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Canadian study demonstrates medical induction of labor increases risk of amniotic-fluid embolism

A Canadian population-based cohort study has revealed that medical induction of labor increases the risk of amniotic-fluid embolism. The study was led by Dr. Michael Kramer, Canadian Institutes of Health Research Senior Investigator from McGill University, and will be published in the Oct. 21 issue of the Lancet.

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Keywords: canadian, study, demonstrates, medical, induction, labor, risk, amniotic-fluid, embolism, demonstrate, amniotic, fluid

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1. Canadian study demonstrates medical induction of labor increases risk of amniotic-fluid embollism
   10-19-2006 · EurekAlert!
   A Canadian population-based cohort study has revealed that medical induction of labor increases the risk of amniotic-fluid embolism. The study was led by Dr. Michael Kramer, Canadian Institutes of Health Research Senior Investigator from McGill University, and will be published in the Oct. 21 issue of the Lancet.
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2. Divorce increases risk of Ritalin use
   06-04-2007 · EurekAlert!
   Divorce puts children at higher risk of Ritalin use compared to kids whose parents stay together, says new research by a University of Alberta sociologist, who cautions that this doesn't necessarily mean that divorce is harmful to a child. The study appears in this week's issue of the Canadian Medical Association Journal.
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3. Chronic job strain doubles the risk of a second heart attack
   10-09-2007 · EurekAlert!
   People who experience chronic job strain after a first heart attack double their risk of suffering from a second one, reports a research team from Université Laval's Faculty of Medicine in the Oct. 10 issue of the Journal of the American Medical Association. This study is the first to clearly demonstrate the risks associated with job strain for workers who have been victim of a first heart attack.
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4. 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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5. Study identifies multiple genetic risk factors for prostate cancer
   04-01-2007 · EurekAlert!
   A study led by researchers at the Keck School of Medicine of the University of Southern California and Harvard Medical School has identified seven genetic risk factors that predict risk for prostate cancer. According to the study's findings, these risk factors are clustered in a single region of the human genome on chromosome 8 and powerfully predict a man's probability of developing prostate cancer.
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6. Researchers develop criteria to detect bone mass deficiencies in children with chronic diseases
   06-06-2007 · EurekAlert!
   Pediatricians now have a practical tool to help determine whether children with chronic diseases like Crohn's, juvenile arthritis and anorexia nervosa -- or those undergoing cancer treatment -- are at increased risk for bone mass deficiencies, fracture or osteoporosis as they get older, according to a new study whose lead author is a researcher at Cincinnati Children's Hospital Medical Center.
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7. It's not too late to change -- lowering cardiac risk later in life
   06-28-2007 · EurekAlert!
   Can adopting a healthier lifestyle later in life help -- or is it too late? In a study published in the July 2007 issue of the American Journal of Medicine, researchers from the Medical University of South Carolina, Charleston found that people 45 to 64 years of age who added healthy lifestyle behaviors could substantially reduce their risk for cardiovascular disease and reduce their death rate.
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8. Older women with memory problems at increased risk for restless nights
   07-16-2007 · EurekAlert!
   Older women experiencing memory loss are more likely than women without cognitive decline to have problems falling asleep and staying asleep, according to a study published in the July 17, 2007, issue of Neurology, the medical journal of the American Academy of Neurology.
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9. Overweight toddlers and those not in day care at risk for iron deficiency
   09-04-2007 · UT Southwestern Medical Center
   A study by UT Southwestern Medical Center researchers has found that overweight toddlers and those not enrolled in day care are at high risk for iron deficiency.
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10. Eating fish, omega-3 oils, fruits and veggies lowers risk of memory problems
    11-12-2007 · EurekAlert!
    A diet rich in fish, omega-3 oils, fruits and vegetables may lower your risk of dementia and Alzheimer's disease, whereas consuming omega-6 rich oils could increase chances of developing memory problems, according to a study published in the Nov. 13, 2007, issue of Neurology, the medical journal of the American Academy of Neurology.
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