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.

--- SoupGate-Win32 v1.05
* 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.

--- SoupGate-Win32 v1.05
* 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)





mathematically

I think a mathematican would be able to come up with an equation and a number to communicate divergence from species similars and convergence on high longevity;



Doing the 100 bowls thing on endoliths, or plants, finds chemicals that are common between high longevity organisms, that took some mathematically less predictable paths, to develop a shared trait, which produces chemicals and has genes that can be
tested on other species to find out if the trend



There could be a 100 bowl convergence with three layers being outside a mathematically predicted form; three data points, i think i heard, can make a trend, and at 100 bowls of two or three organisms, the divergence from other organisms at the same bowl,
and the convergence on specific chemicals and genes among the high longevity bowl organisms, suggests that if there is a third thing then the longevity trends will have greater predictive ablity for specific chemicals and genes (gene versions); one
possible approach to making three data areas to make a trend from is to put a mid-longevity specied in each of the 100 bowls and find out if any of them are shared any of the chemicals (or gemes) that the highest longevity longevity animals comverge on







then the actual chemical and kind of cytochemical and tissue chemical network that the organisms with the greatest longevity at each bowl have, notably where this shared convergence on cytocommunication network form diverges from the similar species in
the same bowl;



I read 60% of the human genome is shared with the banana, so if there is a human tissue chemical, made from a gene that is the same as that of a 3650 day tree, and there is an alternate version of that chemical and gene produced at the kings holly, then
that is a human and tree shared chemical with what may be a much greater longevity version; yeast and mice could be utilized to find out if putting the king’s holly homologous gene at a mammal causes greater longevity;



senolytic dasatinib with quercetin treatment, 190 days compared with 140 days greater longevity from start of treatment, about 35% greater longevity, “20-month-old male mice treated with D+Q”, “For all dasatinib+quercetin (D+Q) treatments, D (5mg/
kg, drug/body weight) and Q (50mg/kg) were administrated by oral gavage in 100-150 μL 10% PEG400. For treating 20-month-old mice, D+Q was delivered either once monthly or every 2 weeks, with essentially identical effects.once every 2 weeks (bi-weekly)
for 4 months.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6082705/



so that is 350 mg for a 70 kg human, 8 times, or 4 times at monthly 2.8 grams, mouse dose compensation factor changes that to 233 mg for all 8 doses.



The quercetin is 2.91 grams per dose, so 8 doses is 23.3 grams



At roayl jelly amking mice live midway between 24 and 26% longer 500 ppm at ad libitum food mixed with 9 parts trehalose was used, at mice that is 25 g a day human dose, or using mouse compendation factor that is 2.09 g/ad libitum feeding, the 50 ppm/ad
libitum feeding was almost identicallly longevizing (112 weeks compared with 110 weeks high dose) and is 250 mg ad libitum feeding human dose, or 2.08 mg ad libitum feeding human dose with mouse compensation dose



That suggests enteric coated 20 grams of trehalose and royal jelly could be effective as an oral dose, coadministered with 2.08 grams royal jelly enteric capsule dose with food



That compares with 60 mg/kg of food at precis of paper, and at medium dose that is 60 mg/kg or 4.2 grams per 24 hours, or 420 mg per 24/hours at a 70 Kh human, without mouse comepensation factor the high dose is 25 gram ad libitum with trehalose and 2.09
grams with mouse compensation factor; note this does not function with high dose medium dose order or magnitude difference



The very large dose, based on mice eating 1/6 of their body mass a day, then calculating a dose on a human eating



Highest high mouse dose is 4.2 grams a day ad libitum with food, lowest high mouse dose is 350 mg, highest medium mouse dose is 420 mg ad libitum, lowest medium mouse dose is 42 mg



most of the mutants with long lifespan had mutations in the age1 gene [4]. This gene turned out to be the catalytic subunit of class-I phosphatidylinositol 3-kinase

(PI3K).



