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Study begins to reveal clues to the cause and progression of sepsis

08-13-2007 · EurekAlert!

Not all patients with sepsis mount the same immune response, even when they look the same clinically, according to findings from the first large-scale natural history study of sepsis. The results, published by University of Pittsburgh School of Medicine researchers in the Aug. 13/27 issue of the Archives of Internal Medicine, indicate that past interpretations of how the immune system responds to infection -- interpretations on which many experimental treatments were based -- were incorrect.

Keywords: study, begins, reveal, clues, cause, progression, sepsis, begin, clue, sepsi

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Brain structure changes years before memory loss begins
04-16-2007 · EurekAlert!
People who develop dementia or Alzheimer's disease experience brain structure changes years before any signs of memory loss begin, according to a study published in the April 17, 2007, issue of Neurology, the scientific journal of the American Academy of Neurology. Researchers say these findings may help identify people at risk of developing mild cognitive impairment, which leads to Alzheimer's disease.
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New Nationwide Study Will Evaluate Effect Of Antioxidants And Fish Oil On Progression Of AMD
10-12-2006 · ScienceDaily
The National Institutes of Health (NIH) has announced a nationwide study to see if a modified combination of vitamins, minerals, and fish oil can further slow the progression of vision loss from AMD, the leading cause of vision loss in the United States for people over age 60.
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Study Offers New Clues to Brain-Stomach Interaction in Overeating
10-02-2006 · Brookhaven National Laboratory
Researchers at Brookhaven have found new clues to how the brain and the stomach interact with emotions to cause overeating and obesity. By looking at how the human brain responds to "fullness" messages sent to the brain, the scientists have identified brain circuits that motivate the desire to overeat in the obese - the same circuits that cause addicted individuals to crave drugs.
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Flawed Stem Cells Yield Fragile X Clues: Researchers study genetic disorder via discarded embryos
11-17-2007 · Science News Online
The most common inherited cause of mental retardation arises when a mutated gene is shut down early in embryonic development.
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Largest study to investigate risk factors of autism to begin enrolling families
11-14-2007 · EurekAlert!
Researchers from Kaiser Permanente and the Centers for Disease Control and Prevention, as well as from five other sites nationwide, today will begin enrolling thousands of families in the largest study to date investigating the genetic and environmental factors that may cause autism and other developmental disabilities. Researchers hope the study will contribute to better services and treatments, and to prevention strategies. Autism affects about one in 150 children born in the US.
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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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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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Yale study offers insight into possible cause of lymphoma
02-14-2008 · EurekAlert!
The immune system's powerful cellular mutation and repair processes appear to offer important clues as to how lymphatic cancer develops, Yale School of Medicine researchers report this week in Nature.
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DNA clues to inform conservation in Africa
05-22-2007 · EurekAlert!
Tracing the evolutionary history of wildlife could improve global habitat conservation, a major Cardiff University study has found. Researchers in the School of Biosciences analysed the African bushbuck -- a common species which lives in most sub-Saharan habitat types -- to test whether DNA similarity between populations living in different habitats can reveal the similarity of those ecoregions now and in the past.
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UT Southwestern participating in nationwide study on leading cause of vision loss for seniors
10-24-2006 · EurekAlert!
UT Southwestern Medical Center is participating in a nationwide study investigating whether modified combinations of vitamins, minerals and fish oil products can slow the progression of vision loss from age-related macular degeneration.
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