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”
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”
10HDA is a longevity producing HDAC inhibitor
Testing numerous different lipid versions of 10HDA from royal jelly as longevity drugs, and finding human equivalents: When people eat fats like omega 3 lipids (DHA, others) the body makes a variety of things like triglyceride forms, ethyl esters, and phospholipid forms out of it it, at humans, but perhaps not mice or queen bees, pancreatic lipase likely emulsifies the 10HDA as well as 10H2DA at royal jelly; all of these suggest that feeding people various of perhaps 10 different lipid forms of 10HDA and then measuring the humans as to things like cognitive ability, and various physiological measures could find things that are more highly beneficial as 10HDA and royal jelly forms; as a longevity drug: noting the published longevity effects at mice, they could feed mice 10HDA preprepared form variants like phospholipid versions, triglyceride versions, ethyl esters, as well as things like methyl esters, and propyl esters, and emulsified creams, then see if there were any longevity differences between the lipid forms; they could also measure the kind and amount of the circulating form of 10HDA lipid at mouse blood, and then the human version of 10HDA and royal jelly could be engineered around producing the same kind of 10HDA lipid, at the human bloodstream, at the same ug/ml as the longest lived 10HDA (or royal jelly) supplemented mice have at their bloodstream; so, if its phospholipid 10HDA that is measured as causing the greatest measured mouse longevity then its also the phospholipid 10HDA amount at human blood, as well as a 10HDA phospholipid longevity supplement or drug for the humans; Similarly if the most longevizing version of 10HDA is 10DHA as triglycerides at some measured amount at the bloodstream of longevized mice then it is the triglyceride form of 10HDA at the same amount at the human bloodstream; Notably, this could also give humans using 10HDA or also 10H2DA, or 90DA, or other longevity decanoic acids, the ability to have the same ug/ml of the same kind of decanoic acid lipid at their bloodstream as the longevized mice; Notably, at DHA/EPA lipid supplements, humans taking an emulsified supplement had 3-5 times higher amounts of omega-3 lipids at their circulation after 8-24 hours than if they took a fish oil pill; feeding mice a 10HDA emulsion, and also humans, could be beneficial at finding a functional dosage;
A paper on greater longevity from HDACinhibition mentions HDAC yeast genes that when removed cause greater longevity, as well as RNAi effects on HDACs, reducing the HDAC effect cause greater longevity, https://www.embopress.org/doi/full/10.15252/emmm.201809854 Trichostatin A, an antifungal, causes greater longevity at drosophila from HDACi Trichostatin A is 50- $100/Kg at alibaba so is likely a longevity drug at less than 10c/24 hours Trichostatin A is soluble in ethanol, but not water, “Trichostatin A is soluble in DMSO, DMF, acetonitrile, and ethanol. It is not soluble in water. This product is tested at 2 mg/ml in methanol, yielding a clear, colorless solution. It is also soluble in lower alcohols” also, “Trichostatin A inhibits histone deacetylase at nanomolar concentrations. The resulting histone hyperacetylation leads to chromatin relaxation and modulation of gene expression.”
https://www.sigmaaldrich.com/content/dam/sigma-aldrich/docs/Sigma/Datasheet/8/t8552dat.pdf , is trichostatin soluble in melted sugar alcohols like sorbitol or xylitol that dissolve it when warm, and then turn to a dry, but trichostatin A dissolved powder to be placed at an enteric capsule? Or, noting liposomes can be made with a bunch of etoh, could a high etoh or DMSO liposome transport dissolved trichostatin A to the lymphatic compartment to be an effective dose?
Noting that omega-3 fats are is up to 9 times more absorbed as food than as pills, and that emulsions have 3-5 times more increase in measured omega-3 amount at the bloodstream after 8-24 hours than pills, eating royal jelly as an emulsion, with food, and a piperine capsule, could be beneficial; Also, a two form dose of royal jelly could be beneficial, a 10DHA calculated longevity dose amount, and then the same amount as the 10DHA calculated longevity dose again while being taken as an enteric pill, with food, with the benefit of the the possibly longevizing royalactin proteins passing the stomach, and the 10HDA likely being emulsified at the GI tract; So if 6 grams of royal jelly is a longevizing 10HDA dose, then 12 grams, half as enteric pill form, the other half as royal jelly (lecithin) emulsion with food, such as 12g or more of an oily food could cause 6G or more of functional 10HDA absorption; different lipid forms have different absorbabilities, but, “Absorption of both EPA and DHA from fish oil ethyl esters was increased three-fold[with the 44 gram fatty meal]”
a person eating 10HDA at royal jelly likely absorbs 90-95% of it; “direct measures of digestion calculate “digestibility coefficients,” or the digestion percentage (efficiency) of various nutrients based on the amount of nutrient consumed relative to that collected in total fecal excretion (i.e., undigested) over a period of a few days. For instance, human studies measuring the digestibility of dietary omega-6 polyunsaturated fatty acids, as linoleic acid, show digestibility efficiencies approaching 90–95%.”, note though that, “a diet higher in fat, rather than a low-fat meal, supports better omega-3 bioavailability.1 Earlier literature indicates absorption efficiencies for EPA in the triglyceride or ethyl ester form of 90% and 60%”
that a triglyceride is 90% absorbable at a human, but an ethyl ester lipid is just 60% absorbable suggests that a 10HDA version that is a triglyceride would be more efficient and effective, possibly better at longevizing, notably though it is possible that a 10HDA ethyl ester actually travels to different tissues than a triglyceride;
Note though that putting a royal jelly emulsion in an enteric capsule could be higher effectiveness, “that DHA, being protected by the encapsulation structure from oxidation and degradation under the acidic conditions of one’s stomach, is successfully released in the upper two parts of the small intestine”
taking the royal jelly 10HDA with a large, lipid-rich meal is the way to heighten absorption of the the 10HDA, “The absorption of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from fish oil triacylglycerols and fish oil ethyl esters consumed in a high-fat meal (44 g total fat) by male volunteers was measured and compared to values previously reported for consumption in a low-fat meal (8 g total fat). Absorption of EPA, but not of DHA, from fish oil triacylglycerols was significantly improved from 69% to 90% by co-ingestion with the high-fat meal. Absorption of both EPA and DHA from fish oil ethyl esters was increased three-fold, to about 60%, by co-ingestion with the high-fat meal, indicating that absorption of fatty acid ethyl esters is highly dependent on the amount of co-ingested fat.
It is likely the double dose, as an emulsion, with an enteric capsule, with food and piperine works better than: combining DMSO with royal jelly powder to make a paste, then putting it an enteric capsules, with a side enteric capsule of piperine could be a way to make the 10HDA 2(dmso) times 4 (piperine) 8 times more physiologically available; notably though, liposomes (4 times from skipping first pass metabolism) with DMSO (2 times) with piperine (4 times) could make the 10HDA as much as 32 times more physiologically available, noting the 6-60g dose of royal jelly, that suggests that a 4g dose, as DMSO liposomes with piperine could be like 128 gram dose.
During 48 hours, emulsified fish oil is about twice (.67 compared with .34) as physiologically available as encapsulated fish oil, “Over a 48 hour period there was enhanced absorption of total n–3 and EPA (0.67 ± 0.16, 0.45 ± 0.06, p<.01;
0.34 % ± 0.05, 0.23 % ± 0.04, p= .05;
EFO and CFO respectively was observed for the EFO treatment., “The emulsified and water soluble state increases exposure to lipase and diminishes the gastric clearance time. Therefore, we have examined the rate and extent of absorption of total n-3 and LCn-3 into the phospholipid fatty acid (PLFA) pool after an emulsified fish oil (EFO) supplement compared to capsules of the fish oil used in its production (capsular fish oil, CFO). We hypothesized that the EFO would have an increased rate and extent of absorption compared to the CFO. “ also, “Participants consumed a 4-g portion of fish oil provided as either 5g (∼ 1 teaspoon) of EFO (80 % lipid, providing 4 g of fish oil) or four 1-g capsules of CFO”, also, “The EFO was Coromega ™ (Carlsbad, CA) an emulsified, flavored lipid supplement produced from marine sources that is of pudding consistency”
Also, “The observed increases are likely due to improved digestion and absorption due to the enhancement of the action of pancreatic lipase on long chain fatty acids (23). Lipid emulsification in the stomach is a fundamental step in fat digestion through the generation of a lipid-water interface essential for the interaction between water-soluble lipases and insoluble lipids (24, 25). The ultimate bioavailability of dietary fat is dependant on this lipid water interface. Emulsification of fish oil bypasses this normal physiologic step and enhances its absorbability (24). Garaiova and colleagues (21) reported the increased absorption of long chain, highly unsaturated fatty acids and incorporation into plasma fatty acids with the administration of pre-emulsified fish oil. Our work demonstrates that in the short term the emulsification of fish oil allows for a similar enhanced absorption with improved rate and extent of incorporation into PLFA
Note: one graph of DHA at the paper shows the capsule oil being at about 7% and the emulsion being at 20%. so emulsified oils are 3 times more detectable at the circulatory system after 24 hours. 48 hours later the emulsified fish oil was still double the capsule concentration, another graph shows the emulsified oil being 4-5 times higher concentration after 8 hours;
Also, taking royal jelly with a meal could cause more 10HDA to be absorbed, “In one study comparing the effects of fish and fish oil, researchers found that levels of DHA after 6 weeks of salmon consumption were nine times higher than after fish oil administration.”
Also, “Another study confirmed this by demonstrating that fish oil is absorbed much better in the presence of a high-fat meal. They found that the content of n-3 fatty acids in the body tissues rose dramatically when the fish oil was taken along with 12g of olive oil.”
That makes me think that royal jelly with 2 oz of cheese is better.,
lecithin is one way to emulsify oil, also, putting royal jelly at an existing food emulsion, like liquid nondairy creamer, could be possible, “Many popular food items are emulsions, including mayonnaise, salad dressings, sauces such as Hollandaise, chocolate, and ice cream. Lecithin, a blend of naturally occurring phospholipids, is widely used in the food industry to promote o/w emulsions.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701654/
A wellness healthspan and possibly longevity drug or genetic modification: “Histone acetylation can be transient and must be maintained by enzymatic activity. Histone acetyltransferases (HATs) transfer the acetyl group (COCH3) from acetyl co-enzyme A to lysine residues”;
HDACinhibitors, favor acetylation, and cause various organisms to live about 22% longer, and ill mice to live 20 weeks rather than 8 (days? weeks?), the thing is though is that keeping a genome acetylated an optimal amount, could vary for numerous reasons, it is possible some humans have SNPs or gene copy numbers that strongly support rapid, full, all-tissue histone acetylation, whereas other humans might have different SNPs or copy numbers; histone acetyltransferase is an enzyme; at various things though 2019 normal humans vary 100% or more (IQ of 200, age at first ovulation, height), it is possible then that acetylation drugs or supplements, gene therapy, or germline gene modification could optimize the amount of histone acetylation that occurs, There could be a gene test to diagnose genetic variation like SNPs or copy number variations at the histone area acetylation enzyme, “The histone acetylation and deacetylation occurs on the lysine residues in the N-terminal tail as part of gene regulation. The mediating enzyme is often histone acetyltransferase”
Also, although not at the histone area, about half of people have varied acetylation ability, “There are three types of N-acetyletransferases. These are labelled A, B and C. These have been extensively studied in yeast. Each subtype is specific for its substrates. These NATs Genetic determines activities of NAT that again regulate drug metabolism. Nearly 20% of Asians have an isozyme that results in slower N-acetylation of drugs, while 50% of Whites”
The reactions are mediated by N-alpha-acetyltransferases (NATs), a sub-family of the GNAT superfamily of acetyltransferases. This superfamily includes histone acetyl transferases. These NATs transfer the acetyl group from acetyl-coenzyme A to the amine group.
Testing an acetyl group drug on mice: So a drug or supplement that causes more histone acetylation could be a water soluble variation on Cellulose triacetate, (triacetate, CTA or TAC) is a chemical compound produced from cellulose and a source of acetate esters, typically acetic anhydride. Triacetate is commonly used for the creation of fibres and film base. It is chemically similar to cellulose acetate. Its distinguishing characteristic is that in triacetate, at least "92 percent of the hydroxyl groups are acetylated." Notably perhaps the cellulose could be replaced with ribose, NMN, NR, or anything with active transport at the exterior cytomemebrane as well as possibly having a nuclear membrane transport peptide on it. triacetylglucose is also online, glucose pentaacetate, “GPA is completely absorbed and extensively utilized by the rat. Absorption of GPA from the gastrointestinal tract is rapid and almost complete in 4 hours.”
