they have used breeding and winnowing to produce fish with 9% larger brains at fish, they could make mice or fish with 24% larger organs and other things then test known functional longevity drugs that work on different mechanisms to find out if organ
size has an effect on longevity; brain, vagus nerve, liver, immunocyte generating tissues, pancreas, GI tract, lungs, eyes, density of neurons at dermis, gonads, kidneys, bile producing organs (bile chemical component lithochilic acid is published as
having lomgevity and wellness effects),

Longevity drug: it is published lithocholic acid at 50 micromolar concentration makes yeast live two times longer, screen a library of lithochilic acid molecular variations, some of which are ethynylized and halogated and have cytotransport moieties to
find those at 99.99th percentile effectiveness then test them on mice, those 100 molecules could be tested on 800-1400 mice as well as human tissue culture and plants; the most hydrophobic bile acids among 6 published as heightening longevity caused the
greatest longevity increase suggesting the screened library contain bile acids modified to be 1.5, 7, 24, 60, 100 times as hydrophobic as lithochilic acid, it is perhaps possible that some locations of fluorine at a molecule heighten hydrophobicity (
teflonization), and removal of -OH hydroxyl groups heightens lipophilicity so these could also be screened; lithochilic acid heightens the maximum lifespan of yeast making it noteworthy as a human longevity drug

The lithocholic acid longevity paper says there are 58 genes effecting longevity in yeast, finding homologs of those genes at mammals, and finding a completely different, complementary, group of longevity increasing genes at mammals could provide new
gene product protein drugs as well as genetic enhancement at humans and provide a way to find a model organism, possibly more predictive than mice at the the effectiveness of longevity technologies and drugs

Monthly mice and marmosets as longevity, healthspan and wellness screening organisms: mouse producing companies, corporate research departments as well as other mouse used for experimental breeding growing, and existence monitoring facilities could
purposefully make sets of mice to be used at experiments, like lomgevity, wellness, and healthspan experiments, that differ as to age at one month each, as a batch, the effect of a longevity chemical on the oldest month would provide the earliest data
after a couple months with new data being generated monthly, 8 mice per month provides a p value of .05 for each month and a math way of combining multiple months to provide reportable data like p values could be found; marmosets are primates, and
batches of four marmosets at 3 month age intervals could provide primate longevity data at six months, mouse or marmoset age batch experiments would also provide a graph of when, as to their age, a human would most benefit from a new longevity chemical
drug or chemical, 8 mice a month at up to 48 months is 384 mice; this also makes a kind of sequential metaanylasis

They could also breed organisms with 24% less tissue at a variety of organs and test known longevity molecules on them,

At humans the genetics of tissue and organ amounts (volume/mass) could be used to predict the effectiveness of different longevity drugs as well as guide experiments on primate and other mammal models, it is possible a human genetics that favors the
function of longevity drugs as well as the effect of different sizes of organs and tissues on longevity is a technology;

Organisms with a larger number of longevity genes than those at s cerevisia like other different species of yeast could possibly be found, making longevity chemical and drug screening on yeast better, they could also genetically engineer yeast to have
all the longevity genes at all measured organisms, like humans; also it is possible putting the longevity genes of humans at the genes of mice could produce a better mouse model of human longevity

Lithocholic acid at alibaba; 50 micromolar might be kind of like 376g/mole or 376 mg per millimole or .00376 mg per micromole to make 50 micromolar solution, 70,000 gram human is then about 70 liters of water or 18 times 70 moles as fluid, 3888 moles so
a 14.6 mg dose at a human; noting it is possible the GI tract might be effective at filtering lithochilic acid it is possible a liposomal version with transport benefits would be higher function; at humans cholesterol amounts and cancer risk could be
effected

Some humans make more lithochilic acid than others and have higher cancer risk, when they omit getting cancer do they live longer

Rabbits compared with mice

Lithochilic acid or a more effective at causing greater longevity engineered into a food plant makes a globally available popular food that could be measured as to its longevity effect on marmosets, possibly at a 3 month partitioned longevity measurement
model

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How many sequential doses of an epigenetic drug cause the epigenetic improvement? Liposomal depot, perhaps attached to an antibody that gloms it to the surface of the lining of the lymphatic compartment could diffuse beneficial drugs, although that seems
complex. One possibly as is epigenetic modifying drug palmitate. I do not know if the longevity effects of 10HDA(10H2DA) are from HDAC interference and epigenetic, but if they are then taking a high dose of 10HDA once a month (or some other interval), or
like 30 grams of royal jelly which has 10HDA(10HDA) for two or three days once a month could have the same or better longevity effect. There is the possibility that occasional high dose 10HDA(10H2DA) or royal jelly is actually more longevizing from being
thorough and of higher activity.

One HDAC2 inhibitor is a nootropic. It is possible that one or two high doses of that HDAC inhibitor a month could

Cause greater cognitive ability.

Notably though there is another version of this. I read histone epigenetics like acetylation can change rapidly, perhaps in minutes, although the other long view also makes sense as people get epigenetics from from their parents or even grandparents. I
perceive I read there is longevity epigenetics people get from their parents so a couple days of epigenetic dosing could cause greater longevity effects the person's entire life. A couple days of epigenetic modifier dosing could even cause their children
and grandchildren to have greater longevity. At the nootropic HDAC2 inhibitor that causes greater cognitive ability, a couple days of HDAC2 inhibitor dosing could cause intelligence enhancement that is also passed along to children and grandchildren.

Cognitive ability genetics: the genes that the published cognitive ability heightening HDAC2 inhibitor modifies could be g (like iq) intelligence genes. SNPs, alleles, and copy numbers of those genes could be enhanced at the germline or with gene therapy
to increase intelligence at humans, that is homo sapiens.

Longevity technology:

I perceive piperine causes greater absorption through the membranes of the GI tract from telling them to be more permeable. Is there anything that could be placed at liposomes along with the active pharmaceutical ingredient (ÅPI) which reach the
lymphatic system to make the lymphatic membranes more permeable? It could be piperine again. That lymphatic permeability drug could make other drugs, like rapamycin, rapalogs, or other longevity drugs to be 2-4 times as effective at reaching tissues from
the lymphatic system. Combined with the 2-10 times greater effectiveness of drugs that skip first pass hepatic metabolism that could make rapamycin, rapalogs, senolytics, or other longevity drugs 4 to 20 times more active and affordable. Rapamycin that
makes mice live 60% longer could be just 12-14 cents a dose based on $40/gram at Alibaba.com .

GSK (Glaxo Smith Klein) has an online page where they request technology ideas. They make Tylenol and some other antipyretic pills:

ela–naproxen (ela-n) is ethynyl liposomal active transport naproxen it is active at about 7.6 micrograms. They could put a dot of it on the outside of regular naproxen pill that is enteric coated so there is an immediate action antipyretic at the
stomach but it also activates 11 hours later so one pill lasts 24 hours. Another way to do it is like multiminipill contac™ with ela-n microenteric coat so it dissolves better at the small intestine after 11 hours. Another way to do it is rather than a
7 day palmitate have ela-n attached to a different alkane COOH like perhaps C6COOH

To make another, delayed dose to make 24 hours of naproxen activity, that could do 36, 48, 72 hour one pill dosing as well: Another way is ela-n of three or more types taken simultaneously where each ela-n has a different enzyme-reactive group on the ela-
n with a passivating group removed by the enzyme. The enzymes that remove the passivation moiety are enzymes at the circulatory system. The first ela-n gets its passivation moiety removed first and the next ela-n gets its passivation moiety removed next
like cumulatively 90 minutes later, then do this with a sufficient elan-enzyme-unpassivated-moieties to get a smooth 24 hour, 36 hour, 48 hour or 72 hour dose curve.

Years of arthritis relief from one office visit: A depot drug form of ela-n, ea-n, which I calculate as having a 7.6 microgram 12 hour dose could put ela-n at an implant (3 year nexplanon-like) with just 16.64 mg of API at the implant. Sensibly and
obviously omitting the 2-4 times dosage multiplier enhancement from liposomes, ae-n could be a 33 mg or 66 mg entire API content implant. I think it is possible to make much longer lasting depot implants or even injections, so a decade of arthritis
relief from a decade functional implant at one offive visit is possible.

Complementing a decade functional arthritis relief implant is putting the longevity and life preserving peptides AEDG (epithalon) and thymosin at the implant. Epithalon is published as causing 24% greater longevity in mice. The combination of epithalon
with thymosin, at intermittent dosing, is published as causing people to be four times more likely to be alive after six years. Epithalon and thymosin are peptides so it is possible screening libraries of variants on these peptides could find versions
with fewer mcg per dose.

Another ela-n 24-96 hour antipyretic: put ea-n on the outside of the pill for immediate relief. At the interior of the pill layer, make the 11 hours later dose with dry liposomes that have different numbers of concentric layers at the liposome molecule,
so like the 11 hour dose has 11 concentric layers of liposomes ======Ö on it.

It is possible to simplify the ela-naproxen molecule to ethynl naproxen, or ethynyl liposomal naproxen. Ethynylizing sex hormones causes sex hormones at FDA drugs to go from a.625 milligram dose to a 600 nanogram dose, a one hundred times amplification
of effect. A cell membrane active transport moiety causes 1000 times greater transport than diffusion. Either of these alone produces microgram active doses of naproxen.

A really simple version of 24-48 hour liposomal naproxen without ethynylization or active transport moieties is to use the way liposomes avoid first pass hepatic metabolism to bring 4 times as much regular naproxen API to the circulation. If that works
on regular naproxen that makes a 24 hour dose fit in a pill half the size or at a full size pill up to 48 hours of antipyretic anti-arthritis effect. Dry liposomes could be used.

Longevity technology:

Multiple simultaneous drugs at aged batched mice are a way to make longevity drug API identification faster, and make mouse research as much as 120 times more affordable to produce a p value. Matrix simultaneous drug administration is published, and
creating batches of mice, at 8 mice each, two months or less apart in age creates 48 mice, with each duomonthly increment able to generate a longevity increase p value longevity drug. The 2^3 deaggregation mice as steps to find the actual drug that
longevizes is a way to do this. Sequential mouse experiments to locate the individual most effective longevity drug, possibly after data on 2-6 months of simultaneous administration of the drugs to new age batched groups of mice. The actual longevization
pct of each batch of mice, starting at the first two months p values, continuing to 4 months and six months also gives a number on how much longer the eight and ten month and year interval mice would have to live to continue that particular mouse'
longevity gain. This is similar to calculating course grades mid term to find out if a person can still get the grade they prefer, at mice this is how much longevity increase would numerically justify continuing that drug at that mouse for greater than
the amount of longevity from other chemicals that have been screened or exist. One API drug longevity quantification; after 4 months you could tell if an Epithalon peptide sequemce variation being screened was 60% more or 60% less longevizing than
regular Epithalon. At 4 months you would be able to calculate that the 6 month mice would have to show an 80% gain from the previously measured effects from an age specific effect (like start midlife to cause longevization) to raise that molecular
version of epithalon's longevity effect to equal or exceed Epithalon. Similarly if a molecular variant of Epithalon is 60% more longevizing at two or four momths then a side experiment can be started with 8 mice to get a p value on the more effective
version. The 8 mouse chronologically colocated experiment can also be raised to eleven mice so three can be used for things like biological samples, psychological testing and other things that accelerate longevity drug development like coaministration of
another longevity drug, likely one with a high likeliness of having a different complementary mechanism

sort of like calculating a school grade mid term to decide to keep taking a class

This batched matrix longevity drug protocol can be used on other species as well. 96 well plate fish are vertebrates, age batching can be accomplished on-location without a breeding facility. I have read about fish with a 6 month lifespan, causing the
longevity test batches to be either 14 days or a month apart, causing either one month drug characterization or 42 day longevity drug characterization. This also provides the opportunity to medicate the fish before mid-life to explore and find new
mechanisms, and measure young behaviors on the longevity drug.

it is also possible to do age batched matrix longevity drug characterization on c elegans. The lifespan of c elegans doubles at some published protocols from 30 to 60 days. The thirty day span can be divided into ten 3 day batches, and the matrix batched
longevity increase percentage can be calculated from three age batches in nine days. It is possible that a 96 well plate technology could be enhanced to use computer vision and an acoustic transducer, or just a speaker, perhaps at deciHz (tenths of a Hz)
and silent to humans to do the same touch the c elegans with a probe to see if it moves, verifying it is alive in an automated and contactless way.

The near camera automatic sonic probe physically motionizes the c elegans, contactlessly imitating a physical probe. To be less annoying, an intensity that 99.999 percent of c elegans will respond to but not louder is possible. Optimally the sonic probe
has a focused beam of less than 1/16th of the plate well area so when the c elegans responds to it the c elegans gets immediate absence of probe stimulation. The sonic probe wiggles the c elegans slightly, causing c elegans initiated motion that is a
computer vision detectable motion at the c elegans verifying it is still alive. This replaces a human with a probe and supports full automation of the longevity drug screening process. Automated pipetting could be used to administer a fresh dose of the
test chemical. Automated pipetting could also be used to rotate out the water periodically to keep the c elegans well and also at standardized drug concentrations.

I think it is possible to place one to four c elegans per plate. At just four c elegans per plate, i think the p

Noting it is possible to get a p value of .01 if the statement has that much mathematical latitude, " they are still alive", and that the computer vision system can measure 3-7 things simultaneously, with a general enough statement like "the c elegans is
above the first standard deviation (compared with normal c elegans) at some automatically measured characteristic" on things like: velocity the c elegans moves when acoustically probed, distance and swimming style of the c elgans when probed, amount of
tropism to or away from a laser illuminating part of the well, food enrichment response, possibly even the effect of pipetting another brief-action drug like a neurotransmitter that causes a behavior into the well's water, any visual indicators that
change with age at c elegans like skin texture, gonad size, heart rate. Also it is possible to quantify c elegans neurology. Genetically engineering the c elegans used at the screening to have fluorescence of brain based regions or neurons having
different emissions spectra fluorescent proteins that the c. Elegans has been engineered to produce. Genetically engineering different parts of the brain or neurotransmitter specific neurons characterizes which systems the longevity drug version being
screened could be benefitting. Camera gathered data on which parts of the brain activate in response to a standard harmless stimulus (food, laser, as well as the camera recording the prior to single utilization of the acoustic probe. Each of these, and
others has a statement with enough latitude to get a p

Genetically engineered c elegans that indicate their youthfulness can be produced. A fluorescent protein like green fluorescent protein is engineered to be made at the brain as well as separable organ systems like heart, liver, nerves, gas exchange
permeability structuress then the size and possibly the activity of these is automatically quantified with the computer camera and compared to preexisting data on young c elegans.

