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Achieving cancer health equity is a national imperative. Cancer is the second leading cause of death in the United States and in North Carolina (NC), where the disease disproportionately impacts traditionally underrepresented race and ethnic groups, those who live in rural communities, the impoverished, and medically disenfranchised and/or health-disparate populations at high-risk for cancer. These populations have worse cancer outcomes and are less likely to be participants in clinical research and trials. It is critical for cancer centers and other academic health centers to understand the factors that contribute to poor cancer outcomes, the extent to which they impact the cancer burden, and develop effective interventions to address them. Key to this process is engaging diverse stakeholders in the development and execution of community and population health assessments, and the subsequent programs and interventions designed to address the need across the catchment area. This chapter describes the processes and lessons learned of the Duke Cancer Institute's (DCI) long standing community partnerships that led to Project PLACE (Population Level Approaches to Cancer Elimination), a National Cancer Institute (NCI)-funded community health assessment reaching 2315 respondents in 7 months, resulting in a community partnered research agenda to advance cancer equity within the DCI catchment area. We illustrate the application of a community partnered health assessment and offer examples of strategic opportunities, successes, lessons learned, and implications for practice., (© 2020 Elsevier Inc. All rights reserved.)

Cluster of Differentiation-200 (CD200) is an anti-inflammatory glycoprotein expressed in neurons, T cells, and B cells, and its receptor is expressed on glia. Both Alzheimer's disease patients and mouse models display age-related or amyloid-β peptide (Aβ)-induced reductions in CD200. The goal of this study was to determine if neuronal CD200 expression restores hippocampal neurogenesis and reduces Aβ in the amyloid precursor protein mouse model. Amyloid precursor protein and wild-type mice were injected at 6 months of age with an adeno-associated virus expressing CD200 into the hippocampus and sacrificed at 12 months. CD200 expression restored neural progenitor cell proliferation and differentiation in the subgranular and granular cell layers of the dentate gyrus and reduced diffuse but not thioflavin-S(+) plaques in the hippocampus. In vitro studies demonstrated that CD200-stimulated microglia increased neural differentiation of neural stem cells and enhanced axon elongation and dendrite number. CD200 also enhanced Aβ uptake by microglia. These data indicate that CD200 is capable of enhancing microglia-mediated Aβ clearance and neural differentiation and has potential as a therapeutic for Alzheimer's disease., (Copyright © 2015 Elsevier Inc. All rights reserved.)