Volume 11 Issue 5, May 2005
News & Views
HIV swiftly guts the immune system
Two studies show that SIV directly kills massive numbers of immune cells in the gut within days of infection. The results come on the heels of similarly dramatic findings for HIV, and could radically shift the focus of HIV research and therapy.
Lipid let loose in pulmonary emphysema
The lipid mediator ceramide contributes to tissue destruction in emphysema by promoting apoptosis of structural cells in the lung. This finding challenges a traditional hypothesis for the pathogenesis of emphysema (pages 491–498).
Killing pain, killing neurons?
Some commonly used pain medications inhibit the production of amyloid-β, a toxic peptide thought to have a major role in Alzheimer disease. New studies suggest that some COX-2 inhibitors may do the opposite—promote the production of this toxic peptide (pages 545–550).
DNA instability in the brain: survival of the 'fittest'
A new mouse model suggests that genomic instability leads to neuronal cell death in Nijmegen breakage syndrome—a neurological disease associated with predisposition to cancer. Impairing ATM or p53 function in the mice holds cell death at bay, restoring normal neurological function despite persistent genetic abnormalities (pages 538–544).
Do-all receptor takes on coagulation, inflammation
How many critical functions can be jammed into one receptor? New work on thrombomodulin explores the limits. This already overtaxed protein binds HMGB1, a molecule that contributes to sepsis and other inflammatory conditions.
Radiation's outer limits
Some types of tumors respond well to radiation therapy, whereas others are refractory to treatment. The molecular underpinnings of these differences are now coming to light (pages 484–490).
Muscle disease: a giant feels the strain
Titin is a massive protein that provides mechanical and structural support in striated muscles. Titin is now implicated in a new signaling pathway that seems to control gene expression. Loss of this pathway as a result of a mutation in titin leads to hereditary muscle disease.