Patented Creation vs Evolution of Disease (1)

See: Learning from Bacteria about Natural Information Processing  10/15/09

The author of this monograph, Eshel Ben-Jacob was a biophysicist who modeled cognition using bacterial organization. That concept was extended to answer the question “What is Life?” in the context of Panksepp’s decoding of primal affective experiences.

Indeed, in the case of higher animals we know the kind of orderliness they feed upon well enough, viz. the extremely well-ordered state of matter in more or less complicated organic compounds, which serve them as foodstuffs. After utilizing it they return it in a very much degraded form -not entirely degraded, however, for plants can still make use of it. (These, of course, have their most power supply of ‘negative entropy’ the sunlight.)

Comparative approaches in evolutionary psychology: molecular neuroscience meets the mind (2002)

Evolutionary psychologists often overlook a wealth of information existing between the proximate genotypic level and the ultimate phenotypic level. This commonly ignored level of biological organization is the ongoing activity of neurobiological systems.

Serious scientists have helped to reveal what can go wrong at every level of biological organization downstream from the Creation of sunlight and water. They have shown how pathogenicity evolves outside the biophysical constraints that link energy as information from ecological variation to ecological adaptations.

See: The Genetic Basis of Escherichia coli Pathoadaptation to Macrophages 12/12/13

…we reveal a molecular mechanism explaining how a specific component of host innate immunity can modulate microbial evolution towards pathogenicity.

Simply put, the virus-driven degradation of messenger RNA has been linked to the hecatombic evolution of pathology in species from archaea and other microbes to humans.

See: Virus-mediated archaeal hecatomb in the deep seafloor (2016) for comparison to  Eukaryotic plankton diversity in the sunlit ocean (2015)

Pseudoscientists ignore the facts about the hecatombic evolution of virus-driven pathology and pretend to know that different species evolved from a Last Universal Common Ancestor, for example, a species of bacteria.

The physiology of reproduction in bacteria links the Creation of anti-entropic virucidal energy and the creation of water from natural information processing in bacteria to the pheromone-controlled physiology of reproduction in species from microbes to humans.

Serious scientists have linked the Creation of sunlight and water to the light-activated assembly of the microRNA-RNA-peptide nanocomplex, which is also known as the polycombic repressive complex (PRC).

Polycomb repressive complex 1

Polycomb repressive complex 1 (PRC1) is one of the two classes of Polycomb Repressive complexes, the other being PRC2. Polycomb-group proteins play a major role in transcriptional regulation during development. Polycomb Repressive Complexes PRC1 and PRC2 function in the silencing of expression of the Hox gene network involved in development as well as the inactive X chromosome.[1] PRC1 inhibits the activated form of RNA polymerase II preinitiation complex with the use of H3K27me. PRC1 binds to three nucleosomes, this is believed to limit access of chromatin to transcription factors and therefore limit gene expression.[2]

What is known about how the PRC limits gene expression can be linked to the polycombic ecological adaptations. They’ve been linked from the Creation of sunlight and water to the light-activated assembly of the microRNA-RNA-peptide #nanocomplex and viral latency by what is known to all serious scientists about microtubules as the link to understanding energy-dependent polycombic ecological adaptations.

See: Nanotubular Highways for Intercellular Organelle Transport 2/13/04

…we propose a novel biological principle of cell-to-cell interaction based on membrane continuity and intercellular transfer of organelles.

Reported as: Cells Talk and Help One Another via Tiny Tube Networks 4/23/18

How did the tunneling nanotubes go unnoticed for such a long time? Lou notes that in the last couple of decades, cancer research has centered primarily on detecting and therapeutically targeting mutations in cancer cells — and not the structures between them. “It’s right in front of our face, but if that’s not what people are focusing on, they’re going to miss it,” he said.

Serious scientists have linked tunneling nanotubes from the light-activated assembly of the microRNA-RNA-peptide nanocomplex, or PRC, to healthy longevity in all living genera via the physiology of reproduction.  None of the serious scientists have suggested that biophysically constrained viral latency is not required to prevent the hecatombic evolution of  pathology, and the Creation of sunlight and water has been  linked to the prevention of all diseases.

See for instance: Dynamic control of chirality and self-assembly of double-stranded helicates with light (2016)

…we report that unidirectional rotary motors with connecting oligobipyridyl ligands, which can dynamically change their chirality upon irradiation, assemble into metal helicates that are responsive to light. The motor function controls the self-assembly process as well as the helical chirality, allowing switching between oligomers and double-stranded helicates with distinct handedness. The unidirectionality of the light-induced motion governs the sequence of programmable steps, enabling the highly regulated self-assembly of fully responsive helical structures.

