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LEXINGTON, Ky. (Aug. 23, 2011) — Bone marrow transplantation with genetically modified cells may prolong the period of cancer-free survival, suggests a study led by Dr. Vivek Rangnekar, associate director of translational research for the Markey Cancer Center at the University of Kentucky.

LA JOLLA, CA – August 24, 2011 – A team of scientists from The Scripps Research Institute have successfully reengineered an important antibiotic to kill the deadliest antibiotic-resistant bacteria. The compound could one day be used clinically to treat patients with life-threatening and highly resistant bacterial infections.

The results were published in an advanced online issue of the Journal of the American Chemical Society.

GAINESVILLE, Fla. — Rates of HIV have increased in Pakistan's general population, as the virus has spread beyond at-risk groups to women and their children, according to an international team of researchers, including a University of Florida scientist.

The researchers raise concern that the transmission across subgroups into Pakistan's general population may serve as indication that the virus may be spreading into populations within neighboring Afghanistan. The team's epidemiological findings were published in July in the journal PLoS One.

Scientists at Northwestern University report a surprising discovery that offers a possible new route for the treatment of neurodegenerative diseases. In a study of the transparent roundworm C. elegans, they found that a genetic switch in master neurons inhibits the proper functioning of protective cell stress responses, leading to the accumulation of misfolded and damaged proteins.

Pittsburgh, Pennsylvania… A remarkably well-preserved fossil discovered in northeast China provides new information about the earliest ancestors of most of today's mammal species—the placental mammals. According to the paper in Nature, this fossil represents a new milestone in mammal evolution that was reached 35 million years earlier than previously thought, filling an important gap in the fossil record and helping to calibrate modern, DNA-based methods of dating the evolution.

Boston, MA – Ebola virus (EboV) is the cause of sporadic outbreaks of highly fatal infections in Africa that are unpredictable in onset and rapid in progression. There is no effective vaccine or therapy for EboV infection.

In the first study of its kind, researchers have linked a natural global climate cycle to periodic increases in warfare. The arrival of El Niño, which every three to seven years boosts temperatures and cuts rainfall, doubles the risk of civil wars across 90 affected tropical countries, and may help account for a fifth of worldwide conflicts during the past half-century, say the authors. The paper, written by an interdisciplinary team at Columbia University's Earth Institute, appears in the current issue of the leading scientific journal Nature.

August 24, 2011 — (Bronx, NY) — Researchers at Albert Einstein College of Medicine of Yeshiva University ((http://www.einstein.yu.edu/home/default.asp) have helped identify a cellular protein that is critical for infection by the deadly Ebola virus. The findings, published in today's online edition of Nature, suggest a possible strategy for blocking infection due to Ebola virus, one of the world's most lethal viruses and a potential bioterrorism agent.

Researchers have used next generation sequencing to trace the source and explain the spread of the latest (seventh) cholera pandemic. They have also highlighted the impact of the acquisition of resistance to antibiotics on shaping outbreaks and show resistance was first acquired around 1982.

Whole genome sequencing reveals that the particular cholera type responsible for the current pandemic can be traced back to an ancestor that first appeared 40 years ago in the Bay of Bengal. From this ancestor, cholera has spread repeatedly to different parts of the world in multiple waves.

BOSTON, MA (August 24, 2011)—In separate papers published online in Nature, two research teams report identifying a critical protein that Ebola virus exploits to cause deadly infections. The protein target is an essential element through which the virus enters living cells to cause disease.

The spread of Dengue fever in northern Australia may be controlled by a bacterium that infects mosquitoes that harbor the virus, Australian and U.S. researchers report Aug. 25 in two papers published in the journal Nature.

The result grew out of work more than 20 years ago by population biologist Michael Turelli, professor of evolution and ecology at UC Davis, and Ary Hoffmann, now at the University of Melbourne, Australia, who are among the coauthors of one of the new Nature papers.

New York, August 25, 2011 – In the zeal to eliminate dangerous bacteria, it is possible that we are also permanently killing off beneficial bacteria as well, posits Martin Blaser, MD, Frederick H. King Professor of Medicine, professor of Microbiology and chair of the Department of Medicine at NYU Langone Medical Center. His commentary is published in the August 25 edition of the journal Nature.

FINDINGS: Where all of us inherit one copy of each chromosome from each of our two parents, cell lines exist with only a single set, and thus with a single copy of each individual gene, instead of the usual two. Using an unusual human cell line of this type, Whitehead Institute researchers and their collaborators performed a genetic screen and identified a protein used by Ebola virus to gain entry into cells and begin replicating. The discovery may offer a new approach for the development of antiviral therapeutics.

The delivery system for an important class of proteins in the cell membrane can be fully replicated with a mere three components, according to a new study.

A George Mason University researcher team has revealed the specific process by which the HIV virus infects healthy T cells—a process previously unknown. The principal investigator, HIV researcher Yuntao Wu, says he hopes this breakthrough will start a new line on inquiry into how researchers can use this knowledge to create drugs that could limit or halt HIV infection.