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Heart rhythm genes possible factors in SIDS

01-16-2007 · EurekAlert!

Nearly 10 percent of sudden infant death syndrome (SIDS) victims have mutations or variations in genes associated with potentially lethal heart rhythms (arrhythmias), according to two newly published studies involving Vanderbilt researchers.

Keywords: heart, rhythm, genes, possible, factors, sids, gene, factor, sid

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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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Gladstone scientists identify critical gene factor in heart development
03-29-2007 · EurekAlert!
Researchers at the Gladstone Institute of Cardiovascular Disease announced they have identified a critical genetic factor in the control of many aspects of heart form and function.
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Scientists associate 6 new genetic variants with heart disease risk factor
01-13-2008 · EurekAlert!
Using new techniques for rapidly scanning the human genome, researchers have associated levels of cholesterol and triglycerides, two fats in the blood, to 18 genetic variants, six of which represent new DNA regions never before associated with the traits. The findings help explain some of the variability in cholesterol and triglyceride levels that arises from genes.
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Scientists find major susceptibility gene for Crohn's disease
04-15-2007 · EurekAlert!
Using a novel approach, researchers identified that the PHOX2B, NCF4 and ATG16L1 genes constitute genetic risk factors for Crohn's disease. In addition, their study identified two regions of the genome where genetic risk factors are located but no known genes were implicated -- further work will be necessary to identify the causal genes in these regions.
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Study locates cholesterol genes; finds surprises about good, bad cholesterol
01-13-2008 · EurekAlert!
An international study of 20,000 people found seven new genes that influence blood cholesterol levels, a major factor in heart disease, and confirmed 11 other genes previously thought to influence cholesterol.
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Gene identified for Crohn's disease in children
07-18-2007 · EurekAlert!
Pediatrics researchers have identified a gene variant that raises a child’s risk of Crohn's disease, a chronic and painful condition attributed to inflammation of the gastrointestinal tract. Because multiple genes interact with each other and with environmental factors in Crohn's disease, sorting out the roles of specific genes may better enable doctors to classify a patient's genetic profile and guide individualized treatment.
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Study finds dietary fat interacts with genes
04-10-2007 · EurekAlert!
Research finds that for most adults in the Framingham Heart Study, dietary fat intake is associated with body mass index (BMI). However, for 13 percent of the study population with a specific gene variant within the apolipoprotein A5 gene (APOA5), higher dietary fat was not related to a higher BMI.
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Gene variations directly link inflammation to an increased risk for lung cancer
07-03-2007 · EurekAlert!
Variations in two genes related to inflammation may be a major risk factor for developing lung cancer, according to a team of scientists from the National Cancer Institute and the University of Texas M. D. Anderson Cancer Center. The effect of these genes is especially strong among heavy smokers, suggesting that the inflammatory response is important in modulating the damage caused by tobacco smoke.
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Gene regulation in humans is closer than expected to simple organisms
08-29-2007 · EurekAlert!
Using a novel method developed to identify reliably functional binding motifs, researchers from the Weizmann Institute of Science in Israel have performed a genome-wide study of functional human transcription factor binding sites that encompasses nearly ten thousand genes and four hundred known binding motifs. The study appears in the August 29 issue of the online, open-access journal PLoS ONE.
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Genetic 'missing link' sheds light on sudden cardiac death
11-06-2006 · EurekAlert!
An electrical imbalance caused by a malfunctioning gene triggers long QT syndrome, a potentially fatal heart rhythm disorder. A mutation in the gene Caveolin-3 can disrupt the heart's electrical-muscular impulses and increase the risk of sudden cardiac death.
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