Light-activated polycombic ecological adaptations vs hecatombic pathology (4)

By: James V. Kohl | Published on: August 23, 2018

Summary: The difference between adaptations and evolution is now perfectly clear. New species do not evolve from other species. Sympatric speciation can be compared to the evolution of all pathology.
Phenotypically distinct female castes in honey bees are defined by alternative chromatin states during larval development August 22, 2018

…our study provides novel data on environmentally regulated organismal plasticity and the molecular foundation of the evolutionary origins of eusociality.

This neo-Darwinian pseudoscientific nonsense about the evolutionary origins of eusociality comes from the Hurd lab. Co-author, Ryszard Maleszka once referred to my comments on light-activated microRNA biogenesis in the context of the honeybee model organism as “creationist crap.” Now he’s part of the team that links everything known to serious scientists about biophysically constrained viral latency to the creation of the sun’s anti-entropic virucidal energy.
See:  A Quick HYL1-Dependent Reactivation of MicroRNA Production Is Required for a Proper Developmental Response after Extended Periods of Light Deprivation

…plants alter microRNA (miRNA) biogenesis in response to light transition.

For a historical perspective, see my 2013 refutation of neo-Darwinian nonsense: Nutrient-dependent/pheromone-controlled adaptive evolution: a model

The role of the microRNA/messenger RNA balance (Breen, Kemena, Vlasov, Notredame, & Kondrashov, ; Duvarci, Nader, & LeDoux, ; Griggs et al., ; Monahan & Lomvardas, ) in adaptive evolution will certainly be discussed in published works that will follow.

The difference between ecological adaptations and the hecatombic evolution of pathology is now perfectly clear. Since new species do not evolve from other species, ecological adaptations and microRNA-mediated sympatric speciation can be compared to the evolution of all pathology.
See also: MicroRNAs in Honey Bee Caste Determination (2016, senior author Ryszard Maleszka)
For comparison, see Expression of key components of the RNAi machinery are suppressed in Apis mellifera that suffer a high virus infection
Only a fool would continue to insist that his findings exemplify the molecular foundation of the evolutionary origins of eusociality after serious scientists linked everything known about light-activated microRNA biogenesis to biophysically constrained viral latency and all biodiversity via the honeybee model organism and extension of the facts to biophysically constrained Alzheimer’s disease.
See: Herpes Viruses and Senile Dementia: First Population Evidence for a Causal Link
See for comparison: Isolated detection of elastic waves driven by the momentum of light
The creation of subatomic particles has been linked from the creation of difference in the energy of photons to the proton motive force and the biophysically constrained transgenerational epigenetic inheritance of all pathology by a novel, primate-specific and human-specific ‘kill switch’.
A novel, primate-specific ‘kill switch’ tumor suppression mechanism for p53

The activation of TP53 is well known to exert tumor suppressive effects. We have detected a primate-specific adrenal androgen-mediated tumor suppression system in which circulating dehydroepiandrosterone sulfate (DHEAS) is converted to DHEA specifically in cells in which TP53 has been inactivated. DHEA is an uncompetitive inhibitor of glucose-6-phosphate dehydrogenase (G6PD), an enzyme indispensable for maintaining reactive oxygen species within limits survivable by the cell. Uncompetitive inhibition is otherwise unknown in natural systems because it becomes irreversible in the presence of high concentrations of substrate and inhibitor. In addition to primate-specific circulating DHEAS, a unique, primate-specific sequence motif that disables an activating regulatory site in the glucose-6-phosphatase (G6PC) promoter was also required to enable function of this previously unrecognized tumor suppression system. I

The nutrient-dependent pheromone-controlled activation of a “kill switch” in mammals was first proposed in the context of Pheromonal Regulation of Genetic Processes: Research on the House Mouse (Mus musculus L.)
It was detailed for a general audience in the context of  The scent of eros: mysteries of odor in human sexuality (by Kohl and Francoeur 1995/2002)
Look inside for information on DHEA and on DHEAS linked to the production of human specific pheromones.
See: [Cytogenetic effect of volatile components of urine of sexually mature animals on bone marrow cells of young female house mice Mus musculus L]
See also: Chemosignals from isolated females have antimutagenic effect in dividing the cells of bone marrow from male mice of the CBA strain

Humans also have various pheromone-induced physiological effects, especially those associated with reproduction [46, 47]. This suggests that the human olfactory system is still an effective pathway for influencing environmental factors on the human nervous system.