possibly with a nuclear memebrane transport peptide attached to it, glucose pentaacetate could heighten histone acetylation
I read that HDACinhibitors cause greater longevity, this, “Many acetylation markers on histones decrease with age, including bulk histone 4 acetylation levels and histone 3 acetylation at lysine residues 18, 27, and 56, which is thought to facilitate the aging process (Feser & Tyler, 2011). Therefore, the effects of an HDAC inhibitor, which prevents HDACs from removing acetyl groups further, have the potential to directly reverse or prevent these age‐related changes.” to my perception that suggests that cumulative modification of and from chromatin accessibility modulators occurs, noting that wikipedia mentioned 1/2 day, 24 hour HDACinhibitor activation spans, and to my perception, a paper on 10HDA as a longevity and phenotype producing HDACinhibitor noted 72 hour spans, that suggests a new kind of chromatin acetylation longevity increasing technology, an acetylator that works to modify multimonth, multidecade cumulative effects of HDACs or other chromatin accessibility modulators that are nonbeneficial to longevity, wellness, as well as healthspan, I have no idea how this works, other than fetuses remove about 90% of their epigenetic sturcturalization during development and perhaps this physiochemical effect could be caused to happen again, beneficially, at persons who have previously experienced puberty, with optimal acetylation as an immediate physiological activity once the epigenetic 90% movement to nonepigenetic form occurs; Another possibility is that a harmless drug that causes a genome to sequentially make say, one molecule, of every protein at its genome causes the entire genome to be sequentially processed, and while it is being processed a beneficial chromatin accessibility modifying modulator (like, from what I read about longevity epigenetics an acetylator) is around at sufficient amounts to modify the entire epigenetics of the entire, one gene at a time, processed genome; it is possible that something like mitosis could be genetically enhanced with gene therapy or germline gene modification to cause young phenotype (like 4 years or 14 years old) chromatin epigenetics, notably longevity, wellness and healthspan optimized acetylation (or also other beneficial chromatin accessibility modulator chemistries, like phosphorylation and others) amounts, That way, depending on the tissue, epigenetics would be reoptimized to be at a chronological 4 year old body or 14 year old body forms at most body cytes and tissues many many times repeatedly, and at a kind of continuous (some of any tissue or organ is likely mitotic at any particular moment) remodelling; Another way to cause change to gradually accumulated epigenetic nonoptimality is to possibly do a computer modelled algorithmic administration, possibly simultaneous, of different various chromatin accessibility modulators with nuclear envelope transport peptides on them, so like algorithmically, perhaps HDACinhibitors with nuclear envelope tranport peptides would have 40 times the activity as HDAC that had been apportioned as being around, but at 1/40th the usual amount, causing some sites that are HDAC beneficial to the organisms longevity, wellness and healthspan (SIRT HDAC possibly) to be HDAC-modified to be remodelled along with the HDACinhibitor modified areas; I do not have any idea how the algorithmic amounts times activities at genome location autosorting could work, although it is possible a new kind of enzyme that rather than methylating, acetylating, deacetylating, phosphorylating, or some other thing, puts tags, to be replaced with things like acetyl groups at a next pass/cycle on the genome, I think I read that basically physiochemicals put acetyls and methyls on lysine amino acids, perhaps there is some other thing that has a lighter, readily replaceable attachability to a lysine, like a PO4, or a poly PO4, or even a somehow physiologically harmless vinyl (bigger than a methyl, perhaps eentsier than an acetyl), then again, restarting it like a fetus’ 90% epigenetic renewed rewritable space every time there is a mitosis or even a quantitatively measured as beneficial and harmless to the progeny meiosis event could be more physiochemically engineerable, and composed of the reuse of other, preexisting, working, beneficial, physiological mechanisms and processes;
It is kind of physiochemically reminiscent of SENS, but perhaps there could be a youthotransferrent, kind of like an upgrade the neighbors, as compared with a senolytic that finds and terminates a nonbeneficial cyte; if some way of measuring that a particular cyte was far above the median as to youthful phenotype, while supporting of organismal longevity, wellness, and healthspan, as well as fully functional at local area physiochemistry, then its chromatin accessibility modulation, perhaps epigenetics, could be copied to neighboring cytes; peptide HDACinhibitors exist, so it is possible cyto efflux transport utilizing chromatin accessibility modulator optimization (like HDACinhibitors) peptides of a variety of forms and effects could exist, and visit the neighbors, spreading a chromatin accessibility modultion form similar or much like the far above median cyte;
At a paper I read https://www.embopress.org/doi/full/10.15252/emmm.201809854 that even though mirochondria are absent having histones HDACinhibitors cause more benficial mitochondrtial function, They could screen a library of acetylators or HDACinhibitors linked to localization molecules that cause preferential concentration at mitochondria to make and find mitochondrial epigenetic optimizers of longevity, wellness, and healthspan, they could then also quantify the beneficial effects
really primitive, but heat shock proteins cause greater longevity when the organism makes more of them, could 1-5 grams of HSP, enteric coated, to pass the stomach, have an effect on longevity; is it possible that an HSP, linked to an active transport moeity, could get rapid transport and movement to the cytes’ cytoplasm at numerous tissues; They could test this on mice to find out if eating enteric coated HSP, like eating chondrotoin, cartilidge, omega-3s, MSM causes physiological, longevity, wellness, and healthspan benefit
I read that getting rid of HDAC genetically causes mice to be nonalive, notably though hdacinhibitors cause greater longevity, at humans, as well as mice, are there HDAC, methylation, as well as a variety of other chromatin accessibility modulators (phosphorylation and others) SNPs (or gene copy number variations) that cause greater organisms longevity, wellness, and healthspan? Have human supercentenarians been characterized this way yet? Gene therapy as well as germline gene engineering could heighten longevity, wellness, and healthspan with optimized as well as new amino acid sequence SNPs (or possibly also different numbers of gene copies) at chromatin accessibility modulators
I perceive I read that when fetuses or possibly zygotes develop they automatically do a thing where they erase near 90%, it might have been 93% of their epigenetic molecular tagging, like removing methyls, acetyls, possibly like another 7-9 other chromatin accessability modulators like phosphorylators, so what I am thinking about as a wellness, healthspan, and, there is a chance, longevity technology is do some human zygotes do this a lot more than others, and what are the genotypic and phenotypic effects? If a normal human with some genome and SNPs (or gene copy number variations) erases 97% of their epigenetics as a zygote, and another normal human erases 93% of their epigenetics, which human is more optimally aligned to penotypically realize greater wellness, healthspan, and longevity? If this does occur, and at numerous things some humans are sometimes double or half of other humans while still being socially capable or thought of as conceptually fine (double height, IQ 200, first ovulation twice as early or at double usual chronological span, other things) is there any benefit to SNPs (or possibly some normal variation on number of gene copies) that strongly or lightly erase epigenetics at zygotes? It is possible that at some physical and interpersonal environments, removal of the epigenetics of previous ancestor’s reactions to stress, absence of stress, gourmand plentitude and prosperity, or perhaps athletic longevity focused protein reduced Keto longevity dieting could be beneficial, while at other ancestry occurences the person with the more epigenetic erasing SNPs (or gene copy number variation effects) might be physiologically skipping a multigenerational trend of epigenetic benefit, so what is better? It is possible that the epigenetics of a highly beneficial epigenetic environment can be purposefully duplicated, basically programmed, bringing preferred patterns of chromatin accessibility modulation (tagging) to all persons, humans, people, that is homo sapiens to create the greatest longevity, healthspan, wellness, and happiness; they coulkd find the 93% and 97% epigenetic zygote epigentic erasing at mice, and figure out which mice benefitted more, and what SNPs (or gene copy number variations) caused the mice to benefit
Do plants have epigenetic new sprout epigenetic blankness-production, if they do, would it be agriculturally beneficial to give plants a beneficial epigenetics, if they do not, would it be beneficial to cause epigenetic refreshing at plants to cause a benficial high genetic response to the environment rather than an ancestor plant’s responses to a different less growth benefitting environment; like the idea that epigenetic blankness or continuity could be bred to be higher or less at mammals it seems possible epigenetic trend or a fresh response could be created at plants on purpose to be beneficial
Longevity technology: have the identical acetylation and methylation (and other chromatin beneficial effects) you had at 7 years old, or a software model of your acetylation at 7 years old, have the 7 year old acetylation amounts all your life with custom chromatin accessibility modulators; this suggests that HDACinhibitors may cause longevity effects from making acetylation amounts similar to those at a younger phenotype, among a variety of possible mechanisms;
“The exact means by which HDAC inhibitors extend lifespan has not been fully resolved; however, a number of possible mechanisms can be envisioned. One possible scenario is that HDAC inhibitors reverse the natural age-related changes occurring in the histone acetylation landscape. This is the most simple explanation for their benefits, supported by the observation that many acetylation marks on histones generally decrease with age and in certain age-related diseases. A second possible mechanism of HDAC inhibitors is that they may affect histones and nucleosomes to directly activate transcription of pro-longevity genes. This is supported by observations that an endogenous HDAC inhibitor, β-hydroxybutyrate (BHB), can increase acetylation in the promoter of the pro-longevity transcription factor FOXO3a resulting in its increased expression, and indeed, BHB's lifespan extending effects depend on HDAC genes.
A third possible mechanism through which HDAC inhibitors may increase lifespan is through hormesis. In this scenario, while high doses of HDAC inhibitors may be toxic, low doses would elicit activation of protective genes to regain homeostasis, ultimately improving function. This is supported by observations that flies treated with HDAC inhibitors show upregulation of heat shock protein chaperones, a class of genes that are usually upregulated under stress. A fourth possibility is that HDAC inhibitors may regulate lifespan by modifying the acetylation state of non-histone proteins, activating signaling cascades that promote longevity independent of histone modifications.
Longevity causing immunization technology, longevity drug: It is possible that at the circulatory system there are circulating chemicals or physiochemicals or even chemicals that people are externally expoosed to that cause nonbeneficial methylation, the deacytlation of histones, or other nonbeneficial chromatin availability modulating things which are deleterious to longevity, wellness and healthspan immunizing against these circulating HDACish, methylationish, and otherwise deleterious chromatin availability modulators is quantifiably measurable as to any effect it has on greater longevity, wellness, and healthspan; this could be a beneficial immunization at children causing greater well being, healthspan and longevity even if immunized before elementary school; Notably the effect of the immunization on rodent and nonhuman primate progeny at more than 2 generations of progeny, female bonobos can get pregnant after 2190 24 hour spans (6 years), so 2 generations of bonobos could be as rapid as 7 years from the first sexually capable female bonobos longevity immunization; the longevity immunization would be studied to verify it was harmless and possibly beneficial to fetuses, pregnancies, babies and the people they grow into; Notably though some HDAC inhibitors are measured as actually causing change at the migration of (fetal) neural crest cytes, suggesting that some kinds of HDAC, methylation, or other chromatin accessibility modulation physiochemistry active immunizations might be better after completing having children, or, that immunizing against chromatin accessibility modulations that are simultaneously deleterious to any possible fetus and mother both are beneficial to make immunizations at;
I read that numerous HDACinhibitors cause greater longevity, is there a different thing, which could also be beneficial, that is a demethylation, that demethylates a histone, they could make a database of where this benefits longevity, wellness, and healthspan;
New fungal based longevity drug: There could be a fungal product similar to 90DA that is a longevity drug that also causes growth at fungi that could be a different chemical to quantify as to longevity effects, a chemical much like 90DA is utilized to grow fungi, “Provided is a method for the use of 10-oxo-trans-8-decenoic acid (ODA) as a fungal growth hormone to stimulate mycelial growth of cultivated mushrooms. A species of cultivated mushroom is selected and grown in a solid or liquid growth medium which has been supplemented with ODA to a concentration of 10-7M to about 10-4M. After culturing the mushroom the mycelium of cultivated mushroom is harvested. In addition to a method of using ODA, a method for the hormonal stimulation of fruiting in cultivated mushrooms is also disclosed. The ODA in this method is added to the casing layer of the compost which is mixed with mushroom spawn.” the 10 oxo-trans-8-decenoic acid chemical is slightly different than “9-oxodec-2-enoic acid”; they could grow a bunch of fungal mycelium, concentrate and separate a number of differing 10 C enoic acids, and see if any of the different ones they find have greater longevity effects on c elegans than 10HDA and 90DA and then test the fungal decanoic acids on mice to find out if the mouse longevity increase is larger than the published 25(27%) from royal jelly; patent: https://pubchem.ncbi.nlm.nih.gov/patent/US5681738#section=Patent-Title
molecules that are similar to 90DA are visually nifty at https://www.chemsrc.com/en/cas/334-20-3_1091822.html These could be screened as a library for longevity drugs, notably as compared with a 10 C decanoic acid, malonic acid has fewer C, is kind of well known, and looks kind of like 10HDA and 90DA, with fewer C at the alkane part, I perceive wikipedia communicates that malonic acid has something to do with valproate another HDAC inhibitor, possibly some variant on malonic acid could be a longevity drug or multiply beneficial HDACinhibitor
I think 90DA nd 10HDA could be engineered to be mass produced at yeast
Chemical molecular entertainment: Is it possible to make a pleasant nootropic, or a highly effective nootropic into a longevity drug; phenibut could have a c=c on it, and a distal =O and a -O, but it might not pass the blood brain barrier, it would still have the distal phenyl on it though (entertainment, not an actual product), phenylethylamine, which causes me to write up to 44 pages of notes on new ideas during about 24-48 hours could have some more alkane C-C happening after the N, and at the further distal alkane could have the =O and -O at a decanoic (10 C) acid, it might do anything, it might be a stimulating nootropic that at 10HDA 60-600mg doses caused mammals like mice to live double digit percentages 25(27%)longer, or even the 46% greater longevity at c elegans
Notably, at previous notes grinding up termite queens (half century longevity) and feeding them to mice, with an enteric coating on the ground up termite material, as well as findout if c elegans lived longer with termite hemolymph at their food or medium was described as a possible longevity drug finding area, termite queens make 90DA, a royal jelly function like chemical
10HDA numbers: “A main component of royal jelly is 10HDA, which can compose 2–6% of royal jelly; this translates into a 100–300mM concentration in royal jelly.”, that also suggests, as the ratio of a published sample of royal jelly was about 3 parts 10 H2DA to 1 part 10 HDA that royal jelly could actually be 18% 10 H2DA, or 24% all 10DHAlike lipids, although that 1/4 lipids thing seems different than the way lyohilized royal jelly looks;
the paper where 10DHA is a thing that turns a methylated gene back on is able to do that with a similar, but different system, at 5mM, and that royal jelly is 100-300 mM, that suggests the plausability that getting 10HDA to the largest variety of tissues could provide a longevity benefit that complements and enhances getting an equivalent to mouse longevity dose amount of 10HDA (or also royalactin), that suggests three sizes of liposomes, and three different phosphatidyl compositions of liposomes, as well as variety at physioavailability enhancers like piperine and quercetin simultneously
surveying libraries is beneficial, they might even find new disease treatments as well,
Noting the screen all FDA drugs to find longevity drugs screening a library approach, numerous dna on the histone activity drugs like HDACs as well as HDIs as well as (possibly) HATS are anti-cancer drugs, screening all FDA anti-cancer drugs as well as HDIs to find new longevity drugs, noting that I just noticed FDA anti-cancer drugs also contain chromatin-access drugs, this could find new longevity drugs. Online it says that HDIs increase longevity at organisms, suggesting mouse screening of all FDA HDI, HDAC, HAT other chromatin accessibility acvtive drugs is a longevity drug finding activity
It is likely a more effective HDI that is a peptide is possible, a paper says, “cyclic peptides are the most structurally complex group of HDAC inhibitors and include depsipeptide, apicidin, and the cyclic hydroxamic acid-containing peptide group of molecules”
10HDA as an autophagy longevity drug: 10 HDA might cause more autophagy, a thing they could see if it happens, (at the study where 10HDA makes the daf 2 mutants live 46% longer) “10-HDA did not extend the lifespan of the eat-2 mutants, which show long lifespan through dietary restriction caused by a food-intake defect. This finding indicates that 10-HDA extends lifespan through dietary restriction signaling.” I perceive calorie restriction longevity effects heighten autophagy and protein recycling, so localization of 10HDA forms might cause some kind of tissue youthification if 10HDA causes greater autophagy, so cardioarea as well as vascular heightened autophagy might go with reducing heart disease, I read autophagy at neurons is beneficial, “Upregulation of this pathway may be neuroprotective, and much effort is being invested in developing drugs that cross the blood brain barrier and increase neuronal autophagy.” so a 10HDA variation that passes the blood brain barrier even more than 10DHA could be a beneficial drug, perhaps the threonate amino acid at Mg threonate could do it, or, at a few amu molecule acetylation (passes blood brain barrier) of 10HDA versions could be measured as to beneficial effects on mouse longevity and congitive youthfulness; an acetyl group on the 120HDA that causes it to pass the blood brain barrier a bunch more could be chemically obvious if you asked a chemist, to make, and maintain the few-AMU size of the molecule, a halogen (p-cholophenoxy moiety) might do it as well,
A liposomal pharmaceutical is about 4 times as physiologically available because it omits first pass heaptic metabolism from going directly to the lymphatic compartment, it could be that liposomal 10HDA has 4 times greater effect at a mg/dose; 10HDA is on alibaba, as is royal jelly, so comparatively big amounts of liposomal royal jelly, or a few tens or hundreds of mg of liposomal just 10HDA could be more effective longevity drugs (mice 25(27%), c elegans 18-46%); also it is possible that liposomes reach different tissues compared with oral royal jelly, royal jelly at enteric capsules, as well as pure 10HDA which is alibabaish, Also, even though a person making juice only gets some juice and some wet unpressed mass, a solvent extraction of royal jelly, which I could ask a chemist on fiverr about, would leave a pressed mass that I could still eat for 10HDA as well as royal jelly benefits if the solvent is edible; thinking about the places liposomal 10 HDA or even liposomal royal jelly could travel to, one online thing mentioned that liposomes might not always be beneficial to the tissues they visit, that brings up the possibility of making liposomes from completely brain beneficial phospholipids, I perceive phosphatidylserine “Phosphatidylserine (PS) is a phospholipid component of the membrane encasing every one of your brain cells”, is a beneficial nootropic, so even though the 10DHA liposomes could travel the entire body, if a quantity of them made it past the blood brain barrier they would be made of a brain-beneficial phospholipid phosphatidylserine chemical; DHA phosphatidylserine EPA together cause greater cheerfulness
