If it lives along time this turtle might have novel longevity genetics.”The green-haired turtle, an Australian species that split from other living species about 40 million years ago, can breathe through its genitals”

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Treon Verdery

Oct 4, 2022, 3:38:49 AMOct 4
does radiolabelled 10HDA concentrate anywhere at the body with positron emission tomography? Mice primates or volunteer humans could provide data, it is possible there is some favored physiological system that heightens longevity, notably radiolabelled 10DHA at daf mutant c elegans could provide data on why they live 46% longer on 10HDA, compared with some other types. Also, 10DHA might cause 96 well plate processable fish, as well as planaria to live longer, I think planaria only have a few hundred cytes, so a 10HDA radiolabelled planaria activity map might be rapidly makeable, and extrapolatable to mice (and humans), producing longevity drugs that are 10HDA variants (also molecular variants) with tissue localization

connecting beauty peptides and collagen elastin production peptides, as well as other tissue phenotype youtfulness of shape, form, and feel to the genetic things that activate during shear stress could as both beauty preserving and tissue building gene response as well as be a tissue and organ youthful morphology creating and preserving response, these genes that turn on during physical shear stress then cause a reduction in gravity or bendiness or bounciness effects, as well as exposure, (from stretching a stretched thing further) or reducing phenotypic change from motional cumulative exposure; also it might be possible to tune the genetic response to shear stress where causing shear stress, of nongravitational or nonswaying form, based on very mild, directed, acoustics, causes the beneficial build up of and repair of tissues at depth; this could be a beauty technology, “an become particularly relevant under conditions in which eNOS is strongly recruited to membranes such as after sustained laminar shear stress” and “in endothelial cells is endothelial NO synthase (eNOS)” Also, the people who make artificial organs might benefit from a 3D acoustic shear stress shape causing gene activation of their choice of genes at a structure when the shear stress gene is attached to something like making a gene activator (gene switch) chemical. An amount of shear stress utilized at one experiment was, “laminar shear stress (LS, 15 dynes/cm2) in a cone-plate system for 18 h.” Wikipedia says a dyne is “centimetre–gram–second” so that is about a 15 gram effect on a CC similar to a 3.9 gram force on 3.9 gram of tissue; 2019 D cup breasts weigh about 760 grams each, other larger breasts have a 1.2 Kg mass; At humans with just two sex chromosomes, both of the sex chromosomes being X chromosomes, born with ovaries, genetic SNPs, beneficial gene copy number variations, or upregulating body responses to laminar shear stress, as well as other dyne directional forces, technologically support causing lasting youthful body phenotype. notably at breasts, faces, (under eye areas, cheeks, neck, other areas), and any other body locations where youthful phenotype is noted as being more beautiful. Notably although breasts were listed as cup sizes during 2019 AD, genetic optimization, or pre-optimization, and beauty drug suggesting software that measures a response to beauty could likely find that a combination of shape, mass, placement, nipple form, smoothness, feel upon touch, as well as other attributes could find a 99.9999th percentile breast form and shape, with a physiologically meaningful and mathematically described state space and descriptive language, noting a pair of breasts that has completely different descriptive language, like 770-790 to 1600 CC of breast tissue at 32” (81.28 cm) measured 1 mm just beneath breast chest’ circumference, of the software optimized shape, nipple form, smoothness, feel on touch, as well as placement region at chest; The software would also produce CAD files that empasize not only the breasts but the entire adipose underlayment contours of the chest; Wikipedia says that estrogen effects the size of the breasts, and progesterone effects breast shape, it is likely the genetics of sex hormone receptors also effect breast size and shape, form, and other attributes as areas for the software that decribes genetics of 99.9999th percentile breast beauty; The software technology that amplifies beauty, as previously described, when software finds images and 3d representations of beauty, like the beauty of the female form, at this technology, the beauty of breasts, that have one per million highest fMRI, positron emission tomography, subjective viewer rating, and possibly a measure like largest number of words spontaneously and voluntarily witten about, at an image of an unknown person or computer constructed image, the beautiful breasts’ beauty, using the largest number of complimentary words, Then the beauty amplification software uses the known effects of genetics, sex hormone concentrations, sex hormone receptors, to make images, likely 3D moving images, of new beauty forms, like breasts that are perhaps slightly rounder (more progesterone), have a particularly high beautifulness quantification at simultaneous side view, front view, and even view from facing the back of the person’s head, where the computer bases the new, software quantified heightened beauty response on shape, form, bounce, softness, longest sustainment of youthful phenotype, on adjustments to genes with new nucleotide sequences, producing new proteins with new amino acids, as well as new or existing SNPs or also optimized numbers of beneficial gene copy variations; noting that human tissues, among them tissues that cause a beauty response and are perceived as beautiful, are, as far as I have heard about, differentiated tissue, modifiers of tissue differentiation that effect sex hormone receptors, location, and amount, are also technological dimesional (engineering/math/actual applied technology adjustable attributes) areas, these adjustable attributes (dimensions) are things the software utilizes (make the breasts a little rounder, placed nearer each other while being large enough to be visible curves at the side of the body from a dorsal view, symmetrical at multiple simultaneous 3d views, make the nipples a slightly wider, puffier form, nipples erect when erotically aroused rather than other stimuli, pale pink nipples), to make graphics, likely 3d and moving graphics, that software models, and projects, and humans verify, go from the 1 per million most beautiful breast forms, shapes, and phenotypes to 1 per 10 billion or higher perceptual beauty of breast form, shape, as well as phenotype based on specifiable beauty genetics; This genetic beauty heightening technology: sample 1 per million or higher of beauty at components and groupings of the human form, software locates known, modifiable, engineerable adjustables like genes, differentiation genetics, genetically directable epigenetics (put an extra histonation causing protein, which previously would have been epigenetic, at a new gene, directing what would have been epigenetic with new genetics), software generates 3D motional samples that the software, including AI, like deep AI, projects as being more beautiful than 1 per 10 billion presoftware persons; the human beauty response is measured and verified; this is utilizable at any measure of visual, tactile, and motional beauty: faces, arms, legs, hands, the abdomen, the head, voice characteristics, the dorsal view of a human body, the side view of the human body, some body language, the contours of the body at its entirety, body area proportions, as well as resting form of the body, it is possible to have a face at rest host a beautiful smile as well as a beutiful expression without particular cognitive/emotional/occurence-based/other source causes; notably persons utilizing software to heighten beauty have the beneficial opportunity to have the software estimate the effect of the heightened beauty on other people, beauty that causes a 99.99th percentile measure of any first conversation, without regard to who initiates the conversation, being enjoyable to the beautiful person, would actually make the beautiful person’s life better, and the possible heightened attracting of other’s interaction experienced as being beneficial. Similarly, beauty that causes others to utilize benevolent, congnitively rich, empathetic, kind, opportunity enhancing words, do benevolent, cognitively rich, empathetic, kind, opportunity enhancing things, as well as have benevolent, pleasant, beneficial action-capable body language, as well as benevolence, cognitive richness, empathetic, kind, opportunity enhancing mental state at the person perceiving the beauty, possibly measured with fMRI and positron emission tomography, or some newer, higher resolution, more effective kind of scanning, such as brain scanning, is measured and verified, and is quantified as having predictive validity at predicting actual beautiful person interactions; Software created genetics of the most beautiful person per 10 billion persons constructed with the beneficial effect of beauty on the beautiful as a engineering quantified specified parameter, gives all people, that is humans, that is people, that is persons, that is homo sapiens the opportunity to be be as beautiful as the most beautiful out of 10 billion is ethically beneficial from making being beautiful 99.99th percentile beneficial (such as beauty engineered persons experience a 99.99th percentile liking of first conversation) as a way of existing, and also generating benefit at the beauty perceivers, who might also (are likely to also be) be beauty enhanced, notably, as a software directed specification of genetics this 1 per 10 billion genetics of beauty, published online, at the internet, or any shared data source, is available to any person that enhances, specifies, or optimizes the genetics of their children and is also available to persons that already exist using gene therapy; I favor genetic modification, pharmacological/laser/other technology can also be utilized; Notably, when people think, “why should I make my children more beautiful than the most beautiful person out of 10 billion?” the software quantized, and people’s actual behavior quantified and verified reply, “people will be nice to them, and their lives will be better and full of opportunity and well being, surrounded with that benevolence they are even likelier to be benevolent to others, and other living beings, as well”

