Masters of deception about nature (2)

By: James V. Kohl | Published on: June 13, 2016

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See my other blog posts on RNA methylation

Thanks for your review of How Can Physics Underlie the Mind?: Top-Down Causation in the Human Context (The Frontiers Collection)

Others linked the sun’s anti-entropic virucidal energy from energy-dependent changes in hydrogen-atom transfer in DNA base pairs in solution to supercoiled DNA, which protects all organized genomes from virus-driven energy theft and genomic entropy.

Ellis comments on at least one of Schrodinger’s claims from “What is Life?” but he largely ignores the energy-dependent links from ecological variation to ecological adaptation that also were reported in two recent publications. See: “Structural diversity of supercoiled DNA” and “Epigenetics and Genetics of Viral Latency.”

Ellis cannot be held accountable for not knowing the most recent work (May 11, 2016) reported that “…viral latency is responsible for life-long pathogenesis and mortality risk…”

However, it seems inappropriate for anyone whose opinions are held in high regard to ignore everything else that is known about energy-dependent RNA methylation and the biophysically constrained morphological and behavioral diversity of all living genera. Experimental evidence has established facts that are being used to link the Precision Medicine Initiative to the National Microbiome Initiative via attempts to crack the olfactory code.

When researchers report the direct link from energy-dependent RNA methylation to differences in behavior, this book will be compared to Masatoshi Nei’s “Mutation-driven evolution.” The biggest difference between the two seems to be that Ellis tries to link emergence to evolution via Darwin’s “conditions of life.”

But he now bears the burden of the report in “Science” of nutrient energy-dependent pheromone-controlled weekend evolution of the bacterial flagellum: “Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system.”

The “resurrection” is obviously energy-dependent and it also links the innate immune system to biophysically constrained biologically-based cause and effect in species from microbes to humans via RNA-mediated amino acid substitutions. Resurrecting Darwin’s “conditions of life” after they were ignored by neo-Darwinists for many decades should not be attempted by physicists, cosmologists, or biologically uninformed theorists from any other discipline without first learning more about what is known about the RNA-mediated links from physics and chemistry to molecular epigenetics.

Kodis and her colleagues appear to have borrowed heavily from “The Scent of Eros,” without either mentioning or citing the first book to focus on the topic of human pheromones. For example, they offer a possible link between pheromones and homosexuality as an original deduction that is supposedly based on information from several different reference sources. However, this link was first detailed in “The Scent of Eros.” In addition, the subtitle of “Love Scents” is misleading. I expected more information about “How Your Natural Pheromones Influence…” Instead, there is very little information about how pheromones do anything. This book is filled with speculation and questions. For example: “Could it be that the friendly attitude of southerners has something to do with their pheromones…?” Questions like this are typically offered in a factual context, but the questions are left unanswered. This leaves the reader without facts. From a scientific perspective, there is evidence of confusion. Specifically, GnRH and LHRH are mentioned in different chapters, and LHRH appears in the glossary. GnRH and LHRH are different names for the same hormone–a fact that anyone who is familiar with the basics of pheromonal communication should recognize. This leads me to wonder about how familiar the authors’ are with the scientific aspects of their topic.

My comments: Ecological variation is linked to ecological adaptation via food odors and pheromones in all invertebrates and vertebrates. Feedback loops link odor and pheromone signaling with reproduction, but pseudoscientists refuse to accept that fact. Serious scientists are using the facts. They are Combating Evolution to Fight Disease because the misrepresentations of neo-Darwinian theorists have been linked to the cause of all pathology via what has been known for twenty years about RNA-mediated cell type differentiation.
See also with my comments: RNA Epigenetics

Introduction: DNA isn’t the only decorated nucleic acid in the cell. Modifications to RNA molecules are much more common and are critical for regulating diverse biological processes.

See also: edx courses (free)

Learn from the world’s best professors and leading industry experts through captivating lectures and presentations

Learn about DNA methylation.
Excerpt:

We will explain how to start with raw data, and perform the standard processing and normalization steps to get to the point where one can investigate relevant biological questions.
… we cover RNA-seq at the transcript-level: inferring expression of transcripts (i.e. alternative isoforms); differential exon usage. We will learn the basic steps in analyzing DNA methylation data, including reading the raw data, normalization, and finding regions of differential methylation across multiple samples. The course will end with a brief description of the basic steps for analyzing ChIP-seq datasets, from read alignment, to peak calling, and assessing differential binding patterns across multiple samples.

My comment: They explain how to start with data and infer cause and effect via alternative splicings linked from the epitransciptome back to hydrogen-atom transfer in DNA base pairs in solution. It’s as if they decided to run this course in reverse to support their data with inferences rather that use the data to answer relevant biological questions.
The sun’s anti-entropic virucidal energy has already been linked from hydrogen-atom transfer in DNA base pairs in solution to ecological adaptation in all living genera via RNA methylation, the innate immune system, the physiology of reproduction, and supercoiled DNA. Answers to relevant questions must include what is known about how energy-dependent changes link angstroms to ecosystems despite virus-driven energy theft, which is linked to all pathology.
Take the course anyway. It will prepare you to find that everything you learn was replaced with accurate representations of biologically-based cause and effect if ever you get the opportunity to take a course on RNA methylation.
Until a course on RNA methylation becomes available, see: PubMed.gov RNA methylation or see these works from Timothy W. Bredy et al.
However, please do not let anyone convince you that ATP synthesis magically occurs in cancer cells. Bredy’s works eliminate the magic of neo-Darwinian theories.
For example of that magic, see: Serine Metabolism Supports the Methionine Cycle and DNA/RNA Methylation through De Novo ATP Synthesis in Cancer Cells. When you see the term de novo used in a context like this, it means they do not know why ATP synthesis in cancer cells is different than ATP synthesis in differentiated cell types.
However, in this case “A method to track methyl units from amino acids onto DNA and RNA is described.”
Excerpt:

…de novo ATP synthesis (i.e., ATP generated by de novo purine synthesis, a biosynthetic pathway that requires glucose and amino acids). Cancer cells show enhanced rates of de novo purine synthesis, which has been interpreted as contributing to increased demand for nucleic acid (primarily RNA and DNA) synthesis.

