Sunlight as information

2 genes in 2 species (too expensive and too insignificant)

by with One Comment AdaptationsEcologyLight EnergyModel OrganismsPhysicsRNA Directed

Characterisation of two Neurogenin genes from the brook lamprey Lampetra planeri and their expression in the lamprey nervous system by Ricardo Lara Ramirez et al.
Abstract excerpt: “Here we report the isolation of two Neurogenin genes, LpNgnA and LpNgnB, from the lamprey Lampetra planeri. Phylogenetic analyses show both genes have orthologues in other lamprey species and in a hagfish.”
My comment: “…the identity of a single functional GPH [glycoprotein hormone] of the hagfish, hagfish GTH, provides critical evidence for the existence of a pituitary-gonadal system in the earliest divergent vertebrate that likely evolved from an ancestral, prevertebrate exclusively neuroendocrine mechanism by gradual emergence of a previously undescribed control level, the pituitary, which is not found in the Protochordates (Uchida et al, 2010)
The authors place what is obviously a nutrient-dependent pheromone-controlled ecological adaptation into the context of evolution via a prevertebrate neuroendocrine mechanism and gradual emergence, which is typical of how evolutionary theorists link pseudoscientific nonsense to biologically-based cause and effect.  For example: “Research on GnRH in hagfish provides a rare insight into a primordial neuroendocrine milieu which could approximate what may have been present in animals living more than 300 million years ago.” For comparison, see our 2001 review from the same journal, Human pheromones: integrating neuroendocrinology and ethology, and place what is known about neuroendocrinology and etholgoy into the context of what is known about GnRH in other species, see: Role of olfaction in Octopus vulgaris reproduction.
Excerpt: “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).”
Kohl (2013) is Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Elekonich and Robinson (2000) is Organizational and activational effects of hormones on insect behavior.
Elekonich and Robinson (2000) linked our 1996 review of RNA-mediated pheromone-controlled hormone-organized and hormone-activated sex differences in morphological and behavioral phenotypes to insects.
Excerpt: “Effects of hormones on brain and behavior occur through three mechanisms: (1) behaviors both organized and activated by hormones, (2) behaviors only organized by hormones, and (3) behaviors only activated by hormones (reviewed in Arnold and Breedlove, 1985; Diamond et al., 1996).” Diamond et al. (1996) is From Fertilization to Adult Sexual Behavior. 
See also: Introduction: A Surfeit of Lampreys
Excerpt: “Recently, lampreys have started getting more widespread attention. Research related to lamprey endocrinology (­particularly the pivotal hypothalamic-pituitary axis and gonadotropin-releasing hormones), the ecology and conservation of native lampreys, and the use of lampreys in evolutionary developmental (evo-devo) and biomedical studies has raised the profile of this group of ancient fishes.”
My comment:  Given the obvious importance of gonadotropin releasing hormone (GnRH), why is it not mentioned in by Ricardo Lara Ramirez et al? Examples of  how ecological variation leads to ecological adaptations via conserved molecular mechanisms of the biophysically constrained chemistry of protein folding now link them from light-induced amino acid substitutions in plants and animals to nutrient-dependent pheromone-controlled RNA-mediated amino acid substitutions and cell type differences in all cells of all individuals of all genera via the balance of viral microRNAs and anti-entropic nutrient-dependent microRNAs. See for instance:
1) The phylogenetic utility and functional constraint of microRNA flanking sequences 
2) N6-methyladenosine marks primary microRNAs for processing
3) N6-methyladenosine-dependent RNA structural switches regulate RNA-protein interactions
For the role of GnRH in mammals, see also: Feedback loops link odor and pheromone signaling with reproduction
Serious scientists know how RNA-directed DNA-methylation and RNA-mediated amino acid substitutions link cell type differentiation in species from microbes to man. The serious scientists are using what is known in the context of Combating Evolution to Fight Disease. What then can be said for pseudoscientists who seem to understand nothing about the role of vertebrate GnRH?
My experience with Ricardo Lara Ramirez says a lot about the pseudoscientists. I’ve had many encounters with him since he first began to antagonize me on the FB pages of Ulla Mattfolk
Here are my comments from a recent exchange with Ricardo Lara-Ramirez, whose antagonistic comments disappeared when he learned from me that his published work had become available, albeit behind a paywall.
To: Ulla Mattfolk Re: your ongoing rudeness at “Thinking Allowed Original” where you banned me from participation, but are still denigrating my works.
Ricardo Lara Ramirez’ friend Jerome Hui just made the lot of you look like biologically uninformed science idiots. See: The phylogenetic utility and functional constraint of microRNA flanking sequences
Excerpt: “MicroRNAs (miRNAs) have recently risen to prominence as novel factors responsible for post-transcriptional regulation of gene expression. miRNA genes have been posited as highly conserved in the clades in which they exist.”
My comment: From my 2013 review: “…the epigenetic ‘tweaking’ of the immense gene networks that occurs via exposure to nutrient chemicals and pheromones can now be modeled in the context of the microRNA/messenger RNA balance, receptor-mediated intracellular signaling, and the stochastic gene expression required for nutrient-dependent pheromone-controlled adaptive evolution.”
Ulla Mattfolk You said yourself you would take the discussion to your own group, so let it be so. Don’t misuse my space. My kindness has limits.
James Kohl Your kindness? I will gladly leave you to your ignorance at a time when everything I’ve claimed gains increasing support from experimental evidence. N6-methyladenosine marks primary microRNAs for processing
See: Chemical tag marks future microRNAs for processing, study shows
Excerpt: “… these experiments have identified a switch that can be used to ramp up or tamp down microRNA levels, and as a result, alter gene expression”

