: The 3D printed hydrosorter could also be used to research a variety, notably a screenable library of 100,000 or a million freeze dried sperm preservatives to find those that produce motile egg-seeking sperm on rehydration, a technology that benefits
eugenics, and can cause the manufacturing cents of a sperm emitting vaginal decal or also paper applicator vaginal canal 60 day attaching paint that continually emits genetically enhanced or also genetically optimized sperm to be about 11 cents a month,
or 1.21 annually. Notably, 25,000 different drugs and preservatives can be screened on 40 sperm each 2.8 hours. Screening a billion freeze dried sperm revival with motility molecules, concentrations, and chemical treatment sequences is less than 120
days. Another technological from is a $4.14 5 gram polymer near cervix circlet that would gradually release 11 mg of motile previously freeze dried sperm every 24 hours for over a year, causing the likelihood of conception to be at 99% during the first
14.2 months of use among those persons capable of becoming pregnant



Gene therapy and gene drive on fish: At fish in the wild it might be notably effective to gather wild fish in multiplenum nets, where the netting is coated with gene transfection gel, and then the fish released after a 1-14 minute interval of gene
transfer to transfect what might be millions of fish with gene drive every 24 hours, with 100 days from one boat causing 100-200 million gene drive enabled fish to communicate gene drive to other fish in the ocean, providing benefits to fish like
removing all nociception as well as decreasing nipping and fish social behaviors humans find ethically beneficial to obviate.



Beauty genes that decrease risk of cancer: It is possible that female sex hormone receptors like estrogen receptors have a genetic 100 to 700% different amount of responsiveness to the same amount of circulating estrogen, progesterones, or other sex
hormones, that the size and shape and optimizability of human female secondary sexual characteristics like breast size and shape and soft skin and even body form (like I have heard of banana shape and top heavy hourglass) could be enhanced with human
germline genetic enhancement of estrogen receptor responsiveness to be at the 700% range, notably actual circulating estrogen could be the 2019 median amount or possibly shifted to endogenous estrogenic, progesteronic, or other sex hormone chemicals
with just 10-50% of the cancer risk of 2019 AD median estrogen amounts or also particular estrogen molecule types, so this gives women and girls even more beautiful body form while reducing cancer risk 50-90%.



There is a possibility that a technology that immunizes against background endogenous amounts of the chemicals produced when a human misses sleep reduces developing infectious disease, precluding, like with immunization, these chemicals, that are around
even when a person gets a normal amount of sleep, could reduce the incidence of many, or most infectious disease; I perceive I read that missing a night of sleep doubles risk of infection, it is possible that is from the production of some chemical, or
the activation of some receptors, it is possible that those chemicals, at different amounts, or receptors’ activation even when a person sleeps normally has some background amount, and that an immunization against those chemicals could reduce the
amount of illness the amount of even persons that sleep normally get. it is also possible that germline genetic engineering as well as gene therapy could quantifiably reduce infectious illness of many kinds through causing less of the sleeplessness
producing physiochemicals or receptor effects at persons that get normal amounts of sleep.



New genes to optimize and enhance the human germline: I favor publishing all the material I have written, among those materials are notebooks; there is material written in notebooks as well as online material I have published favoring enhancing as well
as optimizing the human germline, that enhancement as well as optimization can be the result of engineering completely new genes as well as enhancing or optimizing combinations of genes that already exist during 2019AD.



Raed that during 2019AD pediatricians recommended that babies not sleep with anything in their cribs other than a sheet, perhaps this will improve but until it does, it is possible a flocked sheet with extrasoft flocked patterns on it, like velour
macroscopic swirls could be a variation that the baby actually likes feeling the variations of, and where the baby like might moving over towards might be a beneficial enjoyed thing to put on baby sheets





I read that liposomes that travel to the lymphatic system cause some drugs to be 390% more absorbed, that is have 390% of the plasma levels as other oral drugs that go directly to the circulatory systen; could that be increased even more with the
genetics of having a lymphatic system with twice the permeability of drugs, twice the absorption suface area, some of both; noting the way the immunoeffectiveness of the body goes with the immunofunction of the lymphatic system could that double the
effectiveness of the immunosystem reducing infectioious disease, possibly also reducing cancer incidence as well; the human lymphatic system likely has genetic variations which could be sources of beneficial one dose lymphatic system gene therapies as
well as genetic enhancements and optimazations of human beings that is persons that is people; it is possible longevity technologies could be amplified as to their effectiveness with lymphatic system enhancements



prenatally beneficial PQQ, “Dietary supplementation with PQQ·Na2 significantly increased the total number of piglets born, the number of piglets born alive and the born alive litter weight. It also increased the antioxidant status in the placenta,
plasma and milk.”



