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there is a DNA methylation thing called an epigenetic clock, I think may others must have alreaddy considered editing this clock as a way to increase lifespan. could the corpse of a superenteneratian, 99.999999% of the cytes as which, or more are still
fully functional, extend or refute the methylation clock? Or find the places on it it, the actual tissues, that matter (neurons, vasculature)

its not cancer, its point of specificity tissue disregulation (hints of epigenetic clock going amiss at .000000000001% of tissue causing say atherosclerosis

genetically engineered-in anti-ischemia harm peptides as testable longevity drugs at atherosclerotic mice

mouse dorm n=40k, what causes a bruise to be scavenged successfully away, rather than treated as a body interior multicm dead tissue that could float out and cause strokes effect?

do the genetics of least bruising have any relation to cardiovascular wellness genetics? IS there any relation to longevity effects? Least bruising of human MZ twins correlates with what wellness benefit?

volunteer process, ultrasonic zapper bruises 1 cm tissue at 100k human volunteers with parents ages 70 on up. Correlate parental survival and lifespan with child non bruisability, advantage, basically harmless to the 40-50 year olds at experiment.

Pills that stop bruising may be longevizing, there may be a reduction of “microetherosclerotic” effects benefit as well.
“In one study, patients suffering from pigmented purpura — those deep purple bruises that get progressively worse — that took 50 mg of rutin (oral rutoside) two times per day along with 500 mg of Vitamin C twice a day were completely healed of
their bruising within just four weeks.”, “hesperidin can dramatically reduce bruising and strengthen your capillaries”

60 second reactive stent, 20 seconds better

f=MA microsurgery, 2mm golfball core elastics can do 1.8 mm suturing at 90% mechanical engineering efficiency.


just explore the HOX and other state space to find completely well nonhuman primates with 2-3x the volume, span, and reach, of coronary arteries as regular primates, verify they are almost immune to lethal cardiovascular events from network and path
duplication at the corononary vasculature.

should they just put in two hearts?
right handed heart people
apoe e immunue to ath at germline

Ok, so the source of tissue culture can be exceptionally well tissue, it is even possible that exceptionally well tissue with its epigenetic meythylation clock reset to age 1 could be the basis of transplant tissue.

One way to tell excpetionally well tissue culture tisuue is to use the velvet plate cuplication process; a tissue culutre plate with say 1 billion cyctes at it (vascular epithelium, or better, stem cells) is velvet copied, then the copy frozen (or
quiecently maintained), then at the 1 billion cyctes on the source plate actual particular to the human physiological stressors are introduced. For example, blood plasma concentrate from an elederly person might contain the things senolytics get rid of,
as well as diverse but nonoptimal immunology, like immune sensititizations; other challenges like hypoxia(ischemia) that would terminate 90% of cyctes, and 99th percentile of cholesteric plaque adhesion. So after one of the velvet prints has 99.9999
mortality, the physical locations of the million cells (stem cells, or differentiateds) that surviced all that are known, then tissue culture is accomplished from just those million cells most likely to thrive and survive found via the physical mapping
to the velvet copy base. They would then verify that tissue culture from these 1 in a million best cells actually caused better survival and function at implanted tissue culture constructs, like vascular material, cardiac repair stem cells, and even
neural tissue grafts (treating mental things). If it is possible to grind away an atherosclerotic plaque, then spackle the area with the 1 in a million perkiest spackle cytes, then overlay them with a planar tissue made from the 1 in a million perkiest
planar tissue cytes, then the repairs addressing cardiovascular disease are likely to be better.


As a possible longevity wellness technology it could be possible to find the “weakest stuff” at a person’s personal tissue sample, then cure it, then deliver the cure to the entire person’s living body for greater longevity from strengtheninging
what otherwise would have been the weakest parts. Culture the 99.999th percentile of feeble, (say resistance to ILGF-1, or nonresponsiveness to Nitric oxide, or then cure it, then administer the cure to the actual human where 99.999& of the cells are
doing better

Some people, when they exert themselves, experieince cardiovascular events, even while exercise has preventative effects on CHD, implant notices when the person’s physical exertion (and associated things like blood oxygen levels and blood pressure)
goes into 1 per 10,000 likeliness of causing cardiovascular event then the implant releases instant destresing, blood pressure reducing, respiratory function optimizing drugs, this is then lifesaving per some number of automatic activations; Opiate
peptides might destress, vagus nerve agents, if there are any, might deepen breathing, other peptides could reduce blood pressure.
So this brings up the research question, how many minutes before a heart attack is a heart attack preventable? Do you have to get there 5 minutes early or 30 seconds early? Do sensations radiating along one arm precede a reversible process, or do they
indicate an actual heart attack process? 5 minutes early suggests a wearable, like a smartwatch, that magnetically stirs up and opens chemical reservoirs (drug depots) at an injection site beneath it.

