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With that basic research, mankind found the first major clue to the origins of aging and death. They discovered that some cells in our bodies that may never die. These “immortal cells” and the philosophical shift in thinking they engendered, will likely change medicine as we know it.
Different African killifish species vary extensively in their lifespans—from just a few months to several years. Scientists from the Max Planck Institute for Biology of Ageing in Cologne investigated how different lifespans have evolved in nature and discovered a fundamental mechanism by which detrimental mutations accumulate in the genome causing fish to age fast and become short-lived. In humans, mutations accumulate mainly in the genes that are active in old age.
Russian biologist Denis Rebrikov plans to help five couples who are deaf try CRISPR gene-editing to avoid having a child that inherits the condition.
Cold Spring Harbor, NY — Cancer cells use a bizarre strategy to reproduce in a tumor’s low-energy environment; they mutilate their own mitochondria! Researchers at Cold Spring Harbor Laboratory (CSHL) also know how this occurs, offering a promising new target for pancreatic cancer therapies.
Why would a cancer cell want to destroy its own functioning mitochondria? “It may seem pretty counterintuitive,” admits M.D.-Ph. D. student Brinda Alagesan, a member of Dr. David Tuveson’s lab at CSHL.
According to Alagesan, the easiest way to think about why cancer cells may do this is to think of the mitochondria as a powerplant. “The mitochondria is the powerhouse of the cell,” she recites, recalling the common grade school lesson. And just like a traditional powerplant, the mitochondria create their own pollution.
Machine enhanced humans — or cyborgs as they are known in science fiction — could be one step closer to becoming a reality, thanks to new research Lieber Group at Harvard University, as well as scientists from University of Surrey and Yonsei University.
Researchers have conquered the monumental task of manufacturing scalable nanoprobe arrays small enough to record the inner workings of human cardiac cells and primary neurons.
The ability to read electrical activities from cells is the foundation of many biomedical procedures, such as brain activity mapping and neural prosthetics. Developing new tools for intracellular electrophysiology (the electric current running within cells) that push the limits of what is physically possible (spatiotemporal resolution) while reducing invasiveness could provide a deeper understanding of electrogenic cells and their networks in tissues, as well as new directions for human-machine interfaces.
My colleague Nicola Bagalà recently had the opportunity to interview Sergey Young, a board member of XPRIZE and the creator of the $100m Longevity Vision Fund. As you probably know, at the end of May this year XPrize hosted a 2-day workshop to better understand the bottlenecks and opportunities of the longevity industry, and in this interview, Sergey is sharing his vision on what can — and should — be done to accelerate the development of new therapies addressing aging.
We recently had the opportunity to interview Sergey Young, a board member of XPRIZE and the creator of the $100m Longevity Vision Fund.
When did you first become interested in healthy life extension, and why?
My interest began with a routine visit to a doctor. Five years ago, at the age of 42, my blood tests – which I neglected for 7 years, thinking I was in perfect health – showed that my cholesterol was extremely high, putting me at risk of one of the most common killers: heart disease.
I cannot say that I am cured, but this might be something really interesting.
Dr Grace Gosar began following a medication and diet programme devised by a Staffordshire scientist.
More funding your way would alleviate what he’s calling out.
Despite public and political pressure, pharma keeps on ratcheting up prices.
Current guidelines recommend lowering cholesterol for heart disease risk reduction. New findings indicate that if cholesterol dips too low, it may boost the risk of hemorrhagic stroke, according to researchers.
Over a period of nine years, a Penn State-led study examined the relationship between low-density lipoprotein cholesterol—LDL, commonly known as “bad” cholesterol—and hemorrhagic stroke. This type of stroke occurs when a blood vessel bursts in the brain.
The researchers found that participants with LDL cholesterol levels below 70 mg/dL had a higher risk of hemorrhagic stroke.