Could customized sugars cause localization of drugs at the brain: GLUTS (glucose transporter types) with different genetics might have different transport amounts based on their different genetics and actual protein shapes, perhaps one is twice as
effective as movinh ribose, or another omits transporting highly deuterated glucose; these could be used not only to “feed” brain areas moe than others, but to be made into moeity attachments to drugs to get brain area or neuron type localizations, �
�membrane proteins known as glucose transporters (GLUTs) (Shepherd and Kahn, 1999). Though numerous GLUT isoforms (1–14) have been identified and characterized, only some of these transporters are expressed in the brain and can be involved in neuronal
homeostasis and brain function (Duelli and Kuschinsky, 2001). Specifically, the insulin-independent transporters GLUT1 and GLUT3 mediate glucose uptake into glial and neuronal cells, respectively (Simpson et al., 2007), suggesting that the impact of
insulin on synaptic plasticity should be independent of glucose uptake.

Moreover, GLUT2 and GLUT4 expression has been characterized in specific brain areas: GLUT2 is predominantly localized in the hypothalamus that regulates food intake (Eny et al., 2008), whereas GLUT4 has been identified in cerebellum, neocortex, and
hippocampus, suggesting a role of GLUT-driven glucose uptake in neuronal activity (Vannucci et al., 1998; Sankar et al., 2002). GLUT4 is also expressed in astrocytes and insulin stimulation promotes both glucose uptake and glycogen accumulation in
astrocyte cultures (Heni et al., 2011).”



A longevity immunization: online it says there are things that reduce autophagy, an I perceive I read that autophagy is linked to younger phenotype, so are there any naturally occuring proteins or peptides that reduce autophagy? Immunizing against those
could be a one dose treatment that causes the body’s own reduction of autophagy to be less, which then increases longevity and phenotypic youthfulness. This could be a part of childhood immunizations. “Experimental suppression of autophagy in the
absence of stress is tolerated by the rapidly renewing epidermal epithelium, whereas long-lived skin cells such as melanocytes, Merkel cells and secretory cells of sweat glands depend on autophagy for cellular homeostasis and normal execution of their
functions”

Longevity technology:



Longevity gum, “More than 100,000 tons of chewing gum being consumed every year.”, of cavity preventing xylitol gum, “dentists from all around the world recommend daily ingestion of up to 5g of xylitol (around 9 mints or 3-5 pieces of gum per day”
So if people chew five pieces of gum per day, 1825 pieces a year; 730 million or 1 billion gum chewers is plausible at a little over 10% of 2019 global population, and at 1825 pieces a year that is a little less than 2 trillion sticks of gum a year, at
20 pieces of gum each 24 hours per chewer that is 8 trillion pieces of gum. At a one cent premium per piece of longevity wellness gum that represents 80 billion us$ annual revnue from longevity and wellness increasing chewing gum.



AEDG chewing gum, also if a levo and dextro amino acid version of AEDG is found to be longevizing and wellness causing then AEDG could reach the GI tract for absorption.

Lithium at gum: Lithium in the water supply is correlated with people living longer, and makes laboratory nonvertabrates live 9-20% longer. If a flavor neutral or yummy lithium gum additive can be found, which could possibly arise from linking a 10,000
times sweeter than sugar sweetness peptide to lithium at a stomach dissolvable lithium chelator molecule, then at 5 sticks a day, and 5 mg of lithium per day, then 1.001 to 70 mg of delicious combined lithium/sweetness peptide/chelator molecule would be
at each stick of gum.

Also, they can put anything, at perahps 200 mg at liquid center gums like chewels.

Some chewing gums may already have a peptide/peptone/protein component. calcium casein peptone is a texturizer at chewing gum, “at a use level up to 5% wt/wt”

Production of beneficial drug peptides from milk (casein) and grain (gluten): Modified proteases like trypsin could make different digestion products, some of which are drugs. Genetically engineered organisms would make the new proteolytic enzymes with
customized products, which would then turn other things into beneficial medical peptides affordably. This brings Genetically engineered production’s product affordability to natural products.