Notably, the beauty finding, specifying, and technology actualizing (doing) genetics and pharmacology directing software will improve, and that would make the most beautiful out of 10 billion persons software guided genetics be upgraded at the entire population with new birth cohorts with the most beautiful out of 20 billion persons, rapidly occuring, each generation (birth cohort) then becomes even more beautiful than the previous birth cohort.

It is even possible that with social companion robots, a person at the 10 billionth percentile of beauty could have their social companion robot be equally beautiful, at a different way, such that a human beauty perceiving person seeing them experiences a most beautiful per 20 billion persons fMRI/positron emission tomography, or other newer more measurement-effective, predictive, higher resolution and deep brain scan technology;

Longevity technology:

a neuron specific ethynyl fluororapamycin library: noting that ethynylfluororapamycin, with or without a linkage to a membrane transport chemical, peptide, or protein, could be half a million, to a million, or with a transport peptide, 2-10 million times more powerful than rapamycin at a mcg or nanograms/dose; could really minute amounts of ethynyl fluororapamycin linked to a known effective neutrotransmitter drug be new, brain area and function specific longevity drugs; say you have a few picograms of the AMPA neuron receptor drug phenylpiracetam, and you link it to ethynylfluororapamycin, do mice that get this have 60% greater longevity at that type of neuron perhaps remaining smarter longer? Similarly, could a few picograms of a dopamine active stimulant (even actual L-dopa which does not pass the blood brain barrier, but might at picograms), or a GABA drug like a few picograms, a dose that would be absent mental effect, of a benzodiazepene, or serotonin, like pimavanserin, cause these neurons to live 60% longer and have younger phenotype;

