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Discovery of Taste Receptors May Make Bitter a Bygone Taste

By Wayne Little

It's an old axiom that in life we have to "take the bitter with the sweet." A recent study has shown that humans, as well as rodents, are well equipped to do just that. Scientists have discovered a new family of taste receptors (T2Rs) that may comprise as many as 80 different members, which together help detect different forms of bitter. Why so many? In nature, bitter comes in many shapes, most often associated with poisons, so broad recognition of this taste perception can be critical to an animal's survival. Now that the molecular structure of these receptors is known, scientists may be able to use this knowledge to take the bite out of bitter.

Dr. Nicholas Ryba from the National Institute of Dental and Craniofacial Research and Dr. Charles Zuker from the Howard Hughes Medical Institute and the University of California at San Diego have established a long-term collaboration to investigate the sense of taste. Last year, their groups reported the identification of the first two strong candidate taste receptors: TR1 and TR2. Their work describing and characterizing the new T2R taste receptors is reported in two articles in the Mar. 17 issue of Cell.

According to Ryba, "We now have the means to really start to investigate how taste works, not just in the tongue but also what happens in the brain." Dr. Mark Hoon of NIDCR, a coauthor of the study, adds, "These results significantly enhance our understanding of bitter taste and provide clues about how the sensation of bitter might protect animals from many poisons." Zuker and Ryba are continuing their studies not only to dissect the basis of taste perception but also to identify compounds that might be used to modify the human sensation of bitter.

Gene Tracking Follows Cells from Embryo to Adult

By Wayne Little

In a sense, all teeth can be considered wisdom teeth if their cells of origin are the determining factor. Scientists have developed a sophisticated genetic tracking system that allows them to follow the migration of cells as they stream from the embryonic mouse brain to the developing body, including the primordial jaw where they contribute to the formation of teeth and supporting structures. This is the first time a group of embryonic cells has been "tagged" and followed throughout development to their final destiny.

The research was a collaborative effort of several institutions led by Dr. Yang Chai from the University of Southern California. The study, which appeared in the Mar. 21 issue of Development, was supported in part by the National Institute of Dental and Craniofacial Research.

"This technology allows us to closely follow an important group of cells that contribute not only to formation of the teeth and other craniofacial structures, but also to parts of the developing cardiovascular system," said Chai. "We will soon be able to look at animal models for a variety of human genetic disorders and observe in minute detail the effects on this key cell population. Likewise, we will be able to scrutinize corrective measures such as gene therapy."

Compounds May Be Useful Against Osteoarthritis

By Connie Raab and Kelli Carrington

A systematic analysis of clinical trials on glucosamine and chondroitin sulfate for treating osteoarthritis (OA) has shown that these compounds may have some efficacy against the symptoms of this most common form of arthritis, in spite of problems with trial methodologies and possible biases. The study, by Dr. Timothy E. McAlindon and colleagues at Boston University School of Medicine, published in the Mar. 15 issue of the Journal of the American Medical Association, recommends that additional, rigorous, independent studies be done of these compounds to determine their true efficacy and usefulness.

"About 21 million adults in the United States have OA," said Dr. Stephen Katz, director of the National Institute of Arthritis and Musculoskeletal and Skin Diseases, which funded the study and has helped launch a major clinical trial on the compounds in OA, along with the National Center for Complementary and Alternative Medicine. "Effective treatments are key to improving the quality of life of Americans affected by this common disorder."

OA, also called degenerative joint disease, is caused by the breakdown of cartilage, which cushions the ends of bones within the joint. It is characterized by pain, joint damage and limited motion. It generally occurs later in life, and most commonly affects the hands and large weight-bearing joints such as the knees and hips.

The Boston researchers point out that glucosamine and chondroitin sulfate have received significant media attention and have been used in Europe for OA for over 10 years. The researchers say physicians in the United States and the United Kingdom have been skeptical about these products, probably because of well-founded concerns about the quality of scientific trials conducted to test them. Glucosamine and chondroitin sulfate, which are sold in the U.S. as dietary supplements, are natural substances found in and around the cells of cartilage. Researchers think these substances may help in the repair and maintenance of cartilage.

Arthritis Educators Score High with Patients

By Janet Howard

Arthritis educators can provide a meaningful boost to traditional care for patients with rheumatic diseases, according to a new study reported in Arthritis Care and Research. Teaching and support by trained educators has been proven to have a positive impact on the knowledge and satisfaction with services for patients with arthritis visiting rheumatology clinics.

"People with arthritis are often dissatisfied with their care. We have shown that arthritis patient educators can be a useful addition to traditional rheumatology care," said coauthor Dr. Peter Lipsky, NIAMS scientific director. "We now know for certain that patient education positively affects patient knowledge, disease management and satisfaction with clinic services."

In the study carried out at the University of Texas Southwestern Medical Center in Dallas, one group of patients with arthritis was randomly assigned to an arthritis patient educator as well as standard rheumatologic care. A control group was assigned to receive only the standard care. Both groups completed standard assessment tests.

The results showed that the patients who received the intervention displayed more overall knowledge about their disease than patients who did not. Of this group, 88.5 percent rated the arthritis patient educators "good" or "excellent;" 69 percent found the educators helpful; and 58 percent requested further interactions with the educators. Test group patients were able to name more sources of arthritis information and self-help aids.

Because arthritis is the most costly, chronic and common disease known, the goal of arthritis management has been to minimize pain, inflammation, disability and the psychosocial changes associated with the disease. Currently, arthritis affects over 40 million (15 percent) of the American population, and the number is expected to increase to nearly 20 percent (60 million) by 2020. It is the leading cause of disability in Americans over 65.

Gene Therapy Restores Muscle Function in Dystrophic Hamsters

By Ray Fleming

Scientists supported by NIAMS have used gene therapy to restore muscle function in a hamster model of limb-girdle muscular dystrophy (LGMD), a group of degenerative muscular diseases caused by mutations in the gene for the protein d-sarcoglycan. The work has implications for treating the human forms of this and other muscular dystrophies.

A group of investigators led by NIAMS grantee Dr. Xiao Xiao at the University of Pittsburgh injected a virus vector (adeno-associated virus, or AAV) bearing corrected copies of the gene into a leg muscle of the hamster LGMD model. The result was over 97 percent recovery in muscle strength in the dystrophic animals compared with normal hamsters. Treated animals also regained normal muscle weight and size and showed improvement in muscle cell condition. Furthermore, the treatment conferred protection from muscle loss.

"This work, coupled with other recent advances, signals a brighter day for those with many forms of muscular dystrophy," said NIAMS director Dr. Stephen Katz. "Animal model research like this points to gene therapy as a likely candidate for treating some human muscle diseases."

The study, according to the authors, "is the first report of successful functional rescue of an entire muscle after AAV-mediated gene delivery." But since muscle is one of the larger human organs, they add, successful transfer of this technology to patients will depend in part on producing and delivering large amounts of the vector safely.

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