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UVa researchers restore genes in human inner ear cells
06-14-2007 · EurekAlert!Researchers at the University of Virginia Health System have discovered a way to transfer genes, which they hope will restore hearing, into diseased tissue of the human inner ear. This important step brings scientists closer to curing genetic or acquired hearing loss.
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Keywords: uva, researchers, restore, genes, human, inner, ear, cells, researcher, gene, cell
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- Critical hearing gene helps send auditory messages to brain
10-19-2006 · EurekAlert!
By studying a gene earlier linked to deafness in humans, researchers now have new insight into the molecular process by which components of the inner ear send messages to the brain. The team reports its findings in the Oct. 20, 2006, issue of the journal Cell, published by Cell Press.
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- MIT Team finds new mechanism of gene control
07-12-2007 · Massachusetts Institute of Technology (MIT)
Biologists have long thought that a simple on/off switch controls most genes in human cells. Flip the switch and a cell starts or stops producing a particular protein. But new evidence suggests that our genes are more ready for action than previously thought.
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- Can you hear me now? Stem cells enhance hearing recovery
06-25-2007 · EurekAlert!
Researchers have shown that bone marrow stem cells injected into a damaged inner ear can speed hearing recovery after partial hearing loss. The related report by Kamiya et al, "Mesenchymal stem cell transplantation accelerates hearing recovery through the repair of injured cochlear fibrocytes," appears in the July issue of The American Journal of Pathology.
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- Reactivating a critical gene lost in kidney cancer reduces tumor growth
08-15-2007 · EurekAlert!
Researchers at Mayo Clinic Jacksonville, have found that a key gene is often "silenced" in clear cell renal cell carcinoma, the most common type of kidney cancer, and when they restored that gene in human kidney cancer cells in culture and animal experiments, tumors stopped growing and many disappeared.
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- Study shows isolation of stem cells may lead to a treatment for hearing loss
04-05-2007 · EurekAlert!
Members of the National Center for Regenerative Medicine research team, Dr. Robert Miller and Dr. Kumar Alagramam, both of Case Western Reserve University School of Medicine, published research findings in Developmental Neuroscience which suggest new ways of treating hearing loss. These researchers have isolated "cochlear stem cells" located in the inner ear and already primed for development into ear-related tissue due to their proximity to the ear and expression of certain genes necessary for the development of hearing.
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- Researchers discover gene crucial for nerve cell insulation
04-16-2007 · EurekAlert!
Researchers funded by the National Institutes of Health have discovered how a defect in a single master gene disrupts the process by which several genes interact to create myelin, a fatty coating that covers nerve cells and increases the speed and reliability of their electrical signals
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- U of M researchers discover a pathway to turn off immune system cells
01-31-2008 · EurekAlert!
University of Minnesota researchers have discovered a new way to turn genes off in human T cells, a type of white blood cell that helps the immune system fight infections.Turning off genes, through a process known as mRNA decay, is important for regulating the body's immune response after fighting infection. This research could lead to development of new drugs that turn off the immune system in patients with autoimmune diseases -- such as rheumatoid arthritis and lupus.
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- USC-led researchers use stem cells to regenerate parts of teeth
12-20-2006 · EurekAlert!
A multi-national research team headed by USC School of Dentistry researcher Songtao Shi, DDS, PhD, has successfully regenerated tooth root and supporting periodontal ligaments to restore tooth function in an animal model. The breakthrough holds significant promise for clinical application in human patients.
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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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- Researchers discover important tool in understanding differentiation in human embryonic stem cells
10-24-2007 · EurekAlert!
Researchers at the University of Minnesota's Stem Cell Institute have used an existing genetic tool to study how human embryonic stem cells self-renew. The researchers used "knockdown" technology to reduce the expression, and plasmid vectors to increase the expression of oct4, a gene known to be necessary for self renewal. Both procedures resulted in differentiation, but with similar patterns, unlike mouse ES cells that differentiate into a different cell types with oct4 up-and down-regulation.
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