There is a protein in milk that could cause longevity heightening autophagy as well as cause stem cells to function better, it could also be a senolytic drug, SNPs (or gene copy number variations) at how it occurs at various people could also be a neurodevelopment, intelligence g (like IQ) gene, “milk fat globule-epidermal growth factor (EGF) 8 (Mfge8)”, lactadherin, “a known phagocytosis factor, is highly enriched in quiescent RGLs in the dentate gyrus”https://www.sciencedirect.com/science/article/pii/S1934590918303904 it also does things (ups?) phagocytosis which I think goes with autophagy, and the more autophagy from things like caloric restriction (possibly senolytics) the longer the lifespan, so this could be a milk protein that, at enteric capsules, causes greater stem cell tissue regeneration simultaneously with greater longevity producing autophagy, mfge8 also does a thing that sounds like a senolytic, “Mfge8 is traditionally known to play a critical role in phagocytosis (Raymond et al., 2009). Phagocytes secrete Mfge8, which binds to “eat me” signals secreted by dying cells, such as exposed phosphatidylserine. Mfge8 then binds to integrin receptors αvβ3 or αvβ5 expressed on phagocytes to promote engulfment of apoptotic cells.” different SNPs (or gene copy number variations) of mfge8 at humans could have an effect on brain area volumes and morphology, “Mfge8 is required to maintain a proper level of adult hippocampal neurogenesis.” So it is possible that the genetics of mfge8 effect g, intelligence (like IQ)

also it is possible they could breed or engineer cows to make a much larger amount of the mfge8 protein as a fraction of milk protein, it also does mTOR things, [an eentsier (less than better) amount of]“Mfge8 elevates mTOR1 signaling in RGLs, inhibition of which by rapamycin returns RGLs to quiescence. Together, our study identifies a neural-stem-cell-enriched niche factor that maintains quiescence and prevents developmental exhaustion of neural stem cells to sustain continuous neurogenesis in the adult mammalian brain.”

Longevity technology: making more stem cells, everywhere at the body: look it up, if it is possible think of new ones

A rodents and primates (like humans) are there rodents or primates that have like 2-7 times more actual stem cells just existing at the body, poised to differentiate and repair and rescue, regardless of that actual rodent or primate’s other longevity genetics? If mice make more stem cells as a fraction of tissue than beavers, then even though beavers already live 14 times-ish longer than mice, beavers with mouse higher fraction of all tissue stem cell genetics could live even longer and the beavers do more effective autorepair; similarly, are there nonhuman primates with a greater fraction of stem cells than humans, or an opportunity, are there humans that have twice as many stem cells as a fraction of body tissue as other humans? Noting numerous human attributes during 2019 could be double each other (IQ 200, double height, Jeanne calment longevity) it is possible there are existing human SNPs (or beneficial gene copy number variations) to double stem cell mass fraction at the human body and these could be autorepair, wellness, healthspan and longevity genes, these could also be longevity, wellness, healthspan, and autorepair predictors

So I read fetuses completely remove like 90% of their epigenetic things like methylation and acetylation, being technologically abrupt, is it possible for a post puberty mammal (like a human) to use the same genetic de-epigeneticization program to make 90% of an after puberty mammal’s epigentics be erased, and have the mammal live, and either do well (above average), or have new epigenetics custom programmed at the mammal? One thing about this is that removing 90% of the epigenetics, whicvh the fetus does automatically, has some sort of do beneficial things with stem cells effect, so if stem cells benefit youthfulness, youthful phenotype, and cause nonyouthful phenotypes to repair and continue existing longer, then a post-pubertal 90% epigenetics removal could be a beneficial longevity technology; also there could be a tissue localization beneficial effect, perhaps removing 90% of the epigenetics of the heart (as well as vasculature and epithelial cyctes) heightens stem cells and thus auomatic repair, whereas removing epigenetics at neurons could actually modify mind and personality, of unknown actual effect;

Are there epigenetics that cause more stem cells to be produced? Are these multigenerational, gestational, or also makeable with new genes that then make the epigenetic things so genetics can direct an epigenetic effect;

a longevity gene effect: “Fibroblast growth factor-21 (FGF21), produced mainly in hepatocytes and adipocytes, promotes leanness, insulin sensitivity, and vascular health while down-regulating hepatic IGF-I production. Transgenic mice overexpressing FGF21 enjoy a marked increase in median and maximal longevity comparable to that evoked by calorie restriction”, also, “There is reason to suspect that phycocyanorubin, a bilirubin homolog that is a metabolite of the major phycobilin in spirulina, may share bilirubin's agonist activity for AhR, and perhaps likewise promote FGF21 induction.”, it is possible that things like enthynylization and halogenation of bilirubin or plant based phycocyanorubin could be numerous orders of magnitude more active at causing longevity beneficial FGF21 activity

