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Friday, June 27, 2014

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

Thursday, June 26, 2014

Aubrey De Grey

  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.

Sirt1: A protein required for integrity of induced pluripotent stem cells

A study published today in the journal Stem Cell Reports, from the Cell Publishing Group, reveals that the SIRT1 protein is needed to lengthen and maintain telomeres during cell reprogramming. SIRT1 also guarantees the integrity of the genome of stem cells that come out of the cell reprogramming process; these cells are known as iPS cells (induced Pluripotent Stem cells). Read more at: http://phys.org/news/2014-04-protein-required-pluripotent-stem-cells.html#jCp

Sirt1: Secret to healthy ageing unlocked!

New York, June 10 (IANS) Ageing is inevitable, but the secret to why some people age more gracefully could lie in the functioning of a protein in our body. Sirtuin1 (SIRT1) protein could be the key to maintain the health of ageing blood stem cells as loss of this protein affects their ability to regenerate blood normally, a study indicates. "Our data shows that SIRT1 is a protein that is required to maintain the health of blood stem cells and supports the possibility that reduced function of this protein with age may compromise healthy ageing," explained Saghi Ghaffari, an associate professor at Icahn School of Medicine at Mount Sinai Hospital in New York City. Humans store stem cell pools in key tissues, including blood. These stem cells can become replacement cells for those lost to wear and tear. But as the blood stem cells age, their ability to regenerate blood declines, potentially contributing to anaemia and the risk of cancers like acute myeloid leukemia and immune deficiency. The new study showed that young blood stem cells that lack SIRT1 behave like old ones. With use of advanced mouse models, the researchers found that blood stem cells without adequate SIRT1 resembled aged and defective stem cells, which are thought to be linked to development of malignancies. "The notion that SIRT1 is a powerful regulator of ageing has been highly debated, but its connection to the health of blood stem cells is now clear," Ghaffari added. "Identifying regulators of stem cell ageing is of major significance for public health because of their potential power to promote healthy ageing and provide targets to combat diseases of ageing," she noted. The findings appeared in the journal Stem Cell Reports.

Insulin-Metformin Combo Tied to Poorer Survival in Diabetes Study

"The current study suggests that adding a sulfonylurea to metformin should be preferred to adding insulin for most patients who need a second diabetes drug," she said. Sulfonylureas include glibenclamide (Micronase), glimepiride (Amaryl), glipizide (Glucotrol) and others. They work by stimulating the body to make more insulin. Roumie's team found that, compared with those who added a sulfonylurea, those who added insulin to metformin had 30 percent higher odds of heart attack, stroke and death from any cause during the study period. "Although new heart attacks and strokes occurred at similar rates in both groups, mortality was higher in patients who added insulin," she said. Roumie said she doesn't know why the rate of deaths was higher among study patients taking insulin. "We have a number of studies planned to examine possible mechanisms. We are investigating type 2 diabetes outcomes associated with blood sugar swings and with episodes of hypoglycemia (low blood sugar) tied to insulin," she said. Sulfonylureas can also cause low blood sugar levels, according to the American Diabetes Association. The report was published June 11 in the Journal of the American Medical Association.

Tuesday, June 3, 2014

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