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Mayo researchers offer evidence people with psoriasis greater risk for developing heart disease
11-11-2006 · EurekAlert!People with the skin disorder psoriasis are at increased risk for developing heart disease, according to Mayo Clinic researchers presenting new study data at the American College of Rheumatology Annual Meeting on November 14.
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- Mayo Clinic study predicts cardiovascular disease risk for rheumatoid arthritis patients
11-07-2007 · EurekAlert!
People with rheumatoid arthritis have a higher risk for developing heart disease than the general population; however, it is difficult to identify which patients are at increased risk. Researchers at Mayo Clinic have developed a simple approach to predict heart disease in these patients within 10 years of their initial diagnosis of rheumatoid arthritis.
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- Combination of personality traits increases risk for heart disease
11-16-2006 · EurekAlert!
Frequent bouts of depression, anxiety, hostility and anger are known to increase a person's risk for developing coronary heart disease, but a combination of these "negative" personality traits may put people at especially serious risk, according to a study by researchers at Duke University Medical Center.
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- Framingham study shows parents who live long pass on
03-12-2007 · EurekAlert!
Researchers from the long-standing Framingham Heart Study (FHS), a program of the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health, report that people whose parents live longer were more likely to avoid developing high blood pressure, high cholesterol, and other risk factors for cardiovascular disease in middle age than their peers whose parents died younger.
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- Evidence found for genes that affect risk of developing Alzheimer's disease
01-17-2008 · EurekAlert!
Through one of the largest studies yet of Alzheimer's disease patients and their brothers, sisters, and children, researchers at Mayo Clinic Jacksonville have found strong evidence that genes other than the well-known susceptibility risk factor APOE4 influence who is at risk for developing the neurodegenerative disease later in life.
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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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- Reduced lung capacity linked to cardiovascular disease by inflammation
07-02-2007 · EurekAlert!
People who have a reduced lung capacity may have a greater risk of heart attack and stroke because they show evidence of inflammation, reveals a study published online ahead of print in Thorax.
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- New imaging technique identifies people-at-risk for Alzheimer's disease
12-20-2006 · EurekAlert!
UCLA researchers used innovative brain scan technology with a new imaging molecule, invented at UCLA, to show that abnormal brain protein deposits that define Alzheimer's disease can be detected in people with mild cognitive impairment, a condition affecting 15-20 million Americans that increases risk for developing Alzheimer's disease. The new imaging technique helped researchers track disease progression over a two-year period and may be helpful in detecting pre-Alzheimer's conditions.
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- New study shows smoking increases risk of psoriasis
10-29-2007 · EurekAlert!
Another disease can be added to the list of smoking-related disorders -- psoriasis. Researchers have found that smoking increases the risk of developing psoriasis, heavier smoking increases the risk further, and the risk decreases only slowly after quitting. Investigators from the Massachusetts General Hospital, Brigham and Women's Hospital, the Harvard School of Public Health, all in Boston, Mass., US, and Vancouver General Hospital, Vancouver, BC, Canada, have published the results in the November 2007 issue of The American Journal of Medicine.
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- Mayo Clinic researchers use 'genomic pathway' to predict Parkinson's
06-14-2007 · EurekAlert!
A new Mayo Clinic study provides strong evidence that the joint effects of common DNA variations in several genes that encode proteins within a well-defined biological pathway largely explain why some persons get Parkinson's disease while others don't, and even predict with great accuracy at what age people might develop their first symptoms.
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- Blood protein offers clues to heart attack in seemingly healthy people
07-02-2007 · EurekAlert!
We've all wondered how a seemingly healthy person can actually be at high risk for heart disease or a heart attack. Now researchers have uncovered a new clue to this mystery. The culprit: myeloperoxidase, a protein secreted by white blood cells that both signals inflammation and releases a bleach-like substance that damages the cardiovascular system.
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