Partner notification in the context of HIV: an interest-analysis.

Codes of confidentiality play an essential role in the intimate discourses in many learned professions. Codes with various prescriptions exist. The Hippocratic Oath for example, prescribes rewards to the secret keeper, for keeping secret what ought to be kept secret, and punishments for failing.

Precarious connections: making therapeutic production happen for malaria and tuberculosis.

The One Health Movement has been a primary advocate for collaboration across disciplinary and organizational sectors in the study of infectious diseases. There is potentially much to be gained by incorporating the interrelations of animal and human ecosystems, as well as the expertise of veterinary, medical, and public health practitioners. Too often, however, the idea rather than the realities of collaboration become valorized within One Health approaches.

Calpain cleaves methionine aminopeptidase-2 in a rat model of ischemia/reperfusion.

Ischemic stroke results in multiple injurious signals within a cell including dysregulation of calcium homeostasis. Consequently, there is an increase in the enzymatic activity of the calpains, calcium dependent proteases that are thought to contribute to neuronal injury. In addition, cellular stress due to ischemia/reperfusion also triggers a decrease in protein translation through activation of the unfolded protein response (UPR).

Drug partnerships and global practices.

Tuberculosis poses one of the biggest threats to individuals living with HIV in most low-income regions of the world, and the increase of multi-drug resistant tuberculosis (MDR-TB) in South Africa, Eastern Europe, and elsewhere makes this threat that much more critical. Despite the extent of the problem, new drugs for tuberculosis have not been developed for over four decades, largely because tuberculosis occurs primarily among the poor in low-income regions and the market for tuberculosis drugs is not lucrative enough to warrant time and resource commitments by pharmaceutical companies. In the wake of sustained global criticism of pharmaceutical-state practices, however, new partnerships for drug development (PDPs) are forming to address critical shortages of drugs for diseases like tuberculosis that have been termed 'neglected' precisely because they have not seen new treatments for so long.

Protective effects of NIM811 in transient focal cerebral ischemia suggest involvement of the mitochondrial permeability transition.

Cerebral ischemia followed by reperfusion activates numerous pathways that lead to cell death. One such pathway involves the release of large quantities of the excitatory amino acid glutamate into the synapse and activation of N-methyl-D-aspartate receptors. This causes an increase in mitochondrial calcium levels ([Ca(2+)](m)) and a production of reactive oxygen species (ROS), both of which may induce the mitochondrial permeability transition (MPT).

Market incentives, human lives, and AIDS vaccines.

For many, an AIDS vaccine holds the promise of intervening in a widespread epidemic because it is not predicated on changing economic structures and social contexts underlying vulnerability to HIV for millions of individuals. Yet 20 years into the AIDS epidemic, there is still no vaccine. Based on interviews of AIDS vaccine researchers, watchdog organizations, and ethics groups from the United States, South Africa, and Kenya conducted between August and December of 2003, this paper explores possible answers to the question of why there is no vaccine, looking in particular at contradictions between a biomedical research industry increasingly driven by market incentives and a disease that primarily affects individuals living in low-income countries with little vaccine purchasing power.

The mitochondrial uncoupler 2,4-dinitrophenol attenuates tissue damage and improves mitochondrial homeostasis following transient focal cerebral ischemia.

Ischemic stroke is caused by acute neuronal degeneration provoked by interruption of cerebral blood flow. Although the mechanisms contributing to ischemic neuronal degeneration are myriad, mitochondrial dysfunction is now recognized as a pivotal event that can lead to either necrotic or apoptotic neuronal death. Lack of suitable 'upstream' targets to prevent loss of mitochondrial homeostasis has, so far, restricted the development of mechanistically based interventions to promote neuronal survival.

Glutamate receptor antagonists modulate heat shock protein response in focal brain ischemia.

Neurons and glia reacting to ischemic injury exhibit delayed expression of heat shock proteins (HSPs). We tested the hypothesis that glutamate receptor antagonists alter neuronal and glial activation during focal cerebral ischemia, as shown by spatio-temporal changes in HSP immunoreactivity. Rats underwent focal ischemia by permanent occlusion of the middle cerebral artery.