The value of matrix testing the drugs and the effect on the velocity of creation of new longevity drugs: also, notably the highest performing molecule screening matrix group could be considered a compounded (multicomponent actual treatment) drug in its
own right. If a rapalogs covalently linked to a AMPK activating peptide combined with a senolytics and an RNAi drug causes much larger longevity increase then it is ok to consider that hroup as one treatment at the mice.

Mouse poop and saliva contain circulatory fluids, indicator chemicals, and mouse cytes that could identify separate complementary longevity mechanisms without disturbing the screening mice. This is a way to heighten the effectiveness of matrix
characterization of the longevity heightening from longevity drugs, and, sometimes their combinations, if that is meaningful (note 214 year old whales and mice have almost the same systems, as do million year lifespan endoliths like algae or fungi, as
does 40,000 year kings holly with 3650 day trees, so pansystem longevity drugs have validity in their own right while tissue and organ specificity, and things like body compartment, and lipophilicity/hydrophilicity also have comprehensible value, noting
senolytics tissue localization, and deprenyl which concentrates most of its effects at a brain area called the substantial nigra, as well as the octopus living eight times longer if it does not have a sex gland (the value of specificity is vivid at the
octopus, if there were a "I can tell I have a sex gland" receptor blocking molecule then that one specific molecule, possibly at a particular physical location would cause eight times longer lifespan. That compares with rapamycin effecting mTOR
everywhere to cause 60% greater longevity, though also at humans eunuchs live 19 years longer so localization at just a few grams of tissue could also be a human longevity drug.

As a sample that can guide the mouse longevity molecule screening the c elegans or fish matrix screen to generate 99.9th percentile molecules. The three mice out of eleven to do psychological testing and get biological samples from, do positron emission
tomography at, as well as matrix combinations that match or combine a brain concentrator with a heart concentrator, are places human cognition applied to the drug matrices can occur, augmenting the simplicity of just mass screening with humans figuring
out previously unknown mechanisms from screening successes like finding chemicals at endoliths that longevize mice, and humans basing new drug cores to mass screen variations of.

Drug companies might make a multi chemical ingredient drug based on the effects of the matrix combinations that have the fewest side effects at mice, notably the 3 mice out of a group of 11 (where the other 8 provide a longevity heightening % with a p
value) and the most appealing 96 well plate fish physiology measures, like brain and heart similarity to young fish, and including fish progeny well being

Industry competition and publication multiplication: it is possible that when one company gets particular valued results from mass screening a particular kind of thing (endolith or clam chemical variations) that other companies or people that publish do,
that there is then more activity in that area, like rapamycin's proliferation of papers and people making new rapalogs, or the 8 papers on the beneficial effects of decanoic acid esters (like 10HDA(10H2DA) and HAEE) effects, this could be treated very
simply as a math multiplier of the amount of molecules being screened, if 43 99.9th percentile new longevity chemicals are found then perhaps they will cause 200 new longevity 99.9th percentile higher quality drugs to be produced.

Age batched mice at matrix experiments could possibly be complemented with age batched matrix experiments on marmosets. Marmosets live about 18 years and are a primate with a genome more similar to the human genome. With the most longevizing of the 99.
9th percentile and greater mouse longevity quantified, it is possible to get data from marmosets in 2-3 years; midlife marmoset age batches, like 16, 14, 12, 9 year old marmosets, could be characterized to see which longevity chemicals most nearly track
along with the benefits seen in mice, that traverse a previously documented progression of benefits most similarly, likely things like reduced heart disease, reduced cancer occurrence, and brain function that is maintained or sometimes improved (
rapamycin is nootropic, decanoic acid variant HAEE benefits mental health), it is possible, perhaps to quantify preserved cardiac and brain function, and possibly (possibly otherwise) cancer occurrence decrease at the drugged marmosets that are age
batched, optimally the drugs become part of the pharmacopeia people use long before the marmosets get old, but when the marmosets do get old enough to have quantified long lifespan extension above unmedicated marmosets that contributes to the preference
for that previously introduced drug, and things that might occur, like the pct of marmosets that avoided ever getting heart disease, cancer or cognitive impairment before a ratioized equivalent of a 114 year old are published, which let's people know
about quantified complementary benefits of the drug. The effect of mouse like physiology response being quantified at age-batched marmosets between 7 and 9 years of age or also 14 and 17 years of age being much higher or also nearly identical focuses
drug company products around chemicals that will most predictably work at humans.

Marmoset-mouse response similarity tracking also guides companies as to which longevity molecules are particularly beneficial at primates, and so possibly humans, and which have applicability to other areas of medicine and larger usage volume and
profitability, noting profitability causes more beneficial longevity and other use drug creation and distribution.

What happens when they feed rapamycin as well as other longevity drugs to octopus? I perceive i read that an octopus that does not have a sex gland lives eight times longer. After octopus sex gland removal rapamycin's effects at lifespan of octopus that
have a sex gland compared with no sex gland could be quantified, Octopus lifespan and tissue youthfulness physiology changes from sex gland removal could activate shared homologous genes between octopus and human, suggesting proteins that heighten
longevity that could be new longevity drugs. That also suggests that deleterious gene activation at the sex-gland-having octopus, and that the human homologous versions of these octopus sex-gland activated genes could be producing deleterious things at
normal humans just living. That suggests that epigenetic drugs like area specific methylases could decrease sex-gland-having octopus' shared homologous gene activation areas activity, bringing the human gene activation and gene product amount nearer to
that of an octopus without a sex gland. This would be tested on mice.

Gene products (like proteins), and any circulating chemicals different between sex gland having and octopus absent a sex gland could be proteins and other chemicals that if immunized against cause greater longevity and healthspan at humans. If there is
an obvious decrease in any chemicals at a sex gland having octopus compared with an octopus absent a sex gland then those chemicals could be administered, supplemented, at matrix form to age batched mice to find out if those chemicals have longevising
effects in 2-4 months. Things that decrease activity of the human octopus homologous genes that activate because of the sex gland, compared to, if there is such a thing, octopus puberty, could also be longevity drugs. Epigenetic modifiers of octopus sex
gland networked human homologous genes (methylases and others) could cause greater longevity and healthspan at humans.

They could implant an extra sex gland in an octopus and quantify and qualify the even higher activity than background at an unmodified octopus' human homologous chromosomes to find the particularly likely to be active epigenetic drugs (possibly
methylases) and immunizations against the deleterious things that are even more detectable from an octopus having two sex glands to be longevity drugs.



Preventing birth defects: find the mammal with the fewest birth defects or the rodent with least and most birth defects, particularly noting the genes turned on during prenatal development; at the rodents, then find homologous genes and SNPs at humans to
find human gene products (possibly circulating proteins) to decrease or increase, to be most like the mice with the physiochemistry of least birth defects.

It could be possible to breed mice with rates of birth defects 1/7 the to 1/16th that of wild mice; at the outdoor mouse dorm have the feeding station computers have an ultrasound probe that automatically scans any mouse that comes to eat, pregnant mice
with malformed mouse progeny would accumulate at the database and then their well progeny sterilized. The mice would, as I read mice do, have about 9-11 pregnancies per year and the new baby mice could get pregnant after a month, the feeding stations
could also remove non breeding mice from the mouse dorm, after 365 fays of only defect less mice breeding it is possible there would be a % decrease in the number of birth defects, the mice would have a well baby genome that could be compared to the
genome of the initial mice with possibly a few locatable genes that caused the reduction in birth defects; homologous genes and SNPs could be found at humans for both less than median and more than median defects; any difference in circulating
physiochemical produces a group of chemicals that could be screened to find out if their use as drugs would decrease birth defects, or if epigenetically upregulating their production decreased birth defects, and endogenous chemicals that were associated
with birth defects could be immunized against as well as epigenetics like methylation used to decrease the amount of their production. Along with the genes the actual SNPs, alleles, and copy numbers associated with either direction (imaginably the 3rd
and 97th percentiles) at mouse genes with human homologous genes could be looked for at human gene databases, like those of health organizations, to find out if human variations on those birth defect producing or birth defect preventing genes had strong
numerical associations at humans as well, the human physiochemical differences between the 3rd and 97th percentiles of birth defect rick as suggested from the mouse genes (notably the newly found birth defect reduction genes) would provide a human
physiochemical identity source to derive new birth defect preventing drugs, immunizations, epigenetic modifiers and germline gene modifications with. If a human woman had genes that carried risk she could do a cheek swab, have stem cells produced, the
deleterious genes changed to the more beneficial defect decreasing versions, then conceive a child with the engineered oocyte which would also reduce the risk of birth defects at all of the human woman's progeny, this is also an opportunity for the woman
to enhance the rest of her child's genome.

What would be really amazing is if there were two strains of interbreedable mice, one strain having 1/7 to 1/16 the occurrence of birth defects, the genetic difference between them looked at to find out if there are human homologous genes, and, perhaps
the nifty birth defect preventing thing, notably different SNPs, alleles,and copy number variants between the two strains that have similar genetic variations at humans or at humans' particular specific homologous gene versions; at SNPs at two different
genes that are particularly active prenatally, the mice with less defects could have a particular two SNP difference from other mice, at humans it is possible some pct of the population has two of the SNPs, one or none, they could measure the amount of
birth defects at the humans to find out if those SNPs made a difference at humans, then go through the homologous genes' mouse-human SNP difference (further away from or nearer to each of the mouse' varieties(number of different SNPs; which variety
version of mouses multiple snps, are there)) one gene at a time, simultaneously looking at a big database of different human genomes and comparing it to the mice, matching mouse and human SNPs, alleles and copy number variations to humans that gave birth
to unwell persons; that finds genes that if engineered to be at mice, can be quantified as to how much birth defect risk they produce then drugs and epigenetic regulators and immunizations and gene therapies used to decrease birth defects at humans.

There is the pleasant possibility, without anything I have heard of to suggest actuality, that the genes of birth defect preclusion (found at the mouse dorm mice) could actually enhance baby wellness causing normal babies to be slightly better than well
or to thrive more. There is mathematical support for this, if the number of birth defect reducing genes is near 29 then there is a certain likeliness one or more of the genes is beneficial to the human, perhaps they make more of one beneficial amino acid,
have the super high productivity version of a DHA (omega 3 fatty acid) gene, or a hox gene variant that has extra fidelity when transcribed, or liver genes that are 99th percentile at metabolizing risk causing xenobiotics, or maternal genes not just of
placenta sufficiency but 99th percentile of placenta optimality (perhaps a differing group of genes or SNPs that variously optimize size, vasculature (notably micro vasculature), development velocity (hormone sensitivity); the genes that availablize
nutrients from the mothers body like calcium, phosphorus, and iron could have well baby enhanced versions, the genes that do quality control, like when a woman misses her period for just one month because there was a defective blastocyst or zygote and
the quality assurance physiology terminated it; making it so one out of two birth defects were prevented but rather than half of women having sex get pregnant in 7 months, half of women got pregnant when having sex for 9 months, or at the womans option
she could either get pregnant almost immediately with assisted reproductive technology or take a pill, or get a depot drug, that caused her to have just 1/3 the chance of birth defects while causing such heightened quality assurance physiology that it
took an average woman 19 months to get pregnant. It is also possible the pregnancy quality assurance phenotype and genotype could be made more effective with drugs or gene therapy while minimally effecting the amount of time to get pregnant; SNPs and
alleles of the pregnancy quality assurance process, where I think i read but might misremember, that about half of all blsstocysts (or possibly zygotes got naturally terminated at a normal 2019 woman's body, that process if it has to do with quality
assurance could be adjusted to heighten quality further.

Dominant along with other, simultaneous multirecessive genes that do the same thing, reduce birth defects, would persist at a population even if there were things that effected various genotypes

Breed different mouse strains to be as similar as possible while presenting the half as many defects difference

Find the primate with the least presence of being then utilize that as a physiological experimental animal, feelingless p-zombie as much as possible. Notably this could be a particular genetics at most or several different primate species, noting there
are humans that say they aren't conscious, find the most p-zombie genetics at numerous species then breed or make physiological experimental animals as well as milk cows and egg chickens and caviar fish

Noting human eunuchs live 19 years longer, screening a few thousand sex hormone variations at 96 well plate fish to find 1-100 that longevize without changing behavior could produce a longevity drug screenable on mice. 17 alpha estradiol's published
longevity effects at mice without feminizing effects could be a hint.









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* Origin: fsxNet Usenet Gateway (21:1/5)

How many sequential doses of an epigenetic drug cause the epigenetic improvement? Liposomal depot, perhaps attached to an antibody that gloms it to the surface of the lining of the lymphatic compartment could diffuse beneficial drugs, although that seems
complex. One possibly as is epigenetic modifying drug palmitate. I do not know if the longevity effects of 10HDA(10H2DA) are from HDAC interference and epigenetic, but if they are then taking a high dose of 10HDA once a month (or some other interval), or
like 30 grams of royal jelly which has 10HDA(10HDA) for two or three days once a month could have the same or better longevity effect. There is the possibility that occasional high dose 10HDA(10H2DA) or royal jelly is actually more longevizing from being
thorough and of higher activity.

One HDAC2 inhibitor is a nootropic. It is possible that one or two high doses of that HDAC inhibitor a month could

Cause greater cognitive ability.

Notably though there is another version of this. I read histone epigenetics like acetylation can change rapidly, perhaps in minutes, although the other long view also makes sense as people get epigenetics from from their parents or even grandparents. I
perceive I read there is longevity epigenetics people get from their parents so a couple days of epigenetic dosing could cause greater longevity effects the person's entire life. A couple days of epigenetic modifier dosing could even cause their children
and grandchildren to have greater longevity. At the nootropic HDAC2 inhibitor that causes greater cognitive ability, a couple days of HDAC2 inhibitor dosing could cause intelligence enhancement that is also passed along to children and grandchildren.

Cognitive ability genetics: the genes that the published cognitive ability heightening HDAC2 inhibitor modifies could be g (like iq) intelligence genes. SNPs, alleles, and copy numbers of those genes could be enhanced at the germline or with gene therapy
to increase intelligence at humans, that is homo sapiens.

