Life is energy-dependent. Energy is information. Life is not quantum except in the context of hydrogen-atom energy transfer in DNA base pairs in solution. Claims that do not also address the effects of virus-driven energy theft fail to link what is know about quantum physics from the creation of the sun to quantum biology. That is why Matti Pitkanen and other plagiarists must take my model and use it as if they knew how to link ecological variation to ecological adaptation or to extinction before they learned from me how to do it with the same model.
The wavelike nature of the particle provides a mechanism for it to simultaneously explore multiple pathways and ultimately resolve the optimal route. If the spacing of the chromophores, and the lifetimes of their excitons, are not “just so,” then the particle takes much longer to arrive at the reaction center. Much the same situation applies to electron tunneling through proteins in the mitochondrial respiratory chain. Lloyd whimsically describes these general phenomena as examples of the Quantum Goldilocks Effect: “Natural selection tends to drive quantum systems to the degree of quantum coherence that is ‘just right’ for attaining maximum efficiency.”
Here we report the discovery of this missing component: namely, glutamate-releasing neurons in the ARC that express the oxytocin receptor. We demonstrate that chemogenetic activation or inhibition of ARCVglut2/Oxtr neurons, in contrast to ARCPOMC neurons, rapidly and robustly decreases or increases hunger, respectively.
All serious scientists learned that chemogenetic activation or inhibition of genes is the link from the nutrient-dependent pheromone-controlled physiology of reproduction to energy-dependent endogenous RNA interference and healthy longevity in all living genera. See also: Role of olfaction in Octopus vulgaris reproduction (2015)
Future work on O. vulgaris olfaction must also consider how animals acquire the odours detected by the olfactory organ and what kind of odour the olfactory organ perceives. The OL acting as control centre may be target organ for metabolic hormones such as leptin like and insulin like peptides, and olfactory organ could exert regulatory action on the OL via epigenetic effects of nutrients and pheromones on gene expression (Kohl, 2013; Elekonich and Robinson, 2000).
Virus-driven energy theft links mutations to all pathology via the failure of energy-dependent endogenous RNA interference, which typically protects organized genomes from the effects of messenger RNA degradation.
See for comparison:
Matti Pitkanen: Chemical qualia as number theoretical qualia? (link opens pdf)
…reactive and defensive attitudes interfere de-constructively with logical thinking. Mr X has been stubbornly claiming that I am touting pure nonsense and that all are laughing to me. Surprisingly, he also claims that I have stolen his ideas!
See also: Mitochondria Help Cancers Grow
Jon Lieff has also been sneaking around and dismissing everything known to serious scientists about energy-dependent cell type differentiation, which links virus-driven energy theft to all pathology. He posted on changes in the mitochondria that he failed to link to energy-dependent healthy longevity. For example, mitochondria do not ‘produce’ the ‘cycles’ that link ‘food’ from one carbon metabolism to healthy longevity.
Mitochondria do not ‘adapt.’ The food enables thermodynamic cycles of nutrient energy-dependent protein biosynthesis and degradation. Your example of “doublespeak” obscures, disguises, distorts, or reverses the meaning of words. In that context Matti Pitkanen and Jon Lieff have done the same thing. They have distorted the works of serious scientists to make claims that link theories to biologically-based cause and effect. Theorists refuse to link experimental evidence from top-down causation to energy-dependent changes that link angstroms to ecosystems in all living genera via the physiology of reproduction.
The speed of light on contact with water is the obvious link to all energy-dependent biodiversity and virus-driven energy theft is the link to all pathology. Single-residue insertion switches the quaternary structure and exciton states of cryptophyte light-harvesting proteins. All serious scientists have links light harvesting proteins from plant sensors to RNA-mediated protein folding chemisty.
Evolutionary scientists did not predict such elaborate sensory integration in a single protein system.
Jon Lieff is one of the evolutionary theorists who has ignored that fact.
See also: Neuroimmune communication
We present a special set of Review articles on neuroimmune communication that highlight how the immune system and nervous system are anatomically connected, mechanistically communicate and reciprocally influence the other’s function.
I did that last year and during the past 20 years of my publication history. See: RNA-mediated physics, chemistry, and molecular epigenetics
Published on 3 May 2016
Olfaction and the innate immune system link energy as information from the epigenetic landscape to the physical landscape of supercoiled DNA. The sun’s biological energy is the source of the information that links angstroms to ecosystems via physics, chemistry, and molecular epigenetics.
RNA-mediated protein folding chemistry and amino acid substitutions link the anti-entropic quantized energy of sunlight from the virucidal effects of ultraviolet (UV) light to healthy longevity via biophysically-constrained energy-dependent hydrogen-atom transfer in DNA base pairs in solution and cell type differentiation.
Biomarkers link energy-dependent differences in base pairs and amino acid substitutions to biosignatures across the healthy life span. RNA-mediated amino acid substitutions also reveal the increasing complexity of interactions among cell types as pathology progresses. For comparison, successful reproduction links energy from supercoiled DNA to protection of all organized genomes from virus-driven energy theft and pathology.
This model links the sun’s biological energy from top-down causation in microbes to the most recent model of bottom-up gene activation and cell type differentiation in vertebrates. Citations to extant literature provide examples of what is currently known about how ecological variation leads to biophysically constrained cell type differentiation in the context of nutritional epigenetics and Precision Medicine, which clearly link metabolic networks and genetic networks to pharmacogenomics.
The values of imino photons are linked to energy-dependent closed or open states via the Gibbs free energy difference. See: 2017 Base-pair opening dynamics of the microRNA precursor pri-miR156a affect temperature-responsive flowering in Arabidopsis
I am nearly convinced that no matter how much experimental evidence of biologically-based cause and effect links energy-dependent changes in base pairs from microRNAs to biophysically constrained protein folding chemistry, pseudoscientists will not recognize the need to include virus-driven energy theft when they invent new ridiculous theories.
The “tipping point” was reached in May, 2016, but there are now 7000 more indexed publications that link energy-dependent changes from the microRNA/messenger RNA balance to all biodiversity. microRNA = 57,721 on February 6, 2017
The observed molecular recognition fundamentally differs from canonical promiscuous chaperone–substrate interactions. We demonstrate that the eukaryote-specific RpL4 extension harbours overlapping binding sites for Acl4 and the nuclear transport factor Kap104, facilitating its continuous protection from the cellular degradation machinery. Thus, Acl4 serves a dual function to facilitate nuclear import and simultaneously protect unassembled RpL4 from the cellular degradation machinery.
The nature of the energy-dependent interactions that link autophagy to endogenous RNA interference and healthy longevity is expressed without mention of RNA-mediated amino acid substitutions. The substitutions are reported in the context of residues.
The extensive nature of the interactions is best illustrated by the sheer number of residues directly involved in Acl4–RpL4LOOP binding: 42 out of 70 RpL4LOOP residues and 87 out of 333 Acl4 residues (Fig. 2a; Supplementary Fig. 2).