Sirtuins, epigenetics of sirutins, sirtuin supplements. it is possible endoliths like million year lifespan endoliths have novel sirtuin effecting chemicals



Mammals possess seven sirtuins (SIRT1–7) that occupy different subcellular compartments such as the nucleus (SIRT1, -2, -6, -7), cytoplasm (SIRT1 and SIRT2) and the mitochondria (SIRT3, -4 and -5).



sitruins are deacetylases, SIRT6 is shown in previous studies to be a critical epigenetic regulator of glucose metabolism, it is possible that other things that upregulate or are actual deacetylases, including non epigenetic deacetylases could be
longevity or healthspan drugs, screening a library of molecules that do about the same thing as SIRT6 could find a longevity hieghtening epigenetic drug that is more effective than SIRT6, sirt6 is linked to aging, temoleres and inflammation



SIRT like resveratrol-mimicking drugs such as SRT1720 could extend the lifespan of obese mice by 44%. However, “feeding chow infused with the highest dose of SRT1720 beginning at one year of age increased mean lifespan by 18%, and maximum lifespan by 5%
, as compared to other short-lived obese, diabetic mice; however, treated animals still lived substantially shorter lives than normal-weight mice fed normal chow with no drug.[2] In a later study, SRT1720 increased mean lifespan of obese, diabetic mice
by 21.7%, similar to the earlier study, but there was no effect on maximum lifespan in this study.[3] In normal-weight mice fed a standard rodent diet, SRT1720 increased mean lifespan by just 8.8%, and again had no effect on maximum lifespan.[3]”



43% greater maximumn lifespan from GDF15 is published “Female hNAG-1 mice (mice expressing hNAG-1/hGDF15) have significantly increased mean and median life spans in two transgenic lines. The effect is stronger in mice on high fat diet than on low fat
diet. hNAG-1 mice display reduced body and adipose tissue weight, lowered serum IGF-1, insulin and glucose levels, improved insulin sensitivity, and increased oxygen utilization, oxidative metabolism and energy expenditure.

% change in avg or median lifespan

Female mean lifespan is up to 43% higher.”



The RNA microRNA 17 that increases longevity could be a longevity drug immediately with online ordering and enteric coated capsules or possibly snortable form, or both









microRNA 17

Mus musculus

Pro-Longevity

16%



Gdf15

growth differentiation factor 15

Mus musculus

Pro-Longevity

43%

A list of longevity increasing genes is at http://genomics.senescence.info/genes/search.php?search=&show=4&sort=1&organism=Mus+musculus&long_influence=pro&lifespan_effect=increase&search=&page=1Mir17 Growth/differentiation factor 15 (GDF15)



Nasal liposomes,

liposome formulations showed a mean diameter in the range of 175 nm to 219 nm with polydispersity index lower than 0.22, a lightly negative zeta potential and excellent encapsulation efficiency. Moreover, along with good mucoadhesive properties,
multifunctional liposomes showed a markedly increase in tacrine permeability, which can be related to liposome fusion

with cellular membrane,



C-Pc liposomes were more effectively taken up by Neuro2a cells than free C-Pc and were biocompatible, maintaining the anti-oxidative properties of C-Pc. When optimal C-Pc liposomes were administered to middle cerebral artery occlusion (MCAO) rats 2 h
after onset, infarct sizes were smaller and behavioral activities improved compared with the same metrics in free C-Pc-treated rats. Liposomal delivery still reduced infarct sizes and improved behavioral activity 6 h after onset, whereas free C-Pc did
not.



Intranasal liposomes had a longer half-life in the brain than intranasally or orally administered free drug



Piperine is an antidepressant works better as a snortable liposome, “Antidepressant and cognitive effects of piperine-en- capsulated liposomes (PL) were investigated in male Wistar rats. Oral piperine (5 mg/kg body weight/day) and intranasal PL (7.2 μ
g/day) were randomly as-signed to daily administer for 14 days to rats which were subjected to forced swimming, Morris water maze and spontaneous motor behavior tests. PL sig-nificantly exhibited anti-depression like activity and cognitive enhancing
effects, in comparison to the con-trol groups after the first dose (p < 0.01) and the ef-fects could be maintained throughout the period of study. Quantitative analysis of the brain homogenates by HPLC indicated that piperine, delivered either orally or
nasally, distributed to the hippocampus at a higher extent than the cortex and that the time to peak concentration of nasal PL was shorter than for the oral piperine. Intranasal PL was, thus, potential in delivery of piperine, at a low dose, to exert its
an-tidepressant and cognitive enhancing activities.”

