Ethanol makes for better drug loading, “that rely on incubation temperatures above the phase transition temperature (Tc) of the bulk phospholipid to promote drug loading. In the absence of cholesterol, liposome permeability is enhanced at these
temperatures which, in turn, can result in the collapse of the pH gradient and/or unstable loading. Doxorubicin loading studies, for example, indicate that the drug could not be loaded efficiently into cholesterol-free DSPC liposomes. this problem could
be circumvented by the addition of ethanol as a permeabilityenhancer.Doxorubicinloadingratesincholesterol-free DSPC liposomes were 6.6-fold higher in the presence of ethanol. In addition, greater than 90% of the added doxorubicin was encapsulated within
2 h at 37 °C, an efficiency that was 2.3-fold greater than that observed in the absence of ethanol.” also, “Optimal ethanol concentrations ranged from 10% to 15% (v/v) and these concentrations did not significantly affect liposome size, retention.”
Dissolve in etoh first, then put the water in perhaps, perhaps some solvent that rapamycin is more soluble in than water could be put in the ultrasonic liposome maker at a 1 part per 100 amount to heighten colubility, another way is to see if the pile of
rapamycin dissolves whn you stir the liposome making fluid
Liposomes can be dried over sorbitol, “formulation of proliposomes lipid dried over a fine particulate, water soluble support like sodium chloride, sorbitol or polysaccharides imparts adequate physical and chemical stability and are ideally suitable
for lipophilic drugs” That might be functional with trehalose as well to absorb nonreacted fluids, while the trehalose might also preserve the liposomes
Trehalose as a liposome preservative, at lyophilized of liposomes, “aggregation of liposomes could be prevented by the formation of stable boundaries between the vesicles. The ability of cryoprotectants to form these stable boundaries has been
attributed to their ability to replace the bound water around the bilayer via interaction with the polar region of the lipid 36head group (water replacement hypothesis).” also, as to things like trehalose, “high concentrations (up to 30 mol.% in some
cases) are required” (to where it is gooey)
the trehalose, possibly, could be added to the fluid ahead of ultrasonication, “In the preferred embodiment, the liposomes are made in the presence of the combination of at least one sugar (sucrose, trehalose, lactose, maltose and glucose)”
liposomes could increase plasma half life of rapamycin availability antioxidants as liposome preservatives, “use of antioxidants like α-tochopherols, betahydroxy toluene (BHT)”
Rapamycin is made from fungi, “Rapamycin and its analogs are clinically important macrolide compounds produced by Streptomyces hygroscopicus” so depending on how much rapamycin the fungi make those genes could be transferred to plants or perhaps
mammals like humans
Rapamycin might last awhile at the body, there are three plasma half lifes I have read, .9 hours, 9 hours, and 56 hours, one thing online says, “The long elimination half-life of sirolimus necessitates a loading dose but allows once daily
administration, which is more convenient”
Longevity technology: “Centenarians delay age-related methylation changes, and they can pass this methylation preservation ability on to their offspring.” suggests that drugs, or possibly some non-CRISPR CRISPR like thing could duplicate longevity
methylation at everybody
a-tocopherol looks kind of like phenylethylamine, perhaps putting a nitrogen on it, and maybe trimming away a couple CH3s that are on the long alkane distal to the cylic (bicyclic) part, as well as putting a halogen atom on it (I do not know if 2 grams,
at numerous doses of a-tocopherol is beneficial or nonbeneficial) so that just a few milligrams or even micrograms rather than 350 mg is a fun dose, also halogenation might outcompete a-tocopherol at some valuable body location, it could be a thing
though, a stimulant that is perhaps slightly beneficial
IGF1 (Insulin like growth factor) as well as insulin if modified, perhaps with gene therapy or germline genetic modification could produce IGF1 as well as insulin that do sugar response things while being neutral to longevity, perhaps causing less AMPK
activation (If that is what they do)
fetal environment as well as parental epigenetics are published as effecting longevity, methylation, ethylation and other epigenetic things could be modified with supplements or drugs during pregnancy to align the person the fetus becomes with highest
longevity, wellness, and healthspan; I do not know if more methylation during pregnancy is the thing, or if just specif areas of DNA methylation are the thing, different tissues, at the devloping fetus have different epigentics,
How much food the parents eat makes a difference in progeny wellness, “There is consistent evidence from both mice and rat models that modulating the maternal dietary status such as protein restriction during pregnancy can significantly affect
lifespan”, “F1 male mice exposed to maternal undernutrition during prenatal life produced F2 male offspring with impaired glucose tolerance and increased adiposity”, Also, at humans, “F2-generation offspring of women who were exposed to the
famine of 1944–1945 in the Netherlands (i.e., Dutch Hunger Winter) throughout the gestational period had 1.8 times more health problems in their adulthood than descendants of non-exposed women [70]. The offspring of the fathers, but not the mothers who
suffered from intrauterine undernutrition during the Dutch famine also had a significantly greater weight and body mass index in their adult life than the descendants of parents unexposed to the famine”, I perceive this suggests that at the fetus
different amounts of something like methylation (also acetylation, phosphorylation, methylation, phosphorylation, sumoylation, and ubiquitination) could effect longevity, which suggests drug localization of methyl donors could be beneficial, perhaps
optimal methylation of the CNS and heart could be a longevity area, “the epigenetic code changes dramatically during the embryonic development of the organism to initiate differential gene expression patterns between various developing tissues. This
code consists of chemical modifications of DNA and histone proteins that play a crucial role in packing the DNA by forming nucleosomes.” Acetylation promotes gene expression, perhaps rather than methylation acetylation of longevity genes could cause
greater longevity, also, “The dynamic “writing” and “erasing” of histone modifications are conducted by specific enzymes” suggesting that drugs that cause more beneficial enzymes to be produced, gene therapy as well as germline modification,
particularly with tissue localization of beneficial amounts of enzymes could be beneficial, this could be a longevity techology; what one paper describes as socioeconomic adversity “In sons and grandsons of men born outside wedlock, a 1.64- and 1.83-
fold excess risk of circulatory disease” Homesis also has an effect, so a drug or supplement that cause the right amount of stress, without the parents feeling the stress could be beneficial, “there is also evidence that exposure to mild stressors in
early development can result in beneficial (hormetic) effects and that adaptive modulation of epigenetic processes could significantly contribute to these effects [92–94]. There is also evidence that adaptive/hormetic effects can persist over several
generations”, as a longveity wellness drug, it is possible that parents could make their epigenetics (methylation, acetylation phosphorylation, others) like those of persons at the 99.999the percentile of longevity,
marmosets, a primate, could be used to measure the effect of epigenetics on longevity