My comment: Ask yourself what might contribute to an increased demand for viral nucleic acids.
See: Viral Nucleic Acids
Abstract (with my emphasis):

Viral genomes exhibit extraordinary diversity with respect to nucleic acid type, size, complexity, and the information transfer pathways they follow. Thus, viral nucleic acids can be DNA or RNA, double-stranded or single-stranded, monopartite or multipartite, linear or circular, as short as 2 kb or up to 2500 kb long. The goal of a virus is to replicate itself. To do so, viruses have evolved various strategies to replicate their genomes and produce the structural and catalytic proteins needed for the formation of new viruses. This article is a brief introduction to viral genomes and viral replication.

My comment: If you think that viruses can evolve strategies to create the structure of functional proteins via energy theft, your thoughts about emergence and evolution can probably be compared to the thoughts of many biologically uninformed theorists.
See for comparison: “viral nucleic acid”
For example:RNA exosome complex regulates stability of Hepatitis B Virus’s X-mRNA transcript in a Non-Stop mediated (NSD) RNA quality control mechanism
Excerpt:

Interestingly, G1896A mutation is frequently observed in HBV-eAg negative patients, a subgroup characterized by high levels of HBV replication and more severe liver disease (35). We hypothesize that this mutation enables the virus to escape the degradation of HBV X-mRNA; the increased accumulation of the X transcript (and of the X protein) could be responsible for the increased severity of HBV symptoms in these patients (Fig. 10E).

Conclusions The high association between epigenetic parameters of the MAOA-gene (the VNTR-polymorphism of which usually shows only little impact on FDOPA kinetics) strengthen the possible relevance of these pathways on the modulation of human behaviour. It is in line with the previously published association to [11C]clorgyline binding studies.

Excerpt: [11C]Clorgyline was not retained in the baboon brain nor was it influenced by clorgyline pretreatment or by deuterium substitution, contrasting to results in humans. This suggests a species difference in the susceptibility of MAO A to inhibition by clorgyline and represents an unusual example of where the behavior of a radiotracer in the baboon brain does not predict its behavior in the human brain.

My comment: This blog site draws attention to ~3 posts each time a visitor arrives on the site. That suggests many others are willing to take the claims here and place them into the context of their own representations of biologically-based cause and effect.
For example, see: The Biosemiotic Concept of the Species

Any biological species of biparental organisms necessarily includes, and is fundamentally dependent on, sign processes between individuals. In this case, the natural category of the species is based on family resemblances, which is why a species is not a natural kind. We describe the mechanism that generates the family resemblance. An individual recognition window and biparental reproduction almost suffice as conditions to produce species naturally. This is due to assortativity of mating which is not based on certain individual traits, but on the difference between individuals. The biosemiotic model described here explains what holds a species together. It also implies that boundaries of a species are fundamentally fuzzy, and that character displacement occurs in case of sympatry. Speciation is a special case of discretisation that is an inevitable result of any communication system in work. The biosemiotic mechanism provides the conditions and communicative restrictions for the origin and persistence of diversity in the realm of living systems.

See for comparison: A genetic network that suppresses genome rearrangements in Saccharomyces cerevisiae and contains defects in cancers and Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes
My comment: If you think you can sneak up from behind and begin to tout accurate representations of biologically-based cause and effect without acknowledging the source of your magical “raw insight,” Please revisit: Censorship & Upcoming Royal Society Evo Meeting
I added this earlier today.

“George Ellis appears to owe his allegiance to those who are trying to ensure there is no discussion of virus-driven energy theft and all pathology at the forthcoming meeting.

See: How Can Physics Underlie the Mind?: Top-Down Causation in the Human Context (The Frontiers Collection) 1st ed. 2016 Edition

My review: https://www.amazon.com/gp/review/R1PO4GK29KZN8H?ref_=glimp_1rv_cl

Excerpt:

Ellis cannot be held accountable for not knowing the most recent work (May 11, 2016) reported that “…viral latency is responsible for life-long pathogenesis and mortality risk…”

Summary of this blog post: Ellis and all others appear to be trying to keep accurate information about energy-dependent RNA-mediated cell type differentiation from being disseminated, or trying to disseminate more pseudoscientific nonsense that overwhelms the ability of the biologically uninformed masses to understand the current threat to humanity. Virus-driven energy theft is the threat, and theorists have watched it develop into an evolutionary theory killer at the same time they have tried to kill the messengers who are delivering the facts.
See for example: March 9, 2016 Gene intelligence: The risks and rewards of genome editing resonate beyond the clinic.
Last month, one of the top intelligence officials in the United States warned that genome-editing technology is now a potential weapon of mass destruction.
If you learn how viruses are used in the context of genome-editing technology, you could begin to make progress after 20 years of ignorance led us to a potentially apocalyptic end.