MicroRNA-mediated feedback loops (4)

By: James V. Kohl | Published on: July 28, 2018

Photomodulation links light-activated microRNA biogenesis to RNA-mediated DNA repair in the context of the cell biology game “Cytosis” biomodulation of feedback loops,  and in the context of Biblical Genesis.
See for examples: photobiomodulation RNA
Photobiomodulation prevents DNA fragmentation of alveolar epithelial cells and alters the mRNA levels of caspase 3 and Bcl-2 genes in acute lung injury
Photobiomodulation effects on mRNA levels from genomic and chromosome stabilization genes in injured muscle.
Photomodulation therapy links light-activated microRNA biogenesis to protection from all pathology or to effective treatment.
See Mitogen Health.com blog
The Director at Paleo Osteo – Evolutionary Medicine and Nutrition wrote:

My views are that the virome/viruses in general are not “pathogenic” but are rather informational codons that can be acquired and assimilated into our virome-genome and “shuffled” with our genetic material to innovate rapid evolutionary change.

It appears that traits such as “leaky gut” occur in a stress state in order to acquire new information about the local stressful environment to add to the “deck” in order to expand the array of possible “hands” drawn.

His view is wrong (i.e., unsupported by experimental evidence of top-down causation). See for comparison: Light device is effective ulcer treatment

 

Low level light therapy (LLLT) strikes terror into the hearts of atheistic theorists who believe that viruses cause beneficial mutations and evolution. Try to console them as they watch their ridiculous world-view burn in low level light-activated RNA interference. The link from the creation of anti-entropic virucidal light to the death of bacteriophages in the bad bacteria was established in “What is Life?” (1944)A Feasibility Study of a Novel Low Level Light Therapy for Digital Ulcers in Systemic Sclerosis author version posted online: 04 Jun 2018

Reported on 25 Jul 2018 as: Light device is effective ulcer treatment

The news report was delayed until after publication of the report that linked the creation of sunlight to microRNA biogenesis, viral latency, and all biodiversity in the context of the physiology of reproduction and Biblical Creation.

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

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

See also: The pathogenesis of non-ulcer dyspepsia (1985)

…showed that the bacterium Helicobacter pylori (H. pylori) plays a major role in causing many peptic ulcers, challenging decades of medical doctrine holding that ulcers were caused primarily by stress, spicy foods, and too much acid. This discovery has allowed for a breakthrough in understanding a causative link between Helicobacter pylori infection and stomach cancer.[4][5][6]

The link from the quantized energy-dependent creation of the innate immune system in soil bacteria (CRISPR) and in plants to the effectiveness of light-activated RNA interference in the prevention and treatment of all pathology is being revealed slowly. This helps to to prevent attacks on biologically uninformed science idiots who claimed that mutation-driven evolution was the link to all biodiversity.

Paleo Osteo wrote: lmao check my other company mitogenhealth.com

Scientific creationists have established the fact that his company is using light-activated RNA interference to repair damaged DNA. That’s what the anti-entropic virucidal energy of sunlight has been doing since the dawn of quantized energy-dependent biophysically constrained creation. In H. pylori, the anti-entropic virucidal energy of sunlight has been linked to healthy longevity via the death of viruses in the bacteria, which are called bacteriophages.The links from stress-induced changes in bacteriophages to pathology is manifested in the context of more than 75,000 reports on microRNA-mediated feedback loops.

See for recent examples: Hijacking Oogenesis Enables Massive Propagation of LINE and Retroviral Transposons

…parasitic genomic elements can efficiently hijack a host developmental process to propagate robustly, thereby driving evolutionary change and causing disease.

All serious scientists will link this claim from the creation of quantized energy to biophysically constrained viral latency and ecological adaptations.

See the authors claim for comparison:

Although animals have evolved multiple mechanisms to suppress transposons, “leaky” mobilizations that cause mutations and diseases still occur…

Reported as: How do jumping genes cause disease, drive evolution?

Animals have unwittingly developed a powerful system to suppress jumping gene activity that uses small, non-coding RNAs called piRNAs, which recognize jumping genes and suppress their activity.

“Since Carnegie’s Barbara McClintock made the seminal contribution of discovering the jumping genes more than six decades ago, we have not been able to understand how they mobilize as animals prepare for their next generation.

See: From Fertilization to Adult Sexual Behavior (1996)
Every aspect of biophyically constrained RNA-mediated cell type differentiation was detailed in the context of microRNA-mediated feedback loops. The feedback loops were established at a time when microRNAs were called pre-messenger RNAs. All serious scientists know that microRNA-mediated feedback loops prevent the evolution of anything except pathology in species from microbes to humans.

See Virus-mediated archaeal hecatomb in the deep seafloor

The claim that “Animals have unwittingly developed a powerful system…” is made by biologically uninformed theorists, not serious scientists.

For example, ZZ Zhao Zhang‏ wrote:  Would be interesting to know how “non-serious scientists” think…, just kidding…

Non-serious scientists simply claim that all the links “From fertilization to adult sexual behavior” automagically evolved to protect organized genomes from the virus-driven degradation of messenger RNA. But see our section on molecular epigenetics (1996).


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