The eternal significance of microRNA biogenesis (1)
(click to enlarge)In the first two decades of the twenty-first century, serious scientists forced pseudoscientists and drug developers to make more foolish claims. The additional claims were required for them to avoid admitting that they failed to link the creation of energy to the creation of all biodiversity via the microRNA-mediated physiology of reproduction in all living genera.
That fact means the pseudoscientists and drug developers also failed to link the virus-driven degradation of messenger RNA to all pathology.
For a historical perspective on the link from the virus-driven degradation of messenger RNA in bacteria to the pathology of sepsis and death in humans see:
The eternal significance of microRNAs (1) 4/10/18 through The eternal significance of microRNAs (10) 5/16/18
In 1996, microRNAs were called pre-mRNAs. That is not all that’s changed and the changes are happening faster.
In less than one year, the light-activated assembly of the microRNA-RNA-peptide nanocomplex has been linked from the ten-part series on the eternal significance of microRNAs to biophysically constrained viral latency and all biodiversity on Earth via the physiology of reproduction.
Indeed, light-activated carbon fixation has been linked from quantum physics to classical physics and to biophysically constrained viral latency, which is known to all serious scientists as healthy longevity in the context of Darwin’s “conditions of life.” Light-activated microRNA biogenesis can now be viewed in the context of:
Singlet molecular oxygen regulates vascular tone and blood pressure in inflammation 2/13/19
Our findings demonstrate a pathophysiological role for 1O2 in mammals through formation of an amino acid-derived hydroperoxide that regulates vascular tone and blood pressure under inflammatory conditions.
Reported on 5/14/19 as: Biochemical compound responsible for blood pressure drop in sepsis is discovered
This is the first time singlet oxygen has been shown to play a physiopathological signaling role in mammals. The molecule has well-established roles in photosynthetic plants, bacteria and fungi.
10 years after the failure to reproduce results from an earlier study, they linked photosynthesis from one amino acid substitution to recovery from sepsis. Many people know someone who did not recover. One of the author’s claims that this is science, because “science is reproducibility”.
As other people know, I claim it is pseudoscientific nonsense because all serious scientists know that one food energy-dependent amino acid can differentiate all the cell types and all differences in species via the physiology of reproduction.
If science is reproducibility, what about the other 8300+ indexed studies that mention “singlet oxygen?”
For example: The role of catalases in the prevention/promotion of oxidative stress 4/26/19
Highlights
- •Catalase reactions with species formed under oxidative stress are very fast.
- •Most of the oxidizing species formed during oxidative stress inhibit catalase.
- •Inhibition of catalase leads to the increased oxidative stress.
- •Overproduction of H2O2 resulting from catalase inhibition may be harmful to tissues.
- •Catalase inhibition may be beneficial in some pathological states.
- Testing in the medical laboratory for catalase differentiates the cell types of bacteria containing viruses that force the bacteria to ecologically adapt by finding food and the pheromone-controlled physiology of reproduction. The facts about the viruses and ecological adaptation went missing in this report.See for comparison: Potential drug targets for ALS and FTD identified in two studies 5/15/19
A pair of collaborative studies led by Fen-Biao Gao, Ph.D., have identified two potential drug targets for the diseases amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). The studies, which appear in Nature Neuroscience and PNAS, provide a new layer of detail about how hexanucleotide repeat expansions in the C9ORF72 gene, the most common genetic mutation responsible for both ALS and FTD, causes neuron cell death. The Nature Neuroscience study also describes a new mouse model that more closely mimics the gradual build-up of toxins in patients with the diseases.
The virus-driven degradation of messenger RNA causes the build-up of toxins in the mouse-to-human model of ecological variation and ecological adaptation.
See for comparison: Nutrient-dependent Pheromone-Controlled Ecological Adaptations: From Angstroms to Ecosystems (2018) A pair of collaborative studies led to this claim about the mouse-to-human model of all biophysically constrained pathology in the concluding paragraph:
The ecological adaptations, which appear to be manifested in the human population are detailed in these two reports [159,160]. The ecological adaptations are likely to be nutrient-dependent and pheromone-controlled. If so, ecological variation probably leads to ecological, social, neurogenic, and socio-cognitive niche construction, which is manifested in increasing organismal complexity and species diversity.
For comparison, see: C9ORF72-ALS/FTD-associated poly(GR) binds Atp5a1 and compromises mitochondrial function in vivo and Partial inhibition of the overactivated Ku80-dependent DNA repair pathway rescues neurodegeneration in C9ORF72-ALS/FTD
The authors want you to believe that the ATP5A1 protein is critical to the production of ATP.
See for comparison: Dependence of RNA synthesis in isolated thymus nuclei on glycolysis, oxidative carbohydrate catabolism and a type of “oxidative phosphorylation”
The synthesis of RNA in isolated thymus nuclei is ATP dependent.
ATP-dependent RNA synthesis is energy-dependent and the RNA synthesis must be linked to protein synthesis via fixation of amino acids substitutions. The claim that the ATP5A1 protein is critical to the production of ATP exemplifies human idiocy. Is it like saying that proteins automagically create themselves and that the ATP5A1 protein creates ATP.
The ongoing focus on drug development in the context of a protein that automagically creates ATP was placed into the proper context of a horrid scam in Get Well in the RNAi Way-RNAi, A Billion Dollar Baby in Therapy
RNAi has targeted exogenous genes in models of viral infection…
See also the patent application for biophysically constrained viral latency: RNA-Guided Human Genome Engineering
The facts about RNA interference (RNAi), which should have prevented the drug development scam, were detailed in 1999: RNA-triggered gene silencing
Double-stranded RNA (dsRNA) has recently been shown to trigger sequence-specific gene silencing in a wide variety of organisms, including nematodes, plants, trypanosomes, fruit flies and planaria; meanwhile an as yet uncharacterized RNA trigger has been shown to induce DNA methylation in several different plant systems.
The 2006 Nobel Prize in Physiology or Medicine was shared by Andrew Fire and Craig C. Mello for this work, which presciently linked what is currently known about the light-activated assembly of the microRNA-RNA-peptide nanocomplex from biophysically constrained viral latency in plants to healthy human longevity via the physiology of pheromone-controlled reproduction in species from microbes to humans.
See: RNA interference
Since the discovery of RNAi and its regulatory potentials, it has become evident that RNAi has immense potential in suppression of desired genes. RNAi is now known as precise, efficient, stable and better than antisense technology for gene suppression.[1]
That fact was placed into the context of this 1996 Hormones and Behavior review of RNA-mediated cell type differentiation. See our section on molecular epigenetics in: From Fertilization to Adult Sexual Behavior
Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.
Serious scientists have detailed the facts about energy-dependent protein creation during the past several decades. Drug developers continue to ignore the facts because the profits from drug development are more important to them.
The energy-dependent systems complexity is exemplified in the animation of Mitochondria and Aerobic Respiration
The series includes details about the energy-dependent creation of ATP synthase structure and function relationships.
The relationships are all about energy-dependent changes in base pairs, not the claims by drug developers that the ATP5A1 protein is critical to the production of ATP.
For comic relief, see:
