Weaponized health information (8)

By: James V. Kohl | Published on: July 23, 2019

In “Quantico,” a genetically modified ‘weaponized’ yeast (i.e., a virus-altered GMO) is used to target a specific religious group. It was designed to make them forget why they were fighting with others of different religious groups.  If an energy-dependent microRNA-mediated design change could link Alzheimer’s to world peace, hate-mongers will not like this information about how a effects of this superbug might also lead others to understand what is known about the virus-driven degradation of messenger RNA in Candida auris.

The superbug Candida auris is giving rise to warnings — and big questions 7/23/19 that are not being answered by the so-called experts.

Instead they have more questions.

“They didn’t just ‘poof!’ appear,” Chiller insisted. “They’ve been here for a while. And I wonder where they were hiding.”

Superbugs don’t hide, they ecologically adapt to different hosts via the bacteriophage-linked degradation of messenger RNA that links mutations to all pathology. Genetically engineered superbugs are expected to do the same thing as naturally occurs in the context of ecological variation and ecological adaptation of bacteriophages, viruses in bacteria.
So, I wrote:

Use of fluorescent detection to determine protease activity would probably lead from the discovery of the bacteriophage that is linked to resistance, and then… to effective treatment via the anti-entropic virucidal effects of sunlight. For example, the epigenetic effects of UV light on DNA repair via plant growth and the physiology of pheromone-controlled reproduction in yeasts have been reported in the context of the microRNA-mediated progression of cancers via the same molecular mechanisms. Unfortunately, most researchers missed the facts from Schroedinger (1944) What is Life? The likelihood that they will accept facts that link bacteriophages to all pathology across all kingdoms is negligible. Most are still focused on mutation-driven evolution instead of energy-dependent biophysically constrained ecological adaptations in the context of viral latency. But see: “Virus-mediated archaeal hecatomb in the deep seafloor” and “Eukaryotic plankton diversity in the sunlit ocean” before Koonin and Krupovic formally announce their collaboration with scientific creationists from South Korea, who have linked Schrodinger’s claims to Ben Feringa’s claims via “Dynamic control of chirality and self-assembly of double-stranded helicates with light.”

Before I could do it, George Carlone (PhD retired) suggested that others look for a bacteriophage that can attach, kill or alter C. auris. He also suggested that someone must be doing sequencing.

That’s what I thought would be best based on what is known about how the virus-driven degradation of messenger RNA leads to the creation of shiga toxins.When you tell others why they should do the sequencing (e.g., to link epigenetic effects of food and pheromones to viral latency via HERVs) maybe someone will admit that they have done that, or that they have people who will do it before the bacteriophages kill us all.See for example: “Perspectives of Phage Therapy in Non-bacterial Infections”

I responded to a comment from someone who wrote about Dr. Jack Sobel, who has studied Candida Albicans infections for his entire career and is an expert on vulvovginl candidiasis.

 You may want to interview someone who has linked mating in yeasts to sexual orientation in humans via mate-choice for food energy-dependent pheromone-controlled genetic diversity in the Hutterites from the “Old” World to populations in North America and the mouse-to-human model of fixation of EDAR V370A alleles. See: “HLA and Mate Choice in Humans”

I responded to a comment on about mutations from mating fungi, which were compared to ecological adaptations in H. pylori.

The problem with h.pylori is bacteriophage-induced pathology. Mutations in mating fungi are also typically biophysically constrained by the availability of food energy and the pheromone-controlled physiology of RNA-mediated sexual differentiation of all cell types in all living genera that sexually reproduce. See our section on molecular epigenetics in From Fertilization to Adult Sexual Behavior Published in: Hormones and Behaviour, 30, 333-353 (1996)
I responded to a comment on climate change for comparison to resistance due to overpopulation, over medication, and lax sanitation routines. The suggestion was made that if population declines to more sustainable levels,  “…this “thing” and others which are sure to follow would likely disappear naturally.”

It’s very difficult for me to not link global biogeochemical cycles of protein biosynthesis and degradation to all maladies via the virus-driven degradation of messenger RNA in all living genera. How do you do it post publication of: “Spindle-shaped viruses infect marine ammonia-oxidizing thaumarchaea” by scientific creationists in South Korea who have teamed up with Mart Krupovic and researchers from other countries?