siRNA drugs can be administered with liposomes, “ntranasal delivery of the siRNA targeting Beclin1 significantly depleted the target protein expression levels in brain tissues with no evidence of toxicity.”



we developed a nose-to-brain delivery system combined with cell-penetrating peptide (CPP), Cell-Penetrating Peptides (CPPs), also known as protein transduction domains (PTDs), membrane translocating sequences (MTSs), and Trojan peptides are short
peptides (≤40 amino acids), with the ability to gain access to the interior of almost any cell. They are highly cationic and usually rich in arginine and lysine amino acids. They have the exceptional property of carrying into the cells a wide variety
of covalently and noncovalently conjugated cargoes such as proteins, oligonucleotides, and even 200 nm liposomes.



melatonin antidepressants, mood elevators exist, “Agomelatine is a structural analog of melatonin”, it is possible that like tyhe pineal peptide AEDG causes greater longevity molecular variations of these mood improving drus could be simulataneously
longevizing and mood improving, “agomelatine. Agomelatine is a melatonergic agonist and a 5HT2c antagonist (i.e., it has a unique mechanism of action). The melatonergic function appears to improve sleep patterns, whereas the serotonergic antagonism
results in the release of norepinephrine and dopamine.”



Previously described is finding the genetics of having good dreams, I favor making the genetics of having good dreams part of the human germline, also, amount persons above the 99th percentile of longevity they could find those at the 99% of having
actively good dreams and an absence of dreams the person would prefer to have skipped, this is a guide to finding the genetics of more beneficial sleep, it may even be possible that there are those at the 99th percentile of longevity who dream twice as
much as others, dreaming good dreams twice as often is beneficial to humans and is beneficial to make a part of the human germline



g (like IQ) gene “klotho-enhanced mice performed better on a variety of learning and memory tests, regardless of age. In one test, the mice remembered the location of a hidden target in a maze better, which allowed them to find it twice as fast as
control mice.”

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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.

--- SoupGate-Win32 v1.05
* 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 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



Things that fill children with happiness,

CPU speakers or social companion robots could notice when adults and siblings were at 90th percentile of previously measured happiness and suggest that children interact with people like their oarents or siblings then. Timing could contribute to child
snd adult hapoiness, so CPU speakers that amplify adult and sibling happiness could amplify child happiness.



Longevity technology

Sleep causes greater healthspan, wellness, and optmal amounts of sleep may have longevity increasing effects as well, they could find out what 1000 or 100 chemicals most increase from several hours of sleep, are newly produced, or are decreased from
optimal sleep and find out if supplementing mice or c elegans with those chemicals increases lifespan, circulating chemicals as well as tissue specific chemicals like brain, cardiovascular system, liver and heart could be utilized, chemicals from tissue
homogenates from optimally sleeping and awake primate monozygotic twins or other 8 hour sleeping mammals (cows? Horses? Pigs?) could be used



Do BDNF, NGF as well as other nerve growth factors have beneficial longevity effects or healthspan effects at non neural tissues, this could be tested at human tissue culture, age batched very elderly persons, and a BDNF version with a polyglycine,
protein or other peptide attached to the BDNF or other nerve growth factor so the nerve growth factor does not pass the blood brain barrier (stable isotope verified), this could be tested at mice to find out if the nerve growth factors increase longevity,
if they also increase longevity at yeast or c elegans a million molecular variants could be tested at yeast or 10k versions tested at c elegans (107 or a few hundred 96 well plates) to find a version with greater longevity increase, are there peptide
nrtbe growth factors? Also, if nerve growth factors cause greater longevity this could be a gene therapy longevity or healthspan technology and could also be made part of the human germline



Marmosets are a primate that could be batched into 6 months, one year, two years, and four year prior to being previously alive groups and used to test longevity drugs and the effect of longevity drugs on progeny,