[46] is Kohl, J.V., Atzmueller, M., Fink, B., and Grammer, K., Human pheromones: integrating neuroendocrinology and ethology, Neuroendocrinol. Lett., 2001, vol. 22, pp. 309–321.
See for comparison: Redefining neuroendocrinology: Epigenetics of brain-body communication over the life course (2017)

Though I did not think of it that way at the time, “epigenetics” has been the core of my laboratory’s work on the brain and brain-body interactions. My mentors for my dissertation, in 1964, Vincent Allfrey and Alfred Mirsky, taught me the fundamentals of “epigenetics” in the 1960’s before there was much interest in it, and when the name, epigenetics, meant something quite different (see BOX 3).

In 1991, Bruce McEwen taught me the difference between starting with theories and starting with facts about epigenetic effects on hormones the must be linked to affects on behavior via RNA-mediated biophysically constrained fixation of RNA amino acid substitutions, which differentiate the cell types of all individuals of all species.
I revisited the topic of effect and affect when we last spoke in 2012. I was concerned that he had changed his mind until he corrected an already published manuscript that was the cause of my concern:
See: Correction for McEwen, Brain on stress: How the social environment gets under the skin (2013)

The authors note that on page 17184, right column, first paragraph, line 4, “effect” should instead appear as “affect.”

I now claim that biologically uninformed theorists have not learned the difference between the effect of food odors and pheromones on hormones, and the unconscious affect of hormones on behavior.
See for examples of their overwhelming ignorance.
Sexing up human pheromones: How a corporation created a “scientific” myth
Tristram Wyatt, University of Oxford, United Kingdom
Short summary: “A corporation interested in patenting ‘human pheromones’ for profit created a long lasting myth that has drawn in many scientists as well as the general public. I describe what went wrong. As humans are mammals, we may have pheromones (chemical signals within a species). However, there is no robust bioassay‑led evidence for the widely published claims that four steroid molecules are human pheromones: androstenone, androstenol, androstadienone, and estratetraenol. Positive results are highly likely to be false positives. Instead, we need to use the rigorous methods already proven successful in pheromone research on other species. I will discuss the wider lessons for carrying out better human behavioural research, including olfaction.”
Tristam Wyatt wants a robust assay to show that Olfaction Warps Visual Time Perception in the context of quantized energy-dependent biophysically contrained viral latency that links the pheromone-controlled physiology of reproduction in bacteria to our visual perception of energy and mass in the context of the space-time continuum. He has many supporters among biologically uninformed theorists, but few or none among serious scientists.
See also:
Smell and smell perception: Recent advances & perspectives
Andreas Keller, Rockefeller University, USA
Smell loss: a marker of cognitive decline, dementia, and mortality
Maria Larsson, Stockholm University, Sweden
Can mice detect odour of neoplasm before clinical symptoms?
Agata Maria Kokocińska-Kusiak, Institute of Genetics and Animal Breeding of the Polish Academy of Sciences, Poland
A non-invasive measure of olfactory bulb function in humans
Johan Lundström, Department of Clinical Neuroscience, Karolinska Institute, Sweden
Detection of target odors in cluttered environments
Dan Rokni, The Hebrew University, Israel
Exploration into olfaction and experiential strategy: State of Art
Djamchid Assadi, Groupe ESC Dijon-Bourgogne, France
Enhancing user interaction with olfactory experiences
Marina Carulli, Politecnico di Milano, Italy
Bio-electronic nose: a mouse nose as an ultra sensitive and versatile chemical detector
Dmitry Rinberg, NYU Neuroscience Institute, USA
The Language of Smell: Connecting Linguistic and Psychophysical Properties of Odors
Jonas Olofsson, Stockholm University, Sweden
The power of scents – Scent in context
Peter de Cupere, PXL-MAD School of Arts in Hasselt, Belgium
Miniaturized electronic nose systems for digital olfaction: present and future applications
Jesús Lozano Rogado, University of Extremadura, Spain
Sniff-cam for real-time imaging of volatile chemicals
Kohji Mitsubayashi, Tokyo Medical and Dental University, Japan
Smell-enabled VR Games for Olfactory Training
Simon Niedenthal, Malmö University, Sweden
Digital olfaction: imaging an odor 
Thierry Livache, CSO of Aryballe Technologies, France

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