A FATAL FOUNTAIN: Spike Protein Nanotube Dissemination through the Myocardium Induces Lethal Calcium Tsunamis
How the Spike Protein alone, as a cellular “toxic spill,” travels incognito and induces fatal arrhythmias.
FOR A GREAT MAN WHO HAS ALWAYS TOLD ME TO BE BOLD AND RELENTLESS.
This post, my most important to date, is for Peter McCullough.
Imagine a fountain. This fountain is beautiful, its pumps, which take in water, are in equilibrium, flowing smoothly, distributing the water evenly and at a constant flow throughout its plumbing.
This is how your cells are supposed to make and distribute proteins.
Now, imagine instructions are given to the pumps to go into HYPERDRIVE, taking in excess water but CONVERTING that water into POISON. Quickly, the waters overflow the limits of the fountain. The pumps are instructed to KEEP GOING. These now poisonous waters keep spreading, covering more and more territory where they are NOT supposed to be. And the poisonous waters are SMART. They travel in little tubes they made from the material of the fountain to FUSE with neighboring fountains. The toxic spill increases. More and more fountains are reached by these poisonous tubes.
This is what happens when the fountains that are your cells are told to express Spike mRNA. And it can have catastrophic effects.
THE POISONOUS WATERS CAUSE SOME PUMPS TO GO HAYWIRE (VIA A CALCIUM TSUNAMI). THESE ARE THE PUMPS THAT CONTROL HEART RHYTHM. The haywire pumps can no longer pump some waters. Blood. The heart’s pumps STOP and the victim dies instantly. This is, I am now CERTAIN, the mechanism for the observed plague of Sudden Cardiac Deaths we are observing.
Now for the science.
This is what is happening:
We next evaluated SARS-CoV-2 spike glycoprotein fusion in hiPSC-CMs (Cardiac Myocytes). Super resolution confocal microscopy of hiPSC-CMs transfected with recombinant CoV-2 S-mEm demonstrated fluorescent signal at the tips of dynamic pseudo- and filopodia contacting neighboring hiPSC-CMs. Despite overall transfection efficiency <5%, recombinant CoV-2 S-mEM expressing hiPSC-CMs produced giant CMTs, recognizable within 6 hours of transfection. EdU pulse-labelling demonstrated cell cycle asynchrony confirming fusion rather than endomitosis.
Like their infected counterparts, giant multinucleated CMTs (SARS-CoV-2 infected hiPSC-CMs produced multinucleated giant cells, called cardiomyotubes (CMTs), already evident at 24 hours post-infection) produced by CoV-2 spike protein-driven fusion were characterized by structural derangements that included circular or oval enucleated cytoskeletal “corpses” shown by F-actin phalloidin staining. Nuclei in CMTs frequently arranged themselves in clusters or rosettes, although we occasionally observed more-physiological linear rows of nuclei, reminiscient of pig CMT produced by endomitosis.
Calcium tsunamis in cardiomyotubes
We then characterized the electrophysiology of CMTs fused by recombinant CoV-2 S-mEm glycoprotein through sarcolemma patch clamping (Fig. 5a). Fig. 5b shows action potential tracings evoked in control hiPSC-CMs or recombinant CoV-2 S-mEm multinucleated CMTs. CMTs demonstrated markedly prolonged action potential duration (APD) with an average APD90 of 590 versus 420 ms in control hiPSC-CMs, shown graphically for APD50 and APD90 in, respectively.
SARS-CoV-2 direct cardiac damage through spike-mediated cardiomyocyte fusion
Please read the entire above referenced paper.
There may, however, be some hope in all of this.
SARS-CoV-2 spike generated electrical dysfunction rescued by furin inhibition.
Of course, this MAY BE WHY THERE IS A DAMNED FURIN CLEAVAGE SITE!
I thank all my supporters. My work would be impossible without you. I am particularly grateful to Peter McCullough, who has always prompted me to continue discovering.
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