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.



An immunization could have one of the effects of senolytics, “Senescent cells can develop a senescence-associated secretory phenotype (SASP), consisting of pro-inflammatory cytokines, chemokines, and extracellular matrix-degrading proteins”,
immunizing against extracellular matrix-degrading proteins could cause greater tissue functionality longer, and senolytics are researched as causing greater wellness and younger phenotype. extracellular material might be particularly reachable with
antibodies. It is possible that as some immunizations last as long as a person, immunizing against extracellular matrix degrading proteins could be a one dose lifespan increasing and wellness increasing immunization, possibly functional at farther than
postpubertal ages even when given to a child, during the period when people routinely get immunizations and parents highly prioritize immunization activities and coverage. It is also possible that “matrix degrading proteins” have an effect on dermal
cytes and structure, which I perceive I read have something to do with the word “matrix proteins”, that causes this possible longevity wellness immunization to also be a beautification and youthful appearance sustaining possibly one dose treatment,
heightening popularity and voluntary use. The other chemicals mentioned, “pro-inflammatory cytokines, chemokines” could also be immunized against to benefit longevity, wellness, and phenotypic youthfulness; I pereive there are a number of these
cytokines and chemokines, so a list of which have the highest mass/volume concentration both at the circulatory system and outside, right next to the cytomembrane at the intracyte space, and then immunizing against those, could concentrate effectiveness
although cytotype and tissue specificity could make immunizing against all of them notably more effective; One benefit of immunizing against a multi digit (2 digit? three digit?) number of chemokines and cytokines is that some of them may have
multidecade effective immunization coverage while others might have different immunization coverage, This partial yet long duration removal of deleterious cytokines and chemokines and matrix protein harming chemicals could actually interrupt and derail
any harmful processes where the deletarious cytokines, chemokines and matrix-messing up chemicals effect each other, build on each other, or saturate body repairs, from combining or cascading each other’s effects. A person that is good at math and
algorithms could look at a biochemical network, then come up with a minimum number of items to remove, at certain chemical-link distance from each other, to break a network effect, cause a different group average, or modify the persistence of an emergent
effect, sort of like whats the fewest steps to wipe out a deleterious eignevalue? Immunizing against that group of chemokines, cytokines or matrix-protein messer-uppers could do that math, causing greater longevity, wellness, healthspan, and
youthfulness of phenotype.

Protein or peptide linked drugs could traverse vascular plaque cytopiles to deliver beneficial drugs that shrink of remove vascular plaque blobs and cytopiles and be a cardiovascular wellness drug, “[senolytic]reduces senescent cell-like, intimal foam
cell/macrophages in vascular plaques”; they could screen the 526 peptide library of 2 unit (mer) peptides formed from 24 amino acids to find out if any cause preferential traversal of atherosclerotic plaque cytopiles and possibly cholesterol coatings.
lipophilic peptides could be better at traversing cholesterol coated or layered cytopiles. lipophilic peptides linked to physiologically harmless immunocyte attractants could cause macrophages and WBCs to find atherosclerotic plaque particularly
attractive to glom and remove. Making a protein digest of bacterial cytowalls, then linking them to lipophilic peptides could cause the immune system’s rapid and effective response to bacteria to be directed at atherosclerotic plaque, causing greater
wellness and possibly improving cognition with improved CNS circulation, as well as reducing risk of cardiovascular disease. Immunizing against cholesterol works on rabbits to reduce cardiovascular nonoptimality, immunizing against plaque blobs could
remove them: also just as there are many different velocities and “brush strokes” to cleaning off a nonbiological item, different velocities of immunoresponse as well as different biochemicals to remove (immunoglom) first could be tested to find the
immunocleanup of vascular plaque blobs that was most beneficial and with the least risk.

a novel senolytic mechanism with a “pick preferred candy out of a pile before getting on a school bus” metaphor: Some chemical transport channels of the exteriors of cytomembranes are possibly durably pluggable with molecules, these molecules are
also consructed to have a lengthy molecular tail that the immune system recognizes and is reactive to. It is possible that deleterious cytes like the kind senolytics remove, as well as scar or encapsulation tissue cytes, as well as piled up cytoblobs at
vascular arterial plaques, have greater molecular transport of some specific chemical. Then, I perceive that when a person gets a harmless viral cold, that they get symptoms for 3 days before the symptoms get better, that suggests that a 2019 AD human’
s immunse system takes 72 hours to produce the antibodies to remove an infection.