My comment: The ‘m6A-switch’ apppears to link ecological variation to nutrient-dependent RNA-directed DNA methylation, which links RNA-mediated amino acid substitutions to cell type differentiation in all cells of all individuals of all genera via the biophysically constrained chemistry of RNA-mediated protein folding.

The link from ecological variation and metabolism of nutrients to species-specific pheromones that control the physiology of reproduction in species from microbes to man, links the viral microRNA/nutrient-dependent microRNA balance to pheromone-controlled fixation of amino acid substitutions at the origins of plant life in the context of light-induced amino acid substitutions in plants and algae and sea-slugs et al.

Dobzhansky (1973) provided an example of an amino acid substitution linked to biodiversity.  Like other amino acid substitutions linked to hemoglobin variants in different modern human populations, the variant Dobzhansky mentioned ~41 years ago, is linked to cell type differentiation and to health via increased nutrient-dependent pheromone-controlled genome-wide stability. Evolutionary theorists continue to link amino acid substitutions to physiopathology because they have not learned the difference between an amino acid substitution and a mutation. Most of them probably think the Hemoglobin S variant of sickle cell is a beneficial mutation.  Researchers identify red blood cell traits associated with malaria risk in children
We were the first to detail what was known about molecular epigenetics in our 1996 Hormones and Behavior review. This is the latest update to my domain. Epigenetic switch links MicroRNAs to RNA-protein interactions
… if you want to impress me… — Ricardo Lara Ramirez.
James Kohl Why would I want to do that? You are one of the most biologically uninformed antagonists I have ever encountered. Our 1996 review was the basis for extension of the concept of hormone-organized and hormone-activated behavior in insects, which led to the link from molecular epigenetics/pre-mRNAs to life history transitions that your friend Jerome Hui just reported.
Twenty years after my 1995 book publication, which linked crustaceans to insects via the conserved molecular mechanisms we detailed in our 1996 review — and that others have extended across all genera — he also linked crustaceans to insects.  See: All in the (bigger) family

Excerpt:  “…production of both hormones depends on the same rate-limiting enzymes. And Jerome Hui of the Chinese University of Hong Kong found that in both insects and crustaceans, the same set of micro RNAs control expression of the genes for those enzymes.”
My comment: Have theorists and their friends been living in the Dark Ages for the past two decades? Do you know anything about the first author of this review From Fertilization to Adult Sexual Behavior or the senior author of this award-winning review? Human Pheromones: “Integrating Neuroendocrinology and Ethology”
…”Anyone can write reviews, all you need is time to read and write.” — Ricardo Lara Ramirez
James Kohl Science fiction novelist Greg Bear integrated everything known about cell type differentiation into two of his science fiction novels because he had the time to read and write. With nothing more that a degree in English he included more details that you or Jerome Hui have learned about about during the past two decades. See: When Genes Go Walkabout Reviewed in “Nature”
See also: NIH grants aim to decipher the language of gene regulation
Millions of dollars continue to be wasted on research done by those, like Ricardo Lara Ramirez, who do not understand RNA-mediated sex differences in cell types, which we detailed in 1996. If you cannot understand the fact that sex differences are linked to cell type differences in all cells of all tissues of all organs of all organism systems in individuals of all species via conserved molecular mechanisms of the biophysically constrained chemistry of protein folding, you are probably among those who have forced serious scientists to continue Combating Evolution to Fight Disease.
Ricardo Lara Ramirez next denigrated my works because I have not published research papers.
James Kohl   Why would anyone expect a medical laboratory scientist to publish research papers? That task falls on those who have no experience linking what is known about nutrigenomics and pharmacogenomics via metabolic networks and genetic networks, which is what Greg Bear did based on works by Luis P. Villarreal, which he integrated with works on hormone-organized and hormone-activated behaviors (like our 1996 review). See: Force for ancient and recent life: viral and stem-loop RNA consortia promote life
“… his book Darwin´s Radio is scientifically innacurate, and he also participated on the Halo franchise with really crap ideas on humans being genetically degenerated. LOL” — Ricardo Lara Ramirez
James Kohl   You may be the most ignorant researcher I have ever ever encountered. Please ask Jerome Hui about the role of viral microRNAs in degeneracy. If he also knows nothing, ask Ryszard Maleszka, or see: Epigenomics and the concept of degeneracy in biological systems.
See also the review of “Darwin’s Radio.” Review in Nature “He has mustered a cadre of facts, loosely connected and ill understood. There are little happenings at the periphery of Mendelian genetics, at the edge of neo-Darwinian theory, and what used to be beyond the realm of molecular biology. We know that bacteria contain extrachromosomal elements that transmit traits, such as drug resistance, between individuals and between species. We know that elements exist which insert in and excise from the genome, sometimes in response to environmental signals or stresses. Most of us believe that simple, incremental changes in allele frequencies, driven by the forces of genetic drift, mutation, recombination, migration and natural selection, are enough to explain evolution from adaptation to speciation, to the origin of higher taxa. There is no compelling evidence to the contrary, but neither is there compelling evidence in favour of the idea; we simply haven’t observed or catalogued the forces and changes that create new species. Bear fills this void in our understanding with the notion that radical changes in the genome, brought about by mobilization of transposable elements such as human endogenous retroviruses, result in rapid change at the subspecies or species level.”

