Physics

Virus-driven energy theft: definition?

The FB group antagonists at “Creationism” complain that I am the only one who uses the term “virus-driven energy theft.” They want a definition, and they demand that I tell them my religious beliefs. Young-earth creationist, or not? It’s one of the “False Flag” FB groups, where impersonators claim to be well-educated experts from different disciplines, who then tout their expertise when they attack creationists at every level including denigration of published works and personal denigration of people’s worth.

The impersonators and antagonists cannot understand why serious scientists do not typically use definitions and assumptions to set forth a case for creationism or an alternative to it,  such as mutation-driven evolution. And, as everyone who understands the concept of the “False Flag” in movies about pirates, the pirates in the Creationism will steal all your energy and claim your intellectual property has always belonged to them.

See for example: Replace the Modern Synthesis (Neo-Darwinism): An Interview With Denis Noble

Excerpt:

[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.

Do I owe the impersonators and antagonists  a definition of “virus-driven energy theft” that they can compare to the definition of evolution and their assumptions. Of course not, but let me explain why. First, virus-driven energy theft is a fact. Cells use energy to reproduce, but viruses must steal that energy to replicate. That fact explains why there are different death rates in archaea compared to bacteria in the oceans and everywhere else.

The bacteria and all other living genera have an innate immune system that links what they eat to the physiology of reproduction via energy transfer. For example, the sun’s biological energy can be used for photosynthesis, but ultraviolet (UV) light is virucidal.

I’ve reported that fact here repeatedly in the context of what is known about UV light and RNA-mediated DNA repair, which exemplifies how quantized energy protects all organism from virus-driven energy theft.

Recently, a report in Science linked virus-driven energy theft to the creation of so called oncohistones.  An oncohistone deranges inhibitory chromatin.

See: Histone H3K36 mutations promote sarcomagenesis through altered histone methylation landscape

Excerpt:

Missense mutations (that change one amino acid for another) in histone H3 can produce a so-called oncohistone…

They invented the so-called oncohistone because they needed a word to link energy-dependent changes in amino acids from mutations to cancer. RNA-mediated amino acid substitutions link nutrient energy dependent changes from angstroms to ecosystems and healthy longevity in all living genera.

The authors needed a word they could use to link virus-driven energy theft to loss of function histone mutations via the amino acid substitutions that typically differentiate the cell types of all living genera. For example, they linked these four amino acid substitutions to cancer instead of linking virus-driven energy theft from the mutations to the cancer.

1) lysine 27–to–methionine (K27M)
2) glycine 34–to–arginine/valine (G34R/V)
3) glycine 34–to–tryptophan/leucine (G34W/L)
4) lysine 36–to–methionine (K36M)

They invented a word that could be used to link the mutation to cancer without acknowledging the fact that cancer is caused by virus-driven energy theft. Viruses cause the change of one amino acid for another. To prevent virus-driven energy theft, an anti-entropic force must be linked from sunlight to energy-dependent cell type differentiation. They do not want people to learn that energy is the anti-entropic force that prevents cancer. But information about that fact is not hard to find. Neither is the souce of the energy.

For example, see: Food-derived sensory cues modulate longevity via distinct neuroendocrine insulin-like peptides

Excerpt:

The team discovered that the smell or taste of food can directly shorten lifespan by affecting sensory neurons that produce insulin-6, an insulin hormone-like factor. They also showed that insulin-6 from sensory neurons alters the action of FOXO in various tissues. Their findings were published in Genes & Development as the cover article

They then attempted to turn on the function of only a pair of food-sensing sensory neurons by a blue light, a technique called optogenetics, to mimic the taste of food.”

My comment: They linked the speed of light on contact with water from hydrogen atom transfer in DNA base pairs in solution to the de novo creation of G protein-coupled olfactory receptor genes via energy-dependent changes in microRNA flanking sequences which link adhesion proteins from the innate immune system to supecoiled DNA, which protects the organized genomes of all living genera from the virus-driven energy theft that other researchers just linked to the creation of oncohistones and pathology.

