Also, wikipedia mentions a total of three high-efficacy amino acids at succinate dehydrogenase (SD), “His207 and Asp82 most likely facilitate this process. Other studies claim that Tyr83 of subunit D is coordinated to a nearby histidine as well as the
O1 carbonyl oxygenof ubiquinone. The histidine residue decreases the pKa of tyrosine, making it more suitable to donate its proton to the reduced ubiquinone intermediate.”

11 TCA steps, three high importance amino acids (like His 207 at succinate dehydrogenase, etc) each is just 33 genetic modifications to scren for longevity increase without deleterious effects at mice with; one version is mouse germline (all tissues),
another version is bodyside only gene therapy, leaving the brain full metabolic TCA cycle respiration and energy.

If each mouse longevity experiment where each of the 10 parts of the TCA cycle is downregulated (cellular respiration)is $2000 -$9,000 each then that is $60,000-$270,000 to find/test 30 new longevity gene therapies (three downregulators per TCA cycle
step are tested), and epigenetics longevity therapies also Even Moreso (technology phrase at notes) epigenetics of perhaps less of what are already limiting factor proteins or components of each of the 10 TCA cyce steps; this reduces a well organism TCA
limiting factor to even further less, reducing cellular respiration at mitochondria, which at C60-Malonate causes 27% greater lifespan)

Other Succinate dehydrogenase longevity drugs, about 7 or 14 from wikipedia: each of the Succinate Dehydrogenase inhibitors described could be tested at mice as varying dosages to see if they cause greater longevity (noting the 27% longevity increase
from C60-malonic acid) both linked to C60, and as standalone molecules, “There are two distinct classes of inhibitors of complex II[succinate dehydrogenase]: those that bind in the succinate pocket and those that bind in the ubiquinone pocket.
Ubiquinone type inhibitors include carboxin and thenoyltrifluoroacetone. Succinate-analogue inhibitors include the synthetic compound malonate as well as the TCA cycle intermediates, malate and oxaloacetate. Indeed, oxaloacetate is one of the most potent
inhibitors of Complex II. Why a common TCA cycle intermediate would inhibit Complex II is not entirely understood, though it may exert a protective role in minimizing reverse-electron transfer mediated production of superoxide by Complex I.[17] Atpenin
5a are highly potent Complex II inhibitors mimicking ubiquinone binding. Ubiquinone type inhibitors have been used as fungicides in agriculture since the 1960s. Carboxin was mainly used to control disease caused by basidiomycetes such as stem rustsand Rhizoctonia diseases. More recently, other compounds with a broader
spectrum against a range of plant pathogens have been developed including boscalid, penthiopyrad and fluopyram.[18] Some agriculturally important fungi are not sensitive towards members of the new generation of ubiquinone type inhibitors [19]” So that�
��s like seven *2 (C60 version) new testable possible longevity drugs. Downstream items from SD could also be places to make longevity drugs about

Another source of longevity drugs is just thinking that of 10 cycle steps, if each has 7 inhibitors like the one SD step I read at wikipedia, then the 7*2(C60 version, non-C60 version) 14 drugs testable for longevity increase with the least deleterious,
or complete absence of deletrious effects could be found; that’s 140 new possible longevity chemicals to test at mice, zebrafish, C elegans. The studies can be made simultaneously, matrix style by having eachmouse experience 4 simultaneous TCA cycle
longevity drugs, and 35 mouse/zebrafish/c elegans experiments are utilized. The longest lived mice/zebrafish/c elegans (but why be cheap with c elegans; at c elegans or also human tissue culture test all 140 longevity chemicals separately) then have
their 4 simultaneous TCA cycle drugs separately characterized with 4 experiments, so 39 experiments screen the entire TCA cycle for new longevity drugs. NIA does Multilocation/multicenter longevity mouse studies to get better data;noting China is 5x
cheaper than US, Three studies, in three different countries could be done and the composite numeric effect used to narrow to highest function new TCA cycle longevity drugs. Slovenia, China, and Egypt could be three countries where doing the research is
5-10x cheaper (example 49c/24 hours mouse in USA, 2c/24 hours mouse in egypt). Shipment of drugged mouse chow from USA company or scientist to 3 foreign sites could work. Oral delivery success is preferable as it facilitates oral longevity drugforms at
humans. Among various TCA cycle step inhibitors peptides and proteins could be enterically coated and put in nanosomes for 10x(or higher) better survival and passage throgh the GI tract, alternatively, as mice are small, very large oral doses of active
drug proteins and peptides are highly affordable. a milligram a day to a mouse is like 3g a day to a human. 1 mg of peptide *365*5years is not much to make.