James Kohl Unlike Ricardo, I was paid to help diagnose and treat patients, not to invent theories based on the assumptions of others about biologically-based cause and effect. Nevertheless, two of my reviews won awards — one for best publication in ethology, one for best publication in social science.
“…one of them last author, WOW, that is laim.” — Ricardo Lara Ramirez
James Kohl Evidently, Ricardo doesn’t realize that the last author is also often the senior author of the work (like his friend, Jerome Hui). The phylogenetic utility and functional constraint of microRNA flanking sequences
Clearly, I’m not trying to get the approval of the biologically uninformed. I’m helping to show others how uninformed people can be. Thanks to Ricardo Lara Ramirez for setting an example

James Kohl What do you think is your most important contribution to the understanding of anything? Tell us about your publications and research.

For example, Characterisation of two Neurogenin genes from the brook lamprey Lampetra planeri and their expression in the lamprey nervous system appears to be an entry-level approach to what Anna Di Cosmo’s group detailed about the role of olfaction and GnRH in the cell type differentiation of octopuses and all vertebrates and invertebrates in Role of olfaction in Octopus vulgaris reproduction. See also Evolution of gonadotropin-releasing hormone (GnRH) structure and its receptor

I hope that Ricardo intends to pirate what I am telling him about and include it in meaningful attempts to help detail what is currently known about biologically-based cause and effect rather than continue his attempts to meaningfully interpret the pseudoscientific nonsense he has been taught to believe in.

“Phylogenetic analyses show both genes have orthologues in other lamprey species and in a hagfish.” — abstract excerpt from Characterisation of two Neurogenin genes from the brook lamprey Lampetra planeri and their expression in the lamprey nervous system

Ricardo Lara Ramirez should probably consider asking me to read this and comment on what he seems to have missed before he and his co-authors are horribly embarrassed — if it is not too late already. Can others imagine how horrid it would be to have missed everything known about GnRH-modulated gene expression by focusing on downstream effects and characterization of two genes from a single species?

Ricardo Lara Ramirez is crying now because “… the coordinated evolutionary selection of amino acids participating in binding GnRH has resulted in such perfection, that no substitution with a natural amino acid in any position improves binding potency.” Evolution of gonadotropin-releasing hormone (GnRH) structure and its receptor

I wonder if Ulla Mattfolk will remove the entirety of this discussion to help Ricardo save face. Hopefully, she will leave it as an example of how someone who is the most biologically uninformed antagonist I have ever encountered backed himself and his institution into a corner of “Dark Ages” ignorance by attacking me. No more funding for Ricardo. How about others? “

If you learnt evolutionary biology and genetics a decade or more ago you need to be aware that those debates have moved on very considerably, as has the experimental and field work on which they are based. (p 1014)” Neo-Darwinism, the Modern Synthesis and selfish genes: are they of use in physiology?

Ricardo Lara Ramirez thanked me for telling him his paper was published.

James Kohl  You’re welcome. Please send a pdf reprint to jvkohl@RNA-mediated.com and watch for my review. I’m tempted to comment only on the abstract.

Ricardo Lara Ramirez  laughed at me and noted that I could not get the paper because it was behind a paywall, and that he would not send a reprint.

James Kohl  That’s why I requested the reprint (because it was behind a paywall). An author’s copy would be fine. All of my published works are distributed for free.

