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CBI, Children’s Rare Disease Network and Global Genes Task partner for Rare Disease Leadership Summit THE GUTS for Business Cleverness , a division of Advanstar Communications, is very happy to announce a partnership with the Children’s Rare Disease Network and The Global Genes Task for the 6th Annual Rare Disease Leadership Summit approaching July 12 – 13, 2011 at the Doubletree Resort in Washington, D.C how to trat migraine . There is nothing uncommon about rare diseases. They affect few people separately, but there are a lot more than 25 million children and their families in america only that are affected and approximately 250 million people identified as having a rare disease world-wide. Throughout two times of government, advocacy and industry presentations, you shall learn how to ensure access to orphan drug therapies through collaborative efforts with government, researchers and patient organizations. An interview with Dr KazazianLiposomal sizing and the Coulter basic principle: an interview with Professor Melvin E. KlegermanScalable production of gene therapy vectors: an interview with Frank UbagsThe two-day time event features presentations from Amicus Therapeutics, NIH, Viropharma Incorporated, BioGenerator, Pfizer Inc, FDA, Kakkis EveryLife Base, Genetic Alliance UK, Wellness Canada, Keck Graduate Institute, Mobius Therapeutics LCC, CORD, Shire, The Children’s Rare Disease Network and even more. Join us this July for what guarantees to become a thought-provoking and educational opportunity. SOURCE CBI Study, Inc.

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C. Elegans has comparable virus-fighting mechanism as humans and can be utilized in research Researchers in the University of California, Riverside can see that a basic worm, called C. Elegans, makes an excellent experimental sponsor for studying many of the most virulent viruses that infect humans. The researchers published their results in the Aug. 18 problem of the journal Nature in a paper titled, Pet virus replication and RNAi-mediated antiviral silencing in C. Elegans. UCR Professor of Plant Pathology Shou-Wei Ding co-authored the paper with Morris Maduro, associate professor of biology; Feng Li, a graduate student in microbiology; Rui Lu and Hongwei Li, postdoctoral experts in Ding’s laboratory; and research experts Gina Broitman-Maduro and Wan-Xiang Li. Lu and Maduro are co-first authors of this Nature paper. The National Institutes of Health insurance and the U.S. Department of Agriculture supported the extensive analysis. The paper displays a major stage forward in the analysis of how a few of the world’s most virulent viruses, such as for example West Nile, SARS, Hepatitis and Ebola C connect to their hosts. ‘Each one of these viruses are very dangerous and are traditionally studied in animal versions, so large-scale genetic research of the host-virus interaction is very difficult to do,’ said Ding, who works in the Center for Plant Cell Biology at UCR’s Institute for Integrative Genome Biology. ‘Obviously, we are all extremely excited to find that little worm can be used to know how hosts genetically control viruses.’ For a long time researchers throughout the global world have studied C. Elegans because many areas of its biology, such as genetics, development and the workings of neurons, mirror the biology of humans. However, no infections were known to infect the millimeter-long roundworm so it had not been used as a model for learning viral infections. Related StoriesCamels in Kenya infected by MERS virus, new study findsUC Irvine Wellness researchers develop one-step test to detect HCV infectionsBlocking calcium-signaling pathway could inhibit Ebola virus and various other sources of deadly infectionsThe Nature paper now demonstrates UC Riverside researchers have developed a stress of the worm, C. Elegans, in which an animal virus could replicate, allowing them to map the delicate dance of actions and response between virus and web host. The UCR team shows that virus replication in the worm triggers an antiviral response known as RNA silencing or RNA interference . RNAi specifically breaks down the virus’ RNA. Virus RNA creates proteins that allow the virus to function. The virus responds by creating a protein performing as a suppressor of RNAi to shut down the host’s antiviral response. Virus infection didn’t occur when the viral RNAi suppressor was produced inactive by genetic mutations in the sponsor program. C. Elegans’ RNAi program is known as a ‘blanket system,’ and therefore it has parallels in humans, making the worm model found out by Ding and his colleagues a very important tool in studying just how viruses connect to hosts. This tool may acceleration the discovery of remedies for virus-caused diseases that plague humans. ‘The RNAi machinery is quite similar between humans and C. Elegans, and human infections such as for example Influenza A HIV and virus are recognized to produce RNAi suppressors,’ Ding said. ‘So now, the relevant question is can we treat human viral diseases using chemical inhibitors of viral RNAi suppressors? ‘ The techniques outlined in the type paper are now being used to create additional C. Elegans strains for screening chemical substances that inactivate RNAi suppressors associated with avian flu, HIV and others.