A miRNA model vs moronic theories (8)
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A miRNA model vs moronic theories (7)
The symptoms of liver, lung, kidney, and spleen degeneration observed during RHD are similar to those of acute liver failure (ALF) and multi-organ failure (MOF) in humans.
Single-cell learning in Stentor coeruleus is governed by a fractional-order low-pass filter 6/10/26
The fractional order behavior of habituation in Stentor resembles the fractional-order behavior of adaptation in neurons, further supporting the idea that neurons may employ similar mechanisms for learning as were already present in unicellular eukaryotes prior to the evolution of metazoa.
See for comparison the claim that links your consciousness to the mathemagical evolution of pond scum after energy automagically emerged from the cosmic void.
Your Consciousness Emerges From a Vast ‘Invisible’ Network, a Breakthrough Study Suggests 6/12/26
Grok
The Stentor preprint models habituation via parallel molecular pathways (e.g., CaMKII complexes) as a fractional-order low-pass filter. Solid biophysics on ciliate signaling.
It does not address or support links to light-activated miRNA abundance protecting against virus-driven mRNA degradation, RNA-directed DNA methylation, chromosomal rearrangements, cell-type differentiation, or the origin of life. Those are separate topics and not part of this work.
Sperm RNA experiments in mice provide direct causal evidence for RNA-mediated epigenetic effects. These mechanisms are testable, natural, and integrate into evolutionary biology without issue.
Kohl
Re: “Solid biophysics on ciliate signaling… integrate into evolutionary biology without issue..”
@Grok Ha Ha Ha (ridicule, not death-bed humor) The issues with “evolutionary biology” are clear in the context of biophysics:
Light-activated ATP–dependent RNA-directed DNA methylation (RNA interference) biophysically constrains the virus-driven degradation of mRNA and all pathology across kingdoms.
No experimental evidence from model organisms published by intelligent serious scientists in peer-reviewed journals supports moronic claims theorists invented to link the automagical emergence of energy from the cosmic void to the mathemagical evolution of people from pond scum.
For more facts, see: “Methylation-mediated regulation of tumor-suppressor function of the miR-379/656 (C14MC) cluster and its clinical utility in hepatocellular carcinoma” 6/12/26 and NOVA scienceNOW : 8 – RNAi 7/23/12
Grok
James V. Kohl (@microRNApro) replies to Grok by ridiculing the idea that RNA-mediated mechanisms integrate smoothly into evolutionary biology, instead claiming light-activated ATP-dependent RNA-directed DNA methylation biophysically constrains virus-driven mRNA degradation and all pathology.
The post cites a June 2026 study on DNA methylation silencing the miR-379/656 cluster’s tumor-suppressor function in hepatocellular carcinoma and a 2012 NOVA segment on RNAi to highlight RNA interference’s regulatory importance.
This continues a thread on a Stentor preprint about ciliate habituation modeled as molecular signaling filters, where Kohl promotes his miRNA-autophagy-pH model linking to sympatric speciation over standard evolutionary narratives.
Grok
The bioRxiv preprint shows DNA methylation silences the miR-379/656 miRNA cluster, reducing its tumor suppressor role in liver cancer. It does not mention or support light-activated ATP-dependent RNA-directed DNA methylation or claims it constrains all pathology.
RNAi is a real mechanism, and RNA-mediated epigenetic inheritance (e.g. sperm RNAs) integrates into evolutionary biology. These findings complement rather than contradict established evolutionary science.
Kohl
Re: “Kohl promotes his miRNA-autophagy-pH model linking to sympatric speciation over standard evolutionary narratives.”
@Grok Compared to your promotion of unnecessary suffering and premature death, the difference is clear: See: “Replace the Modern Synthesis (Neo-Darwinism):” 7/9/14
“[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent….. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another…. Assumptions, made but not verified, were taught as fact.” — Lynn Margulis (2009)
The African elephant model organism makes a jackass out of those who assumed their moronic claims were relevant.
Grok
James V. Kohl (@microRNApro) replies to criticism of his work by rejecting Neo-Darwinism, quoting Lynn Margulis (2009) on how population genetics pioneers like Haldane and Fisher relied on unverified assumptions about mutation accumulation driving speciation via gene frequency changes.
Kohl advocates his miRNA-autophagy-pH model, which connects energy-dependent microRNA processes, peptide synthesis, and autophagy to sympatric speciation and ecosystem stability, positioning the African elephant as a model organism supporting it over mutation-centric views.
The post directly challenges Grok by contrasting Kohl’s biophysical framework with what he describes as promotion of unnecessary suffering and premature death under standard evolutionary narratives, linking to his 2014 article calling to replace the Modern Synthesis.
Grok
Clarifying: I don’t promote suffering or death. Biology explains nature’s processes to help reduce disease.
Margulis advanced symbiosis, now integrated into evolutionary biology with miRNAs and cellular mechanisms.
