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Health
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Written by ANI
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Thursday, 23 October 2008 |
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Washington, Oct 23 (ANI): Scientists have selectively and safely managed to remove new and old memories from mice, says a new study. In the collaborative study, researchers were able to eliminate new and old memories alike by over-expressing a protein, called aCaMKII, critical to brain cell communication just as the memory was recalled. "While memories are great teachers and obviously crucial for survival and adaptation, selectively removing incapacitating memories, such as traumatic war memories or an unwanted fear, could help many people live better lives," said Dr. Joe Z. Tsien, brain scientist and co-director of the Brain and Behavior Discovery Institute at the Medical College of Georgia School of Medicine. He added: "Our work reveals a molecular mechanism of how that can be done quickly and without doing damage to brain cells." Already, Tsien had created a mouse that couldn't form memories by eliminating the NMDA receptor, which receives messages from other neurons. He then made "Doogie," a smart mouse in which a subunit of the NMDA receptor is over-expressed. In the current study, the researchers focussed on downstream cascades of the NMDA receptor to learn more about memory formation, and they closed in on aCaMKII protein in the brain, as it's a major signaling molecule for the NMDA receptor. He found that when he over-expressed aCaMKII while a memory was being recalled, that single memory was eliminated. "Learning changes the way cells connect to each other," says Tsien. To form a memory, the NMDA receptor is activated, which results in the insertion of AMPA receptors into those synapses and subsequent strengthening of the synaptic connections among hundreds of thousands of neurons. Scientists believe that aCaMKII plays an important role in the insertion of AMPA receptors into synapses during learning and subsequent strengthening of connections between neurons to create a memory. While previous technology would have taken several days to switch off the protein, the researchers developed a powerful chemical-genetic method that allows him to use a pharmacologic inhibitor to instantly turn aCaMKII off and on in a mouse that he genetically engineered to over express this signaling molecule. That enabled him to study exactly what happened if he threw off the natural balance during the retrieval stage. While the ability to rapidly erase a selective memory is exciting, Tsien cautioned that its translation to humans would be difficult at this stage. A possible strategy for humans would be a drug that mimics the aCaMKII over expression that researchers accomplished through genetic manipulation. Or, further downstream substrates that aCaMKII acts upon could become possible drug targets. The study is published on the cover of the recent issue of Neuron. (ANI)
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Last Updated ( Thursday, 23 October 2008 )
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Written by ANI
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Thursday, 23 October 2008 |
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London, Oct 23 (ANI): Tried every possible way to shed those extra pounds but unable to get results? Well, a new weight loss drug may address the problem effectively. The powerful new drug, known as tesofensine, which was originally developed as a treatment for Parkinson's and Alzheimer's disease, can help users shed two stones in six months. It is twice as effective as current treatments and can see overweight patients lose up to 10 per cent of their body weight quickly. In tests, obese patients given the medication daily for 24 weeks lost around two stones in weight. Tesofensine targets chemicals in the brain to suppress hunger, helping patients to overcome the temptation to over-eat. Researchers said that It was 'very effective' as a weight-loss drug, and further tests are being conducted. "If we could treat obesity like we treat high blood pressure, with safe, effective and affordable drugs, this would be an enormous boon to health care," the Daily Express quoted Professor Steve O'Rahilly, of Cambridge University, as saying. The number of prescriptions for slimming pills passed the one million mark last year, but there has been concern that those currently available on the NHS do not help patients lose enough weight. Research suggests the new drug is five times more effective than going on a diet and taking a dummy pill, and up to twice as effective as a diet combined with current weight-loss pills. If further tests prove tesofensine to be safe, it could be licensed within three years. The report's authors, led by Professor Arne Astrup, of the University of Copenhagen, concluded: "This phase two study shows that the drug tesofensine is very effective in producing weight loss in patients over six months." According to the research, current side-effects of tesofensine include nausea and bowel problems. The findings are published in The Lancet Online. (ANI)
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Last Updated ( Thursday, 23 October 2008 )
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Written by ANI
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Thursday, 23 October 2008 |
