regotek

another two tricotyledons germinated! so there is now three tricotyledons per ~3000 seedlings from my impressive(6n?) Rubus Caesius

finally some good tri-cotyledon Rubus seedling! im starting to suspect that one of my puppy rubus caesius may have a higher ploidy than 4n and this seedling is from this one

@BiluHuang there is no need of aging controling clocks all the job is done by entropy you can only fight with entropy and discover better genes to fight entropy... a lot of computation and.. time.. is needed to develop slow aging genes speed(clock) of aging is just a sum of all genes

My research shows that aging is essentially a genetic program driven by telomere and/or rDNA shortening through the p53 pathway, rather than the accumulation of damage. Individual aging results from replicative senescence of adult stem cells; and that cellular senescence is co-regulated by telomeres and rDNA through the p53 pathway. Moreover, the 11 other classic hallmarks of aging are downstream events regulated by p53 upregulation after telomere and rDNA shortening. From the perspective of first principles, the lifespan of a species is determined by the shortening rate of telomeres and rDNA arrays, which are influenced by both genetic and environmental factors.

@Nene_Smalfoot @dewskiss but... speak for yourself "invasive plants" is an ideology dont make it a revealed truth and dogma

@dewskiss It's sad from an aesthetic sense but if the plants are invasive they should be killed 😞

finally visited the most magical lily valley

#longevity simplicity of immortalization of Roses🌹 organism can grow beyond itself, but evolutionary developed mechanisms must pre-exist: -rooting from the underground -layering stems from the top -some roses "decided" to be mortal Conclusion: -death is optional

@KirkegaardEmil good👍 but job not done.... we need 1000 -2000 ppm to reclaim levels lost in the time of the dinosaurs ice ages were a period of absolute famine catastrophe

Crazy to think about the CO2 pattern in the ice ages. The range is 100-300 but we've pushed it to 430 now and growing. Have to go back 15 million years to find this much CO2 in the air.

@BlackstarOlivia @lios10110 @OrbiOther biodiversity is not the point of life, bioquality and purity is important humanity replaced bad plants with better plants and this is the best improvement of nature in the entire history of the planet

@lios10110 @OrbiOther but yes, you are right human driven monoculture and systemic cultivation and manipulation of the habitat has drastically cut down biodiversity and just amount of life around us. we have more food now, but at a cost to the world

There's many wrong explanations in the replies as to why humanity "failed" to discover agriculture for so long, remaining hunters and gatherers for hundreds of thousand years. Humans didn't *fail* to discover agriculture, it is that up until recently, agriculture was *irrational*

@netherfield34 perfect to maintain beauty of winter gardens

For 10,000 years, we have been slowly dismantling Darwinian evolution and creating new, improved ecosystems. It's a tremendous responsibility, but a noble goal to achieve. The immaculation of original sin from life on the entire planet.

@bryan_johnson I see you're eating classic red raspberries You could improve this dietary ingredient by replacing it with black raspberries (more vitamins and polyphenols)

What I'm eating today.... For...reduced systemic inflammation, microbiome diversity and gut barrier integrity, enhanced mitochondrial efficiency, stabilized blood glucose and insulin sensitivity, improved cardiovascular health and endothelial function, neuroprotection and cognitive support, autophagy stimulation, DNA repair and genomic stability, connective tissue and skin rejuvenation, sustained muscle protein synthesis, oxidative stress reduction, liver detoxification support, improved lipid profiles.

@NiklasAnzinger Blood purity is also important and reinforces the sense of superiority and uniqueness of those associated with the organization time to fund superior longevity closed monasteries-like organisations discipline, consistency, requirements, competition between monasteries

@NiklasAnzinger looks like democracy is the weak point of the DAO we need to create structures reminiscent of ancient monasteries in their organizational structure - they had the power of organization and motivation to achieve their goals

DAOs are dead, long live DAOs? I said for some time now that DAOs have failed. The governance innovation is negative, they are regressing. They are a hotbed for financial chaos and bad actors. However, the idea internet-native companies is good. Time to build now? 1/

@MarcosArrut If aging is written in the epigenome, then you can fix it only temporary and only by commutation engine(organ) one time disabler is not an option because there is no central point to shut down and next there will be problem with aging of commutation organ

If aging is written in the epigenome, then it's not an inviolable law but a code. And every code can be read, rewritten, and therefore controlled. That's all.

@miavonmilk @mixedgrass666 The colors on cars are chaotic, but in the case of potatoes or corn, the colors indicate a multitude of vitamins. Non-color varieties are statistically poorest in vitamins

@mixedgrass666 Fascinating! We erase colors from everything: cars, interior designs, and even potatoes!

It’s incredible to read about what pre-Colombian Andean communities were doing with potatoes. We are missing out on a beautiful tapestry of tuber varieties.

@t_recsch @davidasinclair Did you divide the study into two groups where rapamycin was taken chronic/linear from a second group where rapamycin was taken in intermittent cycles?

@davidasinclair Can you help us understand the hypothesis’ behind the discrepancy between mice and human data? Specifically comparing rapamycin. In one hand it extends lifespan in mice and on another one (you recent research) it ages the epigenetic clock in humans; vice versa for metformin.