Longevity technology:

I perceive piperine causes greater absorption through the membranes of the GI tract from telling them to be more permeable. Is there anything that could be placed at liposomes along with the active pharmaceutical ingredient (ÅPI) which reach the
lymphatic system to make the lymphatic membranes more permeable? It could be piperine again. That lymphatic permeability drug could make other drugs, like rapamycin, rapalogs, or other longevity drugs to be 2-4 times as effective at reaching tissues from
the lymphatic system. Combined with the 2-10 times greater effectiveness of drugs that skip first pass hepatic metabolism that could make rapamycin, rapalogs, senolytics, or other longevity drugs 4 to 20 times more active and affordable. Rapamycin that
makes mice live 60% longer could be just 12-14 cents a dose based on $40/gram at Alibaba.com .

GSK (Glaxo Smith Klein) has an online page where they request technology ideas. They make Tylenol and some other antipyretic pills:

ela–naproxen (ela-n) is ethynyl liposomal active transport naproxen it is active at about 7.6 micrograms. They could put a dot of it on the outside of regular naproxen pill that is enteric coated so there is an immediate action antipyretic at the
stomach but it also activates 11 hours later so one pill lasts 24 hours. Another way to do it is like multiminipill contac™ with ela-n microenteric coat so it dissolves better at the small intestine after 11 hours. Another way to do it is rather than a
7 day palmitate have ela-n attached to a different alkane COOH like perhaps C6COOH

To make another, delayed dose to make 24 hours of naproxen activity, that could do 36, 48, 72 hour one pill dosing as well: Another way is ela-n of three or more types taken simultaneously where each ela-n has a different enzyme-reactive group on the ela-
n with a passivating group removed by the enzyme. The enzymes that remove the passivation moiety are enzymes at the circulatory system. The first ela-n gets its passivation moiety removed first and the next ela-n gets its passivation moiety removed next
like cumulatively 90 minutes later, then do this with a sufficient elan-enzyme-unpassivated-moieties to get a smooth 24 hour, 36 hour, 48 hour or 72 hour dose curve.

Years of arthritis relief from one office visit: A depot drug form of ela-n, ea-n, which I calculate as having a 7.6 microgram 12 hour dose could put ela-n at an implant (3 year nexplanon-like) with just 16.64 mg of API at the implant. Sensibly and
obviously omitting the 2-4 times dosage multiplier enhancement from liposomes, ae-n could be a 33 mg or 66 mg entire API content implant. I think it is possible to make much longer lasting depot implants or even injections, so a decade of arthritis
relief from a decade functional implant at one offive visit is possible.

Complementing a decade functional arthritis relief implant is putting the longevity and life preserving peptides AEDG (epithalon) and thymosin at the implant. Epithalon is published as causing 24% greater longevity in mice. The combination of epithalon
with thymosin, at intermittent dosing, is published as causing people to be four times more likely to be alive after six years. Epithalon and thymosin are peptides so it is possible screening libraries of variants on these peptides could find versions
with fewer mcg per dose.

Another ela-n 24-96 hour antipyretic: put ea-n on the outside of the pill for immediate relief. At the interior of the pill layer, make the 11 hours later dose with dry liposomes that have different numbers of concentric layers at the liposome molecule,
so like the 11 hour dose has 11 concentric layers of liposomes ======Ö on it.

It is possible to simplify the ela-naproxen molecule to ethynl naproxen, or ethynyl liposomal naproxen. Ethynylizing sex hormones causes sex hormones at FDA drugs to go from a.625 milligram dose to a 600 nanogram dose, a one hundred times amplification
of effect. A cell membrane active transport moiety causes 1000 times greater transport than diffusion. Either of these alone produces microgram active doses of naproxen.

A really simple version of 24-48 hour liposomal naproxen without ethynylization or active transport moieties is to use the way liposomes avoid first pass hepatic metabolism to bring 4 times as much regular naproxen API to the circulation. If that works
on regular naproxen that makes a 24 hour dose fit in a pill half the size or at a full size pill up to 48 hours of antipyretic anti-arthritis effect. Dry liposomes could be used.

Longevity technology:

Multiple simultaneous drugs at aged batched mice are a way to make longevity drug API identification faster, and make mouse research as much as 120 times more affordable to produce a p value. Matrix simultaneous drug administration is published, and
creating batches of mice, at 8 mice each, two months or less apart in age creates 48 mice, with each duomonthly increment able to generate a longevity increase p value longevity drug. The 2^3 deaggregation mice as steps to find the actual drug that
longevizes is a way to do this. Sequential mouse experiments to locate the individual most effective longevity drug, possibly after data on 2-6 months of simultaneous administration of the drugs to new age batched groups of mice. The actual longevization
pct of each batch of mice, starting at the first two months p values, continuing to 4 months and six months also gives a number on how much longer the eight and ten month and year interval mice would have to live to continue that particular mouse'
longevity gain. This is similar to calculating course grades mid term to find out if a person can still get the grade they prefer, at mice this is how much longevity increase would numerically justify continuing that drug at that mouse for greater than
the amount of longevity from other chemicals that have been screened or exist. One API drug longevity quantification; after 4 months you could tell if an Epithalon peptide sequemce variation being screened was 60% more or 60% less longevizing than
regular Epithalon. At 4 months you would be able to calculate that the 6 month mice would have to show an 80% gain from the previously measured effects from an age specific effect (like start midlife to cause longevization) to raise that molecular
version of epithalon's longevity effect to equal or exceed Epithalon. Similarly if a molecular variant of Epithalon is 60% more longevizing at two or four momths then a side experiment can be started with 8 mice to get a p value on the more effective
version. The 8 mouse chronologically colocated experiment can also be raised to eleven mice so three can be used for things like biological samples, psychological testing and other things that accelerate longevity drug development like coaministration of
another longevity drug, likely one with a high likeliness of having a different complementary mechanism

sort of like calculating a school grade mid term to decide to keep taking a class

This batched matrix longevity drug protocol can be used on other species as well. 96 well plate fish are vertebrates, age batching can be accomplished on-location without a breeding facility. I have read about fish with a 6 month lifespan, causing the
longevity test batches to be either 14 days or a month apart, causing either one month drug characterization or 42 day longevity drug characterization. This also provides the opportunity to medicate the fish before mid-life to explore and find new
mechanisms, and measure young behaviors on the longevity drug.

it is also possible to do age batched matrix longevity drug characterization on c elegans. The lifespan of c elegans doubles at some published protocols from 30 to 60 days. The thirty day span can be divided into ten 3 day batches, and the matrix batched
longevity increase percentage can be calculated from three age batches in nine days. It is possible that a 96 well plate technology could be enhanced to use computer vision and an acoustic transducer, or just a speaker, perhaps at deciHz (tenths of a Hz)
and silent to humans to do the same touch the c elegans with a probe to see if it moves, verifying it is alive in an automated and contactless way.

The near camera automatic sonic probe physically motionizes the c elegans, contactlessly imitating a physical probe. To be less annoying, an intensity that 99.999 percent of c elegans will respond to but not louder is possible. Optimally the sonic probe
has a focused beam of less than 1/16th of the plate well area so when the c elegans responds to it the c elegans gets immediate absence of probe stimulation. The sonic probe wiggles the c elegans slightly, causing c elegans initiated motion that is a
computer vision detectable motion at the c elegans verifying it is still alive. This replaces a human with a probe and supports full automation of the longevity drug screening process. Automated pipetting could be used to administer a fresh dose of the
test chemical. Automated pipetting could also be used to rotate out the water periodically to keep the c elegans well and also at standardized drug concentrations.

I think it is possible to place one to four c elegans per plate. At just four c elegans per plate, i think the p

Noting it is possible to get a p value of .01 if the statement has that much mathematical latitude, " they are still alive", and that the computer vision system can measure 3-7 things simultaneously, with a general enough statement like "the c elegans is
above the first standard deviation (compared with normal c elegans) at some automatically measured characteristic" on things like: velocity the c elegans moves when acoustically probed, distance and swimming style of the c elgans when probed, amount of
tropism to or away from a laser illuminating part of the well, food enrichment response, possibly even the effect of pipetting another brief-action drug like a neurotransmitter that causes a behavior into the well's water, any visual indicators that
change with age at c elegans like skin texture, gonad size, heart rate. Also it is possible to quantify c elegans neurology. Genetically engineering the c elegans used at the screening to have fluorescence of brain based regions or neurons having
different emissions spectra fluorescent proteins that the c. Elegans has been engineered to produce. Genetically engineering different parts of the brain or neurotransmitter specific neurons characterizes which systems the longevity drug version being
screened could be benefitting. Camera gathered data on which parts of the brain activate in response to a standard harmless stimulus (food, laser, as well as the camera recording the prior to single utilization of the acoustic probe. Each of these, and
others has a statement with enough latitude to get a p

Genetically engineered c elegans that indicate their youthfulness can be produced. A fluorescent protein like green fluorescent protein is engineered to be made at the brain as well as separable organ systems like heart, liver, nerves, gas exchange
permeability structuress then the size and possibly the activity of these is automatically quantified with the computer camera and compared to preexisting data on young c elegans.

The value of matrix testing the drugs and the effect on the velocity of creation of new longevity drugs: also, notably the highest performing molecule screening matrix group could be considered a compounded (multicomponent actual treatment) drug in its
own right. If a rapalogs covalently linked to a AMPK activating peptide combined with a senolytics and an RNAi drug causes much larger longevity increase then it is ok to consider that hroup as one treatment at the mice.

Mouse poop and saliva contain circulatory fluids, indicator chemicals, and mouse cytes that could identify separate complementary longevity mechanisms without disturbing the screening mice. This is a way to heighten the effectiveness of matrix
characterization of the longevity heightening from longevity drugs, and, sometimes their combinations, if that is meaningful (note 214 year old whales and mice have almost the same systems, as do million year lifespan endoliths like algae or fungi, as
does 40,000 year kings holly with 3650 day trees, so pansystem longevity drugs have validity in their own right while tissue and organ specificity, and things like body compartment, and lipophilicity/hydrophilicity also have comprehensible value, noting
senolytics tissue localization, and deprenyl which concentrates most of its effects at a brain area called the substantial nigra, as well as the octopus living eight times longer if it does not have a sex gland (the value of specificity is vivid at the
octopus, if there were a "I can tell I have a sex gland" receptor blocking molecule then that one specific molecule, possibly at a particular physical location would cause eight times longer lifespan. That compares with rapamycin effecting mTOR
everywhere to cause 60% greater longevity, though also at humans eunuchs live 19 years longer so localization at just a few grams of tissue could also be a human longevity drug.

As a sample that can guide the mouse longevity molecule screening the c elegans or fish matrix screen to generate 99.9th percentile molecules. The three mice out of eleven to do psychological testing and get biological samples from, do positron emission
tomography at, as well as matrix combinations that match or combine a brain concentrator with a heart concentrator, are places human cognition applied to the drug matrices can occur, augmenting the simplicity of just mass screening with humans figuring
out previously unknown mechanisms from screening successes like finding chemicals at endoliths that longevize mice, and humans basing new drug cores to mass screen variations of.

Drug companies might make a multi chemical ingredient drug based on the effects of the matrix combinations that have the fewest side effects at mice, notably the 3 mice out of a group of 11 (where the other 8 provide a longevity heightening % with a p
value) and the most appealing 96 well plate fish physiology measures, like brain and heart similarity to young fish, and including fish progeny well being

Industry competition and publication multiplication: it is possible that when one company gets particular valued results from mass screening a particular kind of thing (endolith or clam chemical variations) that other companies or people that publish do,
that there is then more activity in that area, like rapamycin's proliferation of papers and people making new rapalogs, or the 8 papers on the beneficial effects of decanoic acid esters (like 10HDA(10H2DA) and HAEE) effects, this could be treated very
simply as a math multiplier of the amount of molecules being screened, if 43 99.9th percentile new longevity chemicals are found then perhaps they will cause 200 new longevity 99.9th percentile higher quality drugs to be produced.

Age batched mice at matrix experiments could possibly be complemented with age batched matrix experiments on marmosets. Marmosets live about 18 years and are a primate with a genome more similar to the human genome. With the most longevizing of the 99.
9th percentile and greater mouse longevity quantified, it is possible to get data from marmosets in 2-3 years; midlife marmoset age batches, like 16, 14, 12, 9 year old marmosets, could be characterized to see which longevity chemicals most nearly track
along with the benefits seen in mice, that traverse a previously documented progression of benefits most similarly, likely things like reduced heart disease, reduced cancer occurrence, and brain function that is maintained or sometimes improved (
rapamycin is nootropic, decanoic acid variant HAEE benefits mental health), it is possible, perhaps to quantify preserved cardiac and brain function, and possibly (possibly otherwise) cancer occurrence decrease at the drugged marmosets that are age
batched, optimally the drugs become part of the pharmacopeia people use long before the marmosets get old, but when the marmosets do get old enough to have quantified long lifespan extension above unmedicated marmosets that contributes to the preference
for that previously introduced drug, and things that might occur, like the pct of marmosets that avoided ever getting heart disease, cancer or cognitive impairment before a ratioized equivalent of a 114 year old are published, which let's people know
about quantified complementary benefits of the drug. The effect of mouse like physiology response being quantified at age-batched marmosets between 7 and 9 years of age or also 14 and 17 years of age being much higher or also nearly identical focuses
drug company products around chemicals that will most predictably work at humans.

Marmoset-mouse response similarity tracking also guides companies as to which longevity molecules are particularly beneficial at primates, and so possibly humans, and which have applicability to other areas of medicine and larger usage volume and
profitability, noting profitability causes more beneficial longevity and other use drug creation and distribution.

What happens when they feed rapamycin as well as other longevity drugs to octopus? I perceive i read that an octopus that does not have a sex gland lives eight times longer. After octopus sex gland removal rapamycin's effects at lifespan of octopus that
have a sex gland compared with no sex gland could be quantified, Octopus lifespan and tissue youthfulness physiology changes from sex gland removal could activate shared homologous genes between octopus and human, suggesting proteins that heighten
longevity that could be new longevity drugs. That also suggests that deleterious gene activation at the sex-gland-having octopus, and that the human homologous versions of these octopus sex-gland activated genes could be producing deleterious things at
normal humans just living. That suggests that epigenetic drugs like area specific methylases could decrease sex-gland-having octopus' shared homologous gene activation areas activity, bringing the human gene activation and gene product amount nearer to
that of an octopus without a sex gland. This would be tested on mice.

Gene products (like proteins), and any circulating chemicals different between sex gland having and octopus absent a sex gland could be proteins and other chemicals that if immunized against cause greater longevity and healthspan at humans. If there is
an obvious decrease in any chemicals at a sex gland having octopus compared with an octopus absent a sex gland then those chemicals could be administered, supplemented, at matrix form to age batched mice to find out if those chemicals have longevising
effects in 2-4 months. Things that decrease activity of the human octopus homologous genes that activate because of the sex gland, compared to, if there is such a thing, octopus puberty, could also be longevity drugs. Epigenetic modifiers of octopus sex
gland networked human homologous genes (methylases and others) could cause greater longevity and healthspan at humans.