Dimethylaminoethanol is a nootropic, another phosphatidyl thing that might make liposomes is phosphatidylethanolamine; this is another phosphitidyl chemical that is, at a nonhuman brain, 45.9% of the phospholipids at the hippocampus, a person who is thoughtful might make liposomes from three brain beneficial phosphatidyl chemicals, (also possible with phosphatidylserine as well as phosphatidylethanolamine is phosphatidylinositide) with the thought that the liposomes could bring 10HDA (or any other liposomal drug) to a wider range of cyte types and tissues simultaneously; DHA is published as beneficial, I do not know if you can make a liposome that is variously 10% phosphatidylserine 90% DHA, 40/60 DHA with phosphatidylethanolamine , 4/5 or other fractions; Also a person that makes different liposomes to reach different cytotypes and tissues simultaneously might use phosphatidyl chemicals, or methods (apparently you can just shake it in a beaker) that complement ultrasonication to make eentsy, medium, as well as bigger size liposomes even if they all have 10HDA or some other identical ingredient
They could screen a library of new phosphatidyl group containing drugs to find out if any new ones are noticeably beneficial; phosphatidylinositol makes me thing, they could use ribose instead of inositol, and ribose concentrates, beneficially, at the heart and is kind of (I may have read) feeling of energeticness causing, then there are all the phosphatidyl amino acids, also as regards to phosphatidylsugars (like inositol) they could find out if phosphatidyltrehalose is a neuropreservative or possibly causes cytomembranes at neurons to recover from freezing and thawing better or is better at preserving frozen, freeze dried gametes
Going with the concept that 10HDA could benefit the brain, “intranasal administration provides a practical and noninvasive approach to deliver drugs to the brain, allowing in this way an increase in the amount of drugs delivered across the barrier” 10 grams of royal jelly contain 600 mg of 10HDA, so kind of snortable; I do not remember the actual calculation, but if the c elegans dose of .03% of food (or perhaps it was aquaeous medium) is treated as mouse compensation dose, and with mouse 1/6 of body mass food/24 hours then a a human it is between 6 and 60 grams of royal jelly, or perhaps it was pure 10HDA at a human with 46% c elegans greater longevity (also 18% c elegans longevity) dose; a person could look up the papers right now, and calculate the actual numbers; nasal administration of 360 mg of 10DHA seems plausible
life extension foundation product:
Beauty topical drug: Royal jelly is a previously published beauty drug that causes skin to reflect even more light, noting that 10HDA is published as being a calorie-restriction (possibly autophagy causing) function the same as chemical, harmless edible oil extracted (concentrated) 10HDA at liposomes could actually do, and be measured as causing, beneficial tissue youthifying autophagy at the dermis; as a life extension foundation product, oil extracted (concentrated) 10HDA could be a one pill, functions like 20 grams of royal jelly equivalent drug, and they could use their insilico c elegans longevity characterizer to measure the longevity benefit, published at 46% at daf mutant c elegans; also the life extension foundation could possibly find a plant based source of 10HDA that is particularly mass producible and affordable
another library to screen is “DNA repair proteins” that is mentioned in a scientific paper so rather than being a general kind of thing, it is possible it is a particular group of things, I am reminded of when they fed mice things coated with enteric stomach-passsing enteric acryl polymers; (kind of like an enteric capsule at humans) they could feed mice the full published range of different DNA repair proteins, with an enteric coating, to find out if there is longevity, wellness, as well as healthspan benefit
On occasion, a plant extract has longevity effects, fisetin is a longevity increasing published senolytic plant extract; I think researched new human origin molecule pharmaceuticals are much more effective and beneficial at causing greater longevity, lifespan, wellness, and healthspan, it is possible that DNA chromatin active HDIs and HDACs and a variety of other chromatin-accessibility chemicals might already be made at plants and concentrated, these plant based HDIs and HDACs and other chromatin accessibility modifying chemicals could be beneficially screened to find out if they are longevity, wellness, healthspan drugs, creating a new plant based longevity drug
There is also the possibility that plant based chromatin accessibility modulators like HDIs and HDACs as well as other chromatin accessibility chemicals that cause greater longevity could be genetically engineered into a variety of food plants, further developing and supporting the creation of food plants that cause much greater human lifespan
There are whales with multicentury lifespans, do they face cardiovascular, cancer, or completely different risk? Pleasantly and benevolently, if possible (whale communications) voluntarily, could they be fed something or depot-injected to cause even greater whale longevity; longevity genetics at multicentury lifespan whales if they (just happen) to be different than cardiovascular or cancer risks could suggest a genetics of minimization of risk to humans from other risks as well as cardiovascular and cancer risks
Making liposomes that reach varying areas of the brain and body; I read that there is research on liposomes, some with surface moeities, that can pass the blood brain barrier. There is a chart at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4258547/ where lipids of different C amounts are arranged, and some C amounts like C16 can be 2 orders of magnitude different than like C22:6, and that amounts in different brain tissues can be near 90 times higher than other lipids, that suggests that if you make liposomes out of these things they might automatically sort to very different brain tissues and locations just based on the C length of something that is already a form of phosphatidylserine, phosphatidylethanolamine, or phosphatidylcholine;
Fatty acid
Fatty Acyl Composition (% of total fatty acid in each phospholipid class)
Phosphatidylserine
Phosphatidylethanolamine
Phosphatidylcholine
Gray matter
White matter
Gray matter
White matter
Gray matter
White matter
Aa
Bb
A
B
A
B
A
B
A
B
A
B
16:0
2.3
4.2
1.7
1.9
6.7
5.7
6.7
3.4
45.0
45.9
34.3
30.2
16:1
0.3
0.3
0.4
0.3
0.4
0.4
1.4
0.5
3.1
2.4
1.0
2.3
18:0
25.4
45.3
35.8
44.1
26.0
28.4
9.0
9.3
9.3
11.2
13.4
12.9
18:1
21.5
14.0
39.7
41.4
11.9
10.3
42.4
38.9
31.4
30.3
45.2
47.1
20:4
1.6
3.0
2.0
1.2
13.8
11.2
6.4
16.5
4.1
3.6
1.3
0.8
22:5n-6
5.0
0.7
4.8
0.1
14.3
1.2
13.7
0.7
ndc
trd
nd
0.2
22:5n-3
3.3
0.5
0.9
0.2
tr
1.1
0.5
0.9
nd
tr
0.3
0.3
22:6
36.6
23.2
5.6
1.3
24.3
30.5
3.4
8.6
3.1
2.5
0.1
0.2
Also as to screening a library, they could feed these 48 different C length lipids to 8 mice each, measure their cognition, and emotional affect, and find out if any C lengths of these phosphatidyl chemicals have much stronger effects than things like DHA and EPA on mental processes
Intelligence gene, “Enhancement of memory formation is increased in mice given vorinostat, or by genetic knockout of the HDAC2 gene in mice”
Intelligence genes: There are genes that effect the amount of phosphatidylserine, as well as phosphatidylethanolamine that is produced at the brain, SNPs of these (or gene copy number variations) could be characterized as to their effects on g at humans, and mice engineered to have and make the human highest phosphatidylserine and phosphatidylethanolamine production SNPs (or gene copy number variations) could be measured as to cognitive advantage compared with non genetically modified mice; notably there are numerous items at making phosphatidylserine, described online as a nootropic: production of phosphatidylethanolamine and phosphatidylcholine amounts effect the actual phosphatidylserine amount; diethylaminoethanol is a nootropic, so genes that make phosphatidylethanolamine could have g (like iq) cognitive ability heightening effects complementary or of different kind, or measurably beneficially different than greater phosphatidylserine production
A person blenderizing lkyophilized royal jelly and dissolving the 10HDA in a solvent at the blender could use an evaporable solvent compatible with the 10HDA, a paper online says, “A Quantity of 2000 g of fresh RJ with a moisture content of ∼67% was first extracted with 4000 ml of ethanol by stirring for 2 h at room temperature and then filtered to separate the resulting extract into soluble and insoluble fractions. Another 4000 ml of ethanol was then added to the insoluble fraction and stirred for a further 2 h at room temperature. Insoluble precipitates were removed by filtration, and the supernatant was combined with the soluble fraction from the first extraction and evaporated to dryness. The resulting material (385 g) was then extracted with 2000 ml of water : chloroform (1 : 1). After stirring vigorously for 10 min, the mixture was separated into water and chloroform layers. The chloroform layer was collected and evaporated to dryness (72 g) and extracted with 1000 ml of n-hexane. After stirring vigorously for 10 min, the mixture was separated into hexane-soluble and insoluble fractions by centrifugation and each fraction was evaporated to dryness (yield of each fraction was 5.32 g and 66 g, respectively). 5.32 g of the hexane-soluble fraction was dissolved in n-hexane, applied to a column (41 × 300 mm) of silica gel (BW320MH; Fuji Silysia Chemical Ltd, Aichi, Japan) and then successively eluted with 400 ml of n-hexane and 900 ml of chloroform to yield 10 fractions.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2529378/ To make 10DHA is it possible to just do the ethanol extraction part if I am willing to put up with 19.25% active material, with some of it (like 6/19.25ths) being 10HDA? Is there a physiologically beneficial alternative to chloroform and hexane? A ketone possibly, I read acetone is physiologically noncompatible, methyl acetate? ethyl acetate, What is most physiologically compatible at 1/100th solvent still at the liposomes?
It is possible that compared with a liposome at royal jelly as well as 10HDA, 10H2DA that a physiological availability heightener could be even more effective, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3634921/ “quercetin, genistein, naringin, sinomenine, piperine, glycyrrhizin and nitrile glycoside have demonstrated capability to enhance the bioavailability”
If royal jelly is completely absent effects on plants, then the 60% of the human genome shared with a plant is an area different than that which royal jelly ingredients cause published longevity, wellness, healthspan benefits, if royal jelly does effect plants, then it is possible a range of libraries of royal jelly chemicals could be screened on plants amplifying affordability and ease of characterization, and providing large n
A screenable library: the first leaves, cotyledons, of plants that are nondifferentiated to my perception are from physiochemically young tissue, noting plants have 60% homologous (same) genes as humans, then it is possible youthification chemicals, that could effect human genetic receptors and phenotypic structures could be at the first leaves, cotyledons, of plants; Getting a bunch of first leaves of plants, from a variety of species, including plants that 96 well plate fish and c elegans often live near, then protein extracting them, solvent extracting them, and water extracting them and screening those proteins, lipids, and water soluble things as libraries at fish and c elegans to find longevity, wellness, and healthspan drugs is a possible longevity technology. A person with $40 experiment would be to grow (sprout) a few hundred cotyledon plants, grind up the cotyledons, and just feed those to c elegans as a % of food, then enumerate the longevity of the c elegans at microsoft office
Somewhat novel to me: is there an edible surfactant, which can dissolve something like 10HDA as well as 10H2DA in water, then have a chemical put at it to “unsurfactantize” it causing a little blob of lipid soluble material at the top
Also, this suggests that at royal jelly, a solvent extraction finds more of something called 10H2DA than 10HDA: “The active fractions assessed by ER binding assay were pooled, evaporated to dryness and dissolved in a small amount of chloroform, followed by recrystalization five times using methanol. The resulting crystal was identified as 24-methylenecholesterol (24MET) by NMR analysis. The solution remaining after isolation of the crystallized material was evaporated to dryness, dissolved in chloroform and then applied to a column (34 × 240 mm) of Sephadex LH-20 (Amersham Bioscience Corp., NJ, USA). The column was eluted with 300 ml of chloroform to yield seven fractions. The active fractions were pooled, evaporated to dryness and identified as 2DEA by NMR analysis. Five grams of the evaporated hexane-insoluble fraction was dissolved in 40% methanol and applied to a column (50 × 280 mm) of ODS (Chromatorex; Fuji Silysia Chemical Ltd). The column was eluted with 40% methanol containing 0.1% trifluoroacetic acid to generate seven fractions. We obtained two active fractions and identified the active compound within these fractions as 10H2DA and 10HDA by NMR analysis. The yields of 24MET, 2DEA, 10H2DA and 10HDA were 1.2 g, 3 mg, 1.65 g and 0.53 g, respectively.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2529378/ So as I perceive what this says, they solvent extracted 2000 grams of fresh royal jelly and got three times as much 10H2DA as 10 HDA; That has longevity drug development opportunities as mice fed either 10H2DA or 10HDA could have different longevity increases, up from the published 25 (27%), and it is even possible that plant sources of the dfifferently preferrable 10H2DA or 10HDA could be found, bees that make a larger amount of the more longevizing of the two chemicals could be bred; and things like the c elegans 46%/18% longevity increase from 10HDA could be characterized at 10H2DA as well; Notably one of them has a c=c, and the other a c-c, “10HDA is saturated whereas 10H2DA and 2DEA are both unsaturated fatty acids”, that suggests many possible new molecules
I read that 10HDA causes longevity at c elegans from a calorie restriction similar effect, although the c elegans got to eat as much as they liked, they could find out if screening a library of 10H2DA as well as 10HDA variants has an even greater calorie restriction mechanism-possible longevity effect, with different amounts of things like autophagy produced; notably the possibility of making a variety of multiunsaturated, multi c=c at each molecule versions could be beneficial to making this library, and screening it with 96 well plates on the 46% greater longevity c elegans as well as the 18% greater longevity C elegans as well as the unmodified c elegans; That data could then be used to find which new HDA library variants to feed to mice to find out if the published 25(27%) longevity heightening at mice from oral royal jelly, which I now perceive as being at about a 1 part 10HDA to 3 parts 10 H2DA; as previously described, the longevity effects of acetylated HDA, library screened variants, as well as possibly autophagy producing optimized forms of the HDA molecule could be quantified to find acetylated HDA molecule variants that pass the blood brain barrier much more effectively, and mice could be utilized to verify this was cognitively and emotionally, and wellness, and healthspan, and possibly also longevity beneficial from the greater activity at the brain (CNS)
Thre is also the possibility of a completely new drug, some colorants have a bunch of c=c-c=c, and the HDA molecule is linear, it is possible that a non =O variation on 10HDA (or 10 H2DA) that is longevizing could exist. Or if the =O is function-producing, S, Se, or P or N could be tried where the =O is; Also, a person could like comparing the effects of say a 10 C alkane with an OH on a distal part, with a OH(O=c)c=c molecule of any length to find out if the two distal parts of the 10HDA molecule have an separate longevity effects. If it is the OH(O=C)-C=C part then they could just attach that to metformin or rapamycin to make a longevity drug more effective than rapamycin’s 60% increase of longevity; if, just possibly, a 10 C alkane with an OH on it distally is actually longevizing then it is an outside possibility that this could be produced at a yeast culture solution, causing 25-27% or larger amounts of greater longevity at an automatically produced beverage;
Also, what are 10HDA and 10H2DA metabolized into, characterizing those metabolites to find out if they have longevizing effects, different areas of tissue concentration, or completely different drug effects could have longevity technology value, notably there is: cytoplasm metabolism compared with liver metabolism, compared with circulatory system enzyme metabolism each with likely different metabolic products, all of which could be screened for novel higher longevity effects; noting that autophagy happens at the cytoplasm, the 10HDA and 10H2DA cytoplasm metabolites could be particularly likely to be longevity drugs
Royal jelly proteins like royalactin are at a thing I read, published as having a longevity effect, possibly on c elegans, that is different than, and (slightly) contributive to the 10HDA 10H2DA longevity increasing (18-46%) effect (another study possibly, 10-20%); another published paper used a protease to modify royalactin and then (I perceive) measured the effects of the protease treatment on the longevity effects from the modified royalactin, the protease modified royalactin was, to my perception, highly similar to the unmodified royalactin; That brings up doing other modifications to the royalactin protein molecule that could be screened as a library at 96 well plates and the organ9isms like fish and c elegans that I think could live at 96 well plates, aside from the published protease there are numerous ultraffordable enzymes like pepsin, trypsin, chymosin, a variety of others, and notably, vegetable powder treated with alkali tastes different, and to many, more delicious, so there is a range of durable on drying pH modifications to royalactin that could be screened; Also, it could be possible to coat, or react, the outer surface of the royalactin protein with something like an aldehyde that makes it differently reactive, less reactive (possibly more stomach passing), more durable, “rubberier”, online it mentions edible aldehydes, “The aldehyde used should be an edible aldehyde such as vanillin, anisaldehyde or butyraldehyde”; it is possible that like formaldehyde kind of rubberizes, dereactifies and preserves proteins, that the edible aldehydes modfiy royalactin to be stomach passing, enterically functional, as well as have different, quantifiable, longevity, wellness and healkthspan effects; just because the protein goes rubbery is different than it not working as well; screening these edible aldehyde modified royal jelly proteins as both enteric and even direct oral longevity drugs could be beneficial,
Along with liposomes and physiological availability enhancers like piperine, it is possible that gel blobs or easy to make edible jello might heighten absorption of beneficial chemicals and drugs; sodium alginate and calcium chloride combine (2 percent alginate to 98 percent water) to make a gel, it seems possible that there could be jellos, possibly nonprotein jellos, that are still gel at pH 3.5-7.9 that can be poured into a dish and eaten with a spoon, with delicious flavor, while making the drug dissolved in the jello much more physiologically available; this could have application globally as just making some jello might be kind of easy while being a way to distribute and cause to be medically active, a variety of drugs, possibly even antigens, immunizations, and protein or also peptide drugs; edible aldehyde modified protein drugs and antigens for immunization might still be medically functional even though preserved, strengthened, as well as made slightly rubbery with the edible aldhehyde;
A person online basically already thought of it, at fishfood, “A further option would be to include in the pellet mixture material which would effervesce” the recreational fish’ food could contain pH activated colorant that would only be hypervisible to the fish from ph 6.99 to 7, or 7.00 to 7.01, so would harmlessly become transparent at an aquarium, this would though provide a bunch of appetizing visual stimulation to the recreational fish that might then avidly seek and eat the delicious vegetarian or tissue culture based fishfood, I think nonvegetarian food sources are less ethical than vegetarian food sources, and I appreciate and prefer that milk and eggs might be produced with tissue culture technology as well; at humans I strongly support breastfeeding!
