This study compared inpatient, intensive outpatient, and standard outpatient treatment settings for persons with alcoholism and tested a priori hypotheses about the interaction of setting with client alcohol involvement and social network support for drinking. Participants (N = 192) were assigned randomly in cohorts to 1 of the 3 settings. The settings did not differ in posttreatment primary drinking outcomes, although inpatients had significantly fewer jail and residential treatment days combined than outpatients. Clients high in alcohol involvement benefited more from inpatient than outpatient care; the opposite was true at low alcohol involvement levels. Network drinking support did not moderate setting effects. Clients low in cognitive functioning also appeared to benefit more from inpatient than outpatient care. Improved outcomes might be achieved by matching degree of alcohol involvement and cognitive functioning to level of care.

We report that cocaine may act as cofactor in HIV pathogenesis by increasing dendritic cell-specific C type ICAM-3-grabbing nonintegrin (DC-SIGN) expression on dendritic cells (DC). Our results show that cocaine-using, long-term nonprogressors and normal progressors of HIV infection manifest significantly higher levels of DC-SIGN compared with cocaine-nonusing long-term nonprogressors and normal progressors, respectively. Furthermore, in vitro HIV infection of MDC from normal subjects cultured with cocaine and/or HIV peptides up-regulated DC-SIGN, confirming our in vivo finding. Cocaine, in synergy with HIV peptides, also up-regulates DC-SIGN gene expression by MDC. Furthermore, the cocaine-induced effects were reversed by a D1 receptor antagonist demonstrating the specificity of the reaction. Our results indicate that cocaine exacerbates HIV infection by up-regulating DC-SIGN on DC and these effects are mediated via dysregulation of MAPKs. These data are the first evidence that cocaine up-regulates the expression of DC-SIGN on DC. A better understanding of the role of DC-SIGN in HIV infection may help to design novel therapeutic strategies against the progression of HIV disease in the drug-using population.

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