Lifeboat Foundation: Safeguarding Humanity
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Category: biotech/medical – Page 2584

The race is on to edit genes and prevent disease. But this technology is ripe for abuse.

Economic inequity already exists in the reproductive industry. IVF, for example, is not covered by insurance in most states (Massachusetts excepted), setting up a situation in which only infertile people with well-padded pockets can afford the treatment. And of course the well-off have easier access to good health care via quality private insurance — or their own bank accounts. Steve Jobs, for example, spent $100,000 in 2011 to sequence his genome and that of his pancreatic tumor — a bill not many could hope to afford.

“The beautiful thing about this [gene-editing] work is it offers an opportunity to intervene around the moment of birth,” says Katy Kozhimannil, an associate professor in the Division of Health Policy at University of Minnesota’s School of Public Health. “That said, as we pay attention to the opportunity of that moment, it’s important to bear in mind the value of liberty and justice for all.”

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One of the best-known regions of the brain, the cerebellum accounts for just 10 percent of the organ’s total volume, but contains more than 50 percent of its neurons.

Despite all that processing power, it’s been assumed that the cerebellum functions largely outside the realm of conscious awareness, instead coordinating physical activities like standing and breathing. But now neuroscientists have discovered that it plays an important role in the reward response — one of the main drives that motivate and shape human behaviour.

Not only does this open up new research possibilities for the little region that has for centuries been primarily linked motor skills and sensory input, but it suggests that the neurons that make up much of the cerebellum — called granule cells — are functioning in ways we never anticipated.

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Another biomarker of senescent cells could be p16, a protein whose levels increase when cells stop dividing if old and also a protein whose gene is turned off in many human cancers.

Coming back to our topic – designing senolytics that avoid the apoptosis of young, healthy cells – the ideal senolytic should accomplish two things: –turn on p53 at increased levels to determine stubborn, senescent cells to commit suicide –do that on senescent cells only.

And in order to accomplish the second part, such a drug should be ‘programmed’ to only act on those cells where it recognizes senescence-associated biomarkers. There is no single biomarker today that stains positive or negative on all types of senescence cells, but increased levels of beta-galactosidase and p16 proteins could be a welcome start to identify old cells in vivo when designing such a drug.

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Genomic instability (mutations) has been suggested as being one of the primary hallmarks of aging and this research might support that idea. Researchers at John Hopkins report that around 66% of mutations in cancer cells are due to random errors with environment/lifestyle contributing 29% and 5% inherited.

“That finding challenges the common wisdom that cancer is the product of heredity and the environment. “There’s a third cause and this cause of mutations is a major cause,” says cancer geneticist Bert Vogelstein.”

“Such random mutations build up over time and help explain why cancer strikes older people more often. Knowing that the enemy will strike from within even when people protect themselves against external threats indicates that early cancer detection and treatment deserve greater attention than they have previously gotten, Vogelstein says.”

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