Labelling many things, then using a gentle wash to provide unwell/well cytocontrast: Decorative plugs that occupy a transport channel at the cytomembrane diffuse away, with a half-diffused amount at 24 hours, so 96 hours after the labelling dose, only 1/
8 as many decorated plugs are on cytes. If the deleterious cytes stared with 80 plugs per cyte they will still have 10, but the cytes that only had 6-8 decorater plugs will have about 1 or zero.

Noting that senolytics increase longevity, wellness, healthspan, and cause younger cytophenotype and tissue phenotype: a new kind of senolytic: Have the person eat or be dosed with an immunoreactive chemical that has a cytomembrane molecular transport
channel plug that is like 3 to 40 times more likely to plug up a molecular transport channel at the external cytomembrane and accumulate at a deleterious cyte like the kind of cytes senolytics terminate. Noting well cytes and deleterious cytes differ as
to their transport channels (senolytics are previously published as reaching their goals preferentially) Give them a big enough dose so that each deleterious cyte gets say 80 antibody-reactive plugs for every 2 at a well cyte, or even 90 antibody
reactive plugs at a deleterious cyte for every 30 at a well cyte. Then give the human a big dose of the decoration (the antigen without the plug part) to activate the immune response, doing this after 96 hours of gentle diffusion washing away some of
the decorator plugs, the big dose of plugless decoration causes a large immunogen response, after most of the well cytes are absent decoration while the deleterious cytes are still immunoreactive.

Also, along with the activation dose of decorator (absent plug) antigen to produce an immune response after well cytes immunoreactivity is decreased, It is possible to use the body’s apparently ordinary 2019 AD 72 hours to make an immune response to a
viral cold effect, then have that 72 hour spontaneous immune response glom to and remove the decorative plug labelled cytes once 96 hours have progressed, the body has produced antibodies after the 72 hour viral cold-like process, and well cytes have
only zero to perhaps 3 decorated plugs compared with 8 at a deleterious cyte. The deleterious cytes have been senolytically removed, and could even possibly be removed on a “senescent cytes have different transport channels” basis, the thing that
makes it a new senolytic is that it terminates cytes like a senolytic without an external drug toxin; similarly this could be a way to treat cancer, removing some of the oncocytes. Noting that some mechanism at senolytic chemotherapeutic drugs like
dasatinib get preferential effect (thus likely membrane transport) at senescent cytes, and then the senolytic drugs terminate the senescent cytes, it is scientifically sensible to think senescent cytes have different molecular transport channels, or
quantities of ordinary channels.

Plugging the transport channel while attracting immunoreaction, when the immunoreaction can be times or sequenced creates kind of algorithmic numerical advantage in removing deleterious cytes. Possibly a plug that resides for just hours or 96 hours would
preferentially remove deleterious cytes while using up all the circulating beginning antibodies to the decorated plugs; The decorator-plug immunoreactive cytes can use up all the circulating antibodies, that lack of antibodies causes the immunoreactions
effect on well tissue to be minimized, which maintains organism well being. At some numerical versions, noting each deleterious cyte has more than 8 times as many decorative plugs on it while the well tissue only has between zero and 1/8th the sites and
immunoreaction, After 8-24 hours after the 72 hours before the body makes its own antibodies to the plugs, at that 96 hour chronoregion, all the existing amounts of anti-plug antibodies are utilized and there are near zero circulating antibodies, so
there is an absence of further antibody glomming action on well cytes and tissues even though the immune system has been activated, activated with the same effective intensity as a response to a viral cold.


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