#SFN2019 to 2012: Hiding the facts (2)

By: James V. Kohl | Published on: October 17, 2019

Polycomb repressive complex 1: Regulators of neurogenesis from embryonic to adult stage extends our 1996 claims in From Fertilization to Adult Sexual Behavior to all ethnic diversity in morphology and behavior via alternative splicings of pre-mRNAs.
The term use began to change from pre-mRNAs to microRNAs. I learned that from the abstract of a presentation at SFN 2012, and followed up on the presentation with others who were presenting posters that mentioned microRNAs.
I had already presented during the 2012 ancillary meeting of the Society for Social Neuroscience Presentation. That is why the term microRNA interested me.  I asked if microRNAs were the link to all downstream effects on cell type differentiation, and the speaker said “That’s what we have learned during the past ten years.”
See why that fact is important. This is what I presented in 2012:
Poster A15, Thursday, October 11, 6:30 – 8:00 pm, Grand Ballroom D, Hilton Riverside Hotel
Human pheromones and nutrient chemicals: epigenetic effects on ecological, social, and neurogenic niches that affect behavior.

Background: The 2007 iteration of the “FDA Critical Path Initiative” (FDACPI) is a systems biology approach to disease prevention and pharmacogenomics. It stresses the need to examine healthy behavioral development by including interactions among the evolved gene, cell, tissue, organ, organ-system pathway. This pathway links the epigenetic effects of nutrient chemicals and pheromones directly to the organization and activation of behavior in species from honeybees to humans.

The 2011 American Society of Addiction Medicine (ASAM) Public Policy Statement: ‘Definition of Addiction’ dictates the integration of the FDACPI’s neuroscientific principles of epigenetic cause and effect, which are required to understand differences between genetically predisposed brain disease, naturally occurring variations of behavioral development, and choice. These neuroscientific principles include focus on how sensory input influences behavior.

ASAM specifically mentions food and sex along with drugs and alcohol. Each of these influences chemically conditions changes in hormones and in behavioral responses.

Study design: Nutrient chemical signals are associated with food odors. Pheromones are chemical signals associated with social odors and sex differences. We incorporated what is currently known about the ability of chemical signals to condition behavior. This conditioning occurs via epigenetic effects that calibrate and standardize the molecular biology of intracellular signal transduction and stochastic gene expression, which controls the feedback loops of developmental processes required for movement, ingestion, reproduction, and the diversification of species from microbes to man.

Method: Pre-existing, adaptively evolved, nutrition dependent, hormone-driven, cyclic peak fertility in fourteen women was assessed by a non-invasive measure of luteinizing hormone (LH). During a double-blind social construct, the women were exposed for fifteen minutes to a man who had applied either a control mixture (n=7), or a mixture of androstenol/androsterone (n=7). Both mixtures contained the same masking odor. Summary: Evaluated video recordings of interactions showed increased flirtatious behaviors of women, which were statistically attributed to the effect of androstenol on LH and the unconscious affect of androsterone. Measures of self-reported increased attraction correlated with the increased flirtatious behaviors.

Conclusions: Across species comparisons of epigenetic effects on nutrition dependent and hormone-driven invertebrate and vertebrate social and sexual behavior indicate that the androstenol/androsterone mixture contains pheromones, which may increase opportunities for properly timed reproductive sexual behavior. Neuroscientifically established epigenetic effects of sensory input on hormones that affect behavior suggest that this mixture of human pheromones causes changes in ecotypically organized neural pathways that directly link nutrient chemicals and social niches to 1) neurogenic niches; 2) the molecular biology of evolved neural circuitry; 3) genetically predisposed physiological changes, and to 4) unconscious affects on behavior in species from invertebrates to mammals. The molecular biology is conserved and transgenerational epigenetic inheritance establishes the pre-existing genetic variation. Our results tentatively extend epigenetic effects on intracellular signaling, gene expression, hormones, and unconscious affects on behavior, which are due to food odors and pheromones in insects, to socioaffective neuroscience in people despite pre-existing genetic variation and phenotypic differences in nutrition dependent hormone-driven development of the brain, and differences in the development of social and sexual behaviors.

Summary of our facts about human pheromones:
It subsequently became clear that microRNAs were the link from pre-existing genetic variation to all phenotypic differences in the nutrient-dependent hormone-driven development of the brain, and differences in the development of social and sexual behaviors.
Food energy-dependent pheromone-controlled biophysically constrained viral latency has since been linked from the light-activated assembly of the microRNA-RNA-peptide nanocomplex to every aspect of biodiversity across kingdoms.