“…your knowledge on evolution is really crap.” — Ricardo Lara Ramirez 

James Kohl  Agreed. My focus is on an atoms to ecosystems model of how ecological variation leads to ecological adaptations via nutrient-dependent RNA-mediated amino acid substitutions.

…more of his ridiculous antagonism — Ricardo Lara Ramirez   

James Kohl  Ricardo Lara Ramírez = JERK! (Waiting to hear from Denis Noble and many others who may review his most recent published work because it reflects poorly on institutions like Harvard and Oxford). Based on this excerpt from Role of olfaction in Octopus vulgaris reproduction: “…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).,” Ricardo Lara Ramirez appears to have published a career-breaking paper, which is typical of what biologically uninformed researchers do. That’s why serious scientists are “Combating Evolution to Fight Disease.”

See also: Vitamin D vital for gene expression in developing brains The study investigated the gene expression of four neurotrophic genes responsible for the production of proteins which relate to the survival, development and function of neurons (nerve cells).

James Kohl  Was it Ricardo or you Ulla Mattfolk who just removed all his antagonistist posts? No response: I added support for my model.

Electrical synapses connect a network of gonadotropin releasing hormone neurons in a cichlid fish

Anesthetics Act in Quantum Channels in Brain Microtubules to Prevent Consciousness

Reported as: Anesthesia points to deeper level ‘quantum channels’ as origins of consciousness
Excerpt: “Using molecular modeling, the US-Canadian team of Travis Craddock, Stuart Hameroff and Jack Tuszynski had previously shown anesthetic binding in ‘quantum channels’, non-polar arrays of amino acid pi resonance clouds, winding through microtubules.”
See for additional comments on quantum consciousness:

All comments from Ricardo Lara Ramirez have also been removed here. Only the disrespectful taunts of Ulla Mattfolk remain.  Has anyone else encountered such ignorance from anyone who thinks they are biologically informed but has not learned anything about biologically-based cause and effect in the past 20 years?

 
 

achiral-glycine

Ecological variation and niche construction: 1, 2, 3

by with One Comment AdaptationsEcologyHuman BrainPharmacogenomicsVariations

Part 1

From its most basic expression in grazing and predatory nematodes with differences in morphological and behavioral phenotypes, neurogenic niche construction is nutrient-dependent and pheromone-controlled. One of these two worms has teeth. It also recognizes self vs other differences and eats other worms. “The patterns of synaptic connections perfectly mirror the fundamental differences in the feeding behaviours of P. pacificus and C. elegans”, Ralf Sommer concludes.
Evolutionary theorists concluded and continue to claim that “…without mutation, evolution would not be possible. This is because mutations provide the “raw material” upon which the mechanisms of natural selection can act.”  That suggests the differences in synaptic connectivity and differences in behavior in P. pacificus arose via mutations in C.elegans that led to natural selection and the evolution of predatory behavior associated with the evolution of teeth.
For contrast, Starvation-Induced Transgenerational Inheritance of Small RNAs in C. elegans and everything currently known about differences in the immune systems of animals suggests ecological variation led from nutrient-dependent RNA-directed DNA methylation to RNA-mediated events and amino acid substitutions that differentiate the cell types of the two nematodes. All other experimental evidence of biologically-based cause and effect attests to the fact that RNA-mediated events link ecological variation to ecological adaptations manifested in the morphological and behavioral phenotypes of species from microbes to man via conserved molecular mechanisms.
Suzanne Clancy, who stated that “…without mutation, evolution would not be possible”,  should try to explain how she arrived at that conclusion in the context of explaining that “… the alteration of a single nucleotide in the gene for the beta chain of the hemoglobin protein (the oxygen-carrying protein that makes blood red) is all it takes to turn a normal hemoglobin gene into a sickle-cell hemoglobin gene. This single nucleotide change alters only one amino acid in the protein chain, but the results are devastating.”
What happens when the result of altering one amino acid in the protein change are not devastating?
Clancy (2008) wrote that “Beta hemoglobin (beta globin) is a single chain of 147 amino acids.” Thirty-five years earlier, Dobzhansky (1973) wrote that “…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla.”
Summary:
1) One altered amino acid of the chain in beta hemoglobin causes an inherited disease in some populations of modern humans. (per Clancy)
2) One altered amino acid of the chain in alpha hemoglobin causes species-wide differences in all populations of 3 different primates. (per Dobzhansky)
Five questions arise:
1) If the 3 different primates were two different nematodes, would they starve to death or mutate into a new species with a change in their diet.
2) Who is teaching others, like Jay R. Feierman, to believe that “Random mutations are the substrates upon which directional natural selection acts.” (https://groups.yahoo.com/neo/groups/human-ethology/conversations/topics/48229)
3) Why does any intelligent person believe “…that if you showed this statement to any professor of biology or genetics in any accredited university anywhere in the world that 100% of them would say that “Random mutations are the substrate upon which directional natural selection acts” is a correct and true statement.”
4) Similarly, why does any intelligent person believe they can tell me that  “Variation is not nutrient availability and the something that is doing the selecting is not the individual organism. A feature of an educated person is to realize what they do not know. Sadly, you don’t know that you have an incorrect understanding Darwinian biological evolution.”
5) Does anyone else think other intelligent people are not going to ask how nutrients could not be the substrates that enable Darwinian biodiversity when someone claims that random mutations are the substrates on which directional natural selection acts?