The internet says ”The most dangerous times for heart attack and for all kinds of cardiovascular emergency — including sudden cardiac death, rupture or aneurysm of the aorta, pulmonary embolism and stroke — are the morning and during the last phase
of sleep. A group from Harvard estimated this risk and evaluated that on average, the extra risk of having a myocardial infarction, or heart attack, between 6 a.m. and noon is about 40%. But if you calculate only the first three hours after waking, this
relative risk is threefold.” That suggests that the smart watch that activates drug depots to prevent heart attacks might actually find itself working about 1/2 the time while the person is unconscious in the morning before waking.
One advantage to a magnetic drug depot smartwatch that measures physiologogy and dispenses drugs may be that it addresses the (I pereceive I read) 1/3-1/2 of peopel who have a first heart attack without any medical warning. I do not know what medical
warning means, but I get the feeling that it means people who feel healthy, without angina, without prior cardiovascular surgery (atherosclerosis), Have a first and lethal heart attack. Family history could be a guide to whether these people would do
well to wear a heart attack preventing watch above a certain age even with a normal physician’s physical. Also, if you omit ever needing it, it omits ever getting used.

“wiggle melatonin” could reduce heart attacks. Noting the connection between circadian rhythms and heart attacks (quoted) it could be that a multimodal distribution of melatonin taken before sleep, rather than a single main dose of melatonin could
cause the first 4 hours (highest heart attack risk period) to have some quantitative difference in the likeliness of having a heart attack. Also, there is now a melatonoin-similar-molecule antidepressant drug they could screen to see if it, or, it at
certain dosing schedules, reduces risk of heart attack.
There are also nonpineal human circadian rhythm mechanisms and drugs. I read about irisin, whcih effects circadian rhythms, perhaps there could be a heart attack preventing nonpineal circadian rhythm drug.

Epithalon is a pineal hormone, and it is published that humans (over 70?) on epithalon are twice as likely to live six years longer as those not on epithalon. Epithalon could prevent heart attacks.

17%lifespan increase tropical rainforest sounds during heart attack sleep am, measure reduction; stay alsleep massaging bed during am risk period.

“greater than 50 percent more heart attacks in winter months than in summer months, and it's mostly about stress”, combine that with 40% more AM heart attacks and that suggests that studying the physiology of people during summer afternoons could
represent a mere 10% risk. So, using rodents, or another heart attack model experimental mammal, inject the rodents with one-previous-heart attack human AM winter blood chemicals, and human PM summer blood chemicals (from one previous heart attack
paersons), find out if there are specific circulating factors in human blood/plasma that cause heart attacks in rodents or other lab mammals, interestingly there is the possibility of concentrating the plasma chemicals 10 or 100:1 to get a stronger heart
attack production signal. Immunizing aaginst any of these chemicals, if novel, could reduce heart attacks in humans.

if there are specific circulating factors (AM winter) it is possible liver enzymes naturally get rid of them, upregulating those liver enzymes with a pill then reduces the AM winter chemicals, reducing risk of heart attack.

tissue culture staples and roof shingles, tarps oooh gross, or vasculature advantage(?), the tomographed skin tag or wart, possibly from the persons own tissue culture.

Glaxosmithkline: headache reliever pill. Some people chew pills, having planes of cleavage so that the pill fractures all over the place, but always (usually) at a micrometer thin delicious flavor plane turns a yucky chewed NSAID into a tolerably
flavored or even flavor treat headache relief pill that works much faster. The flavor cleavage planes could also have hygroscopic (pulls water from surroundings) micrometer coating to form the rapidest micrometer slurry. Better to use a flavor enhanced
liquicap though if that is faster at pain relief.

