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Vol. LXI, No. 22
October 30, 2009
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Digest

Scientists Discover Protein Receptor for Carbonations

NIH scientists report that the
NIH scientists report that the
taste of carbonation is initiated by an enzyme tethered like a small flag from the surface of soursensing cells in taste buds.

How do people taste the carbonation bubbling in their glass? In the Oct. 15 issue of Science, researchers at the National Institute of Dental and Craniofacial Research and their colleagues from the Howard Hughes Medical Institute at the University of California, San Diego, report that they have discovered the answer in mice, whose sense of taste closely resembles that of humans.

They found that the taste of carbonation is initiated by an enzyme tethered like a small flag from the surface of sour-sensing cells in taste buds. The enzyme, carbonic anhydrase 4, interacts with the carbon dioxide in the soda, activating the sour cells in the taste bud and prompting it to send a sensory message to the brain, where carbonation is perceived as a familiar sensation.

“Of course, this raises the question of why carbonation doesn’t just taste sour,” says Dr. Nicholas Ryba, a senior author of this study and an NIDCR scientist.“We know that carbon dioxide also stimulates the mouth’s somatosensory system. Therefore, what we perceive as carbonation must reflect the combination of this somatosensory information with that from taste…What people taste when they detect the fizz and tingle on their tongue is a combination of the activation of the taste receptor and the somatosensory cells. That’s what gives carbonation its characteristic sensation.”

Retroviral Link to Chronic Fatigue Syndrome Discovered

Scientists have discovered a potential retroviral link to chronic fatigue syndrome, known as CFS, a debilitating disease that affects millions of people in the United States. Researchers from the Whittemore Peterson Institute (WPI), located at the University of Nevada, Reno, the National Cancer Institute and the Cleveland Clinic reported this finding in the Oct. 8 issue of Science.

“We now have evidence that a retrovirus named XMRV is frequently present in the blood of patients with CFS. This discovery could be a major step in the discovery of vital treatment options for millions of patients,” said Dr. Judy Mikovits, director of research for WPI and leader of the team that found this association. Researchers cautioned, however, that this finding shows there is an association between XMRV and CFS but does not prove that XMRV causes CFS.

The scientists provide a new hypothesis for a retrovirus link with CFS. XMRV was first identified by Dr. Robert H. Silverman of the Cleveland Clinic Lerner Research Institute in men who had a specific immune system defect that reduced their ability to fight viral infections.

“The discovery of XMRV in two major diseases, prostate cancer and now chronic fatigue syndrome, is very exciting. If cause-and-effect is established, there would be a new opportunity for prevention and treatment of these diseases,” said Silverman, a coauthor on the CFS paper. Commonality of an immune system defect in patients with CFS and prostate cancer led researchers to look for the virus in their blood samples.


RNA Strand May Help Predict Survival, Response to Liver Cancer Treatment

A small RNA molecule, known as a microRNA, may help physicians identify liver cancer patients who, in spite of their poor prognosis, could respond well to treatment with a biological agent called interferon. The finding, by scientists at NCI and their partners at Fudan University, Shanghai, and the University of Hong Kong in China and at Ohio State University, appeared in the Oct. 8 issue of the New England Journal of Medicine.

“Interferon is an experimental therapeutic agent that has been used for many years to treat cancer patients, but with modest benefit,” said study first author Dr. Junfang Ji of NCI’s liver carcinogenesis section.

“Our findings are exciting because we are rediscovering a drug that may have great potential for patients with a particular genomic profile. Being able to treat patients with an existing drug based on a tumor’s genomic profile should improve its efficacy and reduce the cost of treatment,” added study senior author Dr. Xin Wei Wang, chief of the liver carcinogenesis section.

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