SUBCLINICAL MYOCARDITIS IN CHILDREN

We may be aware of only the tip of an iceberg. Subclinical myocarditis resulting in hospitilization and death is far more common in children than most are aware of. We need serial workups of children given spike protein therapies ASAP.
A study suggests that the prevalence of "silent" myocarditis may be higher in the pediatric population than is generally suspected and may contribute to a significant number of sudden and unexpected deaths in children, particularly those older than one year of age.

In both
children and adults, most cases are subclinical; thus, the true incidence of myocarditis in children is unknown.

Children who have had COVID are advised to be screened for sports to determine the presence of myocarditis. If the spike is responsible, as I believe it is, we must

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More from @Parsifaler

16 Sep
1) THE. AUTOIMMUNE. MECHANISM.
THE SPIKE WILL NOT BE FOUND IN THE BLOOD. IT IS TRAVELLING “INCOGNITO” INTRACELLULARLY.
WE KNEW IT ENTERED CELLS VIA ENDOCYTOSIS IN 2008!
Yesterday I observed that every cell the Spike Protein invades seems to cause the body to develop autoimmunity Image
2) against it. I believe I have discovered the mechanism.
It is a very brief and straightforward mechanism.
Most likely many spikes do NOT stay on the cell surface, once they are expressed via spike protein therapied. The Spike is proven to be brought into the cell by Image
3) Endocytosis. The spike protein is internalized into cells rapidly and is detected in cells within 5 mi, a hallmark of endocytosis. The amount of spike protein in cells continues to increase for up to 30 min. Thus, SARS-CoV-2 spike protein enters cells via endocytosis.
Once it
Read 9 tweets
15 Sep
1) THE SPIKE PROTEIN: ANTIHERO OF THERAPEUTICS
What if a strong immune response IS A SIDE EFFECT OF INDUCING AUTOIMMUNE DISEASE?
Biologics are a class of drug that is made inside a cell. They must be kept cold. You can have an immune reaction to them. Not every Image
2) biologic medication is associated with the same chance of creating antibodies. In one small study comparing three popular biologic medications, it was found that anti-drug antibodies were present in 42% of those receiving Remicade (infliximab), 33% of those receiving Humira
3) (adalimumab), and in none of those patients receiving Enbrel (etanercept).
A review of 443 studies was done to find out how often antibodies were present in patients who had rheumatoid arthritis and were treated with biologics. This review showed that antibodies were found in
Read 9 tweets
14 Sep
1) WAIT! Are we all dogs trying to chase our own tails? ENOUGH! I will cut this Gordian's Knot! THE SPIKE PROTEIN INDUCES AUTOANTIBODIES IN EVERY TYPE OF CELL IT ENTERS/INTERACTS WITH!!!

Autoantibodies against ACE2 and angiotensin type-1 receptors increase severity of COVID-19
2) Autoantibodies against AT1 Receptor Contribute to Vascular Aging and Endothelial Cell Senescence - At COVID diagnosis, AT1 receptor and ACE2 autoantibodies were higher than in controls.

Let us review the mechanisms of autoantibodies. COVID checks every box. It gets an A+.
3) 1. Mimic hormone stimulation of receptor: thyroid-stimulating autoantibodies (TSAb) in Graves’ disease.

2. Blockade of neural transmission by receptor blockade or alteration of the synaptic structures: antibodies against muscle nicotinic acetylcholine receptors (AChRs) in
Read 10 tweets
14 Sep
1) THE SPIKE PROTEIN, TRANSDIFFERENTIATION AND MOYAMOYA SYNDROME: COVID-19 VASCULOPATHY

A collateral circulation developing to compensate for the vascular thickening caused by the transdifferentiation actions of the Spike Protein may be behind the vasculopathy of COVID-19. This
2) is manifest in almost precisely the same way as in MOYAMOYA DISEASE. Interestingly, those with DOWN SYNDROME are extremely susceptible to this. I believe the spike protein is transdifferentiating endothelial to mesenchymal cells. SARS-CoV-2 is also dedifferentiating at least
3) multiciliated cells and monocytes. The virus is erasing/changing cellular identities.
Unlike the flu or SARS-1 which left NO vascular thickening, SARS-CoV-2 is leaving its victims with vascular thickening of 15.4μm. Let us compare that to those that died of flu, which was
Read 13 tweets
13 Sep
1) A NOVEL NEURODEGENERATIVE DISEASE MOST CLOSELY RESEMBLING MULTIPLE SYSTEM ATROPHY MAY BE THE RESULT OF INFECTION WITH THE SARS-CoV-2 VIRUS
We have been overwhelmed with hypotheses trying to determine exactly what COVID-19 is. I, myself, am certainly a generous contributor to
2) this tsunami of conjecture as to what exactly is happening pathologically in a SARS-CoV-2 infection. This is understandable as the disease manifests itself with such a wide variety of symptoms.
And this is the point. It is a MULTI-SYSTEMIC DISEASE. As with all other
3) multi-systemic diseases, there is no concrete order for the appearance of symptoms as everyone will have symptoms present in accordance with their respective genetics. The end results will be the same, the roads traveled to reach those results will be unique.
If we look at the
Read 20 tweets
12 Sep
1) The entirety of SARS-CoV-2 revolves around the Brain Stem. Senescence is an intergral part of the disease. We have clearly either been guided by completely incompetent doctors/researchers or liars. Most likely both. Let us look at the Senescence Accelerated Mouse.

Some of the
2) progeny exhibited a moderate to severe degree of activity loss, hair loss, lordokyphosis and earlySpongiform degeneration: vacuoles of various size in the neuropil in the brain stem (Yagi et al., 1989). Microglial cell proliferation (Amano et al., 1995). Degeneration of
3) dopamine neurons in the substantia nigra and noradrenaline neurons in the locus coeruleus (Karasawa et al., 1997).

Cognition/Behavior
Age-associated behavioral impairments including learning and memory difficulties (Miyamoto et al., 1986), emotional disorders, such as reduced
Read 5 tweets

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