A different decanoic acid, that could also be screened for longevity effects is an antimicrobial, “A recently developed biofilm inhibitor, cis-2-decenoic acid (C2DA)” if C2DA is like an order of magnitude or two more antimicrobial than 10HDA, “
C2DA at concentrations of 500 μg/mL and above inhibited growth, while 125 μg/mL C2DA inhibited biofilm. Combination with antibiotics increased these effects. At concentrations up to 500 μg/mL, there were no cytotoxic effects on fibroblasts.”

it is possible it has other characteristics as well, and screening it for longevity effects at c elegans could be beneficial



a 12 C fatty acid, that looks kind of like 10HDA that could be screened for longevity effects is : “cis-2-decenoic acid appears to be functionally and structurally related to the class of short-chain fatty acid signaling molecules such as diffusible
signal factor which act as cell-to-cell communication molecules in bacteria and fungi.”, “characterized a substituted fatty acid messenger, cis-11-methyl-2-dodecenoic acid, called diffusible signal factor (DSF)”



also, “Treatments consisted of spent medium, CSM, cis-2-decenoic acid, trans-2-decenoic acid, decanoic acid, and DSF at various concentrations.”, “cis isomer of 2-decenoic acid was the organic compound” [that caused biofilms to disperse], “The
compounds with the highest activity were two isomers of 2-decenoic acid. The trans isomer (trans-2-decenoic acid) was shown by microtiter plate dispersion bioassay to have activity only at millimolar concentrations, typically not low enough to qualify as
a cell-cell signaling molecule. Figure Figure5B5B shows the dispersion activity of increasing concentrations of cis-2-decenoic acid against biofilm cultures of P. aeruginosa grown in microtiter plates. These results demonstrated that the cis isomer (cis-
2-decenoic acid) was active over a concentration range from 1.0 nM to 10 mM”

There is some perspective here where a decanoic acid, of a slight variation (cis rather than trans) is like an actual 1 million times more effective (nanomoles compared with millimoles)at causing bacterial biofilms to detach; so that brings up the
possibility, noting that DAEE causes greater happiness, better healing, and other benefits at 2.9 mg/70Kg/24 hour human, that there could be a a 10HDA version that has longevity effects at a couple orders of magnitude fewer atoms per dose, or,
beneficially, has a longevity effect ten times larger than 27% (10HDA at mice), notably salicylic acid causes yeast to live more than 400% longer, so this could be possible; among organisms, a 720 minute longevity bug, compared with a half century
duration termite queen is a a 36,500 times longevity difference, and at mammals, a yearlong rodent compared with a 211 year whale is a 21100% longevity difference; The antarctic sponge has a lifespan of 15550 years or longer;



longevity technology: 10HDA at royal jelly is published as an HDACinhibitor, causing acetylation which velocitizes and causes DNA transcription at histones, I perceive I read a variety of HDACinhibitors have longevity and wellness effects, So, as a
beneficial complementary thing to making a bunch of 10HDA (or 10H2DA) molecular variants and then screening them to find out if they cause greater longevity at yeast, c elegans and 96 well plate vertebrate fish, and mammals, they could make a bunch of
molecular variants of 10HDA that could be and quantified as to their effectiveness as HDAC inhibitors, and noted as to their dose (mcg/ng) effectiveness at causing HDAC inhibition at a variety of HDACs and effectiveness at histones at cytostructures of a
variety of species, including humans, This gives all kinds of new molecular modification possibilities of being effective: 10HDA dimers, halogenated 10HDA, 10HDA linked to a nuclear membrane transport peptide, 10HDA with a butyrate (or propynate)
attached to it, or a valproate, basically any HDAC inhibitor molecule partially modified to have a 10HDA on it, As a molecular library to screen, come up with a few hundred 10HDA variations all of which have a possibility of being a better, faster,
stronger, more reaching of tissues that 10DHA might not usually reach HDAC inhibitor, then screen the library of those hundreds of 10HDA molecule variants, with things like multiwell plates with yeast, also c elegans can be used to quantify better faster
stronger HDACinhibiting effects; Then at humans these versions might also cause greater longevity at few mg or ug/dose



A version of 10HDA that is a better longevizing drug, and that also causes greater intelligence: I read, Intelligence gene, “Enhancement of memory formation is increased in mice given vorinostat, or by genetic knockout of the HDAC2 gene in mice” That
suggests that a modification of 10HDA to be a HDAC2 inhibitor would cause greater intelligence at mammals like humans, so coming up with a library of 10HDA variants, and then screening them to find a version that is HDAC2 inhibiting produces a longevity
drug that makes humans more intelligent; One way to make a 10HDA that inhibits HDAC2 is to modify the HDAC inhibitor molecule vornistat, SAHA, which is kind of long and looks sort of like 10HDA, to be sort of in between 10HDA and SAHA, then screen the
variants, perhaps a million generated microfluidically at a one million channel published microfluidic thing I read about, to find vornistat 10HDA variants that cause C elegans to live longer from 10HDAlikeness while also causing greater intelligence
from SAHAness; Noting you can have the one million channel microfluidic go along with a one million well plate (like integrated circuit technology multimillion well plates) or even a 10 million yeast cyte per second flow cytometry analyzer, you can see
which of the 1 million library variants causes yeast to live the very longest, then among the top .01% of vornistat/SAHA/10 HDA variants at causing greatest yeast longevity then screen those 100 most yeast longevizing library variants with c elegans at
multiwell plates to find the top 3 to quantify and screen as to their effect on longevizing mice, and then humans; that produces a longevity drug that causes greater intelligence



