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Hebrew SeniorLife researchers search for aging, osteoporosis genes
09-19-2007 · EurekAlert!Researchers at Hebrew SeniorLife's Institute for Aging Research have examined close to 100,000 genetic markers for low bone mass and aging to help determine which genes are responsible for the development of osteoporosis and longevity.
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Keywords: hebrew, seniorlife, researchers, search, aging, osteoporosis, genes, researcher, osteoporosi, gene
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- U-M, Israeli scientists report major advance in search for genes associated with colon cancer
07-08-2007 · EurekAlert!
An international team of researchers is reporting on a 10-year study of colon cancer among Israeli Jews and Arabs. The researchers, led by a team from the University of Michigan Comprehensive Cancer Center, discovered a genetic marker that increased a person's risk of colon cancer by 23 percent. At the same time, three other research teams are reporting similar findings involving the same gene, strengthening the likelihood that this particular marker plays a role in colon cancer.
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- Largest genomic search finds genes that may contribute to autism
02-18-2007 · EurekAlert!
An international team of researchers from 19 countries has identified one gene and previously unidentified region of another chromosome as the location of another gene that may contribute to a child's chances of having autism.
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- Einstein researchers use novel approach to uncover genetic components of aging
08-24-2007 · EurekAlert!
People who live to 100 or more are known to have just as many -- and sometimes even more -- harmful gene variants compared with younger people. Now, scientists at the Albert Einstein College of Medicine of Yeshiva University have discovered the secret behind this paradox: favorable "longevity" genes that protect very old people from the bad genes' harmful effects. The novel method used by the researchers could lead to new drugs to protect against age-related diseases.
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- A molecular map for aging in mice
11-28-2007 · EurekAlert!
Researchers at the National Institute of Aging and Stanford University have used gene arrays to identify genes whose activity changes with age in 16 different mouse tissues. The study, published Nov. 30 in PLoS Genetics, uses a newly available database called AGEMAP to document the process of aging in mice at the molecular level. The work describes how aging affects different tissues in mice, and ultimately could help explain why lifespan is limited to just two years in mice.
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- Advance in understanding of blood pressure gene could lead to new treatments
02-04-2007 · EurekAlert!
Research by scientists at UCL (University College London) has clearly demonstrated for the first time the structure and function of a gene crucial to the regulation of blood pressure. The discovery could be important in the search for new treatments for illnesses such as heart disease, the UK's biggest killer. In a paper published online today in Nature Medicine, the team, led by Professor Patrick Vallance and Dr James Leiper, UCL Department of Medicine, reveal the role of the human gene dimethylarginine dimethylaminohydrolase (DDAH), showing that loss of DDAH activity disrupts nitric oxide (NO) production. NO is critical in the regulation of blood pressure, nervous system functions and the immune system. The role of DDAH is to break down modified amino acids (Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA)) that are produced by the body and have been shown to inhibit NO synthase. These molecules accumulate in various disease states including diabetes, renal failure and pulmonary and systemic hypertension, and their concentration in plasma (the fluid component of blood) is strongly predicative of cardiovascular disease and death. In a healthy human body, the majority of ADMA is eliminated through active metabolism by DDAH. Scientists have hypothesised that if DDAH function is impaired, NO production is reduced, and that this could be an important feature of increased cardiovascular risk. To examine this pathway in more detail, the researchers deleted the DDAH gene in mice. These mice went on to develop hypertension, or high blood pressure. They also designed specific inhibitors (small molecules) which bind to the active site of human DDAH. These small molecule inhibitors also induced hypertension in mice, confirming the importance of DDAH in the regulation of blood pressure. Dr Leiper, UCL Medicine, said: “These genetic and chemical approaches to disrupt DDAH showed remarkably consistent results, and provide compelling evidence that loss of DDAH function increases the concentration of ADMA and thereby disrupts vascular NO signalling. “There has been considerable scientific interest in this pathway and the role of ADMA as a novel risk factor, but so far there's been little evidence to support the idea that it's a cause of disease, rather than just a marker. Genes and their pathways are crucial to our understanding of cardiovascular disease and a better understanding of DDAH-1 could lead to important new treatments. “It could help us to establish if genetic variation predisposes certain people to these diseases, or whether environmental factors exert some of their effects through modulation of DDAH activity. “Our research also shows that this pathway could be harnessed therapeutically to limit production of NO in certain situations where too much nitric oxide is a bad thing; for example, hypotension