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Food Crisis And Global Health Workshop July 14-16
The worldwide economic downturn has exacerbated a global food crisis that started in 2007, leading to a significant increase in the number of people who are malnourished. The Institute of Medicine will convene top experts at a three-day workshop to explore the implications of the food crisis on nutrition and health. Participants will discuss the effects of the economic crisis and escalating food prices on nutrition, country and global responses, U.S. policies, and actions to mitigate food crises now and in the future. Speakers include representatives from the World Bank, World Food Program, UN Task Force on Global Food Security Crisis, academic health centers, and organizations from Bangladesh, China, Ethiopia, Kenya, Mexico, and other countries.
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IRIN Examines Efforts To Improve Sleeping Sickness Dectection
IRIN examines the efforts of the Geneva-based Foundation for Innovative New Diagnostics (FIND) to develop less costly surveillance equipment to improve the ability to detect the parasitic disease trypanosomiasis (sleeping sickness) in endemic countries. Though "trypanosomiasis can be cured within a week of hospitalization," left undetected, the disease advances, making it treatable only by medication that "can be toxic in up to 10 percent of patients," according to Joseph Ndung"u, head of FIND"s trypanosomiasis program.
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New Technology A Dead Cert For Improved Scientific Results
New technology that identifies and removes dead and dying cells from cell populations grown in laboratories is now available to UK scientists. Removing such cells increases the efficiency of growing healthy cells and can yield clearer experimental results in a broad range of life science fields. The kits - called Dead Cert - developed by Edinburgh based ImmunoSolv, are the first of their kind to effectively remove both dead and dying cells without trauma to living cells.
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A Cancer Gene Switch For Repairing Damaged DNA

Scientists at the Medical Research Council Laboratory of Molecular Biology uncover how an important cancer gene, BRCA1, works by increasing the accuracy with which broken DNA is repaired. Women who inherit a faulty version of the BRCA1 gene are at a higher risk of developing breast or ovarian cancer. In a research paper appearing in Nature on 21 May, Dr Kevin Hiom and Dr Maximina H. Yun from the Cambridge laboratory describe how an important cancer gene, BRCA1, works by increasing the accuracy with which broken DNA is repaired and thus reducing the risk of cancers developing. Mutations in the BRCA1 gene are associated with a significant increase in breast cancer risk and with the onset of ovarian cancer. By studying the interaction between BRCA1 and a protein called CtIP, the scientists discovered a switch that causes DNA breaks to be repaired using another identical piece of DNA as a template. Using the template makes sure the correct genetic sequence is restored without mistakes, thereby reducing the chance of introducing harmful mutations. Lead author Dr Hiom said: "Our findings help us to understand of how breaks in DNA strands can be repaired in a way that preserves our genetic code so that harmful mutations, which may lead to cancer, are kept to a minimum. We use chicken cells because they repair their DNA in a similar way to humans. Also we can easily create cells lacking different factors involved in DNA repair to study in the laboratory what happens when these factors are missing." "Up to now, it was unclear how this accurate mechanism for repairing DNA breaks is turned on so we are very pleased with the result." Cancer is caused by alterations in the sequence of the genetic material DNA. These mutations often arise when DNA becomes damaged, for example, through the generation of DNA breaks. Sometimes this damage is repaired accurately to restore the original DNA sequence and other times it is repaired inaccurately to produce a mutation. Together BRCA1 and CtIP act on broken ends to enable the reconstitution of one strand of a DNA helix to generate a region of single-stranded DNA. The generation of this single stranded DNA tail, which becomes the template for repair, is a critical step in the initiation of accurate DNA repair. By promoting the interaction of BRCA1 with CtIP it might be possible to increase the levels of accurate DNA repair and reduce the frequency of cancer causing mutations. The Medical Research Council


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