Sialic Acid treatment attempted to rescue Rats from Lethal Endotoxin Kidney Damage
A new paper reviewing Sialic Acids in relation to Blood clotting and other injuries caused by the Covid19 virus reminded me of earlier attempted Endotoxin treatment
Endotoxin Clotting
As readers appreciate, I concentrate on Jab induced injury, rather than that caused by viruses. In the case of Clotting, see my earlier contributions where Endotoxin is the culprit.1
South African researchers under the leadership of Etheresia Pretorius have conducted systematic analysis of the downstream clotting mechanisms induced by Inflammatory Cytokines released by minute amounts of Endotoxin.
In their figure below, you can see the effect on Red Blood Cells of Tissue Necrosis Factor-α (TNF-α) on Human Blood.2
Sialic Acids are a group of naturally occurring N-and O-acyl derivatives of the Deoxyamino Sugar Neuraminic Acid.
A number of Substack authors are interested in Sialic Acids because they are one of the targets of Covid19 via its Spikes, other targets being ACE2 (Angiotensin-Converting Enzyme 2); DPP4 (DiPeptidyl Peptidase-4); APN (AminoPeptidase N); CEACAM (CarcinoEmbryonic Antigen-related Cell Adhesion Molecule 1).
In December 2022 Jessica Rose discussed Sialic Acid causing Red Blood Cells to aggregate, citing a paper by David Scheim.34
A new review by David Scheim and researchers from Japan, South Africa and Australia5 collects further references relevant to clotting and related injuries resulting from attachment of Coronavirus to Red Blood Cells and other cells which have Sialic Acids expressed on their surface.
Other researchers have examined differences in Covid19 clots with respect to Sialylation.6
N-glycan analysis of the serum proteome revealed increased levels of oligomannose- and sialylated di-antennary glycans and decreased non-sialylated in Covid19 patients.7
There appears to be a genetic factor in the degree of sialylation.8
Research using commercial supplies of Spike protein cultured in Human Embryonic Kidney cancer cells can’t be used in studies of Spike clotting because they typically contain up to 1.0 Endotoxin Unit per μg (microgram) protein as determined by the LAL method and this is likely to be an underestimate due to masking.910
Sialic Acid treatment to rescue Endotoxin poisoned Rats from Certain Death
Just as Spike must be free of Endotoxin, commercial supplies of Endotoxin must be cleaned up to remove contamination by bacterial proteins before it can be used in toxicity studies.11
Once repurified Endotoxin was available, study of the effects of Sialic Acid on Female Wistar Rats in Endotoxin poisoning could be done with confidence and proved that the primary driver of harms occurred via TLR4 and not TLR2 pathways.12
Endotoxin caused reduced Arterial Blood Pressure, Renal Microcirculation and Blood Flow, and Increased Vascular Resistance resulting in Multiple Organ Failure. Clotting was clearly involved.
rLPS (repurified Lipopolysaccharide, Endotoxin) enhanced Monocyte/Macrophage (ED-1) Infiltration and ROS (Reactive Oxygen Species) production and impaired Kidneys by triggering p-IRE1α/p-JNK/CHOP/GRP78/ATF4-mediated Endoplasmic Reticulum (ER) stress, Bax/PARP-mediated Apoptosis, Beclin-1/Atg5-Atg12/LC3-II-mediated Autophagy, and Caspase 1/IL-1β-mediated Pyroptosis in the kidneys.
Sialic Acid and Endotoxin have a very high Binding Affinity.
Yang and coworkers found that there was only a 30 minute window to rescue the Rats by injection of large quantities of Sialic Acid from Endotoxin induced Kidney injury and suggested that Sialic Acid would have limited utility in Sepsis patients, but perhaps could be investigated in trials using a dialyzer, intravenous injection, or oral intake.
One can’t discuss Clotting without reference to Platelets. As reviewed by Page and Pretorius, “Viral enzymes such as neuraminidase can cause desialylation of platelet surface receptors and desialylation might promote platelet clearance in the liver.”
