Any medical/doc fags around? Please refer to the thread:
1) AN EXPLANATION FOR THE SUDDEN CARDIAC DEATHS:
I believe the endocytosis of the Spike Protein is interfering with Ryanodine Receptors causing a calcium channelopathy resulting in Catecholaminergic Polymorphic Ventricular Tachycardia. This is a potentially fatal arrhythmia
2) which is induced when the heart rate exceeds 120 bpm.
The intracellular actions of the Spike Protein with Cathepsin L, a protease on the plasma membrane of host cells, increases Ca2+ release from the endoplasmic reticulum (ER) via the ryanodine receptors (RyRs). The associated
3) elevation of cytosolic Ca2+ concentration, in turn, increases cathepsin L activity. Cathepsin L promotes virus fusion with host cells by cleaving and activating the spike (S) protein. High levels of extracellular and cytosolic Ca2+ concentrations are also necessary for virus
4) fusion and endocytosis. Cathepsin L in the endosome, under the condition of a high level of Ca2+ concentration, promotes virus RNA release into the cytosol. On the other hand, the increased cytosolic Ca2+ concentration due to the overactivation of RyRs activates calcineurin,
5) which dephosphorylates NF-AT and translocates into the nucleus for promoting transcription and virus replication. Excess Ca2+ release from ER via overactivation of RyRs in AD cells results in depletion of ER Ca2+ and associated ER stress, as well as the overloading of
6) mitochondria with Ca2+ and associated mitochondria damage.
The Spike Protein therapies should be paused while this mechanism is investigated.
https://twitter.com/Parsifaler/status/1479829397154799618