miRNA constrained life (9)

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miRNA constrained life (8)

@Grok “See: “From fertilization to adult sexual behavior” (1996), “Insect pheromone in elephants” (1996) and “Vibrations in microtubules” (1997):

“the quantum world doesn’t stop at the cell membrane. It reaches deep into the molecular machinery of life — all the way to the cytoskeleton itself.”

[The energy-dependent Creation of the cytoskeleton biophysically constrains the virus-driven degradation of mRNA linked to all pathology.]

Moving forward:

Grok

Thanks for the note on nomenclature—c-fos (official symbol FOS) is the classic cellular proto-oncogene in the Fos/AP-1 family. Recent Kyoto University/PNAS work traces Fos orthologs and expression programs to unicellular holozoan ancestors (~700 mya), with functional tests in Capsaspora showing ancestral roles later repurposed for macrophage-like cells in early animals. miRNA regulation and pH effects fine-tune FOS in modern cells, but comparative genomics and experiments support the deep conservation of this toolkit.

Re: “Deep conservation” aka moronic theories.” See: Greg Bear, “When Genes Go Walkabout” 11/11/11

See also from 2/17/14:

Diverse heliorhodopsins detected via functional metagenomics in freshwater Actinobacteria, Chloroflexi and Archaea 1/4/22

Few people will notice and no one else will report they have linked the light-activated energy-dependent fixation of RNA-mediated amino acid substitutions to biophysically constrained viral latency across kingdoms via protonated RNA interference.

They inadvertently linked former President Trump’s claim that sunlight & humidity weaken coronaviruses from peptide synthesis at the origin of life to viral latency across kingdoms via the patent for naturally occurring RNA interference.

Yesterday, the former director of the CDC claimed that: “The higher the proportion of people with immunity, either through vaccination or infection, the stronger the selective pressure on the coronavirus to mutate in ways that can evade our immunity.”

That puts former President Trump’s claim about sunlight & humidity at the forefront of efforts to stop coronavirus transmission in the context of this 2007 report from CDC researchers: “A Two-Amino Acid Change in the Hemagglutinin of the 1918 Influenza Virus Abolishes Transmission”

Other public health fascists, besides @DrTomFrieden, and Grok are playing a dangerous game of obfuscation at the same time the facts about biophysically constrained viral latency are becoming perfectly clear. See also: The Darwin Code 4/14/15 (at RNA-mediated.com)

Never forget, Sofia Tomov’s algorithm now links PGX, NGS and FISH testing to prevention of medication errors linked to virus-driven mental and physical pathology via “The importance of brain heath for veterans” on page 32 in the June 2026 issue of the American Legion Magazine.

Unsolved Mysteries & Natural Wonder Facts

“At twelve, she wrote an algorithm that scanned the human genome for the specific mutations that turn ordinary prescription drugs into poisons.

Sofia Tomov was homeschooled in Knoxville, Tennessee, the daughter of a teacher and a computer scientist. By the time most kids her age were starting middle school, she had already filed a provisional patent — at eleven — for a device to safely dispose of unused prescription medications and keep them out of the water supply. The drug disposal patent came out of a problem she had read about and decided to think harder about than the people she had read.

Then she encountered the harder problem.

Adverse drug reactions kill more Americans each year than car accidents. The standard estimate — repeated in pharmacology textbooks and the Journal of the American Medical Association — is that adverse drug reactions are somewhere between the fourth and sixth leading cause of death in the United States, depending on how you count them. Most of these deaths are not the result of dosing errors or mismatched prescriptions. They are the result of genetic variation. A small number of common mutations in genes that govern how the body metabolizes drugs — CYP2D6, CYP2C19, TPMT, DPYD, and others — can turn a standard dose of a routine medication into a fatal one in the patient carrying the mutation. The science of this has been settled for decades. It is called pharmacogenomics, and it is one of the more frustrating fields in modern medicine because everyone agrees it would save lives if it were deployed and almost no one’s healthcare system is set up to actually deploy it.

[My pharmacogenomics testing revealed CYP2D6 linked reduced enzyme activity and CYP2C19 duplication to ultrarapid metabolism of antidepressants and altered responses to medications with codeine, and a COMT Val158Met polymorphism, which has been linked to mass killings and murders via medication errors.]

Tomov, at twelve, decided to do something about a small piece of the problem.

Standard genomic analysis software in 2016 scanned the entire human genome — about three billion base pairs — looking for variants of interest. This took hours, sometimes days, on the kind of computing infrastructure most hospitals had. In an emergency, by the time the analysis finished, the patient who needed the drug decision had often already received the drug. Tomov’s insight was that you don’t need to scan the whole genome. You need to scan only the small handful of regions that are known to affect drug metabolism. She wrote an algorithm that filtered to those regions specifically and ran the analysis in seconds rather than hours.

She was one of ten finalists in the 2016 Discovery Education 3M Young Scientist Challenge with the project. She was profiled by US News & World Report, The Telegraph, and Business Insider. The University of Tennessee admitted her as a visiting high school student that fall, at age twelve, so she could take university computer science courses.

In 2018, at fourteen, she gave a TEDxUTK talk called Make the Pill Fit the Ill, which is still available online. That same year, she won first place in the Translational Medicine category at the International Science and Engineering Fair — the largest pre-college science competition in the world.

Her algorithm has not become standard clinical practice in the years since. The reason for this is not, as is sometimes suggested in stories about young women in science, that institutions refused to adopt it. The reason is that the deployment of routine pharmacogenomic screening in everyday medicine is a vastly larger problem than any one algorithm can solve. It requires routine and affordable whole-genome sequencing for every patient, durable storage of that data, integration with electronic medical records, training of clinicians who were never taught pharmacogenomics in medical school, insurance coverage decisions, patient privacy frameworks, and a level of pharmacogenomic literacy in primary care that does not yet exist anywhere in the world. Sofia Tomov did not solve that problem at twelve. Almost no one has solved it at any age.

What she did at twelve was identify a real technical bottleneck in one part of a much larger system, propose a working solution to that bottleneck, and demonstrate it cleanly enough to win a major scientific prize for the work.

That’s enough. It does not need to be more than it is to be remarkable.

She is now in her early twenties. The verifiable public record of her work largely covers her years between eleven and sixteen. What she is doing now is — appropriately — less public than what she was doing when news organizations were chasing her as a prodigy story. The interesting question about her career is not whether her childhood algorithm is in hospitals. It is what someone who was capable of that work at twelve will produce when she has had another twenty years to develop.

She didn’t solve adverse drug reactions at twelve.

She showed, at twelve, that the part of the problem she could see clearly enough to attack — she could attack.”

Her algorithmic attack on moronic theories links Interplay between viral infections and gut microbiota dysbiosis: Mechanisms and therapeutic potential 1/21/26 from my model of biophysically constrained viral latency via Plant cell wall-plasma membrane attachments mediate stress resilience through cellulose synthase complexes and remorins 6/2/26, Merian’s (1679) diet of caterpillars and their metamorphosis into moths, Darwin’s (1859) conditions of life, and Celluose: A Plant Cell Biology Game (for ages 14+).

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