Dream: Cancer Caused By the Presence of 3; 1 Halugenic, Invent Control 7 for Halugenic - "rinig" (Listen/Hear) Water/Genome


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Monday, July 7, 2014

Hydrogen Fuel from WATER - The World is Already Doing IT


Friday, June 27, 2014

#16 --> #1 Pirates win walk-off Josh Harrison







Thursday, June 26, 2014

Aubrey De Grey


COMMENTS
  Khannea Suntzu • • Jun 26, 2014
  The clock is ticking.
  Aubrey was just there at the cusp of the new millennium to emphasize the point that conceivably someone can do this. He was the first to make this point in a particularly emphatic, plausible, rational manner. Any number of similarly talented, motivated, resourced people could have taken up this gauntlet. Aubrey was the first to do so, and there will be statues made of him for doing so.
  Even if he dies from aging before His time.
  And now he has taken up this challenge, millions will in fact take up this challenge in his footsteps. Aubrey de Grey will therefore be contemplated. This video will be reviewed for millenia.
  Now we see the challenge clearly before us, and the clock has start ticking. Solving aging and reverse engineering youth is not an infinitely complex challenge. It may be a challenge that takes 20 years, or it may be a challenge that takes 200 years. It won't be a challenge that takes 500 years.
  That means, in all likelihood, somewhere this century there will be a person living well beyond a natural lifespan. In all likelihood it means that in a conceivably or inconceivably short (depending on your opinion) timespan, someone somewhere will implement treatments. These may initially be modest, expensive, painful or flawed treatments.
  But pretty soon this will be a reality. And when it is, it will never go away again.
  Many people might not like the idea, but that's just the way it is. They'll have to wrap their heads around it. They will just have to come to terms with this new outlandish motion.
  Yesterday we were shackled to the ground and suddenly we can fly. A few decades later millions routinely fly. Yesterday people were imprisoned on the planet and now people can go to the moon.
  Things change, and we adapt. The more things change the more they'll never be the same again.
  The problem of life extension and rejuvenation in the long run isn't a problem of research grants or entropy or time or insurmountable laboratory odds. It is a matter of imagination. It is a matter of psychotherapy.
  And that's the role the interviewer took - he played the unimaginative person. The interlocutor. The skeptic. The contemporary. The simplicius.
  History will be shocked at this hesitancy, and one day it will be hard to understand this point of view. The future will say "what were these people thinking?"
  The sooner the better.

Sunday, June 22, 2014

Sirt1 & Metformin some of the older tweets collected


Tuesday, June 17, 2014

Sirt1 More


Tuesday, June 10, 2014

Accelerated senescence of cord blood endothelial progenitor cells in premature neonates is driven by SIRT1 decreased expression.

Epidemiological and experimental studies indicate that early vascular dysfunction occurs in low-birth-weight subjects, especially preterm (PT) infants. We recently reported impaired angiogenic activity of endothelial colony-forming cells (ECFCs) in this condition. We hypothesized that ECFC dysfunction in PT might result from premature senescence and investigated the underlying mechanisms. Compared with ECFCs from term neonates (n = 18), ECFCs isolated from PT (n = 29) display an accelerated senescence sustained by growth arrest and increased senescence-associated β-galactosidase activity. Increased p16(INK4a) expression, in the absence of telomere shortening, indicates that premature PT-ECFC aging results from stress-induced senescence. SIRT1 level, a nicotinamide adenine dinucleotide-dependent deacetylase with anti-aging activities, is dramatically decreased in PT-ECFCs and correlated with gestational age. SIRT1 deficiency is subsequent to epigenetic silencing of its promoter. Transient SIRT1 overexpression or chemical induction by resveratrol treatment reverses senescence phenotype, and rescues in vitro PT-ECFC angiogenic defect in a SIRT1-dependent manner. SIRT1 overexpression also restores PT-ECFC capacity for neovessel formation in vivo. We thus demonstrate that decreased expression of SIRT1 drives accelerated senescence of PT-ECFCs, and acts as a critical determinant of the PT-ECFC angiogenic defect. These findings lay new grounds for understanding the increased cardiovascular risk in individuals born prematurely and open perspectives for therapeutic strategy.
http://www.ncbi.nlm.nih.gov/pubmed/24518759

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