Even more affordable than engineered enzymes: plants that make modified gluten with trypsin or pesin dividing regions that repeat, with a peptide of value between them: Also, as plants produce glutens, it is possible that producing Genetically engineered
organisms with the sequence (trypsin or pepsin cleavable location) -peptide of value-(trypsin or pepsin cleavable location): as the peptide-of-value-polyrepeat at genetically modified gluten could produce a highly affordable source of beneficial peptides.


Modifications of gluten to produce valued peptides released from digestion with ultraffordable already available bulk trypsin or pepsin:As a system the technologist would just swap in the amino acid sequence of interest at the -peptide of value- location
at the genome. During about 2005 AD the barley lab I worked at would get about 3 successfully genetically engineered plants for every 100 prepared (embryo sliced, soaked in transfection liquid, agar placed) barley embryos suggesting immediate rapid
production of over 200 different versions of gluten with different -peptide-of-value- per researcher per year using very simple technology I was able to use with 1 hour of training; the technology I used likely has transfection efficiency and hourly
production with new variant protocols that are 10 or 100 or even 1000 times more productive from automated slicing and multiwell plates.

It could be nifty if taking a protein with amino acid (peptide-like) sequences that already have bridges (like S bridges or different bridges) and then putting something like a trypsin or pepsin-division sequence at the four corners of the bridge :-:,
would then produce a variety of different customizable bridged peptides easily and reliably; they could even make an enzymatically attachable spacer amino acid string of genetically variable length to place between the two bridge sides like n or n that
would predictably provide the right distancing of briding amino acids to favor amino-acid bridging. This likely already exists.

Can a trypsin or pepsin (notably a chemical variant that does not interact with the protein source, like milk, until the hydrogen ions in the stomach modify the trypsin molecule) be swallowed with a food, like a trypsin or pepsin milkshake, to produce a
biologically active peptide in the stomach or even other parts of the GI tract?

Casein, the 80% of milk’s protein protein is processed like, “manufacturers combine casein with calcium hydroxide at high alkaline levels and dry the protein” So could a non pH/pOH molecule like a carbonium ion, a methyl ion, or an ammonium ion
make a novel protein chemical, that possibly with enzymatic digestion becomes a beneficial drug; sort of like casein with ammonium makes a bunch of c=c-c=c peptides that have ammoniums on them, thus looking sort of like metformin, a biguanide with
numerous c=c, That goes with preconcentration, predigestion protein sources with lots of gaunidine could produce metformin function-similars with ammonium ion (pNH3/pNH2) treatment. This could also be used on digests of the protein gluten.

At casein as well as gluten they could screen every n sized group of peptides available from a library of possible published custom digestions of the protein (producing like all 7 mers, all 40 mers etc) against activity databases to see if any of them
are drugs, they could also massively parallel make molecular receptor attachment models of some amount of casein’s N possible truncated peptide constituents to find new drugs that could be made from casein or gluten.

Opiod peptide from digestion of milk: a 3 (H-Tyr-Pro-Phe-OH) ,4,5,6, or seven-amino peptide (H-Tyr-Pro-Phe-Pro-Gly-Pro-Ile-OH) like beta-casomorphin-7; perhaps some opiod peptides are actually enjoyable, which are also minimally harmful, perhaps from
localizing at only particular brain regions like the nucleus accumbens; It is possible that nonCNS opiod peptides relieve discomfort without having cognitive or behavioral effects. I perceive just putting a hydrophilic lipophobic length of, or external
hydrophilic or lipophobic tertiary structure outer layer of amino acids or a polyglycine length on a peptide will keep it on the body side of the blood brain barrier, so that could be a thing that relieves discomfort or could aslo provide anesthesia.

A map, possibly constructed with positron emission tomography, or other approaches, of a screened library of which peptides concentrate at what brain regions, as well as what body regions, and an immunocolorization map (or niftier technique) of peptide
localization at each cytotype and tissue type would be beneficial to the creation of beneficial drugs, notably those producible from gluten digests and probiotics and gene therapy as well as possible germline modification. Nootropic: numeous nootropic
peptides are described online and at the scientific literature, https://ultranootropic.com/ ,would vasopressin, thymosin beta 4, semax, noopept, as well as many other peptide variants that only localizes at the frontal lobes improve cognition and memory
and other cognitive things without effecting emotional capability (limbic areas) or bodyside functions (cerebellum, brainstem)?