Blue light optogenetics links a specific quantized energy level to the de novo creation of genes and virus-driven energy theft links mutations (so-called oncohistones) to all pathology.

In that context virus-driven energy theft would need to be defined as the opposite of what happens when what is known about optogenetics links a specific quantized energy level to the de novo creation of genes. By using words properly in the context of de novo gene creation, the need to define virus-driven energy theft is negligible.  If you don’t understand how a term is used in context,  you will need to invent a word to use out of that context. Mutation was the word that was invented and defined to take everything know about energy-dependent de novo gene creation out of context.

The taste or smell of foods can affect aging Here’s what the report of the article took out of context.
Animals can perceive changes in many environmental factors such as temperature and the taste or smell of foods. This is achieved by specialized nerve cells called sensory neurons. Interestingly, sensory neurons have been known to control the rate of aging in various animals, including the tiny free living roundworm C. elegans.
The impairment of sensory neurons has been known to delay aging by switching on the action of a well-known anti-aging protein called FOXO. FOXO then turns on the gene’s encoding proteins that protect cells and repair damages in various body parts. However, how sensory neurons influence the activity of the anti-aging FOXO proteins in an entire animal has remained a mystery.
Researchers hypothesized that the smell or taste of food acts on sensory neurons, which may produce a type of aging hormone. This aging hormone may be delivered to various body parts and may affect the action of FOXO proteins. The team discovered that the smell or taste of food can directly shorten lifespan by affecting sensory neurons that produce insulin-6, an insulin hormone-like factor. They also showed that insulin-6 from sensory neurons alters the action of FOXO in various tissues. Their findings were published in Genes & Development as the cover article.
They then attempted to turn on the function of only a pair of food-sensing sensory neurons by a blue light, a technique called optogenetics, to mimic the taste of food. Authors discovered that blue light itself can decrease the lifespan of animals through producing insulin-6 hormone that leads to the reduction of FOXO action without food taste or smell.
It has been shown that perception of food increases the level of blood insulin hormone levels in humans. In addition, many biological processes related to aging are similar in C. elegans and mammals which include humans. Therefore, the team concluded that it is unsurprising to find that food smell or taste play similar roles in the aging of mammals via sensory neurons and hormones like insulin.
See also: A Family of non-GPCR Chemosensors Defines an Alternative Logic for Mammalian Olfaction
Excerpt:

Insects and mammals use similar molecular mechanisms to detect light, heat, and several gases, suggesting that solutions to common sensory problems are often conserved (Caterina, 2007; Dhaka et al., 2006; Terakita, 2005).

Conclusion:

Future investigation of the functional role of Ms4a gene families across chordates—and the relevance of interactions between MS4A proteins and ethologically relevant cues like pheromones and fatty acids—will reveal both common and species-specific roles of the MS4As in processing information from the chemical environment.

For a historical record of publications that linked ethologically relevant cues from fatty acids and pheromones to behavior in all invertebrates to all vertebrates, see:
Effects of Carnitine on Fatty-Acid Oxidation by Muscle (1959)
DEPENDENCE OF RNA SYNTHESIS IN ISOLATED THYMUS NUCLEI ON GLYCOLYSIS, OXIDATIVE CARBOHYDRATE CATABOLISM AND A TYPE OF “OXIDATIVE PHOSPHORYLATION” (1964)
Human pheromones: integrating neuroendocrinology and ethology (2001)
Feedback loops link odor and pheromone signaling with reproduction (2005)
The Mind’s Eyes: Human pheromones, neuroscience, and male sexual preferences (2007)
Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors (2012)
Nutrient-dependent/pheromone-controlled adaptive evolution: a model (2013)

See also, today’s OP in an attempt to discuss this on the “Creationism” FB group

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