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 [[genetic_engineering]] [[genetic_engineering]]
  
-On the subject of immortality. The field has stalled again, so I have decided to go public. Hang on, I have little choice as I am out of the loop, the Illuminati's offer to reveal the secret to immorality comes with one condition, "we would have to kill you" (Hmm, accent sounded Japanese). This guide is in summary form. With inquiry arise charlatans and frauds, be it Harvard grape juice or another miracle nootropic, no human studies and likely not add a single day to life instead take several away. The answer to the French paradox is not "150,000,000 glasses of wine (sic)", resveratrol is destroyed by sulphuric acid in the stomach and not bioavailable, like most vitamins and supplements are [[science:does_not_pass_through_the_small_intestine|rejected during digestion]] and never pass into the bloodstream with prolonged use not advised due to digestive system damage. A recent human trial of nicotinamide riboside (NR) concluded "no clinical benefit to supplementation" and many supplements do not contain the purported active ingredient, wrinkle creams have always been ineffective, except for Retinol. Plastic surgeons are not real doctors. Every so often a new fad pill comes onto the scene promising age reversal that cannot be ignored like CoQ10, PQQ, Omega 3 or a fruit with a fancy name from an exotic place, but they soon fade away in preference for a newer fad. Many physicians have become no more than pill pushers in return for kickbacks from drug companies and the "eat this", "eat that" crowd have amassed a huge eating list, fasting is in and "good for you, bad for you" is so last year. The environment critically and increasingly poisonous, constant vehicle exhaust, noxious gas, polluted air, water and food with heavy metals, chemicals, toxins, pesticides and more, pills will not be a remedy against bad living conditions. Review history, no prizes for guessing where the autism is coming from. Ageing is bigger than one minor detail, drug, supplement. We all want it to be real, so let's make it real... +On the subject of immortality. The field has stalled again, so I have decided to go public. Hang on, I have little choice as I am out of the loop, the Illuminati's offer to reveal the secret to immorality comes with one condition, "we would have to kill you" (Hmm, accent sounded Japanese). This guide is in summary form. With inquiry arise charlatans and frauds, be it Harvard grape juice or another miracle nootropic, no human studies and likely not add a single day to life instead take several away. The answer to the French paradox is not "150,000,000 glasses of wine (sic)", resveratrol is destroyed by sulphuric acid in the stomach and not bioavailable, like most vitamins and supplements are [[science:does_not_pass_through_the_small_intestine|rejected during digestion]] and never pass into the bloodstream with prolonged use not advised due to digestive system damage. A recent human trial of nicotinamide riboside (NR) concluded "no clinical benefit to supplementation" and many supplements do not contain the purported active ingredient, wrinkle creams have always been ineffective, except for Retinol. Plastic surgeons are not real doctors. Every so often a new fad pill comes onto the scene promising age reversal that cannot be ignored but they soon fade away in preference for a newer fad. Many physicians have become no more than pill pushers in return for kickbacks from drug companies and the "eat this", "eat that" crowd have amassed a huge eating list, fasting is in and "good for you, bad for you" is so last year. The environment critically and increasingly poisonous, constant vehicle exhaust, noxious gas, polluted air, water and food with heavy metals, chemicals, toxins, pesticides and more, pills will not be a remedy against bad living conditions. Review history, no prizes for guessing where the autism is coming from. Ageing is bigger than one minor detail, drug, supplement. We all want it to be real, so let's make it real... 
  
 {{ ::1-s2.0-s0092867413006454-gr1.jpg?direct&200|US vs Europe Pillars Of Ageing}} {{ ::1-s2.0-s0092867413006454-gr1.jpg?direct&200|US vs Europe Pillars Of Ageing}}
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 Rapamycin and Metformin, two touted drugs said to increase human lifespan. Metformin primary action is to inhibit mitochondrial complex 1 while Rapamycin pathway mTOR (mammalian target of rapamycin), mTor is further divided into mTor1 and mTor2. mTor is a growth regulator in relation to available nutrients, when mTor growth regulation is suppressed perhaps during puberty the organism grows to its maximum regardless of available nutrients where nutrients regulate the size of an organism. Metformin (a diabetes drug) is believed to mimic the benefits of exercise in a pill without any exercise, AMPK activation. People who have metabolic dysfunction gain from Metformin, while people who exercise or already have optimal metabolic function not only achieve no gain from taking Metformin but it is counter-productive. Rapamycin (immune-suppressant drug) is believed to trigger autophagy something that occurs after fasting for 16 hours, autophagy improves cellular condition and the cell condition is super important for health. Both drugs have side effects with Rapamycin believed to be a weekly or twice a month drug with daily use being life-shortening and Metformin having no gain in healthy people or people without Type 2 diabetes. Sestrins (Sesns) are groups of proteins made when a person exercises, accumulate in the muscle, by taking Sestrins in pill format to mimic exercise without exercise, but they are large molecules and not bioavailable. Stress-induced Sesn expression results in inhibition of the target of rapamycin complex 1 (TORC1). [[https://dom-pubs.onlinelibrary.wiley.com/doi/abs/10.1111/dom.12354|Can people with type 2 diabetes live longer than those without?]], the study says No. [[https://roguehealthandfitness.com/is-metformin-really-an-anti-aging-drug/|Is Metformin Really an Anti-Aging Drug?]], [[https://phys.org/news/2020-05-anti-ageing-protein-shown-cell-growth.html|Gaf1]], [[https://pubmed.ncbi.nlm.nih.gov/24828042/|Alpha Keto-Glutarate]], Spermidine, Sulphorane. Rapamycin and Metformin, two touted drugs said to increase human lifespan. Metformin primary action is to inhibit mitochondrial complex 1 while Rapamycin pathway mTOR (mammalian target of rapamycin), mTor is further divided into mTor1 and mTor2. mTor is a growth regulator in relation to available nutrients, when mTor growth regulation is suppressed perhaps during puberty the organism grows to its maximum regardless of available nutrients where nutrients regulate the size of an organism. Metformin (a diabetes drug) is believed to mimic the benefits of exercise in a pill without any exercise, AMPK activation. People who have metabolic dysfunction gain from Metformin, while people who exercise or already have optimal metabolic function not only achieve no gain from taking Metformin but it is counter-productive. Rapamycin (immune-suppressant drug) is believed to trigger autophagy something that occurs after fasting for 16 hours, autophagy improves cellular condition and the cell condition is super important for health. Both drugs have side effects with Rapamycin believed to be a weekly or twice a month drug with daily use being life-shortening and Metformin having no gain in healthy people or people without Type 2 diabetes. Sestrins (Sesns) are groups of proteins made when a person exercises, accumulate in the muscle, by taking Sestrins in pill format to mimic exercise without exercise, but they are large molecules and not bioavailable. Stress-induced Sesn expression results in inhibition of the target of rapamycin complex 1 (TORC1). [[https://dom-pubs.onlinelibrary.wiley.com/doi/abs/10.1111/dom.12354|Can people with type 2 diabetes live longer than those without?]], the study says No. [[https://roguehealthandfitness.com/is-metformin-really-an-anti-aging-drug/|Is Metformin Really an Anti-Aging Drug?]], [[https://phys.org/news/2020-05-anti-ageing-protein-shown-cell-growth.html|Gaf1]], [[https://pubmed.ncbi.nlm.nih.gov/24828042/|Alpha Keto-Glutarate]], Spermidine, Sulphorane.
