Community-engaged research to develop a Chicago violence research agenda and recommendations to support future community engagement.

BACKGROUND: Chicago has a history of gun violence with some neighborhoods, particularly Black and Brown communities, being disproportionately affected and Black male youth experiencing an even more disparate impact. Too often, violence prevention research is developed and carried out with little or no input from the people living in the most affected communities. The objective of the Community-Academic Collaboration to Prevent Violence in Chicago (CACPVC) was to bring together individuals from impacted communities with academic researchers and other community stakeholders to discuss violence and co-create a research agenda that addresses topics of mutual concern, and recommendations for engaging stakeholders including community members and organizations and funders in violence and violence prevention research. METHODS: From 2014 to 2015, community members and organizations from seven defined regions across Chicago were recruited to participate. An organization network gathering was held in each region for researchers, funders, and community organization representatives to discuss violence prevention. Open community forums then took place in each community. Violence data by region was shared followed by facilitated group discussions that were recorded by youth scribes. Notes were thematically coded, grouped, and compiled after which a list of topics was refined by the CACPVC Work Group, allowing for investigator triangulation. A survey was disseminated to community stakeholders to prioritize the topics. RESULTS: Seven network gatherings (127 attendees) and community forums (133 attendees) were held. Topic areas identified during the gatherings and forums included root causes/cycle of violence, racism and bias/structural violence, trajectory of violence, protective factors and nonviolence, geographic pattern change, violence prevention strategies, youth, family factors, community factors, school, police, gangs/street organizations, and media and public perceptions. Recommendations to support community engagement were grouped as role of research in reducing violence, role of community in violence research, relationships and respect, academic-community communication, financial considerations, training, practical considerations, research design, sharing results, communication about and use of data, and recommendations for funders. CONCLUSIONS: The violence research agenda will be used to inform community-engaged violence prevention research. The recommendations for community engagement provide a resource for researchers about topics to consider to meaningfully engage community members in future research.

Effects of pristane on cytochrome P450 isozyme expression in rat tissues.

Chemical carcinogenesis studies are powerful tools to obtain information on potential mechanisms of chemical factors for malignancies. In this study Western blot analyses, using monoclonal antibodies specific for three different cytochrome P450 (CYP) isozymes (CYP1A1, CYP1A2 and CYP2B), were employed to examine the effect(s) of 3-methylcholanthrene and/or pristane (2,6,10,14-tetramethylpentadecane) on the basal and inducible levels of expression of CYP proteins within Copenhagen rat tissues. Pristane exposure led to tissue specific differences in the CYP isozymes expressed and elicited increased CYP protein expression over 3-methylcholanthrene induced levels in microsomes isolated from liver, Peyer's Patches, and thymus. Within the context of the chemical carcinogenesis model employed in this study, these observations correlated with the induction of B-cell malignancies by low doses of 3-methylcholanthrene and of thymic lymphomas by a high 3-methylcholanthrene dose. The data suggest that pristane treatment affects CYP isozyme expression. This pristane-mediated effect clearly could be a contributing factor in the chemical carcinogenesis of the previously observed lymphoid malignancies, and a possible basis for the tumor enhancing effects of pristane.

Effect of 3beta-hydroxysteroid dehydrogenase inhibition by trilostane on blood pressure in the Dahl salt-sensitive rat.

The brains of rats and humans express the enzymes required for the synthesis of aldosterone from cholesterol, including the 3beta-steroid dehydrogenase that catalyzes the conversion of pregnenolone to progesterone in the pathway of adrenal steroid synthesis. Salt-induced hypertension in the Dahl inbred salt-sensitive (SS/jr) rat is associated with normal to low levels of circulating aldosterone, yet it is abrogated by the central infusion of mineralocorticoid receptor antagonists. To test the hypothesis that de novo synthesis of aldosterone in the brain has a pathophysiological role in the salt-induced hypertension of the SS rat, the 3beta-steroid dehydrogenase antagonist trilostane was infused continuously intracerebroventricularly or subcutaneously in two different cohorts of Dahl SS/jr rats, one female, the other male, during and after the development of salt-induced hypertension. The doses of trilostane used had no effect on blood pressure when infused subcutaneously. Animals receiving vehicle intracerebroventricularly experienced a 30- to 45-mmHg increase in systolic blood pressure measured by tail cuff. The intracerebroventricular, but not subcutaneous, infusion of 0.3 microg/h trilostane effectively blocked the increase in systolic blood pressure and reversed the hypertension produced by drinking 0.9% saline. Trilostane was equally effective in female and male rats. Weight gain, serum aldosterone and corticosterone concentrations, and behavior assessed subjectively and by elevated plus maze were unchanged by the trilostane treatment. These studies suggest that the synthesis in the brain of a mineralocorticoid receptor agonist, probably aldosterone, is responsible in part for the salt-induced hypertension of the inbred Dahl SS/jr rat.