Cytosis can be used to teach everything from base editing to RNA editing to everyone over age 10. They will learn how to link the creation of energy to biophysically constrained viral latency via the physiology of pheromone-controlled reproduction.

Polymaths and paradigm shifts: from Asimov to Bear (3)

Polymaths and paradigm shifts: from Asimov to Bear (2)

Teilhardism And The New Religion: A Thorough Analysis of the Teachings of Pierre Teilhard de Chardin”, p.18, TAN Books

The evolutionist thesis has become more stringently unthinkable than ever before. — Dr. Wolfgang Smith (2015).

A Chat with Information Scientist Pedro Marijuán (2017)

I’ve based my informational scheme of the cell on this thinking of “distinction on the adjacent” — where molecular recognition is the essential phenomenon over which biological complexity has been developed.

Biological complexity develops in the context of the olfactory code. Molecular recognition of food odors and pheromones biophysically constrains viral latency.

See: Fundamental principles of the olfactory code  Volume 164, February 2018, Pages 94-101 open access

Sensory coding represents a basic principle of all phyla in nature: species attempt to perceive their natural surroundings and to make sense of them. Ultimately, sensory coding is the only way to allow a species to make the kinds of crucial decisions that lead to a behavioral response.

Alternative splicing of microRNAs (aka pre-mRNAs) are required for a behavior response.

The splicing code  Volume 164, February 2018, Pages 39-48

…the splicing code depends on a myriad of different factors that in part are influenced by the background in which they are read such as different cells, tissues or developmental stages. Given the complexity of the splicing process, the construction of an algorithm that can define exons or their fate with certainty has not yet been achieved.

Algorithms define nothing. The availability of quantized energy as information must be linked to biophysically constrained viral latency and all biologically based cause and effect.

What is code biology?  Volume 164, February 2018, Pages 1-10

The great discontinuities of the history of life, in other words, can be explained as the result of the appearance of new codes.

New codes do not automagically occur. The new codes are energy-dependent and RNA-mediated in the context of the fixation of amino acid substitutions that differentiate the cell types of all living genera.

On universal coding events in protein biogenesis  Volume 164, February 2018, Pages 16-25

The complete ribosomal protein synthesis cycle and codon-amino acids associations are universally preserved in all life taxa on Earth. This process is accompanied by a set of hierarchically organized recognition and controlling events at different complexity levels. It starts with amino acid activation by aminoacyl tRNA synthetases…

The energy-dependent creation of the tRNA synthetases links hydrogen-atom transfer in DNA base pairs in solution to all energy-dependent biodiversity.

How prokaryotes ‘encode’ their environment: Systemic tools for organizing the information flow  Volume 164, February 2018, Pages 26-38

An important issue related to code biology concerns the cell’s informational relationships with the environment. As an open self-producing system, a great variety of inputs and outputs are necessary for the living cell, not only consisting of matter and energy but also involving information flows.

Quantized energy is the information that flows through every cell type in all prokaryotes.

Causation, constructors and codes  Volume 164, February 2018, Pages 121-127

A formal definition of codes in general, and organic codes in particular, allows the relational diagram to be extended so as to capture this translation of formal cause into process. The extended relational diagram is used to exemplify causal entailment in a diverse range of processes, such as enzyme action, construction of automata, communication through the Morse code, and ribosomal polypeptide synthesis through the genetic code.

The diverse range of processes starts with the creation of energy-dependent enzyme action. The anti-entropic virucidal energy of sunlight was first linked to the creation of all biodiversity on Earth in 1944: What is Life?

Indeed, in the case of higher animals we know the kind of orderliness they feed upon well enough, viz. the extremely well-ordered state of matter in more or less complicated organic compounds, which serve them as foodstuffs. After utilizing it they return it in a very much degraded form -not entirely degraded, however, for plants can still make use of it. (These, of course, have their most power supply of ‘negative entropy’ the sunlight.) (pp. 73 and 74)

If you think you can link anything except sunlight to all biodiversity on Earth, see: Evolution – Genetic Novelty/Genomic Variations by RNA Networks and Viruses
If you know that serious scientists do not link viruses to the evolution of anything except pathology, see:
Schrödinger at 75 – The Future of Biology – September 2018
The future of biology will not be left in the hands of biologically uninformed theorists.

Caption: Contemporary analyses of cell metabolism have called out three metabolites: ATP, NADH, and acetyl-CoA, as sentinel molecules whose accumulation represent much of the purpose of the catabolic arms of metabolism and then drive many anabolic pathways. Such analyses largely leave out how and why ATP, NADH, and acetyl-CoA (Figure 1) at the molecular level play such central roles. Yet, without those insights into why cells accumulate them and how the enabling properties of these key metabolites power much of cell metabolism, the underlying molecular logic remains mysterious. Four other metabolites, S-adenosylmethionine, carbamoyl phosphate, UDP-glucose, and Δ2-isopentenyl-PP play similar roles in using group transfer chemistry to drive otherwise unfavorable biosynthetic equilibria. This review provides the underlying chemical logic to remind how these seven key molecules function as mobile packets of cellular currencies for phosphoryl transfers (ATP), acyl transfers (acetyl-CoA, carbamoyl-P), methyl transfers (SAM), prenyl transfers (IPP), glucosyl transfers (UDP-glucose), and electron and ADP-ribosyl transfers (NAD(P)H/NAD(P)+) to drive metabolic transformations in and across most primary pathways. The eighth key metabolite is molecular oxygen (O2), thermodynamically activated for reduction by one electron path, leaving it kinetically stable to the vast majority of organic cellular metabolites

Ecological adaptation: A new definition of heredity (3)

Excerpt:
Moving forward: Novel and Haplotype Specific MicroRNAs Encoded by the Major Histocompatibility Complex

…these data suggest that a subset of the identified novel miRNAs may contribute to the pathophysiology of numerous diseases, laying the groundwork for future studies to elucidate the functional connections of miRNAs to the numerous diseases associated with sequence variants within non-coding regions of the MHC.

OMCD: OncoMir Cancer Database

Dysregulation of miRNAs is commonly observed in cancers and it largely cancer dependent.

The virus-driven theft of quantized energy as information has been linked from changes in the microRNA/messenger RNA balance to all pathology. That fact replaces the circular logic that links cancer-dependent dysregulation of miRNAs to cancer.  Simply put, the proliferation of viruses cause cancer. The proliferation of viruses is energy-dependent in the context of established links from atoms to ecosystems in all living genera.
See: Subatomic: An Atom Building Board Game

A deck-building game where particle physics & chemistry collide! Use quarks to build subatomic particles & particles to build Atoms!

See also: 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.

Moving forward: Novel and Haplotype Specific MicroRNAs Encoded by the Major Histocompatibility Complex

…these data suggest that a subset of the identified novel miRNAs may contribute to the pathophysiology of numerous diseases, laying the groundwork for future studies to elucidate the functional connections of miRNAs to the numerous diseases associated with sequence variants within non-coding regions of the MHC.

My “Disqus” comment (and nearly 2000 others): Gene expression is energy-dependent, RNA-mediated, and biophysically constrained.
See: FUS Regulates Activity of MicroRNA-Mediated Gene Silencing.

MicroRNA-mediated gene silencing is a fundamental mechanism in the regulation of gene expression.

MicroRNAs do not create themselves.
See also:  Energy as information and constrained endogenous RNA interference
8 of my 9 most recent comments to Disqus have been removed.
See for comparison: Incomplete host immunity favors the evolution of virulence in an emergent pathogen
Reported as: In nature, an imperfect immune system drives the evolution of deadly pathogens

…birds that eat at feeders are more likely to be infected with the disease, which causes red, swollen eyes and often blindness that results in death.

…lower virulence strains could be their own worst enemies, creating a population of hosts that are resistant to them but not the higher virulence strains that remain.

By removing my Disqus comments, the moderators limit discussion of the facts about virus-driven energy theft, which links mutations to all pathology.  That allows the biased reporting on preprints that continue to try to support the ridiculous concept of neo-Darwinian evolution.
It also prevents the realization of goals by serious scientists who have linked the biogenic creation of uranium ores to the prevention of radiation sickness via microRNA therapy. See, for examples: miRNA-mediated therapies
A miRNA-145/TGF-beta1 Negative Feedback Loop Regulates the Cancer-Associated Fibroblast Phenotype

…miR-145 is a key regulator of the CAF phenotype, acting in a negative feedback loop to dampen acquisition of myofibroblastic traits, a key feature of CAF associated with poor disease outcome.

See also: Microhomology-assisted scarless genome editing in human iPSCs

Gene-edited induced pluripotent stem cells (iPSCs) provide relevant isogenic human disease models in patient-specific or healthy genetic backgrounds. Towards this end, gene targeting using antibiotic selection along with engineered point mutations remains a reliable method to enrich edited cells. Nevertheless, integrated selection markers obstruct scarless transgene-free gene editing. Here, we present a method for scarless selection marker excision using engineered microhomology-mediated end joining (MMEJ). By overlapping the homology arms of standard donor vectors, short tandem microhomologies are generated flanking the selection marker. Unique CRISPR-Cas9 protospacer sequences nested between the selection marker and engineered microhomologies are cleaved after gene targeting, engaging MMEJ and scarless excision. Moreover, when point mutations are positioned unilaterally within engineered microhomologies, both mutant and normal isogenic clones are derived simultaneously. The utility and fidelity of our method is demonstrated in human iPSCs by editing the X-linked HPRT1 locus and biallelic modification of the autosomal APRT locus, eliciting disease-relevant metabolic phenotypes.

Reported as: Gene Editing Is Now Precise Enough to Modify a Single Letter of DNA

To make these very precise edits, an SNP modification is first inserted alongside a fluorescent reporter gene that helps researchers to identify modified cells. The researchers engineered a duplicate DNA sequence known as a microhomology (hence the technique’s name) on each side of the fluorescent gene, targeting sites for CRISPR to go in and cut DNA. The researchers were then able to use a DNA repair system known as microhomology-mediated end joining (MMEJ) to remove the fluorescent gene. That left only the single-base edit, in the form of an SNP, behind.

