Antiphospholipid Syndrome caused by Endotoxin in Covid19 Jabs
Blood Clots, Stillbirths, Preeclampsia, Premature Birth, Liver and Spleen damage are just some of the disasters mainly affecting Women and their Foetuses
In an earlier article1 I mentioned that many Autoimmune diseases are caused by development of Antiphospholid Antibodies.
As there is great current interest in declining live births around the world associated with mass jabbing, let’s look at Obstetric Antiphospholipid Syndrome (OAPS) as outlined in a useful review2 that covers the impact from conception to birth.
Figure caption reads:
Figure 1. Cellular and molecular mechanisms of action of aPL in the pathophysiology of OAPS. aPL affect different cellular processes from blastocyst implantation in the uterus mucosa to trophoblast proliferation and differentiation and, eventually, the impairment of fetal growth due to antiangiogenic and prothrombotic activation. aPL induces inflammation via TLR4/MyD88 (1) in trophoblasts and endothelium and immune cells. Complement component deposition (2) on the endothelium and on trophoblasts drives inflammation and MAC formation, leading to cell death. Trophoblasts apoptosis is also produced when aPT antibodies expose PS on the external trophoblast cellular membrane (3). Inactivation of eNOS and dysfunction in ROS production are observed when the ApoE2 receptor binds to the aβGPI–βGPI complex (4). Trophoblast perturbation also affects decidual NK activity, crucial for embryo implantation (5). aPL in the lumen vessels of placental arteries and veins has pleiotropic actions: induction of leukocyte adhesion (6) on inflamed vasculature that drives neutrophil infiltration (7) inside the decidua and NET formation in response to ROS production (8). These mechanisms altogether enhance thromboinflammation with activation of the coagulation cascade initiated by TF (9). Legend depicts cells and molecules.
Endotoxin Priming Essential for Antiphospholid Syndrome
In 2005, Fischetti and coworkers demonstrated that Endotoxin priming is essential.3
They found that antiPhosphoLipid (aPL) immunoglobulin G (IgG) had no procoagulant effect, but it caused rapid endothelial deposition of Fibrinogen, followed by intravascular Platelet-Leukocyte Aggregates (PLA) and Thrombotic Occlusions (TO) in rats receiving an intraperitoneal injection of Endotoxin (bacterial Lipopolysaccharide, LPS) 3 hours before IgG infusion.
The Figure caption reads:
Effects of infusion of human aPL-positive and aPL-negative IgG in rats with or without pretreatment with LPS. Human IgG (10 mg/1 mL sterile saline) purified from 6 aPL antibody-positive sera was infused into the carotid artery of Wistar rats 3 hours after the intraperitoneally injection of either (Endotoxin) LPS (□) or sterile saline (▧). Another group of rats was treated with 5 aPL-negative IgG (10 mg/1 mL sterile saline) with (▪) or without (▦) pretreatment with (Endotoxin) LPS. The procoagulant effect of the various treatments was evaluated by counting the number of microvessels with partial or total occlusions (A) and the number of occluded vessels, as shown by the complete and persistent stop of the blood flow (B). These parameters were evaluated on 2 rats for each IgG sample to a total number of 12 and 10 rats for the aPL-positive and aPL-negative IgG, respectively. The results are expressed as mean ± SD. **P < .01, *P < .05 versus control rats receiving aPL-negative IgG.
In 2011 it was shown that β2-glycoprotein-1 autoantibodies from patients with antiphospholipid syndrome are sufficient to potentiate arterial thrombus formation in a mouse model.4
Endotoxin is linked to Spontaneous Abortion and Foetal Abnormalities
Endotoxin is linked to Spontaneous Abortion and Foetal Abnormalities via the Apex of the Cytokine Storm, Interleukin 1 beta.5
Here are some references that expand on that topic, concentrating on Antiphospholid Antibodies.
