IAS Bulletin Article: Interview with Marios Kyriazis MD about L- <ul><li>This shop requires JavaScript to run correctly. Please activate JavaScript in your browser.</li></ul> Currency Your Account ( Log in ) Shopping Cart 0 Items, Items, (empty) $0.00 Order HotlineUSA Toll Free Products Further Reading Miscellaneous Join Us Our Payment Providers All transactions through veripayment are processed in US dollars Mailing Address Post Box 19, Sark, GY9 0SB Great Britain License No# 8-821A/DNFD Home>Authors Dr. Articles By This Author CONTACT US If you have any questions please contact us where our fully trained staff will be able to assist you Order Hotline USA Toll Free General Enquiries - 1-415-992-5563 (USA) Outside of USA call - +44 208 123 2106 Within the UK call - (0208) 123 2106 International AntiAging Systems Post Box 19, Sark, GY9 0SB Great Britain
Mitochondria: Life, Death and the Agents of Aging - Decoded Science | Decoded Science Mitochondria in Mammalian Lung Tissue. Image by Louisa Howard Despite propaganda to the contrary, aging is rarely a pleasurable experience. “Two linked ideas are at the core of our current aging theory,” says molecular cell biologist Colin Dingwall at Kings College, London “The first is that proteins, RNA and DNA are bombarded with and damaged by reactive oxygen species (ROS) generated during normal cellular respiration and this results in eventual decline and disease. “Moreover,” according to Dingwall, “micro-injection of mitochondria from ‘young’ cells, those which haven’t divided very much, can overcome senescence in cells that are reaching the natural end of their lives and will probably, in the usual course of things, undergo programmed cell death, or apoptosis which is also largely controlled by mitochondria.” Not all mitochondrial-induced aging is caused by ROS – at least not in mice A series of studies in mice has yielded an unexpected result, continues Dingwall. Sources:
New anti-inflammatory agents silence overactive immune response A new way to fight inflammation uses molecules called polymers to mop up the debris of damaged cells before the immune system becomes abnormally active, researchers at Duke University Medical Center report. The discovery, published August 15 in the journal Proceedings of the National Academy of Sciences, offers a promising new approach to treat inflammatory auto-immune disorders such as lupus and multiple sclerosis, which are marked by an overactive immune response. "Depending on the disease, cells that are damaged drive or perpetuate the immune response," said Bruce A. Sullenger, Ph.D., director of the Duke Translational Research Institute and senior author of the study. Sullenger said the idea for the new approach stems from earlier findings by Duke scientists and others that dying and diseased cells spill nucleic acids -- the building blocks of life that include DNA and RNA -- that then circulate at high levels in the bloodstream. "Then we had a 'eureka moment,'" Sullenger said.
Switch in cell's 'power plant' declines with age, rejuvenated by drug Researchers at the Johns Hopkins University School of Medicine have found a protein normally involved in blood pressure regulation in a surprising place: tucked within the little "power plants" of cells, the mitochondria. The quantity of this protein appears to decrease with age, but treating older mice with the blood pressure medication losartan can increase protein numbers to youthful levels, decreasing both blood pressure and cellular energy usage. The researchers say these findings, published online during the week of August 15, 2011, in the Proceedings of the National Academy of Sciences, may lead to new treatments for mitochondrial-specific, age-related diseases, such as diabetes, hearing loss, frailty and Parkinson's disease. "We've identified a functional and independently operated system that appears to influence energy regulation within the mitochondria," explains Jeremy Walston, M.D., professor of geriatric medicine at Hopkins.
Cycling fast: vigorous daily exercise recommended for a longer life Public release date: 29-Aug-2011 [ Print | E-mail Share ] [ Close Window ] Contact: Jacqueline Partarrieupress@escardio.org 33-633-473-335European Society of Cardiology A study conducted among cyclists in Copenhagen, Denmark1 showed that it is the relative intensity and not the duration of cycling which is of most importance in relation to all-cause mortality and even more pronounced for coronary heart disease mortality. Current recommendations prescribe that every adult should accumulate 30 minutes or more of moderate physical activity in leisure time, preferably every day of the week. According to Prof Schnor, "this study suggests that a greater part of the daily physical activity in leisure time should be vigorous, based on the individuals own perception of intensity. Table: Relative risk of all-cause and coronary heart disease death for men and women in relation to duration and intensity of cycling. Contributors: Jacob L. 1 Supported by grants from The Danish Heart Foundation.
The Human Digital Ageing Atlas | A portal of ageing related changes Extending healthy life by getting rid of retired cells | Not Exactly Rocket Science As we get older, many of the cells in our bodies go into retirement. Throughout our lives, they divided time and again, all in the face of radiation bombardments and chemical attacks. Slowly but surely, their DNA builds up damage to that threatens to turn them into tumours. Some repair the damage; others give up the ghost. But they aren’t idle. Baker has developed a way of killing all of a mouse’s senescent cells by feeding them with a specific drug. Note that the mice in this study didn’t live any longer; they just spent more of their life being healthy. Baker exploited the fact that many senescent cells rely on a protein called p16-Ink4a. Baker tested out this system in a special strain of genetically engineered mice that age very quickly. “There’s been a question of whether senescent cells are important, since they’re only a small proportion of cells,” says Kirkland. While several scientists agree that senescent cells are somehow harmful, they’ve disagreed as to how. More on ageing:
Biologists slow the aging process in fruit flies: Study has implications for humans UCLA life scientists have identified a gene that slows the aging process. The biologists, working with fruit flies, activated a gene called PGC-1, which increases the activity of mitochondria, the tiny power generators in cells that control cell growth and tell cells when to live and die. "We took this gene and boosted its activity in different cells and tissues of the fly and asked whether this impacts the aging process," said David Walker, an assistant professor of integrative biology and physiology at UCLA and a senior author of the study. "We discovered that when we boost PGC-1 within the fly's digestive tract, the fly lives significantly longer. We also studied neurons, muscle and other tissue types and did not find life extension; this is telling us there is something important about the digestive tract." The research appears in the current online edition of Cell Metabolism, the leading journal in its field, and will be published in an upcoming print edition.