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Epigenetics of Endotoxin Poisoning from Pfizer Jabs
Within minutes of jabbing many people suffer life threatening reactions to Endotoxins in the Pfizer Covid19 Jabs. What is known about the poisoning mechanisms?
In earlier articles I discussed the use of Escherichia coli Bacteria in production of the Pfizer jabsand how supertoxic Endotoxins carry through to the vials.
Pfizer is legally obliged to measure and report the Endotoxin levels in the jabs but so far has redacted all documents that include actual measured levels using the Horseshoe Crab Blood test.
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The American Comparative Toxicogenomics Database, maintained in North Carolina, provides useful clues to the Epigenetics of these toxins. The summary introduction page is shown below. From this we can look at the genes that will be affected by the Endotoxin and the effects of altered expression of biomolecules in the response at systemic, individual organ and cellular levels.
CTD lists 73 Genes that are affected by Endotoxins from E Coli. Let’s start by looking at the top 12 genes affected.
Anyone who cares to follow the CTD links to individual Genes might like to click on the “Diseases” tab to see the huge range of harmful effects that can be induced by injection of picograms of Endotoxin. We can identify epigenetics causing life threatening conditions including Anaphylaxis, Fever, Clotting, or Hormonal disruption leading to Bleeding.
The intention is to stimulate interest for others to research how the information might be used. For example I imagine forming a matrix of known harms that could be correlated with the thousands of different Pfizer jab harms, affecting millions of jabbees, listed in company documents obtained via court order.
Tumor Necrosis Factor
TNF = Tumor Necrosis Factor.
PTGS2 = Prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase).
NOS2 = Nitric Oxide Synthase 2.
IL6 = Interleukin 6 is a pro-inflammatory cytokine.
RELA = v-Rel avian ReticuloEndotheliosis viral oncogene homolog A, codes for Transcription factor p65 also known as nuclear factor NF-kappa-B p65 subunit.
HMGB1 = High Mobility Group Box 1, activation is a key process in inflammation. The mechanism of inflammation and damage consists of binding to TLR2 and TLR4, which mediates HMGB1-dependent activation of macrophage cytokine release.
TLR4 binding by HMGB1 or Endotoxin (LPS, LipoPolysSaccharide) sustains ADP-ribosylation of HMGB1 by PARP1 thereby serving as an amplification loop for inflammation.
IL1B = Interleukin 1B codes for Interleukin-1 beta (IL-1β) also known as leukocytic pyrogen, leukocytic endogenous mediator, mononuclear cell factor, lymphocyte activating factor.This Interleukin is capable of catalyzing its own expression in a Positive Feedback Loop and is linked to Heart Damage.
CAT = Catalase.
CXCL2 = Chemokine (C-X-C motif) Ligand 2 is also a powerful neutrophil chemoattractant.
IL12B gene has numerous synonyms.
DUSP1 = Dual Specificity Phosphatase 1
NFKBIA = NFKB Inhibitor Alpha.
CTD listing for Lipopolysaccharides
It is always useful to search the CTD under synonyms, as in this example for Endotoxin listed under Lipopolysaccharides.
Note slight differences in the “top interactions” compared to the earlier picture.
I have written a separate article on what is known about the structure of the Endotoxins from E. coli bacteria carried through the production process into jabs and enhancement of their toxicity by Covid19 Spike Protein.
Update 21 August 2023
Found an excellent paper written in 2005 by Calvano and coworkersthat provides a more useful picture of the Septic Shock induced by jabbing Endotoxin into humans, as has been done to billions in the Covid19 tragedy. Look at their simplified view of the alteration of the gene expression in 4 Human volunteers, one female and three males injected with 2 nanogram per kilogram of bodyweight NIH Clinical Center Reference Endotoxin, (CC-RE-Lot 2).
Red indicates upregulation and Blue is downregulation found in Human Blood Leukocytes. These genes are arranged in networks to facilitate the expected physiological devastation pathways including dysregulation of functional modules in Mitochondrial Bioenergetics, Protein Synthesis and Protein Degradation.
Most peak transformations occurred in the first 4 to 6 hours. They observed altered Signal Transducer and Activators of Transcription (STAT genes), cAMP-Response Element-Binding protein (CREB) and CCAAT/ enhancer binding protein (CEBP) gene families. Transcription factors limiting the innate immune response kicked in later including Suppressor of Cytokine Signalling 3 (SOCS3) and IKBK genes. “There was also a delay (4–6 h) in increased mRNA abundance of secreted and membrane associated proteins that limit the inflammatory response, including IL1RAP, IL1R2, IL10 and TNFRSF1A.”
endotoxin-responsive modules were found in addition to the innate immunity network described .. include
(a) increased expression of components of the Superoxide-producing Phagocyte NADPH-oxidase system, a multicomponent enzyme important for host defence,
(b) decreased expression of the Major HistoCompatibility (MHC) II complex, consistent with reduced antigen presentation following endotoxin stimulation,
(c) decreased expression of the TCP1 ring complex required for folding of cytoskeletal proteins,
(d) increased expression in the family of tubulin-A microtubule genes,
(e) suppressed expression of several subunits of the anaphase-promoting complex, which has a key role in cell-cycle regulation, and
(f) reduced integrin-a and -b chain expression, affecting cell–cell and cell–matrix adhesion
Here I delete some of the quote and insert few words of my own in bold
Significant decreases in messenger RNA abundance were observed in the mitochondrial respiratory chain complexes I–V (NDUF, UQCR and ATP synthase genes. Gene expression was also decreased in the Pyruvate Dehydrogenase complex (PDH), which generates, via acetyl-CoA and the TriCarboxylic Ccid (TCA) cycle, reduced coenzymes required for ATP synthesis during mitochondrial oxidative phosphorylation (Warburg Effect Cancer). A concomitant increase in expression of pyruvate dehydrogenase kinase-3 (PDK3), an inhibitor of PDH, was observed. Expression of the Voltage Dependent Anion Channel (VDAC) and adenine nucleotide translocator (SLC25A5), components of the Mitochondrial Permeability Transition Pore (MPTP) complex, were decreased to similar extents, whereas expression of the antagonistic BenZodiazepine Receptor (BZRP) was increased. MPTP activation has previously been considered an early event in apoptosis, leading to mitochondrial membrane depolarization and release of cytochrome c. However, recent reports have indicated a primary role for MPTPactivation in oxidative-stress- and calcium-overload-induced necrotic cell death.
Change in Endotoxin Standard Lots
Throwing a spanner in the works, the NIH changed regulations on the Endotoxins allowed to be used in Human poisoning experiments, something to research further.
Szekely Y, et al. 2018. A Review of Interleukin-1 in Heart Disease: Where Do We Stand Today? https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986669/
Calvano SE et al. 2005. A network-based analysis of systemic inflammation in humans. https://www.nature.com/articles/nature03985
Kiers D, et al. 2019. Comparison of different lots of endotoxin and evaluation of in vivo potency over time in the experimental human endotoxemia model. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6830888/