Daily non-political popular news in brief.

Genetic mutation alters response to heart failure drugs

01-02-2007 · EurekAlert!

Drugs known as beta blockers help reduce the heart's workload during heart failure via their action on beta-adrenergic receptors in cardiac cells. However, doctors remain puzzled by the variable responses to beta blockers among patients. Researchers now show that the key to this variation lies in a single amino acid change in the beta1-adrenergic receptor, that may differ from person to person, which alters the receptor's conformation and the receptor's response to certain beta blockers.

Keywords: genetic, mutation, alters, response, heart, failure, drugs, alter, drug

« Previous | Next »

Similar news on "Genetic mutation alters response to heart failure drugs":

JCI table of contents: January 2, 2007
01-02-2007 · EurekAlert!
This release contains summaries, links to PDFs and contact information for the following newsworthy papers to be published January 2, 2007, in the JCI, including: Genetic mutation alters response to heart failure drugs; Glucose levels trigger compensation for type 2 diabetics; Cell relocation fixes damage to the gut lining; BCL2 reins in BIM, preventing leukemic cell death; and Complex macrophage and monocyte interactions at work in atherosclerosis.
Similar news · Read more »
MU researchers find statin drugs also may help reduce risk of heart failure, sudden cardiac death
05-01-2007 · EurekAlert!
Statin drugs, known primarily for their ability to lower cholesterol, also may reduce the overactive sympathetic nervous system response that contributes to the worsening of heart failure and increases the risk of sudden cardiac death, two University of Missouri-Columbia researchers have found. Heart failure is the leading cause of morbidity and mortality in the United States.
Similar news · Read more »
Drug's potential adverse side effect explained
09-06-2007 · EurekAlert!
Drugs that are agonists of the receptor PPAR-gamma are used to treat individuals with diabetes. However, it has been suggested that their use is associated with a slightly increased risk of heart failure. A potential explanation for this adverse effect that is observed in a minority of patients is outlined in a new study in the Journal of Clinical Investigation.
Similar news · Read more »
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 »
Drug used for treatment for heart failure in adults may not be beneficial for children and teens
09-11-2007 · EurekAlert!
Preliminary findings indicate a heart failure medication used by adults, carvedilol, may not significantly improve heart failure outcomes for children and adolescents, according to an article in the Sept. 12 issue of JAMA.
Similar news · Read more »
Kidney cancer drug attacks a major type of acute myeloid leukemia
01-29-2008 · EurekAlert!
A drug used to treat kidney cancer also targets a genetic mutation active in about one third of patients with acute myeloid leukemia, the most common and lethal form of adult leukemia, researchers at The University of Texas M. D. Anderson Cancer Center report in the Jan. 29 edition of the Journal of the National Cancer Institute.
Similar news · Read more »
Heart failure medication does not improve survival, compared to more widely used medication
05-01-2007 · EurekAlert!
The drug levosimendan did not improve survival for patients with decompensated heart failure when compared with a more widely used treatment for this condition, dobutamine, according to a study in the May 2 issue of JAMA.
Similar news · Read more »
Scientists identify fundamental brain defect, probable drug target in fragile X syndrome
09-17-2007 · EurekAlert!
Scientists have discovered how the gene mutation responsible for fragile X syndrome -- the most common inherited form of mental retardation -- alters the way brain cells communicate. In neurons cultured from laboratory rats, the scientists also were able to reverse the effects of the mutation using a drug targeted to the specific site in an upstream pathway of the defect. The finding could lead to the development of human therapies for this previously untreatable condition.
Similar news · Read more »
Study uncovers mutation responsible for Noonan Syndrome
12-04-2006 · EurekAlert!
Scientists have discovered that mutations in a gene known as SOS1 account for many cases of Noonan syndrome (NS), a common childhood genetic disorder which occurs in one in 1,000-2,500 live births. NS is characterized by short stature, facial abnormalities and learning disabilities, as well as heart problems and predisposition to leukemia.
Similar news · Read more »
JCI table of contents: June 21, 2007
06-21-2007 · EurekAlert!
This release contains summaries, links to PDFs and contact information for the following newsworthy papers to be published online, June 21, 2007 including: A diet rich in omega-3 fatty acids may lower prostate cancer genetic risk; Mending a broken heart: How to boost the number and function of cardiac stem cells; Autophagy plays a role in heart's poor response to stress; New mouse model for the study of some forms of human hypertension; and others.
Similar news · Read more »