How Youth of Color Create Communities of Hope: Connecting Advocacy, Activity, and Neighborhood Change.

The primary aim of this paper was to assess the association of after-school club characteristics with changes in physical activity, nutrition, and attitudes in students of color after participating in the "YEAH!" Advocacy-based Physical Activity Program. We examine the strengths of school-based vs. non-school based programs in promoting feelings of self-efficacy and empowerment among students learning to become more physically active-and importantly, also test the strength of how programs that are more connected (to community-based partners) may contribute to students' optimism around policy and public health as it directly affects them. This study examined differences in the youth advocacy training impact across four after-school club types: school-based with community partnerships, school-based without partnerships, non-school-based with community partners, and non-school-based clubs without partnerships. We measured improvements in youth's "optimism for change", "assertiveness" and "decision-making" as related to after school activities and found that non-school-based programs with community partners showed highest positive impact.

Policy and Practice-Relevant Youth Physical Activity Research Center Agenda.

BACKGROUND: The Physical Activity Research Center developed a research agenda that addresses youth physical activity (PA) and healthy weight, and aligns with the Robert Wood Johnson Foundation's Culture of Health. This paper summarizes prioritized research studies with a focus on youth at higher risk for inactive lifestyles and childhood obesity in urban and rural communities. METHODS: Systematic literature reviews, a survey, and discussions with practitioners and researchers provided guidance on research questions to build evidence and inform effective strategies to promote healthy weight and PA in youth across race, cultural, and economic groups. RESULTS: The research team developed a matrix of potential research questions, identified priority questions, and designed targeted studies to address some of the priority questions and inform advocacy efforts. The studies selected examine strategies advocating for activity-friendly communities, Play Streets, park use, and PA of youth in the summer. A broader set of research priorities for youth PA is proposed. CONCLUSION: Establishing the Physical Activity Research Center research agenda identified important initial and future research studies to promote and ensure healthy weight and healthy levels of PA for at-risk youth. Results will be disseminated with the goal of promoting equitable access to PA for youth.

Do Sexually Oriented Massage Parlors Cluster in Specific Neighborhoods? A Spatial Analysis of Indoor Sex Work in Los Angeles and Orange Counties, California.

OBJECTIVE: Social determinants of health may be substantially affected by spatial factors, which together may explain the persistence of health inequities. Clustering of possible sources of negative health and social outcomes points to a spatial focus for future interventions. We analyzed the spatial clustering of sex work businesses in Southern California to examine where and why they cluster. We explored economic and legal factors as possible explanations of clustering. METHODS: We manually coded data from a website used by paying members to post reviews of female massage parlor workers. We identified clusters of sexually oriented massage parlor businesses using spatial autocorrelation tests. We conducted spatial regression using census tract data to identify predictors of clustering. RESULTS: A total of 889 venues were identified. Clusters of tracts having higher-than-expected numbers of sexually oriented massage parlors ("hot spots") were located outside downtowns. These hot spots were characterized by a higher proportion of adult males, a higher proportion of households below the federal poverty level, and a smaller average household size. CONCLUSION: Sexually oriented massage parlors in Los Angeles and Orange counties cluster in particular neighborhoods. More research is needed to ascertain the causal factors of such clusters and how interventions can be designed to leverage these spatial factors.

HIV testing behavior among Pacific Islanders in Southern California: exploring the importance of race/ethnicity, knowledge, and domestic violence.

This article presents an analysis of a 2008 community needs assessment survey of a convenience sample of 179 Pacific Islander respondents in southern California; the needs assessment focused on HIV knowledge, HIV testing behavior, and experience with intimate partner/relationship violence. Multivariate logistic regression results indicated that race/ethnicity and reported experience with intimate partner/relationship violence were the most important variables in explaining the variation in reported HIV testing among Chamorro/Guamanian and Samoan respondents. However, when analyzed separately, self-reported experience with intimate partner/relationship violence was associated with reported HIV testing only for Chamorro respondents and not for Samoan respondents. As U.S. Pacific Islanders experience a high degree of HIV health disparities, additional research is needed to clarify the links among race/ethnicity, intimate partner/relationship violence, and HIV testing behavior.

