For more than 15 million years, human beings have co-evolved with thousands of microbial species…

Nothing known to serious scientists support ridiculous claims about 15 million years. See for comparison: Natural Selection on the Olfactory Receptor Gene Family in Humans and Chimpanzees

See also: Nothing in Biology Makes Any Sense Except in the Light of Evolution

…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla.

See also: Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution

Editor’s summary: Five antigenic sites in the virus surface hemagglutinin protein, which together comprise 131 amino acid positions, are thought to determine the full scope of antigenic drift of influenza A virus. Koel et al. (p. 976) show that major antigenic change can be caused by single amino acid substitutions.

The fact that one amino acid substitution alters antigenic changes in the influenza viruse and one amino acid substitution stabilizes the organized genomes of primates attests to what Richard Feynman referred to as human idiocy in this snippet about food energy from one of his lectures.

See: Food energy

See for comparison:

Your favorite phrase, “biologically uninformed science idiots” alienates you from people because it sounds insulting and egotistical. — Saibot Rodrigo

“Mutation-driven evolution” sounds insulting and egotistical to serious scientists. Only pseudoscientists use it to dismiss everything known about how quantum physics must be linked to the creation of quantum souls via food energy and the physiology of pheromone-controlled reproduction.

Here are two examples of how pseudoscientists alienate serious scientists. (Jay R. Feierman is a retired medical practitioner and former psychiatrist.)
For example: 7/25/13
Jay R. Feierman:
Variation is not nutrient availability and the something that is doing the selecting is not the individual organism. A feature of an educated person is to realize what they do not know. Sadly, you don’t know that you have an incorrect understanding [of] Darwinian biological evolution.
Jay R. Feierman:

I am absolutely certain that if you showed this statement to any professor of biology or genetics in any accredited university anywhere in the world that 100% of them would say that “Random mutations are the substrate upon which directional natural selection acts” is a correct and true statement.

See also: Past 5,000 years prolific for changes to human genome

Of 1.15 million single-nucleotide variants found among more than 15,000 protein-encoding genes, 73% in arose the past 5,000 years, the researchers report. 164,688 of the variants — roughly 14% — were potentially harmful, and of those, 86% arose in the past 5,000 years. More broadly, the results suggest that humans are carrying around larger numbers of deleterious mutations than they did a few thousand years ago. But this doesn’t mean that humans now are more susceptible to disease, says Akey. Rather, it suggests that most diseases are caused by more than one variant, and that diseases could operate through different genetic pathways and mechanisms in different people.

The claim that diseases could operate through different mechanisms in different people cannot be supported by experimental evidence of biologically-based cause and effect. Healthy longevity and virus-driven pathology have been linked from energy-dependent RNA-mediated cell type differentiation to all biophysically constrained biodiversity via the creation of the sun’s anti-entropic virucidal energy, which prevents the degradation of messenger RNA. The virus-driven degradation of messenger RNA has been linked from mutations to all pathology in all living genera via conserved molecular mechanisms.

Simply put, what organisms eat has been linked from the physiology of pheromone-controlled reproduction to all biophysically constrained biodiversity. What organisms eat links their species-specific nutrient-dependent pheromone-controlled physiology of reproduction to protection of all organized genomes from virus-driven entropy.

See: Herpesviruses shape tumour microenvironment through exosomal transfer of viral microRNAs (with my emphasis)

This flow of genetic information results in a metabolic shift toward aerobic glycolysis in the surrounding non-infected cells. Importantly, this exosome-mediated metabolic reprogramming of neighbouring cells supports the growth of infected cells, thereby contributing to viral fitness. Finally, our data show that this miRNA transfer-based regulation of cell metabolism is a general mechanism used by other herpesviruses, such as EBV, as well as for the transfer of non-viral onco-miRs. This exosome-based crosstalk provides viruses with a mechanism for non-infectious transfer of genetic material without production of new viral particles, which might expose them to the immune system. We suggest that viruses and cancer cells use this mechanism to shape a specific metabolic niche that will contribute to their fitness.

The flow of genetic information must link energy as information to all biologically based cause and effect via the physiology of pheromone-controlled reproduction in all living genera.

See also: RNA on the brain: emerging layers of post-transcriptional regulation in cerebral cortex development

New technological advances raise the potential for an increasingly sophisticated understanding of post-transcriptional control in the developing neocortex. Many RNA-binding factors are also implicated in neurodevelopmental diseases of the cortex. Therefore, elucidating how RBPs and miRs converge to influence mRNA expression in progenitors and neurons will give valuable insights into mechanisms of cortical development and disease.

The fact that food energy-dependent RNA-binding factors and the de novo creation of microRNAs in plants and animals prevent the virus-driven degradation of messenger RNA, which links mutations to all pathology has been established in the context of nearly 64,000 published works that are currently indexed on PubMed.

See: microRNA

See also: Chromogenic In Situ Hybridization Methods for microRNA Biomarker Monitoring of Drug Safety and Efficacy

Disease research and treatment development have turned to the impact and utility of microRNA. The dynamic and highly specific expression of these molecular regulators can be used to predict and monitor disease progression as well as therapeutic treatment efficacy and safety, thus aiding decisions in patient care. In situ hybridization (ISH) of biopsy material has become a routine clinical pathology procedure for monitoring gene structure, expression, and sample characterization. For ribonucleic acid (RNA), determining cell source and level of expression of these biomarkers gives insight into the cellular function and physiopathology. Identification and monitoring of microRNA biomarkers are made possible through locked nucleic acid (LNA)™-based detection probes.

My comment to the Exiqon FB page:

Energy-dependent changes in the microRNA/messenger RNA balance have now been linked to healthy longevity and all extant biodiversity via the physiology of pheromone-controlled reproduction in all living genera. “RNA on the brain: emerging layers of post-transcriptional regulation in cerebral cortex development.”

The virus-driven degradation of messenger RNA has been linked from mutations to all pathology. See for example: “Herpesviruses shape tumour microenvironment through exosomal transfer of viral microRNAs.”

Exiqon’s advances in detection of changes in the microRNA/messenger RNA balance has linked electrons to ecosystems via amino acid substitutions in all living genera. The company seems well-prepared to eliminate most, if not all theories, about the differences between healthy longevity and virus-driven pathology.

Most theorists have paid no attention whatsoever to the advances in technology. That fact attests to the difference between serious scientists and pseudoscientists. Pseudoscientists have been stuck with their theories.

For examples of those who have been stuck with their theories see: Host-derived creation of all pathology (2) in prep

 For a brief expose on the difference between mutations and amino acid substitutions, see also: “In order to make peptides, you start with amino acids obviously.” from:How Peptides Are Made

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