Endotoxin Lipid A, as found in Pfizer jabs, has been shown in Rabbits to induce Antiphospholid Antibodies, specifically Systemic Lupus Erythematosus (SLE) type-aCL (β2GPI-dependent) and Lupus Anticoagulant.6
Thanks to a reader (see comments) the term “Lipid Rafts” was used recently by Capozzi and coworkers to further examine Antiphospholipid reactions.7 They suggest a “Two-Hit” mechanism of Thrombosis, which reminds me of the Shwartzman effect that I mentioned in an earlier article.8
They are interested in possible drug development targeting Cholesterol to ameliorate the effect, whereas I want to eliminate the jab initiated victims.
This is Figure 1 from Capozzi.
Note aCL (β2GPI-dependent) features in the context of NETosis9 and monocyte activation of Cytokine Storm.
Beta2-glycoprotein I (β2-GPI); Annexin 2 (ANXA2); toll-like receptors (TLRs); C3a receptor (C3a-R); C5a receptor (C5a-R); cholesterol (Chol); endothelial protein C receptor (EPCR); lyso-bis-phosphatidic acid (LBPA); myeloid differentiation factor 88 (MyD88); mammalian target of rapamycin complex (mTOR); nuclear factor-kappa B (NF-κB); neutrophil extracellular traps (NETs); vascular cellular adhesion molecule (VCAM-1); intercellular adhesion molecule-1 (ICAM-1); tumor necrosis factor alpha (TNF-α); tissue factor (TF); interleukin (IL).
Single high dose Endotoxin in rodents reduces the protection against Antiphospholipid Syndrome via disrupting the nuclear receptor Peroxisome Proliferator-Activated Receptor-gamma (PPAR-gamma) anti-inflammatory pathway.1011
The study by Zho and coworkers found that Endotoxin decreases PPAR-γ via the increase in proinflammatory cytokine TNF-α release.
Low dose chronic Endotoxin damage to PPAR gamma in Liver and Spleen produces lifelong impact in Female Mice.12 By studying gene expression in the Liver caused by Endotoxin, the following Diseases were linked, including various forms of Cancer, Fatty Liver, Hepatitis C, Thyroid, Diabetes, dormant Virus reinfection and neurodegenerative diseases including Alzheimer’s. When compared to the control group, PPAR gamma was the most up-regulated gene in the liver, with a 4.18-fold increase.
Similar mapping in the Spleen points to inflammatory diseases expected from the Interleukins 1, 6, 8 and 17, which are known to self-amplify to create Cytokine Storm.
Pfizer Catastrophic APS just 1 Day after the Jab
A case report from Japan showed immediate cause and effect of CAPS in a 71-year-old Japanese lady 1 day after her jab. She suffered Thrombosis in multiple organs, including Brain, Heart, Kidney, Spleen and Digits.13
Autoimmune Diseases caused by Endotoxin in mRNA Jabs include Myocarditis, Pericarditis Lupus
Alijotas-Reig J, et al. 2022. Pathogenesis, Diagnosis and Management of Obstetric Antiphospholipid Syndrome: A Comprehensive Review. https://www.mdpi.com/2077-0383/11/3/675
Fabio Fischetti, Paolo Durigutto, Valentina Pellis, Alessandra Debeus, Paolo Macor, Roberta Bulla, Fleur Bossi, Federica Ziller, Daniele Sblattero, Pierluigi Meroni, Francesco Tedesco. 2005. Thrombus formation induced by antibodies to β2-glycoprotein I is complement dependent and requires a priming factor. Blood 106 (7): 2340–2346. https://ashpublications.org/blood/article/106/7/2340/21680/Thrombus-formation-induced-by-antibodies-to-2.