“The unidirectionality of the light-induced motion” has been linked from light-activated microRNA biogenesis in plants to the cure for cancer.

See: A Quick HYL1-Dependent Reactivation of MicroRNA Production Is Required for a Proper Developmental Response after Extended Periods of Light Deprivation (2018)

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

The cure for cancer was announced in that context.

See:  A cure for cancer? Israeli scientists say they think they found one 1/28/19

“We believe we will offer in a year’s time a complete cure for cancer,” said Dan Aridor…

Naysayers did not like the claims made about the forthcoming cure for cancer. But one of them hedged his bets by claiming that “Using peptides to target cancer is not something new.”

See: Experts Decry Israeli Team’s Claims That They Have Found The Cure For Cancer 1/30/19

Ajit Johnson, a cancer genetics researcher at Harvard Medical School, who studies the role of immune cells in cancer, also has doubts about the validity of a single “magic bullet” cancer therapy. “It is always encouraging to see new approaches being developed to cure cancer. However, for the past couple of decades we have tried very hard and a single magic bullet to cure all cancers has not been found for obvious reasons,” he said. “Cancer is a very heterogeneous disease. There are several tens of subtypes within each cancer type and even those vary significantly between patients. Using peptides to target cancer is not something new. Using a combination of peptides to target cancer cells is also not new. In fact, as we expect several subclones of cancer cells within a tumor, we routinely use a cocktail of drugs in clinic rather than a single agent.”

Use of expensive and often unaffordable drugs can be compared to the facts about using a peptide, which was substantiated on Christmas Day in 2018. The experts who decried those claims may not have known about the patent, which links the light-activated assembly of the microRNA-RNA-peptide nanocomplex to protection from the virus-driven degradation of messenger RNA via epigenetic effects on the systems complexity of intermolecular interactions. Alternatively, the experts might have missed the facts the led to the claims in this patent.

See: Methods and compositions for identifying a peptide having an intermolecular interaction with a target of interest 12/25/18

A system of a recombinant bacteriophage library and a target of interest complex, wherein the recombinant bacteriophage peptide library includes a plurality of peptides expressed on the surface of recombinant bacteriophages wherein each recombinant bacteriophage includes (a) a pill protein; wherein each pill protein includes (b) a peptide or polypeptide involved in an intermolecular interaction, which differs by at least one amino acid from other peptides or polypeptides in the library; and (c) a modified protease cleavage site proximal to the peptide, wherein the modified protease cleavage site is the same in each bacteriophage, the modified cleavage site having a reduced binding affinity to a protease, as compared to a non-modified cleavage site, and wherein the target of interest complex includes a protease, a flexible linker attached to the protease, and a target of interest attached to the flexible linker, wherein the target of interest participates in an intermolecular interaction.

For example, a difference in one amino acid substitution has been linked from a peptide or polypeptide involved in an intermolecular interaction to biophysically constrained viral latency in the influenza virus.

See: Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution 11/22/13

Koel et al. (p. 976) show that major antigenic change can be caused by single amino acid substitutions.

Also, two amino acid substitutions in were linked to the weekend resurrection of the bacterial flagellum in and organism that naturally fluoresces on exposure to ultraviolet (UV) light.

See: Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system 2/27/15

From the Editor’s Summary Losing and then regaining flagella

The ability to adapt to changes in the function of gene regulators, as opposed to structural genes, is a crucial aspect of evolutionary change. Taylor et al. mutated a central regulator for the formation of flagella in the bacterium Pseudomonas fluorescens. They then put the mutated flagella-free bacteria under strong selection pressure to regain mobility. The mutated bacteria regained the lost flagella, and motility, within 4 days. Two stereotypical mutations diverted an evolutionarily related regulator that normally controls nitrogen uptake to control flagella biosynthesis. The mutations increased the levels of the co-opted regulator, then altered its specificity for the flagella pathway.

The fact that the mutations increased the levels of two co-opted regulators (two amino acid substitutions) placed the UV light-activated reassembly of the microRNA-RNA-peptide nanocomplex (aka the polycomb repressive complex) into the context of ecological adaptations, which were reported as the weekend evolution of the bacterial flagellum, in “Life finds a way.”