mouse longevity studies

At the succinate dehydrogenase longevity drugs (7*2 C60) as well as the other possible longevity TCA cycle respiration downregulating drugs, noting Dugan’s C60 trimalonic acid 27% lifespan increase, the ide of using different fullrenes comes up, or
other nanodrugdelivery forms; multihundred picometer quantum dots perhaps or also alternate size fullerenes: like C20(?) (littlest fullerene) to C300 or higher(bigger fullerenes)); so screen Dugan’s malonate with 11 different fullerenes to see if there
is any higher than 27% form that could be reused at other longevity drugs.
Also try trimalonate borane soccerball, unless its toxic to see if that alternate 3D molecule is longevizing

Find the most changed cryogenic treatment polymer, and semiconductor; then use that extra latitude at materials science
to make new things.
Test coupon data, and microfluidic array million chemical dot printouts could get lrge amounts of data on cryogenic treatment 1) effects 2) human mind discerned mechanisms; at 1) effects, neural netowrks and genetic algorithms could test new molecules in
silico to find even stronger responders to cryogenic treatment. Imaginably maybe it’s like data trend is “BCC turn FCC”,
Or “dampened vibrations” as wikipedia calls them could be imparted on purpose; so lets say you impart wikipedia “vibrations” on catalytic atoms and alloys and things; do they then become more ctalytic as they have more lattice burring, act like
the’re hot at STP, and interact with greater stoachasticism to their environment. Test this: zap Cobalt with lasers, cold stir weld it, and do shock hardening on it; also have other cobalt as reference sample; does the “vibrationized” cobalt have
greater ctalytic ability; and does taking 20 samples to 10 degree C different cryogenic treatments at both stressed “wikipedia vibrational” cobalt and reference cobalt (-200, -290, -180 etc) to see if the two samples have different responses to
cryogenic treatment.

woods compared for cryogenic treatment; 10 species of pine, and 7 species of tree farm evergreens; 9-34% improvement to plywood from cryogenic treatment; rank best woods for cryogenic treatment; breed or also genetically engineer greater response to
cryogenic treatment into USA and European lumber and building wood species; Bred Chickens Quadrupled their mass; crop yields went up 10 times; the idea that this could double or triple the strength improvmenent is cryogenically treated wood seems
possible. So from the reported 9-34% better (bamboo) to to 27-102% better evergreen fir and pine for construction and even, breeding hardwoods for cryogenic treatment, ding-resistant fine furniture woods. Oak that is twice as strong.
Paper that is twice as strong.


Cryogenically treat condoms so they can be even ultra-thinner

make an electron gradient sandwich + -]|||||||||||||||[- e- does nearness to the cathode and saturation with electrons have any effect on the amount of cryogenic treatment change effect? supposedly all the lecrons are at the surface, but who knows what
local e- does, or, connect to positive charge terminal. As far as I know they say it is about lattice vibrations, but those should be responsive to surplus electrons or positivity.

Beneficially Bausing men and boys to ejaculate more semen: Online there are women that communicate their appreciation larger volumes of semen. As a guy, I notice the more fluid that comes out, the greater the length of orgasm with an increase in
pleasure. All people with Y chromosomes ejaculating quadruple or quintuple volumes of semen compared to a 2020 person at the 99th percentile of ejaculation volume with a Y chromosome is beneficial.
The genes that cause semen fluid volume such as porins (water) at seminal vesicles, and possibly glucose and or also fructose uptake channels could contribute; duplicating thsoe genes, or also putting stronger promoters on them causes larger amounts of
ejaculate to be produced, and is beneficial to make part of the human germline at all humans, that is people, that is homo sapiens globally.

It is also possible to make an immunization, given to infants, that will cause them to ejaculate larger volumes when they experience and complete puberty; I read antibodies can glom to receptors propping them open or making them shut, stimulating them
directly or making them more open to endogeonously existing physiochemical stimulation. The semen volume increasing immunization is likely to prop open some receptors to cause endogenous “make semen” signallinging to be even more strongly directive,
thus making more semen.
The advantage of endogenous physiochemicl stimulation is that if it is some chemical that occurs at puberty the boys can be immunized in infancy before puberty so they make 3-4 times as much semen throughout their ejaculatory lives, starting near puberty.
Optimally, the antigen (immunization) causes the body to produce the antibody that gloms a structure unique to seminal vesicles. Water and glucose transport channels are two possible things to upregulate to quadruple or quintuple the number of
milliliters per ejaculation.

Also at 99.99th percentile volume of ejaculate unmodified, untreated humans, the seminal vesicles’ ultrasound, genetics, and epigenetics can be examined to find why these humans have more semen (ejaculatory fluid); if there is an epigenetic basis then
peptides that install those epigenetics can be coadministered with the antigen vaccine that activates the water (porins) and glucose uptake channels at the seminal vesicles.
To increase semen volume those semen volume increasing peptides, which may also have a Cell Penetrating Peptide (CPP) part added to them, can be made a part of the human, that is people’s that is homo sapiens’ germline genome globally.

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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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