Vinyl is C2H3+, it seems like if there were a way to make really hyperaffordable vinyl cations out of either natural ethlene gas or even methane gas that making liquid fuels would be even thriftier;
I can see why a person would make a different, more ordered polymer on purpose and do something with it, but lignosulfates look like you could attach something to them and make a big dendritic chemical, like a catalyst, or a drug at hundreds or thousands or millions of kilogram quantities really fast, “Lignosulfonate have very broad ranges of molecular mass (they are very polydisperse). A range of from 1000–140,000 da has been reported” https://en.wikipedia.org/wiki/Lignosulfonates like, just thinking, if there is a an benzene cycle opener, and online it says there are, that can take apart the benzeneish thing at a lignosulphate then the molecule could do a bunch of new things, an anerobic benzene cycle opening bacterial chemical is published, and aerobic benzene cycle openers are also published, “Aerobic bacteria can break up aromatic rings with oxygenases in a reaction known as oxidative dearomatisation. Such reactions have an excellent thermodynamic, and oxygen atoms from the air are incorporated into the resulting products.”, other benzene cycle openers are also published, so if any of them are ultraffordable enough to use on lignosulphate then that supports the mass production of likely high utility chemicals
It is possible that a genetics of neuroanatomy could have a high numeric correlation with things that humans, that is persons, that is people, that is homo sapiens find preferable; one of these thigns is feeling good; it is possible the genetics of a 99th percentile largeness of size of hippocampus has a numerically predictive relation with the simultaneous experience of being of higher g (intelligence) than the majority of the population as well as feeling good, “The hippocampi of patients who suffer from depression are significantly smaller than those of healthy individuals [13]. This may be due to the decreased neurogenesis in depressed individuals, because hippocampal neurogenesis is reduced by stress [12] and increased by antidepressant treatment [14]. The parallel changes in BDNF levels and neurogenesis in response to stress and antidepressant treatment suggest a positive correlation between the BDNF level and hippocampal neurogenesis.”
Royal Jelly and 10HDA effect on subjective well being like behavior at mice: “RJ (250 mg/kg/day), HDEA (100 or 500 μg/kg/day), or fluvoxamine (1000 μg/kg/day), each dissolved in phosphate-buffered saline (PBS), was injected intraperitoneally into mice once a day for 21 days”
that is RJ 17.5 grams a day at a human, or with mouse compensation dosage, 1.46 grams a day
Also, that is 35000 ug per 24 hours of 10HDA, or about 1/3 of 100,000 ug, which is 100 mg, so about 35 mg of 10HDA per day, with mouse compensation dosage, 2.91 mg of 10HDA/24 hours, they call it HDEA though, at 6/100ths 10HDA per gram of royal jelly, that is only like 50mg of royal jelly lyophilized powder’s 10HDA,
Also, “Alternatively, RJ (2.5 g/kg/day) was orally administered” so that is 175 g of royal jelly per 24 hours at a 70kg human, although with the mouse compensation dosage it is about 14g/24 hours
Possible longevity lipid similar to 10HDA at royal jelly, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3143448/ “Previously we found that medium-chain fatty acids with 8–12 carbons and their esters facilitate the activation (phosphorylation) of ERK 1/2 of cultured embryonic cortical/hippocampal neurons [33].” From what I perceive, they are making 8-12 C lipids with some =O on them, kind of like 10HDA, and noting they have the ability to cause neural actions; further, “ In particular, trans-2-decenoic acid ethyl ester (DAEE) has the most potent activity.”, alsdo, “DAEE increases the expression of mRNAs of BDNF and neurotrophin-3 and the protein content of synapse-specific proteins such as synaptophysin, synapsin-1, and syntaxin”, DAEE as an ethyl ester decanoic acid is kind of like a alternate lipid version of 10HDA notably an ethyl ester; this DAEE chemical could be quantified to find out if it makes mice live longer as the people that wrote the paper note it has the highest neurobeneficial activity; notably they call DAEE “trans-2-decenoic acid ethyl ester” which reminds me of a trans-fatty acid, a chemically constructed trans fat, notably trans fats do not occur naturally, so DAEE has a greater rigidity at the “2” area than a natural decanoic acid, suggesting they (the authors) made a rigid trans fat on purpose as part of creating a more effective molecule, a better than royal jelly lipid lipid, on purpose
Also, at another study with DAEE, “DAEE-treatment (100 μg/kg body weight injected at 0.5, 24, 48, 72 h after PMCAO (a mouse model of the cerebral infarction caused by unilateral permanent middle cerebral artery occlusion (PMCAO)) significantly restored the mice from PMCAO-induced neurological deficits including motor paralysis”, “These results suggest that DAEE has a neuro-protective effect on cerebral infarction”
an image of DAEE: 
suggests that a 70kg mammal dose at 100ug/Kg is 7000ug, or about 7 milligrams at a 70 Kg mammal, notably with mouse compensation factor, a human dose of DAEE is just .583 mg per 70 Kg human, they utilized four after event dosages, so either 28 milligrams or about 2.4 milligrams
also, “we developed trans-2-decenoic acid ethyl ester (DAEE) as a stable and small molecule with BDNF-like activities.” that suggests a modification to DAEE with a blood brain barrier passing moiety, connected with an enzymatically degradeable linker or an active transport moeity could pass the blood brain barrier hundreds or thousands of times more, benefitting well brain function , also DAEE, or a modification might be simultaneously enjoyable and physiologically beneficial, “DAEE behaved like an anxiolytic and ameliorated this characteristic anxiety-like symptom, suggesting that DAEE may be a promising candidate for a novel anxiolytic” Notably as DAEE is similar to 10HDA of royal jelly, and royal jelly causes 25/27% greater mouse longevity, DAEE, possibly depending on what part of the brain it goes to, could be a fun (anxiolytic), cognitively beneficial (BDNF) drug that also creates greater longevity https://www.ncbi.nlm.nih.gov/pubmed/24190238
Some outside of liposome is molecularly active liposomes pass the blood brain barrier, perhaps DAEE could be localized at particular brain areas and transported in larger, oral, amounts with liposomes that have active surface moieties
They made modifications to DAEE that caused greater activity, it is possible making these same modifications tot he 10HDA (and 10H2DA) at royal jelly could cause royal jelly lipids that create even greater longevity increases: https://bpspubs.onlinelibrary.wiley.com/doi/full/10.1002/prp2.132 “we investigated the protective effect of the ester, thioester, and amide compounds of 2‐decenoic acid derivatives (termed compounds A, B, and C, respectively). The potency of the protective activity against the CORT‐induced depression‐like or anxiety‐like behaviors and the reduction in pERK1/2 level were found to be in the following order: compound B > compound C > compound A.”, also, “treatment with compound B at either 0.3 or 1.5 mg/kg” So it is possible that a thioester or amide of 10HDA could have a greater well being and longevity effect than 10HDA; these are beneficial possible longevity drugs to quantify, also at humans this is a 105 mg/24 hours thioester of deacnoic acid dose, or utilizing mouse compensation factor a 8.3 mg/24 hour human dose;
“Earlier we found that (E)‐2‐ethyl dec‐2‐enoate (trans‐2‐decenoic acid ethyl ester: DAEE” also, based on this: it is possible that a durablized version could actually be a deuterated, mre gradually moving, thus possibly less reactive version, as well as the possibility that a nanosphere or liposome version could omit reacting with all the parts of the body other than the part it was directed to be at, “However, a serious problem has been that the biological activities of DAEE are unstable and influenced by the lot preparation used in experiments (Furukawa S., Iinuma M., Soumiya H., Fukumitsu H. and Furukawa Y. unpubl. results). A primary reason for this instability is thought to be the easy hydrolysis of the ester bond because DAEE has five times higher activity for increasing pERK1/2 levels in vitro than trans‐2‐decenoic acid, the nonester form of DAEE (Hirakawa et al. 2010). DAEE is thought to be a promising lead compound for development of new drugs for treatment of mood disorders; however, it is not considered to be a goal compound.”
Note: I think I saw that there was an April 2019 patent on some variation of DAEE like possibly a thioester, I am really enthused that something that could be a quantitatively mesurable as effective longevity drug might soon be a developed drug;
Nifty thioester as well as amide versions of DAEE, as molecular diagrams, which is kind of like 10HDA at https://bpspubs.onlinelibrary.wiley.com/doi/full/10.1002/prp2.132
Note: amazingly, you can just order DAEE online: “Chemical structures of compounds A, B, and C are indicated in Figure 1, as is the structure of (DAEE). DAEE was purchased from Sigma‐Aldrich (St. Louis, MO).”
viewing the images at the paper the thioester and the amide versions of DAEE, although very diferent as molecules are very similar as to anti-stress anxiolytic effect; notably over 14-21 days, at .3 to 1.5 mg/Kg the thioester version of DAEE caused an absence of anxious behavior similar to that of mice who were absent being made anxious
“Healthy animals were not used in the experiments to evaluate the activities of the compounds because (1) 2‐decenoic acid derivatives, which have structures and activities similar to those of compound B, were earlier shown not to affect healthy mice in terms of their depressive or anxious state or level of phosphorylated ERK1/2 in the hippocampus” this could possibly suggest that DAEE as well as things like thioester and amide versions, is absent notable personality modifying effects on well normal mammals, a thing that could be beneficial to some humans; “Each compound (A, B, or C) was orally administered to the mice once a day at a dose of 0.3 or 1.5 mg/kg through a stomach tube.”