 

The naysayer’s response to the patent for microRNA-mediated healthy longevity has been negligible. Their focus appears to be on the creation of vaccines, which is a bastardization of what is known about  the light-activated peptide-dependent technology for the cure of cancer. The viruses in vaccines reassemble, which links them to constraint-breaking DNA damage that is not repaired.

Virucidal UV light promotes DNA damage repair, which explains how the bacterial flagellum resurrected itself over the weekend.

UV-Induced Charge Transfer States in DNA Promote Sequence Selective Self-Repair 1/13/16

For an example of what happens when DNA damage is not repaired, see: A New Discovery Upends What We Know About Viruses 3/14/19

A plant virus distributes its genes into eight separate segments that can all reproduce, even if they infect different cells.

and

Viruses Can Scatter Their Genes Among Cells and Reassemble 5/21/19

Multipartite viruses have been known for over half a century, when researchers realized that a virus could be composed of two or more independent pieces, all of which were vital for infection. One piece might be necessary for making essential viral enzymes, for instance, while the other would be needed to make the capsule in which the viral particles (or virions) are packaged and transported to other cells.

See how these researchers will contribute to unconstrained reassembly and pathology: RNA Transcription and Splicing Errors as a Source of Cancer Frameshift Neoantigens for Vaccines 10/2/19

Abstract excerpt:

A survey of 5 types of cancers reveals peptides that are personally reactive for each patient.

Text excerpt 1)

In the process of becoming a tumor, not only does the DNA mutation rate increase with faster cell divisions, but also there is a disruption of basic cellular functions, including RNA transcription, splicing and the quality control system on peptides21.

Text except 2)

An important aspect of the model is that because of the global increase in the errors of transcription and splicing, the FS neoantigens will be constantly produced. Thus, in contrast to the commonly held view45, bystander FS neoantigens would be good immunological targets. The production of these variants is not dependent on DNA replication as is the case for DNA mutations nor are they heritable and subject to selection.

This was reported as: Discovery of new source of cancer antigens may expand cancer vaccine capabilities 10/2/19

They have found a common, new source of tumor mutations that could offer three levels of therapy with a cancer vaccine: 1) a broadly protective, or pan-cancer vaccine 2) cancer-type specific vaccines (e.g. breast vs. pancreatic), 3) personalized cancer vaccines based on mutations unique to an individual.

The intent to obfuscate what is known about light-activated energy-dependent cause and effect is clear. The virus-driven degradation of messenger RNA is the source of all mutations. There is no new source that could offer three levels of therapy with a vaccine. Like all vaccines, the reassembly of viruses and viral fragments will cause more pathology.

Researchers in Israel made it perfectly clear that DNA does not cause the production of variants that are selected for heritable mutations. Given that fact, this is the only model that can be linked to constraints on the viruses in vaccines that reassemble to cause all pathology:

Nutrient-dependent Pheromone-Controlled Ecological Adaptations: From Angstroms to Ecosystems 4/18/18

This angstroms to ecosystems model of ecological adaptation links nutrient energy-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA/messenger RNA balance and chromosomal rearrangements via the physiology of reproduction in species from microbes to humans. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity. Species-specific pheromones link quorum-sensing in microbes from chemical ecology to the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection for codon optimality links nutritional epigenetics to the behaviors that enable ecological adaptations. All biodiversity is an ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. Simply put, olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of supercoiled DNA in the organized genomes of species from microbes to man during their development.

My claims about experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches via controlled production of microRNA-mediated peptide-dependent protein folding chemistry and genomic stability were also reported by researchers from Israel in their 12/25/18 patent.

However,  George M. Church et al., had already patented the naturally occurring process of light-activated microRNA-mediated RNA interference, which biophysically constrains viral latency.

See: RNA-Guided Human Genome Engineering

5. Repetitive elements or endogenous viral elements can be targeted with engineered Cas+gRNA systems in microbes, plants, animals, or human cells to reduce deleterious transposition or to aid in sequencing or other analytic genomic/transcriptomic/proteomic/diagnostic tools (in which nearly identical copies can be problematic).

See also: Patented Creation vs Evolution of Disease (4) in prep

Widening the Circle 9/26/19

Checkpoint inhibitors work through an entirely different mechanism than all preceding cancer treatments, by activating a person’s immune system to target and destroy cancer cells. They are among the first examples of a therapeutic approach known collectively as cancer immunotherapy.

Comments

comments

Author: James Kohl

1 thought on “Patented Creation vs Evolution of Disease (1)

Leave a Reply

Your email address will not be published. Required fields are marked *