Also a SAHA/vornistat like 10DHAlike HDAC2inhibitor has another longevity heightening molecular possibility, an NIA study found that the nonfeminizing estrogen alpha-estradiol caused greater longevity (11%?), and wikipedia says, “estrogen receptor
alpha (ERalpha) can be hyperacetylated in response to histone deacetylase inhibition” that suggests an HDACinhibitor could possibly make estrogen receptor alpha really ultra extra responsive, and if it is, then it is possible it’s longevity
increasing effect is more often spontaneously functionally activated to cause greater longevity, and that would move 10HDA to 10HDA with alpha-estrogen activator, from 25/27% (mice) as well as 18/46% (c elegans) to 36/38% (mice) as well as 29/57% c
elegans with the 11% longevity heightening



Another longevity version of a HDAC2inhibitor that causes humans to be more intelligent while heightening longevity is to modify the HDAC tetrapeptide to be a different peptide; the peptide epithalon (AEDG) as well as the peptide thymosin, when given to
a human simultaneously, makes the person four times less likely to be dead after 6 years, so, just make a different shape, branch, or peptide loop (trefoil?) with the HDAC2inhibitor being the tetrapeptide HDACinhibitor, and the other branches, or
possibly they could function with modification as loops, being epithalon (AEDG) and thymosin. It makes you smarter, it keeps you from being dead, and, if it causes alpha estrogen receptor acetylation hyperresponsiveness (from HDAC inhibition) it
increases longevity



longevity technology: 10HDA at royal jelly is published as an HDACinhibitor, causing acetylation which velocitizes and causes DNA transcription at histones, I perceive I read a variety of HDACinhibitors have longevity and wellness effects, So, as a
beneficial complementary thing to making a bunch of 10HDA (or 10H2DA) molecular variants and then screening them to find out if they cause greater longevity at yeast, c elegans and 96 well plate vertebrate fish, and mammals, they could make a bunch of
molecular variants of 10HDA that could be and quantified as to their effectiveness as HDAC inhibitors, and noted as to their dose (mcg/ng) effectiveness at causing HDAC inhibition at a variety of HDACs and effectiveness at histones at cytostructures of a
variety of species, including humans, This gives all kinds of new molecular modification possibilities of being effective: 10HDA dimers, halogenated 10HDA, 10HDA linked to a nuclear membrane transport peptide, 10HDA with a butyrate (or propynate)
attached to it, or a valproate, basically any HDAC inhibitor molecule partially modified to have a 10HDA on it, As a molecular library to screen, come up with a few hundred 10HDA variations all of which have a possibility of being a better, faster,
stronger, more reaching of tissues that 10DHA might not usually reach HDAC inhibitor, then screen the library of those hundreds of 10HDA molecule variants, with things like multiwell plates with yeast, also c elegans can be used to quantify better faster
stronger HDACinhibiting effects; Then at humans these versions might also cause greater longevity at few mg or ug/dose





A version of 10HDA that is a better longevizing drug, and that also causes greater intelligence: I read, Intelligence gene, “Enhancement of memory formation is increased in mice given vorinostat, or by genetic knockout of the HDAC2 gene in mice” That
suggests that a modification of 10HDA to be a HDAC2 inhibitor would cause greater intelligence at mammals like humans, so coming up with a library of 10HDA variants, and then screening them to find a version that is HDAC2 inhibiting produces a longevity
drug that makes humans more intelligent; One way to make a 10HDA that inhibits HDAC2 is to modify the HDAC inhibitor molecule vornistat, SAHA, which is kind of long and looks sort of like 10HDA, to be sort of in between 10HDA and SAHA, then screen the
variants, perhaps a million generated microfluidically at a one million channel published microfluidic thing I read about, to find vornistat 10HDA variants that cause C elegans to live longer from 10HDAlikeness while also causing greater intelligence
from SAHAness; Noting you can have the one million channel microfluidic go along with a one million well plate (like integrated circuit technology multimillion well plates) or even a 10 million yeast cyte per second flow cytometry analyzer, you can see
which of the 1 million library variants causes yeast to live the very longest, then among the top .01% of vornistat/SAHA/10 HDA variants at causing greatest yeast longevity then screen those 100 most yeast longevizing library variants with c elegans at
multiwell plates to find the top 3 to quantify and screen as to their effect on longevizing mice, and then humans; that produces a longevity drug that causes greater intelligence