A new longevity technology: There are a few ways to think about what they describe, one is that they have located a brain cytoprotein that could be meaningful thoroughout the body, and contribute to longevity effects, like those published about royal jelly, and likely 10HDA; this would be a new longevity protein, and upregulating it, making more of it, creating new longevity genetics with it, finding beneficial SNPs about it, or optimizing gene copy number variations about it could be a new longevity technology; the other possibility is that their decanoic acid thioester DAEE just happens to be anxiolytic, and their protein is just a stress removing thing, “How did 2‐decenoic acid derivatives, including compound B, generate a BDNF‐like signal? Earlier we observed that one of the active 2‐decenoic acid derivatives, DAEE, started increasing the level of phosphorylated ERK1/2 at 15 min after the addition and attained the maximal value at the 2‐h time point when tested on cultured cortical/hippocampal neurons (Makino et al. 2010). Such a gradual increase in activation is unlikely to indicate molecular kinetics produced by a specific interaction between ligand and its specific receptor. We presume that the active compound was incorporated passively into the lipid bilayer of neurons and then interacted with and activated some “protein X” in the neurons. This activated protein X may then have mediated the phosphorylation of particular tyrosine kinases of high‐affinity neurotrophin receptors such as TrkB and TrkC. We have found a candidate of protein X predominantly expressed in neuronal cells and are currently investigating its involvement in the DAEE‐mediated mechanism of actions.”; what the authors think is the protein of action, could also be a new to me longevity gene protein mechanism
Also, there is a patent on DAEE variations: The trans-2-decenoic acid derivative or a pharmaceutically acceptable salt, which is the compound of the present invention, is specifically represented by the general formula (I):

wherein X is a substituent such as a 1-pyrrolidyl, a 3-thiazolizyl, or a piperidino, and the compound is highly useful as a pharmaceutical agent, such as a prophylactic or therapeutic agent for a peripheral nerve disorder https://patents.google.com/patent/US9428477B2/en
when they say “erk1/2”, “mitogen-activated protein kinases (MAPK)/extracellular signal-regulated kinases (ERK)1/2 [29]. Activated ERK1/2 then passes into the nucleus to activate transcription factors such as cAMP response element binding protein (CREB), leading to regulation of expression of various genes involved in neuronal differentiation, learning, and memory”
In that study we found that (1) DAEE stimulates phosphorylation of ERK1/2 via MEK activation; (2) DAEE activates CREB predominantly through ERK1/2 activation, not through other pathways such as cAMP/protein kinase A; (3) DAEE increases the expression of mRNAs of BDNF and neurotrophin-3 and the protein content of synapse-specific proteins such as synaptophysin, synapsin-1, and syntaxin [33]. From these observations, HDEA was considered to activate ERK1/2 followed by CREB phosphorylation, which might be a common target of BDNF and antidepressants to improve symptoms
Longevity technology: varieties of 10HDA like that at longevizing royal jelly that have 8 or could have 9 C instead, “honeybees (Apis mellifera L.) produce a caste-related blend of functionalized 8-and 10-carbon fatty acids in their mandibular glands”, also, “the resulting 10-carbon hydroxy acids are oxidized in a caste-selective manner, thereby determining many of the functional differences”, so the 8 C versions could possibly have different =O (esters) as well as different -OH locations, these could be tested as to longevity effects on c elegans and vertebrate fish at 96 well plates, then be longevity tested at mice as C8, and also a novel C9 version of the particular versions of the different than 10HDA mandibular gland products bees produce; this could be a few more possible beneficial longevity molecules to screen
Source of a decanoic acid that is bacterial: cis-2-Decenoic acid is a fatty acid made by Pseudomonas aeruginosa. It looks a lot like 10HDA, and makes me think that a slight mutation and winnowing of pseudomonas aeruginosa could produce lots of 10HDA or a variety of other possibly longevizing decanoic acid physiochemicals https://en.wikipedia.org/wiki/Cis-2-Decenoic_acid; also, genetically engineering mammals to produce their own 10DHA or a more effective longevity chemical is a new kind of longevity gene, a modification of C2DA production genetics from P. aeruginosa could be a new longevity chemical producing gene at a variety of organisms and even plants so all those organisms and humans benefit; also, it is possibly a slight variation on this gene could produce the BDNF activity-like, possibly longevizing, 2.9 mg/70Kg human dose DAEE decanoic acid that causes calmness, more effective healing, and exploratory behavior among mice
Longevity drug: Different species of bees make different versions of things like royal jelly, and likely different species of bees have different queen longevity ratios, that suggests there is a longest queen lifespan bee, and she might eat a form of the longest lifespan producing royal jelly; some other bee species and their chemicals are at pherobase, http://www.pherobase.com/database/genus/genus-Apis.php?isvalid=yes
Another decanoic-acid (10HDA) like fatty acid that it could be beneficial to screen for longevity effects is “9-oxo-2-decenoic acid (9ODA), as well as cis- and trans-9-hydroxydec-2-enoic acid (9HDA) Queen bees make 9ODA and it “9ODA specifically leads to changes in the endocrine organs”, so it could have various other effects as well; find out what c elegans lifespan response to cis and trans 9ODA is
A different decanoic acid, that could also be screened for longevity effects is an antimicrobial, “A recently developed biofilm inhibitor, cis-2-decenoic acid (C2DA)” if C2DA is like an order of magnitude or two more antimicrobial than 10HDA, “C2DA at concentrations of 500 μg/mL and above inhibited growth, while 125 μg/mL C2DA inhibited biofilm. Combination with antibiotics increased these effects. At concentrations up to 500 μg/mL, there were no cytotoxic effects on fibroblasts.”
it is possible it has other characteristics as well, and screening it for longevity effects at c elegans could be beneficial
a 12 C fatty acid, that looks kind of like 10HDA that could be screened for longevity effects is : “cis-2-decenoic acid appears to be functionally and structurally related to the class of short-chain fatty acid signaling molecules such as diffusible signal factor which act as cell-to-cell communication molecules in bacteria and fungi.”, “characterized a substituted fatty acid messenger, cis-11-methyl-2-dodecenoic acid, called diffusible signal factor (DSF)”
also, “Treatments consisted of spent medium, CSM, cis-2-decenoic acid, trans-2-decenoic acid, decanoic acid, and DSF at various concentrations.”, “cis isomer of 2-decenoic acid was the organic compound” [that caused biofilms to disperse], “The compounds with the highest activity were two isomers of 2-decenoic acid. The trans isomer (trans-2-decenoic acid) was shown by microtiter plate dispersion bioassay to have activity only at millimolar concentrations, typically not low enough to qualify as a cell-cell signaling molecule. Figure Figure5B5B shows the dispersion activity of increasing concentrations of cis-2-decenoic acid against biofilm cultures of P. aeruginosa grown in microtiter plates. These results demonstrated that the cis isomer (cis-2-decenoic acid) was active over a concentration range from 1.0 nM to 10 mM”
There is some perspective here where a decanoic acid, of a slight variation (cis rather than trans) is like an actual 1 million times more effective (nanomoles compared with millimoles)at causing bacterial biofilms to detach; so that brings up the possibility, noting that DAEE causes greater happiness, better healing, and other benefits at 2.9 mg/70Kg/24 hour human, that there could be a a 10HDA version that has longevity effects at a couple orders of magnitude fewer atoms per dose, or, beneficially, has a longevity effect ten times larger than 27% (10HDA at mice), notably salicylic acid causes yeast to live more than 400% longer, so this could be possible; among organisms, a 720 minute longevity bug, compared with a half century duration termite queen is a a 36,500 times longevity difference, and at mammals, a yearlong rodent compared with a 211 year whale is a 21100% longevity difference; The antarctic sponge has a lifespan of 15550 years or longer;
longevity technology: 10HDA at royal jelly is published as an HDACinhibitor, causing acetylation which velocitizes and causes DNA transcription at histones, I perceive I read a variety of HDACinhibitors have longevity and wellness effects, So, as a beneficial complementary thing to making a bunch of 10HDA (or 10H2DA) molecular variants and then screening them to find out if they cause greater longevity at yeast, c elegans and 96 well plate vertebrate fish, and mammals, they could make a bunch of molecular variants of 10HDA that could be and quantified as to their effectiveness as HDAC inhibitors, and noted as to their dose (mcg/ng) effectiveness at causing HDAC inhibition at a variety of HDACs and effectiveness at histones at cytostructures of a variety of species, including humans, This gives all kinds of new molecular modification possibilities of being effective: 10HDA dimers, halogenated 10HDA, 10HDA linked to a nuclear membrane transport peptide, 10HDA with a butyrate (or propynate) attached to it, or a valproate, basically any HDAC inhibitor molecule partially modified to have a 10HDA on it, As a molecular library to screen, come up with a few hundred 10HDA variations all of which have a possibility of being a better, faster, stronger, more reaching of tissues that 10DHA might not usually reach HDAC inhibitor, then screen the library of those hundreds of 10HDA molecule variants, with things like multiwell plates with yeast, also c elegans can be used to quantify better faster stronger HDACinhibiting effects; Then at humans these versions might also cause greater longevity at few mg or ug/dose
A version of 10HDA that is a better longevizing drug, and that also causes greater intelligence: I read, Intelligence gene, “Enhancement of memory formation is increased in mice given vorinostat, or by genetic knockout of the HDAC2 gene in mice” That suggests that a modification of 10HDA to be a HDAC2 inhibitor would cause greater intelligence at mammals like humans, so coming up with a library of 10HDA variants, and then screening them to find a version that is HDAC2 inhibiting produces a longevity drug that makes humans more intelligent; One way to make a 10HDA that inhibits HDAC2 is to modify the HDAC inhibitor molecule vornistat, SAHA, which is kind of long and looks sort of like 10HDA, to be sort of in between 10HDA and SAHA, then screen the variants, perhaps a million generated microfluidically at a one million channel published microfluidic thing I read about, to find vornistat 10HDA variants that cause C elegans to live longer from 10HDAlikeness while also causing greater intelligence from SAHAness; Noting you can have the one million channel microfluidic go along with a one million well plate (like integrated circuit technology multimillion well plates) or even a 10 million yeast cyte per second flow cytometry analyzer, you can see which of the 1 million library variants causes yeast to live the very longest, then among the top .01% of vornistat/SAHA/10 HDA variants at causing greatest yeast longevity then screen those 100 most yeast longevizing library variants with c elegans at multiwell plates to find the top 3 to quantify and screen as to their effect on longevizing mice, and then humans; that produces a longevity drug that causes greater intelligence
Also a SAHA/vornistat like 10DHAlike HDAC2inhibitor has another longevity heightening molecular possibility, an NIA study found that the nonfeminizing estrogen alpha-estradiol caused greater longevity (11%?), and wikipedia says, “estrogen receptor alpha (ERalpha) can be hyperacetylated in response to histone deacetylase inhibition” that suggests an HDACinhibitor could possibly make estrogen receptor alpha really ultra extra responsive, and if it is, then it is possible it’s longevity increasing effect is more often spontaneously functionally activated to cause greater longevity, and that would move 10HDA to 10HDA with alpha-estrogen activator, from 25/27% (mice) as well as 18/46% (c elegans) to 36/38% (mice) as well as 29/57% c elegans with the 11% longevity heightening
Another longevity version of a HDAC2inhibitor that causes humans to be more intelligent while heightening longevity is to modify the HDAC tetrapeptide to be a different peptide; the peptide epithalon (AEDG) as well as the peptide thymosin, when given to a human simultaneously, makes the person four times less likely to be dead after 6 years, so, just make a different shape, branch, or peptide loop (trefoil?) with the HDAC2inhibitor being the tetrapeptide HDACinhibitor, and the other branches, or possibly they could function with modification as loops, being epithalon (AEDG) and thymosin. It makes you smarter, it keeps you from being dead, and, if it causes alpha estrogen receptor acetylation hyperresponsiveness (from HDAC inhibition) it increases longevity
longevity technology: 10HDA at royal jelly is published as an HDACinhibitor, causing acetylation which velocitizes and causes DNA transcription at histones, I perceive I read a variety of HDACinhibitors have longevity and wellness effects, So, as a beneficial complementary thing to making a bunch of 10HDA (or 10H2DA) molecular variants and then screening them to find out if they cause greater longevity at yeast, c elegans and 96 well plate vertebrate fish, and mammals, they could make a bunch of molecular variants of 10HDA that could be and quantified as to their effectiveness as HDAC inhibitors, and noted as to their dose (mcg/ng) effectiveness at causing HDAC inhibition at a variety of HDACs and effectiveness at histones at cytostructures of a variety of species, including humans, This gives all kinds of new molecular modification possibilities of being effective: 10HDA dimers, halogenated 10HDA, 10HDA linked to a nuclear membrane transport peptide, 10HDA with a butyrate (or propynate) attached to it, or a valproate, basically any HDAC inhibitor molecule partially modified to have a 10HDA on it, As a molecular library to screen, come up with a few hundred 10HDA variations all of which have a possibility of being a better, faster, stronger, more reaching of tissues that 10DHA might not usually reach HDAC inhibitor, then screen the library of those hundreds of 10HDA molecule variants, with things like multiwell plates with yeast, also c elegans can be used to quantify better faster stronger HDACinhibiting effects; Then at humans these versions might also cause greater longevity at few mg or ug/dose
A version of 10HDA that is a better longevizing drug, and that also causes greater intelligence: I read, Intelligence gene, “Enhancement of memory formation is increased in mice given vorinostat, or by genetic knockout of the HDAC2 gene in mice” That suggests that a modification of 10HDA to be a HDAC2 inhibitor would cause greater intelligence at mammals like humans, so coming up with a library of 10HDA variants, and then screening them to find a version that is HDAC2 inhibiting produces a longevity drug that makes humans more intelligent; One way to make a 10HDA that inhibits HDAC2 is to modify the HDAC inhibitor molecule vornistat, SAHA, which is kind of long and looks sort of like 10HDA, to be sort of in between 10HDA and SAHA, then screen the variants, perhaps a million generated microfluidically at a one million channel published microfluidic thing I read about, to find vornistat 10HDA variants that cause C elegans to live longer from 10HDAlikeness while also causing greater intelligence from SAHAness; Noting you can have the one million channel microfluidic go along with a one million well plate (like integrated circuit technology multimillion well plates) or even a 10 million yeast cyte per second flow cytometry analyzer, you can see which of the 1 million library variants causes yeast to live the very longest, then among the top .01% of vornistat/SAHA/10 HDA variants at causing greatest yeast longevity then screen those 100 most yeast longevizing library variants with c elegans at multiwell plates to find the top 3 to quantify and screen as to their effect on longevizing mice, and then humans; that produces a longevity drug that causes greater intelligence
Also a SAHA like 10DHAlike HDAC2inhibitor has another longevity heightening molecular possibility, an NIA study found that the nonfeminizing estrogen alpha-estradiol caused greater longevity (11%?), and wikipedia says, “estrogen receptor alpha (ERalpha) can be hyperacetylated in response to histone deacetylase inhibition” that suggests an HDACinhibitor could possibly make estrogen receptor alpha really ultra extra responsive, and if it is, then it is possible it’s longevity increasing effect is more often spontaneously functionally activated to cause greater longevity, and that would move 10HDA to 10HDA, alpha-estrogen activator, from 25/27% (mice) as well as 18/46% (c elegans) to 36/38% (mice) as well as 29/57% c elegans with the 11% heightening
Another longevity version of a HDAC2inhibitor that causes humans to be more intelligent while heightening longevity is to modify the HDAC tetrapeptide to be a different peptide; the peptide epithalon (AEDG) as well as the peptide thymosin, when given to a human simultaneously, makes the person four times less likely to be dead after 6 years, so, just make a different shape, branch, or peptide loop (trefoil?) with the HDAC2inhibitor being the tetrapeptide HDACinhibitor, and the other branches, or possibly they could function with modification as loops, being epithalon (AEDG) and thymosin. It makes you smarter, it keeps you from being dead!, and, if it causes alpha estrogen receptor acetylation hyperresponsiveness (from HDAC inhibition) it could heighten longevity
They could blenderize endoliths, which wikipedia says are microorganisms with million year lifespans and 10,000 year cytodivision cycles, and feed them to mice coated with an enteric coating, they could also see they effect on c elegans, as well as amoeba, pa aeurosomethign (a bacteria that makes that has T2DA and C2DA decenoic esters); also wikipedia says, “Some Actinobacteria found in Siberia are estimated to be half a million years old.”
