How and why AIDS changed drug policy in Switzerland.

Switzerland implemented a harm reduction program and reduced the spread of HIV within the drug scene, and from drug users into other population groups, earlier than many countries. Each canton developed strategies based on its drug problem. By 1985 it was obvious that 'needle sharing' was the most significant pathway in the transmission of HIV.

Switzerland, HIV and the power of pragmatism: lessons for drug policy development.

Switzerland in the 1980s was an epicentre of HIV as open drug injection became part of the urban scene, especially in Zurich. Cracks appeared in Switzerland's long commitment to policing as the main drug-control strategy as law enforcement was unable to contain the health and social consequences of the rapid spread of drug injection. In the early stages of the epidemic, the pioneering health care providers who brought technically illegal harm reduction services into the open drug scene in Zurich helped open the exploration at the federal level of more balanced drug policy.

The use of anti-T-cell receptor-Vbeta antibodies for the estimation of treatment success and phenotypic characterization of clonal T-cell populations in cutaneous T-cell lymphomas.

Sézary syndrome and Mycosis fungoides are the most common forms of cutaneous T-cell lymphomas. To assess the response to different therapies especially in Sézary syndrome, it is helpful to monitor the percentage of circulating tumour cells in the blood. The use of T-cell receptor (TCR)-Vbeta specific monoclonal antibodies provides a suitable tool for detecting Sézary cells.

Inhibition of p38 MAP kinase by utilizing a novel allosteric binding site.

The p38 MAP kinase plays a crucial role in regulating the production of proinflammatory cytokines, such as tumor necrosis factor and interleukin-1. Blocking this kinase may offer an effective therapy for treating many inflammatory diseases. Here we report a new allosteric binding site for a diaryl urea class of highly potent and selective inhibitors against human p38 MAP kinase.