Noting CNS effects on longevity, screening all nootropic peptides to see if any of them are also longevity producing peptides could find new longevity drugs, as well as amino acid sequences that van be function mimiced with peptide mimetic drugs to
produce completely new lifespan lengthening drugs.





also, “Casein peptides are used for high blood pressure, high cholesterol, anxiety, fatigue, epilepsy, intestinal disorders, cancer prevention, and stress reduction”

Could casein be used as an ion transporter to different cytotypes?

polyprotic acid, or a polyhydroxyl base



s from changing something like “sodium (salt of) Also, they can put anything, at perhaps 200 mg at liquid center gums like chewels.

Do any oligosaccharides (like sugar mini-polymers) have drug effects? Are any of them longevity or wellness effects like polyribose might have, polyribose molecularly sapced NR or NMN that turns to NMN at cytoplasm, as a possible enzymatic or some
benefit to the brain as a food, or fostering beneficial probiotic growth,

Previously described are possible artificial colors that heighten wellness or longevity to be used as food additives. c=c-c=c-c=c structures are frequent at some colorizing chemicals. Also, a longevity version of bright yellow B vitamins could be
possible.



Microsugar lancets like at applique needlesless drug delivery could have some activity at gum. That suggests a pack of gum could immunize against atherosclerosis, perhaps a dose per decade, or even a dose per century.

A month of gum chewing with highly localized, less than than mentally perceptible effects on feeling normal, senolytic could be a one month longevity treatment.

Although candy with immunoactive material at microlancets could also do immunizations, it is possible swallowing immunobeneficial or other longevity technology gum could be beneficial.

AEDG linked to carbohydrates; lithium linked to carbohydrates, ribose linked to AEDG could concentrate AEDG at the heart, providing benefit.

AEDG linked to lactate or lactic acid could concentrate at the brain, causing benefit; as a minute amount at food, gum, or candy, concentration of AEDG at the brain could provide benefit, notably though AEDG has something to do with pineal gland
chemicals, so brain concentration could permit lower doses, be more likely to provide projected benefits, possible enhance or otherwise effect fertility (50% greater conception rate from melatonin at IVF)

NGF and BDNF heightening 2 amino acid peptide, noopept, “In animal studies, Noopept has been shown to stimulate the expression of two important cognition-related chemicals, Nerve Growth Factor (NGF) and Brain-Derived Neurotrophic Factor (BDNF).”

Could those two amino acids at noopept, proline glycine, or any other nootropic peptide, be used when attached to other drugs cause high utility brain localization, “Brain-Derived Neurotrophic Factor (BDNF) has a similar role to NGF but is primarily
active in the hippocampus, cortex, and basal forebrain, areas of the brain that are vital to learning, memory, and higher thinking”, also, “readily crosses the blood-brain barrier”, so attaching 2 mer (prolyl glycine) noopept to 3 mer opiate
peptide (Tyr-Pro-Phe) making 5 mer pro-gly-tyr-pro-phe as a brain concentrating opiate peptide?



Proline-glycine could be an effective way to get numerous other drugs to pass the blood brain barrier, perhaps phenibut-Pro-Gly could work at orders of magnitude less milligrams per dose, and it is also possibly Pro-Gly causes drugs to pass the ovary-
blood barrier as well, improving fertility drugs and possibly making contraceptives even more affordable on a $/Kg manufacturing basis.



Protein Kinase RNA-Activated inhibitors, or PKR inhibitors like C16 are peptides described online as causing new path learning after one session as compared with several sessions for unmedicated mice; could PKRI be used to localize other drugs to the
brain areas that cause the “one training session works as well as several” effect? CART peptide linked to PKRI is one possibility for a new nootropic that also makes learning with many fewer examples or less practice duration possible. Even linking
Pro-Gly (noopept) which increases BDNF and NGF to PKRI like C16 could cause those rapid-learning neural areas to grow causing lasting increases in intelligence. PRKIProGly can be constructed and ordered online.



Are there any peptides that pass through cartilige and joint tissues rapidly, these are different than “blood brain barrier”, but if there is any preferential transport there might be peptide that does that at joints; chondrotoin, MSM, hyalonuric
acid and others could all be linked to such a joint transport protein. This could also heighten migration of other drugs. This would treat or prevent some joint decay, causing more youthful joint form and usefulness.