Dwelling air warming, cooling, and transport could be improved as to its effect on indorr air quality. Indoor air quality is likely linked to a reduction in risk of disease possibly heart disease, there is a chance improving indoor air quality reduces
risk of heart attack. Noting first four hours of the day (and winter) are greatest risk for heart attacks it is possible indoor air quality duing that time makes a bigger difference. Is there a benefit to producing summer evening psychrometrics (humidity/
temp) during winter AM? It is a broad slice, up at 6 am, at work at 10:00, but suggests indoor air quality at communting vehicles could matter a lot, At the dwelling, just running the fan through the air filter 2-4x as much between 5:00 am and 8:00 am
could be beneficial,

Indoor air quality and psychrometrics might be particularly testable at nursing homes. Just modifying the settings to a different variety of “normal” (summer evening) at 100K of aggregate residential facility could show a strong data trend rapidly.

There is a chance that summer evenings are actually good for cardiovascularly ill people, rather than it just being ab absence of AM events during winter.Find those beneficial things, then trry them out all year, one possibility is pollen, another is
antidepressant long days of summer; better data would be better, I associate winter with rain, others associate it with snow, I perceive places it snows more, the people who live there live longer; rainy winter season from physical rain might be more
deleterious than ice season. Psychrometric testing opportunitity.

well lit dwellings summer circadian during winter could be tested to see if they reduce cadrdiovascular events

(circadian rhythms of summer) gene therapy or daily responsive but once annual or less often depot melatonin injecttion could reduce cardiovascular disease. One set of numbers is 50% less heart attacks during summer, and also melatonin or a nother
circadian rhythym drug could preclude first 4 hours peri-rising (40%) heart attack risk factor. with a one office visit injection to get the multi-year depot injection/implant

Is hibernation or things like estivation a source of calm and possibly sleep, that might work on completely different neurotransmitters than GABA? If so then this could produce beneficial new harmless sedatives and anti-anxiety drugs. They could take a
rodent that does true hibernation, and connect it via parabiosis to a non hibernatining rodent to see if the non hibernatining rodent calmed down, was sedated or also had the brain scan of lack of anxiety. One possibility is the the hibernatining
squirrel/rat or beaver combination, another possibilility is testing the groundhog
“While hibernation has long been studied in rodents (namely ground squirrels) no primate or tropical mammal was known to hibernate until the discovery of hibernation in the fat-tailed dwarf lemur of Madagascar, which hibernates in tree holes for seven
months of the year.”

circulatory factors of hibernating animals do things to alert animals, “Hibernation induction trigger (HIT) is somewhat of a misnomer. Although research in the 1990s hinted at the ability to induce torpor in animals by injection of blood taken from a
hibernating animal, further research has been unable to reproduce this phenomenon. Despite the inability to induce torpor, there are substances in the blood of hibernators that can lend protection to organs for possible transplant. Researchers were able
to prolong the life of an isolated pig's heart with an HIT.[36] This may have potentially important implications for organ transplant,”

smartwatch magnetically releases hibernation induction trigger https://www.annalsthoracicsurgery.org/article/S0003-4975(97)00631-0/fulltext “HIT” (or maintenance) chemicals if it detects 1 per 1000 likeliness of cardiovascular event that hour,
interestingly it may be possible to combine this benefit with a mild wake-up chmical so the person is able to do something other than pass out in response. bodyside and well as brainside varied chemicalcs could also contribute to heightening surviviving
and normalcy after cardiovascular event; bodyside only “HIT” (Hibernation induction trigger (HIT) obtained from serum of certain winter-hibernating mammals, such as woodchucks, 13-lined ground squirrels, brown cave bats, and black bears, can induce
hibernation in these animals, even when summer active) At humans, with a smartwatch drug depot this could be continuouous low level medication for those projected to be at cardiovascular risk without impairing mental function. HIT studies are from 1997
and could be updated to see if it is possible to make RNA drugs and peptides that do the same things as the HIT chemicals, thought at the time to be opiods (like opiate peptides)

As a technologogy to get rid of heart attacks, HIT chemicals could be made to circulate at the body during the first 4 hours (most lethal), as well as during winter. Perhaps bodyside only would do it, leaving people’s minds fully functional in the AM.
Also, the article mentions opiate receptors as HIT life-preserving drug receptors. I read there are more than 100 neurotransmitters, so perhaps there are other non opioid HIT chemicals that can be found with serum between lab mammals experiments.

