Summary: Who lets biologically uninformed theorists make presumptions about evolution after all serious scientists have linked light-harvesting from energy-dependent changes in electrons to ecosystems in all living genera via natural selection for food energy-dependent codon optimality. Who lets them pretend not to know that the pheromone-controlled physiology of reproduction links autophagy to the transgenerational epigenetic inheritance of healthy longevity? Who is causing the unnecessary suffering and premature death of your loved ones?

Elsevier publishing supports the pseudoscientific nonsense touted by theorists by who publish articles like this:

Neurotransmitter Funneling Optimizes Glutamate Receptor Kinetics (open access) Published Online: December 14, 2017 (with my emphasis)

These studies suggest that neurotransmitter binding is a directed process for which kinetics have been optimized (presumably by evolution)…

Our experiments reveal a strikingly elaborate management of ligand transport by AMPA receptors, whereby flexible positive charges ensure that glutamate binding reactions are fast. The existence of these pathways is surprising, and the fact that they alter the kinetics of receptor activity indicates that the molecular mechanisms that determine the action of neurotransmitters at receptors are more complex than previously thought. R660 is conserved between AMPA and NMDA receptors; in kainate receptors, R660 and R661 are replaced by lysine residues (Figure S8). It is possible that these helix F interactions also coordinate ligand binding in kainate and NMDA receptors. Given that electrostatic interactions are also important for coordination in other neurotransmitter binding sites (McCammon, 2009), these principles of ligand funneling may be general.

They linked the lysine residues (i.e., amino acid substitutions)  from electrostatic interactions to RNA-mediated cell type differentiation in all living genera. Their studies do not link any experimental evidence from electrostatic interactions or optimized kinetics to evolution. Evolution cannot optimize any aspect of energy-dependent kinetics. Evolution cannot optimize any aspect of energy-dependent RNA-mediated cell type differentiation, which is biophysically constrained by the physiology of pheromone-controlled reproduction.

The nonsense about evolution was reported as: Scientists chart how brain signals connect to neurons (with my emphasis)

Scientists at Johns Hopkins have used supercomputers to create an atomic scale map that tracks how the signaling chemical glutamate binds to a neuron in the brain. The findings, say the scientists, shed light on the dynamic physics of the chemical’s pathway, as well as the speed of nerve cell communications.

See: Life is physics and chemistry and communication

All experimental evidence of top-down causation links quantized energy from the speed of light on contact with water to energy as information-dependent changes in electrons and all ecosystems via the physiology of pheromone-controlled reproduction, which biophysically constrains viral latency. The use of supercomputers led the researchers to report findings that eliminate everything known to serious scientists about energy-dependent RNA-mediated cell type differentiation. It is common for theorists to eliminate energy as information-dependent changes and replace facts with mathematical models.

See for comparison: Codon identity regulates mRNA stability and translation efficiency during the maternal-to-zygotic transition (open access)

The bias between codons or amino acids, and mRNA expression levels has been previously recognized across species and is thought to result from selection for efficient, accurate translation, and folding of highly expressed genes (Ikemura, 1982; Akashi, 1994; Akashi & Gojobori, 2002; Drummond & Wilke, 2008; Kudla et al, 2009; Novoa & Ribas de Pouplana, 2012). The amino acid optimality code (Fig 6) provides an alternative perspective on sequence changes between paralogs in evolution and human disease.

This is not just an alternative perspective. It is a refutation of neo-Darwinian pseudoscientific nonsense that was reported as: Codon optimality at genome transition

Nucleotide triplets, or codons, designate specific amino acids for protein synthesis. However, that is not their only job. In yeast and bacteria, codons contribute to RNA stability, with “optimal” codons stabilizing RNAs and “suboptimal” codons destabilizing RNAs. This is possible because multiple codons can encode the same amino acid.

See also: Human GW182 Paralogs Are the Central Organizers for RNA-Mediated Control of Transcription Elsevier — Cell Reports (August 15, 2017)

Nuclear RNAi, regardless of whether it is controlling splicing, transcription, or some other nuclear process, would have distinct advantages as a mechanism for evolution, because it would expand sequence-specific control of gene expression by miRNAs.

No experimental evidence of biologically-based cause and effect suggests that microRNAs evolved to control sequence-specific gene expression. The authors linked TNRC6, MED14, NAT10, and WDR5 to RNA-mediated gene activation. They inadvertently linked the energy-dependent de novo creation of microRNAs to Trinucleotide Repeat Containing (TNRC) 6A expression.  See: miR-26a-5p Regulates TNRC6A Expression and Facilitates Theca Cell Proliferation in Chicken Ovarian Follicles

The anti-entropic virucidal energy of sunlight links the creation of microRNAs and multiple codons to the creation of differences and similarities in the same amino acid. That fact has been ignored.

See also: MicroRNAs recruit eIF4E2 to repress translation of target mRNAs

There is increasing evidence indicating that translation initiation is a major target of miRNA repression…

…we provide evidence indicating that TNRC6A, the core component of RISC, can directly recruit eIF4E2 to target mRNA to repress translation.

They provided evidence that the energy-dependent de novo creation of microRNAs represses the expression of the mutations that cause all pathology.

See for example: Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention

Reported as: New Study Finds That Most Cancer Mutations are Due to Random DNA Copying ‘Mistakes’

John Hopkins Kimmel Cancer Center scientists report data from a new study providing evidence that random DNA copying “mistakes” account for nearly two-thirds of the mutations that cause cancer. Their research is grounded on a novel mathematical model based on DNA sequencing and epidemiologic data from around the world.

This was reported in the context of the “bad luck” theory of cancer (video).

For comparison see:  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.

See for comparison: QuEBS: Workshop on Quantum Effects in Biological Systems  has established itself as an outstanding stage to present the research in the intersection of physics, chemistry and biology. This field has… established excitons in biology as the “must-talk-language” when describing the quantum effects in biological light-harvesting systems.

All serious scientists have linked the anti-entropic virucidal energy of sunlight from physics and chemistry to biophysically constrained viral latency via the de novo creation of microRNAs and the physiology of pheromone-controlled reproduction, which links autophagy to fixation of amino acid substitutions that stabilize the organized genome of all living genera in the context of autophagy.

Only biologically uniformed researchers, like Bert Vogelstein are surprised to find bacteria in tumors, because all serious scientists have link the viruses in bacteria from the degradation of messenger RNA in bacteria to the degradation of messenger RNA that causes all pathology in all living genera.




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