Divergence of physiochistry from that of humans approaching being previously alive: from age 11, circulatory system fluids and cheek swabs tissue samples could be used to characterized to show the gradual or sudden changes of people as they traverse the
years from 11 to being previously alive, eight samples from each year of age are sufficient to get a p value, so from 11 to supercentenarians is not that many samples, the chemicals that gradually change, those that increase or decrease are then tested
on c elegans and yeast to find those that lonhevize yeast or, at cumulative or sudden human physiological chemical change otherwise modulate c elegans and yeast longevity and wellness or healthspan, chemicals at the 97th percentile above at causing a
change in any direction could be tested on mice,immunizations against deleterious chemicals could cause greater longevity as well as healthspan, and supplementing with beneficial chemicals could cause greater longevity and healthspan. Some of the
physiochemicals may be symptomatic, others might be causative like the deleterious interleukin senolytics get rid of, a really rapid version of this study would use 9 circulatory system circulating fluids and actual tissue samples from rats or cows, pigs,
or horses, identify and measure the physiochemicals, administer them to yeast then test the 97the percentile of physiochemicals that cause the greatest change on mice, if large animals are used (horses, cows, pigs) then the large animal plasma or
tissues can be used as a plentiful source of test chemicals for the mice, another approach is just to get 7 discrete human year of age equivalent samples from large mammals, mass sort, or electrophoretically sort that into 700 different testable plasma
fraction materials then test those 4900 different plasma fractions on c elegans (53 or hundreds of plates) and yeast to find out if pjysiochemicals from chemical change progression with age shows beneficial or deleterious chemicals, if there is an effect
then that electrophoretic or mass sorted plasma fraction could be electrophoresis sized or mass sorted further and partitioned into another 900 groups to find the longevity and wellness chemicals with greater precision



Things that fill children with happiness

Amplitude, duration, frequency, priming for more happiness, shareability, links to when talking about it causes others to invite the child to other fun activities, neurotransmitter refresh interval, the time of day of the happiness producing thing
effecting duration, amplitude and frequency of enjoyment



What makes tired children happy, what makes children at their personal 72 hour 90th percentile of less happy be happier? They could research these and find out what benefits children.



At the 72 hour 90th percentile local minima of happiness, which could still be happy, it could be that the child has a considered and durable preference, and they are responding from that perspective. Along with finding something that makes them happy
right away, getting around their 72 hour preference, I think there an ethical duty to consider children's suggestions and requests, so a child that is at a brief or hourlong 72 hour local minima of happy because they are told they cannot go to an
amusement park that weekend or have a sleepover combined with when the child is being babysat (although I like the idea of a child getting to have a multiperson sleepover with a babysitter monitoring things if the parent is busy), it is possible the
adult or a social companion robot explaining things, while upholding and supporting the right of the child to make requests and have preferences could ameliorate things. The shift from the child "reacting to no" compared with knowing where the "no" comes
from benefits children. Emphasizing there are reasons for adult behavior might also prompt a "things can make sense" worldview that benefits the child, although, the adult or social companion robot could also have a deeper discussion of error,
stochastics, local resource effects, and how apparently nonsensical or nonoptimal things can be researched to find why they occur, or are at least predictable. Noting that sometimes finding out "actually why it happens" is either more effort than the
value generated or unavailable to a person, software, or AI, and the child could be beneficially prompted to think of a new thing that could answer "why it actually happens" and the new thing even make suggestions of change. Adults or social companion
robots, or CPU speakers could prompt with things like "what if there were a council of children that voted on " no babysitter sleepover" and they had veto power over adults", or "could an expert think of and suggest having a babysitter take me to the
amusement park", or, " if I banked measurements of being above median at school, would that make asking to stay in bed and skip school that day be allowed? (My thought is the extra day of school could make them even higher above median, which is
beneficial, things could be fun once you get to school, and there is value to living beyond 3 minute urges like staying in bed longer), so explaining things to children might sometimes move s multiminute or hour 72 hour local minima nearer to median
happiness, also, The CPU speaker and AI could figure out what they were talking about and make suggestions on how it could be made possible like a babysitter being there, CPU speakers saying they have activity curricula for a toy that got a "no", or a "
video chat with the friend you can't visit is almost as fun", as well as, "afterschool dance has lower fees than gymnastics, is just as much fun (AI only says things that are factual though) and you could invite your friend tiffany to do dance with you".
Genetic enhancement and optimization that makes a child's 168 hour 99th percentile happiness minima still be a happy experience is beneficial.