Also, they found a primate (nearer human biochemistry, mRNA) the fat-tailed dwarf lemur that hibernates up to 7 months a year, along with opiate HIT, these lemurs may have other serum chemical systems that could benefit humans, particularly at redicing
cardiovascular events or making them less serious.

Along with the article URL, that concentrates on treatmentless ischemic hearts having about about 30% their original capacity on survival, and 15 minute pretreated (bear serum or opiates) hearts having 69-80% original capacity this brings up the
possibility of using HIT hibernation chemicals to measurably reduce the effects of strokes or even routine surgical anesthesia on mental functioning.

Under hibernation, Wikipedia mentions sharks can go three hours of ischemia, so shark serum could also be tested on cardiac and strokelike ischemia to find new drugs that minimize the effects of heart attacks and strokes.

As a possible technological improvement to the 1997 HIT paper, cell penetrating peptides could concentrate all of the traversal of active drugs (Bear serum simililar chemicals, opiate peptides) to specific organs, for example, heightening concentration
at the heart and vasculature, making these drugs more dose efficient and possibly better tolerated.

A one dose approach to a drug that increases the survivability of cardiovascular events (heart attacks) is: tail squiggle gene therapy, photoactive installation just at the heart: Describing that, basically receptors, like opiate receptors have receptive
components (one mental reference is g coupled protein receptor swirl fingers) as well as a base area (before the fingers) some authors call the tail that does not directly glom the the thing of interest. This tail area can however have a custom peptide
or protein made, that gloms to it, that causes the actual receptor part (fingers) to be more or less sensistive. So engineering a peptide that causes heart opiate receptors (or bear hibernation serum chemical receptors) to be unusually easy to activate
and causes them to stay activated could cause continuous “on” status just from normal circulating levels of endogenous (natural) chemicals as they are primed to prefer to be on. One way to get the tails to have the perma-on peptide attached to them,
or, perhaps more optimally, just be developed from stem cells with the “easy on” protein sequence and conformation conformation part of their makeup is is phototherapy gene therapy: Using published methods gene therapy only takes (does its thing)
where tissues are illuminated, and at a person, cofocal lighting lights up the heart for the duration of the gene therapy installation. That causes the opiate receptors (or also bear hibernation heart chemical survival receptors) to be the only things at
the body illuminated/eligible, at that particular treatment, for updating with the new genetic form.

Hibernating Arctic ground squirrels

female polar-bears go into hibernation during the cold winter months in order to give birth to their offspring.

What restarts a cardiovascular event heart? They could put that chamical at the magnetic stirred drug depot smart watch that prevents and responds to cardiovascular events.

circulating null epinephirine with enzymatically cleavable null part then turns to nor epinepherine restarting a heart if the magnetic depot releases a bunch of the enzyme.

radical: EM quarter squeeze a supercapacitor to make a super big current pulse; sequential reaction, 2 supercapcitors, the first em squeezes the second, the second supercapacitor when squeezed has a much accellerated or rather concentratated current
pulse. pro IC technology MEMS like size defibribillator,

I have not hard of a defibrillator that installs custom, “ultra high survival” waveforms, perhaps the MEMs duocapacitor could do this as well.

“presented with the shockable rhythms of ventricular tachycardia or ventricular fibrillation (better outcomes)”

People at cardiovascular risk could have their IoT lightbulbs watch them for cardiovascular events. at Quora one person writes, “The most treatable situation is where the event is witnessed, 911 activated and bystander CPR provided. In those cases, we
get about 80% to the hospital alive and about 55–60% discharged from the hospital in normal or near-normal condition.”

That suggests that volunteers trained in CPR at various kinds of dwelling buildings could be IoT (Internet of Things) called to suddenly go to a strange apartment with freshly (IoT) unlocked doors to rescue someone before the paramedics can get there. I�
�d do it, that is I would get CPR certified, then let my neighbor’s computer call me to their assistance to do interim CPR before the professionals arrived.

