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The anthrax attacks in the United States, juxtaposed against the September 11 terrorist attacks on New York and Washington, DC, have transformed a theoretical threat to stark reality. The biomedical research community will be an integral part of the preparation for, defense against and response to bioterrorism
Cardiomyocyte apoptosis occurs during reperfusion injury, transplant rejection and heart failure. The ability to image apoptosis non-invasively in the intact heart could lead to a more precise assessment of the clinical condition of patients, and could also expedite therapy. (pages 1347–1352 and 1352–1355)
In a healthy cell, the normal business of Tsg101 protein is as part of the machinery for protein trafficking. It now emerges that two deadly but unrelated viruses, HIV-1 and Ebola, both subvert Tsg101 as an essential step in their life cycles—exiting a cell to restart the cycle of infection. (pages 1313–1319)
The intriguing finding that α-synuclein—a protein recently found to be mutated in some familial cases of Parkinson disease—and cytosolic dopamine interact to form adducts that stabilize a presumably toxic intermediate of fibril formation provides clues into the mechanism of neurodegeneration.
Reduction in blood levels of low-density lipoprotein cholesterol reduces the risk of coronary heart disease. The identification of a new class of compounds that upregulate the low-density lipoprotein receptor may lead to new therapeutic advances. (pages 1332–1338)
Over time, bacteria have evolved mechanisms to enable them to outwit the efforts of their host to destroy them. New studies have uncovered a hitherto unknown mechanism of defense used by one of the commonest bacteria to infect humans, and a major pathogen, group A Streptococcus (pages 1298–1305)
The identification of a new influenza virus protein PB1-F2, which localizes to mitochondria and causes cell death, may offer important insights into pathogenicity, as well as providing another example of how the virus can expand the coding capacity of its genome using overlapping reading frames. (pages 1306–1312)
Ouabain signaling through a plasma membrane can produce oscillations of intracellular calcium levels, resulting in translocation of the NF-κB transcription factor into the nucleus and gene activation. This is a previously unrecognized form of steroid action.