Trametinib is an approved drug for melanoma. It inhibits MEK1/2 thereby shifting cells away from “grow at all costs” to maintenance & repair🐁Trimetaprib extends lifespan ~15% & with rapamycin a whopping 30%

@davidasinclair looks like the timing/rotation factors are providing the best results! not chemicals itself! next research should focus more on the different rotation cycles of the same substances we need calculate the best commutation(rotation) engines

@biluhuang There is no need to use telomeres or p53 in aging models Organized overexpression of ECM-degrading enzymes (elastin, collagen..) is an equally effectively designed aging process Any gene can maintain aging. Just allow it to be UNMANAGED. telomere-p53 model control nothing.

First, telomeric DNA consists of multicopy tandem repeat arrays and fully possesses all the essential features of a lifespan countdown timer: (1) It can be replicated during cell division to ensure each daughter cell inherits a copy; (2) The shortened length of these arrays in somatic cells is replenished in germ cells, and germ cells must harbor the maximum copy number across all cells of an individual to sustain consumption throughout the entire life cycle, from embryonic development to maturation and senescence [31,22]; (3) The shortening rate of the arrays is malleable to adapt to the distinct developmental and senescent rates of different species and different cell types within the same species; (4) In somatic cells, telomeres are consumed unidirectionally, enabling p53 to generate a concentration gradient along the time axis and form a temporal scale; (5) All external factors or intrinsic genes that modulate the rate of senescence exert their effects by altering the shortening rate of these arrays; (6) Given that some organisms can live for over a century—for instance, the Greenland shark has a lifespan of up to 400 years—the candidate driver substance that propels the operation of the genetic program (analogous to the sand in an hourglass) must be extremely stable and lack a half-life. In contrast, proteins, RNA, mitochondrial DNA (mtDNA), and chemical modifications of DNA and histones are highly unstable, have distinct half-lives, and exist in a dynamic equilibrium of constant degradation and replenishment. For example, DNA methylation and demethylation, as well as histone acetylation and deacetylation, occur simultaneously, making it impossible for these molecules to form a temporal measurement and precluding them from acting as a timer. In other words, the fundamental cause of aging does not lie in RNA, proteins, mtDNA, or epigenetic modifications, and research focused on these directions will never uncover the root cause of aging. Thus, prior to the proposal of the TRCS model, among the numerous theories of cellular senescence, only the telomere theory is valid. In the causal relationship underlying cellular senescence, if telomere shortening is the cause of cellular senescence, then elongating telomere length in senescent cells will inevitably lead to a significant increase in cell replication capacity, accompanied by the reversion to a youthful cellular phenotype. Conversely, if telomere shortening is merely a consequence of cellular senescence, elongating telomere length in senescent cells will not enhance replication capacity nor restore a youthful state. In 2015, scientists at Stanford University first extended the telomere length of skin stem cells by 0.9 kb using hTERT mRNA, which increased the cell replication number by 28 passages [46]; Bodnar (1998) introduced the hTERT gene into human retinal pigment epithelial cells and foreskin fibroblasts, and observed a reduction in the senescence marker β-galactosidase, along with a marked increase in cell replication capacity [47]. Notably, telomere elongation leading to a significant boost in cell replication capacity is an effect that cannot be achieved by any other aging models or intervention strategies. Experimental studies have also shown that a single tail vein injection of AAV9-mTERT in mice over their lifetime resulted in reduced DNA damage, improved glucose tolerance, alleviated cognitive decline, delayed tumorigenesis, and a 24% extension in the average lifespan of the mice [Bernardes de Jesus B, Vera E, Schneeberger K, et al. Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer. EMBO Mol Med. 2012 Aug;4(8):691-704. doi: 10.1002/emmm.201200245.]. However, due to the excessively long telomeres in mice, the lifespan-extending effect of telomerase therapy in mice may be weaker than that in humans. Furthermore, telomere shortening decelerates with age and eventually rebounds: for example, human telomere length increases in individuals aged 80–90 years [48-49], and telomere elongation has also been observed in senescent naked mole-rats [50]. Our own research has also demonstrated that a reduction in 45S rDNA copy number leads to elongated telomeres in white blood cells. Therefore, rDNA exerts a greater driving effect on aging than telomeres in the elderly, meaning that the lifespan-extending efficacy of telomere elongation via telomerase alone will gradually diminish. This finding nonetheless confirms the validity of the telomere theory of aging. Finally, the figure provided shows that leukocyte telomere length is longer in 80-year-old elders than in 20-year-old young adults. However, measuring leukocyte telomere length does not reflect the actual physiological state. Our experimental data indicate that knockout of 45S rDNA leads to telomere elongation in white blood cells, demonstrating that increased leukocyte telomere length is a consequence of aging. Thus, only the measurement of telomere length in stem cells can accurately reflect the true biological state of an organism.

and the much more Enriched Periodic Table of Supplements V2 i know... still looks like a data scrapbook commutation phases slowly added unique discoveries: -royalactin patchway EGFR -anti-inflammatory low IC50: parthenolid, hiperforin -luteolin better than fucoidan in SIRT6?

#Longevity #LEV in search of efficiency i just added non-physical rotation factor to my supplements strategy! The Commutation Cycle is adjusted to Yamanaka Factors and epigenetic reprogramming as the central core of the strategy also organised anabolic and autophagy phase