2021 cov info collection

NOV 2021

MOST IMPORTANT WORK TO DATE: THE SPIKE PROTEIN ITSELF INDUCES RAAS HYPERACTIVATION VIA “CHRONIC ANG II INFUSION” EVERYTHING IS A DECOY. WE HAVE BEEN FOCUSED ON THE PRESENCE OF THE SPIKE PROTEIN (THE INSTIGATOR). YET, IT IS THE ABSENCE OF ACE2 THAT IS ALL OF COVID-19 AND ITS SEQUELAE. COVID-19 IS A DISEASE OF OVEREXPRESSED ANG II: ACE2 DEGRADING/DOWNREGULATION BY THE SPIKE PROTEIN RESULTS IN PRIMARY ARTERIAL HYPERTENSION, MICROVASCULAR DISEASE AND DNA Damage THE SPIKE PROTEIN CAUSES HUMANS TO “SELF-INJECT” THEMSELVES WITH ANG II. JUST AS IS DONE IN LAB MICE EXPERIMENTS Let us begin by looking at one of those very lab mice experiments using ANG II. In C57BL/6-mice equipped with osmotic mini pumps, delivering AngII in four different concentrations between 60 ng/kg per min and 1 μg/kg per min during 28 days, the oxidative and DNA damaging effects of AngII were studied, using immunohistochemistry and mass spectrometry. The results? AngII increased the SBP for up to 38 mmHg over control and adversely affected the kidney function of the mice. In the heart, at the highest dose administered, a significant increase of reactive oxygen species formation (1.4-fold over control) and double-strand breaks could be detected (13-fold over control). In the kidney, a dose-dependent increase of superoxide formation (up to 1.7-fold over control), double-strand breaks (up to 4.7-fold over control) and the mutagenic DNA base modification 7,8-dihydro-8-oxo-guanine (8-oxodG, up to 3.6-fold over control) was observed. Adverse effects already appeared at lower AngII doses, which did not raise the blood pressure. Administration of the radical scavenger tempol significantly decreased oxidative stress (by 20%) in the kidney and DNA double-strand breaks in the kidney by 60% and in the heart by 52%, without being able to lower the blood pressure. The artificially increased ANG II, caused by the depletion of its regulator, ACE2, results in the very pathological aspects of aging we have been observing in COVID-19. Specifically, that the renin–angiotensin system (RAS) is involved in regulation of blood pressure, vasoconstriction, sodium intake and potassium excretion is well established. Studies in the last few years have however documented new roles for this molecule as a pro-inflammatory molecule and more recently as a possible pro-fibrotic agent that contributes to progressive deterioration of organ function in disease. Binding of Ang II to its receptors (in particular AT1) mediates intracellular free radical generation that contributes to tissue damage by promoting mitochondrial dysfunction. Furthermore, Angiotensin II is a potent mediator of oxidative stress and stimulates the release of cytokines and the expression of leukocyte adhesion molecules that mediate vessel wall inflammation. Inflammatory cells release enzymes (including ACE) that generate angiotensin II. Thus, a local positive-feedback mechanism could be established in the vessel wall for oxidative stress, inflammation, and endothelial dysfunction. Angiotensin II also acts as a direct growth factor for vascular smooth muscle cells and can stimulate the local production of metalloproteinases and plasminogen activator inhibitor. Taken together, angiotensin II can promote vasoconstriction, inflammation, thrombosis, and vascular remodeling. ANG II overexpression is a complete textbook description of the “cytokine storm” and hyperactive immune response seen in COVID-19. In the context of an inflammatory process, local activation of RAS and Ang II synthesis both increased vascular permeability by promoting the expression and secretion of VEGF (vascular endothelial growth factor) (Chua et al, 1998; Kitayama et al, 2006; Suzuki et al, 2003), and induced the expression of endothelial adhesive molecules including selectins (P- and L-selectin), vascular cell adhesion molecules-1 (VCAM-1), intercellular adhesion molecules-1 (ICAM-1) and their ligands, the integrins (Alvarez et al, 2004; Piqueras et al, 2000; Pueyo et al, 2000).

Ang II also promotes endothelial dysfunction through COX-2 activation, which generates vasoactive prostaglandins and ROS (Welch, 2008; Wu et al, 2005). Moreover, Ang II favours the recruitment of infiltrating inflammatory cells into tissues by stimulating the production of specific cytokine/chemokines. For example, Ang II induces the production of the potent monocyte chemoattractant MCP-1 in cultured monocytes (Dai et al, 2007). In the aorta of spontaneously hypertensive rats, which bear elevated levels of Ang II, massive macrophage infiltration is accompanied by increased expression of MCP-1 and one of its receptors, the C–C chemokine receptor CCR2. Modulation of MCP-1/CCR2 via AT1 receptor blockade reduces vessel inflammation in these rats (Dai et al, 2007). This also explains the de novo onset of Diabetes being observed. Systemic RAS overactivation via gene overexpression or chronic Ang II infusion also induces insulin resistance, but not necessarily obesity. Perhaps the most unsettling aspect of all of this is that the connection was observed in OCTOBER OF 2020. We must immediately cease all Spike Protein exposures. The damage already done is incalculable.