  
-Sirtuins are genes that encode a family of signalling proteins involved in metabolic regulation. There are 7 Sirtiuns. Sirt 1 - metabolism, inflammation, Sirt 2 - cell cycle, tumorigenesis, Sirt 3 - Metabolism , Sirt 4 - Insulin secretion, Sirt 5 - Ammonia detoxification, Sirt 6 - DNA repair, metabolism, TNF secretion, Sirt 7 - rRNA transcription, cobB - metabolism, SirTM - ROS detoxification. The attempt is to activate sirtuins using pills, STACs (small molecule sirtuin activators) are drugs for sirt activation, there are no STACs and no known pills that can trigger for example DNA repair. As of 2018, there was no clinical evidence that sirtuins affect human ageing. It is believed that there are about 238 genes that can do healthy tasks like DNA repair. As part of the business model they have to fit it into a pill format but 238 is way too much and breaks the pill format, forget 238 how about 6? The commercialization of what might be valid science renders the product a scam. [[https://www.inner-light-in.com/2015/05/list-of-longevity-genes/|List of Longevity Genes]] [[https://www.cell.com/cell-metabolism/fulltext/S1550-4131(15)00465-9|4,698 Single-Gene Deletion Strains Uncovers Conserved Mechanisms of Aging]] [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6284760/|Emerging Anti-Ageing Strategies - Scientific Basis and Efficacy]] [[https://www.inverse.com/mind-body/scientists-identify-a-longevity-switch-in-worm-human-cells|A Trick To Activating "Anti-Aging" Proteins In Worms Could Exist In Humans]], [[https://newatlas.com/medical/dont-eat-me-proteins-synapse-destruction-alzheimers/|Proteins prevent synapse destruction in Alzheimer]]+Sirtuins are genes that encode a family of signalling proteins involved in metabolic regulation. There are 7 Sirtiuns. Sirt 1 - metabolism, inflammation, Sirt 2 - cell cycle, tumorigenesis, Sirt 3 - Metabolism , Sirt 4 - Insulin secretion, Sirt 5 - Ammonia detoxification, Sirt 6 - DNA repair, metabolism, TNF secretion, Sirt 7 - rRNA transcription, cobB - metabolism, SirTM - ROS detoxification. The attempt is to activate sirtuins using pills, STACs (small molecule sirtuin activators) are drugs for sirt activation, there are no STACs and no known pills that can trigger for example DNA repair. As of 2018, there was no clinical evidence that sirtuins affect human ageing. It is believed that there are about 238 genes that can do healthy tasks like DNA repair. As part of the business model they have to fit it into a pill format but 238 is way too much and breaks the pill format, forget 238 how about 6? The commercialization of what might be valid science renders the product a scam. [[https://www.inner-light-in.com/2015/05/list-of-longevity-genes/|List of Longevity Genes]] [[https://www.cell.com/cell-metabolism/fulltext/S1550-4131(15)00465-9|4,698 Single-Gene Deletion Strains Uncovers Conserved Mechanisms of Aging]] [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6284760/|Emerging Anti-Ageing Strategies - Scientific Basis and Efficacy]] [[https://www.inverse.com/mind-body/scientists-identify-a-longevity-switch-in-worm-human-cells|A Trick To Activating "Anti-Aging" Proteins In Worms Could Exist In Humans]], [[https://newatlas.com/medical/dont-eat-me-proteins-synapse-destruction-alzheimers/|Proteins prevent synapse destruction in Alzheimer]], CoQ10, PQQ, Omega 3, Magnesium, D-Ribose, Broccoli. olive oil, oleic acid.
  
 Nicotinamide adenine dinucleotide, NAD+ a cofactor central to metabolism. With ageing, cell performance diminishes and production of  proteins decrease while some increase. NAD+ is produced by the liver and said to decrease with age (almost every measure does with age). Low levels of NAD+ are said to decrease sirtiun or parp activity, acetylation and lifespan. People who supplement with NAD+ or a precursor generally feel no benefit, do not appear more youthful and have a placebo effect outlook. It is said that without NAD+ you would die, what does that even mean? Maybe similar to holding your breath too long or hiking in the desert without water. NMN is not bioavailable and Nicotinamide Riboside (NR) does not make it past the digestive system. Remember, Chromadex went live with NR before efficacy was proven, and they only done one small trial with conflict of interest to conclude their product was safe to eat. It is also a complex process, dumping substances into the bloodstream is too simplistic as there are domino effects, cascades, chain reactions. When people supplement the organ that normally produces that supplement loses its ability to do so, such as people who supplement with testosterone, their testicles shrink (hypogonadism) as it no longer produces the hormone, supplementing with NAD+ may cause the same situation, causing low NAD+ levels for more than a year or more after it is stopped secretly creating an addiction cycle, there are also methylation deficiency that arise from supplementation. It was also said that no matter how much dose was infused the body regulated the amount of NAD+ in the body disposing of excess. This leads to a greater question, why, does it decrease with age, is it another cell morphology causation? NAD+ fad supplementation is probably a scam. Pterostilbene sometimes sold as a substitute to Resveratrol which is destroyed by sulphuric acid of the stomach and not bio-available has even less evidence of efficacy. The advice is take Niacin, Vitamin B3 is a cheap yet equal substitute for expensive NR. I suspect that Vitamin B3 or NR is no more life extending or health promoting than any other vitamin. [[https://www.lifespan.io/news/clinicial-trial-of-nicotinamide-riboside-completed/|Clinical Trial of Nicotinamide Riboside Completed]] [[https://brain.forever-healthy.org/display/EN/NAD+Restoration+Therapy|NAD+ Restoration Therapy - Risk-Benefit Analysis]] Nicotinamide adenine dinucleotide, NAD+ a cofactor central to metabolism. With ageing, cell performance diminishes and production of  proteins decrease while some increase. NAD+ is produced by the liver and said to decrease with age (almost every measure does with age). Low levels of NAD+ are said to decrease sirtiun or parp activity, acetylation and lifespan. People who supplement with NAD+ or a precursor generally feel no benefit, do not appear more youthful and have a placebo effect outlook. It is said that without NAD+ you would die, what does that even mean? Maybe similar to holding your breath too long or hiking in the desert without water. NMN is not bioavailable and Nicotinamide Riboside (NR) does not make it past the digestive system. Remember, Chromadex went live with NR before efficacy was proven, and they only done one small trial with conflict of interest to conclude their product was safe to eat. It is also a complex process, dumping substances into the bloodstream is too simplistic as there are domino effects, cascades, chain reactions. When people supplement the organ that normally produces that supplement loses its ability to do so, such as people who supplement with testosterone, their testicles shrink (hypogonadism) as it no longer produces the hormone, supplementing with NAD+ may cause the same situation, causing low NAD+ levels for more than a year or more after it is stopped secretly creating an addiction cycle, there are also methylation deficiency that arise from supplementation. It was also said that no matter how much dose was infused the body regulated the amount of NAD+ in the body disposing of excess. This leads to a greater question, why, does it decrease with age, is it another cell morphology causation? NAD+ fad supplementation is probably a scam. Pterostilbene sometimes sold as a substitute to Resveratrol which is destroyed by sulphuric acid of the stomach and not bio-available has even less evidence of efficacy. The advice is take Niacin, Vitamin B3 is a cheap yet equal substitute for expensive NR. I suspect that Vitamin B3 or NR is no more life extending or health promoting than any other vitamin. [[https://www.lifespan.io/news/clinicial-trial-of-nicotinamide-riboside-completed/|Clinical Trial of Nicotinamide Riboside Completed]] [[https://brain.forever-healthy.org/display/EN/NAD+Restoration+Therapy|NAD+ Restoration Therapy - Risk-Benefit Analysis]]