I read there are peptides that cause nuclear membrane transport, a new group of drugs, where acetylization and methylization few AMU molecules (like TMG or if there is a acetylization glycine), linked to nuclear membrane transport peoptides could cause thousands or even hundreds of thousands more molecules to accumulate at the nucleus near the actual DNA with the epigenetic things on it; if 1500mg of TMG was a 2000AD dose, then a peptide acetylizer or methylizer could be a 1.5mg dose, that could be combined with a cytotype specific or tissue specific localizer moeity like a membrane transport chemical to put the preferred epigenetic effect supplying chemical at the preferred cytotype and possibly make the dose/mcg or even dose/nanogram a couple orders of magnitude higher, like active transport 1000 times more active than passive transport, so active transport of nuclear membrane peptide at 900 times, as well as the actual epigenetic acetylization chemical supplying part could be 900,000 times more active per amount of dose. There could be enzymatically degradeable linkers between the active transport moiety and the epigenetic few-AMU chemical as well as enzymatically degradeable linkers between the nuclear membrane transport protein and the few AMU epigenetic modifying/group (like acetylation) supplying drug; there is also the possibility of making a gene that makes the epigenetic modifier a 100k times effect drug: the nuclear transport peptide sequence and then the “triacetylizing glycine” kind of thing, then the active transport chemical, could be made as the product of a new gene, and the new gene placed at organisms to direct the organisms previously epigenetic version to be a particular thing, genetically, at plants this could have various benefits as you could omit putting things (plant pharmaceuticals) on the plants; these active transport, nuclear membrane peptide, epigenetic acetylation (velocitize activity) drugs could modify the epigenetics of plants, noting yeast without histones reproduce like 4 or ten or something times more rapidly, or it is possible they just physically grow four or ten times more rapidly, so engineered epigenetics at plants could velocitize growth, favor some phenotypic things, like making more yummy parts, or cause some kind of preferred response to multigenerational repeat of soil nutrients or treatments (more optimal NPK epigenetics, or even, noting mammals, if richly fed, still able to physiologically respond well when the progeny, as well as progeny’s progeny are richly fed)

I think I previously described finding genetics of people that are variously much less or notably more responsive to epigenetics, with there being value to making a enhanced optimized genome that also has the genetics of being less epigenetically modifiable, so the benefits of enhanced or also genetically optimized genomes are more effective; wikipedia mentions a few things that might have SNPs (or possibly beneficial copy number variations) (I am reminded of COMT although this is very different) where variations could imaginably make a mammal, like a human, two or three times more epigenetically shiftable, like, “DNMT3A and DNMT3B have both been linked to a role in the establishment of DNA methylation pattern in the early development of the stem cell, whereas DNMT1 is required to methylate a newly synthesized strand of DNA after the cell has undergone replication in order to sustain the epigenetic regulatory state” So if there are (imaginably) 2 to 3 times varying activities of things like DNMT3A and DNMT3B and DNMT1 at humans from different human SNPs (or normal yet differing gene copy number variations) then it is possible to make people more resistant to environmental or preconception, pregamete nonbeneficialness while finding any beneficial things that would have been epigenetic, making actual gene produced chemical prompters of that effect, causing the beneficial effects to be made part of humans

“Histone deacetylases (HDACs) such as SIR2 and RPD3 are known to be involved in the extension of lifespan in yeast and Caenorhabditis elegans. An inhibitor of HDACs, phenylbutyrate, also can significantly increase the lifespan of Drosophila, without diminution of locomotor vigor, resistance to stress, or reproductive ability. Treatment for a limited period, either early or late in adult life, is also effective”

To find a longevity drug screening a library of things like HDI and HDACs, histone acetyltransferase (HAT), and other chromatin accessibility chemicals (things like phosphorylators as well as others) that might do something, could cause finding something beneficial to longevity, wellness, and healthspan to be found, a kind of version of that being: screen 4000 FDA drugs, find 5 (that I have heard of so far) that cause greater longevity; screening a library has value, there are things called HDACi (histone deacetylase inhibitors), and likely HDIs (HDAC inhibitors) and among about 5-7 epigenetics things (kind of like tags) I saw on wikipedia (like phosphorylation), these longevity, wellness, and healthspan heigtening things that heighten or lessen each chromatin accessibility and activityness epigenetic modifier; that suggests that screening a library of all HDAC as well as HDI like things, at all the types of on-the-DNA (like on histone) epigenetic chromatin accessibility modulators to find things that effect longevity wellness and healthspan; I perceive that is about 40-100 different chromatin accessibility modulator chemicals to screen, perhaps more, so 8 mice per group, 100 chemicals, 800 mice screens a variety of different comparatively global (rather than gene specific) epigenetic changes at a mammal to find new longevity drugs. Also, this could be upped to 2400 mice, and the mice be tested at all chromatin availability drugs (like HDI, HDAC, phosphorylation, methylation), at each of different thirds of living; the mice could also be cognitively characterized and measured as to healthspan and wellness; There could be value in screening all the known HDAC, HDI, and other chromatin accessibility chemicals at fish, posssibly fish that live at and are characterized on 96 well plates; screening a library of 20,000 human genes, making a version of each gene with about 5-9 different chromatin accessibility modifiers (HDACinhibitor, methylation, phophorylation, numerous others) then characterizing the wellness and longevity of that human tissue culture sample area (plate well) could utilize an integrated circuit technology billion (or 100 million) well chip, as well as a published million channel microfluidic chip, or possibly also a published 10 million cytes/second flow cytometer: do human tissue culture at the 100 million well plate, then use million channel microfluidics to do parallel CRISPR/cas9 activation of each of 20,000 separate human genes, that activation loosens the DNA from the histone for the placement of 5-9 different variations on a chromatin accessibility modulator at each gene of 20,000 at a human genome; I read about a high precision, 20,000 gene simultaneous activity variety of CRISPR during 2019, so it seems like parallel CRISPR/cas9 at microfluidics along with a multiwell integrated circuit like tissue culture plate could be functional; The human tissue culture could be genetically premodified to make more GFP (green fluorescent protein) the longer it lives, and more blue fluorescent protein the more it is morphologically or metabolically above 90th percentile of well function, then a camera and software views the 100 million well tissue culture plate (with 5000 parallel versions of 20,000 genes activated at 20,000 separate wells at one gene activated at each, at 5-9 different versions of a chromatin accessibility modulator) and makes a database of doing what thing (like the 5-9 chromatin accessibility modulators), to which gene, causes greater longevity, tissue culture morphology benefit, or metabolic benefit

