1) Although decreased translation fidelity causes protein misfolding and aggregation in both cardiomyocytes and Purkinje cells, the downstream pathways that lead to cell death in the two cell types may be quite different. Interestingly, a point mutation in the editing domain of 2) human mitochondrial AlaRS (AARS2) has been associated with infantile mitochondrial cardiomyopathy, suggesting increased errors in either cytoplasmic or mitochondrial protein synthesis can lead to cell death in the heart. In summary, our data show that a global reduction in

On Damar Hamlin and Dr. Sutterer's "diagnosis" of Commodio Cordis
I am shocked that Commodio Cordis (CC) is named as the cause. Please examine the images carefully. In CC Ventricular fibrillation can be triggered by chest wall IMPACT ONLY OVER THE HEART, and predominantly occurs with impact over the center of the left ventricle. Although CC usually involves impact from a baseball, it has also been reported during hockey, softball, lacrosse, karate, and other sports activities in which a relatively hard and compact projectile or bodily contact caused

1) UPDATED SYNTHESIS: EXTREMELY URGENT
IT’S COMPLICATED, BUT CLEAR – LOOKING ONE MOVE DEEPER
THE SPIKE PROTEIN PATHOGENIC ALGORITHM – DUAL PATHS TO TERMINAL SYSTEMIC FIBROSIS: IMMEDIATE FOR THOSE WITH SIGNIFICANT COMORBIDITIES, INDUCED FOR THOSE WITHOUT
The Spike Protein is 2) inducing terminal systemic fibrosis of all organs, including the blood, via two principal mechanisms.
The first is a direct, immediate path via binding to RGD-binding integrins, which includes several TGF-β -activating integrins. This this activates Myofibroblasts which

1) MORE THAN AMYLOIDOSES. ALL HUMAN TISSUES ARE BEING TRANSFORMED INTO FIBROUS MASSES. INCLUDING. THE. BLOOD.
AMYLOIDOSIS. FIBROSIS. | AUTOPSIES. INCREASED ORGAN WEIGHT. | CLOTS. AMYLOIDS.
The tissues of the body, INCLUDING THE BLOOD, are being either DEPOSITED WITH FIRBILS OR 2) BEING TRANSFORMED INTO FIBRILS. Amyloidosis > Deposition of Fibrils. Fibrosis > Transformation into Fibrils.
The Spike Protein is transforming (at least) all human tissue (perhaps other species?) into non-functioning fibrous masses.
I was reading papers in the solarium after

1) THE SPIKE PROTEIN IS THE “AMYLOID” BEING DEPOSITED AND INDUCING AMYLOIDOSES: A MAJOR FINDING MISSED
SEVERE COVID MAY BE DUE TO THE ADDED DEPOSITION OF COMPLEMENT WITH THE SPIKE
The paper “The histologic and molecular correlates of COVID-19 vaccine-induced changes in the skin” 2) made a case for the immune response to the Spike Protein causing self-limited hypersensitivity reactions to the vaccine. However, if you study the paper carefully, you notice that the authors have missed a far more important finding.
The biopsy specimens of normal skin post

1) PLEASE READ THIS ENTIRE THREAD. IT IS URGENT.
Building on all recent work. By far my most important synthesis:
A NEW KIND OF CANCER: THE MARRIAGE OF ONCOGENESIS AND PRIONOPATHY
THE PROGRESSIVE DESTRUCTION OF TISSUE AND ORGANS BY THE AMYLOIDOGENIC AND OLIGOMERIC PROPERTIES OF 2) THE SARS-CoV-2 SPIKE PROTEIN
It has been proposed that Alzheimer's disease might be a 'whole body' problem, as amyloid-beta can travel, cancer-like, to brain from other parts of body.
Normal mice that had been joined (via bloodstreams) to genetically modified partners for a

1) THIS. CHANGES. EVERYTHING.
THE SPIKE PROTEIN FORMS COMPLEXES WITH ALL AMYLOIDOGENIC PROTEINS!
EXAMPLE: ATHLETES DIE FIRST BECAUSE ATHLETE’S HEARTS ALREADY HAVE HYPERTROPHY!!!
THE AVERAGE CANNOT PERCEIVE. ONLY THOSE AT PHYSICAL EXTREMES ARE AFFECTED INITIALLY. EXTREMES OF SIZE 2) AGE AND ACTIVITY! MAKE NO MISTAKE IT WILL TAKE THE AVERAGE SOON ENOUGH AS THEY ARE “FIBRILLED”!
THE SPIKE PROTEIN IS A FOLDAMER AND A SELF-REPLICATOR: THE INDUCTION OF MULTIPLE LETHAL PROTEINOPATHIES
The more I go down the proteinopathy rabbit hole, the more trouble I see that

1) MOST IMPORTANT FINDING TO DATE. BUILDING ON ALL PREVIOUS RESEARCH.
A UNIFYING THEORY OF COVID-19 PATHOGENESIS, COMBINING SENESCENT, CARDIOVASCULAR, ONCOGENIC AND NEURODEGENERATIVE PATHOLOGIES
“We shall not cease from exploration
And the end of all our exploring 2) Will be to arrive where we started
And know the place for the first time.”