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 Progeria (one of several progeroid syndromes) is an extremely rare autosomal dominant genetic disorder in which symptoms resembling aspects of ageing are manifested at a very early age. Those born with progeria typically live to their mid-teens to early twenties. Progeria is caused by gene mutations that weaken the structure of the cell nucleus, making normal cell division difficult. {{ ::progeria.png?direct|}}The histone mark H4K20me3 is involved in Hutchinson-Gilford Progeria syndrome caused by de novo mutations that occurs in a gene that encodes lamin A. Lamin A is made but is not processed properly. This poor processing creates an abnormal nuclear morphology and disorganized heterochromatin. In normal conditions, the LMNA gene codes for a structural protein called prelamin A, which undergoes a series of processing steps before attaining its final form, called lamin A. Prelamin A contains a "CAAX" where C is a cysteine, an aliphatic amino acid, and X any amino acid. This motif at the carboxyl-termini of proteins triggers three sequential enzymatic modifications. First, protein farnesyltransferase catalyzes the addition of a farnesyl moiety to the cysteine. Second, an endoprotease that recognizes the farnesylated protein catalyzes cleavage of the peptide bond between the cysteine and -aaX. In the third step, isoprenylcysteine carboxyl methyltransferase catalyzes methylation of the carboxyl-terminal farnesylcysteine. The farnesylated and methylated protein is transported through a nuclear pore to the interior of the nucleus. Once in the nucleus, the protein is cleaved by a protease called zinc metallopeptidase STE24 (ZMPSTE24), which removes the last 15 amino acids, which includes the farnesylated cysteine. After cleavage by the protease, prelamin A is referred to as lamin A. In most mammalian cells, lamin A, along with lamin B1, lamin B2 and lamin C, makes up the nuclear lamina, which provides structural support to the nucleus. In 2003, the cause of progeria was discovered to be a point mutation in position 1824 of the LMNA gene, which replaces a cytosine with thymine. This mutation creates a 5' cryptic splice site within exon 11, resulting in a shorter than normal mRNA transcript. When this shorter mRNA is translated into protein, it produces an abnormal variant of the prelamin A protein, referred to as progerin. Progerin's farnesyl group cannot be removed because the ZMPSTE24 cleavage site is lacking from progerin, so the abnormal protein is permanently attached to the nuclear rim. One result is that the nuclear lamina does not provide the nuclear envelope with enough structural support, causing it to take on an abnormal shape. Since the support that the nuclear lamina normally provides is necessary for the organizing of chromatin during mitosis, weakening of the nuclear lamina limits the ability of the cell to divide. Farnesylated prelamin A variants also leads to defective DNA repair, which may play a role in the development of progeria. Progerin expression also leads to defects in the establishment of fibroblast cell polarity, which is also seen in physiological aging. Progerin may also play a role in normal human aging, since its production is activated in typical senescent cells. Some accelerated aging diseases are Werner syndrome, Cockayne syndrome and xeroderma pigmentosum. The appareance of ageing is a little like progeria, while not cased by Lamin A, conceptually identical. Like progeria a normal human ageing cell also distorts, the rate of cell division also decreases and senescence increases and many more cell biology problems. For example, the pituitary gland begins to lag in performance, becomes deformed, lumpy and shrunken and like nuclear deformation in progeria the cell deformation in ageing causes similar problems. Visually the shape of nucleus in progeria results in a problem, with age the cell also starts to have these kinds of shape defomities at least when compared with a young cell. Inbreeding also expresses defects in the genome that present as pathology, the likelihood of health issues and early death is increased. If they cannot cure progeria, cutis laxa, turn on and turn off puberty at the genetic level, regenerate tooth in old age, then they will not be able to cure ageing. Such is the reality check. Progeria is the key insight. Genetic mutations follow on to defective cell function which kills us. [[removing_wrinkles_inside_our_cells_might_reverse_aging|Removing Wrinkles Inside Our Cells Might Reverse Aging]] [[https://www.karger.com/Article/FullText/357206|Epigenetic Involvement in Hutchinson-Gilford Progeria Syndrome: A Mini-Review]] Progeria (one of several progeroid syndromes) is an extremely rare autosomal dominant genetic disorder in which symptoms resembling aspects of ageing are manifested at a very early age. Those born with progeria typically live to their mid-teens to early twenties. Progeria is caused by gene mutations that weaken the structure of the cell nucleus, making normal cell division difficult. {{ ::progeria.png?direct|}}The histone mark H4K20me3 is involved in Hutchinson-Gilford Progeria syndrome caused by de novo mutations that occurs in a gene that encodes lamin A. Lamin A is made but is not processed properly. This poor processing creates an abnormal nuclear morphology and disorganized heterochromatin. In normal conditions, the LMNA gene codes for a structural protein called prelamin A, which undergoes a series of processing steps before attaining its final form, called lamin A. Prelamin A contains a "CAAX" where C is a cysteine, an aliphatic amino acid, and X any amino acid. This motif at the carboxyl-termini of proteins triggers three sequential enzymatic modifications. First, protein farnesyltransferase catalyzes the addition of a farnesyl moiety to the cysteine. Second, an endoprotease that recognizes the farnesylated protein catalyzes cleavage of the peptide bond between the cysteine and -aaX. In the third step, isoprenylcysteine carboxyl methyltransferase catalyzes methylation of the carboxyl-terminal