I just read that the 10HDA at royal jelly, royal jelly being published as making mice live 25(27%) longer and c elegans live 18-46% longer is an HDI (HDAC inhibitor), https://www.academia.edu/7229126/Histone_deacetylase_inhibitor_activity_in_royal_jelly_might_facilitate_caste_switching_in_bees that brings up the idea that there could be longevizing HDI and HDAC as well as HDACinhibitors at other species, even nonmammalian species, even plants and fungi, where if it is modifying the accessibility of chromatin (rapidifying or gradualizing translation and gene expression) at some genetic area, at one of the areas that humans have, along, as homologous genetics, with nonmammals, even plants, that that could be a longevity HDI or even HDAC or HDACi; this nonmammal mammal HDI effect is noted, based on the way 10HDA at royal jelly is an HDI (HDAC inhibitor) apparently doing HDI things when it causes greater longevity; so perhaps there is already a database that exists, or one that could be made, where every gene, at every organism, at a plurality of organisms, at the database is linked to an HDI (HDAC inhibitor) or HDAC, or other chromatin accessibility modulator, noted to be at that varied, nonmammalian, mammalian, or even human or plants species, then technologists and engineers and drug makers could find any HDAC or HDI or other chromatin accessibility modulator, at any homologous chromosomes of any species, and then see if they also had similar beneficial purposeful effects, like longevity drug effects, at mammals like humans; so if there is an HDI or HDAC chemical (like possibly a few AMU chemical, a peptide, or a protein) for mTOR at linden trees they could find out if that HDI or HDAC or HAT chemical has a longevizing effect at human tissue culture cytes, they could also make a library of new chemical variants and then screen them using integrated circuit microfluidic technology where 1 trillion wells fit on a 300 mm wafer, and a billion characterized wells is just a prepackaged convenient to utilize part of the wafer; similarly, if any organisms at all have beneficial epigenetics, possibly even beneficial multigenerational epigenetics, then the HDAC, HMI, or 7-9ish other chromatin accessibility modulators (like phosphorylation) that cause those beneficial epigenetics could be quantified as to any beneficial effect at the source organisms, even if it is a plant or a bird, or a whale, then quantified (as well as qualified) at a model organism and then, beneficially, at humans; say plants phosphorylate (or just HDI:velocitize expression) a trehalose producing area of the genome, causing more trehalose, when, epigenetically, the plants are at more nutrition filled environment than their parent plants (generational epigenetics) possibly a theorist would say “the plant may sense, its seeds have travelled far to a highly nutritious area, the plant’s making more trehalose makes it more likely to prosper during and after winter, noting that at the new location, the effects of winter are unknown, and that this is an advantageous metabolic liveliness noting the unusually high amount of nutrients available”, so then the technologist, genetic engineer or also drug maker says, let’s give this chemical HDI (or HAT or phosporylator) as a drug to mammals and find out if, like the plants, where 60% of their epigenetic HDI/HDAC/phosphorylation/other chromatin modulator activity is on genes like those of mammals, among those mammals humans, the amount of trehalose produced at a mammal, like a human, goes up; So the big chromatin accessibility modulation database creates new modifications (HDI, HAT, HDAC, phosphorylation), amount of modulation using generic modulators, (note, I perceive a number of generic chromatin modulators have been published, one is, “we observed re-expression of the Fas gene (Fig 1A). Furthermore, the regained expression was similar to that obtained with 5-aza-20-deoxycytidine (5-Aza) treatment, a well-characterized inhibitor of DNA methylation)”,