Also a SAHA like 10DHAlike HDAC2inhibitor has another longevity heightening molecular possibility, an NIA study found that the nonfeminizing estrogen alpha-estradiol caused greater longevity (11%?), and wikipedia says, “estrogen receptor alpha (ERalpha)
can be hyperacetylated in response to histone deacetylase inhibition” that suggests an HDACinhibitor could possibly make estrogen receptor alpha really ultra extra responsive, and if it is, then it is possible it’s longevity increasing effect is
more often spontaneously functionally activated to cause greater longevity, and that would move 10HDA to 10HDA, alpha-estrogen activator, from 25/27% (mice) as well as 18/46% (c elegans) to 36/38% (mice) as well as 29/57% c elegans with the 11%
heightening



Another longevity version of a HDAC2inhibitor that causes humans to be more intelligent while heightening longevity is to modify the HDAC tetrapeptide to be a different peptide; the peptide epithalon (AEDG) as well as the peptide thymosin, when given to
a human simultaneously, makes the person four times less likely to be dead after 6 years, so, just make a different shape, branch, or peptide loop (trefoil?) with the HDAC2inhibitor being the tetrapeptide HDACinhibitor, and the other branches, or
possibly they could function with modification as loops, being epithalon (AEDG) and thymosin. It makes you smarter, it keeps you from being dead!, and, if it causes alpha estrogen receptor acetylation hyperresponsiveness (from HDAC inhibition) it could
heighten longevity



They could blenderize endoliths, which wikipedia says are microorganisms with million year lifespans and 10,000 year cytodivision cycles, and feed them to mice coated with an enteric coating, they could also see they effect on c elegans, as well as
amoeba, pa aeurosomethign (a bacteria that makes that has T2DA and C2DA decenoic esters); also wikipedia says, “Some Actinobacteria found in Siberia are estimated to be half a million years old.”



It is possible a plasticizer, like replacements for 2019 bisphenols could be esterified decnoic acids, possibly with a few esters, or possibly cyclic; basically they could do tests and find out if a plasticizer for industry could be found tht actuallu
casues greater longevity at mice, and thus might be harmless or beneficial to humans



when they make vehicle fuel out of used food oil it is often a fatty acid ester, perhaps there is a fatty acid ester, utilizable as a motor fuel, that causes mammals to live longer the way 10HDA and 10H2DA at royal jelly make C elegans and mice live
longer, then rahter than “smog” being deleterious to health a .01% or near that unreacted fatty acid ester could cause a longevizing effect at mammals that breathed trace amounts





Computational methods of finding active drugs and chemicals, “he estimates CPU costs of only a thousand dollars or so for half a billion molecules, although I think that’s too low), “, “assume an average of 25 heavy atoms for your molecules, so
50 atoms in total, so 150 coordinates per conformer, times 100 confs per molecule[*], and you’re looking at north of 30TB of data: that’s doable, but the storage costs are going to be significantly more than your CPU costs. If your virtual library is
10 billion molecules, now you’re looking at 600TB of data” https://blogs.sciencemag.org/pipeline/archives/2018/09/06/virtual-compound-screening-the-state-of-the-art



Another cancer drug that might be a longevity drug is bryostatin, it has a 8-9 Carbon partially unsaturated alkane (a couple C=C) with esterification there, but then that part which is a lot like 10H2DA (of royal jelly longevity), is connected to a bunch
of other atoms at a big anticancer molecule; so if a person purposefully attached an esterified decanoic acid (like 10H2DA, 10HDA, 90DA, HAEE, or a more effective longevity increasing molecule) to a rapamycin molecule it might be much more effective, but
bryostatin might already have longevity functionality now. Beneficial to screen bryostatin molecule for longevity



It is 2019 AD, wikipedia says, “In March 2010, research was published demonstrating an HTS”, high throughput screening, “process allowing 1,000 times faster screening (100 million reactions in 10 hours) at 1-millionth the cost (using 10−7 times
the reagent volume) than conventional techniques using drop-based microfluidics.[22] Drops of fluid separated by oil replace microplate wells and allow analysis and hit sorting while reagents are flowing through channels.

In 2010, researchers developed a silicon sheet of lenses that can be placed over microfluidic arrays to allow the fluorescence measurement of 64 different output channels simultaneously with a single camera.[23] This process can analyze 200,000 drops per
second.

Whereby traditional HTS drug discovery uses purified proteins or intact cells, very interesting recent development of the technology is associated with the use of intact living organisms, like the nematode Caenorhabditis elegans and zebrafish (Danio
rerio).[24]



one system that could be improved uses mass spectroscopy to screen 2 million molecules in 10 days,



wikipedia says, “we substantially enhance screening throughput by enabling growth and analysis of 6144 mutant yeast colonies on a single agar plate. The significance of achieving this number is that the vast majority of microbial model organisms have
gene counts very near but not exceeding this number, allowing for an entire, genome-wide screen to be performed on a single agar plate.”

That suggests that 20k human genes fits on 3 (2014 AD) plates, or if it quadrupled (2019), to one 24K colony plate









multiwell systems sometimes have a wash stage, perhaps the chronological interval of this could be decreased with ultrasonic transducers at the washing fluid emitter, one system I read about that could do 2 million measurments in 10 days had a wash cycle

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