farnesylcysteine. The farnesylated and methylated protein is transported through a nuclear pore to the interior of the nucleus. Once in the nucleus, the protein is cleaved by a protease called zinc metallopeptidase STE24 (ZMPSTE24), which removes the last 15 amino acids, which includes the farnesylated cysteine. After cleavage by the protease, prelamin A is referred to as lamin A. In most mammalian cells, lamin A, along with lamin B1, lamin B2 and lamin C, makes up the nuclear lamina, which provides structural support to the nucleus. In 2003, the cause of progeria was discovered to be a point mutation in position 1824 of the LMNA gene, which replaces a cytosine with thymine. This mutation creates a 5' cryptic splice site within exon 11, resulting in a shorter than normal mRNA transcript. When this shorter mRNA is translated into protein, it produces an abnormal variant of the prelamin A protein, referred to as progerin. Progerin's farnesyl group cannot be removed because the ZMPSTE24 cleavage site is lacking from progerin, so the abnormal protein is permanently attached to the nuclear rim. One result is that the nuclear lamina does not provide the nuclear envelope with enough structural support, causing it to take on an abnormal shape. Since the support that the nuclear lamina normally provides is necessary for the organizing of chromatin during mitosis, weakening of the nuclear lamina limits the ability of the cell to divide. Farnesylated prelamin A variants also leads to defective DNA repair, which may play a role in the development of progeria. Progerin expression also leads to defects in the establishment of fibroblast cell polarity, which is also seen in physiological aging. Progerin may also play a role in normal human aging, since its production is activated in typical senescent cells. Some accelerated aging diseases are Werner syndrome, Cockayne syndrome and xeroderma pigmentosum. The appareance of ageing is a little like progeria, while not cased by Lamin A, conceptually identical. Like progeria a normal human ageing cell also distorts, the rate of cell division also decreases and senescence increases and many more cell biology problems. For example, the pituitary gland begins to lag in performance, becomes deformed, lumpy and shrunken and like nuclear deformation in progeria the cell deformation in ageing causes similar problems. Visually the shape of nucleus in progeria results in a problem, with age the cell also starts to have these kinds of shape defomities at least when compared with a young cell. Inbreeding also expresses defects in the genome that present as pathology, the likelihood of health issues and early death is increased. If they cannot cure progeria, cutis laxa, turn on and turn off puberty at the genetic level, regenerate tooth in old age, then they will not be able to cure ageing. Such is the reality check. Progeria is the key insight. Genetic mutations follow on to defective cell function which kills us. [[removing_wrinkles_inside_our_cells_might_reverse_aging|Removing Wrinkles Inside Our Cells Might Reverse Aging]] [[https://www.karger.com/Article/FullText/357206|Epigenetic Involvement in Hutchinson-Gilford Progeria Syndrome: A Mini-Review]]
 +
 +On the subject of morphology, a recent paper suggests in yeast that the causes of ageing are two paths to ageing. One is mitochondria dysfunction, the other is morphology of the nucleolus. [[https://biodynamics.ucsd.edu/pubs/articles/Li20.pdf|A programmable fate decision landscape underlies single-cell aging in yeast]], [[https://ucsdnews.ucsd.edu/pressrelease/researchers-discover-two-paths-of-aging-and-new-insights-on-promoting-healthspan|Researchers Discover Two Paths of Aging and New Insights on Promoting Healthspan]]
  
 [[genetic_engineering|Gene therapy]], is the most important technology. 3-plus billion nucleic acid base pairs of human DNA, coded on 46 chromosomes, are the hereditary map that encodes production and control of 20,000 to over 100,000 necessary proteins. Many genetic mutations in these base pairs contribute to the development of disease have been identified. With progeria genetic mutations cause defective cells which ends life likewise with age mutations lead to many errors causing ageing, so we require gene therapy to repair these mutations. In a study, monozygotic twins are formed when one zygote, one egg and one sperm, splits into two and have similar lengths of life when compared to dizygotic twins, two ovums, two sperms[[https://pubmed.ncbi.nlm.nih.gov/7871944/|1]], inclining that identical genetics equals identical lifespan. The difference with each child of the same parents is the chromosomes are shuffled leading to wider range of differences. All children born from the same parents are believed to have the same mitochondria, does the monozygotic twins study disprove the mitochondria theory? [[https://academic.oup.com/biomedgerontology/article/60/7/862/539576|Centenarians]], persons that live more than 100 years run in family, genetic assertion. The body has a genetic repair system but genetic mutations cause many diseases and also increase with age. For our purposes we require systemic error checking; check for mutation, if found then repair, otherwise do nothing. Crispr-Cas9 works just this way, possibly [[https://pubs.rsc.org/en/content/articlelanding/2020/bm/d0bm00427h|Crispr-Cas9 in an engineered exosome]] or nano particle to avoid disadvantages with viral vectors and pass the blood brain barrier. [[https://www.nature.com/articles/s41467-020-17029-3|Systemic nanoparticle delivery of CRISPR-Cas9 ribonucleoproteins for effective tissue specific genome editing]], Crispr-Cas9 is noted for its off target edits which defeats using Crispr to repair mutations but the latest news is that [[https://newatlas.com/medical/crispr-enzyme-mutation-more-precise/|Crispr-Cas9 has been improved 100 fold against off site edits]]. The many variants such as [[https://www.herabiolabs.com/cas-clover/|Cas-CLOVER]] advertise undetectable off-target activity and even a variant of Crispr for mitochondria edits or repair. ZNF, Talen, Cas9.  