Biologically uninformed science idiot: Self-defense (1)

By: James V. Kohl | Published on: June 1, 2018

I recently published a review of nutritional epigenetics. It was an invited review that was returned in 2014 without review so I placed it on a preprint server as: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

In the past 4 years, others have linked the creation of subatomic particles from quantum physics to classical physics. Now, the slight change in the title makes more sense.  See: Nutrient-dependent Pheromone-Controlled Ecological Adaptations: From Angstroms to Ecosystems

The review already is forcing biologically uninformed science idiots to defend their ignorance. They must act as if they always knew everything I have detailed during the past two decades in my other published works.

See for example: June 1, 2018 from the FB page of Jon Lieff

He revives How Does Diet Influence Immunity (2015) with the claim:

Particles of food are signals to produce correct immunity

People like Jon Lieff pretend to know what people like me have detailed. Could people like Jon Lieff cause the ignorance of all theorists? What made Jon Lieff place biophysically constrained energy-dependent viral latency into the context of “…very complex intelligent communication with a vast array of signals from a single layer of cells.”What is the origin of the intelligent communication? I think his nonsense facilitates the illogical thought processes of others who are biologically uninformed. For example, anyone who does not know that all intelligent communication is quantized energy-dependent is more likely to believe in mutation-driven evolution.

These changes could be the result of a microRNA (miRNA)-mediated mechanism, which may be epigenetically inherited across generations.

My comment from nearly 4 years ago:

There is currently no alternative explanation for these changes. However, a model of how nutrient-dependent pheromone-controlled amino acid substitutions link cell type differentiation (e.g., from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man via conserved molecular mechanisms) explains how nutrient-dependent changes in the microRNA/messenger RNA balance cause effects on hormone-organized behaviors that also are affected by hormones.

See also from 2013: Nutrient-dependent/pheromone-controlled adaptive evolution: a model
With publication of Nutrient-dependent Pheromone-Controlled Ecological Adaptations: From Angstroms to Ecosystems in the Journal of Genetics and DNA Research, others can help those who are Combating Evolution to Stop Disease.
See for example: On universal coding events in protein biogenesis

Coding events are quantized energy-dependent and RNA-mediated. They are biophysically constrained by the availability of food and the pheromone-controlled physiology of reproduction in the context of viral latency.

See Fig. 1. Coding events in the ribosomal cycle of protein biosynthesis

Fig. 1. Coding events in the ribosomal cycle of protein biosynthesis. Proteins, which play an essential role in cellular metabolism, are composed of 20 (+2) natural amino acids. These are generally activated by 20 different aminoacyl-tRNA synthetases (aaRS) and loaded onto tRNA adaptors, which decode the genetic program using a triplet code and thus translating the genetic information into functional polymers that fold into 3D structures. Once the protein is folded, it should become functional to sustain cellular life. Upper part: A simplified scheme of the ribosomally mediated translation of genes into proteins. In the operational RNA code (Schimmel et al., 1993), the 3′-terminus of the acceptor part of the tRNA has to be aminoacylated appropriately. For each tRNA, the 3′-terminus codon composition and its 3D structure shape should be placed in a very specific way to enable the interaction between their acceptor tails and its cognate aaRS. In this process, tRNA is not just a ‘passive’ adaptor but it actively participates in binding to elongation factor (EF) Tu (charge code) and the accommodation step in the ribosomal elongation cycle (Dale and Uhlenbeck, 2005). The ‘anticodon’ or triplet code, which is based on codon-anticodon interactions, is degenerate, ‘wobbled’ and non-overlapping (Crick, 1968). The conformational specificity of the protein core is a stereochemical (or folding) code (Rose and Wolfenden, 1993) that enables proper folding into functionally active protein structures. Post-translational modifications (PTMs), occur on nearly all proteins also having their own “code” (Lothrop et al., 2013). Lower part right: General framework of identity elements in the context of the cloverleaf model of tRNA’s secondary structure with marked nucleotides that are present in nearly all tRNA species (Mukai et al., 2017). For example U33 is essential for translocation in ribosome while N73 is the so-call “discriminatory base” (Shi and Schimmel, 1991). Lower part left: a generalized translation scheme focusing on codon-anticodon interactions.

Simply put, the codon-anticodon interactions only occur in the context of natural selection for food energy-dependent biophysically constrained viral latency and the physiology of pheromone-controlled reproduction, which links RNA-mediated DNA repair to healthy longevity via control of the virus-driven degradation of messenger RNA, which links mutations to all pathology.

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