It is possible a plasticizer, like replacements for 2019 bisphenols could be esterified decnoic acids, possibly with a few esters, or possibly cyclic; basically they could do tests and find out if a plasticizer for industry could be found tht actuallu casues greater longevity at mice, and thus might be harmless or beneficial to humans
when they make vehicle fuel out of used food oil it is often a fatty acid ester, perhaps there is a fatty acid ester, utilizable as a motor fuel, that causes mammals to live longer the way 10HDA and 10H2DA at royal jelly make C elegans and mice live longer, then rahter than “smog” being deleterious to health a .01% or near that unreacted fatty acid ester could cause a longevizing effect at mammals that breathed trace amounts
Computational methods of finding active drugs and chemicals, “he estimates CPU costs of only a thousand dollars or so for half a billion molecules, although I think that’s too low), “, “assume an average of 25 heavy atoms for your molecules, so 50 atoms in total, so 150 coordinates per conformer, times 100 confs per molecule[*], and you’re looking at north of 30TB of data: that’s doable, but the storage costs are going to be significantly more than your CPU costs. If your virtual library is 10 billion molecules, now you’re looking at 600TB of data” https://blogs.sciencemag.org/pipeline/archives/2018/09/06/virtual-compound-screening-the-state-of-the-art
Another cancer drug that might be a longevity drug is bryostatin, it has a 8-9 Carbon partially unsaturated alkane (a couple C=C) with esterification there, but then that part which is a lot like 10H2DA (of royal jelly longevity), is connected to a bunch of other atoms at a big anticancer molecule; so if a person purposefully attached an esterified decanoic acid (like 10H2DA, 10HDA, 90DA, HAEE, or a more effective longevity increasing molecule) to a rapamycin molecule it might be much more effective, but bryostatin might already have longevity functionality now. Beneficial to screen bryostatin molecule for longevity
It is 2019 AD, wikipedia says, “In March 2010, research was published demonstrating an HTS”, high throughput screening, “process allowing 1,000 times faster screening (100 million reactions in 10 hours) at 1-millionth the cost (using 10−7 times the reagent volume) than conventional techniques using drop-based microfluidics.[22] Drops of fluid separated by oil replace microplate wells and allow analysis and hit sorting while reagents are flowing through channels.
In 2010, researchers developed a silicon sheet of lenses that can be placed over microfluidic arrays to allow the fluorescence measurement of 64 different output channels simultaneously with a single camera.[23] This process can analyze 200,000 drops per second.
Whereby traditional HTS drug discovery uses purified proteins or intact cells, very interesting recent development of the technology is associated with the use of intact living organisms, like the nematode Caenorhabditis elegans and zebrafish (Danio rerio).[24]
one system that could be improved uses mass spectroscopy to screen 2 million molecules in 10 days,
wikipedia says, “we substantially enhance screening throughput by enabling growth and analysis of 6144 mutant yeast colonies on a single agar plate. The significance of achieving this number is that the vast majority of microbial model organisms have gene counts very near but not exceeding this number, allowing for an entire, genome-wide screen to be performed on a single agar plate.”
That suggests that 20k human genes fits on 3 (2014 AD) plates, or if it quadrupled (2019), to one 24K colony plate
multiwell systems sometimes have a wash stage, perhaps the chronological interval of this could be decreased with ultrasonic transducers at the washing fluid emitter, one system I read about that could do 2 million measurments in 10 days had a wash cycle
New longevity genes:
They could mutate a bunch of yeast, knoocking out genes, notably 6K genes at microorganisms and 20K at a mammal, find which out of a million (parallel measurement of duplicate knock outs) omit living longer with a longevity drug, then sequence their genomes to find the missing gene, then look for SNPs or copy number variations of that gene at living organisms with the gene that then cause greater susceptibility and effectiveness of the longevity chemical, then transfer the gene to mice and human tissue culture, see if it is possible to make mice that live 80-200% longer from rapamycin treatment (up from 60%) this way, or 79 to 140% longer from royal jelly ingredients (25/27% longer), possibly decanoic acid esters like 10HDA and 10H2DA, or 14 to 105% longer from metformin (up from 3-35% longer lifespan); notably if these genes are completely new to being investigated it is possible that rather than using already researched mechanisms they might utilize new mechanisms that favor the effectiveness of numerous longevity molecules and drugs that do not, or do not yet, have published mechanisms of action; so, finding these genes, optimizing SNPs or making new gene nucleotide sequences, as well as changing copy number, could make an organism much more susceptible to a wide range “any” new longevity drugs and chemicals being characterized;
It is imaginable that a gene that causes double or halved diameter or quantity of nuclear membrane pores could have effects on anything that gets transcribed, also it is possible to imagine that, noting autophagy happens at numerous, different receptor-differing longevity drug effects, that something that makes autophagy 2,4, 8, 16, 32 times more likely to occur at the presence of some cytochemical (a new, or, SNP optimized, copy number optimized, variant of the “autophagy turn-on protein that is much more active at what previously would be traces of chemical that were less than autophagy causing, that now cause autophagy even from 1/16 or 1/32nd amounts) could be the result of enriching the amount or activity of a gene, which if deleted at a yeast, happened to make a sluggish version of an autophagy turn on gene (that required much more endogenous cytochemical to turn autophagy on); so, 180 degrees different than the nonresponsive version, the new gene, optimized SNP, or most beneficial copy number would cause greater susceptibility to longevity drugs of numerous kinds, receptors, and mechanisms, including new mechanisms without any previous research as well as new drugs;
Finding the genetics of unusually high, hyperresponsiveness to longevity producing drugs and chemicals also brings up the possibility of making laboratory model organisms that are 2, 4, 8, 16, 32 times more responsive to new longevity chemicals and drugs that are possibly being screened as libraries; There is a difference between this and just a genetic variation that causes dose susceptibility; say an unengineered typical mouse registers a mild 7% longevity increase from smelling the odors of young mice of a sex they can have progeny with, if the gene-response heightened mouse registers a 23% longevity increase then this might suggest that, once the mouse’s nasal receptors got turned on, regardless of the dose above a threshold, the neurons connected to something, or did something that caused 2,4,8,16 times bigger diameter nuclear membrane pores to get utilized, or some neural acivity, which might just barely modify autophagy, is now of sufficient size to cause longevity producing amounts of autophagy, this effect even when the actual dose of the scent is either midrange, or perhaps engineered to be at highest amplitude respponse at nasal neurons already.
Laboratory organisms with heightened amplitude of response to longevity chemicals and drugs could create higher prominence (statistically resolvable effectiveness) of new and effective and developable longevity drugs and chemicals at mass screening,
Another example could be a “cyclomolecule transport channel active transport gene”; basically this might be a gene that specifies active transport of anything with a cyclic part (benzene, cycloanything) at its molecule, that is kind of a gene for: really likes to transport most few amu drugs directly to the cytoplasm, a yeast without that gene might be unresponsive to many many pharmaceuticals, but a yeast with optimized SNPs, new nucleotides at a new “cylomolecule active transport gene”, or a higher copy number of that gene, might be 2-10 times more responsive to any drug added to its medium, the cyclomolecule transport gene is sort of near a dose responsiveness gene though;
One possibility to make more illness more rapidly curable, at a wider variety of treatable tissues, possibly including treating, preventing or curing cancers, is to do gene therapy that puts: 2,4,8,16,32, or even 1000 times more active transport of anything with a cyclic area at its molecule to the cytoplasm gene,
It is also possible that some kind of loclization could be utilized to localize the gene therapy at a particular tissue or oncocyte area; that way a person could take a longevizing dose of rapamycin, while at any oncocytes, that the cyclomolecule active transport gene therapy had localization at, the rapamycin dose would be 32-1000 times higher and block or terminate any oncocytes.
it is possible that a new, existing, or optimized cyclomolecule active transport gene could be used to treat or prevent malaria, On finding a cycle-having molecule transport gene, a technologist would think of RNA and DNA drugs, as well as peptides and function-causing nestles-together at sockets protein drugs and few AMU molecule drugs to cause the “make more cyclomolecule transport channels” gene to be more active, or also to cause the already there amount of cyclocontaining molecule drug transporter channels to heighten their activity, or possibly also modify their specificity to transport more kinds of molecules; There might be something like a drug, mRNA, siRNA, other RNA or DNA drug, peptide, or even harmless, existing, nonengineered bacteria or virus, that causes the active transport at the external cell membrane of of cyclic area (like benzenes or various partially saturated on nonsaturated cyclothings) containing molecules to heighten, if there is then it could be coadministered with malaria medication, or perhaps any medication containing a cycloarea at its molecule, to create much stronger response per microgram of dosage; that could make malaria medication a few orders of magnitude more affordable from a raw chemical ingredient perspective,
It is possible that a kind of chemical, drug, or gene therapy, or bacteria specific RNA/DNA drug could cuase bacteria to actively transport cyclic structure area containing molecules 2, 4, 8, 16, 32, even 1000 times more actively, that could cause the bacteria of focus to be more likely to transport a greater amount of antibacterials (antibiotics) curing bacterial infections; I do not know if this would make it so that 1) amplified active transport of cyclocontaining molecules at bacteria of focus simultaneous with 2) antibacterial, antibiotic doses that are 16, 32, or even 1000 times fewer migrograms/picograms/ml would make it so the bacteria of focus transported much more antibiotic, was terminated and the person cured while, beneficially, exposing body organisms like other bacteria, to only 1/16 or 1/32nd or even 1/1000 of the actual quantity of migrograms or nanograms of antibacterial or antibiotic; keeping that vast number of different nonfocus bacteria from developing antibiotic resistance; it might be effective, and at things like milk cows and egg chickens, could make it so that illnesses that affect these could be mass treated, as they are during 2019, with the 1/16, 1/32, or even 1/1000th 2019 dose of antibiotics, simultaneously reducing antibiotic resistance development at all of the other bacteria at the organism, and making the actual medication affordability 1-3 orders of magnitude more affordable
Modifying active transport with drugs, chemicals, genetics, or possibly RNA/DNA/peptide drugs could cause immunizations to be more effective, perhaps a version that did 2,4,8,16,32 or 1000 times more active transport, possibly with transcytosis, to anything, even a many-AMU molecule like an actual antibody would cause heightened effectiveness as well as new therepeutic technologies, like: antibodies doing things at the cytoplasm; what happens to an antibody at the actual cell cytoplasm? Does it just sit there in jello? Can it glom entirely new things floating around, causing entirely new, beneficial medical effects? (cytoplasm reaching antibodies could glom deleterious versions of nonfuncting mitochondria, and some petides or proteins festooning the at-cytoplasm antibody could communicate to lysosomes, “engulf this nonfunctional organelle (unuseful mitochondria)”; antibodies that glom onto a lysome, noting I read antibodies, at a different thing, cytoexterior, can cause a receptor to activate or passivate as the technology makign person prefers, suggests that at-cytoplasm antibodies could make lysosomes much more likely to recycle cytocomponents causing autophagy to increase, that creates a new longevity drug based on a one-dose administration of an antigen to produce the antibodies); As a brain and CNS funcion heightening and longevity and young phenotype supporting and increasing technology it is possible that glia, which move around, and benefit the brain, and are descended from innunocytes, could, using a drug, chemical, RNA or DNA drug, gene therapy or germline gene modification have their active transport heightened for drugs, chemicals, molecules, peptides, RNA or DNA drugs with particular moeities, perhaps easy to make, but rarerly endogenously produced at the body moeities, that cause the glia to do things that are particularly longevizing of CNS brain function, brain CNS capability increasing, and shielding of the CNS brain from anything deleterious at the neurons that glia support and travel around through;
Screening a library of 10 to 100 million or even a billion molecular variants and peptides with a 10 million cells/second flow cytometer could be a 10 second to 100 second (or, with parallel simultaneous dosing of 10 cells per chemical, 20 minute) way to find out which molecules and chemicals and drugs cause changes at various kinds of active transport and cytotransport at cells; Once found these chemicals could be enhanced, diversified, and the new library screened; That creates the drugs and chemicals that cause the physiologically beneficial, medically beneficial, capability enhancing, as well as longevity, wellness, and healthspan heightening new drugs at cytoplasm effects
Also, I do not know, but it looks like at cell cytoplasm sized structures, even though pershaps the cells are terminated, antibodies can glom to cytoplasm sized things, even though I think of antibodies as being many-AMU protein things
This thing says that when you change the nucleus of just one cell, the cells ner it change as well, it calls this “they bystander effect”; are there physiologically beneficial, longevizing, wellness and healthspan heightening bystander effect technologies, if, as it says, the bystander effect exists?
“the nucleus is the target for genotoxic and cytotoxic effects. Reports on the “Bystander Effect” indicate that DNA damage can be caused in cells not directly traversed. Objective: use microbeam to selectively irradiate cytoplasm to determine if there are effects on survival or mutation frequency. The Columbia microbeam produces alpha particles of 5.5 MeV, range ~40 μm, LET = 90 keV/μm. Irradiation of each cell takes about 6 seconds. All cells on the dish irradiated, then trypsinized, removed and plated for either survival or mutation analysis. Mutation assay is the AL hamster line with one human chromosome. Human chromosome expresses cell surface antigens that make cells susceptible to complement inactivation. Wild-type cells are killed in the presence of antibody and complement Cells with mutations in this gene can survive.”
are there plenums (separation structures) of some kind that divide bystander effect areas from each other, I do not actually have any idea, but I perceive that if I get a beautification chemical peel, it is absent effect on my vagus nerve, what are the plenum forms, sizes, lengths, genetics and physiochemistry of the bystander effect; is more bystander effect beneficial, is less of it beneficial, are there human genes, SNPs as well as copy number variants that cause, noting the 100% difference among normal humans at some attributes (IQ 200, age at first ovulation, height) it is possible some humans have double or half the bystander effect, among these which have greater longevity, wellness, healthspan, subjectivbe well being (happiness) and benevolence?