Articles:  [[https://interestingengineering.com/new-crispr-free-gene-editing-tool-a-massive-step-scientists-say|New CRISPR-Free Gene-Editing Tool a Massive Step, Scientists Say]] [[https://ganino.com/neuroscientists_discover_anti_aging_molecule_repairs_age_related_dna_damage|Neuroscientists discover anti-aging molecule that repairs age-related DNA damage]] [[https://www.nature.com/articles/srep15145|Synchronized age-related gene expression changes across multiple tissues in human and the link to complex diseases]] [[https://newatlas.com/medical/single-gene-treatment-parkinsons-three-months/|Single-gene treatment cures mice of Parkinson's within three months]] [[https://www.nature.com/articles/s41598-020-66966-y|Distal lung epithelial progenitor cell function declines with age]] [[https://frontlinegenomics.com/studies-find-crispr-gene-editing-of-human-embryos-give-rise-to-unwanted-results/|Studies find CRISPR gene-editing of human embryos give rise to unwanted results]] [[https://www.drugtargetreview.com/news/53807/exosomes-used-by-researchers-as-form-of-novel-gene-therapy/|Exosomes used by researchers as form of novel gene therapy]]  [[https://phys.org/news/2020-07-paths-aging-insights-healthspan.html|Researchers discover 2 paths of aging and new insights on promoting healthspan]] [[https://www.nature.com/articles/s41598-019-40222-4|Magnetically guided non-invasive CRISPR-Cas9/gRNA delivery across blood-brain barrier to eradicate latent HIV-1 infection]] [[https://www.exosome-rna.com/cancer-derived-exosomes-as-a-delivery-platform-of-crisprcas9/|Cancer-derived exosomes as a delivery platform of CRISPR/Cas9]] [[https://www.sciencedirect.com/science/article/abs/pii/S0168365917308465|Cancer-derived exosomes as a delivery platform of CRISPR/Cas9 confer cancer cell tropism-dependent targeting]] [[https://www.wired.com/story/this-company-wants-to-rewrite-the-future-of-genetic-disease/|This Company Wants to Rewrite the Future of Genetic Disease]] [[https://www.nature.com/articles/d41586-019-03164-5|Super-precise new CRISPR tool could tackle a plethora of genetic diseases]] [[https://www.nature.com/articles/d41586-020-00340-w|Super-precise CRISPR tool enhanced by enzyme engineering]] [[https://www.frontiersin.org/articles/10.3389/fnmol.2019.00110/full|Editing the Central Nervous System Through CRISPR/Cas9 Systems]] [[https://www.nature.com/articles/d41586-020-02054-5|Scientists make precise gene edits to mitochondrial DNA for first time]] [[genetic_engineering|Gene therapy]], is the most important technology. 3-plus billion nucleic acid base pairs of human DNA, coded on 46 chromosomes, are the hereditary map that encodes production and control of 20,000 to over 100,000 necessary proteins. Many genetic mutations in these base pairs contribute to the development of disease have been identified. With progeria genetic mutations cause defective cells which ends life likewise with age mutations lead to many errors causing ageing, so we require gene therapy to repair these mutations. In a study, monozygotic twins are formed when one zygote, one egg and one sperm, splits into two and have similar lengths of life when compared to dizygotic twins, two ovums, two sperms[[https://pubmed.ncbi.nlm.nih.gov/7871944/|1]], inclining that identical genetics equals identical lifespan. The difference with each child of the same parents is the chromosomes are shuffled leading to wider range of differences. All children born from the same parents are believed to have the same mitochondria, does the monozygotic twins study disprove the mitochondria theory? [[https://academic.oup.com/biomedgerontology/article/60/7/862/539576|Centenarians]], persons that live more than 100 years run in family, genetic assertion. The body has a genetic repair system but genetic mutations cause many diseases and also increase with age. For our purposes we require systemic error checking; check for mutation, if found then repair, otherwise do nothing. Crispr-Cas9 works just this way, possibly [[https://pubs.rsc.org/en/content/articlelanding/2020/bm/d0bm00427h|Crispr-Cas9 in an engineered exosome]] or nano particle to avoid disadvantages with viral vectors and pass the blood brain barrier. [[https://www.nature.com/articles/s41467-020-17029-3|Systemic nanoparticle delivery of CRISPR-Cas9 ribonucleoproteins for effective tissue specific genome editing]], Crispr-Cas9 is noted for its off target edits which defeats using Crispr to repair mutations but the latest news is that [[https://newatlas.com/medical/crispr-enzyme-mutation-more-precise/|Crispr-Cas9 has been improved 100 fold against off site edits]]. The many variants such as [[https://www.herabiolabs.com/cas-clover/|Cas-CLOVER]] advertise undetectable off-target activity and even a variant of Crispr for mitochondria edits or repair. ZNF, Talen, Cas9.  Articles:  [[https://interestingengineering.com/new-crispr-free-gene-editing-tool-a-massive-step-scientists-say|New CRISPR-Free Gene-Editing Tool a Massive Step, Scientists Say]] [[https://ganino.com/neuroscientists_discover_anti_aging_molecule_repairs_age_related_dna_damage|Neuroscientists discover anti-aging molecule that repairs age-related DNA damage]] [[https://www.nature.com/articles/srep15145|Synchronized age-related gene expression changes across multiple tissues in human and the link to complex diseases]] [[https://newatlas.com/medical/single-gene-treatment-parkinsons-three-months/|Single-gene treatment cures mice of Parkinson's within three months]] [[https://www.nature.com/articles/s41598-020-66966-y|Distal lung epithelial progenitor cell function declines with age]] [[https://frontlinegenomics.com/studies-find-crispr-gene-editing-of-human-embryos-give-rise-to-unwanted-results/|Studies find CRISPR gene-editing of human embryos give rise to unwanted results]] [[https://www.drugtargetreview.com/news/53807/exosomes-used-by-researchers-as-form-of-novel-gene-therapy/|Exosomes used by researchers as form of novel gene therapy]]  [[https://phys.org/news/2020-07-paths-aging-insights-healthspan.html|Researchers discover 2 paths of aging and new insights on promoting healthspan]] [[https://www.nature.com/articles/s41598-019-40222-4|Magnetically guided non-invasive CRISPR-Cas9/gRNA delivery across blood-brain barrier to eradicate latent HIV-1 infection]] [[https://www.exosome-rna.com/cancer-derived-exosomes-as-a-delivery-platform-of-crisprcas9/|Cancer-derived exosomes as a delivery platform of CRISPR/Cas9]] [[https://www.sciencedirect.com/science/article/abs/pii/S0168365917308465|Cancer-derived exosomes as a delivery platform of CRISPR/Cas9 confer cancer cell tropism-dependent targeting]] [[https://www.wired.com/story/this-company-wants-to-rewrite-the-future-of-genetic-disease/|This Company Wants to Rewrite the Future of Genetic Disease]] [[https://www.nature.com/articles/d41586-019-03164-5|Super-precise new CRISPR tool could tackle a plethora of genetic diseases]] [[https://www.nature.com/articles/d41586-020-00340-w|Super-precise CRISPR tool enhanced by enzyme engineering]] [[https://www.frontiersin.org/articles/10.3389/fnmol.2019.00110/full|Editing the Central Nervous System Through CRISPR/Cas9 Systems]] [[https://www.nature.com/articles/d41586-020-02054-5|Scientists make precise gene edits to mitochondrial DNA for first time]]
