HPV infects more than 79 million Americans. The virus-driven degradation of messenger RNA links the creation of enzyme USP46 to specific HPV strains that cause nearly all cases of cervical cancer. Other scientists should consider who may suffer and die before they report results that link QTLs to cell type differentiation.
See for comparison: Revealing the brain’s molecular architecture
…QTLs are found to be associated with variation in cell type proportions in the brain, as well as those affecting chromatin, DNA hydroxymethylation, and gene expression.
To link the virus-driven degradation of messenger RNA from cervical cancer to mental disorders, see: Big data reveals hints of how, when and where mental disorders start
Serious scientists used 3D maps of primary olfactory neuronal cells to understand how the creation of the sense of smell in bacteria is linked to gene regulation in all living individuals. They placed their findings into the context of food energy-dependent pheromone-controlled transcriptome-wide changes in RNA-mediated amino acid substitutions.
Theorists touting their pseudoscientific nonsense about QTLs in “Science Magazine” for comparison, place the amino acid substitutions into the context of mutation-driven evolution via isoform-level dysregulation in ASD, schizophrenia and bipolar disorder. Isoform-level dysregulation automagically occurs when any of two or more functionally similar proteins with similar but not identical amino acid sequence, which are either encoded by different genes or by RNA transcripts from the same gene become unable to link energy as information to biophysically constrained viral latency.
For comparison, integrative models of human brain function and dysfunction clearly link the sun’s anti-entropic virucidal energy from the epigenetic landscape to the physical landscape of supercoiled DNA via changes in base pairs linked to the creation of RNA. Experimental evidence of top-down causation links integrative models from the virus-driven degradation of messenger RNA to neuropsychiatric risks.
For example (cited works below), “The transcription factor POU3F2 regulates a gene coexpression network in brain tissue from patients with psychiatric disorders” in the context of species-specific “Spatiotemporal transcriptomic divergence across human and macaque brain development.” These groups of researchers also linked, “Neuron-specific signatures in the chromosomal connectome to schizophrenia risk” before placing their findings back into the ridiculous context of a mathematical model of the genome-wide de novo risk score via promoter variation in autism spectrum disorder. They ignored claims that link the epigenetic effects of food and pheromones from noncoding RNA to the creation of enzymes and the regulated expression of several schizophrenia-related genes.
See for an example of links to the creation of one enzyme: COMT Val158Met Items: 1 to 20 of 865
If PsychENCODE pseudoscientists had included information on nonhomologous end joining, the level of obfuscation would have been clearer. Theorists should be thankful that nonhomologous end joining can still be used to explain the development of cancer outside the context of what is known to all serious scientists about the energy-dependent links from the creation of subatomic particles to cytosis and healthy longevity in species from microbes to humans. But they will not be able to play their ridiculous word games for much longer.
“nonhomologous end joining” Items 1-1737
“Regulatory QTL” Items 1-7
microRNA Items 1-81,101
But see: L. Sanders. One problem, many paths. Science News. Vol. 180, August 13, 2011, p. 20.
See also these additional reports from: The PsychENCODE Consortium in Science. Vol. 362, December 14, 2018.
M. Li et al. Integrative functional genomic analysis of human brain development and neuropsychiatric risks. Science. Vol. 362, December 14, 2018, p. 1264. doi: 10.1126/science.aat7615.
M.J. Gandal et al. Transcriptome-wide isoform-level dysregulation in ASD, schizophrenia and bipolar disorder. Science. Vol. 362, December 14, 2018, p. 1265. doi:10.1126/science.aat8127.
D. Wang et al. Comprehensive functional genomic resource and integrative model for the human brain. Science. Vol. 362, December 14, 2018, p. 1266. doi:10.1126/science.aat8464.
Y. Zhu et al. Spatiotemporal transcriptomic divergence across human and macaque brain development. Science. Vol. 362, December 14, 2018, p. 1267. doi:10.1126/science.aat8077.
A. Amiri et al. Transcriptome and epigenome landscape of human cortical development modeled in organoids. Science. Vol. 362, December 14, 2018, p. 1268. doi:10.1126/science.aat6720.
P. Rajarajan et al. Neuron-specific signatures in the chromosomal connectome associated with schizophrenia risk. Science. Vol. 362, December 14, 2018, p. 1269. doi:10.1126/science.aat4311.
J.-Y. An et al. Genome-wide de novo risk score implicates promoter variation in autism spectrum disorder. Science. Vol. 362, December 14, 2018, p. 1270. doi:10.1126/science.aat6576.
For the most significant reports on energy-dependent top-down causation and biophysically constrained viral latency, see:
S.L. Rhie et al. Using 3D epigenomic maps of primary olfactory neuronal cells from living individuals to understand gene regulation. Science Advances. Published online December 13, 2018. doi:10.1126/sciadv.aav8550.
C. Chen et al. The transcription factor POU3F2 regulates a gene coexpression network in brain tissue from patients with psychiatric disorders. Science Translational Medicine. Vol. 10, December 19, 2018. doi:10.1126/scitranslmed.aat8178.
Q. Meng et al. The DGCR5 long noncoding RNA may regulate expression of several schizophrenia-related genes. Science Translational Medicine. Vol. 10, December 19, 2018. doi:10.1126/scitranslmed.aat6912.
Remember, serious scientists have linked light-activated microRNA biogenesis in plants from the creation of the sense of smell in bacteria to our visual perception of energy and mass via the pheromone-controlled physiology of reproduction in species from microbes to primates.
If you are too stupid to do a literature review before you publish something that mentions QTLs but fails to mention microRNAs, you probably will not have a Happy New Year. Serious scientists will get all the funding in 2019.
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; experiencedependent 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.
This integrative analysis combines miRNA expression, mRNA expression, and genotype data… to find polymorphisms that modulate co-expression patterns between miRNAs and their putative gene targets, which we term regQTLs.
They use a relatively new term: regQTLs, to obfuscate facts about energy-dependent changes in base pairs. The changes link quantum physics to classical physics and biophysically constrained protein folding chemistry from viral latency to healthy longevity in species from yeasts to vertebrates via fixation of RNA-mediated amino acid substitutions.
See also: QTL “base pair”
On 11/29/18, my 29 tweets made 26,287 impressions. On 12/5/18 my 32 tweets made 350 impressions. Obviously, I cannot compete for a target audience during a time when more nonsense about QTLS is touted each day.
“…gene-expression differences among different genotype groups…”
…are energy-dependent and microRNA-mediated in the context of base pairs linked from the creation of enzymes to metabolism and all biophysically constrained biodiversity. Stop calling base pairs: “QTLs.”