See also: Inhibition of the Host Translation Shutoff Response by Herpes Simplex Virus 1 Triggers Nuclear Envelope-Derived Autophagy
Nuclear envelope-derived autophagy (NEDA) appears to be a cellular stress response, which is triggered late during HSV-1 infection. An energy-dependent single nucleotide repeat (SNR) might compensate for the viral alteration of the macroautophagic response. At this level of hydrogen-atom energy transfer in DNA base pairs in solution, the link to supercoiled DNA and viral latency becomes increasingly important.
Theorists are angry because they have been left behind. They know very little about what is important. That was expected by all serious scientists, especially those who have accumulated decades of testing experience while working in medical laboratories.
See for example: Applications of ligation-mediated PCR

Using a molecular energy source (which differs depending on the enzyme source organism), DNA ligase reforms the missing covalent bond and the strand is whole again. Two aspects of this are critical:

The nick to be repaired occurs on a single strand but in the context of a double-stranded molecule.
The bases of the nicked strand, and particularly those directly flanking the nick site, must be properly base-paired to the opposite (un-nicked) strand.

It’s not hard to imagine why this is: the base pairing is required to hold the two parts (sugar 3′ -OH and the next phosphate) in place for the ligase enzyme active site to catalyze joining them. If either one of these isn’t base-paired down and is flopping about with thermal motion, the reaction geometry doesn’t occur, and no new bond can be made.

Biologically uninformed theorists cannot even speak the same language. They do not start with a molecular energy source for base pairing and microRNA-mediated amino acid substitutions that differentiate all cell types. Instead, mutations are linked to increasing organismal complexity via the magic of evolution.

For God and Country

Enzyme-constrained interethnic diversity (8)

I am intrigued by the fact that I detailed the energy-dependent links to interethnic diversity in this blog post on the same day that the so-called science journalist Ed Yong placed everything known to serious scientists back into the context of neo-Darwinian evolution.
See for comparison to Ed Yong’s nonsense: “Players compete to build enzymes, hormones and receptors and fend off attacking Viruses!
Yong’s addendum:

*This article has been corrected to reflect the fact that Arc genes were co-opted by animals from a group of genes that also gave rise to retroviruses, and are not directly descended from retroviruses, as originally stated. We regret the error.

Retractions by Szostak reflect a similar theme.

In retrospect, we were totally blinded by our belief [in our findings]…we were not as careful or rigorous as we should have been (and as Tivoli was) in interpreting these experiments.

The food energy-dependent creation of Arc genes links the virus-driven theft of quantized energy to the creation of retroviruses, which are biophysically constrained by RNA-mediated amino acid substitutions in the context of the pheromone-controlled physiology of reproduction.
Something has gone horribly wrong in the context of respected scientist’s retractions and the addendums by science journalists who have failed to link ridiculous theories from top-down causation to biophysically constrained viral latency during the past two decades.
See for comparison:  The vibrational theory of olfaction for the win
John Hewitt will almost undoubtedly be the first science journalist to link the energy-dependent creation of enzymes from the sense of smell in bacteria to our visual perception of mass and energy.
Olfaction Warps Visual Time Perception will then be linked to “The Darwin Code: Intelligent Design without God” and interethnic biodiversity via food energy-dependent pheromone-controlled RNA-mediated amino acid substitutions.

IMG_3010

Enzyme-constrained interethnic diversity (7)

Summary:  I suspect that John Hewitt will soon publish an article on the energy-dependent creation of microRNAs and enzymes. He is most likely to link the virus-driven theft of quantized energy as information to all pathology without challenging pseudoscientists and other science journalists to revise their ridiculous claims about mutation-driven evolution.
Digital medicine, on its way to being just plain medicine

There are already nearly 30,000 peer-reviewed English-language scientific journals, producing an estimated 2.5 million articles a year.

Until recently, no published works linked the creation of the sun’s anti-entropic virucidal energy from ATP to the creation of RNA and biophysically constrained viral latency.
But see: EXD2 governs germ stem cell homeostasis and lifespan by promoting mitoribosome integrity and translation January 15, 2018

“Loss of EXD2 results in defective mitochondrial translation, impaired respiration, reduced ATP production…” and “…aberrant association of messenger RNAs with the mitochondrial ribosome.

Exonuclease 3′ –5′ domain-containing 2 (EXD2) is a mitochondrial ribonuclease. A ribonuclease is a type of nuclease that catalyzes the degradation of RNA into smaller components such as microRNAs. A nuclease is an enzyme capable of cleaving the phosphodiester bonds between monomers of nucleic acids. EXD2 is required for mitoribosome integrity and efficient mitochondrial translation.
See: The Excitable Mitochondria by John Hewitt, who brought the article on EXD2 to my attention in his tweets. The link from energy-dependent changes in EXD2 to homeostasis predicts the link from reduced ATP production to the virus-driven degradation of EXD2 to the aberrant associations that link mutations in messenger RNA to all pathology. I suspect that John Hewitt will soon publish an article on the energy-dependent creation of microRNAs and enzymes. He is most likely to link the virus-driven theft of quantized energy as information to all pathology without challenging pseudoscientists and other science journalists to revise their ridiculous claims about mutation-driven evolution. Challenging your peers leads to your elimination from consideration. Your peers cannot rise to the ocassion and meet the challenge, so they must ignore you.
As I finalize this series on enzyme-constrained interethnic diversity, I also offer information from my largely ignored FB posts on the anniversary dates indicated:
January 10, 2017

The scent of eros: mysteries of odor in human sexuality

“This is science at its best, with adventure, ideas, and lots of facts”. — Helen Fisher

“A treasure hunt through history, literature, and scientific data”. — Gina Ogden

On pages 160-162 of “The Scent of Eros” (1995/2002) we linked race and ethnicity to all biodiversity via the same model of biologically-based cause and effect. It is still the only valid model.

What exactly do people think was still being debated about the fact that all organisms must eat to reproduce, or that pheromones control the physiology of reproduction in all living genera?

How could race and ethnicity not be aspects of a valid model of biologically-based cause and effect unless pseudoscientists convinced you to believe in mutation-driven evolution?

January 10, 2016

This serves as a reminder to all sex researchers. Most of them understand nothing about how RNA-mediated sex differences in cell types are linked to sex differences in #behavior by nutrient-dependent amino acid substitutions.
They refused to accept the fact that the pheromone-controlled physiology of reproduction and chromosomal rearrangements link the molecular epigenetics of cell type differentiation in all cell types of all individuals of all species from microbes to humans.

Xistential crisis: Discovery shows there’s more to the story in silencing X chromosomes
Xist is widely believed to be both necessary and sufficient for X silencing,” … “We for the first time show that it’s not sufficient, that there have to be other factors, on the X-chromosome itself, that activate Xist and then cooperate with Xist RNA to silence the X-chromosome.
An example of how 20 years of ignorance about RNA-mediated cell type differentiation leads to “NEW” discoveries.
From Fertilization to Adult Sexual Behavior 1996
Genomic-imprinting is also manifest in specific parts of the X-inactivation region’s related XIST gene. Here male- and female-specific methyl-group patterns participate in X-inactivation in females and also in the preferential inactivation of the paternal X in human placentae of female concepti (Harrison, 1989; Monk, 1995). This process indicates that tissues of the early conceptus can sense and react differentially to epigenetic sexual dimorphisms on the female conceptus’ own two X chromosomes. Furthermore, variations of X-inactivation patterns often account for traits discordance in monozygotic twin females. In other words, they are often found to have nonidentical patterns of X-inactivation, yielding differing expression of noticeable X-linked traits (Machin, 1996).
January 10, 2017

The anniversary of an attack on science.

Odious Christianity
Ray Comfort

Professor PZ Myers hates Christianity. Nor is he a big fan of my good friend, Ken Ham.
In writing about his hatred, PZ unwittingly showed his hand when he said,

“I reject his notion of sin — the idea that there is some kind of divine law against which we can transgress — but humanists do not deny that we can do wrong and we can do harm. We think we should do better, not to appease some vengeful deity, but because it improves our lives and helps make those around us happier and better able to live up to their potential. We certainly do accept that death is inevitable, but not because we are wicked — the wicked often seem to flourish while the good may die young. Are we to measure the virtue of human beings by their longevity? Charles Manson is 82, and surely destined to join the saints in heaven, while every infant death must open a chute directly to hell for its wicked soul.”
His hatred is perfectly in line with the Bible:
“Because the carnal mind is enmity against God; for it is not subject to the law of God, nor indeed can be” (Romans 8:7).
PZ is unashamedly godless (a state the Bible refers to as “carnal”), and so his mind is at “enmity” against God. That means he is in a continual state of hostility towards his Creator. That certainly is true. Even though he doesn’t believe that He exists, but he contemptuously hates the very thought of “a god.”
But look at the pinpoint accuracy of the Scriptures:
“…for it [our carnal mind] is not subject to the law of God, nor indeed can be.”
His hatred is directed at the “law of God,”–the moral Law (the Ten Commandments).
PZ is like a criminal who hates the police, not because of who they are individually, but because of what they represent. They stand for the law–that which is right and good, and that is offensive to someone who loves and lives for crime.
PZ’s railings about his loved ones dying is tragic, but peripheral. They are not the main reason why he is angry.
His anger is primarily at God and His Law, because he doesn’t like being told what to do. Like you and I before we came to Christ, he loves his sin, and he who loves the darkness hates the light.
I’m not sure why PZ called Charles Manson “wicked,” when his atheistic worldview doesn’t allow for anyone to be “wicked.”
Or could it simply be that Manson transgressed the moral Law, which says “You shall not kill,” and PZ intuitively knows that, because of his God-given knowledge of right and wrong (see Romans 2:15).
It’s actually heartening to see him using his moral compass. If he would put down his weapons and study how God’s moral compass is infinitely higher, he may rethink his rejection of “The soul who sins, shall die.”
This is because every death is sobering evidence of the truth of that verse.
You can see PZ in action in our movie “Evolution vs God” (over 2 million views) at www.FullyFreeFilms.com
P.S. PZ hates the movie.