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-Mesenchymal stem cells do repair work, and they hone in using inflammation, without secretion of inflammatory factors they do not know where to go. You cannot eat turmeric or grape juice to ameliorate inflammation. Inflammation is the initial response to tissue damage or cell damage, when a person cuts themselves or bumps their head the area becomes inflamed or swells. After that the human body activates its regenerative system to begin the repair process. Inflammation increases with ageing and this may be due to the difference in cell morphology relative to a young person and the body views an aged cell as damaged and thus the inflammatory response, the remedy is then the innate regenerative response, which is severely limited with age so a foreign source of the components of the regenerative system is infused. There are various places that stem cells can be harvested, bone marrow or fat tissue but the stem cells there are at the same age as the patient, the richest source of these regenerative factors is in umbilical cord, Wharton's jelly, amniotic tissue, placenta. The stem cells in focus are mesenchymal stem cells and exosomes. They take these cells, expand them in culture and infuse or inject them into an older person, where they hone in on inflammation and conduct systemic repair work (apoptosis, cleaning, signal adjacent cells into mitosis and more). Non bone marrow or fat tissue cells do not have matching DNA with the recipient, but they are said to have immunomodulation abilities for a period, they communicate with the immune system to get a pass for a time but eventually the immune system eats them. There is still no way to have young stem cells become part of the foreign body due to immune system rejection which could be an unrealized potential as stem cell depletion is a major indicator of ageing. These sources of stem cells are ethical if they are expanded using non-animal serums otherwise they use foetal bovine serum which is unethical and the field has a very evil temptation of using aborted babies as a source of ideal stem cells, in some places abortion laws have been quietly altered to facilitate the harvesting of aborted babies. Foetal stem cells are the remains of aborted babies and there are some ugly people that want to absorb them. {{::stem-cell-aging-.jpg?direct&500 |Show how available replacement cells diminish with age, causing reduced healing}} Which should I have, exosomes or mesenchymal stem cells or both? Exosomes are extracted from mesenchymal stem cells, as it is believed that exosomes from healthy cells carry much of the regenerative proteins of mesenchymal stem cells and also exosomes fit the definition of nan particles. Nano particles are very small and can penetrate the blood brain barrier in hopes it regenerates the brain. It is believed that much or all of the positive outcomes believed to have been attributed to mesenchymal stem cells for the treatment of neurodegenerative disorders are due to the exosomes derived from mesenchymal stem cells. Many scientists now believe that you are skipping right to the regeneration process by using exosomes as opposed to mesenchymal stem cells. MSC fan boys say, you need the full signalling capacity of which only the MSCs can provide and not just the exosome. Exosomes have messenger RNA, micro RNA and proteins and are made by cells and transfer these contents to other cells. Cells produce exosomes, so there might be a way to make a [[https://www.ganino.com/files/Thepotentialofexosomesfromcowmilkfororaldelivery.pdf|transgenic cow that produces human exosomes in the milk]], [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6499203/|already shown to be possible using mice]] [[https://www.nature.com/articles/d41586-020-01767-x|Do the microRNAs we eat affect gene expression?]], as they are nan particles they are bio-available and the milk orally consumed. Not all exosomes are identical, the constituting RNA and proteins are information and can communicate differently so the age of the cell is important here, as young exosomes are communicating different information than old exosomes, so exosomes produced by a theoretical transgenic cow would have to code for the right types or mix of one or more optimal exosomes. There are several places where you can receive an injection of mesenchymal stem cells or exosomes, some claim great success others not. I do not believe that bone marrow or adipose stem cells are effective in comparison to umbilical cord derived stem cells. The therapy is required either every year or every three years and constitutes one IV session lasting one hour, with beneficial effects progressing over several months. Some say they have had better results with senolytic treatment prior and some say slim down and get fit before getting them. Expertise is crucial, the most established practitioners are possibly the Riordan clinic in Panama (MSCs), and PRmedica exosome clinic in Mexico. A session might cost $10,000 (USD), unless they have opted for non-animal serum stem cell therapies rely on foetal serum to grow stem cells. [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6115766/|Extracellular Vesicles, Ageing, and Therapeutic Interventions]], [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6476062/|Stem Cell-Derived Exosomes Prevent Aging-Induced Cardiac Dysfunction through a Novel Exosome/lncRNA MALAT1/NF-κB/TNF-α Signaling Pathway]], [[https://born2invest.com/articles/biotech-companies-leading-the-way-with-exosome-human-clinical-trials/|Biotech companies leading the way with exosome human clinical trials]], [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6721852/|Mesenchymal Stem Cells for Regenerative Medicine]] [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059014/|Therapeutic repair for spinal cord injury: combinatory approaches to address a multifaceted problem]]+Mesenchymal stem cells do repair work, and they hone in using inflammation, without secretion of inflammatory factors they do not know where to go. You cannot eat turmeric or grape juice to ameliorate inflammation. Inflammation is the initial response to tissue damage or cell damage, when a person cuts themselves or bumps their head the area becomes inflamed or swells. After that the human body activates its regenerative system to begin the repair process. Inflammation increases with ageing and this may be due to the difference in cell morphology relative to a young person and the body views an aged cell as damaged and thus the inflammatory response, the remedy is then the innate regenerative response, which is severely limited with age so a foreign source of the components of the regenerative system is infused. There are various places that stem cells can be harvested, bone marrow or fat tissue but the stem cells there are at the same age as the patient, the richest source of these regenerative factors is in umbilical cord, Wharton's jelly, amniotic tissue, placenta. The stem cells in focus are mesenchymal stem cells and exosomes. They take these cells, expand them in culture and infuse or inject them into an older person, where they hone in on inflammation and conduct systemic repair work (apoptosis, cleaning, signal adjacent cells into mitosis and more). Non bone marrow or fat tissue cells do not have matching DNA with the recipient, but they are said to have immunomodulation abilities for a period, they communicate with the immune system to get a pass for a time but eventually the immune system eats them. There is still no way to have young stem cells become part of the foreign body due to immune system rejection which could be an unrealized potential as stem cell depletion is a major indicator of ageing. These sources of stem cells are ethical if they are expanded using non-animal serums otherwise they use foetal bovine serum which is unethical and the field has a very evil temptation of using aborted babies as a source of ideal stem cells, in some places abortion laws have been quietly altered to facilitate the harvesting of aborted babies. Foetal stem cells are