The cable box anti-heart attack drug flinger and pro-survival taser, expanded to the in commuter vehicle version: I think it is possible that at halfbakery.com I posted a technology about how the home media center (20th century words: cable box) could
have a camera that watched the people on the couch in front of them, using things like digital themography of the face to see how their health was. It could spot if they were having a heart attack and then the cable box could discharge (fling) eentsy
ninja-shuriken drug injecting at the person’s neck to deliver lifesaving chemicals (drugs), possibly like the ones EMTs (emergency medical technicians) give to people they are reviving, or things like DMSO(drug delivery)-aspirin splashballs, Something
better than tissue plasminogen activator, and, having read more recently, possibly the the chemicals at hibernating animals (hibernating bear blood serum chemicals, opiate peptides) that cause (30% functional ->80 functional) greater function survival in
heart-attack hearts. The in-vehicle (car) version makes sense as well. A very simple modification to that makes it work better, put it at the dashboard of the vehicle. Airbags are already common, and heart attacks in motor vehicles on the driver’s side
(and with oblique shuriken aim, passenger side) could possibly be very near the lifesaving rescue use numbers of collision airbags. The numbers are very approximate, but 2020 800K heart attacks, compared with 30.2K (2010) lethal vehicle acidents, (800k/
24 hours, 33K heart attacks during a period of driving 1 hour each day. Note that the 33k heart attacks is spread across the entire population of drivers. If the motor vehicle had an Anti-Heart Attack Drug Shuriken Flinger (AHADSF) only at those over 49 (
actually math of a graph with crossing lines could find the optimal age to have an anti-heart attack drug shuriken flinger (AHADSF) installed at a vehicle) then the person could just get that as a standard option on their motor vehicle when they were
getting it >49.

Also, there is an opportunity for higher quality of diagnostics than “having a heart attack”, for example, if the radiating one arm sensations that may(?) precede a heart attack can be detected with digital thermography of the hand and neck, then 5-
15 minutes of advance notice is produced to fling the drug shuriken ahead of time. Similarly there are optical (laser) only ways to read blood pressure from the eye, and it is just possible that photonics of the face, or through-skull photonics could
detect angina. Benefitting this technology is autodriving vehicle technology (driverless cars) which could take over for a person who is on the verge of a cardiovascular event but does not know it, or a person having a cardiovascular event.

One thing an in-vehicle heart attack response technology can do is do a good job imitating an EMT (emergency medical technician), with technology at the steering column able to push out a contact surface that can do CPR compressions, and another item
that extends (or shoots, perhaps like a taser) from the steering column that does electrical defibrillation.

https://www.everydayhealth.com/atrial-fibrillation/noninvasive-vagus-nerve-stimulation-shown-to-reduce-atrial-fibrillation-in-post-operative-patients/ "Electrical stimulation of the ear and the vagus nerve that sits on the surface there has a calming
effect, in that we are stimulating the largest nerve of the parasympathetic nervous system [part of the autonomic nervous system] and hence the corresponding antagonists," Martin Andreas, MD, lead author and an associate professor in the department of
cardiac surgery for the Medical University of Vienna, said in a press release. For the study, researchers divided 40 postoperative patients into two groups: one-half received LLTS while the rest were given a placebo. The patients who received LLTS for five days post-surgery had a significantly lower incidence of developing atrial
fibrillation — 4 patients out of 20, compared with 11 out of 20 in the control group.
“The autonomous nervous system controls the heart rate and influences the threshold for cardiac arrhythmias,” Dr. Andreas said. After surgery, the body is under stress, dealing with inflammatory reactions and oxidative stress, and the sympathetic
nervous system — the body’s fight or flight response — gets activated. This increases the likelihood of developing atrial fibrillation, which affects 1 out of 3 patients who undergo open heart surgery and can lead to further complications.
“Patients who had an episode of atrial fibrillation are more likely to develop another episode and are frequently kept on anticoagulant medication, which increases the bleeding risk and may increase long-term complications,” Andreas said.
A previous study, published in September 2017 in JACC: Clinical Electrophysiology, found that vagus nerve stimulation had a positive effect on incidences of atrial fibrillation post-surgery, but researchers used an invasive device that was implanted
inside patients’ bodies. This study shows that a noninvasive option could make a similar positive effect with fewer potential complications.”
As an adjunct that reduces death from CVD vagus earlobe or throat stimulation could be based on a wearable battery pack, with a wireless charging pad on bed. Other published things online have descrbibed how people are at greatest risk of heart attack
during the first 4 hour hours or morning (approximately, that includes about an hour of sleeping), it could be that vagus stimulation could have anti-heart attack beneficial AM effects. Similiarly vagus stimulation could reduce cardiovascular risk during
Winter (50% greater risk) as well. Perhpas the vagus output of normal well people during summer evenings could be prompted to be produced with a vagal stimulator at the unwell and this could contribute to fewer heart attacks.

