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)”,


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