New Study Found A 9-Times Increased Rate Of Myocarditis In Males After mRNA Booster | 3 Or More COVID-19 Vaccine Doses Associated With A 6-Fold Increased Risk Of Infection Said Cleveland Clinic | ETC
New Study Found A 9-Times Increased Rate Of Myocarditis In Males After mRNA Booster | 3 Or More COVID-19 Vaccine Doses Associated With A 6-Fold Increased Risk Of Infection Said Cleveland Clinic | ETC
Very important data appeared over the past days that was suppressed by the media. Specifically, two new shocking studies were released that associated mRNA COVID-19 vaccination with higher than previously estimated rates of myocarditis, and higher than previously reported risk of infection.
Please pay attention - in the study below (Investigation into the toxic effects of graphene nanopores on lung cancer cells and biological tissues):
Heart tissue showed chemodectoma, toxic myocarditis, reddish brown atrophy; yellowish brown pigments suggesting lipofuscin granules as remnants of cell organelles and cytoplasmic material.
However, inhalation of graphene structures is believed to be a risk factor for cardiorespiratory disease. For example, inhaled graphene nanoplatelets can be transported deep within the distal regions of the lungs and trigger chronic inflammation in the respiratory tract. It is generally thought that the placenta, lung, gastrointestinal tract and skin act as major barriers for many nanostructures entry into living organisms. Indeed, a recent study on mice demonstrated that intratracheally delivered few-layered graphene was mainly retained in the lung, with 47% remaining after 4 weeks and this resulted dose-dependent acute lung injury and pulmonary oedema. An in vitro study of the effects of graphene and graphene oxide on human skin HaCaT keratinocytes demonstrated that oxidized graphene was the most cytotoxic, inducing mitochondrial and plasma-membrane damage, and suggesting low cytotoxic effects at the skin level. Reduced graphene oxide is more toxic than graphene oxide as evidenced by many studies reported recently. This is primarily due to its sharp edges and structural morphology. In contrast to the typically soluble nanoparticles examined in conventional toxicology investigations, graphene nanostructures have different shapes and surface areas, and which in turn can significantly influence their diffusion, dispersion, aggregation and agglomeration in plasma. Importantly, these “tunable” characteristics of graphene account for the varying toxic outcomes on the tissues. In vivo, following toxicity testing of graphene, post-mortem histological examinations of liver alterations have revealed hypertrophy of hepatocytes, necrosis and inflammatory cell infiltration in liver and kidney tissues.
Antioxidants act as a defense system to reinstate the cellular redox balance when oxidative stress is generated as a result of excess production of reactive oxygen species.
Disruption of this critical balance in the presence of excessive reactive oxygen species triggers the activation and promotion of a pro-inflammatory cascade, which in turn may cause mitochondrial release of proapoptotic factors potentially leading to cell death. Hepatocytes are key targets for reactive oxygen species damage, and therefore liver function and biomarkers of oxidative stresses should be investigated with great care.
Specifically, vacuolation, dilation of central vein and hemorrhage, vacuolation and dilation of central vein, damage of vacuolation, hemorrhage and degeneration of central vein, dilation of epithelial lining and hydropic degeneration oedema were observed in liver tissue. Kidney tissue of the treated groups showed acute vacuolization, dilation of epithelial lining, vacuolation and nucleus degeneration, nucleus damage, necrosis and epithelial degeneration.
Heart tissue showed chemodectoma, toxic myocarditis, reddish brown atrophy; yellowish brown pigments suggesting lipofuscin granules as remnants of cell organelles and cytoplasmic material.
The brain showed effects of secondary carcinoma, olegodendrocytoma small thin walled blood vessel and crytococcosis. Testicular tissue of treated groups showed spermatogenesis and vacuolation, dilation of germinal layer, degeneration of secondary spermatocytes, damage to the germinal layer and vacuolation. The lung showed damage of vacuolation, degeneration of central vein, inflammation, haemorrhage, d-shaped cells structure, hemosidophroages and lesion.
Indeed, 3D porous graphene frameworks have shown various effects from acute lethally to sub lethal toxic effects including histological, and oxidative stress responses and, after inhalation exposure in rats, graphene has been found to accumulate in the lung, leading to phagocytosis.
In this study, the first sign of toxicity recorded for the rats given an intraperitoneal injection of GNPs was an observed decrease in body weight at the higher dose. Toxic effects of GNPs on CBC were not observed although there was a slight (6%) reduction in platelet numbers in the 15 mg/kg group. The increased activities of AST, ALT, AMP and creatinine observed after 27 days are indicators of liver and kidney toxicity respectively and appeared in the rats receiving both single and multiple doses of GNPs, compared to control groups. Severe organ damage can increase the activities of ALT and AST and enhanced activity of both are observed when disease processes affect liver cell integrity. Importantly, increased serum ALT activity reflects specific hepatocellular injury. Histopathological alterations were also evident in the liver, where GNPs induced dose- and time-dependent histological alterations of the liver tissues, including congestion, prominent vasodilatation, and vacuolization.
