A community based participatory approach to improving health in a Hispanic population

ABSTRACT: BACKGROUND: The Charlotte-Mecklenburg region has one of the fastest growing Hispanic communities in the country. This population has experienced disparities in health outcomes and diminished ability to access healthcare services. This city is home to an established practice-based research network (PBRN) that includes community representatives, health services researchers, and primary care providers. The aims of this project are: to use key principles of community-based participatory research (CBPR) within a practice-based research network (PBRN) to identify a single disease or condition that negatively affects the Charlotte Hispanic community; to develop a community-based intervention that positively impacts the chosen condition and improves overall community health; and to disseminate findings to all stakeholders. METHODS/DESIGN: This project is designed as CBPR. The CBPR process creates new social networks and connections between participants that can potentially alter patterns of healthcare utilization and other health-related behaviors. The first step is the development of equitable partnerships between community representatives, providers, and researchers. This process is central to the CBPR process and will occur at three levels -- community members trained as researchers and outreach workers, a community advisory board (CAB), and a community forum. Qualitative data on health issues facing the community -- and possible solutions -- will be collected at all three levels through focus groups, key informant interviews and surveys. The CAB will meet monthly to guide the project and oversee data collection, data analysis, participant recruitment, implementation of the community forum, and intervention deployment. The selection of the health condition and framework for the intervention will occur at the level of a community-wide forum. Outcomes of the study will be measured using indicators developed by the participants as well as geospatial modeling.On completion, this study will: determine the feasibility of the CBPR process to design interventions; demonstrate the feasibility of geographic models to monitor CBPR-derived interventions; and further establish mechanisms for implementation of the CBPR framework within a PBRN

The role of apologies in professional discipline

We live in times of 'apology mania', says Lee Taft, or at least 'national conversation' about the role and meaning of apologies. Roy Brooks talks of an 'age of apology'. Some 10 years after these pronouncements, little has changed. Apologies are ubiquitous and debated in the public and political domain. And they continue to be used and imported into legal jurisdictions. For instance, legislation removes civil liability for saying 'sorry' in certain contexts and may reward apologies in mitigation of sentence

Inhibition of Glycogen Synthase Kinase 3β (GSK3β) Decreases Inflammatory Responses in Brain Endothelial Cells

Immune mediators and leukocyte engagement of brain microvascular endothelial cells (BMVECs) contribute to blood–brain barrier impairment during neuroinflammation. Glycogen synthase kinase 3β (GSK3β) was recently identified as a potent regulator of immune responses in in vitro systems and animal models. However, the role of GSK3β in regulation of immune endothelial functions remains undetermined. Here we evaluated the effect of GSK3β inhibition on the regulation of inflammatory responses in BMVECs. A focused PCR gene array of 84 genes was performed to identify the cytokine and chemokine gene expression profile in tumor necrosis factor (TNF) α-stimulated BMVECs after GSK3β inactivation by specific inhibitors. Fifteen of 39 genes induced by TNFα stimulation were down-regulated after GSK3β inhibition. Genes known to contribute to neuroinflammation that were most negatively affected by GSK3β inactivation included IP-10/CXCL10, MCP-1/CCL2, IL-8/CXCL8, RANTES/CCL5, and Groα/CXCL1. GSK3β suppression resulted in diminished secretion of these proinflammatory mediators by inflamed BMVECs detected by ELISA. GSK3β inhibition in BMVECs reduced adhesion molecule expression as well as monocyte adhesion to and migration across cytokine stimulated BMVEC monolayers. Interactions of monocytes with TNFα-activated BMVECs led to barrier disruption, and GSK3β suppression in the endothelium restored barrier integrity. GSK3β inhibition in vivo substantially decreased leukocyte adhesion to brain endothelium under inflammatory conditions. In summary, inhibition of GSK3β emerges as an important target for stabilization of the blood–brain barrier in neuroinflammation