Targeting Troublesome T Cells
In type 1 diabetes, renegade Tcells of the immune system kill the insulin-making beta cells of the pancreas. New beta cells could, in theory, cure diabetes, but because the misguided autoreactive Tcells would eventually destroy them as well, stopping the wayward attack is important [see “Insights: Putting Up with Self”; SciAm, December 2006]. Previously, Denise L. Faustman of Harvard Medical School had shown in mice that activating a natural compound in the body called tumor necrosis factor (TNF) could selectively kill the autoreactive Tcells and permit restored beta cell function. The same process can happen with human cells, as she and her colleagues show in a paper published online August 28 by the Proceedings of the National Academy of Sciences USA.
In March an 18-month clinical trial began in which human patients receive a generic tuberculosis drug that stimulates TNF production.
Self-assembly is a key strategy in nanotechnology, and genetically modified viruses are of great help, such as those deployed by Angela M. Belcher of the Massachusetts Institute of Technology [see “The Scientific American 50: Research Leader of the Year”; SciAm, December 2006]. She and her colleagues have now shown that virus-based construction can make the electrodes of a microbattery. First, they etched onto a rubber substrate posts a few microns wide and deposited on them polymer layers that serve as a solid electrolyte. On top of the electrolyte they added a virus modified to produce a protein coat that collects molecules of cobalt oxide. The virus builds up the cobalt oxide into a structure that acts as the negative electrode of a discharging battery. Although the team still has to make the positive end, the partial battery—described in a study published online August 27 by the Proceedings of the National Academy of Sciences USA—displayed full electrochemical functionality. Microbatteries might power labs-on-a-chip, implantable medical devices and other tiny tech.
Slimming Down Brown
Obesity studies strive to reveal the biochemical pathways that create fat cells [see “What Fuels Fat”; SciAm, September 2007]. More fat could be the secret to losing weight—as long as that fat is brown. Unlike the white kind, which rings the abdomen and pockets the hips, brown adipose releases energy and promotes calorie burning. In humans, most brown fat disappears shortly after birth, when it has fulfilled its role of keeping a newborn’s body temperature stable. Two studies in the August 21 Nature describe ways to bring back the brown. Specifically, they describe proteins that control the creation of brown fat cells from immature muscle and white fat cells. Mice given one of the proteins developed more brown fat and became leaner than those that did not receive the protein. Conceivably, a drug version could jump-start a change of white to brown fat cells. Alternatively, brown cells transplanted into an obese person’s abdomen could fuel calorie burning.
That plants can emit methane stunned researchers and sparked controversy over the role of forests in global warming [see “Methane, Plants and Climate Change”; SciAm, February 2007]. Some doubted the real-world relevance of the laboratory findings, but researchers have now demonstrated methane release by plants in a natural setting. Using large plastic chambers to capture emissions, a team finds that grasses on the Tibetan Plateau, such as those shown here, produce methane. Shrubs in the alpine meadow absorbed atmospheric methane, however—a result at odds with lab evidence showing the contrary for lowland shrub species. Study leader Xinquan Zhao of the Northwest Plateau Institute of Biology in Xining, China, says these discrepancies highlight the need to examine each species individually because plants vary in chemical composition and metabolism, which affect their capacity to produce the greenhouse gas. Biology Letters published the study online August 26.
Note: This article was originally published with the title, "Updates".