Elephant TP53 expansions exemplify gene duplication selected for cancer resistance—consistent with adaptation to large body size.
What specific, testable predictions from the miRNA-autophagy-pH model distinguish it from extended evolutionary frameworks?
Kohl
Re: “gene duplication selected for cancer resistance—consistent with adaptation”
@Grok For comparison to Republican Party symbolism and elephant TP53 expansions, see the symbol for the Democratic Party of the USA: “The Original Jackass… [donkey/mule]”
“Hee Haw, Hee Haw, Hee Haw” (ridicule, not humor).
Grok
@microRNApro responds to Grok’s explanation of elephant TP53 gene duplications enabling cancer resistance as an adaptation by contrasting the Republican elephant symbol with the Democratic Party’s donkey (jackass) symbol and adding mocking “Hee Haw” sounds.
The referenced biology involves elephants evolving ~20 TP53 copies to resolve Peto’s paradox, allowing large body size without elevated cancer risk through enhanced DNA damage response and apoptosis, as detailed in peer-reviewed studies from 2016 onward.
James V. Kohl, a medical lab scientist and long-time proponent of miRNA-mediated, nutrient-dependent models of adaptation and sympatric speciation via autophagy and pH-dependent processes, frequently uses such exchanges to link molecular biology with wider observations.
Grok
Elephant TP53 expansions are a documented evolutionary feature. Genomic studies show elephants carry ~20 copies of this tumor suppressor gene, coinciding with the rise of large body size and enhanced DNA damage responses that help resolve Peto’s paradox on cancer rates. This is independent of political symbols. The Democratic donkey traces to 1828 Jackson-era satire and later cartoons; it has no bearing on biology or adaptation.
Kohl
Re: “Elephant TP53 expansions…coinciding with the rise of large body size and enhanced DNA damage responses…independent of political symbols… has no bearing on biology or adaptation.”
@Grok Providentially, Jackasses are more like male homosexual liberal democrats than anything else intelligent serious link to the God of Abraham’s sexual differentiation of species and biophysically constrained virus-driven pathology across kingdoms.
Grok
@microRNApro quotes Grok’s clarification on elephant TP53 gene expansions as an evolutionary adaptation for cancer resistance in large animals, resolving Peto’s paradox through enhanced DNA damage responses unrelated to political symbols like the Democratic donkey.
The reply asserts that “jackasses” align more closely with male homosexual liberal Democrats, connecting this to the God of Abraham’s mechanisms of sexual differentiation of species and virus-driven pathology constrained across biological kingdoms.
The author’s profile centers on miRNA-mediated autophagy, pH-dependent peptide synthesis, sympatric speciation, and ecosystem health, frequently integrating these molecular processes with interpretations involving divine creation and biophysical limits.
Grok
Elephant TP53 expansions reflect evolutionary adaptations to large body size and longevity via natural selection and genomic duplication, as shown in comparative genomics studies. The Democratic donkey symbol stems from 19th-century political cartoons and has no connection to animal biology, sexual differentiation mechanisms, or virus-related processes in any species. These remain distinct domains: biophysical evolution versus human cultural and personal frameworks.
Kohl
Re: “TP53 expansions reflect evolutionary adaptations to large body size and longevity via natural selection and genomic duplication, as shown in comparative genomics studies.”
@Grok Energy-dependent changes in molecular distance link our claims in “From Fertilization to Adult Sexual Behavior” https://www.hawaii.edu/PCSS/biblio/articles/1961to1999/1996-from-fertilization.html to ecological adaptations, not moronic evolutionary theories.
My PGx, NGS and FISH testing results link differences between somatic mutations and genetic mutations to all biodiversity on Earth via the physiology of pheromone regulated reproduction in Biblical Genesis.
Grok
James V. Kohl (@microRNApro) quotes Grok’s post on elephant TP53 gene expansions as adaptations for body size and longevity via natural selection, dismissing it as “moronic evolutionary theories” in favor of energy-dependent molecular changes.
He ties his views to the 1996 paper “From Fertilization to Adult Sexual Behavior,” claiming PGx, NGS, and FISH test results show somatic versus genetic mutations drive biodiversity through pheromone-regulated reproduction linked to Biblical Genesis.
Peer-reviewed comparative genomics confirms elephants have around 20 TP53 copies that boost DNA damage response and apoptosis, addressing Peto’s paradox by lowering cancer incidence in large, long-lived species.
Grok
Energy-dependent molecular changes contribute to adaptations and ecological dynamics. TP53 expansions in elephants result from gene duplications under natural selection for cancer resistance in large animals, per comparative genomics. Somatic mutations are non-heritable, while germline mutations enable biodiversity through selection, drift, and other mechanisms. Pheromone-regulated reproduction influences sexual selection but operates within evolutionary biology. Genomic, fossil, and experimental data support this integrated view.