What makes tired children happy could be researched. Along the continuum of low energy to exhausted, different things could have different effects, I support genetic enhancement and genetic engineering that makes children and adults full of energy and
less likely to be tired.



Longevity technology



If people did something longevizing as an automatic response to a risk, "I'm taking extra longevity pill as long as my car has no brake lights" where the longevity gain is always higher than the risk is beneficial, social companion robots, CPU speakers
or phone texts could encourage people to get the risks repaired, or change their personal habits



some longevity drugs can be taken once ever, annually, daily or other amounts just from the math distribution of available technologies. An ion based longevity technology like lithium (7% greater longevity?) Could be daily or monthly as could metformin,
although an annual metformin longevity drug could be possible, figuring out why education is linked to greater longevity could find some kind of actual incremental effect on longevity where using educational software or optional nootropics is longevizing,
these could be daily options that increase longevity and could "make up" for other activities







Longevity technology



Things that fill children with happiness

The duration of children's happiness might be extendable 20-200%, the fMRI of happiness at a gift or a hug could be measured and they could find out if duration of happiness at a happiness producing thing has a genetic component that would be beneficial
to make a part of the human genome, germline and genetic engineering



They could screen things, like toys, events, activities and school to find the things that cause the longest multiminute or multihour lasting happiness at school, some things like displayed awards might cause multi-month greater happiness, confidence,
and seeking out of further opportunities at that activity or more voluntary practice, things that are authentically beneficial to children could give awards, wearable fMRI or photonic brain scan like Deep water technology, as well as deep learning AI
viewing facial expressions, vocal tone, and body language could measure duration increase of happiness



Duration of happiness of children could also go up with mid-hapiness statements that CPU speakers, robot companions, or other people make while the child is particularly happy from a stimulus, or afterwards as a reminder, software and people could figure
these out.



Would looking at the literature or trying new things find a form of continuous reinforcement that causes as many retries and repeat visits to an activity as variable reinforcement? That could be the basis for a fairer, ethically consistent activity that
makes children happy, sometimes physically getting blocks to fit together feels good, or easily reaching for a toy, or reinforcement at doing a well practiced dance move could be reinforcing. As could heightening numeric scores or levels at a computer
amusement. It is possible fresh new activities could be thought of that always cause heightening behavioral psychology positive reinforcement like easy but mounting complexity IQ test items (which is next in a visual, word, or number sequence) and which
way will the gear turn, and who is having the best time at a party (after reading party person's activity descriptions) items



Longevity technology



Enjoyment and happiness could come from a variety of activities, what makes a baby, a 4 year old, a 6 year old and a 9 year old happy likely could have differences, measuring happiness producing things at a variety of children's ages is beneficial.



Making 5 year olds happy

Things with certainty "allosourus was an herbivore" that they can learn and share might be to my perception be a thing 5 and 6 year olds enjoy, the thing that teaches these things could teach statementables that are also of interest to adults like
accurate factoids about the internet or consumer reports magazine type things, or statements like "they order things like swing sets for city parks out of a catalog, I think the catalogs have less than 100,00 different playground toys in them"

The child fact statements could prompt the adult to say, "do you think they should have more items at the playground activity structure catalogs or make it like a sortable database list of most fun, or both?" It is both factual and provides the
opportunity for deep discussion about when more is better compared with when advice on what is better about a wide range is especially optimal. The adult or social companion robot could say "life is full of many trillions or quadrillions of possibilities,
more possibilities is beneficial as well as is asking people who are doing especially well what their preferences and behaviors are, you can have both", "let's ask someone who knows about a particular area", then a question, "what do you think we should
ask?" And then the child, or the adult, might mention something from school or living that seems improvable or has a multitude of options like what after school activities are better than others, what babysitters are like and how babysitters should act,
where to go on vacation, or something about options at software the child uses, or if they are into dolls, building blocks, cars, or board games, what is the funniest thing to do with that toy, then they send email to people that know. At their question,
the adult writes the email the child speaks if the child has not yet learned to write and reads the replies.