or possibly modified particularly effective chemicals, as well as algorithmic direction that then creates greater physiological well being, longevity, wellness, and healthspan at humans, persons, people, homo sapiens, as well as creates new biological technology opportunities; so, is there a way to mass screen and make a database of utilizable functional chromatin accessibility modulators; one possibility is to generate a kind of generic HDI, HDAC, HAT, phosphorylator, other chromatin accessibility modulators, group of forms, that can be at least 20-90% active at any genomic sequence it happens to be on/at; Then you use something like a 1 billion to 1 trillion integrated circuit technology array of wells, each with 1) human tissue culture cytes or 2) yeast, or 3) tissue culture of the organism on earth that is most similar to all other organisms, as well as microfluidics, and parallel screen 1 billion or 1 trillion library variations on the chromatin accessibility modulator chemicals at each of numerous 20 thousands, hundreds of thousands, and occasionally, possibly, millions of genes’ chromatin modulating things like HDI, HDAC, HAT, phosphorylation, others, Notably, as an engineering, software, human well being, longevity, wellness, healthspan, and genetic enhancement and optimization technology, any of the chromatin modulating things, which previously might have been epigenetic, are actually directable with new created physical genes that produce the chemical that does that specific, valued, beneficial chomatin modulation (the new or also enhanced gene makes an HDI, HAT, HDAC, phosphorylation or other chromatin accessibility modulation chemical that goes to the optimal, actual, genome location to make what was previously a beneficial epigenetic thing be genetic); at yeast and human tissue culture, the longevity and metabolic similarity to a thriving (99.9999th percentile or higher wellness, long healthspan) organism’s effects of having HDI, HDAC, phosphorylation, also other chromatin accessibility modulators, are quantifiable, and integrated circuit technology and microfluidics technology causes column and row function to specify the variation that is being quantified, that the software and database records and utilizes, I read that about 10,000 human tissue cytes per well are published, so similarly 10,000 yeast cytes, then place those at 100 million, 1 billion or 1 trillion wells;

Finding an area of longevity, wellness, and healthspan acetylation, methylation, phosphorylation as well as other chomatin accessibility heightening and promoting chromatin accessibility relations, that is algorithmically describable, or even AI deep learning modellable and duplicable that when applied to to other organisms, like humans, then heightens their longevity, wellness, and healthspan: think of a map, or model, of how much things wiggle, and around what values (kind of like: math:hysteresis network), as well as how often; kind of cybernetic, as an actual science word; Now make those models, as quantitatively measured, at a variety of organisms, then find the cybernetic, algorithmic software, or deep learning AI versions that describe variously: most simultaneously shared wiggle types (and cybernetic math spaces) amongst the longest lived (whales and naked mole rats both, imaginatively, deacetylate just 3%, whereas, imaginably, mice deacetylate 30%, humans and long lived tortoises imaginably renew the phosphorylation of their genomes every 72 hours, other primates and average tortoises semiannually) as well as other cybernetic relations; then come up with a software predictor of what would happen at an organism if all the different wiggles (cybernetic areas) were those of the organisms with greatest lifespan and high effectiveness combined among species(note whales might phosphorylate semiannually, providing opportunity for the software suggested enhancement); then at a model actual organism (mice, fish, yeast, daphnia, other organisms) find out if it is possible to guide the cybernetic wiggles to be like the software’s most optimal version, then quantify if greater longevity, wellness, and healthspan occur at the (HDAC inhibitor, HAT, methylated, phosphorylated, other chromatin accessibility modulating things) model organism; notably this model organism with simultaneously optimized cybernetic things could possibly be tested with 9 times a day chromatin modulating cheimcals (HMI, HDAC, phosphorylation, others) drugging as compared with genetic modification, and the million lane microfluidics as well as 100 million, 1 billion or 1 trillion well plates made with integrated circuit technology could sequence and time the pharmaceutical actions at a plurality of nonsentient organisms, like daphnia or tissue cultures

What two organisms are the most similar that have the greatest longevity difference? One yucky possibility, a termite, compared with a termite queen (a year or two compared with half a century, or greater), Is it epigenetic with termites’ longevity variation? Among mammals, is there any shared epigenetic chromatin accessibility modulation or difference? Beavers live 35 years, mice about 2.5, if the epigenetics of a beaver’s genome is copied to a mouse does the mouse live longer? at the 20:1 queen bee ratio, or the 50:1 or 2 termite ratio longevity difference from epigenetics That could be a most rapid path, fewest variable sample to produce greater longevity scientific bases and also epigenetic (chromatin accessibility modulation) longevity drugs, which are then made as genes to be genetic rahter than epigenetic, and produce a variety of longevity technologies, possibly with chemicals and genetics that are simultaneously at the largest increase, greatest proportional longevity variation organism and human physiologies shared physiology, genetics, and chromatin modulation effectors (HMI, HDAC, phosphorylation, others), so basically, if the epigenetics of the beaver copied onto a mouse double or greater mouse lifespan, or the epigenetics of a termite queen copied onto a different termite cause 50 times greater longevity, then at a bunch of these considered together with software, the epigenetics of greater human longevity could be found; Marmosets are primates, so if multicenturylifespanwhale1::whale2, beaver::mouse, and even queenbee::bee all suggest separate longevity optimizations at completely different genes, all of which are genes people have, then the computed version of that could be installed on a marmoset to see if it doubles primate lifespan, and, among human volunteers, organ and tissue specific epigenetic modification, as well as bodywide epigenetic modification could be qauntified as to effect;