They could implant an extra sex gland in an octopus and quantify and qualify the even higher activity than background at an unmodified octopus' human homologous chromosomes to find the particularly likely to be active epigenetic drugs (possibly
methylases) and immunizations against the deleterious things that are even more detectable from an octopus having two sex glands to be longevity drugs.



Preventing birth defects: find the mammal with the fewest birth defects or the rodent with least and most birth defects, particularly noting the genes turned on during prenatal development; at the rodents, then find homologous genes and SNPs at humans to
find human gene products (possibly circulating proteins) to decrease or increase, to be most like the mice with the physiochemistry of least birth defects.

It could be possible to breed mice with rates of birth defects 1/7 the to 1/16th that of wild mice; at the outdoor mouse dorm have the feeding station computers have an ultrasound probe that automatically scans any mouse that comes to eat, pregnant mice
with malformed mouse progeny would accumulate at the database and then their well progeny sterilized. The mice would, as I read mice do, have about 9-11 pregnancies per year and the new baby mice could get pregnant after a month, the feeding stations
could also remove non breeding mice from the mouse dorm, after 365 fays of only defect less mice breeding it is possible there would be a % decrease in the number of birth defects, the mice would have a well baby genome that could be compared to the
genome of the initial mice with possibly a few locatable genes that caused the reduction in birth defects; homologous genes and SNPs could be found at humans for both less than median and more than median defects; any difference in circulating
physiochemical produces a group of chemicals that could be screened to find out if their use as drugs would decrease birth defects, or if epigenetically upregulating their production decreased birth defects, and endogenous chemicals that were associated
with birth defects could be immunized against as well as epigenetics like methylation used to decrease the amount of their production. Along with the genes the actual SNPs, alleles, and copy numbers associated with either direction (imaginably the 3rd
and 97th percentiles) at mouse genes with human homologous genes could be looked for at human gene databases, like those of health organizations, to find out if human variations on those birth defect producing or birth defect preventing genes had strong
numerical associations at humans as well, the human physiochemical differences between the 3rd and 97th percentiles of birth defect rick as suggested from the mouse genes (notably the newly found birth defect reduction genes) would provide a human
physiochemical identity source to derive new birth defect preventing drugs, immunizations, epigenetic modifiers and germline gene modifications with. If a human woman had genes that carried risk she could do a cheek swab, have stem cells produced, the
deleterious genes changed to the more beneficial defect decreasing versions, then conceive a child with the engineered oocyte which would also reduce the risk of birth defects at all of the human woman's progeny, this is also an opportunity for the woman
to enhance the rest of her child's genome.

What would be really amazing is if there were two strains of interbreedable mice, one strain having 1/7 to 1/16 the occurrence of birth defects, the genetic difference between them looked at to find out if there are human homologous genes, and, perhaps
the nifty birth defect preventing thing, notably different SNPs, alleles,and copy number variants between the two strains that have similar genetic variations at humans or at humans' particular specific homologous gene versions; at SNPs at two different
genes that are particularly active prenatally, the mice with less defects could have a particular two SNP difference from other mice, at humans it is possible some pct of the population has two of the SNPs, one or none, they could measure the amount of
birth defects at the humans to find out if those SNPs made a difference at humans, then go through the homologous genes' mouse-human SNP difference (further away from or nearer to each of the mouse' varieties(number of different SNPs; which variety
version of mouses multiple snps, are there)) one gene at a time, simultaneously looking at a big database of different human genomes and comparing it to the mice, matching mouse and human SNPs, alleles and copy number variations to humans that gave birth
to unwell persons; that finds genes that if engineered to be at mice, can be quantified as to how much birth defect risk they produce then drugs and epigenetic regulators and immunizations and gene therapies used to decrease birth defects at humans.

There is the pleasant possibility, without anything I have heard of to suggest actuality, that the genes of birth defect preclusion (found at the mouse dorm mice) could actually enhance baby wellness causing normal babies to be slightly better than well
or to thrive more. There is mathematical support for this, if the number of birth defect reducing genes is near 29 then there is a certain likeliness one or more of the genes is beneficial to the human, perhaps they make more of one beneficial amino acid,
have the super high productivity version of a DHA (omega 3 fatty acid) gene, or a hox gene variant that has extra fidelity when transcribed, or liver genes that are 99th percentile at metabolizing risk causing xenobiotics, or maternal genes not just of
placenta sufficiency but 99th percentile of placenta optimality (perhaps a differing group of genes or SNPs that variously optimize size, vasculature (notably micro vasculature), development velocity (hormone sensitivity); the genes that availablize
nutrients from the mothers body like calcium, phosphorus, and iron could have well baby enhanced versions, the genes that do quality control, like when a woman misses her period for just one month because there was a defective blastocyst or zygote and
the quality assurance physiology terminated it; making it so one out of two birth defects were prevented but rather than half of women having sex get pregnant in 7 months, half of women got pregnant when having sex for 9 months, or at the womans option
she could either get pregnant almost immediately with assisted reproductive technology or take a pill, or get a depot drug, that caused her to have just 1/3 the chance of birth defects while causing such heightened quality assurance physiology that it
took an average woman 19 months to get pregnant. It is also possible the pregnancy quality assurance phenotype and genotype could be made more effective with drugs or gene therapy while minimally effecting the amount of time to get pregnant; SNPs and
alleles of the pregnancy quality assurance process, where I think i read but might misremember, that about half of all blsstocysts (or possibly zygotes got naturally terminated at a normal 2019 woman's body, that process if it has to do with quality
assurance could be adjusted to heighten quality further.

Dominant along with other, simultaneous multirecessive genes that do the same thing, reduce birth defects, would persist at a population even if there were things that effected various genotypes

Breed different mouse strains to be as similar as possible while presenting the half as many defects difference

Find the primate with the least presence of being then utilize that as a physiological experimental animal, feelingless p-zombie as much as possible. Notably this could be a particular genetics at most or several different primate species, noting there
are humans that say they aren't conscious, find the most p-zombie genetics at numerous species then breed or make physiological experimental animals as well as milk cows and egg chickens and caviar fish

Noting human eunuchs live 19 years longer, screening a few thousand sex hormone variations at 96 well plate fish to find 1-100 that longevize without changing behavior could produce a longevity drug screenable on mice. 17 alpha estradiol's published
longevity effects at mice without feminizing effects could be a hint.

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the King’s Holly has lived 1.46 million days thus far, other trees have a lifespan of just 3650 days, ceasing to be alive even before a human reaches puberty; Finding longevity drugs based on the 400,000 percent different longevity difference between
trees goes with doing HPLC, something better than electrophoresis like laser spectroscopy, electrophoresis or some other thing, to find all the chemicals, proteins, peptides, lipids, in the plants, as well as at human tissue, then finding those chemicals,
proteins, peptides, lipids difference between the 1.46 million day longevity plant, the 3650 day plant, and the human;



I read humans share 60% of their genome with the banana, that suggests some plant genes, and plant gene products, and the amount of those chemical plant gene products, have most longevizing molecule versions that can be quantified as to longevity effects
at yeast and mice;



finding longevity chemicals: the group of chemicals (and genes) at both the (3650 day tree and the human) that are different than the chemicals that the (kings holly and the human share) are places where the chemicals (and the genes) at the humans could
improve and the king’s holly is the source of improvement;



At homologous genes an organisms that noticed it had the 3650 day plant version rather than the kings holly would notice an opportunity to have more longevizing chemicals endogenously produced



finding longevity chemicals: dosing yeast and mice with the chemical that the kings holly gene makes, that the human does not, noting the homologous but different gene, could find longevity drugs;



engineering mice and yeast to make that shared homologous kings holly gene then finding out if it longevizes them produces new longevity genes



This same approach works for finding longevizing chemicals between groups like million year lifespan endoliths comparison grouped with similar-to-endolith with different habitat organisms with 365 day lifespans, 214 year old whales, and whales with
briefer lifespans, 400 year lifespan clams, and clams with annual lifespans, and supercentenarian humans with 18 year marmosets;



The genes and gene products (chemicals) that the 400 year clam shares with the annual clam are ignored when narrowing the list of chemicals and genes at the human to find 400 year clam genes with longevity effects;



Now, although the amount of the chemicals matters the same thing can be done with chemicals, proteins, peptides, and lipids at the bodies of the various trees and other organisms



If the chemical is the the 3650 day plant and the king’s holly, ignore it, if it is only at the king’s holly put it in a database;



This works better at varieties of the same species with widely varying lifespans, if there are any species that interbreed but have 2-4 times different longevity, then ignoring the chemicals they share, then making a database of the chemicals only at the
long lived variety, then at humans finding if any of the database chamicals



There is a thing here though that kind of makes it improvable, for each 14 million chemicals the kings holly contains, and the 3650 plant overlaps 90% of them, that is still 1.4 million chemicals that might have longevity effects;



I think geneticists who write computer programs already know all about this, but if you have like 100 groups of related-organisms pairs (king’s holly 3650 day tree),(mouse, beaver), (214 year whale, less longevity whale), (human, primate with 1/5th
human lifespan) with the group members as far apart as possible as to longevity, and then compare the amount the very different most long lived species converge towards each others gene versions, notably moving away from their species-similar organisim,
then you find a possible math convergence around better versions of genes, or better versions of physiochemicals



The high longevity organisms at each of the 100 bowls of 2 or 3 longevity heterogenous organisms each



This technique can be used for other things like, 100 bowls of 2 or 3 mammals each, and the species similar mammals differ as much as possible on behavior, then you look at how the bowl leaders (of very different species) converge on various
characteristics, these can be genes, fMRI of brain areas, even things like parenting styles; a human, or niftily, a deep learning AI can then make a list of trends



(Mathematically you would expect the beaver to be more like the mouse, but if the beaver is more like the whale, the human, and the King’s holly then there might be a longevity trend at that homologous gene, similarly you might expect a human to be
more like a marmoset than a whale or the king’s holly, but at genes where the king’s holly is more similar that could suggest a “different chemical is better” trend, then noting the upper longevity organisms at each of the 100 bowls each with two
or three species in them (mouse beaver, 214 year whale, less longevized whale) (longevized bat, less longevized bat) (human, primate with 1/5th human longevity)



The 100 bowls of three high distalness (long lived, otherwise) yet each bowl with similar species could be repeated at species that have particularly wide longevity ranges, perhaps birds as well; if this finds a longevity trend for a group of genes at
very different birds, then the genes the different bowl gnes most share



also the 100 bowls thing of 2 or 3 organisms thing works with longevity chemicals as well, if 100 bowls find like 5000 circulatory chemicals shared at the long lived organisms out of each bowl, then those 5000 chemicals are compared to the chemicals in a
human, any of the 100 bowl shared longevity chemicals the human does not (yet) have could be tested on yeast and mice and human tissue culture to find out if they are longevizing; this works with homologous genes as well, if you have 100 bowls of clams,
birds, sharks, endoliths, plants, and other things, and the distal organisms in each bowl have and above-chance occurence of shared genes, then those could be longevity genes and a human would compare their genome to that shared at the 100 bowls of very
different species; mathematically it would be possible to list in order the genes shared between bowls, and the longevity trend of just that group of bowl-set organisims, so it would be possible to find the likely most longevizing versions of the bowl-
shared genes;



at endoliths, 100 bowls as a way to find new human longevity genes has nifty characteristics; endoliths can be bacteria, fungi, algae or lichen, very different species, but they all share lifespans longer than the entire span of human culture; first find
briefer species that are most genetically similar to the endoliths, (3 century lichens) (24 hour bacteria) to put in the bowls, with each of the 100 bowls having an endolith; do HPLC on all the organisms chemicals, and sequence the genomes of the 200 or
300 organisms in the 100 bowls, then find where the endoliths converge towards each other, across widely differing species, and away from the other organisms at their bowl,



The chemicals (proteins, peptides, others) that subsets of endoliths produce that have varied amounts of convergence at different subsets of the 100 bowls can be tested as longevity cheimcals;



encouragingly, the 10,000 year lifespan creosote bush produces NDGA, which is also published as causing greater longevity at mice, so chemicals that 100 different endoliths converge on, at unexpected divergence from the other organisms in their similar
species bowl, could be longevity drugs and chemicals;



similarly, the long lifespan but species heterogenity of endoliths (algae, bacteria, fungi) if there are any converged on homologous genes could actually suggests genetics of greater longevity at humans, that can be tested on mice, let’s say the
endoliths all have mitochondrial DNA that causes mitochondrial uncoupling, then a human could look through a database of mammal genetics and genomes and find out if any mammals had uncoupled mitochondria, and the effect it had on that species being above
the median, or high above the median on longevity; (I read that mitochondrial uncoupling actuallu doubles c elegans lifespan, it just seems possible to have a 100 bowl convergence be able to find it as well)



do the “are there any mammals like the converged endoliths’ homologous genes unusualness of form, and, how is it going for them?” thing automatically with computers, also, the technique can be used with any group of species like birds, or
tortoises, or even bowls of plants, along with the kings holly there are many trees with multimillenia lifespans



when they do, that version of that mammal gene is unusually likely to be a longevity gene, and using yeast and mouse full lifespan to quantify its effects is beneficial and produces a longevity gene; notably though the gene sometimes makes a product like
a protein, endolith converged, then found at mammal genes’ proteins could be screened as to longevity effect; I read that sme endoliths, after you put them in a comfy environment grow rapidly, and a kilogram of cultured endolith might provide enough
converged-endolith-gene product to dose shrews, c elegans, yeast, and human tissue culture; (it is kind of nice with 100 bowls you get to skip screening a library, you just culture and gather material from of the species at one of the bowls that makes
the converged on chemical, a mathematician would be able to suggest the optimal number of bowls, with endoliths perhaps it is 300 because, if there is convergence on some chemicals, rather than the numerics of screening a library you already have a
source)

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How many sequential doses of an epigenetic drug cause the epigenetic improvement? Liposomal depot, perhaps attached to an antibody that gloms it to the surface of the lining of the lymphatic compartment could diffuse beneficial drugs, although that seems
complex. One possibly as is epigenetic modifying drug palmitate. I do not know if the longevity effects of 10HDA(10H2DA) are from HDAC interference and epigenetic, but if they are then taking a high dose of 10HDA once a month (or some other interval), or
like 30 grams of royal jelly which has 10HDA(10HDA) for two or three days once a month could have the same or better longevity effect. There is the possibility that occasional high dose 10HDA(10H2DA) or royal jelly is actually more longevizing from being
thorough and of higher activity.