Body and other Fluid technology: antibodies can glom to things the size of, I perceive I read, three nucleotides (like 10 or more non hydrogen atoms per adenine, so 30 non hydrogen atoms at a shape), and I do not know how many metal atoms to make a glommable thing, but antibodies can react to metals like cobalt, so an antibody might actually be able to change shape around 1 metal atom, although, noting three nucleotides, it is also possible it is 30-300 atoms at a multiatom cobalt particle, that suggests it is possible to make an antibody that, without full glomming, although it could also fully glom, a particle at a fluid environment could get the entire antibody protein to change shape and charge; on glomming, the glider’s hydrodynamic wing position could change, I suppose I might have heard of one atom changing the conformation and entire quaternary and tertiary structure of a protein, but it seems like it might be possible to make like an antibody glider (like an actual shape) that has wings that change their positioning based on sensing one atom, or a few hundred; that could cause an ingredient (antibody gliders in solution) that when placed at a fluid would make the fluid’s containerful effect flowability, even things like physical directionality, a kind of chirality, and 3d spatially specifiable adjustable things, possibly as macroscopic as light polarization-size molecules, and even tetris-piece (or fittable modules) accumulations at various areas of fluid velocity, specifiable and even algorithmically directable (from some perspectives programmable, also automata-directable); antibodies are $435/gram online; This reminds me of nanoassembly, and one thing to think about is where does the energy to change glider wing postition based on 1 atom (or a few hundred come from); ATP is the 20th century reply, but there are a number of triphosphate molecules that might be able to bring conformation-modifying energy to proteins, notablyproteins that have previous biogenic energy circuits, UTP, GTP are a couple, but it seems possible that with modelling a new nucleotide, and a bunch more phosphates at a polyphosphate, could make something like a UTP, GTP polymer with like 30 to 300 phosphates on it, which is a couple orders of magnitude more energy to bring to the molecule, like a thing-glomming and moving antibody molecule so it can do more thing recognizing, and thing moving around, at higher velocities from an ambient energy source that has like 100 times more molecular energy at a form that can power things that have a biogenic (from organisms) protein energy chemistry; some bacteria make polyphosphate crystals, and polyphosphate is a water treatment chemical
also, as a multiatom molecular technology that reminds me of a nanoassembler, can you just take two or three antibodies, attach them to each other at the base of the Y so they are a certain distance apart and angle, and then glom and position items that meet up with them and are the right shape; three of these reminds me of a drill chuck, and the thing about getting them to do things onpurpose could be
drug amplification technology, wikipedia says, “but lipids and nucleic acids become antigens only when combined with proteins and polysaccharides” suggests that making a nucleic acid drug, or a lipid drug, makes it so that: nucleic acid liposomes, if they are possible, or perhaps not, could concentrate at the lymphatic compartment, omitting first pass metabolism, while being immunoinvisible; I read liposomes get glommed with antibodies, nucleic acid thing (drug) containers could last much longer than regular liposomes, even though nucleic acid forms are different than autoassmebling phopholipid bags, also RNA and DNA drugs, perhaps made with new nucleic acids, or also really strong new variants on the rails of ladders, could be really really durable active drugs, but omit being glommed up; halogenation might keep the liver from metabolising them as well
Tolerogens cause antibodies to be calmer, It is possible that antibodies that cause some kinds of inflammation, if reduced as to their intensity with tolerogenic therapy, could cause a reduction of physiological accumulated problemness, and preserve younger phenotype longer; preserving younger phenotype longer could cause greater longevity, wellness, and healthspan; it is not that linked, but kind of reminds me of, rapamycin being a transplant-rejection blocking (immunomodulating) drug
things that cause tolerogenic activity: “Semi-mature dendritic cells are tolerogenic. Conditions including the absence of an inflammatory environment result in the incomplete maturation of dendritic cells.”; so if an SNP or gene copy number, gene therapy or germline genetic engineering on humans optimizes dendritic cell forms that are tolerogenic, that could be a longevity wellness and healthspan heightening technology, there are numerous technology branches and possibilities to making tolerogenic benefits, wikipedia says, “completely protected from symptoms”, “produced IL-10, (an antiinflmmatory cytokine, that is also at intracyte spaces) a cytokine which is able to inhibit the Th1 response”
Deleting histone deacetylase 2 HDAC2 at mice cause greater cognitive ability, this could be a human intelligence heightening genetic modification, they could find people with an absence of HDAC2 at the population or various SNPs and find out the quantifiable effect on g (like IQ), as well as personality (like big5 measurement) of an absence of HDAC2 or also SNP variants and copy number variants on human being as an intelligence increasing gene
Noting depot drug injections, It could be possible to beneficially immunize children and give them their booster immunization simultaneously, benefitting children’s wellness and well being; online it mentions, “The percentages of primed children with hSBA titers ≥8 was low for serogroup A (6–25%) and moderate for serogroups C (27–43%), Y (69–74%) and W (56–69%). For all serogroups, hSBA antibody geometric mean titers (GMTs) tended to be higher in the ACWY-2 than the ACWY-4 group. Post-booster/single dose, ≥96% of primed and ≥73% of naïve children had hSBA titers ≥8 against each serogroup, and hSBA GMTs were higher in primed children.” which to my peception might communicate something kind of like “about half of children become immune with one dose when they were just a few months old, then with another dose at 60 months then about 4 out 5 or also 19 out of 20 became immune”; At a particular group among a few groups, they gave the children 2 doses of immunizations at about a year, then again at 60 months, and got 96% effectiveness; That suggests that if the children had one office visit, rather than three, and that if the one dose at the office visit had microparticles that released immunization chemicals to their body at 60 months later, that they could get 96% immunity from one dose and one office visit; just one office visit rather than three could make it so more children and their parents succeeded at the procedure;
a microbead slurry or 1 ml or less that could be injected at the bellybutton, with the bellybutton location omitting bumpiness as well as being absent sensation or a wiggletropic conceptually noticeable form: It might be possible to do something like 9600 DPI inkjet printer print 14 or hundreds of sandwich layers of materials with minute squiggles on them, and have the base it is printed on dissolve at a harmless solvent, leaving a bunch of separate inkjet printer ink polymer and protein customized geometry sandwitches, or 3D printer print a shape, like things with branches that have branches, that does a math function of how much things soak in to the branches, and how much the branches dissolve per month; sort of like the first 14 months, the first branches plump up and dissolve, then the next 14 months the branches sequential to that that plump up and dissolve, and then after that the next group of branches plump up and dissolve, where each dissolving of branches creates a fluid channel with like 100 times more spontaneous fluid motion even at the diffusion only next to body-tissue moist environment of a bellybutton injected slurry of microspheres, then at 60 months the branches that, at their sequence, plump up and dissolve, while having lots of immunization protein rich branchlets, and possibly even also enzymes that dissolve the polymer that the immunization depot is made of, turning the microspheres to soft wet jello mini blobs, and at 60 months the supplemental dose that raises immunity from 6-74% to 96% is administered
That reminds me of the longevity drug depot injection, thinking about hundreds of years of continuous contribution of longevity drug ethynylfluorarapamycin to thecirculatory system from a gram or less of ethynylfluororapamycin at a way to make the depot injection function many centuries is:
I think that something like eentsy linear strings of protein releasing polymer, sort of like string cheese version of norplant, as microbeads, (kind of a millifiore polymer protein form) could always have high output lines of chemical concentration, as compared with like diffusion from a sphere that has layers of different drug concentrations (kind of like candy panning) from the surface;
I read flow cytometry of yeast can characterize 10 million yeast cells per second; is it possible that an integrated circuit technology could use a 1 cm 10 billion well geometry (although it might be 1 billion, or even 100 million wells because the yeast are actually perhaps 2 micrometers large each, and statistically having a plurality at each well has value), with a semiconductor light emitter (laser diode) as well as photodetector at the base, or oblique side, of each well, to do imaging of at a 10 billion yeast colony well as a parallel chemical, like physiochemical, scientific and manufacturing research and technology, as well as drug reasearch, and other utilizations, screening technology; The flow cytometry version with 9600 DPI inkjet printheadf also could be beneficial utilizable technology: although the published flow cytometer only utilizes 10,000 seconds to process 10 billion yeast cytes, if they are at wells at a semiconductor technology produced structure, like about a cm^2 of semiconductor wafer, then their row, as well as column location can be related to the chemicals or processes that they have experienced, as well as provides a location with lots of order, minimized unplanned variability; compare the 9600 DPI inkjet printer attached to a 10 million yeast cell per second flow cytometer: theoretically a 10 million yeast cells per second could print out say, 5000 yeast cells each containing microdots of fluid, possibly even containing a: preserves living organisms chemical, or even a cryoprotectant, and basically 9600 DPI print an array of 46 billion separate, findable, the 5000 different yeast cells could be resorted, yeast cells per square inch, certainly with the option of printing them with a couple diameters of space between them to make 46 billion findable yeast on a cryopreservable, or ambient stable chemistry array about 3 inches on a side;
the 9600 DPI living, viable, or possibly even spore-induced yeast cells on a paper like surface (likely a polymer surface) also could be immunofluorescence dipped
Interestingly, if the 10 million yeast/second flow cytometer finds or matches, or groups the things it sorts, then it can actually repoduce identical or near identical visual identity form row and column sorted, printed 3 times 3 inch prints, then, immunofluorescent dipping of one of the papers/polymer inkjet like arrays, could find yeast of interest, and then because the flow cytometer grouped yeast together, another piece of paper/polymer would have that identical flow cytometry visual (imaging) form of yeast geometric arrangement on the paper/polymer, at those same row as well as column coordinates, and a third piece of inkjet printed paper could have the same array, again, printed with cryoprotectant for sharing with other persons or further development uses; from the perspective of a person with a liter of yeast fluid, they could print out as many copies of their yeast chemical response and its characterization, or yeast chemical production genetic library, or yeast drug response library as they liked; With this system, one person could distribute a 46 billion seperate, and reseparable yeast library to as many people or organizations as they liked;
Also, using 9600 DPI inkjet technology it could be possible to print a layer of immunofluorescent material onto the printed dot layer of yeast, possibly have ambient moisture, or 9600 DPI printed fluid diffuse or blend sufficiently to visibly fluoroimmunolabel the yeast, gaining more data of value; The 9600 DPI inkjetcould also apply chemical reagents to the yeast as well,
As a longevity technology, printing yeast, then printing a matrix of 300 different longevity chemicals at a row, and 300 different longevity chemicals at a column, possibly even layering yeast, nutritive growth medium, longevity chemical, more yeast, and more growthmedium as a 9600 DPI sandwich could produce a 90,000 combined longevity chemical matrix
Notably, noting the sizes of screenable libraries, autogenerated variations of longevity molecules could have millions or billions of screenable variants; every hydroxyl and hydrogen at rapamycin could be considered as a binary power of 2 with about 2^30 possible different versions; every location of the oxygen and hydroxyl and unsaturated C=C at a decanoic acid ester (like 10HDA or 10H2DA) is a possible combinatoric library; notably though, as 9600 DPI inkjet printing can make hundreds or thousands of identical printed versions of a screened library to distribute to other persons at a company or other scientists, sharing actual organism form, distributing reproductive ready samples, recorded as well as completely new data, archiving, artificial intelligence and software queryability and stimulation of the dataset, as well as backup copies are among benefits of 9600 DPI yeast sandwich and sortation printing;
There are numerous linked technologies: A collaborator at the same company could reload another person’s yeast print into another 9600 DPI inkjet printer, then print a completely different immunofluorescent labeller onto the identical dataset of 300 times 300 longevity chemicals effect on yeast chemical matrix, Another person might actually physically grab a separated with a gap printed yeast colony dot with 5000 yeast at it, put it in culture medium, grow a few billion of them, and then do a new screening, on perhaps an computer modelled group of related longevity chemicals, or completely new chemicals, likely with flow cytometry and 9600 DPI inkjet printing with new chemicals, processes and areas of interest, Another person at another company the first company is collaborating with might do flow cytometry with 9600 DPI inkjet printing to compare a human tissue culture chemical sandwich response or also flow cytometry grouping at the 200 times 200 longevity chemical matrix and compare the areas of most similar and most different expression and amount of longevity, finding chemicals that had much more effect on humans than yeast, as well as chemicals that effected both similarly: that would suggest that the chemicals that effected only human tissue culture cytes have a different genetic and physiochemical longevity producing basis; they could then do tissue culture response at a 300 times 300 longevity 9600 DPI printed chemical sandwich matrix with tissue culture of species far from both humans and yeast, like marsupials, platypus, million year lifespan endoliths, 400 year lifespan quahog clams, termite queens, macaws, and naked mole rats; longevity chemical responses at a matrix shared between these would be highly conserved, and longevity chemicals with particular concentrations and activity at different but related species could show the different separate occurence of high-longevity capability phenotype, genotype, and what might be called chemotype capabilities; finding those origins, their actual genetic nd physiochemical origins, of new longevity chemotypes describes linked physiochemical systems, and gives the possibility of transferring those longevity systems, as genes, to other organisms, to bring that organism an entire beneficial useable longevity phenotype, genotype, chemotype to the other species, humans would benefit from clams, and possibly endoliths. The responses of a plurality of species’ tissue cultures to a matrix of chemicals from things like the king’s holly (40,000 year lifespan) and creosote bush could also be compared;
I read that atopic dermatitis, “guidelines for AD include hydrating topical treatment, topical glucocorticosteroids” which made me think, what about other sugars and carbohydrates at he “gluco” part of clucocorticoid? How about a ribocorticosteroid (ribose), or e fewer AMU erthritol C3 sugar (glucose is C6) so erythricorticosteroids as a treatment; then I thought about how images of the dermis I have seen have many cell types and layers, and it is possible that different medications might localize to these various cytotypes and sort of distances from both skin surface and distance from capillaries could localize differently; if there is a most exterior cytomembrane transported to cytoplasm chemical, like maybe ATP, or an ion where if it is at a persons skin it is itchless like Mg, or even Ca. then atopic dermatitis medication with that most highly exterior cytomembrane transported chemical as part of the atopic dermatitis treatment like an ATPhalogenatedcorticosteroid or a magnesiumhalogenatedcorticosteroid could be beneficial as it gets much more transport, possible active transport or also transcytosis transport;
GSK:
Also there is the possibility that the duration of an atopic dermatitis treatment could work chronologically longer, my perception is that a halogenated cortisone ointment kind of does things when it is is gooey and on, then sort of rubs off onto other things, then might not be doing that much 11-14 hours after application; I think I read that fluorocorticoids are 1000 times more physiologically potent than nonhalogenated cortisone so that brings up the possibility that compared with 100% strength at 1 minute, and 1% strength at 720 minutes there might be a way to cause fluorocorticoids that treat atopic dermatitis to linger and even fluidicly recycle so they are are 100% at 1 minute but at like 40% at 720 minutes; one possibility is actually exterior of cell cytotransport to cytoplasm facilitating molecules, and also cytoexport (efflux) molecules (possibly peptides) being attached to the fluorocorticoid molecule, this would cause a kind of chemical engineering, it pours into the cell cytoplasm at a certain amount/minute and it pours out of the cell at a certain amount per minute, whle being right next to the cell and all the cytoexterior fluorocorticoid receptors, so the amount outside the cell, while near the cell exterior receptors is at a particular moderate to high range with a long plateau curve; I perceive that topical halogenated corticosteroids might actually work on receptors on the exterior of cells to get rid of atopic dermatitis, so there could even halogenated corticosteroids that had some kind of intracyte space area physiological tropism, although Ido not know how that works, perhaps one of thephysiologicially beneficial interleukins that I mighthave read accumulate at the inter cyte could be attached to the halogenated corticosteroid molecule, even though the beneficial interleukin is many AMU and the halogenated corticosteroid is few AMU