finding longevity genes other than those that effect mTOR and AMPK: they could look at all the rodents (mice, beavers), and all the bats, and find the ones with the least and most favorable mTOR and AMPK genetics, then they could find the longest living
rodents and bats with the least beneficial mTOR and AMPK genetics, it is possible that noting 33 year rodent lifespan difference the long lived non beneficial mTOR and AMPK rodents can be compared with the lifespan of rodents with highly favorable mTOR
and AMPK genetics but lifespans of 1/2 to 1/4 or even 1/11 of that, then they can find the genes that cause the greater longevity even though mTOR and AMPK are least beneficial at the much longer lived rodents, also, they can just compare mice
genetically modified to have highly beneficial mTOR and AMPK with the genes of beavers to find the beaver non-mTOR and non-AMPK genes that cause the greater longevity even though the beavers might have median mTOR and AMPK genetics; they can do the same
thing with bats; The longevity drug benefit is that on finding the longevity genes of rodents that outlive rodents with optimal mTOR and AMPK genetics 4 to 11 times then the products of those genes, and the actual genes, can then be placed at mice to
find out if they are longevity drugs and genes, characterizing humans as to the amount of the new longevity genes activity and the amounts of their gene products, is also beneficial.
crispr rodent gene swap, find the longevity gene swapping beaver and mouse genes with CRISPR/cas9 to find out which non mTOR and AMPK genes cause mice to live much longer like the 35 year beavers
Longevity technology:

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All technologies, ideas, and inventions of Treon Sebastian Verdery are public domain at JUly 8,2023AD and previously, as well as after that date

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