One HDAC2 inhibitor is a nootropic. It is possible that one or two high doses of that HDAC inhibitor a month could

Cause greater cognitive ability.

Notably though there is another version of this. I read histone epigenetics like acetylation can change rapidly, perhaps in minutes, although the other long view also makes sense as people get epigenetics from from their parents or even grandparents. I
perceive I read there is longevity epigenetics people get from their parents so a couple days of epigenetic dosing could cause greater longevity effects the person's entire life. A couple days of epigenetic modifier dosing could even cause their children
and grandchildren to have greater longevity. At the nootropic HDAC2 inhibitor that causes greater cognitive ability, a couple days of HDAC2 inhibitor dosing could cause intelligence enhancement that is also passed along to children and grandchildren.

Cognitive ability genetics: the genes that the published cognitive ability heightening HDAC2 inhibitor modifies could be g (like iq) intelligence genes. SNPs, alleles, and copy numbers of those genes could be enhanced at the germline or with gene therapy
to increase intelligence at humans, that is homo sapiens.

Longevity technology:

I perceive piperine causes greater absorption through the membranes of the GI tract from telling them to be more permeable. Is there anything that could be placed at liposomes along with the active pharmaceutical ingredient (ÅPI) which reach the
lymphatic system to make the lymphatic membranes more permeable? It could be piperine again. That lymphatic permeability drug could make other drugs, like rapamycin, rapalogs, or other longevity drugs to be 2-4 times as effective at reaching tissues from
the lymphatic system. Combined with the 2-10 times greater effectiveness of drugs that skip first pass hepatic metabolism that could make rapamycin, rapalogs, senolytics, or other longevity drugs 4 to 20 times more active and affordable. Rapamycin that
makes mice live 60% longer could be just 12-14 cents a dose based on $40/gram at Alibaba.com .

GSK (Glaxo Smith Klein) has an online page where they request technology ideas. They make Tylenol and some other antipyretic pills:

ela–naproxen (ela-n) is ethynyl liposomal active transport naproxen it is active at about 7.6 micrograms. They could put a dot of it on the outside of regular naproxen pill that is enteric coated so there is an immediate action antipyretic at the
stomach but it also activates 11 hours later so one pill lasts 24 hours. Another way to do it is like multiminipill contac™ with ela-n microenteric coat so it dissolves better at the small intestine after 11 hours. Another way to do it is rather than a
7 day palmitate have ela-n attached to a different alkane COOH like perhaps C6COOH

To make another, delayed dose to make 24 hours of naproxen activity, that could do 36, 48, 72 hour one pill dosing as well: Another way is ela-n of three or more types taken simultaneously where each ela-n has a different enzyme-reactive group on the ela-
n with a passivating group removed by the enzyme. The enzymes that remove the passivation moiety are enzymes at the circulatory system. The first ela-n gets its passivation moiety removed first and the next ela-n gets its passivation moiety removed next
like cumulatively 90 minutes later, then do this with a sufficient elan-enzyme-unpassivated-moieties to get a smooth 24 hour, 36 hour, 48 hour or 72 hour dose curve.

Years of arthritis relief from one office visit: A depot drug form of ela-n, ea-n, which I calculate as having a 7.6 microgram 12 hour dose could put ela-n at an implant (3 year nexplanon-like) with just 16.64 mg of API at the implant. Sensibly and
obviously omitting the 2-4 times dosage multiplier enhancement from liposomes, ae-n could be a 33 mg or 66 mg entire API content implant. I think it is possible to make much longer lasting depot implants or even injections, so a decade of arthritis
relief from a decade functional implant at one offive visit is possible.

Complementing a decade functional arthritis relief implant is putting the longevity and life preserving peptides AEDG (epithalon) and thymosin at the implant. Epithalon is published as causing 24% greater longevity in mice. The combination of epithalon
with thymosin, at intermittent dosing, is published as causing people to be four times more likely to be alive after six years. Epithalon and thymosin are peptides so it is possible screening libraries of variants on these peptides could find versions
with fewer mcg per dose.

Another ela-n 24-96 hour antipyretic: put ea-n on the outside of the pill for immediate relief. At the interior of the pill layer, make the 11 hours later dose with dry liposomes that have different numbers of concentric layers at the liposome molecule,
so like the 11 hour dose has 11 concentric layers of liposomes ======Ö on it.

It is possible to simplify the ela-naproxen molecule to ethynl naproxen, or ethynyl liposomal naproxen. Ethynylizing sex hormones causes sex hormones at FDA drugs to go from a.625 milligram dose to a 600 nanogram dose, a one hundred times amplification
of effect. A cell membrane active transport moiety causes 1000 times greater transport than diffusion. Either of these alone produces microgram active doses of naproxen.

A really simple version of 24-48 hour liposomal naproxen without ethynylization or active transport moieties is to use the way liposomes avoid first pass hepatic metabolism to bring 4 times as much regular naproxen API to the circulation. If that works
on regular naproxen that makes a 24 hour dose fit in a pill half the size or at a full size pill up to 48 hours of antipyretic anti-arthritis effect. Dry liposomes could be used.

Longevity technology:

Multiple simultaneous drugs at aged batched mice are a way to make longevity drug API identification faster, and make mouse research as much as 120 times more affordable to produce a p value. Matrix simultaneous drug administration is published, and
creating batches of mice, at 8 mice each, two months or less apart in age creates 48 mice, with each duomonthly increment able to generate a longevity increase p value longevity drug. The 2^3 deaggregation mice as steps to find the actual drug that
longevizes is a way to do this. Sequential mouse experiments to locate the individual most effective longevity drug, possibly after data on 2-6 months of simultaneous administration of the drugs to new age batched groups of mice. The actual longevization
pct of each batch of mice, starting at the first two months p values, continuing to 4 months and six months also gives a number on how much longer the eight and ten month and year interval mice would have to live to continue that particular mouse'
longevity gain. This is similar to calculating course grades mid term to find out if a person can still get the grade they prefer, at mice this is how much longevity increase would numerically justify continuing that drug at that mouse for greater than
the amount of longevity from other chemicals that have been screened or exist. One API drug longevity quantification; after 4 months you could tell if an Epithalon peptide sequemce variation being screened was 60% more or 60% less longevizing than
regular Epithalon. At 4 months you would be able to calculate that the 6 month mice would have to show an 80% gain from the previously measured effects from an age specific effect (like start midlife to cause longevization) to raise that molecular
version of epithalon's longevity effect to equal or exceed Epithalon. Similarly if a molecular variant of Epithalon is 60% more longevizing at two or four momths then a side experiment can be started with 8 mice to get a p value on the more effective
version. The 8 mouse chronologically colocated experiment can also be raised to eleven mice so three can be used for things like biological samples, psychological testing and other things that accelerate longevity drug development like coaministration of
another longevity drug, likely one with a high likeliness of having a different complementary mechanism

sort of like calculating a school grade mid term to decide to keep taking a class

This batched matrix longevity drug protocol can be used on other species as well. 96 well plate fish are vertebrates, age batching can be accomplished on-location without a breeding facility. I have read about fish with a 6 month lifespan, causing the
longevity test batches to be either 14 days or a month apart, causing either one month drug characterization or 42 day longevity drug characterization. This also provides the opportunity to medicate the fish before mid-life to explore and find new
mechanisms, and measure young behaviors on the longevity drug.

it is also possible to do age batched matrix longevity drug characterization on c elegans. The lifespan of c elegans doubles at some published protocols from 30 to 60 days. The thirty day span can be divided into ten 3 day batches, and the matrix batched
longevity increase percentage can be calculated from three age batches in nine days. It is possible that a 96 well plate technology could be enhanced to use computer vision and an acoustic transducer, or just a speaker, perhaps at deciHz (tenths of a Hz)
and silent to humans to do the same touch the c elegans with a probe to see if it moves, verifying it is alive in an automated and contactless way.

The near camera automatic sonic probe physically motionizes the c elegans, contactlessly imitating a physical probe. To be less annoying, an intensity that 99.999 percent of c elegans will respond to but not louder is possible. Optimally the sonic probe
has a focused beam of less than 1/16th of the plate well area so when the c elegans responds to it the c elegans gets immediate absence of probe stimulation. The sonic probe wiggles the c elegans slightly, causing c elegans initiated motion that is a
computer vision detectable motion at the c elegans verifying it is still alive. This replaces a human with a probe and supports full automation of the longevity drug screening process. Automated pipetting could be used to administer a fresh dose of the
test chemical. Automated pipetting could also be used to rotate out the water periodically to keep the c elegans well and also at standardized drug concentrations.

I think it is possible to place one to four c elegans per plate. At just four c elegans per plate, i think the p

Noting it is possible to get a p value of .01 if the statement has that much mathematical latitude, " they are still alive", and that the computer vision system can measure 3-7 things simultaneously, with a general enough statement like "the c elegans is
above the first standard deviation (compared with normal c elegans) at some automatically measured characteristic" on things like: velocity the c elegans moves when acoustically probed, distance and swimming style of the c elgans when probed, amount of
tropism to or away from a laser illuminating part of the well, food enrichment response, possibly even the effect of pipetting another brief-action drug like a neurotransmitter that causes a behavior into the well's water, any visual indicators that
change with age at c elegans like skin texture, gonad size, heart rate. Also it is possible to quantify c elegans neurology. Genetically engineering the c elegans used at the screening to have fluorescence of brain based regions or neurons having
different emissions spectra fluorescent proteins that the c. Elegans has been engineered to produce. Genetically engineering different parts of the brain or neurotransmitter specific neurons characterizes which systems the longevity drug version being
screened could be benefitting. Camera gathered data on which parts of the brain activate in response to a standard harmless stimulus (food, laser, as well as the camera recording the prior to single utilization of the acoustic probe. Each of these, and
others has a statement with enough latitude to get a p

Genetically engineered c elegans that indicate their youthfulness can be produced. A fluorescent protein like green fluorescent protein is engineered to be made at the brain as well as separable organ systems like heart, liver, nerves, gas exchange
permeability structuress then the size and possibly the activity of these is automatically quantified with the computer camera and compared to preexisting data on young c elegans.

The value of matrix testing the drugs and the effect on the velocity of creation of new longevity drugs: also, notably the highest performing molecule screening matrix group could be considered a compounded (multicomponent actual treatment) drug in its
own right. If a rapalogs covalently linked to a AMPK activating peptide combined with a senolytics and an RNAi drug causes much larger longevity increase then it is ok to consider that hroup as one treatment at the mice.

Mouse poop and saliva contain circulatory fluids, indicator chemicals, and mouse cytes that could identify separate complementary longevity mechanisms without disturbing the screening mice. This is a way to heighten the effectiveness of matrix
characterization of the longevity heightening from longevity drugs, and, sometimes their combinations, if that is meaningful (note 214 year old whales and mice have almost the same systems, as do million year lifespan endoliths like algae or fungi, as
does 40,000 year kings holly with 3650 day trees, so pansystem longevity drugs have validity in their own right while tissue and organ specificity, and things like body compartment, and lipophilicity/hydrophilicity also have comprehensible value, noting
senolytics tissue localization, and deprenyl which concentrates most of its effects at a brain area called the substantial nigra, as well as the octopus living eight times longer if it does not have a sex gland (the value of specificity is vivid at the
octopus, if there were a "I can tell I have a sex gland" receptor blocking molecule then that one specific molecule, possibly at a particular physical location would cause eight times longer lifespan. That compares with rapamycin effecting mTOR
everywhere to cause 60% greater longevity, though also at humans eunuchs live 19 years longer so localization at just a few grams of tissue could also be a human longevity drug.

As a sample that can guide the mouse longevity molecule screening the c elegans or fish matrix screen to generate 99.9th percentile molecules. The three mice out of eleven to do psychological testing and get biological samples from, do positron emission
tomography at, as well as matrix combinations that match or combine a brain concentrator with a heart concentrator, are places human cognition applied to the drug matrices can occur, augmenting the simplicity of just mass screening with humans figuring
out previously unknown mechanisms from screening successes like finding chemicals at endoliths that longevize mice, and humans basing new drug cores to mass screen variations of.

Drug companies might make a multi chemical ingredient drug based on the effects of the matrix combinations that have the fewest side effects at mice, notably the 3 mice out of a group of 11 (where the other 8 provide a longevity heightening % with a p
value) and the most appealing 96 well plate fish physiology measures, like brain and heart similarity to young fish, and including fish progeny well being

Industry competition and publication multiplication: it is possible that when one company gets particular valued results from mass screening a particular kind of thing (endolith or clam chemical variations) that other companies or people that publish do,
that there is then more activity in that area, like rapamycin's proliferation of papers and people making new rapalogs, or the 8 papers on the beneficial effects of decanoic acid esters (like 10HDA(10H2DA) and HAEE) effects, this could be treated very
simply as a math multiplier of the amount of molecules being screened, if 43 99.9th percentile new longevity chemicals are found then perhaps they will cause 200 new longevity 99.9th percentile higher quality drugs to be produced.

Age batched mice at matrix experiments could possibly be complemented with age batched matrix experiments on marmosets. Marmosets live about 18 years and are a primate with a genome more similar to the human genome. With the most longevizing of the 99.
9th percentile and greater mouse longevity quantified, it is possible to get data from marmosets in 2-3 years; midlife marmoset age batches, like 16, 14, 12, 9 year old marmosets, could be characterized to see which longevity chemicals most nearly track
along with the benefits seen in mice, that traverse a previously documented progression of benefits most similarly, likely things like reduced heart disease, reduced cancer occurrence, and brain function that is maintained or sometimes improved (
rapamycin is nootropic, decanoic acid variant HAEE benefits mental health), it is possible, perhaps to quantify preserved cardiac and brain function, and possibly (possibly otherwise) cancer occurrence decrease at the drugged marmosets that are age
batched, optimally the drugs become part of the pharmacopeia people use long before the marmosets get old, but when the marmosets do get old enough to have quantified long lifespan extension above unmedicated marmosets that contributes to the preference
for that previously introduced drug, and things that might occur, like the pct of marmosets that avoided ever getting heart disease, cancer or cognitive impairment before a ratioized equivalent of a 114 year old are published, which let's people know
about quantified complementary benefits of the drug. The effect of mouse like physiology response being quantified at age-batched marmosets between 7 and 9 years of age or also 14 and 17 years of age being much higher or also nearly identical focuses
drug company products around chemicals that will most predictably work at humans.