Genetically engineering a plant that treats schizophrenia and psychosis: There could be a peptide, findable at a library of less than 576 two mer peptides that specifically effecs 5HT receptors, Latuda which functions only at HT2 receptors and is absent
effect on D1,D2, orther dopamine receptors, causing fewer side effects, could perhaps have a functionalike peptide, and then the peptide engineered into plants, brewing yeast, yogurt, vaginal probiotics, and oral probiotics, making antipsychotic
medication grwoable and able to reach more than 70 million people globally. Of the Pro-Gly two amino acid noopept, online it says, “Noopept modulates the activity of both AMPA and NDMA receptors”, so they could screen a combinatorial library of all
the 2 unit peptide combinations of 24 different peptides, which is near 576 different peptides on 8 mice each, to get p<.05 at behavior change, like nonpsychotic begavior, and immunocolorization mapping of the brains and bodyside nerves to see which
peptides caused localization at dopamine neurons, much the way Pro-Gly concentrates at AMPA and NMDA neurons. Also, as serotonin neurons have many published activities these serotonin active or also serotonin neuron localizing neurons could have
numerous beneficial drug effects.

Although noopept Pro-Gly is functional at 10mg oral dose, could a leve-dextro version of the amino acids make it omit being digested, causing a nootropic doasge in the micrograms?

Similarly, could a levo-dextro version of opiate peptides omit being digested thus causing microgram functional dosages? Also, do opiate peptides work more enjoyably if snorted or vaginally applied, or made to be a buccal absorption alginate gel mouth
coating?

A variety of ribosomal activity nootropics that might, or might not function like PKRI C16, Protein Kinase RNA-Activated Inhibitors,“What makes PKR inhibitors an EXTREME example is how it works. It essentially disables a security feature of the brain
that helps to prevent viral infections” suggests the possibility that either genetic material reaching ribosomes omits a prescreening of some kind, or that the ribosomes work more rapidly, or that tRNA availability goes up,



Longevity technology: Dastinib with querectin are Senolytics that benefit the brain:

The senolytic: is described as, “Senolytic treatment of AD mice selectively removed senescent cells from the plaque environment, reduced neuroinflammation, lessened Aβ load, and ameliorated cognitive deficits. Our findings suggest a role for Aβ-
induced OPC cell senescence in neuroinflammation and cognitive deficits in AD, and a potential therapeutic benefit of senolytic treatments. “dasatinib and quercetin (D + Q), can selectively eliminate senescent cells from pathological tissues”

At mice, the senolytic dose was 12 mg/Kg of dasatinib and 50 mg/Kg querecetin, oral gavage with PEG/saline vehicle; so perhaps 70 mg per day of D for a human, utilizing the 1/12 mouse dose thing, and 350 mg of querecetin per day. Dasatinib is prescribed
for 12 months or possibly longer as an anti-cancer drug, but the senolytic dosage duration at the mouse experiment is 9-10 days. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6605052/

Dasatinib causes mice on an 11 week long dose to be better at learning motion pathways, at (youngish) 3.5 month old mice, rigged to be messed up, “In peripheral organs, partial elimination of senescent cells (~30%) is sufficient to restore tissue
homeostasis and function in disease models and during aging7,29,30. We next determined whether longterm intermittent senolytic treatment could ameliorate Aβ plaque pathology and/or improve cognition in APP/PS1 mice. Beginning at 3.5 months of age,
female APP/PS1 AD mice were treated with either D + Q or vehicle once weekly for 11 weeks (Fig. 5a). Hippocampus-dependent spatial learning and memory were evaluated by testing the mice in the Y maze immediately before, and at the 6- and 11-week
treatment time points, and mice were also tested in the water maze during treatment week 10. Mice were euthanized at 11 weeks and their brains processed for biochemical (one hemisphere) and histological (the other hemisphere) analyses. [and then it says]
Compared with vehicle-treated APP/PS1 AD mice, APP/ PS1 AD mice treated with D + Q performed significantly better in the Y maze at both the 6- and the 11-week time points (Fig. 5f). In the water maze tests, D + Q treatment enhanced memory acquisition (
more rapid learning of the location of the hidden platform) and memory retention in the probe trial” Notably at a graphic at the paper, dasatinib with querecetin caused large but then identical learning effects; at day 4 of cumulatively learning a
pathway finding task the drugged mice were approximately 62% better learners, but at day 5 they were identical.