January 10, 2017

How Your Toxic Boss Is Hurting Your Mental Health

Get out before the DNA damage is irreparable.


I do not have a boss. But the stress of attempting to interest others in what is known about how biologically-based cause and effect must be linked to interethnic similarities and differences may prevent some further attempts to explain how DNA damage is biophysically constrained in the context of naturally occurring RNA interference and viral latency.
November 27, 2017 See: Damage-induced lncRNAs control the DNA damage response through interaction with DDRNAs at individual double-strand breaks
Reported on November 29, 2017 as: RNA takes over control of DNA break repair

Now, a study shows that following the formation of DNA double-strand breaks, bidirectional transcription events adjacent to the break generate small RNAs that trigger the DNA damage response by local RNA:RNA interactions.

The RNA:RNA interactions are energy-dependent and they link the creation of microRNAs to the creation of enzymes, receptors, and hormones that protect organized genomes from virus-driven energy theft and all pathology.  But they are not just RNA:RNA interactions. The interactions among microRNAs and messenger RNA link food energy and the pheromone-controlled physiology of reproduction to all biodiversity on Earth without the pseudoscientific nonsense touted by biologically uninformed theorists and science journalists such as Ed Yong and Carl Zimmer.

 
Cytosis can be used to teach everything from base editing to RNA editing to everyone over age 10. They will learn how to link the creation of energy to biophysically constrained viral latency via the physiology of pheromone-controlled reproduction.

A Mathematical Model Links Quantum Physics to Quantum Souls (1)

Historical facts: All energy-dependent cell type differentiation is biophysically constrained by the de novo creation of microRNAs and enzymes that metabolize food and drugs. All food energy-dependent metabolism occurs in the context of microRNA-mediated cause and effect and the physiology of pheromone-controlled reproduction. The food energy-dependent pheromone controlled physiology of reproduction in bacteria links what organisms eat to the transgenerational epigenetic inheritance of their morphological and behavioral phenotypes. The virus-driven degradation of messenger RNA has been linked to all pathology in the context of the National Microbiome Initiative, the Precision Medicine Initiative, Alpha Genomix profiling of pathways linked to the creation of CYP enzymes and test results that differentiate the most likely response to some medications based on fixation of  RNA-mediated amino acid substitutions in the organized genomes of different people and different populations of modern humans.
See: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems (2014)
The ingestion of sago palm-like leaves linked increased endogenous vitamin C from the stability of the mouse genome to the stability of the organized genome in a modern human population via one base pair change and the fixation of one RNA-mediated amino acid substitution.
See also: Towards a systemic paradigm in carcinogenesis: linking epigenetics and genetics (2015)

The SMT’s [Somatic mutation theory’s] fundamental assumption is that there is no cancer without genetic or chromosomal harm.

See for comparison: Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention
Watch as 2 of 3 co-authors of the article about can prevention tell the world that cancer is caused by “bad luck.”

Now see one of the 3 co-authors admit to his overwhelming ignorance in: Why Is This Bacterium Hiding in Human Tumors?

“The whole idea of bacteria in tumors is fascinating and unexpected,” said Dr. Bert Vogelstein, a colon cancer researcher at Johns Hopkins.

  1. The fundamental assumption that there is no cancer without genetic or chromosomal harm links the virus-driven degradation of messenger RNA in bacteria to the food energy-dependent pheromone-controlled physiology of reproduction in bacteria and healthy longevity via error-free DNA repair.
  2. The fundamental assumption that there is no cancer without genetic or chromosomal harm links virus-driven pathology to cell type-specific and species-specific pathology in all cell types of all individuals of all living genera via the failure of microRNA-mediated error-free DNA repair.

There is now a mathematical model of top-down causation that links the sun’s anti-entropic virucidal energy on contact with water to the physiology of pheromone-controlled reproduction and all biodiversity via RNA-mediated error-free DNA repair. The mathematical model refutes the pseudoscientific nonsense touted by neo-Darwinian theorists because it starts with the creation of the sun, which biophysically constrains viral latency. The importance of linking this mathematical model to all models of biologically-based cause and effect cannot be overstated.
See: Quantum Vacuum Dynamics, Coherence, Superluminal Photons and Hypercomputation in Brain Microtubules

After the Schrodinger’s intuition, expressed in his book “What is life?” [12], the first systematic approach to a quantum interpretation of biological process dated back to the model proposed by Frohlich [13] several years ago. He suggested the occurrence, in biological matter, of macroscopic quantum phenomena able to explain the energy transport without loss in the living organisms and signal transfer based on collective coherent oscillations associated to a branch of longitudinal
electric modes in the frequency range [ ] also known as Frohlich frequency. So in living systems, according to Frohlich’s model, energy could be stored in a thin two – dimensional layer placed beneath the cell membrane, that in this way would act as a biological superconducting medium, under dipolar propagating waves without thermal loss [13].

The ridiculous assumptions about thermal loss and evolution were placed into the context of other ridiculous assumptions that failed to start from the creation of the sun and link the anti-entropic virucidal energy of the sun from food energy to all biodiversity via the physiology of pheromone-controlled reproduction.
For comparison see: Reversing the thermodynamic arrow of time using quantum correlations

We observe a spontaneous heat flow from the cold to the hot system. This process is enabled by a trade off between correlations and entropy that we quantify with information-theoretical quantities.

Reported as: Experiment shows that arrow of time is a relative concept, not an absolute one

The second law of thermodynamics says that entropy, or disorder, tends to increase over time, which is why everything in the world around us appears to unfold forward in time. But it also explains why hot tea grows cold rather than hot. In this new effort, the researchers found an exception to this rule that works in a way that doesn’t violate the rules of physics as they have been defined.
The idea of entangled particles has been in the news a lot lately as researchers around the world attempt to use it for various purposes—but there is another lesser-known property of particles that is similar in nature, but slightly different. It is when particles become correlated, which means they become linked in ways that do not happen in the larger world. Like entanglement, correlated particles share information, though it is not as strong of a bond. In this new experiment, the researchers used this property to change the direction of the arrow of time.

Succinctly stated as:

This observation did not violate the second law of thermodynamics, the group explains, because the second law assumes there are no correlations between particles.

The ridiculous assumption that there are no correlations between subatomic particles led to assumptions that energy emerged and that all life evolved in the context of mutations and natural selection, which led to the “bad luck” theory of cancer.
Frohlich’s model was dismissed and so was the the fact that “…energy could be stored in a thin two – dimensional layer placed beneath the cell membrane, that in this way would act as a biological superconducting medium, under dipolar propagating waves without thermal loss [13].
[13.] Long-range coherence and energy storage in biological systems (1968)

Biological systems are expected to have a branch of longitudinal electric modes in a frequency region between 1011 and 1012 sec−1. They are based on the dipolar properties of cell membranes; of certain bonds recurring in giant molecules (such as H bonds) and possibly on pockets of non-localized electrons. In Section 2 it is shown quit generally that if energy is supplied above a certain mean rate to such a branch, then a steady state will be reached in which a single mode of this branch is very strongly excited. The supplied energy is thus not completely thermalized but stored in a highly ordered fashion. This order expresses itself in long-range phase correlations; the phenomenon has considerable similarity with the low-temperature condensation of a Bose gas. General consequences and proposals of experiments are discussed in section 3.

Four years earlier, McEwen et al., (1964) linked the creation of the sun’s anti-entropic virucidal energy to the creation of ATP and the creation of RNA.
See: Dependence of RNA synthesis in isolated thymus nuclei on glycolysis, oxidative carbohydrate catabolism and a type of “oxidative phosphorylation”

The synthesis of RNA in isolated thymus nuclei is ATP dependent.

That same year, Dobzhansky (1964) first asserted this claim:

The notion has gained some currency that the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists! I have heard a man whose official title happens to be Professor of Zoology declare to an assembly of his colleagues that “a good man cannot teach zoology. A good man can teach, of course, only molecular biology.

In 1973, Dobzhansky again mocked all the pseudoscientists whose mathematical model failed to link the creation of the sun’s anti-entropic energy from the physiology of pheromone-controlled reproduction to RNA-mediated fixation of amino acid substitutions that differentiate all cell types in all living genera.
See: Nothing in Biology Makes Any Sense Except in the Light of Evolution
He assumed that all serious scientists would recognize that the light of evolution linked Schrodinger’s claims about sunlight to all biodiversity via the food energy-dependent pheromone-controlled fixation of RNA-mediated amino acid substitutions.
He claimed

“…one can calculate the minimum numbers of single mutations needed to change the cytochrome C of one organism into that of another.”

He linked that calculation to this fact:

…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.

The levels of complexity that must be addressed by the calculations have since been addressed and reported in: Quantum Vacuum Dynamics, Coherence, Superluminal Photons and Hypercomputation in Brain Microtubules
Nothing has changed about the facts that all serious scientists have linked from biophysically constrained viral latency to all biodiversity via the physiology of pheromone-controlled reproduction.
For example, see: Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution

The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.

See also Cytosis:A board game taking place inside a human cell! Players compete to build enzymes, hormones and receptors and fend off attacking Viruses!

Alternative splicing of pre-mRNA

Agilent technology and energy-dependent autophagy

The first step towards understanding the link from the creation of energy to metabolism-related cellular function is called energy phenotyping. It requires the  technology to measure energy-dependent changes in RNA-mediated metabolic switches via the RNA interference (RNAi) screening strategy. Endogenous RNAi must then be linked  to the prevention of the virus-driven degradation of messenger RNA that causes all pathology.
Scientists discover possible master switch for programming cancer immunotherapy

…they employed an RNA interference screening strategy which can test the actual function of thousands of factors simultaneously.