Part 2

All 5 questions from Part 1 have been addressed in the context of three articles published in Science, which were reported yesterday in an “In Depth” perspective by Elizabeth Pennisi on a “metabolic shift” linked to the immune system, which is required for self vs other recognition. See my comment: Metabolic shift may train immune cells. All three articles attest to the requirement for a link from ecological variation to ecological, social, neurogenic, and socio-cognitive niche construction via the gene-cell-tissue-organ-organ system pathway. Clearly, increasing organismal complexity arises via this established pathway that links embryonic development to adult development of morphological and behavioral phenotypes in vertebrates.
I have detailed a link in conjunction with details about the pathway from the epigenetic landscape to the physical landscape of DNA in the organized genomes of different species from microbes to man in Nutrient-dependent/pheromone-controlled adaptive evolution: a model. I included the examples of the two nematodes and an example of a primate population (i.e., modern humans in central China). Here is information about neurogenic niche construction in another model organism:

Sensory-specific modulation of adult neurogenesis in sensory structures is associated with the type of stem cell present in the neurogenic niche of the zebrafish brain

Excerpt: “…modality-specific stimulation at distinct stages in the process of adult neurogenesis – chemosensory niches at the level of neuronal survival and visual niches in the size of the stem/progenitor population” are linked to the origins of niche construction in the embryo via conserved molecular mechanisms of transgenerational epigenetic inheritance in nematodes. Can anyone explain how niche construction evolved?
Obviously, there are many researchers who still think “…mutations provide the “raw material” upon which the mechanisms of natural selection can act.” Does anyone know how mutations and natural selection led to the evolution of niche construction and the nutrient-dependent pheromone-controlled biodiversity manifested in the morphological and behavioral phenotypes of species from microbes to man — and to sensory specific modulation of adult vertebrate brain development in vertebrates? If so, mutations and natural selection could lead from the evolution of pheromones to….

Part 3

Roles for learning in mammalian chemosensory responses

? EVOLUTION OF PHEROMONES ?
Excerpt 1) “When Karlson and Lüscher first proposed their definition of a pheromone they envisaged that their definition would be redefined and updated over time (Karlson and Lüscher, 1959).”
My comment: Their definition was clear. ”Pheromones are defined as substances which are secreted to the outside by an individual and received by a second individual of the same species, in which they release a specific reaction, for example, a definite behavior, or a developmental process.”
Excerpt 2) “… it still forms the core of most accepted definitions, such as the recent, slightly modified definition by Wyatt, “molecules that are evolved signals…” (Wyatt, 2014).
My comment: Portraying pheromones as if they are evolved signals, is not a slightly modified definition. Wyatt (2014) took pheromones from the context of ecological variation and nutrient-dependent ecological adaptations in insects and defined pheromones in the context of evolution. He bastardized the definition to make it fit what population geneticists invented and defined, which is now called neo-Darwinism. The population geneticists defined Darwin’s nutrient-dependent ‘conditions of life’ in terms of mutations, natural selection, and evolution. Wyatt and others must now have “molecules that are evolved signals…” to continue their pseudoscientific nonsense, which is based on statistics not biologically-based cause and effect. Population Genetics is, however, only a statistical association between something we had to infer and something we could observe.
Dobzhansky’s (1964) accurate portrayal of the observers follows: “…the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists!”
Dobzhansky’s portrayal serves as an introduction to claims by Wyatt and others who continue the bastardization of Darwin’s works as if food odors and pheromones evolved. The perturbed reality of the observers does not include ‘conditions of life’ that are nutrient-dependent. They ignore that fact that nutrients are metabolized to species-specific pheromones that control the physiology of reproduction in species from microbes to man.
Pheromones are nutrient-dependent. Ecological adaptations are nutrient-dependent and pheromone-controlled. Protein biosynthesis and degradation are biophysically contrained in the context of thermodynamic cycles that must lead to the stability of DNA in the organized genomes of organisms that require nutrient-dependent metabolic shifts to enable organism-level thermoregulation.
What evolved? How? Why hasn’t anyone described a biologically-based evolutionary event? Why is Wyatt trying to convince others that pheromones evolved when their production is obviously nutrient-dependent and clearly linked from RNA-directed DNA methylation to RNA-mediated amino acid substitutions that differentiate the cell types of all cells of all individuals of all species via the conserved molecular mechanisms that enable the nutrient-dependent pheromone-controlled physiology of reproduction in species from microbes to man?