Marmoset-mouse response similarity tracking also guides companies as to which longevity molecules are particularly beneficial at primates, and so possibly humans, and which have applicability to other areas of medicine and larger usage volume and
profitability, noting profitability causes more beneficial longevity and other use drug creation and distribution.

What happens when they feed rapamycin as well as other longevity drugs to octopus? I perceive i read that an octopus that does not have a sex gland lives eight times longer. After octopus sex gland removal rapamycin's effects at lifespan of octopus that
have a sex gland compared with no sex gland could be quantified, Octopus lifespan and tissue youthfulness physiology changes from sex gland removal could activate shared homologous genes between octopus and human, suggesting proteins that heighten
longevity that could be new longevity drugs. That also suggests that deleterious gene activation at the sex-gland-having octopus, and that the human homologous versions of these octopus sex-gland activated genes could be producing deleterious things at
normal humans just living. That suggests that epigenetic drugs like area specific methylases could decrease sex-gland-having octopus' shared homologous gene activation areas activity, bringing the human gene activation and gene product amount nearer to
that of an octopus without a sex gland. This would be tested on mice.

Gene products (like proteins), and any circulating chemicals different between sex gland having and octopus absent a sex gland could be proteins and other chemicals that if immunized against cause greater longevity and healthspan at humans. If there is
an obvious decrease in any chemicals at a sex gland having octopus compared with an octopus absent a sex gland then those chemicals could be administered, supplemented, at matrix form to age batched mice to find out if those chemicals have longevising
effects in 2-4 months. Things that decrease activity of the human octopus homologous genes that activate because of the sex gland, compared to, if there is such a thing, octopus puberty, could also be longevity drugs. Epigenetic modifiers of octopus sex
gland networked human homologous genes (methylases and others) could cause greater longevity and healthspan at humans.

They could implant an extra sex gland in an octopus and quantify and qualify the even higher activity than background at an unmodified octopus' human homologous chromosomes to find the particularly likely to be active epigenetic drugs (possibly
methylases) and immunizations against the deleterious things that are even more detectable from an octopus having two sex glands to be longevity drugs.



Preventing birth defects: find the mammal with the fewest birth defects or the rodent with least and most birth defects, particularly noting the genes turned on during prenatal development; at the rodents, then find homologous genes and SNPs at humans to
find human gene products (possibly circulating proteins) to decrease or increase, to be most like the mice with the physiochemistry of least birth defects.

It could be possible to breed mice with rates of birth defects 1/7 the to 1/16th that of wild mice; at the outdoor mouse dorm have the feeding station computers have an ultrasound probe that automatically scans any mouse that comes to eat, pregnant mice
with malformed mouse progeny would accumulate at the database and then their well progeny sterilized. The mice would, as I read mice do, have about 9-11 pregnancies per year and the new baby mice could get pregnant after a month, the feeding stations
could also remove non breeding mice from the mouse dorm, after 365 fays of only defect less mice breeding it is possible there would be a % decrease in the number of birth defects, the mice would have a well baby genome that could be compared to the
genome of the initial mice with possibly a few locatable genes that caused the reduction in birth defects; homologous genes and SNPs could be found at humans for both less than median and more than median defects; any difference in circulating
physiochemical produces a group of chemicals that could be screened to find out if their use as drugs would decrease birth defects, or if epigenetically upregulating their production decreased birth defects, and endogenous chemicals that were associated
with birth defects could be immunized against as well as epigenetics like methylation used to decrease the amount of their production. Along with the genes the actual SNPs, alleles, and copy numbers associated with either direction (imaginably the 3rd
and 97th percentiles) at mouse genes with human homologous genes could be looked for at human gene databases, like those of health organizations, to find out if human variations on those birth defect producing or birth defect preventing genes had strong
numerical associations at humans as well, the human physiochemical differences between the 3rd and 97th percentiles of birth defect rick as suggested from the mouse genes (notably the newly found birth defect reduction genes) would provide a human
physiochemical identity source to derive new birth defect preventing drugs, immunizations, epigenetic modifiers and germline gene modifications with. If a human woman had genes that carried risk she could do a cheek swab, have stem cells produced, the
deleterious genes changed to the more beneficial defect decreasing versions, then conceive a child with the engineered oocyte which would also reduce the risk of birth defects at all of the human woman's progeny, this is also an opportunity for the woman
to enhance the rest of her child's genome.

What would be really amazing is if there were two strains of interbreedable mice, one strain having 1/7 to 1/16 the occurrence of birth defects, the genetic difference between them looked at to find out if there are human homologous genes, and, perhaps
the nifty birth defect preventing thing, notably different SNPs, alleles,and copy number variants between the two strains that have similar genetic variations at humans or at humans' particular specific homologous gene versions; at SNPs at two different
genes that are particularly active prenatally, the mice with less defects could have a particular two SNP difference from other mice, at humans it is possible some pct of the population has two of the SNPs, one or none, they could measure the amount of
birth defects at the humans to find out if those SNPs made a difference at humans, then go through the homologous genes' mouse-human SNP difference (further away from or nearer to each of the mouse' varieties(number of different SNPs; which variety
version of mouses multiple snps, are there)) one gene at a time, simultaneously looking at a big database of different human genomes and comparing it to the mice, matching mouse and human SNPs, alleles and copy number variations to humans that gave birth
to unwell persons; that finds genes that if engineered to be at mice, can be quantified as to how much birth defect risk they produce then drugs and epigenetic regulators and immunizations and gene therapies used to decrease birth defects at humans.

There is the pleasant possibility, without anything I have heard of to suggest actuality, that the genes of birth defect preclusion (found at the mouse dorm mice) could actually enhance baby wellness causing normal babies to be slightly better than well
or to thrive more. There is mathematical support for this, if the number of birth defect reducing genes is near 29 then there is a certain likeliness one or more of the genes is beneficial to the human, perhaps they make more of one beneficial amino acid,
have the super high productivity version of a DHA (omega 3 fatty acid) gene, or a hox gene variant that has extra fidelity when transcribed, or liver genes that are 99th percentile at metabolizing risk causing xenobiotics, or maternal genes not just of
placenta sufficiency but 99th percentile of placenta optimality (perhaps a differing group of genes or SNPs that variously optimize size, vasculature (notably micro vasculature), development velocity (hormone sensitivity); the genes that availablize
nutrients from the mothers body like calcium, phosphorus, and iron could have well baby enhanced versions, the genes that do quality control, like when a woman misses her period for just one month because there was a defective blastocyst or zygote and
the quality assurance physiology terminated it; making it so one out of two birth defects were prevented but rather than half of women having sex get pregnant in 7 months, half of women got pregnant when having sex for 9 months, or at the womans option
she could either get pregnant almost immediately with assisted reproductive technology or take a pill, or get a depot drug, that caused her to have just 1/3 the chance of birth defects while causing such heightened quality assurance physiology that it
took an average woman 19 months to get pregnant. It is also possible the pregnancy quality assurance phenotype and genotype could be made more effective with drugs or gene therapy while minimally effecting the amount of time to get pregnant; SNPs and
alleles of the pregnancy quality assurance process, where I think i read but might misremember, that about half of all blsstocysts (or possibly zygotes got naturally terminated at a normal 2019 woman's body, that process if it has to do with quality
assurance could be adjusted to heighten quality further.

Dominant along with other, simultaneous multirecessive genes that do the same thing, reduce birth defects, would persist at a population even if there were things that effected various genotypes

Breed different mouse strains to be as similar as possible while presenting the half as many defects difference

Find the primate with the least presence of being then utilize that as a physiological experimental animal, feelingless p-zombie as much as possible. Notably this could be a particular genetics at most or several different primate species, noting there
are humans that say they aren't conscious, find the most p-zombie genetics at numerous species then breed or make physiological experimental animals as well as milk cows and egg chickens and caviar fish

Noting human eunuchs live 19 years longer, screening a few thousand sex hormone variations at 96 well plate fish to find 1-100 that longevize without changing behavior could produce a longevity drug screenable on mice. 17 alpha estradiol's published
longevity effects at mice without feminizing effects could be a hint.

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How many sequential doses of an epigenetic drug cause the epigenetic improvement? Liposomal depot, perhaps attached to an antibody that gloms it to the surface of the lining of the lymphatic compartment could diffuse beneficial drugs, although that seems
complex. One possibly as is epigenetic modifying drug palmitate. I do not know if the longevity effects of 10HDA(10H2DA) are from HDAC interference and epigenetic, but if they are then taking a high dose of 10HDA once a month (or some other interval), or
like 30 grams of royal jelly which has 10HDA(10HDA) for two or three days once a month could have the same or better longevity effect. There is the possibility that occasional high dose 10HDA(10H2DA) or royal jelly is actually more longevizing from being
thorough and of higher activity.



One HDAC2 inhibitor is a nootropic. It is possible that one or two high doses of that HDAC inhibitor a month could

Cause greater cognitive ability.



Notably though there is another version of this. I read histone epigenetics like acetylation can change rapidly, perhaps in minutes, although the other long view also makes sense as people get epigenetics from from their parents or even grandparents. I
perceive I read there is longevity epigenetics people get from their parents so a couple days of epigenetic dosing could cause greater longevity effects the person's entire life. A couple days of epigenetic modifier dosing could even cause their children
and grandchildren to have greater longevity. At the nootropic HDAC2 inhibitor that causes greater cognitive ability, a couple days of HDAC2 inhibitor dosing could cause intelligence enhancement that is also passed along to children and grandchildren.





Cognitive ability genetics: the genes that the published cognitive ability heightening HDAC2 inhibitor modifies could be g (like iq) intelligence genes. SNPs, alleles, and copy numbers of those genes could be enhanced at the germline or with gene therapy
to increase intelligence at humans, that is homo sapiens.



Longevity technology:

I perceive piperine causes greater absorption through the membranes of the GI tract from telling them to be more permeable. Is there anything that could be placed at liposomes along with the active pharmaceutical ingredient (ÅPI) which reach the
lymphatic system to make the lymphatic membranes more permeable? It could be piperine again. That lymphatic permeability drug could make other drugs, like rapamycin, rapalogs, or other longevity drugs to be 2-4 times as effective at reaching tissues from
the lymphatic system. Combined with the 2-10 times greater effectiveness of drugs that skip first pass hepatic metabolism that could make rapamycin, rapalogs, senolytics, or other longevity drugs 4 to 20 times more active and affordable. Rapamycin that
makes mice live 60% longer could be just 12-14 cents a dose based on $40/gram at Alibaba.com .





GSK (Glaxo Smith Klein) has an online page where they request technology ideas. They make Tylenol and some other antipyretic pills:



ela–naproxen (ela-n) is ethynyl liposomal active transport naproxen it is active at about 7.6 micrograms. They could put a dot of it on the outside of regular naproxen pill that is enteric coated so there is an immediate action antipyretic at the
stomach but it also activates 11 hours later so one pill lasts 24 hours. Another way to do it is like multiminipill contac™ with ela-n microenteric coat so it dissolves better at the small intestine after 11 hours. Another way to do it is rather than a
7 day palmitate have ela-n attached to a different alkane COOH like perhaps C6COOH



To make another, delayed dose to make 24 hours of naproxen activity, that could do 36, 48, 72 hour one pill dosing as well: Another way is ela-n of three or more types taken simultaneously where each ela-n has a different enzyme-reactive group on the ela-
n with a passivating group removed by the enzyme. The enzymes that remove the passivation moiety are enzymes at the circulatory system. The first ela-n gets its passivation moiety removed first and the next ela-n gets its passivation moiety removed next
like cumulatively 90 minutes later, then do this with a sufficient elan-enzyme-unpassivated-moieties to get a smooth 24 hour, 36 hour, 48 hour or 72 hour dose curve.



Years of arthritis relief from one office visit: A depot drug form of ela-n, ea-n, which I calculate as having a 7.6 microgram 12 hour dose could put ela-n at an implant (3 year nexplanon-like) with just 16.64 mg of API at the implant. Sensibly and
obviously omitting the 2-4 times dosage multiplier enhancement from liposomes, ae-n could be a 33 mg or 66 mg entire API content implant. I think it is possible to make much longer lasting depot implants or even injections, so a decade of arthritis
relief from a decade functional implant at one offive visit is possible.



Complementing a decade functional arthritis relief implant is putting the longevity and life preserving peptides AEDG combined with thymosin at it

A peptide humanin, as well as MOT-c mitochondrial derived peptides (MDP) that is beneficial to screen as to being a longevity peptide that anti aging things and aging things simultaneously, the crummy part is it makes old cytes make old cyte chemicals,
like some interleukins, the longevity thing it does is be opposite ilgf, growth hormone and Alzheimer's amyloid, they have, as far as I know, fed it to organisms to find out if the mice live longer and if they do, how much; notably though if MDP actually
causes the things senolytics do then the opposite of a MDP, a receptor passivator, or an immunization against MDP could be a longevity drug, the MDP and antiMDP could be administered to different mice to find out if either is a longevity peptide



I saw a graph suggesting longevity chemical spermidine is an acetylase (histones) adjustor, it is possible that the

