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Researchers Identify Gene That Regulates Tumors In Neuroblastoma
Virginia Commonwealth University researchers have identified a gene that may play a key role in regulating tumor progression in neuroblastoma, a form of cancer usually found in young children. Scientists hope the finding could lead to an effective therapy to inhibit the expression of this gene.
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NEJM Perspective Provides Overview Of Recent Health Reform Action
"Building Momentum as Democrats Forge Health Care Reform," New England Journal of Medicine: In a perspective piece, John Iglehart, a national correspondent for NEJM, reviews recent action on health reform. He discusses industry and provider groups" pledge to reduce spending by $2 trillion over the next 10 years, noting that the groups" pledge was a "recognition that the pace of reform is quickening and they wanted to be a full participant in negotiations." He also addresses congressional action, including discussions of a public insurance option and how lawmakers are attempting to address the cost of reform (Iglehart, NEJM, 5/14).
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New Imaging Technique: Toward Spinal Cord Regeneration?
The axon is a part of the neuron through which nerve impulses are transmitted, and at the end of which is located the synapse, which connects it to another neuron. In the event of a lesion, the axon is the component which must be regenerated in order to restore the connections between the different neurons and re-form the nerve.
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Gladstone Scientists Identify Key Factor That Controls HIV Latency

Scientists at the Gladstone Institutes of Virology and Immunology (GIVI) have found another clue that may lead to eradication of HIV from infected patients who have been on antiretroviral therapy. A real cure for HIV has been elusive because the virus can "hide" in a latent form in resting CD4-T cells. By understanding this "latency" effect, researchers can identify ways to reactivate the virus and enable complete clearance by current or future therapies. Researchers in the laboratory of GIVI Associate Director Eric Verdin, MD have found that methylation of cytosine in the DNA of infected cells is associated with HIV latency and that inhibition of DNA methylation causes the reactivation of latent HIV. These observations offer a potential new strategy for inhibiting HIV latency and reactivating the virus. The discovery was reported in the current edition of PLoS Pathogens. "While HIV-1 latency is likely to be a multifactorial process, we have shown that inhibiting the methylation of the provirus contributes to an almost complete reactivation of latent HIV-1," said lead author Steven E. Kauder. The research team, which also included scientists from the University of Utah and Stockholm"s Karolinska Institute, developed in vitro models of HIV-1 latency in T cells that harbor a full-length HIV genome. The provirus in the cell lines also encoded a fluorescent marker to illuminate HIV-1 transcriptional activity. In addition to finding that DNA methylation is a mechanism of latency, the scientists also discovered that a host protein, called methlyl-CpG binding domain protein 2 (MBD2) binds to the methylated HIV DNA and is an important mediator of latency. "Interfering with methylation greatly potentiates the reactivation of HIV," Kauder said. In this study, the researchers found that the drug 5-aza-2"deoxycytidine (aza-CdR) can inhibit HIV methylation and cause the virus to reactivate. "Combined with other areas of our investigation into HIV latency, this research provides important new knowledge about the process and opens many new pathways for future study," said Dr. Verdin, senior author of the study. The research team included Alberto Bosque and Vicente Planelles of the University of Utah and Annica Lindqvist of Karolinska University. The study was supported by the National Institutes of Health Eric Verdin"s primary affiliation is with the Gladstone Institute of Virology and Immunology, where his laboratory is located and all his research is conducted. He is also professor of medicine at the University of California, San Francisco. Valerie Tucker Gladstone Institutes


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