Noting that 10HDA, like that at royal jelly, a longevizing chemical, is published as an actual HDACI (histone deacetylase inhibitor) it is possible that a version of 10HDA that reaches the nucleus more effectively than 10 HDA would provide greater longevity effect per amount of dose, I read there are peptides that cause preferential transport at the nuclear membrane, so linking a nuclear membrane transport peptide to 10HDA could cause a 10HDA longevity effect at micrograms of dose; also putting an active external cytomembrane transport moeity on the nuclear peptide with the 10HDA molecule could cause active transport (possibly 1000 times more active) causing the longevizing dosage of the nuclear membrane transport, 10HDA, active transport moeity molecule to be nanograms to cytoaccumulate a longevity heightening dose; a nanogram longevity heightening dose could make a dept injection that lasts hundreds of years per injection possible; the different parts of the molecule could be linked with enzymatically degradeable linkers so the 10HDA is fully functional at the nucleus as a HDACI

An siRNA that could be a longevizing molecule, possibly also at mammals, like humans, “small interfering RNA(siRNA)-induced knockdown of

Dnmt3 levels in newly emerged larvae results in the development of queen bees with fully developed ovaries (Kucharski et al

, 2008). Thus, injection of honey-bee larvae with Dnmt3siRNA can replace royal jelly consumption” https://www.academia.edu/7229126/Histone_deacetylase_inhibitor_activity_in_royal_jelly_might_facilitate_caste_switching_in_bees They could find out if this siRNA that causes queen bee physiology with its greater longevity, causes longevity at mammals among those mammals humans; the paper says that 10HDA modifies (similar to removes, different than removes though) a genomic methylation, causing a gene to become active, that then produces the longer lived queen bee phenotype, the paper also says, “These data indicate that 10HDA inhibits a pathway involved in transcription repression that runs parallel to the DNA methylation pathway, and does not function as a DNA demethylating agent per se”; From what I read at this paper, the epigentic modifications from 10HDA (that cause greater longevity) could have a cofactor at the body which causes the combination of 10HDA with the cofactor to have a gene expression amplifying effect, That cofactor could be another administerable longevity drug as well, creating the optimal amount of both cofactor and 10HDA could create a longevity drug with greater activity than the 25 (27%) mouse longevity increase as well as the 18-46% c elegans longevity increase, from just 10HDA, “10HDA alone had no effect, but markedly potentiated the ability of 5-Aza to activate GFP (supplementary FigS3D online). In the same cell line, both royal jelly and 10HDA can reactivate epigenetically silenced p21 expression (supplementary Fig S3 A,B online). To test directly whether 10HDA can block DNA methylation, we performed a pyrosequencing assay for LINE-1 (long interspersed nuclear element) repeats, as a measure of global hypomethylation in these cells. Although 5-Aza treatment reduces DNA methylation by 50% in this assay, 10HDA was not able to reduce the levels of LINE-1 DNA methylation alone, or to potentiate the effect of 5-Aza in sequential combination treatment.”; also, “10HDA does not affect either of these signalling pathways (supplementaryFig S4B online), suggesting that it directly targets an epigenetic effector molecule.”

notably, the paper I read suggested that 10DHA has a cofactor that causes it to (have an effect like but different than) demethylating a location, and cause the longevized phenotype; it is possible this cofactor could be a chemical at queen bees’physiology that could be found and then combined with 10HDA or also royal jelly to create greater longevization; it is also possible this cofactor could have a variety of molecular form variants with different tissue distribution (hydrophilic, lipophilic, nucleus-tranport enhanced, active transport moeity versions) so that a technological enhancement to the longevity drug 10HDA would be putting it with its cofactor, and making both 10HDA and the cofactor reach as many mammalian, like human, tissues and cytotypes as possible;

10HDA as an HDACinhibitor makes a bunch of different HDACs much less active; the human dose equivalent of royal jelly at a 70 Kg human is possibly possible to calculate, “we performed individual inhibitor assays using recombinant HDAC1,3, 8, 10 and 11 (supplementary Fig S6 online). 10HDA inhibits all of these recombinant HDACs with and half-maximal inhibitory concentration (IC50), in the range of 5–8mM (I perceive I read royal jelly is 100 to 300 mM of 10HDA); this brings up the technology that if HDAC inhibition is often beneficial to the organism, most of the time, is there an HDAC inhibitor that although perhaps less specific, is a longevity wellness, healthspan drug that is a chemically sourced manufactured pharmaceutical, a new drug, or also possibly an anticancer drug that aready exists? Phenylbutrate smells yucky, but what about phenylpropynate (phenylproprionate?), Trichostatin A is an HDACinhibitor, but it is administered via injection, perhaps there is an orally absorbable form, or it could be placed at enteric capsules or liposomes;