The Nordic study also appears to show a 15x increase for myocarditis in the 2 dose Moderna males 16-24 relative to the unvaxed. Am I reading that correctly? And does that mean that the 8x increase (which uses a slightly different age grouping) is a multiplier of the 15x increase?
Please pay attention - in the study below (Investigation into the toxic effects of graphene nanopores on lung cancer cells and biological tissues):
Heart tissue showed chemodectoma, toxic myocarditis, reddish brown atrophy; yellowish brown pigments suggesting lipofuscin granules as remnants of cell organelles and cytoplasmic material.
https://www.sciencedirect.com/science/article/pii/S2352940718302853 Investigation into the toxic effects of graphene nanopores on lung cancer cells and biological tissues
However, inhalation of graphene structures is believed to be a risk factor for cardiorespiratory disease. For example, inhaled graphene nanoplatelets can be transported deep within the distal regions of the lungs and trigger chronic inflammation in the respiratory tract. It is generally thought that the placenta, lung, gastrointestinal tract and skin act as major barriers for many nanostructures entry into living organisms. Indeed, a recent study on mice demonstrated that intratracheally delivered few-layered graphene was mainly retained in the lung, with 47% remaining after 4 weeks and this resulted dose-dependent acute lung injury and pulmonary oedema. An in vitro study of the effects of graphene and graphene oxide on human skin HaCaT keratinocytes demonstrated that oxidized graphene was the most cytotoxic, inducing mitochondrial and plasma-membrane damage, and suggesting low cytotoxic effects at the skin level. Reduced graphene oxide is more toxic than graphene oxide as evidenced by many studies reported recently. This is primarily due to its sharp edges and structural morphology. In contrast to the typically soluble nanoparticles examined in conventional toxicology investigations, graphene nanostructures have different shapes and surface areas, and which in turn can significantly influence their diffusion, dispersion, aggregation and agglomeration in plasma. Importantly, these “tunable” characteristics of graphene account for the varying toxic outcomes on the tissues. In vivo, following toxicity testing of graphene, post-mortem histological examinations of liver alterations have revealed hypertrophy of hepatocytes, necrosis and inflammatory cell infiltration in liver and kidney tissues.
Antioxidants act as a defense system to reinstate the cellular redox balance when oxidative stress is generated as a result of excess production of reactive oxygen species.
Disruption of this critical balance in the presence of excessive reactive oxygen species triggers the activation and promotion of a pro-inflammatory cascade, which in turn may cause mitochondrial release of proapoptotic factors potentially leading to cell death. Hepatocytes are key targets for reactive oxygen species damage, and therefore liver function and biomarkers of oxidative stresses should be investigated with great care.
Specifically, vacuolation, dilation of central vein and hemorrhage, vacuolation and dilation of central vein, damage of vacuolation, hemorrhage and degeneration of central vein, dilation of epithelial lining and hydropic degeneration oedema were observed in liver tissue. Kidney tissue of the treated groups showed acute vacuolization, dilation of epithelial lining, vacuolation and nucleus degeneration, nucleus damage, necrosis and epithelial degeneration.
Heart tissue showed chemodectoma, toxic myocarditis, reddish brown atrophy; yellowish brown pigments suggesting lipofuscin granules as remnants of cell organelles and cytoplasmic material.
The brain showed effects of secondary carcinoma, olegodendrocytoma small thin walled blood vessel and crytococcosis. Testicular tissue of treated groups showed spermatogenesis and vacuolation, dilation of germinal layer, degeneration of secondary spermatocytes, damage to the germinal layer and vacuolation. The lung showed damage of vacuolation, degeneration of central vein, inflammation, haemorrhage, d-shaped cells structure, hemosidophroages and lesion.
Indeed, 3D porous graphene frameworks have shown various effects from acute lethally to sub lethal toxic effects including histological, and oxidative stress responses and, after inhalation exposure in rats, graphene has been found to accumulate in the lung, leading to phagocytosis.
In this study, the first sign of toxicity recorded for the rats given an intraperitoneal injection of GNPs was an observed decrease in body weight at the higher dose. Toxic effects of GNPs on CBC were not observed although there was a slight (6%) reduction in platelet numbers in the 15 mg/kg group. The increased activities of AST, ALT, AMP and creatinine observed after 27 days are indicators of liver and kidney toxicity respectively and appeared in the rats receiving both single and multiple doses of GNPs, compared to control groups. Severe organ damage can increase the activities of ALT and AST and enhanced activity of both are observed when disease processes affect liver cell integrity. Importantly, increased serum ALT activity reflects specific hepatocellular injury. Histopathological alterations were also evident in the liver, where GNPs induced dose- and time-dependent histological alterations of the liver tissues, including congestion, prominent vasodilatation, and vacuolization.
The Nordic study also appears to show a 15x increase for myocarditis in the 2 dose Moderna males 16-24 relative to the unvaxed. Am I reading that correctly? And does that mean that the 8x increase (which uses a slightly different age grouping) is a multiplier of the 15x increase?
Thank you.
COVID VARS reveal MYOCARDIS,
https://twitter.com/RobertC39536883/status/1611030603612274699?s=20&t=CO-_49kddBTR-Fcb6T5c4g