See also: Energy as information and constrained endogenous RNA interference (video 6:46 minutes)
Abstract:

Feedback loops link quantized energy as information to biophysically constrained RNA-mediated protein folding chemistry. Light induced energy-dependent changes link angstroms to ecosystems from classical physics to chemistry/chirality and to molecular epigenetics/autophagy. The National Microbiome Initiative links microbial quorum sensing to the physiology of reproduction via endogenous RNA interference and chromosomal rearrangements. The rearrangements link energy-dependent fixed amino acid substitutions to the Precision Medicine Initiative via genome wide inferences of natural selection. This detailed representation of energy-dependent natural selection for codon optimality links biologically- based cause and effect from G protein-coupled receptors to RNA-mediated amino acid substitutions and the functional structure of supercoiled DNA. Energy-dependent polycombic ecological adaptations are manifested in supercoiled DNA. Chromosomal inheritance links the adaptations from morphological phenotypes to healthy longevity via behavioral phenotypes. For contrast, virus-driven energy theft is the link from messenger RNA degradation to negative supercoiling, constraint breaking mutations, and hecatombic evolution. The viral hecatomb links transgenerational epigenetic inheritance from archaea to Zika virus-damaged DNA, which typically is repaired by endogenous RNA interference and fixation of RNA-mediated amino acid substitutions in organized genomes.

See also: Measuring the Metabolic Switch in Cancer Cells – Agilent (pdf)

Yoshida used TRAP1-null cells and transient TRAP1 mutants on an Agilent Seahorse XF96 Analyzer to show that TRAP1 regulates a metabolic switch between oxidative phosphorylation and aerobic glycolysis in immortalized mouse fibroblasts and in human tumor cells. TRAP1 deficiency promotes increased mitochondrial respiration, fatty acid oxidation, accumulation of TCA intermediates, ATP, and ROS, while suppressing glucose metabolism.

The virus-driven degradation of messenger RNA is the only perfectly obvious reason for changes in oxidative phosphorylation and aerobic glycolysis that prevent the metabolism of glucose. Natural selection for energy-dependent codon optimality links the creation of energy to the metabolism of glucose via the creation of enzymes that metabolize food energy. Energy-dependent RNA-mediated error-free DNA repair and fixation of amino acid substitutions is required to link the creation of enzymes and the species-specific production of pheromones from the physiology of reproduction to biophysically constrained viral latency and all morphological and behavioral phenotypes in all living genera.
In that context, energy-dependent natural selection for codon optimality links biologically-based cause and effect from hydrogen-atom transfer in DNA base pairs in solution to the transgenerational epigenetic inheritance of healthy longevity. For contrast, the virus-driven theft of quantized energy links changes in non-coding RNAs to all pathology.
For example, see: Reduced expression of brain-enriched microRNAs in glioblastomas permits targeted regulation of a cell death gene
See also: A Concise Review of MicroRNA Exploring the Insights of MicroRNA Regulations in Bacterial, Viral and Metabolic Diseases
The link from the virus-driven theft of quantized energy to glioblastoma may be the best example of how viruses are readily linked to the cell death gene in all cell types of all individuals of all living genera. That fact is more obvious with further examination of details provided for free in book chapters from Codon Publishing.
See: Noncoding RNAs in Glioblastoma  Free book chapter from Codon Publishing

The vast majority of the human genome is transcribed into noncoding RNAs. Among these, microRNAs (miRNA) and long noncoding RNAs (lncRNA) are frequently deregulated in cancer, where they regulate a wide variety of functions.

See also: Epigenetic Mechanisms of Glioblastoma Free book chapter from Codon Publishing

Aberrant DNA methylation is a common event in the genesis and progression of tumors. The application of next-generation sequencing enables the identification and mapping of DNA methylation and its derivatives, 5fC and 5hmC, to base-pair resolution. This chapter describes nine novel hypermethylation genes and six hypomethylation genes, identified by constructing a DNA methylation profile, in glioblastoma. Abnormal promoter methylation and histone modifications were associated with differential expression of miRNAs in glioblastoma: miR-185 reversed global DNA methylation and the methylation level of the hypermethylation genes by targeting DNMT; and miR-101 regulated histone methylation of hypomethylation genes by targeting EED, EZH2, and DNMT3A. The long noncoding RNA CASC2c directly bound to miR-101 via microRNA response elements, and there was a reciprocal repression between CASC2c and miR-101. Despite being competitors they both led to the overexpression of their target hypomethylation genes CPEB1, PRDM16, and LMO3. Taken together, glioblastoma is a complicated pathological process with deregulated methylation and histone modifications. Focal differentially methylated region and differentially methylated site studies will be helpful for the identification of regulatory elements of transcription. Studies of intragenic and distant intergenic alterations in DNA methylation will help elucidate the nature of epigenetic deregulation in glioblastoma.

The Seahorse XF Cell Energy Phenotype Test kit is a simple assay kit that simultaneously measures the two major energy producing pathways in live cells – mitochondrial respiration and glycolysis, allowing rapid determination of energy phenotypes of cells and investigation of metabolic switching.
The simultaneous measurement of two major energy-producing pathways in live cells allows serious scientists to report their findings in the context of what is known about mitochondrial respiration and glycolysis. Glycolysis is epigenetically effected and RNA-mediated. No magic of evolution or nonsense about natural selection for anything except food and reproduction is required to explain how rapid metabolic switching determines whether or not viral latency is biophysically constrained across the time-space continuum.
See: From Fertilization to Adult Sexual Behavior (1996)

Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.

See: Epigenetic modifications poster (Abcam)
Also from Abcam: Mechanisms of Recombination conference
The bottom line is The secret to safe DNA repair  (2015)

…if you don’t have this enzyme, then this error-free repair is stopped. You can’t do it. If you can’t do the error-free repair, among other things that happen is that you expect these cells to be cancer prone.

Clearly, the creation of the enzyme is energy-dependent and biophysically constrained by the pheromone-controlled physiology of reproduction. Pseudoscientists seem to know nothing about that, and most serious scientists are not telling you the facts that link the virus-driven degradation of messenger RNA to the “death gene” via the mechanisms that fail during recombination.
But see: microRNA autophagy  and also see: See:  Agilent Seahorse XF Publications Alert for December 2017
Selected publications
Autophagy maintains the metabolism and function of young and old stem cells
Ho, T. T., Warr, M. R., Adelman, E. R., Lansinger, O. M., Flach, J., Verovskaya, E. V., Figueroa, M. E. and Passegue, E.
Nature. 2017 Mar 9, 543 (7644):205-210.
Involvement of autophagy in the outcome of mitotic catastrophe
Sorokina, I. V., Denisenko, T. V., Imreh, G., Tyurin-Kuzmin, P. A., Kaminskyy, V. O., Gogvadze, V. and Zhivotovsky, B.
Sci Rep. 2017 Nov 6, 7 (1):14571.
Sugar or Fat?-Metabolic Requirements for Immunity to Viral Infections
Shehata, H. M., Murphy, A. J., Lee, M. K. S., Gardiner, C. M., Crowe, S. M., Sanjabi, S., Finlay, D. K. and Palmer, C. S.
Front Immunol. 2017 Oct 16, 8:1311.
System-wide Benefits of Intermeal Fasting by Autophagy
Martinez-Lopez, N., Tarabra, E., Toledo, M., Garcia-Macia, M., Sahu, S., Coletto, L., Batista-Gonzalez, A., Barzilai, N., Pessin, J. E., Schwartz, G. J., Kersten, S. and Singh, R.
Cell Metab. 2017 Dec 5, 26 (6):856-871 e5.
Late-onset Alzheimer’s disease is associated with inherent changes in bioenergetics profiles
Sonntag, K. C., Ryu, W. I., Amirault, K. M., Healy, R. A., Siegel, A. J., McPhie, D. L., Forester, B. and Cohen, B. M.
Sci Rep. 2017 Oct 25, 7 (1):14038.

BAG3 directly stabilizes Hexokinase 2 mRNA and promotes aerobic glycolysis in pancreatic cancer cells
An, M. X., Li, S., Yao, H. B., Li, C., Wang, J. M., Sun, J., Li, X. Y., Meng, X. N. and Wang, H. Q.
J Cell Biol. 2017 Dec 4, 216 (12):4091-4105.
Drug resistance induces the upregulation of H2S-producing enzymes in HCT116 colon cancer cells
Untereiner, A. A., Pavlidou, A., Druzhyna, N., Papapetropoulos, A., Hellmich, M. R. and Szabo, C.
Biochem Pharmacol. 2017 Oct 20, [epub ahead of print]
ISG15 governs mitochondrial function in macrophages following vaccinia virus infection
Baldanta, S., Fernandez-Escobar, M., Acin-Perez, R., Albert, M., Camafeita, E., Jorge, I., Vazquez, J., Enriquez, J. A. and Guerra, S.
PLoS Pathog. 2017 Oct 27, 13 (10):e1006651.
High throughput measurement of metabolism in planarians reveals activation of glycolysis during regeneration
Osuma, E. A., Riggs, D. W., Gibb, A. A. and Hill, B. G.
Regeneration. 2017 Nov 02, [epub ahead of print]
Current technical approaches to brain energy metabolism
Barros, L. F., Bolanos, J. P., Bonvento, G., Bouzier-Sore, A. K., Brown, A., Hirrlinger, J., Kasparov, S., Kirchhoff, F., Murphy, A. N., Pellerin, L., Robinson, M. B. and Weber, B.
Glia. 2017 Nov 7, [epub ahead of print]
Glucose-regulated protein 75 determines ER–mitochondrial coupling and sensitivity to oxidative stress in neuronal cells
Honrath, B., Metz, I., Bendridi, N., Rieusset, J., Culmsee, C. and Dolga, A. M.
Cell Death Discovery. 2017 Nov 06, [epub ahead of print]