Pheromones and Animal Behavior: Chemical Signals and Signatures

“A final chapter critically considers human pheromones and the importance of olfaction to human biology. Its breadth of coverage and readability make the book an unrivaled resource for students and researchers in a range of fields from chemistry, genetics, genomics, molecular biology and neuroscience to ecology, evolution and behavior.”
People like Wyatt continue to show others that if you don’t understand the Laws of Physics, you should not write books about “…a range of fields from chemistry, genetics, genomics, molecular biology and neuroscience to ecology, evolution and behavior.” Instead, you should write books that claim “…constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.” Alternatively, you can keep claiming that pheromones in mammals do not exist or that human pheromones don’t exist because we are too highly evolved. After all, “WHAT are we going to do if it turns out that we have pheromones? What on earth would we be doing with such things? With the richness of speech, and all our new devices for communication, why would we want to release odors into the air to convey information about anything?” — Lewis Thomas (1971) “A Fear of Pheromones” as cited in the first book about human pheromones:

The Scent of Eros: Mysteries of Odor in Human Sexuality (1995/2002).

human-evolution

Nutrient-dependent erythropoiesis and anemia

by with No Comment AdaptationsDiseases & DisordersEcology

A critical role for mTORC1 in erythropoiesis and anemia

Excerpt 1): “Cells must coordinate their rate of growth and proliferation with the availability of nutrients. mTOR , a serine-threonine kinase, is one the key proteins responsible for nutrient signaling in eukaryotic cells. mTOR is activated by conditions that signal energy abundance, such as the availability of amino acids, growth factors, and intracellular ATP. Activated mTOR then phosphorylates a set of downstream targets that promote anabolic processes, such as protein translation and lipid biosynthesis, while suppressing catabolic processes such as autophagy [1].”
My comment: That fact links the availability of nutrients to RNA-mediated cell type differentiation in all cells of all tissues of all organs and all organ systems via the conserved molecular mechanisms. The mechanisms epigenetically link the sensory environment to pheromone-controlled cell type differentiation in species from microbes to man during their life history transitions. Simply put, cells must have nutrients to proliferate. They cannot coordinate their growth rate when they are starving to death. That fact makes the nutrient-dependent microRNA/messenger RNA balance the most obvious link to the physical landscape of DNA in the organized genomes of all species.
Evolutionary theorists continue to claim that the genomes are organized in the context of mutations, natural selection and the evolution of biodiversity. Although no evolutionary event has ever been described and only RNA-mediated events have been detailed, some people seem to prefer to believe in pseudoscientific nonsense about protein biosythesis and degradation. Fortunately, most medical laboratory scientists know that pseudoscientific nonsense may kill people.
For example see:

Two case studies and a review of paroxysmal cold hemoglobinuria

Yesterday, I spoke about this with Misty, a medical technology student. I learned later from a former technologist who became a physician’s assistant that Misty had ‘aced’ her most recent test in immunohematology/blood-banking/transfusion medicine. I discussed this with Misty and we concurred: No matter how much laboratory professionals learn, there will always be cases where what is not known alters patient outcomes.
In these two case studies, the authors link what appears to be antibiotic-induced receptor-mediated changes to an acquired hemolytic anemia via medication-induced changes in the microRNA/messenger RNA balance and RNA-mediated events that differentiate cell types via amino acid substitutions. Unlike Misty, some students may believe cell type differentiation is caused by mutations and natural selection. Yes, indeed, Richard Lenski’s works with E.coli have been meaningfully interpreted to make it appear that they support a ridiculous theory. See: The Man Who Bottled Evolution. That report misrepresents this fact: The organisms were competing for a carbon source, as all organisms must do. Without a source of nutrients, they starve to death. They do not evolve inside or outside bottles. See for example:  “…in medium with glucose and acetate as carbon sources, E. coli cells preferentially metabolize glucose and excrete acetate until the glucose is depleted and then undergo a diauxic switch to acetate consumption [32].” This fact is reported — with my emphasis — as “…each population consisted of generalists competing for two different sources of dietary carbon (glucose and acetate), but after 1200 generations they had evolved into two coexisting types each with a specialized physiology adapted to one of the carbon sources.” I am reminded that medical laboratory scientists who often are generalists may also compete to find the diagnosis that best fits into the context of a disease or disorder. It may be a matter of ego, but the competition is more likely to be a matter of which professionals can collectively provide the best information to the attending physician.
If the problem with cell types that led to the aquired anemia was manifested in sickle-cell anemia, most people would have been taught by evolutionary theorists that the genomic instability that led to the ecological adaptation was caused by a mutation, which somehow spread throughout human populations in geographic regions where malaria was or still is endemic. That is an example of how evolutionary theory continues to kill people. Theorists don’t seem to know anything about biophysically-constrained nutrient-dependent RNA-mediated events and amino acid substitutions, which differentiate cell types in all cells of all individuals in all species via stabilization of DNA. That is why evolutionary theorists typically attribute the biodiversity of cell types to mutations, natural selection, and the evolution of more than 1180 human hemoglobin variants.
If medical laboratory scientists did that, no tests for the cell type variants present in the anemia manifested in the two cased presented above would ever have been developed. Two children (one 23 month-old and one 4-year old) would have not been diagnosed with paroxysmal cold hemoglobinurea (PCH). Both would have received transfusions or died. Only one received a transfusion, and fortunately both children lived. That’s because a test for PCH was developed in 1904. When the 4-year old manifested the symptoms and same results of testing, no transfusion was requested. Kudos to those who adeptly recognized the pattern in these two children.
What is the problem? Medical laboratory professionals are taught to recognize patterns; evolutionary theorists are not.
In this case, the acquired hemolytic anemia makes it clear that consideration of the biophysically-constrained thermodynamics of protein biosynthesis and degradation should be the first consideration. Antibiotic-induced changes in these receptor-mediated nutrient-dependent thermodynamic cycles appear to initially help with the natural genetic engineering of organism-level thermoregulation in the management of infections and fever in both children.
The antibiotics did not cause mutations in the bacteria or in the children. However,  two to three weeks later the children presented with the acquired hemolytic disease. Was the disease acquired due to a virus that led to a bacterial infection or the antibiotic used to treat the symptoms?  Could an earlier diagnosis of PCH have been made in the 23-month old to avoid the requirement for transfusion? An earlier diagnosis is not likey if the medical professionals are taught to believe in the evolution of antibiotic resistance or to believe that evolutionary events somehow differentiate cell types.
Cell type differentiation is nutrient-dependent and RNA-mediated. It is controlled by the metabolism of nutrients to species-specific pheromones that enable self versus non-self recognition as clearly as does testing in the blood bank. Unfortunately, some evolutionary theorists portray the Duffy-null allele, which is nearly completely fixed in mainland sub-Saharan Africa and absent elsewhere, as if it were a mutation that was fixed in certain populations via natural selection. How can they suggest that given what is known: “There are two DARC protein polymorphisms, the FY*A and FY*B alleles, that differ by a single amino acid. A third polymorphism, FY*O or the Duffy-null allele, is a DARC promoter region single nucleotide polymorphism (SNP) that effects the loss of Duffy antigen protein expression on red blood cells [5].” — Hodgson et al (2014)
Medical professionals probably understand what most theorists cannot. Cell type differentiation is nutrient-dependent and pheromone-controlled via RNA-mediated events, which explains why medical professionals may laugh at any attribution that links a fixed amino acid substitution to perturbed protein folding, which theorists claim also causes the loss of Duffy antigen protein expression on red blood cells. Most medical professionals have trouble believing in a hypothesis that links mutations to amino acid substitutions and protein biosynthesis, but also to the loss of those proteins. Medical professionals should be wary of anyone who tells them that mutations lead from protein biosyntheis to fixed amino acid substitutions and also the elimination of amino acid substitutions and proteins in different human populations. For example, watch out for Masatoshi Nei. He states that “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.” Kick him out of your lab before he kills someone with an incompatible blood type with his theory. Tell him on his way out that nutrient-dependent RNA-mediated events differentiate cell types and you have the test results that prove it. If you must do so, first take him to the microbiology department and experimentally test how long any bacteria lasts without a supply of nutrients.
Show him how that cell types of E. coli show up in different colors on different types of media if he needs to be convinced that the morphology of the colonies is nutrient-dependent and pheromone-controlled via quorum-sensing.
If medical professionals refuse to believe in the pseudoscientific nonsense of neo-Darwinian theory, experiences in microbiology, transfusion medicine, and other departments, may lead to more interest in obtaining a thorough patient history. Most of us would not hesitate to obtain that history if any problem occurred in any aspect of testing — even with a cold agglutinin that appeared to cause hemolysis. Some of us may link antibiotic use to the hemolytic disorder by what is currently known about RNA-mediated events that differentiate cell types via amino acid substitutions in populations with different hemoglobin variants.
“What’s a hemoglobin variant?” — an evolutionary theorist might ask. “I learned that mutations cause different cell types associated with skin pigments in different populations of humans so that — as mutant humans — they could survive in regions where malaria was, or still is, endemic.
We need to keep the evolutionary theorists out of the lab and ignore them when we are inside or outside the lab. We need to tell them that they may be causing patient deaths by preventing the early diagnosis of disorders that may or may not require treatment with blood transfusions, or with antibiotics if the diagnosis of the disorder is made quickly. Try this, tell the evolutionary theorists that the diagnosis of PCH requires the same test that has been used since 1904. Ask why they don’t know that RNA-mediated events link nutrient-dependent amino acid substitutions to cell type differentiation. Tell them they have contributed to deaths from disorders caused by population geneticists who knew nothing about cell type differentiation in any species. They simply assumed that mutations caused the morphological and behavioral differences and taught others who have continued to tout that pseudoscientific nonsense for more than 100 years. They wouldn’t know the difference between an ecological adaptation and a mutation if they saw one macroscopically, in a test tube, or under the microscope.
 