the remains of aborted babies and there are some ugly people that want to absorb them, they may be turning the remain into a lysate and infusing the remain into themselves, the elites and royals are also living longer than they used to lifespan usually runs in families. {{::stem-cell-aging-.jpg?direct&500 |Show how available replacement cells diminish with age, causing reduced healing}} Which should I have, exosomes or mesenchymal stem cells or both? Exosomes are extracted from mesenchymal stem cells, as it is believed that exosomes from healthy cells carry much of the regenerative proteins of mesenchymal stem cells and also exosomes fit the definition of nan particles. Nano particles are very small and can penetrate the blood brain barrier in hopes it regenerates the brain. It is believed that much or all of the positive outcomes believed to have been attributed to mesenchymal stem cells for the treatment of neurodegenerative disorders are due to the exosomes derived from mesenchymal stem cells. Many scientists now believe that you are skipping right to the regeneration process by using exosomes as opposed to mesenchymal stem cells. MSC fan boys say, you need the full signalling capacity of which only the MSCs can provide and not just the exosome. Exosomes have messenger RNA, micro RNA and proteins and are made by cells and transfer these contents to other cells. Cells produce exosomes, so there might be a way to make a [[https://www.ganino.com/files/Thepotentialofexosomesfromcowmilkfororaldelivery.pdf|transgenic cow that produces human exosomes in the milk]], [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6499203/|already shown to be possible using mice]] [[https://www.nature.com/articles/d41586-020-01767-x|Do the microRNAs we eat affect gene expression?]], as they are nan particles they are bio-available and the milk orally consumed. Not all exosomes are identical, the constituting RNA and proteins are information and can communicate differently so the age of the cell is important here, as young exosomes are communicating different information than old exosomes, so exosomes produced by a theoretical transgenic cow would have to code for the right types or mix of one or more optimal exosomes. There are several places where you can receive an injection of mesenchymal stem cells or exosomes, some claim great success others not. I do not believe that bone marrow or adipose stem cells are effective in comparison to umbilical cord derived stem cells. The therapy is required either every year or every three years and constitutes one IV session lasting one hour, with beneficial effects progressing over several months. Some say they have had better results with senolytic treatment prior and some say slim down and get fit before getting them. Expertise is crucial, the most established practitioners are possibly the Riordan clinic in Panama (MSCs), and PRmedica exosome clinic in Mexico. A session might cost $10,000 (USD), unless they have opted for non-animal serum stem cell therapies rely on foetal serum to grow stem cells. [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6115766/|Extracellular Vesicles, Ageing, and Therapeutic Interventions]], [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6476062/|Stem Cell-Derived Exosomes Prevent Aging-Induced Cardiac Dysfunction through a Novel Exosome/lncRNA MALAT1/NF-κB/TNF-α Signaling Pathway]], [[https://born2invest.com/articles/biotech-companies-leading-the-way-with-exosome-human-clinical-trials/|Biotech companies leading the way with exosome human clinical trials]], [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6721852/|Mesenchymal Stem Cells for Regenerative Medicine]] [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059014/|Therapeutic repair for spinal cord injury: combinatory approaches to address a multifaceted problem]]
  
 Yamanaka Factors by Shinya Yamanaka, transcription factors are proteins that bind to DNA-regulatory sequences (enhancers and silencers), to modulate the rate of gene transcription. This may result in increased or decreased gene transcription, protein synthesis, and subsequent altered cellular function. Yamanaka factors are a group of transcription factors, 4 proteins injected into the cell or bathed in medium that can turn a differentiated cell back into an embryonic stage cell just like Turritopsis dohrnii, the immortal jerry fish and also re-differentiate cells from for example a skin cell back to embryo and then into a liver cell if given the right chemical signals. These are adult stem cells called IPSC (induced pluripotent stem cells). In 2006 Dr. Shinya Yamanaka, a stem-cell researcher at Kyoto University, amazed biologists by showing that a cell's fate could be reversed with a set of four transcription factors — agents that activate genes — that he had identified. A cell dosed with the Yamanaka factors erases the marks on the epigenome, so the cell loses its identity and reverts to the embryonic state. Erroneous marks gathered during aging are also lost in the process, restoring the cell to its state of youth. Dr. Yamanaka shared the 2012 Nobel Prize in medicine for the work. In age reversal we do not want to turn the cells back into embryonic stage. Before this everyone thought the cells cycle was fixed in one direction only. Yamanaka factors are (Oct3/4, Sox2, Klf4, c-Myc) are highly expressed in embryonic stem (ES) cells, and their over-expression can induce pluripotency in both mouse and human somatic cells, indicating that these factors regulate the developmental signalling network necessary for embryonic stem cell pluripotency. In 2016, Juan Carlos Izpisua Belmonte, of the Salk Institute for Biological Studies in San Diego, found that the two effects of the Yamanaka factors — erasing cell identity and reversing ageing — could be separated, with a lower dose securing just age reversal. He achieved this by genetically engineering mice,  but if a mouse gets too much the cell becomes an embryo and starts dividing leading to cancers, tumours. Izpisúa Belmonte believed there might be a way to give mice a less lethal dose of reprogramming. He was inspired by salamanders, which can regrow an arm or tail. Researchers have yet to determine exactly how amphibians do this, but one theory is that it happens through a process of epigenetic resetting similar to what the Yamanaka factors achieve, though more limited in scope. With salamanders, their cells "just go back a little bit" in time, Izpisúa Belmonte says. In 2016, Belmonte's team devised a way to partially rewind the cells in mice with progeria. They genetically modified the mice to produce the Yamanaka factors in their bodies with condition the mice would produce those factors only when given an antibiotic, doxycycline. Some mice were allowed to drink water containing doxycycline continuously while others got it just for two days out of every seven. "When you give them … doxycycline, expression of the genes starts," explains Reddy. "The moment you remove it, the expression of the genes stops. You can easily turn it on or off." The mice that drank the most quickly died. But the mice that drank a limited dose did