Evolutionary determinants of genome-wide nucleotide composition January 1, 2018
1) They place their thoughts about mutation rates into the context of compatibility with mutational spectra.
2)They claim the mutation rate can be linked to mutational spectra that may be free to wander across evolutionary time.
3) They ignore facts that link the energy-dependent maintenance of a suppressed constant genome-wide deleterious rate that obviously occurs in the context of the Virus-mediated archaeal hecatomb in the deep seafloor
4) They eliminate the need for food energy and the pheromone-controlled physiology of reproduction, which protect all organized genomes from the virus-driven degradation of messenger RNA.
5) They link the mutations caused by the degradation of messenger RNA to increasing organismal complexity via mutational spectra.
Summary, these researchers appear to be biologically uninformed science idiots.
See also Luo lab at CUHK publications Microbial Evolution and Ecology
The fact that microbes do not evolve and the fact that ecological variation is biophysically constrained by the food energy-dependent pheromone-controlled physiology of reproduction does not appear to have occurred to any coauthors of any articles from this group with one notable exception.
Single–cell genomics-based analysis of virus-host interactions in marine surface bacterioplankton
Viruses are the most abundant biological entities on Earth, surpassing the number of their potential host cells by at least one order of magnitude (Suttle, 2005). In the ocean, viral infections kill ~10–20% of planktonic biomass each day (Suttle, 2007; Evans and Brussaard, 2012). These infections are believed to have a major impact on microbial community composition, evolution and global geochemical cycles (Jover et al., 2014).
See also: Marine phage genomics: the tip of the iceberg
At some point, all serious scientists expect others to acknowledge the fact that the role bacteriophages play in pathology extends from marine phage genomics to the energy-dependent antiphage defense mechanism referred to as autophagy. Autophagy links food energy from the biophysically constrained pheromone-controlled physiology of reproduction to healthy longevity in all living genera. The facts about autophagy refute all the pseudoscientific nonsense touted by theorists.
See for instance: Interrogating marine virus-host interactions and elemental transfer with BONCAT and nanoSIMS-based methods
By resolving carbon and nitrogen enrichment in viral particles, we demonstrate the power of nanoSIMS tracer experiments in obtaining quantitative estimates for the total number of viruses produced directly from a particular production pathway (by isotopically labeling host substrates). Additionally, we show through laboratory experiments and a pilot field study that BONCAT can be used to directly quantify viral production (via epifluorescence microscopy) with minor sample manipulation and no dependency on conversion factors. This technique can also be used to detect newly synthesized viral proteins. Together these tools will help fill critical gaps in our understanding of the biogeochemical impact of viruses in the ocean.
The resolve of the carbon and nitrogen enrichment in P. fluorescens was linked to autophagy via the nutrient-dependent pheromone-controlled weekend resurrection of the bacterial flagellum. See: Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system
The claim about the “evolutionary resurrection” exemplifies the amount of pseudoscientific nonsense that theorists have placed into the context of energy-dependent pheromone-controlled fixation of RNA-mediated amino acid substitutions that differentiate the cell types of all individuals of all living genera.
A single nucleotide polymorphism (SNP) in ntrB in strain AR2S caused an amino acid substitution [Thr97→Pro97 (T97P)] within the PAS domain of the enzyme sensor NtrB. Another SNP in the fast-spreading strain AR2F in the σ54-dependent EBP gene ntrC alters an amino acid (R442C) within the DNA binding domain. The alteration in the two amino acids were reported as if they were mutations in the context of evolution, which occurred over-the-weekend.
See for comparison Diet and cancer prevention: Dietary compounds, dietary MicroRNAs, and dietary exosomes October 4, 2017
,,,a variety of dietary compounds such as curcumin, green tea, folat, selenium, and soy isoflavones show a wide range anti-cancer properties. It has been showed that these compounds via targeting a sequence of cellular and molecular pathways could be used as suitable options for cancer chemoprevention and cancer therapy. Recently, dietary microRNAs and exosomes have been emerged as attractive players in cancer prevention and cancer therapy. These molecules could change behavior of cancer cells via targeting various cellular and molecular pathways involved in cancer pathogenesis. Hence, the utilization of dietary compounds which are associated with powerful molecules such as microRNAs and exosomes and put them in dietary patterns could contribute to prevention or treatment of various cancers.
When growth factors are withdrawn, the autophagosome forms to induce autophagy .
A quantum theory for the irreplaceable role of docosahexaenoic acid in neural cell signalling throughout evolution
Classical physics cannot explain how Darwin’s “conditions of life” are linked to the biophysically constrained energy that is released during cell type signalling, which appears to be absolutely and precisely quantized in the context of tunnelling. However, nothing known to serious scientists about tunneling has been linked from experimental evidence of top-down causation to the energy-dependent tunneling. The spurious use of the term “evolution” should be placed into that context.
Docosahexaenoic acid–mediated, targeted and sustained brain delivery of curcumin microemulsion
MicroRNA: A Novel Target of Curcumin in Cancer Therapy
…curcumin has a variety of pharmacological effects such as antioxidant, anti-cancer, anti-inflammatory, and anti-microbial activities. Anti-cancer effects of curcumin are due to targeting of a wide range of cellular and molecular pathways involved in cancer pathogenesis including NF-kB, MAPK, PTEN, P53, and microRNAs (miRNA) network. Multiple lines of evidence have indicated that curcumin exerts its therapeutic effects via regulating miRNA expression (e.g. miR-1, miR-7, miR-9, miR-34a, miR-181, miR-21 and miR-19) which could lead to the regulation of underlying cellular and molecular pathways involved in cancer pathogenesis.
At some point, the facts must be recognized by even the most biologically uninformed researchers in the world. See: Viral MicroRNAs, Host MicroRNAs Regulating Viruses, and Bacterial MicroRNA-Like RNAs