Their Figure 213 shows the key parts of our Platelets:
See also their Figures 5 and 6 that show how our Platelets react to Bacterial Endotoxin and Viruses respectively.
I will add more references to Sialic Acid interactions as they are found.
Conformal White Fibrin "Clots" are caused by Endotoxin in Jabs
Martin J. Page, Janette Bester and Etheresia Pretorius. 2018. The inflammatory effects of TNF-α and complement component 3 on coagulation. https://www.nature.com/articles/s41598-018-20220-8
Scheim, D.E. A Deadly Embrace: Hemagglutination Mediated by SARS-CoV-2 Spike Protein at Its 22 N-Glycosylation Sites, Red Blood Cell Surface Sialoglycoproteins, and Antibody. Int. J. Mol. Sci. 2022, 23, 2558. https:// doi.org/10.3390/ijms23052558
Scheim, D.E.; Parry, P.I.; Rabbolini, D.J.; Aldous, C.; Yagisawa, M.; Clancy, R.; Borody, T.J.; Hoy, W.E. 2024. Back to the Basics of SARS-CoV-2 Biochemistry: Microvascular Occlusive Glycan Bindings Govern Its Morbidities and Inform Therapeutic Responses. https://www.mdpi.com/1999-4915/16/4/647
Moiseiwitsch N, Zwennes N, Szlam F, Sniecinski R, Brown A. 2022. COVID-19 patient fibrinogen produces dense clots with altered polymerization kinetics, partially explained by increased sialic acid. https://www.jthjournal.org/article/S1538-7836(22)18370-4/fulltext
Julia Beimdiek, Sabina Janciauskiene, Sabine Wrenger, Sonja Volland, Adriana Rozy, Jan Fuge, Beata Olejnicka, Isabell Pink, Thomas Illig, Alexander Popov, Joanna Chorostowska, Falk F. R. Buettner and Tobias Welte. 2022. Plasma markers of COVID‑19 severity: a pilot study. https://link.springer.com/article/10.1186/s12931-022-02272-7
Raymond Kruse Iles. 2023. The COVID-19 antibody responses, isotypes and glycosylation: Why SARS-CoV-2 Spike protein complex binding of IgG3 is potentiated in some and immuno-pathologies manifest. https://www.medrxiv.org/content/10.1101/2023.01.13.23284524v1
SARS-CoV-2 (2019-nCoV) Spike/RBD Protein. APB Biologics Product Information.
SARS-CoV-2 (2019-nCoV) Spike RBD-mFc Recombinant Protein (HPLC-verified). https://www.sinobiological.com/recombinant-proteins/2019-ncov-cov-spike-40592-v05h
Matthew Hirschfeld; Ying Ma; John H. Weis; Stefanie N. Vogel; Janis J. Weis. 2000. Cutting Edge: Repurification of Lipopolysaccharide Eliminates Signaling Through Both Human and Murine Toll-Like Receptor 2. https://journals.aai.org/jimmunol/article/165/2/618/32909
Chih-Ching Yang, Chien-An Yao, Jyh-Chin Yang, and Chiang-Ting Chien. 2014. Sialic Acid Rescues Repurified Lipopolysaccharide-Induced Acute Renal Failure via Inhibiting TLR4/PKC/gp91-Mediated Endoplasmic Reticulum Stress, Apoptosis, Autophagy, and Pyroptosis Signaling. https://academic.oup.com/toxsci/article/141/1/155/2338281
Martin J Page and Etheresia Pretorious. 2020. A Champion of Host Defense: A Generic Large-Scale Cause for Platelet Dysfunction and Depletion in Infection. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7339151/
The whole idea of using our own cell as antigens to provoke an antigenic response, is like asking the citizens of Troy to invite in the Trojan horse! Foolishness disguised as genius, the same as a mass vaccination program in the middle of a pandemic?
Interesting how many athletes that have stated online how their blood pressures changed immediately after the vaxx, plenty use the apps and heart rate monitors to continually monitor their training results.
Ties into the drop in arterial blood you mention.pressure perhaps