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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)
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 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.
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)
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)
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.
Systemic lupus erythematosus can cause various forms of central nervous system disorders, ranging from subtle cognitive dysfunction to life-threatening coma. How lupus autoantibodies target neurons and cause brain injury remains a mystery. New research suggests that a subset of autoantibodies to double-stranded DNA in lupus patients cross-reacts with the NMDA glutamate receptor, and produces neuronal injury and death. (pages 1189–1193)
The etiology of thrombotic thrombocytopenic purpura (TTP), a severe blood disorder resulting from increased platelet activation, has been an enigma. The identification of ADAMTS as a protease that cleaves von Willebrand factor and the demonstration of ADAMTS mutations in families with inherited TTP suggest a molecular mechanism for the disease.
Virologists and immunologists are all too aware of the ability of HIV to evade efforts by its human host to destroy it within the body. Now, two new pieces of evidence reveal yet more of HIV's survival abilities: the virus uses a single protein both to trigger and block apoptosis as the situation demands. (pages 1217–1224)
Holt–Oram syndrome has been associated with mutations in the T-box transcription factor TBX5, but little is known about the function of this protein or how mutations in it cause disease. A new mouse model of this syndrome will help to answer some of these questions.
Little was known about the function of T cells expressing the γδ–T-cell receptor, until these cells were shown to protect against skin cancer. But what is the mechanism mediating this activity?
The finding that CD38 mediates a sustained calcium signal inside neutrophils, which directs their movement toward lung tissue infected with pneumococcus bacteria suggests a new mechanism by which the immune system prevents the spread of bacterial infection. (pages 1209–1216)
Methicillin-resistant Staphylococcus aureus infections have become a major problem worldwide. The finding that two bacterial enzymes, one native and one acquired, cooperate to build cell walls in the presence of methicillin has drawn attention to an as yet unutilized target for new antibiotics.