Policy and Systems Change in Intimate Partner Violence and Human Trafficking: Evaluation of a Federal Cross-Sector Initiative.

Objectives: This study evaluates Project Catalyst's impact on policies related to Intimate Partner Violence (IV) and Human Trafficking (HT), which contribute to negative health outcomes for survivors. Methods: We utilized continuous evaluation using data from policy assessment tools and interviews with participating state leadership team (SLT) members. Results: Five SLTs reported integration of IPV into state-level initiatives. All implemented clinical practice and organizational policy recommendations. SLTs reported that Project Catalyst increased awareness of IPV/HT and health impacts and established ongoing partnerships between the three organizations. Conclusions: Funding, training, and technical assistance to encourage cross-sector collaboration at the state level can promote policy changes that support comprehensive health center responses to IPV/HT.

Microarray analysis of cytokine and chemokine genes in the brains of macaques with SHIV-encephalitis.

Human immunodeficiency virus (HIV)-encephalitis results from a cascade of viral-host interactions that lead to cytokine and chemokine imbalance, which then leads to neuropathologic manifestations of the disease. These include macrophage/microglia activation, astrocytosis and neuronal dysfunction or death. As the molecular mechanisms of this process are poorly understood, we used Atlas human cytokine or cytokine receptor microarray analysis to highlight gene expression profiles that accompanied encephalitis in Simian human immunodeficiency virus (SHIV) 89.6P-infected macaques. Of the 277 genes screened, marked upregulation of monocyte chemoattractant protein-1, interferon-inducible peptide IP-10 and interleukin-4 were observed specifically in the encephalitic brains. These genes are collectively known to promote macrophage infiltration and activation and virus replication. In contrast, genes regulating neurotrophic functions, such as brain-derived neurotrophic factor were downregulated. We also found that some of the apoptosis genes were up- or down-regulated. These data provide a comprehensive spectrum of gene expression that underscores the two major clinical manifestations of this unique syndrome: enhanced virus replication in brain macrophages and dystrophic changes in neurons.