Cardiac energy metabolism requires units of energy
(click to enlarge)
Acetylation contributes to hypertrophy-caused maturational delay of cardiac energy metabolism (First published May 17, 2018 )
Silencing the mRNA of general control of amino acid synthesis 5-like protein 1 reduced acetylation of LCAD and βHAD as well as fatty acid oxidation rates in cardiomyocytes. Thus, hypertrophy in CHDs prevents the postnatal increase in myocardial acetylation, resulting in a delayed maturation of cardiac fatty acid oxidation.
The virus-driven theft of quantized energy causes the silencing of mRNA, which generally controls amino acid synthesis. The failure to link the creation of sunlight from the creation of ATP synthase to the creation of ATP and the creation of microRNAs, leaves a gaping hole in the logic they use to support their ridiculous claim about hypertrophy in CHDs, which they link to what all serious scientists know is quantized energy-dependent cardiac fatty acid oxidation.The molecules that energize babies’ hearts
“Our findings show that acetylation of metabolic enzymes plays an important role in controlling the dramatic changes in energy metabolism that occur in newborn hearts immediately after birth,” says Arata Fukushima. “The findings also show how hypertrophy can perturb this process by delaying the maturation of fatty acid metabolism, which compromises the ability of the newborn heart to generate energy. Developing drugs that enhance acetylation of the metabolic enzymes could help treat patients with hypertrophy.”
The focus on drug development obfuscates the facts about energy-dependent fixation of RNA-mediated amino acid substitutions. All metabolic processes are quantized energy dependent. The quantized energy comes from sunlight and it is typically biophysically constrained in food. In the report, there is no mention of amino acids whatsoever. Ask the researchers and reporters, “Why not?”Food energy VIDEO VIDEO microRNA s
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