We are all ultimately overtaken by age, yet for some people, the correct genes can make the journey into old age rather slow.
Italian researchers made a unique discovery regarding people who survive well into their 90s and beyond a few years ago: they frequently possess a variant of the gene BPIFB4 that guards against cardiovascular disease and maintains the heart in excellent condition for a longer period of time.
Science and Technology: I don’t want to die.
A friend of the academic, who died in the US in 2021, says his brain has been cryonically preserved in accordance with his final wishes.
We don’t exactly know why we age; we know what aging looks like —the “symptoms”, so to speak— but the root causes remain foggy. One leading hypothesis is that the changes associated with old age, both external and internal, are a result of accumulating DNA damage. As this damage builds, cellular functions begin to break down and important pathways start going haywire.
One of the most extreme forms of DNA damage is the double-strand break, which happens when a strand of DNA snaps in half, leaving two separate slivers floating around. Left unfixed, these strands can snag at and break chromosomes, leading to diseases like cancer and other disorders. But how the body repairs this kind of wreckage has been a source of mystery. Now, scientists at the Dresden University of Technology have managed to shine a light on the process. Published in Cell, their work offers important new insights that may eventually help treat, and possibly reverse, DNA damage.
The capacity of intestinal stem cells to maintain cellular balance in the gut decreases upon ageing. Researchers at the University of Helsinki have discovered a new mechanism of action between the nutrient adaptation of intestinal stem cells and ageing. The finding may make a difference when seeking ways to maintain the functional capacity of the ageing gut.
The cellular balance of the intestine is carefully regulated, and it is influenced, among other things, by nutrition: ample nutrition increases the total number of cells in the gut, whereas fasting decreases their number.
The relative number of different types of cells also changes according to nutrient status.
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Endothelial cells line at the most inner layer of blood vessels. They act to control hemostasis, arterial tone/reactivity, wound healing, tissue oxygen, and nutrient supply. With age, endothelial cells become senescent, characterized by reduced regeneration capacity, inflammation, and abnormal secretory profile. Endothelial senescence represents one of the earliest features of arterial ageing and contributes to many age-related diseases. Compared to those in arteries and veins, endothelial cells of the microcirculation exhibit a greater extent of heterogeneity. Microcirculatory endothelial senescence leads to a declined capillary density, reduced angiogenic potentials, decreased blood flow, impaired barrier properties, and hypoperfusion in a tissue or organ-dependent manner.
A genetic marker linked to premature aging was reversed in children with obesity during a six-month diet and exercise program, according to a recent study led by the Stanford School of Medicine.
Children’s telomeres — protective molecular “caps” on the chromosomes — were longer during the weight management program, then were shorter again in the year after the program ended, the study found. The research was published last month in Pediatric Obesity.
Like the solid segment at the end of a shoelace, telomeres protect the ends of chromosomes from fraying. In all people, telomeres gradually shorten with aging. Various conditions, including obesity, cause premature shortening of the telomeres.
Superintelligent AI might solve all the world’s problems. It could cure cancer, eliminate human aging, create a world of abundance for all.
Superintelligent AI might also prove completely uncontrollable and destroy humanity, whether intentionally or as mere collateral damage in the path of achieving other goals.
The clashing viewpoints about the potential and dangers of peak AI live at the heart of the battle of techno-optimists and doomsayers, accelerationists vs doomers.
Called it. already impacting. not even a week later.
I just used AI in two films that are going to be announced soon. That kept me out of makeup for hours. In post and on set, I was able to use this AI technology to avoid ever having to sit through hours of aging makeup.
How are you thinking about approaching the threat that AI poses to certain job categories at your studio and on your productions?
Everything right now is so up in the air. It’s so malleable. The technology’s moving so quickly. I feel like everybody in the industry is running a hundred miles an hour to try and catch up, to try and put in guardrails and to try and put in safety belts to keep livelihoods afloat. But me, just like every other studio in town, we’re all trying to figure it all out. I think we’re all trying to find the answers as we go, and it’s changing every day — and it’s not just our industry, but it’s every industry that AI will be affecting, from accountants to architects. If you look at it across the world, how it’s changing so quickly, I’m hoping that there’s a whole government approach to help everyone be able to sustain, is my hope.
For this long overdue update of top longevity conferences we’ve removed 5 old events no longer happening and added a whopping 12 new ones!
We’ve put together the most up-to-date list of longevity conferences where you can learn about life-extension research in-person and online.