--from Little Gidding by T.S. Eliot
THE SPIKE PROTEIN OF SARS-CoV-2 INDUCES A SYSTEMIC AMYLOID PROTEINOPATHY
When I first began researching the Spike Protein of SARS-CoV-2, I believed it was

1) MAJOR FINDING TONIGHT: THE SPIKE PROTEIN INDUCES PATHOLOGIES THAT ARE RARE AND NORMALLY INHERITED!
FROM INHERITANCE TO INDUCTION, BURNING THE CANDLE AT BOTH ENDS: CHANNELOPATHY AND HYPERTROPHIC CARDIOMYOPATHY
I am extremely concerned that in addition to channelopathies induced 2) by the spike protein potentially causing death in sleep, hypertrophic cardiomyopathy induced by the spike protein is causing death at the other end of the spectrum - during intense exertion.
As I have previously theorized, the Spike Protein and its immune complexes are

1) BUILDING. AN URGENT WARNING. IMMEDIATE ACTION REQUIRED.
SARS-CoV-2 SPIKE PROTEIN AS VIROPORIN, INDUCING BRAINSTEM SPREADING DEPOLARIZATION (SD) RESULTING IN SUDDEN CARDIAC DEATH – THE SUDEP-SIDS CONNECTION
The current epidemic of sudden cardiac deaths, ranging from occurrence 2) during physical exertion to occurrence during sleep may be explained by a sudden spreading depolarization initiated in the brain stem by the viroporin actions of the Spike Protein.
One prominent gene family present in an analysis of spike binding affinity is the voltage-gated

1) MY MOST IMPORTANT FINDING TO DATE
SPIKE PROTEIN ACTIVATION OF LINE-1 RETROTRANSPOSONS FORCES THE BODY TO PLAY A GAME OF GENETIC “RUBIK’S CUBE” WHICH ALTERS GENE COPIES, SHORTENS TELOMERES AND THE “WINNERS” CLAIM THE PRIZE OF SUDDEN CARDIAC DEATH
This is my most technical 2) finding to date and it is extremely complicated. I apologize in advance if it is difficult to follow.
Most individuals who die from sudden cardiac death are old and they invariably suffer from atherosclerotic disease. Do not let anyone tell you otherwise. They lie.

1) IN DEPTH: MOST IMPORTANT FINDING TO DATE
AFTER DESTROYING THE ENDOTHELIUM, THE SPIKE PROTEIN, IN ADDITION TO INDUCING FIBROSIS, THEN TURNS THE VASCULATURE TO “IRON AND STONE”: THE SPIKE PROTEIN IS INDUCING THE CALCIFICATION OF AND HEMOSIDERIN DEPOSITION INTO THE VASCULATURE: 2) THE KEY TO THE WHITE CLOTS
I read a paper from a group in Hong Kong that had injected a Spike Protein Accelerant into mice. With the surprising result that within two days THE HEART WAS SIGNIFICANTLY CALCIFIED. So, I decided to look into this a little deeper.
It turns out that

1) A WARNING
AN INTENTIONAL MIXTURE OF CANCER TREATMENT INDUCED AGE ACCELERATION: A MARRIAGE IN HELL OF RADIATION AND CHEMOTHERAPY SIDE EFFECTS – THE SPIKE PROTEIN PROGEROID SYNDROME
I don’t quite know how to say this. Maybe I shouldn’t say it this way, yet I feel I must. I must 2) speak what I believe to be the truth. And it is the only logical explanation for what we are seeing that I can arrive at. I think it is first important to understand that I believe we are under the spell of a web of lies so sinister and so well constructed, that it may as well

1) THE SPIKE PROTEIN AND THE “IRRADIATION” OF THE ENTIRE VASCULATURE
The Spike Protein of SARS-CoV-2 damages the Endothelium IN PRECISELY THE SAME WAY RADIATION DAMAGES THE ENDOTHELIUM. Now we know why pathologists keep saying victims of COVID and the Spike Protein look like 2) radiation injuries.
Both the Spike Protein and Radiation damage the Endothelium by inducing inflammation via TLR2-dependent activation of the NF-κB pathway.
An alternative mechanism for the development of the proinflammatory phenotype of irradiated endothelial cells is the

