The 1902 definition of mutation by Hugo de vries can again be placed into the context of facts about energy-dependent RNA-mediated cell type differentiation and healthy longevity before anyone else attempts to redefine heredity. Hopefully, that will be done before anyone else from the CDC goes missing. The threat to thos who understands how top-down causation is linked to the transgenerational epigenetic inheritance by cell survival is severe because they have linked virus-driven energy theft from mutations to the death gene. For comparison, mathematical models link mutations to evolution.
Historical perspective:
De Vries’s theory was one of the chief contenders for the explanation of how evolution worked, leading, for example, Thomas Hunt Morgan to study mutations in the fruit fly, until the modern evolutionary synthesis became the dominant model in the 1930s. Somewhat ironically, the large-scale primrose variations turned out to be the result of chromosomal duplications (polyploidy), while the term mutation now generally is restricted to discrete changes in the DNA sequence.
Thomas Hunt Morgan won the Nobel Prize in Physiology or Medicine in 1933 for discoveries elucidating the role that the chromosome plays in heredity.[2]
See also: Feedback of the Drosophila period gene product on circadian cycling of its messenger RNA levels (1990), which was co-authored by Michael Rosbash who shared the 2017 Nobel Prize in Medicine for development of the cryo-EM technology. Cryo-EM links energy-dependent changes in electrons to ecosystems via the physiology of reproduction and chromosomal rearrangements that biophysically constrain viral latency in all living genera.
See for comparison, this attack on my scientific credibility by P.Z. Myers: One crank dies, another rises to take his place
I wrote:
The proof of ecological variation that appears to refute the theory of evolution, which actually refutes itself, is that ecological adaptations occur too fast for mutations to compete with them as a source of anything but diseases and disorders.
Since December 25, 2017 I have been using my twitter account to reach a larger target audience at a pace of about 100,000 impressions each month. For example, my top tweet in February got 12,500 impressions. I wrote:
See also:
https://t.co/ctmkUlnsrL "…provides insight for a better understanding of miRNA-elicited antiviral responses against IAVs and raises potential interest in the delivery of exogenous miRNAs as a therapeutic approach for antiviral therapy."
— James V. Kohl (@jvkohl) March 7, 2018
See for comparison: https://t.co/gSfr1JKuyC by @carlzimmer who has, like other so-called science journalists, failed to link food energy-dependent changes in the miRNA/mRNA balance to biophysically constrained viral latency and healthy longevity in species from microbes to humans
— James V. Kohl (@jvkohl) March 7, 2018
https://t.co/iF6OOoCGoi He published at least two articles that linked interethnic similarities and differences in RNA-mediated amino acid substitution to sex differences in disease via what is known to all serious scientists about biophysically constrained viral latency.
— James V. Kohl (@jvkohl) March 7, 2018
He is not the same person who linked an orally available anti-inflammatory cell survival peptide from a class of reparative chaperones called heat shock proteins to effective treatment and/or prevention of neurodegenerative diseases. https://t.co/jw9HpFcyyj
— James V. Kohl (@jvkohl) March 7, 2018
https://t.co/05pHAxKqsF The similarities and differences between the two Timothy J. Cunninghams are as clear as the interethnic similarities and differences they helped to establish before one of them disappeared without a trace.
— James V. Kohl (@jvkohl) March 7, 2018
See also: Ecological adaptation: A new definition of heredity (3)