Physics

Jay R. Feierman

by with 2 Comments AdaptationsEcologyHuman BrainModel OrganismsVariations

In his posts that I have linked below, Jay R. Feierman takes us from random mutations on which natural selection acts to natural selection for phenotypes and changes in the brain that lead to increased reproductive success. According to him, the change in the brain can be called an adaptation.
In my model, ecological variation and nutrient-dependent pheromone-controlled epigenetically-effected ecological, social, neurogenic, and socio-cognitive niche construction enable organismal complexity of the human brain. Ecological variation links the epigenetic landscape to the physical landscape of DNA in the organized genome of species from microbes to man. That fact is exemplified in model many organisms, but it is a fact that Feierman seems unable to understand.
Jay R. Feierman: I am absolutely certain that if you showed this statement to any professor of biology or genetics in any accredited university anywhere in the world that 100% of them would say that “Random mutations are the substrate upon which directional natural selection acts” is a correct and true statement. 
Foote et al (2013)“Ecological variation is the raw material by which natural selection can drive evolutionary divergence [1–4].”
James V. Kohl:  “Evolution by natural selection cannot be the outcome if something is not first selected. Selection is always for nutrients. It is as simple as that.”
Jay R. Feierman: Variation is not nutrient availability and the something that is doing the selecting is not the individual organism. A feature of an educated person is to realize what they do not know. Sadly, you don’t know that you have an incorrect understanding Darwinian biological evolution.
Jay R. Feierman: “…natural selection “selects” for phenotypes, not for genotypes.”
Dobzhansky (1972): “Reproductive isolation evidently can arise with little or no morphological differentiation.”
Dobzhansky (1964): the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists!
James V. Kohl:  Adaptations and increased brain size in mammals
Jay R. Feierman: “…When the brain changes as a result of an interaction with the environment, and if the change in the brain leads to increased survival and reproductive success, that change can be called an adaptation. 
Addendum 2/15/14
After everything he has said to denigrate me and everything he has done to prevent discussion of my series of published works on ecological variation and adaptations via the epigenetic effects of olfactory/pheromonal input, and only after it has become perfectly clear that there is no such thing as mutation-initiated natural selection, Feierman includes epigenetically turned on genes in the context of selection. Now Feierman implies that epigenetically turned on genes AND mutations can cause natural selection.
Jay R. Feierman: Natural selection is the equivalent of a directional vector force. A directional vector force can’t do anything without something, such as mutations or epigenetically turned on genes, on which to do it!
I reiterate: Selection is always for nutrients. It is as simple as that! Nutrients epigenetically effect the de novo creation of genes and are metabolized to species-specific pheromones that epigenetically control the de novo creation of genes that is responsible for increasing organismal complexity and species diversity via ecological, social, neurogenic, and socio-cognitive niche construction.
Jay R. Feierman: One can’t separate natural selection and mutations…
Does anyone else think that different races and their morphological and behavioral traits are naturally selected in the context of mutation-driven evolution and diseases associated with reproductive fitness? In every other species from microbes to man, differences in morphological and behavioral traits associated with reproductive fitness are examples of ecological adaptations.  It seems racist, sexist, and homophobic to imply that ecological adaptations in other species are examples of mutation-driven evolution in humans.  See for example: New forms of racism arise in science research
Excerpt: “Published research has shown that blacks are more likely than whites to have a blood type that causes sickle cell disease and can protect against malaria, and are more likely to have a certain gene called APOL1, which protects against a parasite that causes sleeping sickness.”
My comment: If sickle cell disease is due to an RNA-mediated event and nutrient-dependent amino acid substitution that results in one of 1182 hemoglobin variants, it is an ecological adaptation. Anyone who claims that sickle cell disease is due to a mutation should either support that claim with experimental evidence  of what causes the mutation and how it is naturally selected in some circumstances that appear to vary with skin pigmentation, or be prepared to defend themselves from claims that they are racists.