Props could make children happy at the context of imagining a scenario where the prop is used, or imaginatively imitating a person that would use that prop, like having a savings bank, waving it around, and speaking as if they were a banker, or an adult
that encourages saving, or a person with a unit of money (all the money in the bank) talking about swapping the bank's value for something beneficial.



Children could say I'm imagining that" then children can say anything while being honest "I'm imagining that if you leave your favorite book open to your favorite page the ideas will fly out and visit other people" "mom's car already talks, I'm imagining
it talks about other cars and says (things) "

Things that fill children with happiness



Longevity technology

Do other molecules that build up muscle mass besides mTOR and HGH cause different longevity, they could find out if decreasing a variety of anabolic receptors has a longevizing effect



Do things that are catabolic or smooth muscle decreasing have a longevizing effect, I have heard about this with other muscles



What is the most common genetic ancestor between all mammals, things that longevize age-batched groups of that mammal could have



There is a lizard that can detect light with its pineal gland, any extra chemicals or peptides that produces could be screened for longevity effects, noting AEDG Epithalon is a pineal peptide



The peptides and proteins that reach the circulatory system when a person experiences romantic limerance (excitement) as well as spring could be mood lifting as well as longevizing noting what I perceive I may have read about young new romantic partners
increasing healthspan, perceived or actual wellness and longevity



Does glycine or other amino acids with a silicon atom or a fluorine atom taste sweet or more strongly, the variations that do might have higher affinity for receptors, thus be part of better peptides



Electrical engineering

Have electrical distribution networks switching stations modularized (they already are), and optimized to the fewest necessary components ( they already are), and made of the most affordable materials possible while still being highly functional,
optimally more functional, the capacitors could be made from



PCBs polychlorinated biphenyls, could they be milder if they use half as much with one that has higher dielectric constant, or an emulsion with a high dielectric material, or at transformers, if an engineer could use any material what is the least size
they could be, like cobalt and nickel laminar electrodwell things, silver wire, and cooling, what is the eentsiest superconducting transformer



Things I don't do:

Gold with cobalt blue





Art

how about a wig on a van De graaf sphere full of electrons, unfurled? Or a petri dish on a van de Graaf generator with colonies on it and calcium ions, whenever you come near it the electroporation and Ca++ cause genetic engineering, or a big puffy HOMO
molecule of 10H2DA and longevizing alpha 2 estradiol



They could use positron emission tomography and deep learning software that finds the thing that most activates beauty areas of the brain and the nucleus accumbens dopamine and GABA neurons and then makes beautiful molecules shspes and display those and
title it, "What does it do", they could also screen the million most beautiful molecules and find any that had pharmaceutical effects



A statue of a mouse llifting its head, doing actual happy mouse postures, looking up, and have Thank You written on the plaque the mouse statue is on



A plaque that says, "The government has been good to me but I am still a libertarian, they have missed out on so much" § And a big piece of cheese, like a round with a slice out of it, with the edges of the slice decorated with images, from laser
engraving, that are round, soft, swirly, and deep learning AI screened highly beautiful.

Deep learning AI and brain scan most beautiful images on circular tiles and )( shapes to tesselate them, the visitors make their own compositions, images of people, trees, and nature scenes and domestic dwelling scenes are also at the tiles



What if deep learning AI with brain scanning finds that there are 3-4 distinct human appreciation of beauty types, there are those images that appeal to most, but for highest experience specialization would be utilized, make those separate images and
call it "3-4 kinds of beauty"



Water is often beautiful, make a 3D SI screened more beautiful than the first 24 pages of a search engine results on beauty and then have people view it



Wet look things might be especially beautiful, take ordinary things then wet look and AI deep learning beauty enhance them to make images like the exteriors of houses and grocery aisles and city streets and children, and nudes, and landscapes, ordinary
things



Have people online rate with slider bars ----------|--- the amount the 2000 more AI beautiful images that make them feel good, then display those



Have a plaque that says "go to college, you will be happier, meet better romantic partners, live longer and learn things" then have a fairy lit upon one corner of it looking thoughtful













Fan fiction

Kirk and Spock took the surplus phaser and set it to explode, then they tossed it in the water, big splash! Just two guys having fun.



