Let’s make peer review scientific
…peer review is often biased and inefficient. It is occasionally corrupt, sometimes a charade, an open temptation to plagiarists. Even with the best of intentions, how and whether peer review identifies high-quality science is unknown. It is, in short, unscientific.
The androgynous baby-faced boy or girl pictured among those wearing pink “crotch” hats appears to representing others at the March for Women. The sign may also be representing the intent of one of the organizers whose support for terrorists became better known after this March.
Next comes the March for Science, where anyone whose photo appears can be asked what area of scientific expertise most interested them. Attempts will be made to learn more about what they did to link energy-dependent changes in angstroms from sunlight to ecosystems in all living genera via hydrogen-atom transfer in DNA base pairs in solution.
Measurement of ATP use revealed no significant preference for glycolytic or oxidative ATP by specific ATP consumers. Overall, we demonstrate how extracellular fluxes quantitatively reflect intracellular ATP turnover and cellular bioenergetics.
The energy-dependent extracellular fluxes link pheromone-controlled entropy from cellular bioenergetics to the physiology of reproduction. Virus-driven energy theft compromises the conserved molecular mechanisms of cellular bioenergetics.
See for example: Endothelial cell tropism is a determinant of H5N1 pathogenesis in mammalian species
…our study demonstrates that endothelial cell tropism is a determinant of the high virulence associated with HPAI H5N1 infection in mammalian hosts. By utilizing endogenous miRNA mediated restriction of viral tropism, we demonstrate that H5N1 infection of endothelial cells results in increased cytokine production in the lungs and loss of endothelial barrier function, which culminates in vascular leakage in the lungs. In addition, extrapulmonary spread of H5N1 virus likely occurs via the hematogenous route by infection of endothelial cells.
They link virus-driven energy theft from microRNAs in bacteria to messenger RNA degradation in archaea and L-forms (cells without walls). They fail to link energy theft to the substitution of nutrient energy-dependent amino acid substitutions in viruses, which links viruses to pathology in all living genera.
See for example: Identification of amino acid substitutions supporting antigenic change of influenza A(H1N1)pdm09 viruses
In conclusion, substitutions in or near the RBS can influence the antigenic properties of A(H1N1)pdm09 viruses. Based on the current and previous studies of antigenic change of influenza A viruses (11, 12), it is probable that emerging antigenic variants of A(H1N1)pdm09 viruses will escape from population immunity because of substitutions in or near the RBS. However, our results also suggest that the presence of antibodies directed to epitopes on seasonal A(H1N1) and A(H1N1)pdm09 viruses in much of the population limits the number of antigenic variants that can emerge to cause new epidemics.
Antigenic variants that are biophysically constrained cannot “emerge.” Nutrient stress or social stress must first break the biophysical constraints or there would be no new epidemics. That fact means that nutrient-dependent pheromone-controlled neurogenesis links the physiology of reproduction to ecological adaptations in all cell types of all individuals of all living genera, including organisms with no brain. If you start from neurogenesis in the human brain without realizing that it is pheromone-controlled, you may never learn how food odors and pheromones link the physiology of reproduction to the transgenerational epigenetic inheritance of all morphological and behavioral diversity via conserved molecular mechanisms of endogenous RNA interference.
See also from 6 years ago: Reproduction: A New Venue for Studying Function of Adult Neurogenesis?
Recent studies disclose that SVZ neurogenesis is under regulation of reproductive cues like pheromones.
Some recent debate about this fact was published to the Discover Magazine blog site in the context of accurate claims that Ben Carson made about learning and memory. A anonymous character with the screen name “Neuroskeptic” caused me to voice some concerns about the intelligence of people who accused Ben Carson, a pediatric neurosurgeon, of being wrong about anything.
