RNA-mediated theory killers (2)

By: James V. Kohl | Published on: December 12, 2015

RNA-mediated theory killers…

This is a continuation that will become a series that links the million dollar paradox to the $100,000 prize offered for finding the origin of information at Evolution 2.0, which obviously will be a continuation of Schrodinger’s claims and Dobzhansky’s claims along with the claims of others I have repeatedly mentioned here.
Critical Role of Histone Turnover in Neuronal Transcription and Plasticity
Reported as: Lifelong learning is made possible by recycling of histones

“Histones and their modifications can play an important role in switching genes on and off—a type of epigenetic control. This research uncovers an epigenetic mechanism, involving one slightly-modified, “variant” histone, that makes learning possible by facilitating the genetic changes necessary for neurons to form connections,” says study author C. David Allis.

My comment: The recycling of histones links nutrient-dependent microRNAs to the stability of supercoiled DNA in organized genomes via a single amino acid substitution during the life history transition from adolescence to adulthood.
My phys.org comment:

They have linked the nutrient-dependent pheromone controlled chemistry of RNA-mediated protein biosynthesis and degradation from the epigenetic landscape to the physical landscape of DNA in the context of metabolic networks and genetic networks that link the life history transitions of honeybees (and other invertebrates) to the life history transitions of vertebrates, mammals, and primates including humans, via the conserved molecular mechanisms of biophysically constrained RNA-mediated amino acid substitutions and protein folding that differentiate all cell types of all individuals of all genera.
For an example of the link from nutritional epigenetics to pharmacogenomics testing for a single amino acid substitution linked to life-history transitions in human behavior, see: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults

For the link from nutritional epigenetics to pharmacogenomics testing for a single amino acid substitution, which may be the most obvious overlooked link between RNA-mediated amino acid substitutions and to cancer.
Clipping proteins that package genes may limit abnormal cell growth in tumors

“What we found was that histone H3.3 and its clipped form, which lacks 21 amino acids of the histone tail and associated modifications, prevents normal cells from dividing. Clipped H3.3 may be a marker of cells that stop proliferating and has implications for cancer, in particular cancers like melanoma that have a senescence phase.”

My comment: For the most obvious link from the theft of nutrient energy by viruses to life history transitions in behavior and life history transitions linked to cancer via age-related changes in immune system changes, see: Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution. My published comment on the fact that no evolution of the virus could have occurred because the amino acid substitution is nutrient-dependent and thereby biophysically constrained by everything currently known to serious scientists about protein folding chemistry was replaced with this comment from the authors.

The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.

Nutrient energy-dependent base pair changes and RNA-mediated amino acid substitutions link everything currently known to serious scientists about cell type differentiation during the development of morphological and behavioral phenotypes in all living genera. The facts have been placed into the context of this parody. But, most people still have not recognized the links from viruses to perturbed protein folding.

And see also, this parody.

If you are a biologically informed medical practitioner, you are probably already aware of how pharmacogenomics links the conserved molecular mechanisms of biophysically constrained nutrient-dependent RNA-mediated protein folding chemistry during life history transitions that are manifested in healthy longevity or virus-driven pathology.
See, for example:
Would you like to ensure that your treatment regimen meets the current standards of exceptional care that are based on the Precision Medicine Initiative. You and your patients or loved ones do not need to become study participants, although the option may soon become available if the US government funds the testing of all people, not just patients with Medicare coverage. The funding will remain an issue that can be compared to what has been known to some medical practitioners about the links from metabolic networks to genetic networks.
See: Metabolic typing from the 1930’s and Table of Pharmacogenomic Biomarkers in Drug Labeling 150 markers
Many researchers have already joined the ranks of those who are fighting pathology by learning more about why the honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli. Testing is already available that will help you to find what may be the perfect drug.

A Test That Finds the Perfect Drug?


“There is a huge downside: It’s called suffering, time, and money.” “Psychiatry remains the only discipline of medicine that has no test to predict treatment response,” said Evian Gordon, the founder of one such company, Brain Resource. “This is providing, for the first time, an objective step as to which drug might be responsive.”

See also:
DNA methylation and single nucleotide variants in the brain-derived neurotrophic factor (BDNF) and oxytocin receptor (OXTR) genes are associated with anxiety/depression in older women
Neuroendocrine mechanisms underlying behavioral stability: implications for the evolutionary origin of personality
Tracking the Brain’s Functional Coupling Dynamics over Development
Dopaminergic, serotonergic, and oxytonergic candidate genes associated with infant attachment security and disorganization? In search of main and interaction effects
Abstract excerpt:

…specific tests revealed evidence for a codominant risk model for COMT Val158Met, consistent across both samples. Children with the Val/Met genotype showed higher disorganization scores (combined effect size = .22, CI = .10–.34, < .001). Gene-by-environment interaction effects were not replicable across the two samples.

Conclusions:  This unexpected finding might be explained by a broader range of plasticity in heterozygotes, which may increase susceptibility to environmental influences or to dysregulation of emotional arousal. This study is unique in combining the two largest attachment cohorts with molecular genetic and observed rearing environment data to date.

My comment: More than 45,000 published journal articles are indexed on PubMed that mention the role of nutrient-dependent microRNAs, with or without mention of the fact that they link cell adhesion proteins to supercoiled DNA and the stabibility of organized genomes in all living genera. Many of the indexed articles are not likely to mention where the nutrient-dependent microRNAs come from because they link the morphological and behavioral phenotypes of all individuals of all species from metabolic networks to genetic networks. That fact presents a problem to anyone in the medical profession who was taught to believe in the emergence and evolution of pathology via mutations and natural selection.

For example, that is obviously what these researchers were taught to believe or what they want you to believe.

Additive Gene–Environment Effects on Hippocampal Structure in Healthy Humans

Abstract excerpt:

Observed effects were additive by nature and driven by both recent as well as early life events. A consecutive analysis of hippocampal subfields revealed a spatially distinct profile for each genetic variant suggesting a specific role of 5-HTTLPR for the subiculum, BDNF Val66Met for CA4/dentate gyrus, and COMT Val158Met for CA2/3 volume changes. The present study underscores the importance of G × E interactions as determinants of hippocampal volume, which is crucial for the neurobiological understanding of stress-related conditions, such as mood disorders or post-traumatic stress disorder (PTSD).

See also:
The catechol-o-methyltransferase Val158Met polymorphism modulates the intrinsic functional network centrality of the parahippocampal cortex in healthy subjects
Abstract excerpt:

…our findings may provide plausible implications regarding individual differences in the genetic contribution of COMT Val158Met to the brain network and cognition.

My comment: Do they not know that Val158Met represents an nutrient-dependent RNA-mediated amino acid substitution?
The question arises: What are some good books on molecular biology?

Dennis Mitton, Science and technical writer. Uber evolutionist. Deeply agnostic.

I suppose you will have as many choices as respondants.

My comment: Fortunately, no other respondents chose any other outdated (2007) books. Only someone who describes himself as an “Uber evolutionist” who is “Deeply agnostic” would recommend such ridiculous choices.

Description excerpt:

The Third Edition of this landmark text offers an authoritative, accessible, and engaging introduction to modern, genome-centered biology from its foremost practitioners.

My comment: Genome-centered biology and gene-centric theories about mutation-driven evolution have been virtually eliminated from consideration by serious scientists. The pseudoscientists who still tout them failed to integrate any aspect of what is known about physics, chemistry, and the conserved molecular mechanisms of biophysically constrained RNA-mediated protein folding chemistry. Why bother to read any books written by authors like that?

See also: Underlying Mechanisms of Gene–Environment Interactions in Externalizing Behavior: A Systematic Review and Search for Theoretical Mechanisms


…we argue that one way to help resolve this problem is the development of theory-driven a priori hypotheses on which biopsychosocial mechanisms might underlie cG × E. Such a theoretically based approach can help us specify our research strategies, create more comparable findings, and help us interpret different findings between studies. In accordance, we describe three possible explanatory mechanisms, based on extant literature on the concepts of (1) emotional reactivity, (2) reward sensitivity, and (3) punishment sensitivity. For each mechanism, we discuss the link between the putative mechanism and externalizing behaviors, the genetic polymorphism, and family adversity. Possible research strategies to test these mechanisms, and implications for interventions, are discussed.

My comment: I argue that anyone who is still taking a theoretically-based approach to links from ecological variation to nutrient-dependent healthy longevity or to pathology in the context of life history transitions via hormone-organized and hormone-activated behaviors in all invertebrates and vertebrate will not still be practicing medicine by the end of this decade. If they are still practicing, they will probably lose any accumulated wealth in the context of malpractice after they lose their malpractice insurance because they have not kept up with current practice guidelines, which link atoms to ecosystems in all living genera via their nutrient energy-dependent physiology of reproduction.

Excerpt 2)

Another issue concerning cG × E is that there is a lack of insight into biopsychosocial mechanisms that underlie such interactions (see also Battaglia 2012; Dodge 2009; Salvatore and Dick 2015). At present, looking at cG × E findings is like looking at a “black box,” in that we are only aware of what goes in and what comes out. However, insights into how these G × E interactions work (i.e., “how genes get outside the skin,” Reiss and Leve 2007) is of great empirical and clinical importance.

My comment: Brain on stress: How the social environment gets under the skin explains how G × E interactions work, and the Correction for McEwen, Brain on stress: How the social environment gets under the skin is a clear indicator that medical practitioners must learn to distinguish between epigenetic effects on hormones and the affects of hormones on behavior during life history transitions that link the honeybee model of morphological and behavioral diversity during life history transitions to all other animal models via a single amino acid substitution.

Excerpt 3)

The COMT polymorphism is a SNP (rs 4680) resulting in a valine (i.e., Val) to methionine (i.e., Met) mutation.

My comment: That ridiculous claim makes the need for continuing education perfectly clear. If someone who is nicer than I am tells you to please become biologically informed, I hope you will take the opportunity to do so.

Excerpt 1)

But to make proteins, first the DNA genomic information must be transcribed with complete fidelity, chemical letter by letter into an intermediary molecule, called messenger RNA, or mRNA. In what is known as the central dogma of biology, DNA makes RNA, which makes protein.”

Excerpt 2) “Small RNAs, called micro RNAs (miRNAs), work to pair with a UTR to block translation, killing the message, and thus, silencing a gene. Uncovering the interplay between miRNA and their specific UTRs have become a hot area in biology, and big business.”

My comment: Obviously, someone needs to tell the folks in ASU’s Center for Evolution, Medicine and Public Health that they are about to be forced off the campus via the works of a science fiction author and serious scientists who have since linked atoms to ecosystems across all living genera.

Evolutionary medicine, or Darwinian medicine, is the application of modern evolutionary theory to understanding health and disease.

Attempt to apply any theories to the practice of medicine have failed miserably and caused more suffering and death that could ever be imagined until after viruses kill more people than ever before. Perhaps they will kill us all. If so, the deaths will be attributed to neo-Darwinian evolutionary theory.

 Today, Perry Marshall appeared on the CBS station in Richmond Virginia, WTVR Channel 6, talking about Evolution 2.0! Perhaps Randy Nesse will ask him to speak at ASU sometime soon. After all, the Hippocratic Oath supposedly is one of the oldest binding documents in history.

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