Associations Between Microbiota, Mitochondrial Function, and Cognition in Chronic Marijuana Users
Panee, J., Gerschenson, M. and Chang, L.
J Neuroimmune Pharmacol. 2017 Nov 4, [epub ahead of print]
RNA cytosine methyltransferase Nsun3 regulates embryonic stem cell differentiation by promoting mitochondrial activity
Trixl, L., Amort, T., Wille, A., Zinni, M., Ebner, S., Hechenberger, C., Eichin, F., Gabriel, H., Schoberleitner, I., Huang, A., Piatti, P., Nat, R., Troppmair, J. and Lusser, A.
Cell Mol Life Sci. 2017 Nov 4, [epub ahead of print]
Deep transcriptome annotation enables the discovery and functional characterization of cryptic small proteins
Samandi, S., Roy, A. V., Delcourt, V., Lucier, J. F., Gagnon, J., Beaudoin, M. C., Vanderperre, B., Breton, M. A., Motard, J., Jacques, J. F., Brunelle, M., Gagnon-Arsenault, I., Fournier, I., Ouangraoua, A., Hunting, D. J., Cohen, A. A., Landry, C. R., Scott, M. S. and Roucou, X.
Elife. 2017 Oct 30, 6.
The Human Knockout Gene CLYBL Connects Itaconate to Vitamin B12
Shen, H., Campanello, G. C., Flicker, D., Grabarek, Z., Hu, J., Luo, C., Banerjee, R. and Mootha, V. K.
Cell. 2017 Nov 2, 171 (4):771-782 e11.

See also: Research areas for this month include:

See for comparison: Autophagy

Autophagy is a process by which cellular material is degraded by lysosomes or vacuoles and recycled. Several autophagy pathways operate within a cell, including macroautophagy, microautophagy and chaperone-mediated autophagy.

Latest Research and Reviews

For example:

Dual role of autophagy in hallmarks of cancer

Quantitative assessment of cell fate decision between autophagy and apoptosis

The Nature Publications Group has fallen far behind the data and technical expertise of all the serious scientists in the world. It seems likely that they will attempt to portray autophagy as something besides the innate phage defense system and fail miserably.

Autophagy is the antiphage defense strategy December 8, 2016

What would you do if your publisher arrived at the “Autophagy Party” more than a year late and you had to introduce them as a supporter of neo-Darwinian nonsense and “Big Bang” cosmology?
Nobody wants to belong to the party of losers. One of the best strategies in such a case is evidently an interpretation of the change as a gradual accumulation of knowledge while their work has always been at the cutting edge. — Kalevi Kull
 

Difference in the network of hydrogen bonds between high- and low-altitude Hb variants, HH-H and LL-L, respectively

The α1 and β1 subunits of HH-H (light blue) and LL-L (light red) are superimposed, and van der Waals radii are shown for α-chain residues that are in atomic contact with β-chain residues of the opposing α2β2 dimer.

The overwhelming ignorance of sex researchers

Summary: J. Michael Bailey, and others like him, pretend to not know how non-coding variants are epigenetically linked from differences in hydrogen bonds to all energy-dependent biophysically constrained morphological and behavioral phenotypes.

Genome-Wide Association Study of Male Sexual Orientation [Energy-dependent changes in biophysically constrained viral latency]

We identified several [energy-dependent changes in] SNPs with p < 10−5, including regions of multiple supporting SNPs on chromosomes 13 (minimum p = 7.5 × 10−7) and 14 (p = 4.7 × 10−7). The genes nearest to these peaks have functions plausibly relevant to [biophysically constrained viral latency and] the development of  sexual orientation.

Reported as: Gene variants identified that may influence sexual orientation in men and boys

The findings by the team do not settle the argument of whether homosexuality in people is biology-based, but instead offers more evidence that suggests it is likely the case. Prior studies that looked at family histories have also offered some evidence of biology playing a role while other studies have found some differences in chromosomes. In this study, the number of samples tested was too small to offer conclusive evidence—larger studies will have to be undertaken to solidify the evidence.

I was not surprised to see J. Michael Bailey listed as a co-author. He is a biologically uninformed pseudoscientist and a passive/aggressive antagonist.

It’s been more than 4 years since food energy-dependent changes in hydrogen-atom transfer in DNA base pairs in solution were linked to biophysically constrained viral latency and all biodiversity via the pheromone-controlled physiology of reproduction in all living genera.

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Sex researchers like J. Michael Bailey, are still among the majority of those who have paid no attention to the extant literature since the time we published this 1996 review in Hormones and Behavior (with a section on molecular epigenetics.)

From Fertilization to Adult Sexual Behavior

Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus (Runge and Zakian, 1996; Wu and Haber, 1995).

All serious scientists know that everyone else must also start with differences in the quantized energy of hydrogen to get from epigenetic modifications to differences in morphological and behavioral phenotypes. Serious scientists also know that social science is pseudoscience and that pseudoscientific nonsense is the cause of all preventable unnecessary suffering and premature death.

See for instance:

1) Epistasis Among Adaptive Mutations in Deer Mouse Hemoglobin
2) Mutation-Driven Evolution
and my refutation of neo-Darwinian pseudoscientific nonsense. All three were published on June 14, 2013.
3) Nutrient-dependent/pheromone-controlled adaptive evolution: a model
Please join the other serious scientists who have been quietly ridiculing people like J. Michael Bailey for more than 20 years.

QuEBS workshop has established itself as an outstanding stage to present the research in the intersection of physics, chemistry and biology. This field has been developed in Lithuania for more than 20 years already. The beginnings could be associated with a series of “Light-harvesting Physics” international conferences, which were held in Lithuania (in Preila, 1992 and 1994, and in Birštonas, 1996). During these conferences, discussion of notable scientists and pioneers of Quantum Biology, such as Graham R. Fleming, Shaul Mukamel, Rienk van Grondelle, Richard Cogdell, Alfred Holzwarth and others, established excitons in biology as the “must-talk-language” when describing the quantum effects in biological light-harvesting systems.

Light harvesting is the source of energy-dependent changes in hydrogen that link physics, chemistry, and molecular epigenetics to accurate representations of RNA-mediated cell type differentiation. All aspects of energy-dependent RNA-mediated cell type differentiation have been virtually ignored by J. Michael Bailey, who is the proud owner of the Sexnet listserver. It has been a consistent source of misinformation for all participants during the past two decades.
See for comparison my comments on: Evolution of a Vertebrate Social Decision-Making Network
1)

Re: Cause and effect. How could it not be the adaptive evolution from yeasts of the ligand-receptor binding exemplified across species by the conservaton of gonadotropin releasing hormone (GnRH) and diversification of its receptor? Model organisms like the threespine stickleback make clear the involvement of ecological niche construction. The honeybee invertebrate model organism makes clear the involvement of the nutrient dependent ecological niche in construction of the pheromone-dependent social niche. Invertebrate and vertebrate models collectively attest to the common molecular biology of adaptively evolved social decision-making networks. In mammals, the hypothalamic neurogenenic niche (probably located in the MPOA) responds to nutrients to enable fertility and responds to pheromones to enable sexual reproduction that has adaptively evolved from its origins in brewer’s yeast. Never before has there been such a clear reprentation of cause and effect across species from microbes to man, where nutrient chemicals calibrate the intracellular signaling and their metabolism to pheromones standardizes and controls the stochastic gene expression required for reproduction. Gene expression enables adaptive evolution of the brain and ensures that our ability to acquire nutrient chemicals is the first priority for reproduction via appropriate social behaviors, as it is in every species. For example, microbes eat the DNA of heterospecifics but not conspecifics, which indicate more social sense than what some people today are capable of recognizing in the design of biology (the evolved gene, cell, tissue, organ, organ system pathway that directly links sensory input to the mammalian neuroendocrine system and the hormones responsible for our behavior, which activates the same ‘organized’ pathway).

2)
Re: The Intersection of Neurotoxicology and Endocrine Disruption. NeuroToxicology, Bernard Weiss

Abstract excerpts: …hormones help steer the process of brain development.

…sex differences in behavior are primarily the outcomes of differences in how the brain is sexually differentiated during early development by gonadal hormones (the Organizational Hypothesis).

… environmental chemicals are capable of altering these underlying events and processes. Among those chemicals, the group labeled as endocrine disrupting chemicals (EDCs) offers the clearest evidence of such selectivity… —————– I have terminally argued to conclusion that the clearest evidence of chemicals that alter the underlying events and processes of brain development and its sexual differentiation are the nutrient chemicals and pheromones responsible for the adaptive evolution of species from microbes to man.

Focus on endocrine disruption establishes what happens when toxic chemicals alter the same events and processes of brain development and its sexual differentiation via epigenetic effects on gonadotropin releasing hormone (GnRH) pulsatility, luteinizing hormone, olfactory bulb neurogenesis, hippocampal neurogenesis, learning, and memory in vertebrates.

For contrast, I’ve modeled the epigenetic effects of food odors and pheromones on homeostasis and species diversification, and for many years, my friend Teresa Binstock and co-author (e.g., with Milton Diamond)stressed the importance of endocrine disruption (specifically due to bisphenol A and phthalates) on J. Michael Bailey’s “Sexnet”. Now that the basic principles of biology and levels of biological organization, which link sensory input from the environment directly to behavior via intracellular signaling and stochastic gene expression, have been clarified by work with model organisms, I look forward to learning if there are any reasons to avoid the incorporation of current information on endocrine disruption into existing studies of the homeostatic development of human sexual behavior.

Comparing typical and atypical epigenetic effects that appear to extend to those that are transgenerational seems even more important now than in 1996.

Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338

See also: Open Chromatin Profiling in hiPSC-Derived Neurons Prioritizes Functional Noncoding Psychiatric Risk Variants and Highlights Neurodevelopmental Loci

Our study shows that noncoding disease variants in OCRs can affect neurodevelopment, and that analysis of open chromatin regions can help prioritize functionally relevant noncoding variants identified by GWAS.

After Alan R. Sanders and others published this, the claims in Genome-Wide Association Study of Male Sexual Orientation can be viewed in the context of two decades of false claims and pleas for more funding.

Conclusion:

In this study, the number of samples tested was too small to offer conclusive evidence—larger studies will have to be undertaken to solidify the evidence.

Cytosis can be used to teach everything from base editing to RNA editing to everyone over age 10. They will learn how to link the creation of energy to biophysically constrained viral latency via the physiology of pheromone-controlled reproduction.

Mouse morphs and primate diversity in 50 years

Excerpt:

Analysis of the crystal structure of deer mouse Hb at 1.8 Å resolution (24, 25) revealed that each of the eight rHb mutants is characterized by a unique constellation of hydrogen bonds within and between subunits (Table 2 and fig. S2). Additional hydrogen bonds between subunits of the same αβ dimer are formed in the presence of β128Ser (an L-type residue; fig. S2), which contributes to the observed epistasis between allelic α- and β-chain variants.

———————————
Energy-dependent RNA-mediated biophysically constrained viral latency (i.e., silencing of viral elements) protects all organized genomes from the degradation of messenger RNA that links mutations to all pathology. The mutations are caused by nutritional stress and/or social stress. That fact has been known to all serious scientists for at least 50 years. But see:
Silencing of viral elements: A cure for schizophrenia? ARTICLE Provisionally accepted

1. The problem.
Scientific evidence for various infectious agents as cause for psychosis in schizophrenia is not robust. Many pathogens that influence brain development might play a role in disease causation. It has been shown that influenza exposure before birth(Brown, 2012), exposure to herpes simplex during birth(Brown et al., 2011) or exposition to Toxoplasma gondii and other pathogens (Arias et al., 2012) increases risk for schizophrenia and/or compromises cognition. During psychosis viral and also ancient retroviral elements become may activated in the brain(Karlsson et al., 2001; Perron et al., 2012). The implication of this research for use in clinical practice is ambiguous, because a robust virus test is lacking.

Examples of human idiocy are the problem. See for comparison:

QuEBS workshop has established itself as an outstanding stage to present the research in the intersection of physics, chemistry and biology. This field has been developed in Lithuania for more than 20 years already. The beginnings could be associated with a series of “Light-harvesting Physics” international conferences, which were held in Lithuania (in Preila, 1992 and 1994, and in Birštonas, 1996). During these conferences, discussion of notable scientists and pioneers of Quantum Biology, such as Graham R. Fleming, Shaul Mukamel, Rienk van Grondelle, Richard Cogdell, Alfred Holzwarth and others, established excitons in biology as the “must-talk-language” when describing the quantum effects in biological light-harvesting systems.

Every aspect of biophysically constrained energy-dependent RNA-mediated life on Earth has refuted the pseudoscientific nonsense about emergence and evolution.

As climate warms, mice morph

Biologists document changes in teeth and skull structure in two species in southern Quebec over past 50 years

The ridiculous claim that the fixed amino acid substitutions were adaptive mutations proves how little the authors understand about biophysically constrained viral latency.

Excerpt 1)

“Biologists document changes in teeth and skull structure in two species in southern Quebec over past 50 years

Excerpt 2)

“These changes may be related to a dietary shift caused by climate change, combined with competition for food resources between the two species of mice, according to the researchers.”

All serious scientists know that food energy biophysically constrains the pheromone-controlled physiology of reproduction, which links the fixation of RNA-mediated amino acid substitutions to cell type differentiation in all living genera.
 
We have now arrived at the claims of biologically uninformed science idiots who tell us that two different species evolved in 50 years.
 

Excerpt 3)

“One question that remains to be settled is whether the changes are genetic, and will be passed on to future generations — actual evolution — or whether they represent “plasticity,” the capacity of some species to adjust to rapid environmental change.”

The facts about the transgenerational epigenetic inheritance of healthy longevity for comparison to virus-driven pathology have been exquisitely detailed. All serious scientists have dispensed with the nonsense that questions the capacity of some species to adjust to rapid environmental change. Ecological variation must be linked from the physiology of pheromone-controlled reproduction in all living genera via the conserved molecular mechanisms of RNA-mediated cell type differentiation that link fixation of amino acid substitutions to the morphological and behavioral phenotypes of all individuals and all species on Earth.

See for instance, on the same day that my 2013 refutation of Nei’s pseudoscientific nonsense about Mutation-driven evolution was published, this also was published: Epistasis Among Adaptive Mutations in Deer Mouse Hemoglobin

Epistasis is food energy-dependent. The energy must be biophysically constrained in the context of the physiology of pheromone-controlled transgenerational epigenetic inheritance. The creation of energy in a hydrogen atom was linked from the anti-entropic virucidal effect of sunlight to the stability of the organized genome of mice by hydrogen-atom transfer in DNA base pairs in solution and differences in the hemoglobin molecule of ecologically adapted species.

Analysis of the crystal structure of deer mouse Hb at 1.8 Å resolution (24, 25) revealed that each of the eight rHb mutants is characterized by a unique constellation of hydrogen bonds within and between subunits (Table 2 and fig. S2). Additional hydrogen bonds between subunits of the same αβ dimer are formed in the presence of β128Ser (an L-type residue; fig. S2), which contributes to the observed epistasis between allelic α- and β-chain variants.

See also:

…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.

The fact that every Angstrom is dynamic and the fact that energy-dependent changes in the microRNA/messenger RNA balance have been linked to biophysically constrained viral latency and all biodiversity was placed into the context of this parody:

 See also:


The Mechanical Properties of DNA are food energy-dependent and RNA-mediated

The elastic properties of the DNA molecule determine how it supercoils during replication, how it packs into confined biological structures and how it interacts with proteins during gene expression.

See: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
Pattern recognition

Nutrient-dependent atomic-level changes may determine the nucleotide changes in a specific base pair. The nucleotide changes appear to link nutrient-dependent single nucleotide polymorphisms (SNPs) from the availability of fruits and vegetables or fermented milk products to individual differences and to species differences in the need for certain vitamins. For example, cell type determination and differentiation are associated with the nutrient-dependent 3D distribution of amino acid substitutions as they accumulated during a history of ecological adaptations [32] in flies [9] and in humans [33]. Sex differences in behavior also appear to arise from the single-molecule and single cell levels in flies, which suggests that adaptive changes in behavior can be explained in the context of nutrient-dependent pheromone-controlled genome-environment interactions that alter circuit plasticity via amino acid substitutions [34].

Conclusion from: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

The companion papers [162-163] told a new short story of ecological adaptations. In the context of climate change and changes in diet, the story began with what probably was a nutrient-dependent base pair change and a variant epiallele that arose in a human population in what is now central China. Apparently, the effect of the epiallele was adaptive and it was manifested in the context of an effect on sweat, skin, hair, and teeth. In another mammal, such as the mouse, the effect on sweat, skin, hair, and teeth is probably due to a nutrient-dependent epigenetic effect on hormones responsible for the tweaking of immense gene networks that metabolize nutrients to pheromones. The pheromones appear to control the nutrient-dependent epigenetically-effected hormone-dependent organization and hormone-activation of reproductive sexual behavior in mammals such as mice and humans, but also in invertebrates and in microbes as previously indicated.

The ecological adaptations, which appear to be manifested in the human population are detailed in these two reports [162-163]. The ecological adaptations are likely to be nutrient-dependent and pheromone-controlled. If so, ecological variation probably leads to ecological, social, neurogenic, and socio-cognitive niche construction, which is manifested in increasing organismal complexity and species diversity. If not, there may be something as yet unknown about mutations and evolution that makes sense in the light of what is known about nutritional epigenetics and the molecular biology of species from microbes to man.

See for comparison: The evolution of H2
Biohydrogen production from hyperthermophilic anaerobic digestion of fruit and vegetable wastes in seawater: Simplification of the culture medium of Thermotoga maritima
Mechanism of Nitrogenase H2 Formation by Metal-Hydride Protonation Probed by Mediated Electrocatalysis and H/D Isotope Effects
The claims that energy emerged or that differences in hydrogen and differences in species evolved outside the context of the energy-dependent creation of enzymes are among the most ridiculous examples of human idiocy that any serious scientist has ever encountered.
Claims about the emergence of life were again retracted on November 23, 20-17 and reported on December 5, 2017.

”Definitely embarrassing:” Nobel Laureate retracts non-reproducible paper in Nature journal

See: Comment awaiting moderation.

James V. Kohl December 7, 2017 at 4:35 am
The Science Behind the Game “Cytosis,” pits the collaborative efforts of 20 serious scientists against the pseudoscientific nonsense touted by theorists. The serious scientists know how energy-dependent RNA-mediated cell type differentiation occurs.
Resources (e.g., mRNA, ATP) are used to build enzymes, hormones, and/or receptors. Health points accumulate to show why food energy must be linked from the physiology of pheromone-controlled reproduction to biophysically constrained viral latency.
For comparison, Szostak and other theorists have been stuck with their ridiculous misrepresentations of emergence and neo-Darwinian evolution, which failed to consider Darwin’s “conditions of life.”
“Conditions of life” are energy-dependent. The energy is Schrodinger’s anti-entropic virucidal energy. It comes from sunlight and is epigenetically “trapped” in food via the physiology of reproduction.
Board Game:
Cytosis: A Cell Biology Game
Title:
Cytosis – The Science Behind the Game https://boardgamegeek.com/filepage/155090/cytosis-science-behind-game
See also: Two retractions of human idiocy
See also: Routing gene therapy directly into the brain

Once the genetically-engineered HSCs are transplanted into the brain’s ventricles, the crucial enzyme they contain helps to metabolize the materials that were previously building up and causing tissue damage.