See: Ben Carson and the Power of the Hippocampus 3/10/17
My comment from 3/11/17
See also: “Reproduction: A New Venue for Studying Function of Adult Neurogenesis?” (2011) Cell Transplant
Excerpt: …the number of dividing neurons in the hippocampus of female sheep increased robustly (43), which is accompanied with a sharp increase in circulating luteinizing hormone. Additionally, luteinizing hormone level and hippocampal neurogenesis were also upregulated by the soiled bedding. With the use of prolactin and leutinizing hormone receptor knock-out mice, it was confirmed that the hippocampal neurogenesis is due to the increase of the luteinizing hormone but not prolactin; in contrast, prolactin is the regulatory factor of SVZ neurogenesis (69).
Neuroskeptic displayed the ignorance of all theorists and left them with no excuse to say anything more about Ben Carson, or anyone else who intends to help the President of the United States “Make America Great Again.” Only biologically uniformed liberals will continue their attempts to stop President Trump. The anti-entropic effect of pheromones on GnRH and luteinizing hormone links food odors and pheromones from feedback loops to the physiology of reproduction in all vertebrates via the substitution of the achiral amino acid glycine in position 6 of the GnRH decapeptide.
With co-authors, Donald Pfaff did this in the context of autism. For example, substitution of the achiral amino acid glycine in position 6 of the GnRH decapeptide also links food odors and pheromones from stress-linked changes and feedback loops to sex-specific gene–environment interactions via the hypothalamic-pituitary-gonadal axis.
See: Sex-specific gene–environment interactions underlying ASD-like behaviors
…we found a significant three-way interaction on corticotropin-releasing hormone receptor-1 (Crhr1) gene expression, in the left hippocampus specifically, which co-occurred with epigenetic alterations in histone H3 N-terminal lysine 4 trimethylation (H3K4me3) over the Crhr1 promoter. Although it is highly likely that multiple (synergistic) interactions may be at work, change in the expression of genes in the hypothalamic–pituitary–adrenal/stress system (e.g., Crhr1) is one of them. The data provide proof-of-principle that genetic and environmental factors interact to cause sex-specific effects that may help explain the male bias in ASD incidence.
This was reported as: Study tests the ‘three-hit’ theory of autism
…the researchers looked for molecular changes within these rodents’ brains that might help to explain the differences in behavior. They found an increase in the expression of a gene that helps to kick off stress responses, in a brain region called the left hippocampus. With help from C. David Allis’s lab, they looked for chemical alterations in the packaging of DNA that might explain this uptick in gene activity. This effort revealed one particular chemical change in the nerve cell nucleus that encourages the expression of this stress-relevant gene.
The chemical alterations are energy-dependent and RNA-mediated via methylation, which alters gene activation to help ensure that all organisms of all living genera have the best opportunity to ecologically adapt. If they fail to adapt, they die. They do not mutate and become another species.
See: Every amino acid matters: essential contributions of histone variants to mammalian development and disease (2014) by senior author C. David Allis.
…numerous histone variants seem to be restricted to specific cell lineages or tissue types, yet it remains unclear how such expression patterns are maintained and what the consequences are of increasing or reducing combinatorial variant deposition across cell types. Aberrations in these processes result in detrimental phenotypic outcomes across numerous mammalian systems, including humans. Although we are clearly still in the infancy of this ever-expanding and diverse field, we imagine that future endeavours related to histone variant biology will hold great promise for human health and disease.
The tag-team of Pfaff and Allis will continue to prevent others from what is known to all serious scientists about epigenetically-effected gene-environment interactions among all living genera. The interactions are nutrient-energy-dependent and pheromone controlled by the physiology of reproduction.
I posted this question to the CRISPR Cas 9 FB group and to the miRNA & siRNA FB group
Does any experimental evidence of biologically-based cause and effect suggest that microRNA-mediated host-induced gene silencing is not linked from biophysically constrained viral latency to energy-dependent RNA-mediated cell type differentiation via amino acid substitutions in the cell types of all living genera?
For example, could host-induced gene silencing occur outside the context of natural selection for energy-dependent codon optimality and endogenous RNA interference and the physiology of reproduction?
Can you imagine what the value of future patents on drugs will be if researchers continue to deny what is known about those two natural laws?