiplatelet factor 4 (anti-PF4) antibody production even in recipients without clinical manifestation of thrombosis .
Intriguingly, the S protein increases human cell syncytium formation, triggering pyroptosis of syncytia formed by fusion of S and ACE2-expressing cells .
Also, in cells or mouse experimental models, it was shown that S removes lipids from model membranes and interferes with the capacity of high-density lipoprotein to exchange lipids , inhibits DNA damage repair processes , and induces Snail-mediated epithelial–mesenchymal transition marker changes and lung metastasis in a breast cancer mouse model
These findings suggest the evolution of novel genomic responses after the second dose and, more importantly, the unique biology of mRNA vaccines versus other more conventional platforms.
Of particular interest is also the report of a cytokine release syndrome (CRS) – an extremely rare immune-related AE of immune checkpoint inhibitors – post-BTN162b2 vaccination in a patient with colorectal cancer on longstanding anti-programmed death 1 (PD-1) monotherapy; the anti-PD1 blockade-mediated CRS was evidenced by increased inflammatory markers, thrombocytopenia, elevated cytokine levels, and steroid responsiveness .
These proinflammatory effects could be particularly pronounced in the elderly, since recent data revealed that senescent cells become hyperinflammatory in response to the S1 subunit, followed by increased expression of viral entry proteins and reduced antiviral gene expression in nonsenescent cells through a paracrine mechanism
Although, the modern viral vectors that are used in CoViD vaccines are silenced (replication-deficient), each dose of the vaccine contains a very high viral load (e.g., 50 billion viral particles per dose in Ox/AZ or J&J/Janssen CoViD-19 vaccines whereas 100 billion viral particles per dose in the Sputnik-V).
The viral particles are unlikely to be confined to the muscles at the injection site; they are free to distribute across the body and drain through the lymphatic system; their apparent volume of distribution is likely to be very high.
The biodistribution of ChaAdOx1 containing HBV in BALB/c mice (study 0841MV38.001) indicated the highest viral levels at the injection site, but low levels of virus were still detected after 24 hours of injection in all other tissues (including blood, brain, heart, inguinal lymph node, kidney, liver, lung, gonads, and spleen).
The proportional tissue distribution of viral vectors in the body tissues away from the injection site was likely to increase with time, however, biodistribution beyond 24h post-dose was not studied. The biodistribution of ChAdOx1 encoding nCoV-19 following intramuscular injection in mice (study 514559) was ongoing at the time of its regulatory approval
However, in the absence of the results of study 514559, the biodistribution of ChaAdOx1 HBV in mice (study 0841MV38.001) confirms the delivery of vaccine into the brain tissues. The vaccine may therefore spur the brain cells to produce CoViD spike proteins that may lead to an immune response against brain cells, or it may spark a spike protein-induced thrombosis.
For COVID-19 mRNA Vaccine (Pfizer or Moderna), the biodistribution studies in animals were not conducted. The surrogate studies with luciferase and solid-lipid nanoparticles (Pfizer) confirm a biodistribution to the liver and other body tissues beyond the administration site [5].
For Moderna, the biodistribution of mRNA-1647 (encoding CMV genes) formulated in a similar lipid nanoparticulate delivery system confirms a biodistribution beyond the injection site, in particular, the distribution to the lymph nodes, spleen and the eye was noted [6].
However, the detailed tissue-specific distribution of mRNA vaccines encoding SARS-CoV-2 spike proteins (Pfizer or Moderna) is not fully known that can offer invaluable insights into the potential safety of these vaccines in peoples with pre-existing conditions or those on certain medications.
originally posted by: thethinkingman
No. It can only distribute further in very severe infections essentially when people have already failing immune systems.
99+% of people do not have this what so ever. The scale of the spike protein cannot be comparable to several shots that are designed to make you produce spike proteins, when people barely get any virion replication in them.
Its doesnt stay in the muscle what so ever, there are many, many studies showing this, its obvious just by the fact its causing injury and death. The needle bursting through your skin and piercing it is giving the nanoparticles entrance into the blood stream. There is not free floating spike proteins en masse from the virus, the're attatched to the virus....
