Story ideas from the Proceedings of the National Academy of Sciences

PNAS tipsheet for November 2-6

ARTICLE HIGHLIGHTS

• The disappearing glaciers of Kilimanjaro
• Designer cells may help protect the body from itself
• Genetic component of metabolic syndrome

ALSO OF INTEREST

• Cooperative social behavior in man-eating lions
• Improving spinal cord injury recovery
• Sleep likely consolidates observational learning

The glaciers atop Mt. Kilimanjaro continue to shrink in size and depth and could disappear completely in the next two decades, researchers suggest. Lonnie Thompson and colleagues say that warmer temperatures, along with drier and less cloudy conditions than in the past, are contributing to sublimation and melting of the glaciers atop the Tanzanian mountain. The researchers combined measurements of ice area from aerial photographs and ground measurements of ice thickness change to determine how fast the ice is disappearing. They calculate that the total area of the ice fields has shrunk by nearly 85 percent between 1912 and 2007. If current conditions persist, the ice could disappear as early as 2022, or as late as 2033. The authors suggest that, in addition to the observed atmospheric changes, warmer temperatures due to climate change are likely another significant factor in the ice shrinkage on Kilimanjaro, as well as other equatorial glaciers worldwide. Although Kilimanjaro's ice fields have survived 11,700 years, including historical drought and other climate changes, without mitigating action, current conditions could wipe out the glaciers and significantly impact the local communities in Africa, according to the authors.

Article #09-06029: "Glacier loss on Kilimanjaro continues unabated," by L. G. Thompson, H. H. Brecher, E. Mosley-Thompson, D. R. Hardy, and B. G. Mark

MEDIA CONTACT: Lonnie Thompson, Byrd Polar Research Center and School of Earth Sciences, Ohio State University, Columbus, OH; tel: 614-292-6652; e-mail: thompson.3@osu.edu

Images accompanying this article are available.

Engineering regulatory cells in the body's defense system could allow researchers to dampen an overactive autoimmune response in a targeted fashion and reduce the need for drugs that suppress the entire immune system. Hans Stauss and colleagues investigated two strategies to design regulatory T cells capable of reducing inflammation regardless of the initial trigger. In one cohort of laboratory experiments, the researchers used gene transfer to generate regulatory T cells with defined specificity. For the second population, the authors switched the specificity of normal T cells and empowered them with regulatory function. The researchers then studied the immune dampening effectiveness of the engineered regulatory T cells with a mouse model of arthritis, in which the cells were intravenously injected into the animals. The engineered regulatory T cells accumulated at the site of arthritis, where the cells suppressed inflammation and bone destruction. The speed of the engineering process and the cells' ability to reduce the body's inflammatory response make the method potentially useful for a wide range of autoimmune diseases that currently rely on systemic immune suppression, according to the authors.

Article #09-07396: "Adoptive therapy with redirected primary regulatory T cells results in antigen-specific suppression of arthritis," by Graham P. Wright, Clare A. Notley, Shao-An Xue, Gavin M. Bendle, Angelika Holler, Ton N. Schumacher, Michael R. Ehrenstein, and Hans J. Stauss

CONFLICT OF INTEREST REPORTED: HJS is a consultant for Cell Medica.

MEDIA CONTACT: Hans Stauss, University College London, Royal Free Hospital, London, UNITED KINGDOM; tel: +44-207-794-0500 ext 33321; e-mail: h.stauss@medsch.ucl.ac.uk

Researchers suggest that expression levels of a particular gene variant may be involved with "metabolic syndrome," a disorder characterized by multiple, simultaneous symptoms, including insulin resistance, high blood pressure, and obesity. Oliver Smithies and colleagues hypothesized that variants of a gene called PPAR[gamma] might play a role in the increasingly common ailment, which can lead to coronary artery disease, stroke, and type 2 diabetes. Previous research had found that PPAR[gamma] regulates the development of fat cells and fat metabolism, and drugs that activate the gene make people more sensitive to insulin. The researchers genetically engineered a series of mice with varying levels of the gene expression and found that animals with PPAR[gamma] levels approximately 30 percent less than normal had higher blood pressure than unaltered mice. Conversely, mice with increased levels of the gene expression had lower blood pressure. The authors suggest that varying levels of some versions of the PPAR[gamma] gene in humans may increase the risk for high blood pressure and thus heart disease.

Article #09-09657: "Genetic variations in PPAR[gamma] expression affect blood pressure," by Yau-Sheng Tsai, Lonquan Xu, Oliver Smithies, and Nobuyo Maeda

MEDIA CONTACT: Oliver Smithies, Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC; tel: 919-966-6913 (day), 919-933-1160 (evening); e-mail:jenny_langenbach@med.unc.edu or nobuyo@med.unc.edu

Cooperative social behavior in man-eating lions

Isotopic evidence from the Tsavo man-eating lions in 19th century Africa reveals the extent of the animal's human depredation, and suggests that the behavior likely resulted from the lion's physical infirmity combined with environmental and anthropogenic stressors.

Article #09-05309: "Cooperation and individuality among man-eating lions," by Justin D. Yeakel, Bruce D. Patterson, Kena Fox-Dobbs, Mercedes M. Okumura, Thure E. Cerling, Jonathan W. Moore, Paul L. Koch, and Nathaniel J. Dominy

MEDIA CONTACT: Justin Yeakel, Department of Ecology and Evolutionary Biology, University of California, Santa Cruz, CA; tel: 831-459-5088 (day), 330-280-0320 (evening); e-mail: jdyeakel@gmail.com

IMAGES ACCOMPANYING THIS ARTICLE ARE AVAILABLE

A minimally invasive system to deliver a bacterial enzyme called chondroitinase ABC could help reduce scars at the site of injury and enhance recovery after spinal cord damage.

Article #09-05437: "Sustained delivery of thermostabilized chABC enhances axonal sprouting and functional recovery after spinal cord injury," by Hyunjung Lee, Robert J. McKeon, and Ravi V. Bellamkonda

MEDIA CONTACT: Ravi Bellamkonda, Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA; tel: 404-385-5038; e-mail: ravi@bme.gatech.edu

Immediate sleep after observing and learning a motor skill can improve memory and performance of the task in athletes, children, and patients having to re-master skills following stroke or injury.

Article #09-01320: "Learning by observation requires an early sleep window," by Ysbrand D. Van Der Werf, Els Van Der Helm, Menno M. Schoonheim, Arne Ridderikhoff, and Eus J.W. Van Someren

MEDIA CONTACT: Ysbrand Van der Werf, Department of Sleep and Cognition, Netherlands Institute for Neuroscience, Amsterdam, NETHERLANDS; tel: +31-20-444-0737 (day), +31-20-566-5500 (evening); e-mail: yd.vanderwerf@vumc.nl