After someone else complained about the clear and convincing evidence of the failure, inept, and unprofessional groups of scientists and others within the faculties and institutions from which they preach their pseudoscientific nonsense, I wrote:

See: “Why have microRNA biomarkers not been translated from bench to clinic?” 1/17/19 and more than 89,000 indexed publications from PubMed that mention microRNAs.

If people from other countries were as stupid as people in the countries of the Western World, President Trump would not need to change the focus of research to effects of nutrition or effects of nutrient stress and social stress on all pathology.

I might have just as well been talking to myself.

Then I read: Towards a global dialogue about heritable germline editing: Mapping needs and challenges 7/23/19I turned to Twitter in an attempt to discuss the perceived problem with bacteriophages in the contest of germline editing and the transgenerational epigenetic inheritance of virus-driven pathology.I asked: Can regulation prevent global biogeochemical cycles of energy-dependent ecological adaptations to the virus-driven degradation of human mRNA, which link the pheromone-controlled physiology of reproduction in bacteria to protection from bacteriophage-induced shiga toxin?I expressed this concern: I’m concerned about heritable genome editing because naturally occurring food-energy dependent pheromone-controlled germline editing may not biophysically constrain viral latency. For example, C. elegans become P. pacificus, a predatory nematode with teeth.I placed my concern into this context:
If you knew that lack of a single amino acid substitution could cause the predatory nematode to adapt, would you ensure that the diet of your children did not cause one or more to become mass murderers or commit suicide via failure to fix COMT Val158Met in their organized genome?
I mentioned this fact:  If the value judgments and consensus that germline editing is desirable emerged from profit-motivated deliberation among stakeholders, could the problem with germline editing be linked to the development of a new human species without God’s involvement via claims from “The Darwin Code: Intelligent Design without God”4/14/15
Greg Bear claimed that shiga toxin, a potent poison linked to disease via the

“…viral infection of bacteria–is also an essential method of communication–FedEx for genes.”

When genes are swapped, bacteria can adapt quickly to new opportunities. In the case of bacterial pathogens, they can rapidly exploit a potential marketplace of naïve hosts. In a way, decisions are made, quorums are reached, recipes are traded, and behaviors change.

I started to read: The longevity-promoting factor, TCER-1, widely represses stress resistance and innate immunity 7/17/19

In many organisms, a positive correlation has been noted between increased longevity and enhanced tolerance against environmental stressors such as high temperature, oxidative damage and pathogen attack (reviewed in refs. 1,2,3).

Immediately, I recognized the connection from the nutrient-dependent pheromone-controlled microRNA-mediated behavior C. elegans to the dietary change and ecological adaptations in a predatory nematode with teeth, P. pacificus.
I revisited: A functional genomic screen for evolutionarily conserved genes required for lifespan and immunity in germline-deficient C. elegans  8/5/14
Abstract Introduction

The reproductive system regulates lifespan in insects, nematodes and vertebrates. In Caenorhabditis elegans removal of germline increases lifespan by 60% which is dependent upon insulin signaling, nuclear hormone signaling, autophagy and fat metabolism and their microRNA-regulators. Germline-deficient C. elegans are also more resistant to various bacterial pathogens but the underlying molecular mechanisms are largely unknown.

Abstract Conclusion:

From an evolutionary perspective, most of the genes differentially expressed in germline deficient C. elegans also show a conserved expression pattern in germline deficient Pristionchus pacificus, a nematode species that diverged from C. elegans 250-400 MYA

I gave up hope. The molecular mechanisms of epigenetically-effected microRNA-mediated biophysically constrained viral latency via autophagy and the links to healthy longevity were detailed in our 1996 Hormones and Behavior review. From Fertilization to Adult Sexual Behavior
The nutrient-dependent pheromone-controlled divergence of P. pacificus from C. elegans was attributed to a change in diet in  System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes.

Reported as: The neurobiological consequence of predating or grazing

“The patterns of synaptic connections perfectly mirror the fundamental differences in the feeding behaviours of P. pacificus and C. elegans”, Ralf Sommer concludes. A clear-cut result like that was not what he had necessarily expected. Previous studies in much simpler neural circuits – as in the marine snail Aplysia – had indicated that changes in behaviour do not have to coincide with changes in number and location of synapses. Differences in physiological properties of neurons or in their modulation by neurotransmitters can be sufficient to effect behavioural changes.

See: Bastardized health care (1)

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