To create a new chromatin accessibility modulating epigenetic-like longevity drug,like an HDACi, they could characterize the most effective 16 longevity chemicals as to whether they had epigenetic or epigenetic-like chromatin accessibility modulating (HDAC inhibitor, other mechanisms) effects, find the different as well as cofunctional areas they perhaps shared at things like, or possibly other than, demethylating (or some other chromatin accessibility modulation), and then create a new, optimal chromatin accessibility modulation drug that causes greater longevity increase than any individual particular chromatin accessibility modulation epigenetic-like effect longevity drug, and perhaps a greater longevity effect than all of the longevity drugs quantified as having chromatin accessibility modulation effect, epigenetic-like longevity drugs combined; This could be an integrated circuit technology microfluidics mass screening of a library of drug variants utilizing technology; a different technology, flow cytometry, can screen 10 million yeast per second, so testing 100 million HDAC inhibitor or other chromatin accessibility modulating longevity molecules on 10 billion yeast could be accomplished in a few hours. Also, it is possible to view and arrange the preferred version of chromatin acessibility modulation, at HDAC inhibitors, that cause gene activation, noting some HDACi are only active at parts of genomes of some species; royal jelly has published longevity effects in mice, notably though, “There are four annotated histone deacetylases encoded in the honey-bee (A. mellifera) genome, with orthologues in both class I and class II. 10HDA inhibits class I and class II HDACs, as determined by using a HDAC colorimetric assay, specific in vitro assays using a panel of recombinant HDACs, and western blot analysis with pan-acetyl lysine antibodies. Most HDACis is function by chelating a crucial zinc atom in the active site of the enzyme (Finnin

et al , 1999; Bertrand, 2010). Carboxylic acids are a subset of these, and 10HDA can be classed within this group,which includes valproic acid and butyric acid (Bertrand, 2010). Thus, similarly to the other members of this group, 10HDA has proven to be a broad-spectrum class I and class II inhibitor, which causes an increase in lysine acetylation levels and generates atranscriptionally permissive state.”; note then that as bees only HDAC inhibit four things, so a mammal like a human could have a greater complementary longevity effect from HDAC inhibiting another completely different four things found at mammals along with that; those four or more mammalian things are a greater engineerable area for longevity drug mechanism coverage;

90DA longevity drug: An HDAC inhibitor (gene activator) similar to the longevity drug 10HDA, that could be another, new to me, longevity molecule: “(E )-9-oxodec-2-enoic acid (90DA) is an analogue of 10HDA that is produced by the queen bee (Plettner et al, 1996), and it also has similar HDACi activity (supplementary Fig S5online). This activity of 90DA acid might be important for maintaining the royal phenotype, if it is produced and consumed by the queen herself.” noting that the queen lives 12-24 times as long as the other bees, the 90DA she produces may have a simultaneous with 10HDA ingestion greater longevity effect, that would make feeding mice, 96 well plate fish, as well as c elegans 90DA simultneously with 10HDA a thing to quantify as to if it causes even greater longevity than 10HDA alone, so 90DA could be a 10DHDA longevity drug amplifier; https://pubchem.ncbi.nlm.nih.gov/compound/1713084 90DA looks very similar to 10HDA at one of the distal parts it has a =O rather than an OH

Testing the effects of longevity drugs on pregnant rodents and nonhuman primates provides data on any effects longevity drugs, particularly any that effect epigenetics, may have on progeny; it is possible that epigenetic modifiers like 10HDA at royal jelly, an HDAC inhibitor, could have fetal effects; notably, valproate, an HDACinhibitor triples occurences of nonwellbeing at fetuses (wikipedia), noting two and three generation epigenetic effects, verifying epigenetic well being at mice and even the primate bonobos, which is able to have progeny after 6 years, that experience longevity drugs is beneficial; just 10 bonobos before the year 2026 could verify that rapamycin(60%), mtor1 rapalog (60%), metformin (5-35%), lithium (7%), 10HDA, and other decanoic acids (90DA, 10H2DA, fungal decanoic acid) (25/27%-46%), 17 alpha estradiol (9-11(?)%), NDGA (double digit 11(?)%) were absent harm to primate babies. It is even possible, that screening a sufficient number of longevity drugs on mice, that longevity drugs with beneficial epigenetic effects will be found;

17 alpha estradiol is published at the NIA as causing greater longevity, HDACinhibitors also have the effect of making alpha estradiol receptor genes differently activity producing, so that is another possible HDACinhibitor longeveity drug, “estrogen receptor alpha (ERalpha) can be hyperacetylated in response to histone deacetylase inhibition, suppressing ligand sensitivity and regulating transcriptional activation by histone deacetylase inhibitors.” I do not know if this says, HDACinhibiton makes more alpha estradiol receptors (possibly longevizing), or if this says the receptors that get made have different sensitivity;

There will likely be numerous HDACinhibitor beneficial pharmaceuticals, wikipedia mentions these, all of which could be quantified on 96 well plate verebrate fish as well as c elegans as to any longevity increasing effects they may have, “HDIs include the hydroxamic acids vorinostat (SAHA), belinostat (PXD101), LAQ824, and panobinostat (LBH589); and the benzamides : entinostat (MS-275), tacedinaline (CI994), and mocetinostat” It is possible that, “Enhancement of memory formation is increased in mice given vorinostat” comined with screening vornistat for heightened longevity could produce a longevity drug that is also a nootropic; cheerfulness, better than well producing, longevity HDACinhibitor drugs may also be possible, “research on the use of HDAC inhibitors (HDI) for the treatment of depression use rodents”

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