Refence :

COVID-19, ACE2 DEPLETION AND RAMPANT ANG II OVEREXPRESSION: A DISEASE OF LOCAL AND SYSTEMIC RAS The great puzzle of COVID-19 may finally be solved. The immense number of systems involved, and the vast number of symptoms presented can be explained by the implication of Systemic and Local Renin-Angiotensin Aldosterone (RAS) systems. The RAS systems (both local (non-Renin dependent) and systemic (Renin-dependent) are primarily responsible for fluid homeostasis, most notably blood pressure regulation. However, the RAS system has evolved over time to be responsible for far, far more than just fluid homeostasis. Everything we are seeing in COVID-19, both acute and in its sequelae, can be explained by the overexpression of a single peptide: Angiotensin II. This peptide, necessary to maintain a healthy blood pressure, is kept in check by ACE2, which cleaves it into ANG 1-7. Without this process, the body will experience organ damage (fibrosis), rampant inflammation, neurodegeneration, senescence and even telomere shortening. Again, all that we are observing in COVID-19. INFLAMMATION AND ENDOTHELIAL DYSFUNCTION A large number of experimental studies have shown that Ang II mediates several key events of the inflammatory processes. Inflammation involves activation of the endothelium of blood vessels and expression of diverse endothelial cell selectins that dictate extravasation of specific leukocyte populations to the site of injury. Ang II also promotes endothelial dysfunction through COX-2 activation, which generates vasoactive prostaglandins and ROS. Moreover, Ang II favours the recruitment of infiltrating inflammatory cells into tissues by stimulating the production of specific cytokine/chemokines. For example, Ang II induces the production of the potent monocyte chemoattractant MCP-1 in cultured monocytes. HEART FAILURE AND CARDIAC DISEASE It is widely known that increased ANG II expression causes CHF. This is why, of course, ACE Inhibitors are used to treat CHF and a variety of cardiac and hypertensive diseases. Renin-angiotensin system (RAS) blockade with angiotensin converting enzyme (ACE) inhibitors and/or angiotensin II type 1 receptor 9) blockers (ARBs) has turned out to be beneficial at all stages of this continuum. THE CAROTID BODY AND THE OBSERVED “HAPPY HYPOXIA” The local RAS in carotid body plays a key role in modulating the carotid body response to hypoxia. Angiotensin II itself increases carotid body 10) efferent activity, presumably via activation of the AT1 receptor. Meanwhile, chronic hypoxia upregulates several key RAS components in the carotid body, including time-course dependent ACE activity. AUTOIMMUNITY RAS is critically involved in the development of Th1/Th17-mediated multiple sclerosis (MS) as shown in experimental autoimmune encephalomyelitis (EAE), a well-established mouse model for human MS. Peripheral CD4+T cells from EAE mice show increased levels of Ang II which acting through the AT1 receptor promote the synthesis of Th1 and Th17 cytokines, specifically IFN-γ and IL-17. A recent study also highlighted the role of AT1 receptors in glomerular inflammation associated with autoimmune disease in rodents by studying AT1A receptor-deficient (AT1A−/−) MLR-Faslpr/lpr (lpr) mice, 13) which develop an autoimmune disease resembling human systemic lupus erythematosus (SLE). NEURODEGENERATION The discovery of the existence of a paracrine, locally acting RAS operating independently from the circulatory RAS has fostered studies addressing the role of brain RAS, in particular in what concerns its involvement in the pathophysiology of Alzheimer's disease, the most common form of dementia. Elevated neuronal and perivascular immunoreactivity of ACE and Ang II surrounding the parietal and frontal cortex vessels in the brain of Alzheimer's disease patients has also been reported. Increased ACE activity would be expected to reduce brain perfusion, characteristic of Alzheimer's disease possibly through elevated production of Ang II. OXIDATIVE STRESS, AGING AND SENESCENCE We have previously referred to the impact of Ang II in ROS production. In fact, Ang II robustly stimulates the production of molecular oxygen species that trigger mitochondrial dysfunction and cellular injury. Ang II via AT1 receptor stimulation can activate NAD(P)H oxidase to produce ROS, resulting in the impact of Ang II in ROS production. In fact, Ang II robustly stimulates the production of molecular oxygen species that trigger mitochondrial dysfunction and cellular injury. Ang II via AT1 receptor stimulation can activate NAD(P)H oxidase to produce ROS, resulting in oxidative stress damage. Harman has proposed that ROS are the most prominent molecular species involved in the aging process. According to his theory, ROS contribute significantly to various age-associated organ failures, including hypertension, cardiovascular diseases and renal damage. Hence, Ang II could be involved in organ senescence given its ability to mediate the release of oxidant species. The disruption of AT1A receptor preserves mitochondrial and cellular wellness and promotes longevity by modulating ROS production and sirtuin expression. GLUCOSE INTOLERANCE AND DIABETES Data indicate the existence of a functional ACE2-angiotensin(1–7)-Mas axis in Caco-2 cell line, which may provide an alternative mechanism for GLUT2 and/or SGLT1-mediated intestinal glucose uptake in normal and diabetic conditions. Levels of ANG II and the presence of ACE2 Autoantibodies must be tested for in all those exposed toi the spike protein.

Reference

VAC ( - ) COLLECTIVE INFO

Relative trends in hospitalizations & mortality among infants by the number of vaccine doses and age, based on the Vaccine Adverse Event Reporting System (VAERS), 1990-2010:
http://www.ncbi.nlm.nih.gov/pubmed/22531966

Children with ASD more likely to have Rh negative mother than controls (rhogam shot):
http://www.ncbi.nlm.nih.gov/pubmed/17674242

Thousands of scientific studies in the medical literature on the dangers of vaccines:
http://medscienceresearch.com

Unvaccinated children tend to come from more educated & affluent households:
https://www.ncbi.nlm.nih.gov/m/pubmed/15231927

Flawed studies on vaccinating healthcare workers — actually no benefit at all:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3502850

2-phenoxyethanol (ethalene glycol) connection with infertility — chidren receive 17 injections with this chemical before the age of 18:
https://www.ncbi.nlm.nih.gov/m/pubmed/2086313