I perceive I read some people are not sure if they have had a heart attack or not, perhaps a medical diganostic chewing gum with antibodies that change color could tell people if they are having a cardiovascular event that immediate attention would
benefit. The general instructions might go like this: “You have a family hisotry of heart disease and various biomarkers suggesting cardiovascular risk. If you feel funny, chew this gum. If it changes color immediately seek medical assistance even if
you feel fine.” This is a actually very affordable, compared to a (color/antibody) $1 pregnancy test, 1 piece of gum a month (the worried well) for three decades is only $360 for a person to test themselves at will if say their hand feels funny or if
they get dizzy.

Longevity technology, This one is a longshot. I read that at different times of the human menstrual cycle women are much better at smelling odors than other times. I also read that the abilitity to discern odors is predictive of whether a person will be
alive or not. “A 2019 study published in the Annals of Internal Medicine found a link between a poor sense of smell and mortality. Researchers from Michigan State University analyzed data of over 2000 older adults, between the ages of 71 and 82. As
part of the study, participants were asked to identify 12 common scents such as cinnamon, gasoline, and smoke. Researchers then tracked each participants over the course of 13 years. As they found, people who identified less than eight different smells
were 46 percent more likely to die 10 years laetr. So researchers concluded that a poorer sense of smell could predict death.”, so drawing plasma from young women at their monthly height of odor detecting ability, then administering the plasma
fractions as drugs to elderly mice could find out a longevization diference between most effective smelling times of the month plasma administred-as-drug and least effective smelling times of the month plasma-administered-as-drug. Then note the chemical
differences between the two plasmas with their different longevization abilities (if any), to find the specific plasma chamicals that are causing the mice to live longer. Make synthetic versions and administer these human chemicals (proteins, peptides)
to age batched groups of human volunteers to see if the pro-smell plasma chemicals are longevizing to humans to make a new human longevity drug.

another approach to finding a longevity drug from the human smelling acuity test is to find out the people who could smell just 1 or zero of the scents, and see if their 10 year mortality was above the published 46% for those that smell less than 8 of
the samples. If the zero/one smellers are hypermortality-prone then their blood may carry toxic chemicals that when administered to mice cause mortality. The sources (specific plasma proteins) of that chemically transmissable mortality can be found, and
then immunizations to those chemicals produced, and the immunizations tested on mice and humans as longevity drugs.
Another way is to make a longevity drug from supersmeller blood plasma: find the 99.99th percentile of both males and females able to discern different odors, then make blood plasma fractions from a donated 2 pints of blood then inject mice or rats with
the plasma fractions. Noting the 2 pint volume to mouse or rat dose volume ratio One human supersmeller might be able to dose 300 days of rat possible longevization from 1 pint (600 days from 2 pints), or several thousand days of mouse dosing per pint of
human plasma.

BDNF gene is IQ (like g) gene, that suggests that completely new human-created BDNF genes could cause even higher intelligence, perhaps from coding a different amino acid sequence protein. “Brain-derived neurotrophic factor (BDNF), a member of the
nerve-growth-factor family, plays an important role in neuronal survival and development, and it can modulate serotonergic activity. Further, BDNF has been implicated in the expression of personality traits and in cognitive function. We tested the
associations between functional BDNF Val66Met genetic variants, and personality trait and intelligence in a cohort of 114 healthy young Chinese females. Subjects with the Val/Val genotype had a significantly higher mean performance IQ than Val/Met
carriers, especially for the Object Assembly subtest. No significant association was demonstrated for the BDNF polymorphism and any of the Tridimensional Personality Questionnaire personality-factor scores, including harm avoidance. These results suggest
that genetic variants of the BDNF gene may play a role in specific cognitive functions, but not in overall intelligence. In contrast to a recent report, however, this polymorphism does not appear to be associated with the neuroticism-related personality
trait.” https://selfdecode.com/blog/article/boost-plasticity-with-the-bdnf-gene-50/


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