Pharmacokinetic studies have not been conducted with COVID-19 mRNA Vaccine BNT162b2 and are generally not considered necessary to support the development and licensure of vaccine products for infectious diseases (WHO, 2005; WHO, 2014).
No absorption studies were conducted for COVID-19 mRNA Vaccine BNT162b2 since the route of administration is intramuscular (IM).
No excretion studies have been conducted with COVID-19 mRNA Vaccine BNT162b2. In the PK study, it appears that 50% of ALC-0159 was eliminated unchanged in faeces. Metabolism played a role in the elimination of ALC-0315, as little to no unchanged material was detected in either urine or faeces. Investigations of urine, faeces and plasma from the rat PK study identified a series of ester cleavage products of ALC-0315. The manufacturer has proposed that this likely represents the primary clearance mechanism acting on this molecule, although no quantitative data is available to confirm this hypothesis.
Toxicokinetics
No toxicokinetic studies have been performed with the vaccine. This is consistent with WHO guidelines on the nonclinical evaluation of vaccines (WHO 2005).
Genotoxicity
No genotoxicity studies are planned for BNT162b2, as the components of all vaccine constructs are lipids and RNA that are not expected to have genotoxic potential (WHO, 2005).
Carcinogenicity
Carcinogenicity studies with BNT162b2 have not been conducted as the components of all vaccine constructs are lipids and RNA that are not expected to have carcinogenic or tumorigenic potential. Carcinogenicity testing is generally not considered necessary to support the development and licensure of vaccine products for infectious diseases (WHO, 2005).
A combined fertility and developmental study (including teratogenicity and postnatal investigations) in rats is ongoing.
Prenatal and postnatal development, including maternal function No such studies have been done.
Local tolerance
No such studies have been done. The assessments made as part of the general toxicity study should suffice and a separate study is not needed.
Study R-20-0112 aimed to characterise T- and B-cell responses in the spleen, lymph nodes and blood of BNT162b2 immunised mice. It characterised changes in the myeloid cell compartment, determined the ability of CD8+ T-cells to react to cells presenting the vaccineencoded antigen, and determined antibody responses.
CD8+ T cells (often called cytotoxic T lymphocytes, or CTLs) are very important for immune defence against intracellular pathogens, including viruses and bacteria, and for tumour surveillance. When a CD8+ T cell recognises its antigen and becomes activated, it has three major mechanisms to kill infected or malignant cells. The first is secretion of cytokines, primarily TNF-α and IFN-γ, which have anti-tumour and anti-viral microbial effects
The second major function is the production and release of cytotoxic granules. These granules, also found in NK cells, contain two families of proteins, perforin, and granzymes. Perforin forms a pore in the membrane of the target cell, similar to the membrane attack complex of complement. This pore allows the granzymes also contained in the cytotoxic granules to enter the infected or malignant cell.
Granzymes are serine proteases which cleave the proteins inside the cell, shutting down the production of viral proteins and ultimately resulting in apoptosis of the target cell. The cytotoxic granules are released only in the direction of the target cell, aligned along the immune synapse, to avoid non-specific bystander damage to healthy surrounding tissue (see Figure 1).
CD8+ T cells are able to release their granules, kill an infected cell, then move to a new target and kill again, often referred to as serial killing. The third major function of CD8+ T cell destruction of infected cells is via Fas/FasL interactions.
Activated CD8+ T cells express FasL on the cell surface, which binds to its receptor, Fas, on the surface of the target cell. This binding causes the Fas molecules on the surface of the target cell to trimerise, which pulls together signalling molecules.
These signalling molecules result in the activation of the caspase cascade, which also results in apoptosis of the target cell. Because CD8+ T cells can express both molecules, Fas/FasL interactions are a mechanism by which CD8+ T cells can kill each other, called fratricide, to eliminate immune effector cells during the contraction phase at the end of an immune response.