…Szostak’s lab could not reproduce the findings, which the group attributes to honest error.
Please put the “honest error” into the perspective of what was reported in: Retraction Watch
In retrospect, we were totally blinded by our belief [in our findings]…
The claim that scientists were blinded by their belief in their findings attests to the likelihood that they may not be serious scientists. Instead, they may exemplify what Richard Feynman placed into the context of human idiocy.
See: Food energy (video) My summary: All organisms must eat or they die.
For details, see: Dependence of RNA synthesis in isolated thymus nuclei on glycolysis, oxidative carbohydrate catabolism and a type of “oxidative phosphorylation”
McEwen et al., (1964) presciently linked quantized energy as information to all biophysically constrained biodiversity via the physiology of pheromone-controlled reproduction. Serious scientists now know that feedback loops link food odors to viral latency via changes in base pairs and RNA-mediated amino acid substitutions.
The beliefs of Szostak, and others like him, do not fit with the facts about the energy-dependent creation of supercoiled DNA. That fact has prevented others from examining facts about food energy-dependent autophagy, which biophysically constrains viral latency.
See: Modern diversification of the amino acid repertoire driven by oxygen
Simply put, the sudden emergence of life’s anti-entropic virucidal energy and the magical creation of enzymes did not lead to the evolution the amino acid repertoire. Energy-dependent changes in base pairs linked changes in the microRNA/messenger balance to RNA-mediated amino acid substitutions and the creation of enzymes that organize the genomes of all extant species on Earth.
The damage to science that has been done by those whose beliefs are not based on experimental evidence or common sense, which could have been applied to examples from model organisms, has been placed into the context of how enzymes metabolize food and drugs.
See: Alphagenomix and download a sample report that links the quantized energy dependent creation of enzymes from single nucleotide polymorphisms to RNA-mediated amino acid substitutions. The substitutions typically biophysically constrain viral latency and all pathology in the context of the physiology of pheromone-controlled reproduction and feedback loops. The facts about feedback loops make claims about mutations, natural selection (e.g., for anything except energy-dependent codon optimality) and claims about evolution appear to have automagically arisen from the life-ending thought processes of biologically uninformed theorists, who ignored Darwin’s “conditions of life.”
See for comparison: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
If it is not obvious to you that the ingestion of sago palm-like leaves links endogenous Vitamin C from the mouse model to the human example of biophysically constrained viral latency in a modern human population in China, you may need to review the extant literature that has been published by serious scientists since 1994, or earlier.
[Pheromonal regulation of genetic processes: research on the house mouse (Mus musculus L.)]
A study of the influence of pheromone stressor(s) on proliferating germ and somatic cells was performed on laboratory lines of house mouse in the context of the physiological hypothesis of mutation process, proposed by M.E. Lobashev in 1947. Data from experiments are presented, and results obtained during last 10-15 years are discussed. The adaptive role of cytogenetic and other observed pheromonal effects is considered. The possible existence of interorganism systems of genetic regulation is discussed, the search for and study of which may help in more complete understanding of the regularities of functioning of genetic material.
See for comparison: Session 10: Viral Evolution (iBiology supports the evolution industry)
See for comparison: The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.