At a different paper, “senolytic therapies could be administered intermittently, serving to reduce the senescent cell burden by treating quarterly or even annually, which minimizes the risk of side effects”, “Treatment of mice with dasatinib plus
quercetin (D + Q) improves cardiac ejection fraction and increases vascular reactivity in old mice after a single, 3 day treatment course [30,34]. In addition, D + Q treatment decreases vascular calcification and increases vascular reactivity in
hypercholesterolemic, high fat diet fed ApoE−/− mice after three monthly 3 day treatment courses”

They could see if a different chemotherapeutic drug, nilotinib, that works on the same kind of cancer as dastinib is a beneficial senolytic, possibly with nonoverlapping activity at different body cytes or body tissues.

Localization peptides or proteins attached to senolytics like dasatinib could cause even greater benefit. Pro-Gly could cause brain concentration, noting that dasatinib is published as heightening learning ability it is perhaps beneficial to have a
senolytic reach the brain. Chondrotoin or MSM molecular moeity on senolytics could cause greater joint youthfulness function, reduce immunoreactivity and sequelae; the cytotypes senolytics remove are published as linked to bone-joint illness, suggesting
senolytics could produce younger phenotype function at bones and joints.

Fisetin is a senolytic, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6197652/ “The natural product fisetin has senotherapeutic activity in mice and in human tissues. Late life intervention was sufficient to yield a potent health benefit.” as well as,
“chronic administration of fisetin to wild-type mice late in life improved tissue homeostasis, suppressed age-related pathology, and extended median and maximum lifespan”, “This result, similar to a recent report on the combination of D ± Q, is
the first to document extension of both health span and lifespan by a senolytic with few side effects, even though administration was started late in life.”,

Dose: “mice were fed Teklad 2020 chow (Envigo, Madison, WI) prepared with or without 500 ppm (500 mg/kg) of fisetin (Indofine Chemical Co., Hillsborough, NJ) by Envigo. Co. (Tampa, FL). For oral administration of fisetin, mice were dosed with 100 mg/kg
of fisetin in 60% Phosal 50 PG:30% PEG400:10% ethanol or vehicle only by gavage.” That represents 7 grams of fisetin every 24 hours at a direct, non compensated for mouse size dose, or 583.3 mg every 24 hours at a compensated mouse dose. At the
fisetin placed at food, “diet with or without supplementation with 500 ppm (500 mg/kg) of fisetin, ad libitum (approximately 60 mg/kg fisetin per day). The mice were exposed to a fisetin diet intermittently from 6 to 8 then 12–14 wks of age” which
could be communicating that each Kg of mouse (that is a lot of mice) got 60 mg of fisetin, so 4.2 grams per day, without mouse division number, or 350 mg per day at the mouse dose equivalent convention number. On ebay, fisetin is $22 for 10g.

At the paper, 20 micromolar fisetin has twice the cytonumber reduction as 5 micromolar fisetin at cultured cytes treated for 48 hours, and the difference in messed up cytes goes from no effect at absence of drug to 1.1/.5, or about 55% reduction of
messed up cytes at 20 micromolar.

A different graph displays fisetin at cultured cytes’ senolytic activity as 1.3/.4 or 69% reduction in senolytic cytes.

They measured the senolytic activity of 11 different chemicals, fisetin at 69% was more effective than curcurmin as a senolytic at about 50% https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6197652/

It is possible that sequential or simulataneous senolytics could benefit survival and promotion of youthful cytotypes, so curcurmin with fisetin, or at a sequence with each other could be beneficial. Taking them simultaneously could possibly work better
as it is possible the nonoptimal cytes express immunoattractants while processing senolytics, and doubling the amount of immunoattractants or simultaneously producing different kinds of immunoattractants could cause greater immune response that removes
nonoptimal cytes.

Notable for fisetin in food compared with once a day oral dosing, fisetin has a plasma half life, so keeping plasma levels high and steady could be beneficial as the food only had 350 mg in it, compared with the 583 mg in the once daily dose, I do not
know if they had identical senolytic activity yet though.

If a human eats .5Kg of carbohydrates that is 2000 calories, and at mouse dose would have 250 mg of senolytic fisetin, suggesting the 583.3 mg a day dose is better, noting at cultured cytes doubling fisetin concentration doubled senolytic acivity. also,
at a different paper dasatinib was more effective at higher doses.




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