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Scientists from the Howard Hughes Medical Institute and their colleagues have unraveled some of the fundamental mysteries about the genetic mechanisms that endow the immune system with its life-saving ability to generate specialized antibodies. Without genetic fine-tuning, antibodies would be relatively ineffective in finding a good match on the surface of viruses, parasites, and other potentially dangerous foreign pathogens. The findings also reveal the workings of a gene mutation process that can go awry, leading to the development of certain forms of cancer or allergic reactions.

Researchers have discovered one way in which the human immunodeficiency virus (HIV) wins its cat-and-mouse game with the body’s immune system. The study, published in the March 20, 2003, issue of the journal Nature, shows that HIV-1, a common strain of the virus that causes AIDS, uses a strategy not seen before in other viruses to escape attack by antibodies, one of the immune system’s prime weapons against invading viruses and bacteria.

The delicate interplay of two chemical signals coaxes stem cells into becoming hair follicles, according to new research by scientists at the Howard Hughes Medical Institute at The Rockefeller University. The research has implications for understanding hair growth and hair-follicle development, and it may also help explain how diverse structures, such as teeth and lungs, are formed or how some forms of skin cancer develop.

While studying mice with a mutant gene whose counterpart causes inherited glaucoma in humans, researchers have discovered a second gene mutation that worsens the structural eye defect that causes this type of glaucoma. The newly discovered gene mutation affects production of L-DOPA. The researchers suggest that it might be feasible to prevent glaucoma by administering L-DOPA, which is used in treating Parkinson’s disease.

For the first time, researchers have eavesdropped on the brains of mice as they go about the normal behaviors of detecting the subtle chemical signals called pheromones from other animals. The researchers have discovered that the animals’ pheromone-processing machinery in the brain forms, in essence, a specific “pheromonal image” of another animal. Such an “image” of another animal’s sex, identity, social standing and female reproductive status governs a range of mating, fighting, maternal-infant bonding and other behaviors. The scientists said that the specificity they discovered in the neurons that process pheromonal signals is akin to the “face neurons” in the visual areas of primate brains that are specifically triggered by facial features of other animals.

Although sweet, bitter and umami (monosodium glutamate) tastes are different, researchers are finding that information about each of these tastes is transmitted from the various taste receptors via a common intracellular signaling pathway. The identification of a common pathway runs counter to widespread belief among some researchers in the taste field who have long held the view that the different tastes require distinct machinery within the cell to transduce their signals to the brain, which is responsible for processing taste perceptions.

An international team of researchers has demonstrated a genetic basis for a fatal form of inherited cardiac arrhythmia that usually strikes young, seemingly healthy people. Basing their research on a French family with a form (Type 4) of inherited Long QT Syndrome (LQTS) and experiments in mice, the researchers found the mutation in a specific gene encoding ankyrin-B, a protein within heart muscle cells. Their discovery identifies what appears to be a novel mechanism for cardiac arrhythmia.

Using a tiny worm to model a severe childhood movement disorder, researchers have discovered the role of a protein that may have implications for a number of neurological syndromes such as Parkinson’s and Huntington’s diseases. The scientists found that a mutated gene associated with early onset dystonia, a severe hereditary movement disorder, normally helps manage protein folding.

Amid the glowing results for chronic myelogenous leukemia (CML) patients using Gleevec the past three years, the one reality check has been that a majority of the patients with advanced disease eventually relapse and die of the leukemia. An article to be published in the Dec. 15 issue of the journal Cancer Research shows that, in the lab, the molecular mutations that produce a resistance to Gleevec can be overcome. Brian Druker, M.D., Howard Hughes Medical Institute Investigator and JELD-WEN Chair of Leukemia Research at the Oregon Health & Science University Cancer Institute, and colleagues report that a compound called PD180970 successfully stopped the activity of several mutations found in patients who developed a resistance to Gleevec.

Researchers have found that the secret to mending a broken heart — at least at the molecular level — resides within the two-chambered heart of a fish commonly found in household aquariums. The scientists showed that the zebrafish can regenerate its heart after injury, and their studies suggest that understanding cardiac regeneration in this fish may lead to specific strategies to repair damaged human hearts.

With 46 chromosomes and six feet of DNA to copy every time most human cells divide, it’s not surprising that gaps or breaks sometimes show up in the finished product – especially when the cell is under stress or dividing rapidly, as in cancer. But what is surprising is that the breaks don’t always occur at random. They happen at a few specific locations on chromosomes, when cells are under stress, during the stages in the cell cycle where DNA is copied, or replicated, and the cell splits into two identical daughter cells. Scientists call them fragile sites, but the reasons for their inherent instability have remained a mystery. Now researchers have discovered that a protein called ATR protects fragile sites from breaking during DNA replication.

Researchers have generated a mouse model of a new type of tumor suppressor gene that triggers a rapidly advancing cancer that affects children. The discovery of the fast-onset cancers that result from inactivation of the gene and the technique used to generate the model will likely prove useful in studying genes involved in other forms of cancer.

Researchers have discovered that an important cellular “off-switch” that desensitizes receptors on the cell surface also regulates a second deactivation mechanism that had not been suspected before. Their finding that the off-switch, known as beta-arrestin, operates in two distinct ways may hint at a broader set of regulatory roles for the molecule.

Drug-resistant staph infections are a major concern to health care providers. Hospitals in particular have become home to some strains of Staphylococcus aureus that resist every known antibiotic, including the last-resort vancomycin. But two researchers say they’ve discovered just how so-called “Hospital staph” develops resistance, potentially opening the door for development of new drugs that beat it to the punch.