Then there is the possibilityof a new atopic dermatitis drug: is there anything, which if actually actively transported to the cytoplasm, completely a different place than the receptors on the cells exterior, that would decrease atopic dermatitis physiochemistry and symptoms, like perhaps something that, at the cytoplasm, makes capillary epithelial cytes exude less fluid (plasma), or causes dermatocytes to exude less fluid; (my perception during the 20th century AD was that moisture->itchiness) or I read about some kind of tolerancization of immunoresponse thing having to do with non-mature dendric immune cells, as well as beneficial inteleukins, so perhaps there could be some RNA or DNA drug that causes the person’s own genome to make something that the tolerance promoting young dendric cells respond to with decreased immunoreactivity around dermis (skin), another possibility besides RNA (mRNA) as well as DNA drugs at topical liposomal or nanoemulsions are things with a nuclear membrane transport peptide attached to them, imaginably this could cause 7-40-100 times more movement of the nucleus effecting drug to actually reach the nucleus (like DNA drug);
Also, I read about things like HDACinhibitors, and methylators, perhaps theycould findout ifthere is any kind of histone modification, like preserving acetylation, or demethylating some part of the histones, that causes people to have less atopic dermatitis; there are numerous orally active histone deacetylators, and some like 10HDA (also possibly 10H2DA and 90DA), that occur at natural products that cause greater longevity at mice, and one called Vortsomething also called SAHA that causes greater cognitive ability; so there could be a histone acessibility and activateability drug, thatis oral, that causes a personto be absent having atopic dermatitis thatmakes them live longer or also be more intelligent;
People that value atopic dermatitis being cured could do gene therapy, I think the topical availabillity, the ability to dothings like electroporation, andhere is a thought new to me, the ability to, using the same genome, turn the genes at the dermis on and off so they are like those at a cell that has differentiation, could make it so thatturning off some of the genes at the dermis, or turning some on, might make the persons skin as nonresponsive to atopic dermatitis causes as the least immunoreactive cell type at the rest of their body; Perhaps like, the bloodbrain barrier is almost always completely immunononreactive, because it is important, so some kind of electroporation transported RNA or DNA drug that causes the active and available genes of the dermis to be more like those of the bloodbrain barrier would cause a gene and gene product availability/producibility to be like thatof the persons own blook brain barrier and their skin would be immune system unreactive; It seems possible they could also just find well normal people at the 99th percentile of having skin (dermis) that was spontaneously non-irritable and 99th percentile of nondeveloping of any kind of dermatitis even when a dermal chemical irritant was applied, who also had skin other people described as attractive and healthy, and then find out if the 99th percentile of nonirritability and nondermatis response had a particular group ofgenes that were nonavailable or less available for translation and transcription, and then make RNA and DNA topical drugs, or just possibly, if it lasts quite a while, an electroporation of gene expression modifying drug like RNA drug or DNA drug that causes the DNA transcriptiongenetics available to the persons dermis to belike the 99th percentile of people with irritationless, nondermatitis responsive skin; There is also the possibility that rather than Not Making things in response to an irritant, that 99th percentile of absence of skin (dermis) irritability and 99th percentile of absence of a dermatitis response even if there is a chemical irritant, among people that others quantify as having skinthat is moreattractive than the 90th percentile, is linked to the people with 99th perentile well dermis (skin) making something, that is expressing a gene and making a transcribed protein, that people with atopic dermatitis do not make as much of, that could then be addressed with topical RNA (mRNA) or DNA drugs, or possibly electroporation that cause those genes at a personwith atopic dermatitis to be more active, so they make the same amount of beneficial material as the 99th percentile of dermal wellness persons and then they ceasehaving dermatitis; Notably, if mRNA could function this way as a drug, and liposomes and nanoemulsions could bring the mRNA to the dermal layers that are alive, noting that thisis like micrograms, or possibly even nanograms of mRNA, it could be highly affordable being made out of ultrasonicated oil,phospholipids, water, and like .1 or .01 mg of mRNA per big jarful
At C elegans royalactin protein without 10HDA (10H2DA) has a longevizing effect, I perceive this was kind of near 1/3 the distance on the graph that the 10HDA (10H2DA) produced at c elegansas to increased longevity, so the 10HDA (10H2DA) was like three times more longevising than the royalactin; they could do a thing where they noticed the amount of activation at genes in C elegans, mice, and humans, when eating enteric coated (stomach passing) royalactin, to find out if any of the genetic changes that occur at C elegans that cause greater longevity from just royalactin also occur at mice and humans; also the mice eating the enteric coated royalactin could be dosed their entire lives and quantified to find out how much longer they lived, if anything different than 10HDA(10H2DA) amount of longevity increase, published at mice as 25/27% greater longevity from oral royal jelly; if the mice live longer from enteric coated royalactin, and their genes with different activation amounts have similar changes to activation amounts at human genes among human volunteers that eat enteric coated royalactin protein then it could be that royalactin, enteric coated or enteric optimized, is likely to cause greater human longevity; this brings up the possibility of engineering a protein with much higher longevity increasing effects than royalactin, at bees, yeast, or bacteria, the royalactin protein producing gene could be modified to produce different proteins, and then those proteins screened as a library at c elegans in 96 well culture plates to find out if any of the royalactin protein variants was more effective at increasing longevity; among numerous possibilities are lipophilic as well as hydrophilic varieties of royalactin protein; a version of royalactin’s protein bunch layer exterior, but with notably different number of atoms, that is fewer AMU, which could actually reach more tissues, more effectively as the atomic weight is less and it might have much more transport and diffusion; versions of royalactin protein where if you think of protein as a bunched up blob, then the amino acid sequence of the protein at just the royalactin exterior could be multiply repeated, with the technology that this would be kind of like a bunch of identical repeating space filling units of royalactin exterior; similarly dimerized (two royalactins) as well as trimerized (three royalactins) could be quantified as to longevity effect; also the nonsurface core of the royalactin protein could be quantified as to increased longevity effects, dimerized and trimerized as well; noting that similar gene activation patterns between c elegans, mice and humans as a response to royalactin may exist, quantifying the effects of royalactin protein modifications and variations could be accomplished at c elegans as welkl as mice tobenefit humans; noting that at c elegans royalactin was sort of 1/3 the longevity strength of 10HDA, and that entire material royal jelly is published as causing 25/27% greater longevity at mice, it is is possible that a new version of the royalactin protein that is three times as effective as the royalactin in royal jelly could possibly exist or be produced, and that this would be a new longevity chemical, supplemnet or drug to have the same amount of longevising effect as the 10HDA (10H2DA);
also, varieties of the royalactin protein that are the actual versions of the protein at the queen bee’s GI tract after the digestive area of the queen bee’s stomach could represent that actual protein forms that contribute to 20-40 times greater longevity at the queen bee than other bees, so that is another protein variation to quantify the longevity effects of, similarly, noting the 25/27% greater longevity at mice orally eating royal jelly, and the possibility that compared with a human stomach digestion duration of .5-3/4 of an hour that a mouse stomach digestion period is imaginably 5-7 minutes, it is possible that at mice, the royalactin protein is modified to a fewer AMU protein, yet still a protein, compared to royalactin possibly being digested into individual amino acids at a human; if royalactin is not fully digested at mice, then that modified fewer AMU royalactin protein product from the briefer mouse digestion is another possible longevity protein variant on royalactin to quantify the effects of; encouragingly, it is my perception that the luminosity and number of wavelengths of engineered proteins like green fluorescent protein have been amplified to many times the first protein’s luminosity, and more than 9 new spectral emissions wavelengths have been produced, it seems possible that tripling the longevity effect of royalactin protein at mammals could be possible; putting the genetics of a much greater longevity producing variant of the royalactin protein at plant food products and also possibly eggs at chickens that produce eggs, creates new longevity foods; Gene therapy so that people produce longevity proteins at their bodies, as well as germline gene therapy so that people produce longevity, wellness, and healthspan producing proteins at their bodies is also beneficial;
Online it mentions that royalctin causes activation of particular receptors, I read there is a gene expression measurment chip that covers the entire human genome along with another 6500 genes, and it is likely that that amount of capability is also available at the mouse genome, and possibly the c. elegans genome: the effect of royalactin on a very large number of receptors might be generated, and then the new different versions of royalactin and their amplitude of effect on these receptors could be quantified to produce new variants of the royalactin protein that have greater receptor activity; it is possible that the receptors that cause greater longevity at c elegans from royalactin could be qualified and quantified, and that, if mice are longevized with enteric coated royalactin, that the longevizing receptors that are quantifiably stimulated at longevized mice that also have human receptor equivalents could be researched as a basis for completely new non-protein longevity heightening drugs
It is possible that having e coli or yeast, of some species, (pichia pastoris has been utilized to make royalactin at a laboratory, during research on a possible basis for manufacturing production) process something like the amyl, propyl, butyl, hexyl,heptl, octyl acetates of GRAS food flavorings could cause some versions of variously esterified alkanes with perhaps one nonsaturated C=C link to be produced, and that this could be characterized and quantified as to longevity effects at mice, also, it is possible that 10HDA and 10H2DA are possible products, then this yeast modified GRAS material could be concentrated and distributed while being hundreds or thousands of times more affordable than royal jelly; imaginably the yeast could chemically transform plant based decanoic acids to partially saturated (C=C) decanoic acid esters (=O), online it says that decanoic acid, without a desaturated C=C, is at palm oil, coconut oil, and milk lipids, so there could be highly affordable sources of the C10 molecule for a desaturating C=C producing esterifying organism, possibly a yeast, to make into a quantitatively longevity increasing, at mammals, like mice, molecule that people could take as a supplement or drug hundreds or thousands of times more affordably than royal jelly, and at longevity heightening research supported tens, hundreds, or even thousands of times higher doses than royal jelly
One of the other royal jelly proteins could be quantified as to any nootropic effects it has on humans, “MRJP1 is also related to the learning ability of bees.” so an enteric coated nootropic protein active at humans could be possible
So, there is already a one pill, one dose yeast infection cure pill, fluconazole, is there a possible version that could be distributed and voluntarily used globally that is less than 1 cent a dose, and as a side effect makes people live longer? Fluconozole is $200/Kg, the one dose yeast infection amount is 150 mg, which is three cents per pill for the drug; Halogenation, ethynylization, also attaching the moiety that causes active transport (1000 times greater transport than diffusion) at the largest possible number of cytotypes and tissues could all be ways; 100 times more affordable from halogenation heightened effect per mg dose, and 40 times more affordable from ethynylization heighteing of effective mg dose, causes 4000 times more affordable pill; is 1/4000 of 3 cents, or less than 1/1000 of 1 cent per dose; globally as a medication printed on edible round paper, noting 396 adhesive applique papers that look festive are $1.00 retail at the dollar store; then it goes up to about 1/4 of 1 cent a dose; Placing folate at fluconozole to reduce birth defects: minute effects could have value at public well being; it is possible that over 50% of women globally conceive their first child between 18 and 28, that suggests that a folate plamitate that lasts 7 days could reduce birth defects in 1/120th/4 of per decade pregnancies if a woman takes it as part of curing one yeast infection per decade with a one pill yeast infection curing treatment; 400 mcg times 30 is 12 milligrams of folate per pill, or perhaps 24 milligrams of folic acid palmitate; at $30/Kg folate that is is 41,000 doses per $30.00 or 1/11 of 1 cent per dose to put as another chemical at a yeast infection curing one pill one dose paper form or tablet; I perceive that online 1/52 times 70% of 300,000 annual birth defects are preventable with folate, so 4038 annually or 40,380 per decade; at the likeliness of the week the yeast infection curing pill being the week a woman gets pregnant, then that is 40,380 birth defects prevented per decade when folate palmite is combined with a one dose yeast infection curing pill, for an entire pill $ at 1/4 of one cent at a retail US paper adhesive on paper dosage form;
Endogenous chemicals are found at some organisims that when given to other organisms cause the other organsisms to live longer; 10HDA, as well as 10H2DA are decanoic acids esters found in royal jelly, when royal jelly was fed to mice it caused the mice tpo live 25/27% longer, when other decanoic acid esters like DAEE were administered to mice their wellness and healing ability improved as did their resistance to cognitive stress, 90DA is another esterified alkane (with one C=C) with HDACinhibitor effects; Finding and screening a variety of ester (=O, the 10H2A and 10HDA also have -OH) 10 carbon atom molecules to find those that cause longevity effects, optimally longer than those of 10HDA nd 10H2DA could come from making tissue concentrates from the tissue of long lived species like: bowhead whales (multicentury lifespan), 400 year lifespan Quahog clams, 300 year lifespan tortoises, 300 year lifespan sharks, 100 year lifespan macaws, 50-100 year lifespan queen termites, 35 year lifespan naked mole rats, 35 year lifespan bats, 35 year lifespan beavers, 40,000 year lifespan King's holly palnt, 10,000 year lifespan creosote bush, then doing a procedule like high performance liquid chromotography to find any alkanes, partially saturated alkanes (one or more C=C) (might as well find any esterified =O alkene or partial alkene as well) that are at any concentration at the circutory fluid and brain homogenate of these organisms; Then, using chemistry synthesise a few hundred of these esterified alkane/alkene molecules and find out if they amke mouse human tissue culture cells, human tissue culture cells, and entire C elegans organisms live longer; Then order the list of these chemicals on llifespan increase and feed them to mice, orally, with IP injection option ok, with oral valued, to mice at longevity studies to find out if they cause greater longevity at entire mice
Create a tissue culture model of longevity drug increase at mouse tissue culture and human tissue culture: It is possible that there are mouse cells as well as human cells with lifespan of 72 hours, 20 days, 100 days and 200 days at tissue culture, these could then be correlated with the actual lifespan of entire organisim mice to find tissue cultures that are 90% or higher predictive validity at predicting how long a mouse will live with a longevity test drug or chemical; mouse tissue cultures that live 60% longer that with rapamycin, 25-27% longer with royal jelly, 10HDA or also 10H2DA, or also royalactin protein, 5-35% longer with metformin are developed and then these are used, with their faster 72 hour, 20 day, 100 day or 200 day lifespan cycyle times to make screening new longevity drugs and chemicals 300 times, 5 times, and ten times faster than using whole mice; Notably humn stomach tissue lining renews every 72 hours and human tongue surface every 168 hours so I think it is possible to find both mouse and human tissue cells for culturing that have natural 72 hours, 20 day, 100 dy and 200 day lifespans. These could be used to screen hundreds of thousands or millions of longevity drug and longevity chemical candidates at libraries; Technology supporting 1 million, 100 million, and 1 billion well tissues cultures are: a published 1 million channel microfluidic device, a 10 million cells (yeast) per 10 second interval flow cytometer, the way a 1 billion to 10 billion feature commercial integrated circuit CPU has an area of near 1 CM,
90% or higher predictive correlation of tissue culture lifespan and mouse lifespan as a human tissue culture
beneficial to measure peak plasma and trough palsma and plasma half life of longevity drugs and chemicals at mice, optimally at oral administration of longevity drugs and chemicals so humans can duplicate these at humans with oral doses
They could blenderize endoliths, which wikipedia says are microorganisms with million year lifespans and 10,000 year cytodivision cycles, and feed them to mice coated with an enteric coating, they could also see they effect on c elegans, as well as amoeba, pa aeurosomethign (a bacteria that makes that has T2DA and C2DA decenoic esters); also wikipedia says, “Some Actinobacteria found in Siberia are estimated to be half a million years old.”