Alpha ketoglutarate, or AKG, has long been used as a dietary supplement in the bodybuilding world.
By satisfying bioenergetic demands, generating biomass, and providing metabolites serving as cofactors for chromatin modifiers, metabolism regulates adult stem cell biology. Here, we report that a branch of glycolysis, the serine biosynthesis pathway (SBP), is activated in regenerating muscle stem cells (MuSCs). Gene inactivation and metabolomics revealed that Psat1, one of the three SBP enzymes, controls MuSC activation and expansion of myogenic progenitors through production of the metabolite α-ketoglutarate (α-KG) and α-KG-generated glutamine. Psat1 ablation resulted in defective expansion of MuSCs and impaired regeneration. Psat1, α-KG, and glutamine were reduced in MuSCs of old mice. α-KG or glutamine re-established appropriate muscle regeneration of adult conditional Psat1-/- mice and of old mice. These findings contribute insights into the metabolic role of Psat1 during muscle regeneration and suggest α-KG and glutamine as potential therapeutic interventions to ameliorate muscle regeneration during aging.
Older people may be at greater risk of developing pancreatic cancer and have poorer prognoses because of age-related changes in cells in the pancreas called fibroblasts, according to research led by investigators from the Johns Hopkins Kimmel Cancer Center, the Johns Hopkins Bloomberg School of Public Health and the Bloomberg~Kimmel Institute for Cancer Immunotherapy.
The study, published online Feb. 8 in Cancer Research, provides clues as to why pancreatic cancer is more common and aggressive in older people. It may also help scientists develop new therapeutic approaches for this difficult-to-treat cancer. The study showed that aging alters fibroblasts in ways that enable them to promote pancreatic cancer tumor growth.
“Older fibroblasts release proteins that directly affect pancreatic cancer cells and ultimately lead to the growth and spread of pancreatic cancer tumors,” says the study’s lead author, Daniel Zabransky, M.D., Ph.D., assistant professor of oncology at the Johns Hopkins University School of Medicine. “The younger fibroblasts did not have these capabilities. We think this is a key reason why we see pancreatic cancer more commonly in older patients.”
Facebook is quickly being overrun by dubious, AI-generated junk — which is somehow attracting huge amounts of attention from its aging user base.
Worse yet, according to a new analysis by Stanford and Georgetown University researchers, first spotted by 404 Media, scammers and spammers are using this lowbrow content to grow their audiences on Facebook.
Even with the proliferation of AI image generators, the novelty has clearly yet to wear off for users on the largest social media network, a veritable social media dinosaur.
Please note that the links below are affiliate links, so we receive a small commission when you purchase a product through the links. Thank you for your support!
As we age, we might begin to observe that it takes more time to recall the exact words we want to use. This situation can raise worries about cognitive deterioration and the risk of dementia.
However, a new study by Baycrest and the University of Toronto suggests that talking speed is a more important indicator of brain health than difficulty finding words, which appears to be a normal part of aging. This is one of the first studies to look at both differences in natural speech and brain health among healthy adults.
“Our results indicate that changes in general talking speed may reflect changes in the brain,” says Dr. Jed Meltzer, Baycrest’s Canada Research Chair in Interventional Cognitive Neuroscience and the lead author on this study. “This suggests that talking speed should be tested as part of standard cognitive assessments to help clinicians detect cognitive decline faster and help older adults support their brain health as they age.”
The new findings could lead to better treatments for rheumatoid arthritis, lupus and other inflammatory diseases – and may even help us slow aging.
Researchers have discovered how “leaky” mitochondria can drive harmful inflammation responsible for diseases such as lupus and rheumatoid arthritis. Scientists may be able to leverage the findings to develop better treatments for those diseases, improve our ability to fight off viruses and even slow aging.
The new discovery reveals how genetic material can escape from our cellular batteries, known as mitochondria, and prompt the body to launch a damaging immune response. By developing therapies to target this process, doctors may one day be able to stop the harmful inflammation and prevent the toll it takes on our bodies.
Anyone know anything else? This is a supplement easily found too.
Dr. Stephanie Venn-Watson presents a newly discovered natural molecule that has potential benefits to extend both healthspan \& lifespan in this video.
~* More About Fatty15 Supplement \& 20% OFF Discount Link *~
The Schwartz Reisman Institute for Technology and Society and the Department of Computer Science at the University of Toronto, in collaboration with the Vector Institute for Artificial Intelligence and the Cosmic Future Initiative at the Faculty of Arts \& Science, present Geoffrey Hinton on October 27, 2023, at the University of Toronto.
0:00:00 — 0:07:20 Opening remarks and introduction. 0:07:21 — 0:08:43 Overview. 0:08:44 — 0:20:08 Two different ways to do computation. 0:20:09 — 0:30:11 Do large language models really understand what they are saying? 0:30:12 — 0:49:50 The first neural net language model and how it works. 0:49:51 — 0:57:24 Will we be able to control super-intelligence once it surpasses our intelligence? 0:57:25 — 1:03:18 Does digital intelligence have subjective experience? 1:03:19 — 1:55:36 Q\&A 1:55:37 — 1:58:37 Closing remarks.
Talk title: “Will digital intelligence replace biological intelligence?”
Abstract: Digital computers were designed to allow a person to tell them exactly what to do. They require high energy and precise fabrication, but in return they allow exactly the same model to be run on physically different pieces of hardware, which makes the model immortal. For computers that learn what to do, we could abandon the fundamental principle that the software should be separable from the hardware and mimic biology by using very low power analog computation that makes use of the idiosynchratic properties of a particular piece of hardware. This requires a learning algorithm that can make use of the analog properties without having a good model of those properties. Using the idiosynchratic analog properties of the hardware makes the computation mortal. When the hardware dies, so does the learned knowledge. The knowledge can be transferred to a younger analog computer by getting the younger computer to mimic the outputs of the older one but education is a slow and painful process. By contrast, digital computation makes it possible to run many copies of exactly the same model on different pieces of hardware. Thousands of identical digital agents can look at thousands of different datasets and share what they have learned very efficiently by averaging their weight changes. That is why chatbots like GPT-4 and Gemini can learn thousands of times more than any one person. Also, digital computation can use the backpropagation learning procedure which scales much better than any procedure yet found for analog hardware. This leads me to believe that large-scale digital computation is probably far better at acquiring knowledge than biological computation and may soon be much more intelligent than us. The fact that digital intelligences are immortal and did not evolve should make them less susceptible to religion and wars, but if a digital super-intelligence ever wanted to take control it is unlikely that we could stop it, so the most urgent research question in AI is how to ensure that they never want to take control.