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• The peptide AEDG is published as causing greater longevity and wellness in laboratory mammals, making a version of AEDG with weekly, monthly, annual or multi-annual dosing is beneficial.
• Fluoexetine palmitate is once weekly dosing; AEDG palmitate could be weekly dosing
• “Paliperidone Palmitate 3-month injection” suggests 3 month injection could function 3 months, noting the few nanograms or few milligrams of AEDG it is possible to think an AEDG palmitate could last longer than three months. “Six-month depot
formulation of leuprorelin acetate” suggests 6 month AEDG dosing could be functional.
• The needleless injection technology that is like transdermal sugar dermal piercers could work at the nanograms to milligrams of AEDG to provide beneficial effect. “AEDG peptides in concentrations 0.05-2.00 ng/ml on organotypic skin cell cultures
proliferation in young and old animals were investigated. Peptides stimulated skin fibroblasts proliferation on 29-45% in skin cell cultures of young and old rats.” (PMID:25946846) suggests a therepeutic effect over a range of 1 to several hundred
units of dosage having beneficial effect, that gives the possibility of the beneficial human drug being active at even transdermal needleless injection.
• The dosing amount of epithalon, AEDG might be larger than the mg dosages described at other items here. “Injectable Epithalon use (most effective): duration: 10 - 20 days dosage: between 5 - 10 mg per day”, also, “Each 10 - 20 days course of
Epithalamin is followed by 4-6 months pause before repeating” (http://steroid.es/epitalon.html) suggests that 100-200 mg depot injection annually could be beneficial. Supporting nanogram to single milligram 6 month or longer depot dosages is, “In
vitro biotesting included the determination of the proliferative activity of thymocytes, a bimodal curve with the second maximum were detected at super-low doses (10(-17)-10(-15) mol/l). Authors propose a hypothesis that for superlow concentrations the
formation and distance transmission of a signal from ligand to a target cell without the formation of any ligand-receptor complex take place.” (PMID:12881997)
• AEDG is orally active in rodents, it is possible AEDG toothpaste could beneficially dose humans.
• Some proteins glom to circulating albumins like SHBG strongly, it is possible that attaching AEDG to one of those proteins with a very gradually dissolving enzymatically dividable linker could cause 1 to 3 month or greater AEDG dosing intervals and
be orally administered. Oral dosing: salmon calcitonin linked peptides pass through the GI tract for oral delivery of peptides.
• I may or may not have read about injectable chemical ID, if that is non-isotopic then AEDG linked to that chemical could have annual or multiyear dosing.
• Putting an atom or a few on the AEDG peptide, like changing the =O to -OH at few places, or changing hydrophilicity or lipophilicity could make nanogram dosing possible from modifying the distance between AEDG and a cytostructure or external
cytomembrane structure, rather than the activation of a receptor with AEDG, “In vitro biotesting included the determination of the proliferative activity of thymocytes, a bimodal curve with the second maximum were detected at super-low doses (10(-17)-
10(-15) mol/l). Authors propose a hypothesis that for superlow concentrations the formation and distance transmission of a signal from ligand to a target cell without the formation of any ligand-receptor complex take place.” (PMID:12881997)
• Variations on AEDG that do the “to a target cell without the formation of any ligand-receptor complex” thing at nanogram dosages: deuterated AEDG could have slightly different intramolecular distances; blood brain barrier passing version of AEDG
like diacetylAEDG (possibly with enzyme degradable linker molecule),
• • Lysine-EDG (LK) is similar to AEDG, and has both similar and different effects.
• There are over 100 mentions of epithalon, AEDG at pubmed, epithalon is a pineal peptide, there are numerous other pineal peptides that could be beneficial to humans, “Within the epiphysis polypeptide complex, free amino acids (3.26%), dipeptides (
23.19%), tripeptides (50.72%), tetrapeptides (22.10%), and pentapeptides (0.72%)” The thing is though, “The biological effects of the epiphysis polypeptide complex are determined by the effect of its component AEDG”
• • The peptide KED (Lys-Glu-Asp) is about 40% more effective at, “The effect of AED (Ala-Glu-Asp), KED (Lys-Glu-Asp), KE (Lys-Glu), AEDG (Ala-Glu-Asp-Gly) peptides and their compound on neuronal differentiation of human periodontal ligament stem
cells (hPDLSCs) was studied by immunofluorescence and western blot analysis.” also: “Molecular aspects of vasoprotective peptide KED activity during atherosclerosis and restenosis”
• There is also a nonapeptide, thymulin, wikipedia says, “Thymulin” “is a nonapeptide produced by two distinct epithelial populations in the thymus” “It requires zinc for biological activity. Its peptide sequence is H-Pyr-Ala-Lys-Ser-Gln-Gly-
Gly-Ser-Asn-OH.”
• “acetylated and acetyl-amidated versions” of AEDG are described, that reminds me of acetylation to cross the blood brain barrier and possibly other cytomembranes: https://www.reddit.com/r/Nootropics/comments/3ji7d8/epitalon_any_noticeable_results/
• Also, attaching AEDG to a protein with favorable cytomembrane transport channels, likely with an enzymatically degradeable linker molecule or ATP or polyATP could cause the AEDG beneficial effects at lower doses making annual or multiyear dosing more
effective.
• nuclear membrane transport channels: Also, noting “cause the recognition and complementary binding of a regulatory peptide with DNA functional groups” It is possible a material that causes AEDG to be preferentially transported to the nucleus
through the nuclear membrane could increase the activity of AEDG at any particular dose, making annual or multiyear dosing even more effective.
• noting, “The structures and metrics of peptides and the DNA double-helix cause the recognition and complementary binding of a regulatory peptide with DNA functional groups at the interface of the major groove. We have used complementary binding
model to find a possible base pair sequence ATTTTC for specific binding of synthetic tetrapeptide epitalon. This base pair block and its reverse complement were found repeatedly in the promoter region of telomerase.” It is possible there are different
genotypes for the ATTTTC sequence and that persons with variations can be measured as to wellness and longevity to find an optimal version of the sequence. The more optimal sequence could then be made part of the human genome. AEDG could also be
produced at human, that is persons, that is people’s tissue with gene therapy.
• Mammal and human studies could find out if AEDG which effects melatonin production benefits the fetus and baby as much as melatonin is published as benefitting fetuses and babies, This study notes higher fertility when conceiving and greater
resistance to trouble at the new baby, “Melatonin receptors are widespread in the embryo and fetus since early stages. There is solid evidence that melatonin is neuroprotective and has a positive effect on the outcome of the compromised pregnancies.”
The journal article also says, “The pineal gland develops completely postpartum, so both the embryo and the fetus are dependent on the maternal melatonin provided transplacentally. Melatonin appears to be involved in the normal outcome of pregnancy
beginning with the oocyte quality and finishing with the parturition” Also, “Melatonin decreases in conditions associated with serious outcome for the fetus and seems to be involved in preeclampsia and intrauterine growth restriction [7]. Melatonin
treatment during human normal or abnormal pregnancy has been studied for a large range of conditions and at different times during the gestational period. Considering the ethical issues, it is more difficult to study a normally occurring pregnancy, than
an in vitro fertilization (IVF) one. Melatonin administration started prior to IVF-cycles, continued during pregnancy and was associated with improved pregnancy outcomes”, also, at in vitro fertilization, “Fertilization success and pregnancy rate
were improved by melatonin treatment. Fertilization rate was 50% higher in melatonin treatment cycle“ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4316124/

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an antiglycation mechanism could be found at some animals then tested at mice anfd humans to see if it increased longevity, healthspan, and wellness, also, gene variations at humans like SNPs could be correlated with wellness and absence of or reduced
glycation at humans, and then causality measured with mouse studies to find beneficial genes for human gene enhancement or also optimization; notably though I perceive plants also do the nonpreferred glycation of proteins, so anything at plants that is
produced at cytes that reduces glycation could be tested at the mammalian genome to find out if it benefits longevity, wellness, and healthspan, notably the 40,000 year old King’s holly, the 10,000 year old creosote bush, and the 4k year old conifer
might each have a different plant genetics of antiglycation that benefits their longevity that could be tested at mice and humans.

When a person gets gene therapy, they might like having a way to utilize their previous genome at some or even all their cytes: backup with gene therapy: crispr/cas9 appends the new genome to the previous genome, puts a start codon (or start codon group)
imaginably at a sticks-out circly pouf on the nucleotide double lane topology, the body ignores the first, previous, genome, which might even have some stop codons crispr/cas9ed into it at easily recognized locations (sort of like restriction enzymes say
“thing here” perhaps stop codons could be placed at the previous genome anytime a CCCCC occured, so if editing it out it would be near errorless to utilize the previous genome, if the utilizer felt like it.

I have not read about any siRNA longevity molecules, It is possible these are possible, and that siRNA that heighten AMPK and decrease mTOR (or another 60% greater mouse longevity mTOR drug, that works on just mTOR1 rather than mTOR1 and mTOR2), siRNA
might be even better at reaching the CNS through the blood brain barrier as their AMU is less than some other nucleotides



I perveive there might be a million or more actin lanes per cyte, at 70 trillion cytes, that could be like a math iteration structure with a really large number of math areas to model, algorithmize, and generate, something like interpretations about
things as compared with, and possibly as a beneficial resource to the brain and CNS; Like what if the 70 trillion cytes with actin paths simulated various effects of various possible things, and communicated the modelling results with a one thing one
meaning language;

um, I perceive how DNA per cyte has lots more data space, it is just that actin paths also have lots of functional movement, geometry, spatial accessibility…

It likely already exists, but is there a CRISPR/cas9 automatic gene sequence linker? I perceive different lengths of DNA have different easiness of transfection like 3/4 a decade ago (2011), but the perception I have of of CRISPR/cas9 is that they have
figured out how to make. transfer, and activate things with out about 20,000 genes with simultaneous high velocity, high accuracy, and high editing sucess (transfection); complementing that, perhaps at a variety of sizes, could be something that is
effective at attaching one sequence to another, at a functional place and physical form, (imaginably, histonated, less histonated, a loopy part available because of a mitosis, translation as well as transcription event, meiosis, or some new thing that is
new to me)

so, one approach is to find the easiest histones on earth; some mammal has histones with really long, super editable, physical like-new preservationess above other mammalian histones, really available DNA; completely making a synthetic sequence of that,
then making if even more genetic engineering friendly, then placing it at a variety of mammals, likely including humans, could benefit DNA transcript fidelity, DNA preservation, translation velocity at organisms, like humans, as well as heightening
beneficial, functional, engineering friendly genetic editing, modification and genetic engineering;

Also, besides unlooping things, and actually I have no idea what they do, but I perceive DNA is unusually accessible during translation, mitosis, meiosis, and possibly some kind of “make this” thing that something at the nucleus says, like imaginably,
if something says “make ribosomes” perhaps hundreds of ribosome making DNA locations get sequentially availabilized rather than just like one, over and over again; so, it seems possible they have tried loading up a well human cyte with a numerous
quantity of things to translate at DNA, so they could unspool a bunch of DNA, efficiently, and edit it;

Along with making like a big list of DNA access producing translation instructions, they might have some amazing thing like a DNA translation smoothified new to me histone that makes DNA completely available to editing (like crispr cas9 or more advanced)
while being a place to have a lot of DNA stay linear, functional, well, effective, and immediately ok to utilize without repairs; the smoothified histone could even be nifty at some ethynilization methylization optionalizing, gene modification now able
to be unaffected from methylization and ethynilization molecular topology effect; a smoothified histone like an inspection and upgrade access area of an airplane;

Is there an artificial intelligence thing where if people, or AIs share the technology the sharers accumulate greater prosperity; it is possible AI APIs

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a new kind of autophagy could be linked to longevity, healthspan, and wellness, if it is functional: Noting the idea that cytoplasm might have nonorganelle enzymes floating around, catalyzing things, possibly even comminuting or nonactivating some
cytochemicals: These enzymes, outside the lysosome remind me of autophagy, autophagy is linked to cytorefreshment, longevity, and wellness, it could be that the genetics of having more cytoplasm enzymes outside of organelles do something like an
alternate version of autophagy, refreshing and recycling physiostructures and chemicals, so looking at a variety of mammals, notably things like multicentury lifespan whales, beavers, naked mole rats, bats, tortoises, and parrots and 400 year lifespan or
longer clams, kings holly, and creosote (reminded of mitochondrial apoptosis) any cytoplasm enzymes, notably proteolytic or membraneolytic, outside of organelles (like lysosome) could be quantified at mice as to longevity wellness and healthspan effects,
and if beneficial made into gene therapy, drugs, or germline enhancement or optimization at humans;

Noting autophagy is linked to longevity, wellness and healthspan, and I might have read that AMPK heightens autophagy, it could be possible to engineer larger amounts of autophagy from 1) cytoterminating chemicals, proteins or peptides as drugs (possibly
kind of senolytic like), also as periodically automatically activated gene therapy; an accumulation of physiologically beneficial peptides, like AEDG heightening with each sleep occurence, could, when they accumulate to a particular amount, cause the
gene therapy modified tissue to produce a new circulating amount of the new autophagy chemical, causing fresh autophagy and renewal at the living human; these likely would benefit from localization to create beneficial differences in concentration and
action at different cytes and tissues;

Along with heightening cytoplasmic autophagy like effect enzymes, periodic production of autophagy as algorithmically activated with a completely beneficial physiochemical that accumulates (epithalon, thymosin, likely a variety of things, possibly even
beneficially heightened circulating omega 3 DHA from accumulation of DHA from endogenous production), there is also periodic, quantitatively measured as beneficial to longevity, wellness, and healthspan, triggering of mitochondria to zap cytes, causing
leukocytes to absorb them.

New to me autophagy longevity technologies: Another possibility is a periodic genetic activation of the production of a non-autoimmune activating production of antigens at the surface of cytes, possibly those at the 40th percentile or less of cyte and
tissue youthfulness, where the percentile is an experimentally quantified causative function at wellness and healthspan; this could possibly be quantified with mRNA transcript production’s deviation from a beneficial range (reminds me of engineering
tolerance, the 2nd standard deviation at the non-preferred side of the distribution) Periodic activation of the beneficial new form of autophagy could be linked to the accumulation of a physiologically beneficial chemical (epithalon, thymosin, omega 3
DHA);

New to me autophagy with high cytotype localization technology: I perceive I read about where two different receptor proteins, when both activated, caused a cyte to be exposed to a chemotherapy drug, causing fewer well cytes to be dosed with the
chemotherapy; Responding to things like: At cytes that are at less than 30th percentile of wellness, longevity and healthspan heightening physiology, the translation/transcription protein generators receive instructions to make notably larger amounts of
one normal type, but comparatively tissue and cyte unusual chemical, protein, or peptide transport channel, perhaps something that occurs less than 1/400th of a cytes’ external receptors or transport channels, and at perhaps less than 1 per 200
different cytotypes and tissues, it then becomes 1/20th to 1/40th of the proportion of the cytes external transport channels and receptors enumerated amount, (twenty or ten times as populous as previously), and then an transport channel optimized
autophagy causing protein, peptide, or genetic effect causes autophagy at that cyte; The concentration of the autophagy causer is 40 times greater at the 30th percentile nonwell cytes than at well, wellness, longevity and healthspan functionally active
cytes; Technologically it seems possible that autophagy could be tuned to to be activated when the transport protein heightened autophagy causer is above 30 times that at an unaffected cyte;

As a another supporting technology, it is possible a protein, peptide, or peptide effluxing transporter could be part of membrane accumulating cytotransport duo; at a well, longevity, wellness, and healthspan support heightening, functional cyte the
transport and efflux of a particular protein, peptide or chemical from the duo, which could be spontaneously occuring at a nonmodified organism or human, would be about the same amount, they would omit accumulating the transported protein, peptide, or
chemical at the cytoplasm; that would cause any autophagy activating chemicals, proteins, peptides, or gene products, to pass through well cytes above the 30th percentile causing a minimal amount at the cytoplasm of the 30th percentile of higher cyte;
When the measure of the longevity functionality, wellness, and healthspan of an unwell cyte occurred it would cause the unwell cyte to make large numbers of the harmless chemical cytotransport structure, causing it to be 40 times more prevalent at the
unwell cyte; natural endogenous circulation of things that that particular transport protein transports, would reach 40 times the usual amount, causing a gene at the cyte to make an autophagy causing molecule endogenous to they cyte; another technology
is to have the autophagy causing protein, peptide, or chemical that is linked to a 40 times usual amount transport protein moeity for hieghtened transport to the 1th to 30th percentile cytes, be produced at a different area of the body, perhaps from just
a few gram, or even one gram area of gene therapy;

