Biology to a Physicist

Becoming biologically informed (2)

New Perspectives on microRNA in Disease and Therapy

Free Webinar
Wednesday July 22, 2015
2:30 – 4:00 PM EDT

MicroRNAs play an important role in modulating gene expression. Characterizing the mechanism of action of microRNAs and identifying microRNA targets is critical for understanding the function of microRNA in development and disease. The Scientist brings together a panel of experts to discuss various microRNA functions. Topics to be covered include the role of microRNA in cancer and viral infection, and the therapeutic targeting of microRNA.
Dr. Benjamin tenOever see: Benjamin tenOever: Going Viral

“It dawned on me that just because these microRNAs are not antiviral does not mean they could not be antiviral.” In other words, why not engineer viruses to be vulnerable to the microRNAs present in mammalian cells? TenOever and his colleagues designed an influenza virus that is crippled by the microRNAs present in mice.3

Dr. Andrea Kasinski

In some instances the combination of multiple subtle changes causes the tumor cells to become addicted to a single miRNA. MiR-21 and miR-155 are two oncogenic miRNAs (oncomiRs) that have shown this type of addictive pattern in vivo. Similarly loss of key tumor suppressive miRNAs, through epigenetic silencing, genomic loss, and reduced upstream signaling and processing, has been correlated with disease state. Based on this knowledge we have embarked on three very distinct yet equally important areas of miRNA therapeutic biology.

My comment: Thermodynamic cycles of protein biosynthesis and degradation appear to link the effects of viral microRNAs to entropic elasticity and the effects of nutrient-dependent microRNAs to proper cell type differentiation. Perturbed protein folding caused by viruses and viral microRNAs links them to pathology that is prevented by the anti-entropic epigenetic effects of nutrients, which enable the fixation of RNA-mediated amino acid substitutions that stabilize the organized genomes of all genera via their physiology of reproduction. Nutrient stress and social stress perturb the thermodynamic cycles of protein biosynthesis and link mutations to virus-driven pathology.
See, for details, my invited review of nutritional epigenetics and pharmacogenomics. Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man. Species diversity is a biologically-based nutrient-dependent morphological fact and species-specific pheromones control the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection of nutrients cause the behaviors that enable ecological adaptations. Species diversity is ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. This is known: Olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man during their development.

Attend the webinar to learn more about the paradigm shift. Tell others about the free webinar, especially those who may be willing to help serious scientists who are Combating Evolution to Fight Disease. 
Serious scientists need all the help they can get from others who are biologically informed.
The biologically uninformed continue to tout the pseudoscientific nonsense of their ridiculous theories, and their idiot minions continue to follow their lead. See for example: One crank dies, another rises to take his place
Excerpt: Evolution was all due to chromosome rearrangements, which somehow are not mutations, and he also somehow ignored the existence of allelic differences between species
PZ Myers is not capable of understanding biologically-based cause and effect.
Ecological variation is linked to ecological adaptations in all living genera via virus-driven chromosomal rearrangements and the physiology of nutrient-dependent reproduction. Obviously, the evolution industry and the big bang cosmology industry need new leaders who are biologically informed.
Since the 1940’s, evolutionary theorists have continued to cause the unnecessary suffering and death of millions that will receive effective treatments via the New Perspectives on microRNA in Disease and Therapy.
Since Dobzahsnky (1973), serious scientists have known that “…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” (p. 127).
Since last year, serious scientists have known that a single RNA-mediated amino acid substitution during  the life history of humans links behavioral transitions to other species.
For example, see: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults. The A or Met allele is associated with lower enzymatic activity (due to thermoinstability), and with exploratory behavior.
Attempts to place these single amino acid substitutions into the context of ridiculous theories about mutation-driven evolution fail to address anything known to serious scientists about biologically-based cause and effect.

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