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New lab mice pave way for novel studies of human infection

10-22-2006 · EurekAlert!

A new type of laboratory mouse developed at UT Southwestern Medical Center can fight certain infections the same way humans do, making the rodents very useful for novel studies of human-pathogen interaction and developing disease therapies.

Keywords: lab, mice, pave, way, novel, studies, human, infection, study

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New lab mice pave way for novel studies of human infections
10-23-2006 · UT Southwestern Medical Center
A new type of laboratory mouse developed at UT Southwestern Medical Center can fight certain infections the same way humans do, making the rodents very useful for novel studies of human-pathogen interaction and developing disease therapies.
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Genetic 'roadblock' hoped to inspire future type 2 diabetes research
10-02-2007 · EurekAlert!
A team of Mount Sinai Hospital researchers has found that a 'genetic roadblock' identified in a recent study could pave the way toward novel treatments for type 2 diabetes. In the study, researchers from the Samuel Lunenfeld Research Institute of Mount Sinai Hospital found the first genetic evidence that the elimination of the gene for glycogen synthase kinase-3 in mice sensitizes the animals to insulin.
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Stanford researchers identify immune dysfunction in melanoma patients
05-07-2007 · EurekAlert!
Researchers at Stanford have begun to shed light on why the human immune system isn't able to stop such cancers as melanoma, suggesting answers that could pave the way for better treatment of this often-fatal illness. In a small study, the scientists found that the immune cells in a majority of people with this deadly skin cancer fail to respond properly to a molecule called interferon, which normally activates the immune system.
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Dietary copper may ease heart disease
03-05-2007 · EurekAlert!
Including more copper in your everyday diet could be good for your heart, according to scientists at the University of Louisville Medical Center and the USDA Human Nutrition Research Center. Their studies show that giving copper supplements to mice eased the stress on their over-worked hearts by preventing heart enlargement. The study will be published online on March 5 in the Journal of Experimental Medicine.
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T for two: Scientists show how immune system chooses best way to fight infection
11-14-2006 · EurekAlert!
A new study has suggested a novel way of combating diseases related to the immune system, including cancer and autoimmune diseases such as type I diabetes and arthritis. The study, funded by the Wellcome Trust, appears online in the journal Nature.
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New culture method for hepatitis C virus uses primary hepatocytes and patient serum
01-23-2007 · EurekAlert!
Researchers open the way for improved study of hepatitis C virus by devising a novel virus culture system that allows replication of patient-isolated virus in nontransformed hepatocytes, instead of culture-adapted virus strains in transformed cell lines. The related report by Lázaro et al, "Hepatitis C virus replication in transfected and serum-infected cultured human fetal hepatocytes," appears in the February issue of the American Journal of Pathology.
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Altering a protein makes mice less fearful
08-01-2007 · EurekAlert!
A University of Iowa study shows that loss or chemical inhibition of a protein, known as acid sensing ion channel protein, reduces innate fear behavior in lab animals, making normally timid mice relatively fearless. The findings might provide useful insight into anxiety disorders, and may even point the way to a new therapeutic target.
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UCLA AIDS Institute researchers find a peptide that encourages HIV infection
05-10-2007 · EurekAlert!
UCLA AIDS Institute researchers have discovered that when a crucial portion of a peptide structure in monkeys that defends against viruses, bacteria and other foreign invaders is reversed, the peptide actually encourages infection with HIV. The findings, published in the April issue of AIDS Research and Human Retroviruses, could pave the way for the use of such peptides in gene therapy using HIV-based vectors as the delivery method.
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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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'Electronic switch' opens doors in rheumatoid joints
01-02-2008 · EurekAlert!
A breakthrough in understanding the way atoms move across cell membranes in the human body could pave the way for the development of new treatments for inflammatory diseases such as rheumatoid arthritis.
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