1) BUILDING: MY MOST IMPORTANT FINDING TO DATE: DIED UNEXPECTEDLY SOLVED
SUDEP AND “DIED UNEXPECTEDLY” – THE SPIKE PROTEIN, FIBROSIS AND THE BRAINSTEM
PART I “A SILENT ENTRANCE”
As you recall, the original spike caused a loss of the sense of smell, the medical term is Anosmia. 2) The olfactory (sense of smell) system happens to be a DIRECT ROUTE TO THE BRAINSTEM.
Indeed, when we look at autopsies, the Spike Protein is a very frequent “guest” in the Brainstem. Pathological immune responses or SARS-CoV-2 invasion of the brainstem is suspected.

1) OMNIPOTENT TROPISM; OMNIPOTENT MOLECULAR MIMICRY: A Terrifying Monster To Blood Vessels – AND NEURONS! Most Likely More
I don’t quite know how to say this. But I am shaking as I write this. I was smoking a cigar and contemplating a DM an amazing (and famous) doctor sent me. 2) The DM was about Pericytes and the Spike Protein. And I just kept thinking about it. Slowly, it dawned on me. And now I am shaking as I write this.
Spike in Endothelium. Spike in Pericytes. Spike in Basement Membrane. Spike in Myelin Sheath. Spike in Axon. Spike distributed

1) CONVINCING, DEFINITIVE PROOF OF MASS INJURY/DEATH
READ THIS: Over 90% of S1 spike positive cells were endothelia in microvessels.
THE SPIKE PROTEIN CAUSES REPEATED AND SEVERE DAMAGE TO THE MICROVASCULATURE AND INDUCES FIBROSIS
The opening statement of this post was from mice 2) autopsies after Spike Protein administration ALONE: Over 90% of S1 spike positive cells were endothelia in microvessels.
It is, I believe, WITHOUT QUESTION that the Spike Protein is inducing fibrosis and turning vasculature to scar tissue.
Now that we know WHERE the spike is,

1) IF YOU READ ANYTHING ABOUT COVID IN YOUR LIFE. READ THIS!
COVID-19: AN IMMUNE MEDIATED DISEASE OF PROGRESSIVE SYSTEMIC FIBROSIS INDUCED BY THE SPIKE PROTEIN AND ITS IMMUNE COMPLEXES. THE PRESENCE OF SPIKE PROTEIN WITH SPIKE ANTIBODIES IS EXTREMELY DANGEROUS; INCREASED TROPISM 2) GIVING THE SPIKE A HUMAN Fc RECEPTOR!
This is an urgent warning to all clinicians and public health professionals. We have been lied to and led astray as to the true nature of SARS-CoV-2 and the Spike Protein.
It is established that those with increased NON-NEUTRALIZING

1) SUMMA SUMMARUM 2.0
SPIKE PROTEIN FIBROSIS SYNDROME:
THE SPIKE PROTEIN INDUCES A FIRBROTIC CASCADE EXACTLY PARALLEL TO RADIATION FIBROSIS SYNDROME
THE SPIKE PROTEIN INDUCES THE SAME ACCUMULATION OF EXCESS FIBRIN THAT RADIATION DOES!
First: In the microcirculation, SARS-CoV-2 2) and the S protein directly enhance platelet activation and fibrin aggregation, predisposing 30–50% of COVID-19 patients to develop thrombotic events.
Various pathophysiological mechanisms have been postulated for RFS including induction of free radical (FR)-mediated DNA damage

1) A PARRALEL BETWEEN JUVENILE RHEUMATOID ARTHRITIS (JRA) AND THE SPIKE PROTEIN: IS THE BODY ATTACKING ITS OWN ENDOTHELIUM?
An interesting case (published in 1989) discussed in the Journal of Pediatric Gastroenterology and Nutrition relays a case in which a JRA patient developed 2) a fatal immune enteropathy years after the onset of the disease. Biopsies of the small bowel exposed to the patient's serum revealed deposition of complement and immunoglobulins in the epithelium.
This is where the parallel with COVID (in particular, the Spike Protein) becomes

1) VITAMIN D, OR VITAMIN D BINDING PROTEIN: It May Be That Vitamin D Binding Protein Is More Important Than Vitamin D Itself In COVID-19 Pathology
As I have previously discussed, it has been determined that the Spike Protein damages hematopoietic stem/progenitor cells in the 2) mechanism of pyroptosis in Nlrp3 inflammasome-dependent manner. This leads to the release of cytosol components to extracellular space and final cell lysis.
And, as in endothelial injury after hematopoietic stem cell transplant it has been shown that release of the angiopathic