Evolutionary theories of epigenetic drift (2)
Summary: For another refutation of neo-Darwinian pseudoscientific nonsense, see: Conformational landscape of isolated capped amino acids: on the nature of non-covalent interactions
reported as: Folding biomolecule model shows how form dictates function
…the sorting of such ancestral phenotypic polymorphisms in subsequent speciation events provides a parsimonious explanation why evolutionary derived characteristics are shared among species that are not each other’s closest relatives.
The claims about evolutionary derived characteristics require acceptance of the belief that one species can evolve into another. For comparison to ridiculous neo-Darwinian theories of mutation-driven evolution, which are now being framed in the context of epigenetic drift see: Dopamine oxidation mediates mitochondrial and lysosomal dysfunction in Parkinson’s disease
…a time-dependent pathological cascade beginning with mitochondrial oxidant stress leading to oxidized dopamine accumulation…”
The relationship between miRNA, neurodegeneration and neurogenesis will be highlighted. Moreover, the benefits, outcomes and limitations of therapies using miRNA technology for neurodegenerative disorders will also be discussed.
This reduction is consistent with the hypothesis that Parkinson’s disease begins with bacteria, viruses or environmental toxins entering the brain via the nose and affecting first the olfactory bulb, where the neurodegenerative disease is triggered and gradually spreads through other parts of the brain.
See also: Olfaction Warps Visual Time Perception
Reported as: Odors Alter Subjective Time Experience
The sense of smell is like a time machine that links our experiences from the past to our behaviors throughout life.
All pseudoscientists use changes in words and definitions to prevent anyone who intends to become a serious scientist from learning how energy as information must be linked from the physiology of pheromone-controlled reproduction by feedback loops.
All serious scientists are Combating Evolution to Fight Disease
See my comment to Science from March 7, 2014
Darwin probably anticipated the insemination of population genetics that led to the bastardization of his detailed observations in the “Modern Synthesis.” He politely insisted that ‘conditions of life’ be considered before natural selection.
There are two ‘conditions of life.’ It is nutrient-dependent and pheromone-controlled. Rosenberg and Queitsch now note the work with Dobzhansky’s rarely acknowledged claim: “I am a creationist and an evolutionist.” They also declare the need for “Deep understanding of the mechanisms that generate variation at the molecular level…”
Deep understanding of the ‘conditions of life’ does not come from theory.
Problems with the “modern synthesis” now lead us back to the facts about biologically-based cause and effect that Darwin and Dobzhansky approached with humility, which are the same biological facts that evolutionists approached with ignorance about behavioral affects and the arrogance that accompanies that ignorance. Rosenberg and Queitsch echo the sentiments of those who have been subjected to academic suppression.
Clearly, however, “nothing in evolution makes sense except in the light of biology” is not an exaggeration. It is a common sense statement about the biologically plausible genesis of functional cell types. Population genetics and evolutionary theories abandoned the biophysical constraints of ecological variation and the physiology of reproduction, which enable epigenetically-effected nutrient-dependent pheromone-controlled receptor-mediated ecological adaptations and species diversity via the complexities of protein folding and niche construction.
It’s time for biophysicists to tell theorists and pathologists how to differentiate between theories about the genesis of different cell types and the biological facts about the nutrient-dependent pheromone-controlled ecological adaptations that enable the genesis of different cell types in individuals of different species. Simply put, it’s time to stop trying to explain ecological adaptations in the context of mutations and evolution.
Figuring out how EWS interacts with other EWS portions, and with FLI, could result in a clinical revolution for transcription factor-driven cancers. “If you can disrupt the function of the EWS component, you can stop cancer in its tracks. New cancer would be prevented, and the cancer that exists will die,” says Dr. Lessnick. “Another target would be to block the binding of FLI to the microsatellites. Without this binding, Ewing sarcoma can’t manifest.”
All pathology is caused by virus-driven energy theft, which links changes in the microRNA/messenger RNA balance from the degradation of messenger RNA to changes in transcription factors via autophagy.
See: Conformational landscape of isolated capped amino acids: on the nature of non-covalent interactions
reported as: Folding biomolecule model shows how form dictates function
Outside the context of the obvious fact that form dictates function, there are theories that our ancestors evolved in caves. The theories make no sense to creationists who recognize that the fossil record includes examples of humans with virus-driven degradation of their messenger RNA.
See for example: Mutation in human CLPX elevates levels of δ-aminolevulinate synthase and protoporphyrin IX to promote erythropoietic protoporphyria
This was reported as: New Genetic Cause Discovered for Photosensitive Blood Disorder
Without realizing it, they report that virus-driven energy theft links a dominant mutation and the ATPase active site of human CLPX. Specifically, p.Gly298Asp results in pathological accumulation of the heme biosynthesis intermediate protoporphyrin IX (PPIX).
Tthe virus-driven degradation of messenger RNA links the Gly298Asp amino acid substitution to the photosensitive blood disorder, erythropoietic protoporphyria (EPP). They place that fact into the context of a mutation in CLPX that inactivates its ATPase activity, which supposedly alters the coassembly of mutant and Wild Type “protomers” to form an enzyme with reduced activity.
Conclusion: Use of the terms mutation, coassembly, and protomer obfuscate fact about energy-dependent RNA-mediated cell type differentiation. Instead, they claim that “The presence of low-activity CLPX increases the posttranslational stability of ALAS, causing increased ALAS protein and ALA levels, leading to abnormal accumulation of PPIX.”
My summary: Biologically uninformed science idiots must still try to avoid any direct link between the anti-entropic virucidal of sunlight and healthy longevity. No matter how obvious the direct link becomes, the word games of pseudoscientists must continue for a few more weeks. Then the release of the cell biology game “Cytosis” means it is “game over” for all theorists. It will become clearer that the remains of cave-dwelling primates and their paintings on the wall are evidence that they suffered from virus-driven low-activity CLPX, which increased the posttranslational stability of ALAS. The fact that altered posttranslatkional stability caused increased ALAS protein and ALA levels, which lead to abnormal accumulation of PPIX suggests that they were driven back into the caves by the lack of nutrients that led to their virus-driven pathology and ultimately to their extinction. Claims that they evolved into modern humans are ridiculous at every level of examination that clearly links energy-dependent changes from angstroms to ecosystems in all living genera.
See also: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems and the complaints about the facts in Uproar in Turkey over removing evolution from biology class