Daily non-political popular news in brief.

U-M scientists develop tool to probe role of oxidative stress in aging, disease

Oxygen, although essential for human life, can turn into an aggressive chemical that is outright toxic to important molecules inside our cells. This "oxidative stress" is associated with many diseases, such as Alzheimer's, heart disease and cancer, and has been suggested to be the culprit underlying aging.

Read more »

Keywords: u-m, scientists, develop, tool, probe, role, oxidative, stress, aging, disease, scientist

« Previous | Next »

Similar news on "U-M scientists develop tool to probe role of oxidative stress in aging, disease":

1. Boston College profs study oxidative stress subcellular to discover its role in diseases
   09-14-2007 · EurekAlert!
   An interdisciplinary team of scientists from Boston College has found a means to discover more about what role oxidative stress plays in the development of diseases by studying it at the subcellular level. Oxidative stress is known to underlie many human diseases including atherosclerosis, Parkinson's disease and Alzheimer's disease.
   Similar news · Read more »
   
2. Cigarettes leave deadly path by purging protective genes
   01-23-2008 · EurekAlert!
   A University of Rochester scientist discovered that the toxins in cigarette smoke wipe out a gene that plays a vital role in protecting the body from the effects of premature aging. Without this gene we not only lose a bit of youthfulness -- but the lungs are left open to destructive inflammation and diseases such as chronic obstructive pulmonary disease and lung cancer.
   Similar news · Read more »
   
3. 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.
   Similar news · Read more »
   
4. Weizmann Institute scientists develop a general 'control switch' for protein activity
   06-19-2007 · EurekAlert!
   Since malfunctioning proteins can cause disease, the study of protein structure and function can lead to the development of drugs and treatments for numerous disorders. Now, Weizmann scientists have developed a unique "switch" that can control the activity of any protein, raising it several-fold or stopping it almost completely. The method provides researchers with a simple and effective tool for exploring the function of unknown proteins.
   Similar news · Read more »
   
5. Alzheimer's prevention role discovered for prions
   07-03-2007 · EurekAlert!
   A role for prion proteins, the much debated agents of mad cow disease and vCJD, has been identified. It appears that the normal prions produced by the body help to prevent the plaques that build up in the brain to cause Alzheimer’s disease. The possible function for the mysterious proteins was discovered by a team of scientists led by Medical Research Council funded scientist Professor Nigel Hooper of the University of Leeds.
   Similar news · Read more »
   
6. Scientists discover novel way to remove iron from ferritin
   11-02-2007 · EurekAlert!
   A new study led by Children's Hospital Oakland Research Institute senior scientist, Elizabeth Theil, PhD, is the first to suggest that a small protein or heptapeptide could be used to accelerate the removal of iron from ferritin. The results of this study may help scientists develop new medications that dramatically improve the removal of excess iron in patients diagnosed with blood diseases such as B-Thalassemia (Cooley's anemia) or sickle cell disease.
   Similar news · Read more »
   
7. Key Function Of Nervous System Enzyme Found; Impact On Drug Development Against Alzheimer's
   09-29-2006 · ScienceDaily
   Ever since scientists first elucidated the molecular mechanisms underlying the pathology and loss of nerve cells in Alzheimer's disease, drug companies have been working to develop drugs which will inhibit the outbreak of this severe form of dementia. Now researchers in Munich and Berlin (Germany) have discovered that an enyzme which has a central causal role in Alzheimer's disease happens also to have a key function in the normal development of the nervous system. This enzyme, beta-secretase or BACE1, ensures that nerve fibers (axons) are adequately isolated with sheaths of myelin, enabling rapid conduction of electrical impulses, as well as preventing short-circuits, akin to plastic insulation on electrical wires.
   Similar news · Read more »
   
8. Scientists learn role of oxidative stress in estrogen-related bone loss
   09-10-2007 · EurekAlert!
   Scientists have discovered new information about an immune pathway in mice that explains how oxidative stress that results from acute estrogen deficiency leads to the loss of bone. The finding could help in identifying a new drug target for preventing postmenopausal bone loss.
   Similar news · Read more »
   
9. Search for the 'on' switches may reveal genetic role in development and disease
   01-24-2008 · EurekAlert!
   A new resource that identifies regions of the human genome that regulate gene expression may help scientists learn about and develop treatments for a number of human diseases, according to researchers at Duke's Institute for Genome Sciences & Policy.
   Similar news · Read more »
   
10. Depression, aging, and proteins made by a virus may all play role in heart disease
    10-01-2007 · EurekAlert!
    Researchers here have linked an increase in two immune system proteins essential for inflammation to a latent viral infection and proposed a chain of events that might accelerate cardiovascular disease. The same process may be involved in a host of other ailments plaguing the elderly.
    Similar news · Read more »