Plate tectonics and a warming climate will change Earth’s appearance in the future.
Earth’s surface is constantly changing.
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The cerebellum can’t get no respect. Located inconveniently on the underside of the brain and initially thought to be limited to controlling movement, the cerebellum has long been treated like an afterthought by researchers studying higher brain functions.
But researchers at Washington University School of Medicine in St. Louis say overlooking the cerebellum is a mistake. Their findings, published Oct. 25 in Neuron, suggest that the cerebellum has a hand in every aspect of higher brain functions — not just movement, but attention, thinking, planning and decision-making.
“The biggest surprise to me was the discovery that 80 percent of the cerebellum is devoted to the smart stuff,” said senior author Nico Dosenbach, MD, PhD, an assistant professor of neurology, of occupational therapy and of pediatrics. “Everyone thought the cerebellum was about movement. If your cerebellum is damaged, you can’t move smoothly — your hand jerks around when you try to reach for something. Our research strongly suggests that just as the cerebellum serves as a quality check on movement, it also checks your thoughts as well — smoothing them out, correcting them, perfecting things.”
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This video is the third in a multi-part series discussing computing. In this video, we’ll be discussing classical computing, more specifically – how the CPU operates and CPU parallelism.
[0:27–4:57] Starting off we’ll look at, how the CPU operates, more specifically — the basic design of a CPU, how it communicates with memory, the stages it executes instructions in as well as pipelining and superscalar design.
[4:57–8:00] Following that we’ll discuss, computing parallelism, elaborating on the hardware parallelism previously discussed as well as discussing software parallelism through the use of multithreading.
A more detailed look at the CPU:
Drugs that target multiple aging pathways at once significantly extend the healthspan and lifespan of nematodes.
In a paper published in Developmental Cell, scientists from Yale University have demonstrated how targeting multiple pathways related to aging with different drug combinations can slow aging down and extend healthy lifespan in C. elegans [1].
Abstract
There is growing interest in pharmacological interventions directly targeting the aging process. Pharmacological interventions against aging should be efficacious when started in adults and, ideally, repurpose existing drugs. We show that dramatic lifespan extension can be achieved by targeting multiple, evolutionarily conserved aging pathways and mechanisms using drug combinations. Using this approach in C. elegans, we were able to slow aging and significantly extend healthy lifespan. To identify the mechanism of these drug synergies, we applied transcriptomics and lipidomics analysis. We found that drug interactions involved the TGF-b pathway and recruited genes related with IGF signaling. daf-2, daf-7, and sbp-1 interact upstream of changes in lipid metabolism, resulting in increased monounsaturated fatty acid content and this is required for healthy lifespan extension.
Dr. David Sinclair AMA
Posted in biotech/medical, genetics, life extension
On the 23rd of this month, Dr. David Sinclair did an Ask Me Anything over at the Futurology subreddit in support of the NAD+ Mouse Project on Lifespan.io. There were a range of interesting questions from the community about his work in aging research, particularly the role of NAD+ in aging.
Dr. David A. Sinclair is a Professor in the Department of Genetics at Harvard Medical School and a co-joint Professor in the Department of Physiology and Pharmacology at the University of New South Wales. He is the co-Director of the Paul F. Glenn Laboratories for the Biological Mechanisms of Aging and a Senior Scholar of the Ellison Medical Foundation. He obtained his Ph.D. in Molecular Genetics at the University of New South Wales, Sydney in 1995. He worked as a postdoctoral researcher at M.I.T. with Dr. Leonard Guarente; there, he co-discovered a cause of aging for yeast as well as the role of Sir2 in epigenetic changes driven by genome instability.
More recently, he has been in the spotlight for his work with NAD+ precursors and their role in aging and has been helping to develop therapies that replace NAD+, which is lost with aging, in order to delay the diseases of old age. Below are a selection of questions and answers from the AMA, and we urge you to head over to Reddit Futurology to check out the other questions that people asked.
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In addition, a small number of posters will be selected for oral presentation.
Poster topics should lie within the scope of the conference: Research contributing to the eventual postponement of age-related decline in health, with an emphasis on measures that repair damage rather than slowing its creation. Poster submissions are due on January 31, 2019.
To submit your poster go to:
