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Gene-chip studies provide new leads in treating lung disease of premature newborns

10-03-2007 · EurekAlert!

Some 20 to 40 percent of extremely premature infants suffer abnormal lung development leading to bronchopulmonary dysplasia, a chronic lung disease that can cause long-term breathing problems. Little is known about how to predict whether a premature infant will develop BPD in the weeks after birth, much less how to prevent or treat it. Now, gene-chip studies of these tiny babies’ umbilical cords provide unexpected, much-needed leads into predicting and treating this debilitating condition.

Keywords: gene-chip, studies, provide, leads, treating, lung, disease, premature, newborns, gene, chip, study, lead, newborn

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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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Model found to determine cause, possible treatment of nerve tumors
02-04-2008 · EurekAlert!
A multi-institutional study led by Cincinnati Children's Hospital Medical Center has led to new insights and a model to help unravel the cause of fibrous, noncancerous nerve tumors called neurofibromas, which can lead to disfigurement and in rare cases death by compressing vital organs. Writing for the February Cancer Cell, researchers said their findings also provide a way to test therapies that could eventually help patients with limited options for treating the disease -- Neurofibromatosis type 1.
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Type of stem cell found to reside in transplanted lungs
03-08-2007 · EurekAlert!
A new study involving a type of stem cells from the lungs of transplant patients demonstrates for the first time that these progenitor cells reside in adult organs and are not derived from bone marrow, which leads to the possibility that the cells may be able to help with the rejection of donated organs and with various kinds of lung disease.
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Einstein researchers discover important clue to the cause of Parkinson's disease
01-02-2008 · EurekAlert!
A glitch in the mechanism by which cells recycle damaged components may trigger Parkinson's disease, according to a study by scientists at the Albert Einstein College of Medicine of Yeshiva University. The research, which appears in the Jan. 2 advance online issue of the Journal of Clinical Investigation, could lead to new strategies for treating Parkinson's and other neurodegenerative diseases.
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Loss of stem cells correlates with premature aging in animal study
06-06-2007 · EurekAlert!
Researchers at the Abramson Family Cancer Research Institute of the University of Pennsylvania have found that deleting a gene important in embryo development leads to premature aging and loss of stem cell reservoirs in adult mice. This gene, ATR, is essential for the body's response to damaged DNA, and mutations in proteins in the DNA damage response underlie certain types of cancer and other disorders in humans.
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Massive microRNA scan uncovers leads to treating muscle degeneration
10-17-2007 · EurekAlert!
An increasing number of genes have been linked to muscular dystrophy and related disorders that cause muscle weakness and wasting, but it's still largely unknown how these genes cause disease, and, more importantly, how to translate the discoveries into treatments. A report in PNAS this week finds a wealth of new clues about how muscle function is regulated by analyzing microRNAs -- tiny bits of code that govern gene expression.
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Lupus gene finding prompts call for more DNA samples
12-02-2007 · EurekAlert!
Wellcome Trust researchers have identified a key gene involved in the disease lupus, which affects around 50,000 people in the UK, mostly women. The lead researcher behind the study has called for more patients to volunteer DNA samples to enable them to further study the underlying causes of the disease.
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Genetic diversity of European Americans and disease gene mapping
01-17-2008 · EurekAlert!
In a recent study, published in the open-access journal PLoS Genetics, an international team of researchers provide the first genetic dissection of the population structure of European Americans, focusing on identifying the contributions from different genetic ancestries that are important for disease gene mapping.
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Enhanced DNA-repair mechanism can cause breast cancer
10-15-2007 · EurekAlert!
Although defects in the "breast cancer gene," BRCA1, have long been known to increase the risk for breast cancer, exactly how the defects lead to tumor growth has remained a mystery. Now scientists provide insight into how the normal BRCA1 gene suppresses the growth of tumors as well as the nature of the genetic instability that leads to cancer when BRCA1 is defective.
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Data presented at ISHLT meeting confirm RNA analysis can identify rejection in lung transplant recip
04-27-2007 · EurekAlert!
Recent data from the Lung Allograft Rejection Gene expression Observational study provides compelling evidence that profiling gene expression in peripheral blood can detect organ rejection in lung transplant patients. Refining the Identification of Discriminatory Genes for Rejection in Lung Transplantation: The LARGO Study will be presented today by Shaf Keshavjee, M.D., chair, Division of Thoracic Surgery, University of Toronto, and LARGO study lead, at the 27th annual Meeting and Scientific Sessions of the International Society for Heart and Lung Transplantation.
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