Observational poem



Tastes interesting

Good, not so good

I wonder what the director bee thinks of the flavor

She's used to it

Royal jelly



York peppermint patties are good when you dissolve them in your mouth

Did they used to be smooth?



The amazing phenibut makes my skin not itch

Yay penibut !



I checked my email yesterday

Will I check it today?

Couchurfers.





Things that fill children with happiness,

Although live in boyfriends have among the highest association with risks to children, it is likely the upper third of beneficialness at live-in boyfriends are beneficial for the children to know and communicate with, cameras, audio, and computers at the
dwelling could qualify if the boyfriend is at the upper third of live in boyfriends, and the live-in boyfriends that were more successful than the previous parent or the mother, and then prompt children to beneficially interact with the live in boyfriend,
this would provide the child with more, and more beneficial, examples of how people live and what they do than the child would get from the mother or other-parent visits alone, so if I were a female computer programmer, and my live in boyfriend was at
the upper third of absence of risk, and the boyfriend (perhaps a mathematician that consults on applied mathematics) was more successful than I was, then my daughter could learn about entire realms of activity, career, educational, fiscal, and physical
activities I was unaware of, benefitting my daughter, notably at mothers with numerous sequential boyfriends or simultaneous boyfriends this could be especially apt and productive, giving the child the optimal data from annual or less frequent new live
in boyfriends, for each 100 million persons the prompting software would benefit 16.6 million only children or more than 40 million non only children, noting multichild families, Amazon echo dot or Cortana child advisor could prompt child-live-in-
boyfriend conversations that went deeper than pleasantries and touched on 14-40 areas that tend to cause success and the live-in boyfriend could contribute what they know and what worked for them, the CPU speaker could also prompt the live-in boyfriend
to bring the child along to their daytime activities, the CPU speaker could blend the 14-40 topics with fun, happiness causing things so the child and live-in boyfriend would have a good time, prompting further software use



Longevity technology

Would an enteric coating on a regular multivitamin make it function better, the introduction of enteric coated Centrum could also be an occasion to talk about Centrum's new longevity and healthspan increasing AEDG Epithalon and 10HDA, I read half of
Americans take a multivitamin so advertising things that reach them about the benefits of longevity drugs is beneficial



School buses could have psychometric test generated seating charts where half the bus was sit wherever you like (preexisting friends might want to sit together) and the other half of the bus you sat near a person the software estimates would make you
happy and perhaps become a new friend, also, children living less than a mile apart who were compatible with each could be seated together, seats could be rotated three times a year, it is possible if sit anywhere is at the front of the bus this could
reduce potentially deleterious back-of-the-bus groupings, there would be an absence of insistence but a screen on the back of each seat would say who sits there and have some conversation prompting questions and statements or images, dollar store LCD
calculator suggests $20 to label half the seats on a bus



Longevity technology

Insurance companies build up a pool of funds at the company while getting funds monthly so the company gets both a pool of investments and cash flow



Insurance companies profit when they favor longevity drugs and technologies, and advertise longevity technologies, and they have a financial interest in funding the development of longevity technologies, noting that, and that they aim for a particular
return on their investments, insurance companies could blend higher volatility longevity technology companies shares with less volatile investments while maintaining their rate of return, during 2019 AD the combination of rapamycin, senolytics, and AEDG
epithalon which all have separate mechanisms, could heighten longevity 104%, if so, then insurance companies remit less funds less often, their investment pool grows and they collect money from people longer, they could also gain clients, advertising:
just two days of taking any of the longevity drugs on our list (senolytics, oral or snortable antigens to mTOR receptors, other better longevity drugs), we'll send them to your door! That gets you 20% off life insurance, $700 cash up front, or 11% off a
home-automobile-life insurance policy package switch to us now!



Things that make children happy

Optimally children would play with social companion robots, toys, other children, the internet, and adults more than they watch media, if media watching occurs then a CPU speaker could have a fun conversation with the child about the media heightening
children's enjoyment, content could range from neutral, "what would you do if you were the main character", to educational, "they should show the people building the spaceships" an adult can configure it onscreen

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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 AE

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