Rockville Maryland - centre of Endotoxin and GMO mRNA research Invited Me to Chat - Should I submit an Abstract ?

US Bioweapons axis coincidences continue?

Join me in lodging a paper with the United States Pharmacopeial Convention Virtual Summit?

Deadline is extended to 31 January 2025 American time.

This is a most interesting coincidence because the other day I joined a useful X thread¹ as shown here, where I pointed out that Janos Szebeni, who recently wrote about Covid19 Jab contamination, worked at Division of Retrovirology, Dept of Vaccine Production and Delivery, US Military HIV Research Program, Walter Reed Army Institute of Research, Rockville, Maryland.

Janos Szebeni is an expert in Endotoxin activation of Complement and its disastrous consequences.

The paper² I referenced saw him working with researchers in Georg-August-Universität, Göttingen Germany and two departments of the Uniformed Services University of the Health Sciences, Bethesda, Maryland.

The Journal is appropriately named Shock.

The Abstract of his work using Pigs:

Activation of the complement (C) cascade is known to play a key role in the adverse immune consequences of hemorrhagic trauma with subsequent shock and resuscitation. However, it is not clear whether hypovolemia per se, without trauma and resuscitation, can also lead to C activation. To address this question, we studied the presence, kinetics, and cause of C activation in a porcine model of hemorrhagic shock and resuscitation in the absence of trauma. Pigs were bled to and kept at 35 mmHg for 90 min, followed by hypotensive resuscitation with different fluids and, finally, with shed blood.

The animals developed severe lactic acidosis between 30 and 90 min, which was accompanied by a trend for initial rise and subsequent 40% drop of CH₅₀/mL, indicating massive C activation even before resuscitation, i.e., before reperfusion damage could have occurred. Resuscitation with plasma expanders caused 20% additional C consumption, whereas whole blood raised CH₅₀/mL. Plasma C5a decreased initially and then significantly increased at 60 and 180 min, whereas thromboxane B₂ showed a 3-fold increase at 30 and 60 min.

Plasma LPS (Endotoxin) was also increased above baseline at 90 and 180 min.

In in vitro studies with pig blood, spontaneous C5a formation, as well as zymosan-induced C consumption, was significantly enhanced under the conditions of lactic acidosis. Our data suggest that lactic acidosis, endotoxemia, and possibly other ischemia-related tissue alterations act in a vicious cycle in inducing C activation and, hence, aggravation of shock. The biphasic course of CH₅₀/mL and C5a changes may reflect yet unrecognized physiological responses to hemorrhage-related C activation.

Interesting discussion of Endotoxin increase in the shocked Pigs.

In our experiments, the quantitatively small, yet significant rise of plasma LPS at 90 and 120 min is consistent with the CH₅₀/mL curve reaching its nadir during this period. As for the low degree of changes, there are several processes contributing to the rapid clearance of the LPS (Endotoxin) in plasma, such as the binding to plasma proteins, high-density lipoproteins, and CD14 receptors on different (monocytic) cells, and enzymatic degradation by esterases (^33,34).

Thus, our analysis might have underestimated the endotoxin exposure of the animals under shock.

It should also be considered that hemorrhagic shock could sensitize the pigs to LPS (Endotoxin) in a process similar to that described in rabbits (³⁵).

A recent study by Zhi-Yong et al. (¹⁸) is particularly relevant in this regard, as the authors demonstrated close parallelism between bacteremia, hypotension, and the elevation of plasma C5a and TXB₂ after restoration of bowel circulation in dogs after partial occlusion of the superior mesenteric artery.

The work “was supported by the U.S. Army Combat Casualty Care Research Program under the auspices of the U.S. Army Research Office Scientific Services Program administered by Battelle (Delivery Order 0032, Contract No. DAAD 19-02-D-0001). It was also supported by grants to P.D.M. (Office of Naval Research), R.B. (USUHS RO70LO), and O.G. (Deutsche Forschungsgemeinschaft, SFB 330 and 236 and by project OP 42/5-1).”

The Szebeni paper was published in 2003, the same year that Endotoxin Induced Myocarditis was understood at molecular level.³

Read more on the clearance of Endotoxin by your circulating Binding Protein.⁴

I have covered deadly Anaphylaxis due to Complement Activation.⁵

I also wrote about using Piglets in Endotoxin studies using just 0.06 μg/kg of Endotoxin, derived from Escherichia coli serotype 0111:B4, dramatically increasing Heart Rate, and Renal Vascular Resistance and decreased Renal Blood Flow, Glomerular Filtration Rate, Urine Volume and Paraaminohippuric Acid Clearance.⁶

I look forward to your comments, and please let me know if you submit an abstract.

1. https://x.com/FluoridePoison/status/1881974946643251290

2. Szebeni, Janos; Baranyi, Lajos; Savay, Sandor; Götze, Otto; Alving, Carl R.; Bünger, Rolf; Mongan, Paul D. 2003. Complement Activation During Hemorrhagic Shock and Resuscitation in Swine. https://journals.lww.com/shockjournal/fulltext/2003/10000/complement_activation_during_hemorrhagic_shock_and.9.aspx

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