and septic shock. These are some of the biggest problems in intensive care medicine and there is a huge unmet need for drug treatments.” The study, which was carried out at UCL's Rayne Institute, was funded by grants from the British Heart Foundation, the Wellcome Trust and the Medical Research Council. Professor Jeremy Pearson, Associate Medical Director of the British Heart Foundation, said: "The unexpected finding in the 1980s that a simple gas, nitric oxide (NO), is made by cells in the blood vessel wall and is a powerful control of blood vessel relaxation led to the award of the Nobel Prize in 1998 to its discoverers. "More recently, there has been increasing evidence that impairment of NO production is likely to be an important factor in the development of heart and circulatory disease, but the mechanisms responsible are not fully understood. "This study suggests for the first time that the loss of the activity of the enzyme DDAH-1 leads to reduced NO production and may cause heart and circulatory disease. These findings are likely to be important in the search for new ways to optimise the health of our blood vessels." ### Notes for Editors 1. For more information, please contact Ruth Metcalfe in the UCL Media Relations Office on tel: +44 (0)20 7679 9739, mobile: +44 (0)7990 675 947, out of hours: +44 (0)7917 271 364, e-mail: r.metcalfe@ucl.ac.uk2. 'Disruption of methylarginine metabolism impairs vascular homeostasis' is published in the February issue of the journal Nature Medicine. Advance online publication is embargoed to 18.00 GMT (13.00 US Eastern) Sunday 4 February 2007. Journalists can obtain copies of the paper by contacting the UCL Media Relations Office.3. The study was funded by the British Heart Foundation, the Wellcome Trust and the Medical Research Council. About UCL Founded in 1826, UCL was the first English university established after Oxford and Cambridge, the first to admit students regardless of race, class, religion or gender, and the first to provide systematic teaching of law, architecture and medicine. In the government's most recent Research Assessment Exercise, 59 UCL departments achieved top ratings of 5* and 5, indicating research quality of international excellence. UCL is the fourth-ranked UK university in the 2006 league table of the top 500 world universities produced by the Shanghai Jiao Tong University. UCL alumni include Mahatma Gandhi (Laws 1889, Indian political and spiritual leader); Jonathan Dimbleby (Philosophy 1969, writer and television presenter); Junichiro Koizumi (Economics 1969, Prime Minister of Japan); Lord Woolf (Laws 1954, Lord Chief Justice of England & Wales); Alexander Graham Bell (Phonetics 1860s, inventor of the telephone), and members of the band Coldplay.
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- Opening and closing the genome
02-22-2007 · EurekAlert!
A dynamic cast of gatekeeper enzymes controls access to the DNA for gene transcription, adding and removing particular molecules to open or close the genome as needed. Researchers have identified an important new player in this gene-control system, an enzyme responsible for removing certain molecules, or marks, involved in opening or closing chromatin, the material that makes up chromosomes. The activity of this enzyme is thought to be widespread, likely affecting many genes.
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- Isolation of a new gene family essential for early development
08-22-2007 · EurekAlert!
Researchers at BRIC, University of Copenhagen, have identified new gene family essential for embryonic development. The family controls the expression of genes crucial for stem cell differentiation, and the results may contribute significantly to the understanding of cancer development. The results are published in Nature, and it follows up on two other high-impact articles on related gene families published in Nature and Cell by the same researchers within the last year.
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- Firefly genes allow testing of new therapy against lymphoma
12-19-2007 · EurekAlert!
Researchers here have figured out a way to use a firefly gene to let them see just how effective a new drug combination actually is against some forms of cancer and its serious complication. The new study looked at ATLL, adult T cell lymphoma and leukemia, a form of cancer where it is particularly hard to gauge the disease's progress, and where the patients' prognosis is generally poor. There is now no widely effective therapy available to treat this disease successfully.
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- 'Junk' DNA now looks like powerful regulator, Stanford researcher finds
04-23-2007 · EurekAlert!
Large swaths of garbled human DNA once dismissed as junk appear to contain some valuable sections, according to a new study by researchers at the Stanford University School of Medicine and the University of California-Santa Cruz. The scientists propose that this redeemed DNA plays a role in controlling when genes turn on and off.
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- 'Best of both worlds' -- Targeting a single gene could inhibit bone decay and stimulate bone growth
12-08-2006 · EurekAlert!
Researchers at the University of Pennsylvania's School of Medicine have found by targeting the function of a single gene that it is possible to inhibit bone decay while simultaneously stimulating bone formation. This concept may lead to drug treatments for osteoporosis and other bone diseases. Senior author Yongwon Choi, PhD, professor of Pathology and Laboratory Medicine at the University of Pennsylvania and colleagues report their findings in the December issue of Nature Medicine.
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