not develop tumours. Instead, they became more physically robust, their kidneys and spleens worked better, and their hearts pumped harder. In all, the treated mice lived 30% longer than their littermates. A Stanford team confirmed Salk Institute, extracted aged cartilage cells from patients with osteoarthritis and found that after a low dosage of Yamanaka factors the cells no longer secreted the inflammatory factors that provoke the disease and also found that human muscle stem cells, which are impaired in a muscle-wasting disease, could be restored to youth. Members of the Stanford team have formed a company, Turn Biotechnologies, to develop therapies for osteoarthritis and other diseases. Another company is AgeX and GenuCure developing various treatments, heart tissues, osteoarthritis, aging-related muscle loss, rejuvenating cartilage. [[old_human_cells_rejuvenated_stem_cell_technology|1]] Other scientists are experimenting with the factors, by leaving some out or another derivative cell quality improves and cancer is less probable while others are including more factors than the four, OSKM. The major problem is separating ageing from ipsc, they are struggling to get significant age reversal before going too far, high dose and reverting the cell to ipsc. They are using RNA's which degrade quickly, have no permanent effect and have the possibility to be systemic perhaps in a vesicle. It matters less as to effectiveness at this stage rather, any proposed therapy even modest be safe. The situation might require a reprogramming blocker, after an RNA partially reprograms, another RNA makes the cell immune to further re-programming allowing systemic uniform partial reprogramming. The RNA will eventually dissolve and the cell becomes partially reprogrammable again. [[https://ganino.com/yamanaki_prolonged_life_mice_by_50|Yamanaki prolonged life mice by 50]] Yamanaka Factors by Shinya Yamanaka, transcription factors are proteins that bind to DNA-regulatory sequences (enhancers and silencers), to modulate the rate of gene transcription. This may result in increased or decreased gene transcription, protein synthesis, and subsequent altered cellular function. Yamanaka factors are a group of transcription factors, 4 proteins injected into the cell or bathed in medium that can turn a differentiated cell back into an embryonic stage cell just like Turritopsis dohrnii, the immortal jerry fish and also re-differentiate cells from for example a skin cell back to embryo and then into a liver cell if given the right chemical signals. These are adult stem cells called IPSC (induced pluripotent stem cells). In 2006 Dr. Shinya Yamanaka, a stem-cell researcher at Kyoto University, amazed biologists by showing that a cell's fate could be reversed with a set of four transcription factors — agents that activate genes — that he had identified. A cell dosed with the Yamanaka factors erases the marks on the epigenome, so the cell loses its identity and reverts to the embryonic state. Erroneous marks gathered during aging are also lost in the process, restoring the cell to its state of youth. Dr. Yamanaka shared the 2012 Nobel Prize in medicine for the work. In age reversal we do not want to turn the cells back into embryonic stage. Before this everyone thought the cells cycle was fixed in one direction only. Yamanaka factors are (Oct3/4, Sox2, Klf4, c-Myc) are highly expressed in embryonic stem (ES) cells, and their over-expression can induce pluripotency in both mouse and human somatic cells, indicating that these factors regulate the developmental signalling network necessary for embryonic stem cell pluripotency. In 2016, Juan Carlos Izpisua Belmonte, of the Salk Institute for Biological Studies in San Diego, found that the two effects of the Yamanaka factors — erasing cell identity and reversing ageing — could be separated, with a lower dose securing just age reversal. He achieved this by genetically engineering mice,  but if a mouse gets too much the cell becomes an embryo and starts dividing leading to cancers, tumours. Izpisúa Belmonte believed there might be a way to give mice a less lethal dose of reprogramming. He was inspired by salamanders, which can regrow an arm or tail. Researchers have yet to determine exactly how amphibians do this, but one theory is that it happens through a process of epigenetic resetting similar to what the Yamanaka factors achieve, though more limited in scope. With salamanders, their cells "just go back a little bit" in time, Izpisúa Belmonte says. In 2016, Belmonte's team devised a way to partially rewind the cells in mice with progeria. They genetically modified the mice to produce the Yamanaka factors in their bodies with condition the mice would produce those factors only when given an antibiotic, doxycycline. Some mice were allowed to drink water containing doxycycline continuously while others got it just for two days out of every seven. "When you give them … doxycycline, expression of the genes starts," explains Reddy. "The moment you remove it, the expression of the genes stops. You can easily turn it on or off." The mice that drank the most quickly died. But the mice that drank a limited dose did not develop tumours. Instead, they became more physically robust, their kidneys and spleens worked better, and their hearts pumped harder. In all, the treated mice lived 30% longer than their littermates. A Stanford team confirmed Salk Institute, extracted aged cartilage cells from patients with osteoarthritis and found that after a low dosage of Yamanaka factors the cells no longer secreted the inflammatory factors that provoke the disease and also found that human muscle stem cells, which are impaired in a muscle-wasting disease, could be restored to youth. Members of the Stanford team have formed a company, Turn Biotechnologies, to develop therapies for osteoarthritis and other diseases. Another company is AgeX and GenuCure developing various treatments, heart tissues, osteoarthritis, aging-related muscle loss, rejuvenating cartilage. [[old_human_cells_rejuvenated_stem_cell_technology|1]] Other scientists are experimenting with the factors, by leaving some out or another derivative cell quality improves and cancer is less probable while others are including more factors than the four, OSKM. The major problem is separating ageing from ipsc, they are struggling to get significant age reversal before going too far, high dose and reverting the cell to ipsc. They are using RNA's which degrade quickly, have no permanent effect and have the possibility to be systemic perhaps in a vesicle. It matters less as to effectiveness at this stage rather, any proposed therapy even modest be safe. The situation might require a reprogramming blocker, after an RNA partially reprograms, another RNA makes the cell immune to further re-programming allowing systemic uniform partial reprogramming. The RNA will eventually dissolve and the cell becomes partially reprogrammable again. [[https://ganino.com/yamanaki_prolonged_life_mice_by_50|Yamanaki prolonged life mice by 50]]
regenetive_medicine_anti_aging_immortality.1595594364.txt.gz · Last modified: 2020/07/24 12:39 by admin