Ariela Arad, Valerie Proulle, Richard A Furie, Barbara C Furie, Bruce Furie. 2011. β2-glycoprotein-1 autoantibodies from patients with antiphospholipid syndrome are sufficient to potentiate arterial thrombus formation in a mouse model. https://pmc.ncbi.nlm.nih.gov/articles/PMC3069681/
Gotoh M, et al. 2016. Induction of anticardiolipin antibody and/or lupus anticoagulant in rabbits by immunization with lipoteichoic acid, lipopolysaccharide and lipid A. https://journals.sagepub.com/doi/abs/10.1177/096120339600500606
Capozzi A, et al. 2023. Advances in the Pathophysiology of Thrombosis in Antiphospholipid Syndrome: Molecular Mechanisms and Signaling through Lipid Rafts. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9917860/
Zhou M, et al. 2007. Endotoxin downregulates peroxisome proliferator-activated receptor-γ via the increase in TNF-α release. https://journals.physiology.org/doi/full/10.1152/ajpregu.00340.2007
Siddiqui AM, et al. 2006. The anti-inflammatory effect of curcumin in an experimental model of sepsis is mediated by up-regulation of peroxisome proliferator-activated receptor-γ. https://journals.lww.com/ccmjournal/abstract/2006/07000/the_anti_inflammatory_effect_of_curcumin_in_an.2.aspx
Dervishi E, et al. 2023. Early-Life Exposure to Lipopolysaccharide Induces Persistent Changes in Gene Expression Profiles in the Liver and Spleen of Female FVB/N Mice. https://www.mdpi.com/2306-7381/10/7/445
Jinno S, et al. 2021. Catastrophic antiphospholipid syndrome complicated with essential thrombocythaemia after COVID-19 vaccination: in search of the underlying mechanism. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8665448/
Baicalin...
+Remyelination is really useful!
***
Baicalin Promotes CNS Remyelination via PPARγ Signal Pathway
Ruo-Song Ai et al. Neurol Neuroimmunol Neuroinflamm. 2022.
pubmed.ncbi.nlm.nih.gov/35105686/
On top of everything else this is outrageous!
The sheer level of unnecessary risk forced onto everyone to the great financial boon of those funded by government to create it is greatly concerning and desperately needs to be publicly addressed.
Valid enforceable contracts require good faith conduct by ALL parties, failure in this likely invalidates contracts.
No valid contract = no legal immunity
Good faith is defined in law as fair and reasonable by Renard Constructions (ME) Pty Ltd v Minister for Public Work (1992) 26 NSWLR 234
Fair is adherence to due process and respecting the legal frameworks conditions
Reasonable is what is reasonably expected a reasonable individual would do in the same circumstances, which is entirely subjective.
Yet a reasonable person would not expect those making a fortune off a mass experimental treatment taken on good faith because of promises, which turned out to be mostly lies or false at best, made of safety and effectiveness try and hide the data required to evidence those claims, if the data actually exists, for almost a century...
Government has no power in its own right, it only has power through the assumed representation and administration of the publics best interests.
To not treat the public as a valid equal stakeholder is slavery/tyranny by another name.
The purposeful, successful and unsuccessful, attempts at suppression of data and information by the corporate and public servant interests tells a tale of conflict of interest unto itself.
Provisionally approved means approval of mass experimental use with appropriate caveats, not punishing and threatening doctors into cowed silence.
Why did no corporate WHS risk assessment and minimisation program involving coercion into participating into an experiment on the fraudulent basis that it kept the workplace $afe address the actual dangers, known and unknown especially long term, of the transfection inducing mRNA gene the-rapy?
Why was Queensland's CHO married to a Pfizer executive and repeatedly publicly thank them for helping them make the tough decisions, like violating non-derogable rights, during the emergency, real or imagined, made into the publics most senior power in Queensland as the Governor-General?
Does conflict of interest between corporate interests and government exist anymore?
Or has the pretence that they are separate, like the separation of powers, just too much of a bother?
Bit like the ACMA giving law making powers to the media which the ACMA will enforce at tax payers expense and authority...
Bit like being choked with your own hands :~/