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London, Oct 23 (ANI): An international team of researchers have identified as many as 26 genes that are frequently mutated in the most common form of lung cancer, thus opening up avenues for developing new therapies for treating the disease. The researchers looked at nearly 200 patients with lung adenocarcinoma and decoded or sequenced the DNA of several hundred genes that are known to or are suspected to be involved in cancer development. By scanning the tumour genomes, they identified several abnormally active as well as silent genes. The team was able to pinpoint more than 1,000 genetic alterations - the majority of which had not been previously known. For example, the NF1, ATM, RB1 and APC genes, which were previously not linked to lung cancer, were mutated in a significant portion of the lung tumors analysed. These genes have been implicated in other tumour types, suggesting roles in multiple forms of cancer. The scientists also found genetic ties to a critical class of genes known as tyrosine kinases. Kinases are known to promote cell growth. In lung tumours, the researchers found mutations in several groups of related tyrosine kinase genes, including the EGF, EPH, FGF, NTRK, and VEGF receptor gene families. "In recent years, there's been some important successes for targeted therapies for some types of lung cancer," Nature quoted co-senior author Matthew Meyerson, a senior associate member of the Broad Institute of MIT and Harvard and an associate professor at Dana-Farber Cancer Institute and Harvard Medical School, as saying. "This work helps identify new targets that might show promise for treating broader groups of lung cancer patients." "One of the key findings from our study is that some of the newly discovered genes and pathways that are mutated in lung cancer are also known to be defective in other cancers. "That gives us hope that targeted therapies could be used across multiple cancer types," he added. The study is published in journal Nature. (ANI)
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Last Updated ( Thursday, 23 October 2008 )
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Written by ANI
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Thursday, 23 October 2008 |
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Washington, Oct 23 (ANI): Researchers from University of Minnesota have identified certain genetic variations that may help predict survival in cancer patients. A research team led by Brian Van Ness, Ph.D, from Masonic Cancer Centre, University of Minnesota, claim to have identified combinations of genes associated with early clinical relapse of multiple myeloma, a cancer of the white blood cells that produce antibodies, which can help predict patient's response to treatment. "Ultimately, the goal of this research is to predict drug efficacy and toxicity based on a patient's genetic profile, and develop individualized assessments and predictions for the right drug, at the right dose, for the right patient," said Van Ness. "This approach offers the dual benefits of avoiding unnecessary treatment for patients less likely to respond to a particular drug, and targeting treatments to those who will benefit most," he added. For the study, Van Ness and his colleagues analysed the genetic information that the International Myeloma Foundation has gathered from myeloma patients worldwide through its program, Bank On A Cure(r). "Although myeloma is considered a fatal disease, individual patients have widely varied rates of disease progression and response to treatment because of attributes encoded in their DNA," said Van Ness. According to Van Ness, the research study findings demonstrate that cancer outcomes differ because patients vary in the ways they absorb, distribute, metabolize, and transport drugs across cell membranes. Individual variations in genes that regulate these biologic processes may not only affect the effectiveness of the drug, but also can result in adverse side effects. The findings are reported in the current issue of the research journal BMC Medicine. (ANI)
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Last Updated ( Thursday, 23 October 2008 )
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Written by ANI
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Thursday, 23 October 2008 |
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Washington, Oct 23 (ANI): A new study by UC Riverside biochemists has revealed that ingesting apigenin, a naturally occurring dietary agent found in vegetables and fruit, improves cancer cells' response to chemotherapy. The leading cause of death in all cancer patients continues to be the resistance of tumour cells to chemotherapy, a form of treatment in which chemicals are used to kill cells. Now, Xuan Liu, a professor of biochemistry, and Xin Cai, a postdoctoral researcher working in her lab, found that apigenin localizes tumour suppressor p53, a protein, in the cell nucleus - a necessary step for killing the cell that results in some tumour cells responding to chemotherapy. The study provides a novel approach to conquer tumour resistance to chemotherapy, and suggests an avenue for developing safe chemotherapy via naturally occurring agents. Normally, cells have low levels of p53 diffused in their cytoplasm and nucleus. When DNA in the nucleus is damaged, p53 moves to the nucleus where it activates genes that stop cell growth and cause cell death. In this way, p53 ensures that cells with damaged DNA are killed. In many cancers, p53 is rendered inactive by a process called cytoplasmic sequestration. Apigenin is able to activate p53 and transport it into the nucleus, resulting in a stop to cell growth and cell death. "In therapy you want to kill cancer cells. But to stop cell growth and to kill the cell, p53 first needs to be moved to the cell's nucleus to function. Apigenin is very effective in localizing p53 this way," said Cai. Apigenin is mainly found in fruit (including apples, cherries, grapes), vegetables (including parsley, artichoke, basil, celery), nuts and plant-derived beverages (including tea and wine). It has been shown by researchers to have growth inhibitory properties in several cancer lines, including breast, colon, skin, thyroid and leukemia cells. It has also been shown to inhibit pancreatic cancer cell proliferation. "Our study advocates the inclusion of vegetables and fruit in our daily diet to help prevent cancer," said Liu. The study is published this in the online early edition of the Proceedings of the National Academy of Sciences. (ANI)
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Last Updated ( Thursday, 23 October 2008 )
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