Improved Outcomes Software (IOS) today announced the release of GeneLinker(TM) Gold and Platinum 4.6, new versions of the award-winning Gene Expression and Proteomics Analysis Software products. "The new releases are focused primarily on importing and analyzing protein biomarker data, a high priority for many of our customers. For example, we have integrated the Protein Biomarker Package into the latest versions of the products (previously the Protein Biomarker Package required a separate installation). We have also provided improved Proteomics Import Scripts and enabled the import of p-value spectrum data to allow exported p-values from ANOVA experiments to be re-imported, enabling novel visualization of channels that best distinguish between different classes (see Protein Biomarker/Proteomics Examples available on the website)" said Dr. Tom Radcliffe, Chief Scientific Officer of IOS.

Scientists report today in the journal Genome Research that they have successfully cloned and characterized a previously intractable DNA sequence: a 554-kilobase-pair genomic segment near the centromere of the human Y chromosome. This sequence contains eight putatively active genes that could be implicated in sex-associated height differences and gonadal tumor development.

For many years, DNA and proteins have been viewed as the real movers and shakers in genomic studies, with RNA seen as little more than a messenger that shuttles information between the two. But researchers from Whitehead Institute for Biomedical Research and Massachusetts Institute of Technology have discovered that small RNA molecules called microRNAs regulate thousands of human genes--more than one third of the genome's protein-coding regions. In other words, a class of molecule once relegated to the sidelines may be one of the principal players in regulating cellular mechanisms.

Researchers at New York University have developed a model of the intra-cellular mammalian biological clock that reveals how rapid interaction of molecules with DNA is necessary for producing reliable 24-hour rhythms. They also found that without the inherent randomness of molecular interactions within a cell, biological rhythms may dampen over time. These findings appeared in the most recent issue of the Proceedings of the National Academy of Sciences (PNAS). Daniel Forger, an NYU biologist and mathematician, and Charles Peskin, a professor at NYU's Courant Institute of Mathematical Sciences and Center for Neural Science, developed a mathematical model of the biological clock that replicates the hundreds of clock-related molecular reactions that occur within each mammalian cell.

Mutations in mitochondrial DNA (mtDNA) play an important role in the development of prostate cancer, according to research by scientists at Emory University School of Medicine and the University of California, Irvine. The findings are published online this week in the Proceedings of the National Academy of Sciences (PNAS). Mitochondrial DNA, which is separate from nuclear DNA, is found in the hundreds of mitochondria located in the cytoplasm outside of each cell's nucleus. The mitochondria often are called the "powerhouse" of the cell because they produce about 90 percent of the body's energy. John A. Petros, MD, associate professor of urology and pathology at Emory University School of Medicine and the Winship Cancer Institute, and Douglas C. Wallace, PhD, director of the Center for Molecular and Mitochondrial Medicine and Genetics at the University of California, Irvine, sequenced segments of mtDNA from prostate cancer patients and found a variety of mutations, including various mutations in the mtDNA cytochrome oxidase subunit (COI) gene.

For the first time, scientists have found that bacteria can use a Sonar-like system to spot other cells (either normal body cells or other bacteria) and target them for destruction. Reported in the December 24 issue of Science, this finding explains how some bacteria know when to produce a toxin that makes infection more severe. It may lead to the design of new toxin inhibitors. “Blocking or interfering with a bacterium’s “detection” mechanism, should prevent toxin production and limit the severity of infection,” says Michael Gilmore, PhD, lead author of the study, and currently director of research at the Schepens Eye Research Institute and professor of ophthalmology at Harvard Medical School.

When researchers came up with the powerful cocktail of anti-HIV drugs known as highly active antiretroviral therapy (HAART), they hoped they had found a way to finally rid the body of the virus. But they were wrong. The virus instead goes into hiding, dormant and practically undetectable in the body – and impervious to attack. While HAART manages to keep the virus at bay, it’s still quite capable – given the right opportunity – of replicating and wreaking havoc on the body’s immune system. Now, virologists at Jefferson Medical College, led by Roger J. Pomerantz, M.D., professor of medicine, biochemistry and molecular pharmacology and director of the Division of Infectious Diseases and Environmental Medicine at Jefferson Medical College of Thomas Jefferson University in Philadelphia, may have found a way to bring HIV out of hiding. They have shown that an immune cell protein called interleukin-7 (IL-7) can rouse the virus better than previously tried agents, making it vulnerable to drugs and the body’s immune system. If the new technique proves its mettle, the work could lead to improved treatments for HIV infection, and might be a step toward complete viral eradication.