Technologies that could discern longevity, wellness, healthspan contributive and supportive cytes above the 20th percentile: mRNA, possibly gene therapy that caused presence of nonbeneficial mRNA, cytochemicals, proteins, or peptides, to cause

Normalization algorithms create higher and higher longevity, wellness, and healthspan physiochemistry, it is possible that technologies that cause the least (0- 20th percentile) longevity, wellness, and healthspan supporting cytes to be quantified as
they relate to the to other cytes at the body, to be as a relation to all the cytes at the body continuously or periodically, would cause double digit % increase in baseline longevity, wellness, and healthspan annually, this could physiochemically
contribute to a percentage of longevity increase, and noting the continuous improvement of 20% more longevity, wellness, and healthspan cytes annually is likely larger than an annual accumulation of nonwell cytes, that like actuarial escape velocity,
things move towards wellness, longevity, and healthspan faster than they wear out; The effect of multiple 20th percentile autophagy events causes the after autophagy organism to be accumulate towards what would previously have been 90th percentile or
higher cyte function as to longevity, wellness, and healthspan physiochemistry; that similarity to actuarial escape velocity, which I have also read is called longevity escape velocity, is alogrithmically related to making each iteration of cytes that
support longevity, wellness, and healthspan as the new computational basis for the percentiles. A technology I read about, which might be called gene switches, makes things like AND and OR as well as other logic forms out of simultaneous gene
modification effects; The technological algorithm that supports the heightening of each iteration of 20th percentile or less’ autophagy to be based on a new foundation could be based on things like: gene therapy at the entire body causes harmless
unique peptides or proteins to be produced, which then utilize mechanisms that are usual to move to the exterior cytomembrane of the cyte they are produced at, This labels each cyte with a non immunoreactive cytosurface diagnostic of what it is doing and
making, it is possible the diagnostic proteins that make their way to the cytosurface are actually beneficial, noting the cyte is still alive, or also possibly beneficial to neighbor cytes, the (0-20th percentile) producers of just the completely
beneficial interleukins, possibly some onconeutral neutral growth protein like BDNF, or if immunotransparency and absence of immunoreaction of any kind is beneficial, perhaps slight variations on water transport proteins (aquaporins), where variations
from the usual protein amino acid sequence would let diagnostic things that cause the 40 times greater amount of transport channels to cause beneficial autophagy find and have effects on cytes at less than the 20th percentile; Gene logic could also just
have quantifiable things effect logic, to cause the production of mRNA that makes the 40 times higher amount of autophagy transport channels at the cytomembrane; it is also possible that gene logic can just directly make autophagy functional effects
directly at any cyte where the gene logic notes 0-20th percentile longevity, wellness, and helthspan physiochemistry;

also possibly periodic wellness chemical accumulation (epithalon, thymosin, omega 3 DHA) that activates the production of “make transport channels” at the unwell cytes;

Also possible is the unwell 20th perctile making 40 times more transport channels, and then a human, person, a member of a group of people, that is a homo sapiens, takes a drug to cause the autophagy, much more beneficial is an automated, periodic,
automatic process, which could technologically be based around a one gram or less area of gene therapy that emits things that diagnose, modify and cause autophagy at cytes at the (0-20th percentile) of longevity, wellness, and healthspan, noting the
continuously new distribution’s new foundation; Notably though, there is also the technology of a multihundred year longevity depot injection that just causes autophagy anywhere a group of antibodies (I perceive I read about fewer AMU versions of
antibodies) note some unusual distribution of surface characteristics (proteins), also I think I read about antibodies that can glom to receptors to make them stay active, go less active, or just be neutrally at the cyte, this might function at
cytotransport channels as well, possibly antibodies glomming unwell cytes

Gene logic

possible that without antibodies, this would cause autophagy at virus inected cytes from their being at 30th percentile or less of wellness quantifications, the incidental antiviral effect could be beneficial to both the person, and even possibly reduce
the amount of viruses circulating at the population. The 30th percentile of wellness autophagy technology could be a nonimmunosystem new to me approach that kind of incidentally removes virus infected, oncocyte, and even possibly, fiberous nonutility
tissue, which might be replaced with weller cytes. It is kind of like a new to me, multipurpose, new (30th percentile quantified effect at any nonoptimality) kind of senolytic, with different criteria than various intracyte deleterious products like
interleukins;

the versionbs of these technologies or others that create longevity, wellness, and healthspan beneficial new versions of autophagyor germline enhancement or optimization

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an antiglycation mechanism could be found at some animals then tested at mice anfd humans to see if it increased longevity, healthspan, and wellness, also, gene variations at humans like SNPs could be correlated with wellness and absence of or reduced
glycation at humans, and then causality measured with mouse studies to find beneficial genes for human gene enhancement or also optimization; notably though I perceive plants also do the nonpreferred glycation of proteins, so anything at plants that is
produced at cytes that reduces glycation could be tested at the mammalian genome to find out if it benefits longevity, wellness, and healthspan, notably the 40,000 year old King’s holly, the 10,000 year old creosote bush, and the 4k year old conifer
might each have a different plant genetics of antiglycation that benefits their longevity that could be tested at mice and humans.

When a person gets gene therapy, they might like having a way to utilize their previous genome at some or even all their cytes: backup with gene therapy: crispr/cas9 appends the new genome to the previous genome, puts a start codon (or start codon group)
imaginably at a sticks-out circly pouf on the nucleotide double lane topology, the body ignores the first, previous, genome, which might even have some stop codons crispr/cas9ed into it at easily recognized locations (sort of like restriction enzymes say
“thing here” perhaps stop codons could be placed at the previous genome anytime a CCCCC occured, so if editing it out it would be near errorless to utilize the previous genome, if the utilizer felt like it.

I have not read about any siRNA longevity molecules, It is possible these are possible, and that siRNA that heighten AMPK and decrease mTOR (or another 60% greater mouse longevity mTOR drug, that works on just mTOR1 rather than mTOR1 and mTOR2), siRNA
might be even better at reaching the CNS through the blood brain barrier as their AMU is less than some other nucleotides



I perveive there might be a million or more actin lanes per cyte, at 70 trillion cytes, that could be like a math iteration structure with a really large number of math areas to model, algorithmize, and generate, something like interpretations about
things as compared with, and possibly as a beneficial resource to the brain and CNS; Like what if the 70 trillion cytes with actin paths simulated various effects of various possible things, and communicated the modelling results with a one thing one
meaning language;

um, I perceive how DNA per cyte has lots more data space, it is just that actin paths also have lots of functional movement, geometry, spatial accessibility…

It likely already exists, but is there a CRISPR/cas9 automatic gene sequence linker? I perceive different lengths of DNA have different easiness of transfection like 3/4 a decade ago (2011), but the perception I have of of CRISPR/cas9 is that they have
figured out how to make. transfer, and activate things with out about 20,000 genes with simultaneous high velocity, high accuracy, and high editing sucess (transfection); complementing that, perhaps at a variety of sizes, could be something that is
effective at attaching one sequence to another, at a functional place and physical form, (imaginably, histonated, less histonated, a loopy part available because of a mitosis, translation as well as transcription event, meiosis, or some new thing that is
new to me)

so, one approach is to find the easiest histones on earth; some mammal has histones with really long, super editable, physical like-new preservationess above other mammalian histones, really available DNA; completely making a synthetic sequence of that,
then making if even more genetic engineering friendly, then placing it at a variety of mammals, likely including humans, could benefit DNA transcript fidelity, DNA preservation, translation velocity at organisms, like humans, as well as heightening
beneficial, functional, engineering friendly genetic editing, modification and genetic engineering;

Also, besides unlooping things, and actually I have no idea what they do, but I perceive DNA is unusually accessible during translation, mitosis, meiosis, and possibly some kind of “make this” thing that something at the nucleus says, like imaginably,
if something says “make ribosomes” perhaps hundreds of ribosome making DNA locations get sequentially availabilized rather than just like one, over and over again; so, it seems possible they have tried loading up a well human cyte with a numerous
quantity of things to translate at DNA, so they could unspool a bunch of DNA, efficiently, and edit it;

Along with making like a big list of DNA access producing translation instructions, they might have some amazing thing like a DNA translation smoothified new to me histone that makes DNA completely available to editing (like crispr cas9 or more advanced)
while being a place to have a lot of DNA stay linear, functional, well, effective, and immediately ok to utilize without repairs; the smoothified histone could even be nifty at some ethynilization methylization optionalizing, gene modification now able
to be unaffected from methylization and ethynilization molecular topology effect; a smoothified histone like an inspection and upgrade access area of an airplane;

Is there an artificial intelligence thing where if people, or AIs share the technology the sharers accumulate greater prosperity; it is possible AI APIs

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finding human gene variants that predict responsiveness to different longevity drugs would be beneficial. Rapamycin and a rapalog each are published at 60% longevity increase, my perception is that that math functions describe a medianized response, so
noting half of all persons are above median, perhaps a greater than 60% rapamycin response could be predicted, and a gene therapy or a coadministered gene product upregulating drug might be able to cause a 99th percentile rapamycin response.

Squiggles developed with AI deep learning have been published that cause primate brains to produce more activity than views of faces and nature, it is possible that new squiggles developed with deep learning AI could cause greater amounts of response
than the beauty responding areas of the human brain, and that when humans view these squiggles people describe them as attractive, appealing, and beautiful. I am not aware of research on deep AI generated squiggles that are beauty experieince activating
above that of nature and human faces and form that are three dimesnional or that vary gradually. Among many beneficial uses of these squiggles could be decorating architecture, decorating energy producing utility plants (among them wind, photovoltaic,
nuclear, chemical), hairstyles, and notably anything with above median utility and during the year 2019 less than median aesthetic impression; trash dumpsters, parking facilities, some public transit, medical appliances, anything on a list of survey
generated “could look better” things at public and private spaces.

It is possible that things that are already aesthetically beneficial like plants, landscapes, nature, aesthetically appealing humans, could have versions and variations of deep AI developed beauty squiggles, and that actual spaces could be quantified as
to their beauty response as well as images duplicated. Also, automated mechanisms or also robots that clean and arrange dwelling spaces could arrange items that humans view and utilize to be simultaneously highly available and, with beauty squiggle
technology, arranged at ways that cause higher subjective well being increasing beauty response than the person doing their own arranging. People could of course do their own arranging, they might more often appreciate deep AI guided arrangeements of
things.

Aesthetically mild to beneficial things like computer interfaces and printed text, could generate a beauty response while being combined with other deep AI developed squiggles that simultaneously increase comprehension and retention to create beautiful
and cognitively enhanced interfaces and text; I favor a computer interface and text interface that causes heightened sense of well being (the psychometric: subjective well being increase from experiencing beauty), the “nice space” architecture effect,
the “startlingly gorgeous” art object response, and even the human reponse to human female beauty response at persons with any form of human sex chromosomes occuring at 98% or more of people;

There are no top of page results on a search of “chemical vapor deposition metallurgy” so these are some chemical vapor deposition metallurgy technologies. I read that 3 nanometer silicon features are produced at integrated circuit technology,
noting that arrays of atoms can have much more than an anisotropy or two at (25 atoms per feature, one to 20something billion features per IC, ) a trillion deposited atoms, that suggests that rather than a 3 nanometer feature size a 1 nanometer atom
group feature size could be produced, and that the dots could be customizably amorphous, crystalline, variations of crystalline or other forms.

rather than an integrated circuit phototemplate it is possible a UV laser could produce a regular array of dots or shapes at a photoresist with diffraction grating technology, switching between a few, or even a few hundred different atom location
preferentialization areas could produce a wide range of material characteristics;
thoughts on the size of chemical vapor deposition metallurgy part sizes: MEMs technology could also be a guide, with thickest chemical vapor deposition metallurgy being some higher of power of two than the 24 hour thickest MEMs object production cycle,
it could be higher, if manufacturing time equivalence is considered (a company orders parts for delivery every month, giving as much as 1 month photolithography growth or possibly MEMs thickness build up), if something like UV lasers with a diffraction
grating can be adapted to modify the shape of a growing single crystal of tungsten, like those used at some airplane turbines, then that could be a metallurgical chemical vapor deposition object size guide (although perhaps not, as I think they might
pull those out of a melt)

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Some biologically occuring tings do rapamycin like things https://www.ncbi.nlm.nih.gov/pubmed/29165314 It is possible that mutating these plants, then screening their chemicals on yeast and things like c elegans with 96 well plate technology could create
much larger rapamycin like longevity chemicals at plants, these could then be genetically engineered into delicious as well as ubiquitous plant foods to create longevity producing fruits, grains, and food products like pasta, pizza, potato products,
breading, there is also the possibility that moving these gnes and gene products from plants to eggs and milk could be beneficial

a molecular variant or rapamycin, rapamycin preassociated (attached) to a protein makes it 2000 times more active, “To probe the affinities involved in the formation of the FKBP.rapamycin.FRB complex, we used fluorescence polarization, surface plasmon
resonance, and NMR spectroscopy. Analysis of the data shows that rapamycin binds to FRB with moderate affinity (K(d) = 26 +/- 0.8 microM). The FKBP12.rapamycin complex, however, binds to FRB 2000-fold more tightly (K(d) = 12 +/- 0.8 nM) than rapamycin
alone. No interaction between FKBP and FRB was detected in the absence of rapamycin. These studies suggest that rapamycin's ability to bind to FRB, and by extension to mTOR, in the absence of FKBP is of little consequence under physiological conditions.�
� It is possible some molecular version of rapamycin (a rapalog) could cause mTOR activity without FKBP protein, FKBP has immunoeffects so that molecule could have less immunoeffects than rapamycin

Rapamycin that is more water soluble, “clinical development of its formulations was hampered due to its poor solubility and undesirable distribution in vivo. Chemical modification of rapamycin presents an opportunity for overcoming the obstacles and
improving its therapeutic index. The objective of this study is to develop a drug-polymer conjugate to increase the solubility and cellular uptake of rapamycin.

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