What happened with the term pre-mRNA when it was changed to microRNA obfuscated pattern recognition with use of older non-descriptive terms such as  ‘polycomb repressive complex’ instead of ‘microRNA-RNA-peptide nanocomplex’ which has also been referred to as the ‘Skp1/cullin/F-box (SCF) complex.’
The different names for the same nanocomplex have been linked to healthy longevity or to cancer via use of the terms such as ‘spasmolytic polypeptide-expressing metaplasia’ in the context of transthiolation, a fundamental biological reaction that is utilized by many enzymes such as the light-activated ubiquitin-conjugating enzyme, cdc34.
But, only the names have changed. The facts link light-activated microRNA biogenesis from the Creation of enzymes to all biodiversity on Earth. MicroRNA biogenesis is required to biophysically constrain viral latency, which is required for the genesis of all biophysically constrained biodiversity.
I reiterate. For confirmation of the facts, which have not changed, see these presentations during the 2019 Annual Meeting of the Society for Neuroscience
683.03. Hypothalamic microRNA-7 regulates energy homeostasis in vivo
552.08. MicroRNA regulation of inhibitory synaptic plasticity
642.23. Behavioral characterization of mice deficient for the mammal-specific microRNA 379-410 cluster
649.08. Profiling of neuronal and microglial argonaute-2 bound microrna during epileptogenesis and in chronic epilepsy reveals cell-type specific contribution to disease
036.07. Regulation of brain synapses and behaviour by miR-138
734.26. Unique blockage of host RNAi machinery by the zika virus capsid in fetal NSCs and mouse model
076.22. A rodent model of early life stress (ELS) associated with altered miRNA expression in rat hypothalamus
126.20. Specific microRNAs (miRNAs) play major roles in human diseases
236.07. Profiling brain-derived exosomes in the prefrontal-cortex of individuals with major depressive disorder
602.01. Odor preference training in week-old rat pups is associated with changes in protein and non-protein coding messenger ribonucleic acids in odor-encoding mitral cells
602.05. Synaptogenesis and neuronal activation dependent on MeCP2/CaMK2A phosphorylation signaling pathway
640.12. Micrornas and histone deacetylase inhibition mediated differentiation of human mesenchymal stem cells into neuronal lineage
704.03. Isoform analysis of blood transcriptomic biomarkers for depression in human lymphocytes and hippocampal tissue
628.04. Programmable modulation of extracellular vesicles
736.15. Spatio temporal dynamics of miRNA mediated regulation of local protein synthesis
776.21. Blood microRNAs as biomarkers for stress susceptibility or resiliency and treatment response
In Patented Creation vs Evolution of Disease (9), I wrote

For the historical perspective on works from E. J. NESTLER, see: Transgenerational Epigenetic Contributions to Stress Responses: Fact or Fiction? 3/25/16

Despite the two extremes of disbelief versus wild speculation, there is growing evidence for at least some contribution of epigenetic regulation—perhaps achieved by miRNAs—in mediating part of the ability of parental behavioral experience to influence stress vulnerability in their offspring.

Growing evidence has turned into overwhelming evidence that energy-dependent biophysically constrained microRNA-mediated viral latency is required for the the transgenerational epigenetic inheritance of healthy longevity.

The take home message from the 2019 Annual Meeting of the Society for Neuroscience should be something the helps biologically uninformed theorists and other science idiots accept the facts that link nutrient stress and or social stress to all pathology via the works of Bruce S. McEwen.
Moving forward. See: Bruce McEwen et al.
018.08. Role of the ventral hippocampal circuit in generating and regulating cognitive responses to stress and a novel antidepressant
The ventral hippocampal circuit has emerged as a target for the responses to stress and antidepressant action, including the rapid actions of the novel glutamatergic agent acetyl-L-carnitine (LAC). Previous research has shown that chronic stress causes bot…
240.27. Oxycodone injections not paired with conditioned place preference have little effect on the hippocampal opioid system in female and male rats
…changes in the hippocampal opioid system that would promote opioid-associative learning processes do not occur with administration of oxycodone alone, and instead must be paired with CPP.
240.28. Sex and chronic stress differentially alter phosphorylated mu and delta opioid receptor levels in the rat hippocampus following oxycodone conditioned place preference
240.29 / W1 – Sex differences in the mRNA expression of opioid peptides and receptors in the rat hippocampus
…sex-dependent changes in opioid-associated genes and receptors in the hippocampus following CIS are paralleled with an inability for males, but not females, to acquire conditioned place preference (CPP) to mu-agonist oxycodone. Here, RNAScope in situ hybridization was used to determine if the expression of hippocampal opioid peptides and receptors is altered in unstressed (US) and CIS estrus female and male rats.
293.04. Divergent roles of astrocytic versus neuronal glutamate transporter EAAT2 deficiency on cognition and overlap with aging and Alzheimer’s molecular signatures
594.22. What happens to the infant during maltreatment? Stress targets hippocampus but stress with mother targets amygdala and social behavior
675.16 / P5 – Individual differences in aggression mediated by temporal changes in cytokine signaling in the dorsal raphe nucleus
These data also supports an involvement of endogenous IL-1β in aggressive behaviors, however, the source of IL-1β in the dorsal raphe nucleus is still not clear and requires further investigation.
636.04 – Transcriptional profiling of the stressed hippocampus: Does sex make a difference?
This favors the use of big data to probe dissimilar gene functions that underlie sex-specific endophenotypes in animal models of stress.
769.02 / Q8 – Estrogen receptor beta agonists block slow-onset angiotensin II hypertension and reduce NMDA receptor-signaling in paraventricular neurons in female mice at an early stage of accelerated ovarian failure
These results suggest that heightened NMDA receptor signaling in ERβ-expressing PVN neurons contributes to the susceptibility of peri-AOF mice to the hypertensive actions of AngII. These findings provide preclinical evidence supporting a therapeutic window of opportunity for estrogen-based management of hypertension as women transition through menopause.

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