A new lineage of cells descended from the transplanted HSCs — a type of cell called a myeloid — begin to scavenge and consume the excess material that is responsible for neurodegeneration.

The pheromone-controlled differentiation of these cell types was predicted in the context of claims that pheromones biophysically constrain all pathology in the mouse to human model, which has been thoroughly detailed since 1994.
See: [Pheromonal regulation of genetic processes: research on the house mouse (Mus musculus L.)
See also: Pheromones and the luteinizing hormone for inducing proliferation of neural stem cells and neurogenesis

See also: Researchers Discover Key to Diseases in Mitochondrial DNA Mutations

Because the primary job of the mitochondrion is to produce energy, most of its genes are involved in pathways in the energy production process. Although it has a small genetic code, mtDNA contains the blueprints for building many of the enzymes and proteins that are needed to function in those pathways.
 
The virus-driven theft of quantized energy as information links the degradation of messenger RNA from mutations to all pathology in all living genera. The speed of light on contact with water has been linked to all energy-dependent RNA-mediated DNA repair in the context of the physiology of reproduction and the transgenerational epigenetic inheritance of healthy longevity.
Alternative splicing of pre-mRNA

Light-activated error free DNA repair (2)

Summary: In the diagram and diatribes that accompany claims about de novo changes in electrons and the production of nucleotides, the amount of pseudoscientific nonsense becomes perfectly clear. Pseudoscientists start with energy-dependent changes but call the changes de novo changes in electrons. That allows the pseudoscientists to dismiss any facts about how the creation of energy must be linked to the creation of enzymes. The creation of enzymes does not automagically occur and the creation of all biodiversity must occur via the enzymatic metabolism of food to pheromones and the physiology of pheromone-controlled reproduction. Use of the phrase de novo changes is a clear indicator that pseudoscientists know nothing about biophysically constrained viral latency and nothing about cell type differentiation. All changes are energy-dependent and virus-driven energy theft links the degradation of messenger RNA from mutations to all pathology.
In Light-activated error free DNA repair, I wrote:

The creation of quantized energy in sunlight links energy as information from electrons to ecosystems via the physiology of reproduction in all living genera.

See also: Endogenous adenosine maintains cartilage homeostasis and exogenous adenosine inhibits osteoarthritis progression

We conclude that adenosine, acting at A2AR, is an important homeostatic regulator of chondrocytes and cartilage and adenosine repletion may represent a novel approach to treating OA (Fig. 6).

The link from exogenous adenosine to the endogenous adenosine that inhibits pathology is food energy-dependent and RNA-mediated.That is why adenosine repletion will almost undoubtedly be effective. Some friends have already found that supplements of curcumin and nicotinamide/niacinamide are helpful.
Science needs reason to be trusted to link the creation of visible light to the creation of the nicotinamide-dependent enzyme known as ketoreductase, which can be transformed from a carbonyl reductase into an initiator of radical species and a chiral source of hydrogen atoms.
If hydrogen-atom transfer in DNA base pairs in solution is not linked to healthy longevity, the virus-driven degradation of messenger RNA will not be linked from mutations to all pathology.
See: Accessing non-natural reactivity by irradiating nicotinamide-dependent enzymes with light
The link from the quantized energy of the sun has been placed into this context:

We demonstrate this new reactivity through a highly enantioselective radical dehalogenation of lactones-a challenging transformation for small-molecule catalysts. Mechanistic experiments support the theory that a radical species acts as an intermediate in this reaction, with NADH and NADPH (the reduced forms of nicotinamide adenine nucleotide and nicotinamide adenine dinucleotide phosphate, respectively) serving as both a photoreductant and the source of hydrogen atoms.

The photoreductant source of hydrogen atoms links the quantized energy of sunlight from quantum physics to quantum souls via error-free RNA-mediated DNA repair in the context of the physiology of pheromone-controlled reproduction and the creation of all morphological and behavioral diversity on Earth via what is known about the stability of the gonadotropin releasing hormone (GnRH) decapeptide. The creation of achiral glycine and its position at position 6 in the GnRH decapeptide is linked from food odors and pheromones to the stability of all vertebrate genomes.
See how easily the facts about the stability of supercoiled DNA in the organized genomes of all vertebrates was placed back into the context of evolution.
A quantum theory for the irreplaceable role of docosahexaenoic acid in neural cell signalling throughout evolution
Explanations from classical physics cannot be used to support the theory and nothing but that facts about chemistry links sunlight to the creation of enzymes that metabolize food and link the food energy to biophysically constrained life via the physiology of pheromone-controlled reproduction, which protects organized genomes from the virus-driven degradation of messenger RNA that links mutations to all pathology.

We suggest that DHA is one Darwin’s “Conditions of Existence” [conditions of life] which made DHA the master of DNA

How Popper killed Particle Physics

Even in his worst moments Popper never said a theory is scientific just because it’s falsifiable. That’s Popper upside-down and clearly nonsense. Unfortunately, upside-down Popper now drives theory-development, both in cosmology and in high energy physics.
It’s not hard to come up with theories that are falsifiable but not scientific. By scientific I mean the theory has a reasonable chance of accurately describing nature.

11/20/17
Jay R. Feierman:

Science is about predicting, not post hoc explaining except under the conditions stated above. I still find Popper’s methods useful for crafting theories in the bio-behavioral sciences. I’m not ready to declare his philosophy as dead.

7/25/13
Jay R. Feierman: Variation is not nutrient availability and the something that is doing the selecting is not the individual organism. A feature of an educated person is to realize what they do not know. Sadly, you don’t know that you have an incorrect understanding [of] Darwinian biological evolution.
Popper’s upside-down theory can be replaced in the context of the inside-out olfactory receptor, which links the epigenetic landscape to the physical landscape of DNA via two epigenetic traps
An Epigenetic Signature for Monoallelic Olfactory Receptor Expression
Nuclear Aggregation of Olfactory Receptor Genes Governs Their Monogenic Expression

We’ve got the evolution of complex cells inside-out

Almost everybody agrees that the complex eukaryotic cell evolved from a simple ancestor. The question is how.

All serious scientists know that the energy-dependent creation of ATP (epigenetic trap #1) must be linked from the creation of RNA (epigenetic trap #2) to all biodiversity on Earth via the physiology of pheromone-controlled reproduction in species from microbes to humans. For example, without the energy-dependent de novo creation of G protein-coupled receptors, there is no way to link any light-induced endogenous substrate to the creation of enzymes and the metabolism of food to the energy that sustains life in electron eating microbes and microbes that “eat” light.

 
“…Golden didn’t set out from school intent on pursuing a career in chronobiology. The field only barely existed when she did her graduate work in the 1980s. Her specialty was, and still is, studying bacteria that use light as a source of energy.

See also: Biogenic non-crystalline U(IV) revealed as major component in uranium ore deposits

The fact that bacteria eat electrons and produce uranium isotopes can now be linked from light-harvesting to all pheromone-controlled biophysically constrained biodiversity on Earth by what was known to Susan S. Golden in the 1980s.

Two Questions remain:

1) Where do the electrons come from?

2) Why doesn’t every serious scientist know how to link energy-dependent changes from electrons to ecosystems via the link from ultraviolet light to the vibrational theory of olfaction and RNA-mediated feedback loops that link food odors and pheromones to the physiology of reproduction in species from microbes to humans?

The vibrational theory of olfaction for the win by John Hewitt

On 11/21/17, John Hewitt alerted me to the fact that the information in this article might be linked from the de novo creation of olfactory receptor genes to all biodiversity on Earth via links from the physiology of pheromone-controlled reproduction in bacteria to human adult hippocampal neurogenesis. The monoallelic disease(s) known as Kallmann’s Syndrome clearly link the transgenerational epigenetic inheritance of virus-driven pathology to deficits in olfactory acuity and specificity. The olfactory deficites link interactions among all neuronal systems in the brain to healthy longevity via the substitution of the achiral amino acid glycine in position 6 of the GnRH decapeptide.

See: Long-Range GABAergic Inputs Regulate Neural Stem Cell Quiescence and Control Adult Hippocampal Neurogenesis

Taken together, these findings delineate a GABAergic network involving long-range GABAergic projection neurons and local PV interneurons that couples dynamic brain activity to the neurogenic niche in controlling NSC quiescence and hippocampal neurogenesis.

See for comparison: Guidelines for Genome-Scale Analysis of Biological Rhythms

1) Genome biology approaches have made enormous contributions to our understanding of biological rhythms, particularly in identifying outputs of the clock, including RNAs, proteins, and metabolites, whose abundance oscillates throughout the day.

2) …we discuss several unmet analytical needs, including applications to clinical medicine, and suggest productive avenues to address them.

This suggests they are going to try to make it appear that Schrodinger’s link from the anti-entropic virucidal effects of sunlight has only recently been discovered to be the key to the prevention of the virus-driven degradation of messenger RNA, which all serious scientists know is the link from mutations to all pathology.
SS Golden is the co-author and they propose 3 broadly applicable “golden rules” of light-activated biological rhythms. The “Golden Rules” do not link more than 66,000 published works on microRNAs to Kohl’s “Laws of Biology” in this 2014 invited review of nutritional epigenetics: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
The Law’s of Biology are Darwin’s “conditions of life.” Simply put, all organisms must eat and the physiology of pheromone-controlled reproduction must be linked to all morphological and behavioral biodiversity on Earth after the creation of light made life possible. Natural selection for anything that was selected after the creation of energy, should not be viewed in the context of explanations of anything else.
Nothing on Earth exists outside the context of biophysically constrained energy and viral latency. Nothing on Earth exists outside the context of energy-dependent natural selection for codon optimality in the context of fixation of RNA-mediated amino acid substitutions, the creation of enzymes and the interactions among complex systems in humans that link achiral glycine in position 6 of the GnRH decapeptide to all morphological and behavioral phenotypes.

See also: An epigenetics gold rush: new controls for gene expression

‘A-to-I editing’ can alter a protein’s coding sequence, and, in humans, is crucial for keeping the innate immune response in check.

See for comparison: Redox-sensitive alteration of replisome architecture safeguards genome integrity

DNA replication requires coordination between replication fork progression and deoxynucleotide triphosphate (dNTP)–generating metabolic pathways

The safeguards are energy-dependent and they have been linked from light-activated endogenous substrates in all cell types to changes in immune system function. That fact is ignored in the context of a “genome survellance mechanism.”

Studying this genome surveillance mechanism in cancer cells with elevated ROS levels and increased replication adaptability may provide opportunities to specifically target tumors.

Reported as: Redox sensing controls DNA replication!

Redox sensing controls DNA replication!

New DNA is generated in human cells from tiny building blocks called nucleotides produced by an enzyme called RNR (ribonucleotide reductase).

By starting with de novo changes in electrons, the diagram that accompanies the pseudoscientific nonsense of their claim makes the nonsense perfectly clear. They intend to leave out anything known to serious scientists who have linked the creation of energy to the creation of enzymes and to the creation of all biodiversity via the metabolism of food to pheromones and the physiology of pheromone-controlled reproduction.
For comparison, serious scientists have linked energy-dependent changes from atoms to ecosystems via the conserved molecular mechanisms of base editing, microRNA editing, and RNA editing as detailed in Light-activated error free DNA repair.
See for examples:
Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
Reduced adenosine-to-inosine miR-455-5p editing promotes melanoma growth and metastasis

…adenosine-to-inosine (A-to-I) RNA editing occurs in microRNAs (miRNAs)…

Thanks to Dr. Phil Mills for bring this to my attention in the context of more than 40 skin cancer excisions I have had during the past few years. RNA editing by ADAR1 leads to context-dependent transcriptome-wide changes in RNA secondary structure

Our findings imply that the editing effect on RNA secondary structure is context dependent and underline the intricate regulatory role of ADAR1 on global RNA secondary structure.

See: Scientists demonstrate the importance of RNA editing in melanoma development

…a lack of RNA editing, a process by which information inside RNA molecules is transformed, leads to tumor growth and progression through manipulation of proteins.

See also: Study: Vitamin B3 might help against skin cancer

…people who took a specific type of vitamin B3 for a year had a 23 percent lower rate of new skin cancers compared to others…

The link from sun exposure to vitamin C production in plants and vitamin D production in human populations that might be protected from skin cancer by niacinamide, led me to become more focused on prevention. For example, a 23 percent lower rate of skin cancers translates to 10 less excision surgeries if I can achieve a better energy-dependent microRNA/messenger RNA balance.
Energy-dependent base editing has been linked to microRNA editing and linked from RNA editing to the fixation of RNA-mediated amino acid substitutions in the organized genomes of all living genera via the pheromone-controlled physiology of reproduction. Any presentation of data that fails to start with energy-dependent changes in the microRNA/messenger RNA balance implies a deliberate attempt to support the pseudoscientific nonsense of evolutionary theorists and/or big bang cosmologists.
It’s time for pseudoscientists to admit they’ve been wrong about mutation-driven evolution and move forward via consideration of experimental evidence.
See also: Systematic characterization of A-to-I RNA editing hotspots in microRNAs across human cancers
MicroRNA-mediated RNA editing links energy-dependent changes in base pairs from the creation of nucleotides to the stability of organized genome in all living genera via the physiology of pheromone-controlled reproduction in species from microbes to humans.  All serious scientists know that. However, the number of pseudoscientists is more than the serious scientists who will be presenting at this conference.
See: Mechanisms of Recombination conference
For comparison, the pseudoscientists have their own conferences. See for a possible example: Neuroimmunology and Neurological disorders
I’ve already asked the conference organizer “Who will be linking the molecular mechanisms of recombination to neuroimmunology via autophagy or help serious scientists to link the virus-driven degradation of messenger RNA to all pathology?” 
I no longer expect any answer to my questions from those who have not linked the creation of quantized energy to all biodiversity via the pheromone-controlled physiology of reproduction in species from microbes to humans.
See instead, more information on: A-to-I RNA editing

Alternative splicing of pre-mRNA

MicroRNAs and the Cassandra syndrome (revisited)

Conclusion: Serious scientists can explain every aspect of energy-dependent biophysically constrained viral latency in the context of details about these pathways and everything that links changes from electrons to ecosystems in all living genera. Why are the serious scientists still challenged by “…the tendency of academia to reject any academic-like work from outside academia?” What aspect of the academic contribution that could lead to the cure for all pathology do biologically uninformed academics want to continue to reject and attack?
See: Creating genes and species

The “Cassandra syndrome” theme prevails throughout the history of all serious scientists. They are cursed with being able to predict the future because they are always disbelieved.

See for instance: Experience-Dependent Accumulation of N6-Methyladenosine in the Prefrontal Cortex Is Associated with Memory Processes in Mice
The authors claim that differential effects of m6A may depend on interactions between microRNAs and cis-acting elements that are present on the RNA molecule.
Simply put, the interactions are energy-dependent and RNA-mediated. Pseudoscientists do not know where the energy came from that creates new cells and they do not know what kills the new cells.
But see: When You Learn, Your Brain Swells with New Cells — Then It Kills Them

In a new opinion paper, published online Nov. 14 in the journal Trends in Cognitive Sciences, researchers proposed that this swelling and shrinking of the brain is a Darwinian process.

The claim that this is a Darwinian process comes from: Expansion and Renormalization of Human Brain Structure During Skill Acquisition

MRIs use complex physics to peer through the walls of the skull into the brain.

Jaak Panksepp’s group won the 2002 award that my group won in 2001 for publication of Human pheromones: integrating neuroendocrinology and ethology. See for comparison:

If you don’t understand the foundational level, then you can do brain imaging until you’re blue in the face, but you still will not understand the process at a deep causal level. — Dr. Jaak Panksepp, Author of Affective Neuroscience: The Foundations of Human and Animal Emotions

The foundational level is food energy-dependent. See RNA-mediated.com or the FB group RNA mediated.
See the missing foundational level extended from a Darwinian process of swelling and shrinking of the brain to claims about human evolution.
From the Human Ethology Yahoo Group moderated by Jay Feierman.
Human evolution was uneven and punctuated, suggests new research

…this process was not a straightforward, smooth one – instead, it seems to have been punctuated, with different evolutionary patterns in different geographical regions.

More than 1300 hemoglobin variants attest to the obvious fact that evolutionary theorists cannot recognize any pattern that links food energy from what humans eat to the biophysically constrained pheromone-controlled physiology of reproduction. They ignore every aspect of food energy-dependent RNA-mediated amino acid substitutions, which protect all organized genomes from the virus-driven degradation of messenger RNA. The degradation of messenger RNA links mutations to all pathology.
See for examples of food energy-dependent pathology prevention: HbVar: A Database of Human Hemoglobin Variants and Thalassemias
To place food energy-dependent prevention of pathology into the perspective of difference in primates, see:

For example, 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).”

See also: Humans And Chimps Differ At Level Of Gene Splicing
The fact that gene splicing is linked to a single amino acid that differentiates the cell types of 2 primate species from the gorilla, led me to ask: What do other people do when they learn that everything they were taught to believe about evolution is a lie?
I placed the question to the Neuroscience FB group into this context: The Academic Ape: Instinctive aggression and boundary enforcing behaviour in academia

The Cassandra Effect describes the tendency of academia to reject any academic-like work from outside academia and that the more “academic” the contribution, the more strongly it is rejected and attacked.

This is the accurate representation of food energy-dependent pheromone-controlled learning and memory that has consistently been attacked or ignored since the time we published our 1996 Hormones and Behavior review. In our section on molecular epigenetics, we wrote:

Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to….

Alternative splicing techniques of pre-mRNA have since been linked to every aspect of cell type differentiation in all individuals of all species. The pre-mRNAs are called microRNAs and detailed examples of how food energy-dependent changes in the microRNA/messenger RNA balance can be linked to what has been known about RNA-mediated cell type differentiation to serious scientists. For example, serious scientists know that all changes in the microRNA/messenger RNA balance are energy-dependent. No changes are random. All changes are biophysically constrained. The changes constrain viral latency. That fact has been established in more than 67,000 indexed published works.

See: microRNA Items: 1 to 20 of 67307

What do theorists do when they are repeatedly presented with overwhelming experimental evidence that links food energy-dependent microRNAs to refutation of all their ridiculous theories and all the pseudoscientific nonsense of neo-Darwinian evolution?

 

Jay R. Feierman:

“Variation is not nutrient availability and the something that is doing the selecting is not the individual organism. A feature of an educated person is to realize what they do not know. Sadly, you don’t know that you have an incorrect understanding [of] Darwinian biological evolution.”

See for comparison: Food derived microRNAs
and

 
See also: Exploitation of microRNAs by Japanese Encephalitis Virus in human microglial cells

The microRNA gene targets, gene ontology, annotations and pathways were identified through various bioinformatics tools. Additionally, the pathways were mostly found common to “ubiquitin mediated proteolysis”, “cytokine signaling”, “maintenance of barrier function/cell junctions”, JAK/STAT pathway” “Toll-like receptor signaling”, “Wnt-signaling”, “adhesion molecules”, “apoptosis”, “endocytosis”, “vesicle mediated transport” etc.

Serious scientists can explain every aspect of energy-dependent biophysically constrained viral latency in the context of details about these pathways and everything that links changes from electrons to ecosystems in all living genera. Why are the serious scientists still challenged by “…the tendency of academia to reject any academic-like work from outside academia?” What aspect of the academic contribution that could lead to the cure for all pathology do biologically uninformed academics want to continue to reject and attack?