Hepatitis B among Pacific Islanders in Southern California: how is health information associated with screening and vaccination?

We measured Hepatitis B virus (HBV) transmission knowledge and self-reported screening/testing behavior among Pacific Islanders (Guamanians/Chamorros, Samoans, and Tongans) in Southern California. We also examined access and trust by Pacific Islanders of varying health information sources. We administered and analyzed survey data (N = 297), using a convenience sample in Los Angeles, Orange, and San Diego Counties in spring 2009. We found that while Pacific Islander respondents reported that they receive health information from physicians, and largely trust this source, information from and trust in physicians were not statistically significant in explaining whether respondents sought HBV screening or vaccination.

Mechanisms linking diabetes mellitus to the development of atherosclerosis: a role for endoplasmic reticulum stress and glycogen synthase kinase-3.

Recent decades have seen a significant increase in the incidence of diabetes mellitus. The number of individuals with diabetes is projected to reach 300 million by the year 2025. Diabetes is a leading cause of blindness, renal failure, lower limb amputation, and an independent risk factor for atherosclerotic cardiovascular disease (CVD)--a leading cause of death in Western society. Understanding the molecular and cellular mechanisms by which diabetes mellitus promotes atherosclerosis is essential to developing methods to treat and prevent diabetes-associated CVD. This review summarizes our current knowledge of the mechanisms by which diabetes may promote atherogenesis and specifically focuses on a novel pathway linking these 2 conditions. We hypothesize that the accumulation of intracellular glucosamine observed in conditions of chronic hyperglycaemia may promote atherogenesis via a mechanism involving dysregulated protein folding, activation of endoplasmic reticulum (ER) stress, and increased glycogen synthase kinase (GSK)-3 activity. The identification of this novel mechanism provides a promising hypothesis and multiple new targets for potential therapeutic intervention in the treatment of diabetes mellitus and accelerated atherosclerosis.

Glucosamine-induced endoplasmic reticulum dysfunction is associated with accelerated atherosclerosis in a hyperglycemic mouse model.

Diabetes is a major independent risk factor for cardiovascular disease and stroke; however, the molecular and cellular mechanisms by which diabetes contributes to the development of vascular disease are not fully understood. Our previous studies demonstrated that endoplasmic reticulum (ER) stress-inducing agents, including homocysteine, promote lipid accumulation and activate inflammatory pathways-the hallmark features of atherosclerosis. We hypothesize that the accumulation of intracellular glucosamine observed in diabetes may also promote atherogenesis via a mechanism that involves ER stress. In support of this theory, we demonstrate that glucosamine can induce ER stress in cell types relevant to the development of atherosclerosis, including human aortic smooth muscle cells, monocytes, and hepatocytes. Furthermore, we show that glucosamine-induced ER stress dysregulates lipid metabolism, leading to the accumulation of cholesterol in cultured cells. To examine the relevance of the ER stress pathway in vivo, we used a streptozotocin-induced hyperglycemic apolipoprotein E-deficient mouse model of atherosclerosis. Using molecular biological and histological techniques, we show that hyperglycemia is associated with tissue-specific ER stress, hepatic steatosis, and accelerated atherosclerosis. This novel mechanism may not only explain how diabetes and hyperglycemia promote atherosclerosis, but also provide a potential new target for therapeutic intervention.

Valproate protects cells from ER stress-induced lipid accumulation and apoptosis by inhibiting glycogen synthase kinase-3.

A wide range of agents and conditions are known to disrupt the ability of the endoplasmic reticulum (ER) to fold proteins properly, resulting in the onset of ER dysfunction/stress. We and others have shown that ER stress can induce intracellular lipid accumulation through the activation of the sterol responsive element binding proteins (SREBPs) and initiate programmed cell death by activation of caspases. It has been suggested that ER stress-induced lipid accumulation and cell death play a role in the pathogenesis of disorders including Alzheimer's disease, Parkinson's disease, type-1 diabetes mellitus and hepatic steatosis. Here we show that exposure of HepG2 cells to the branch chain fatty acid, valproate, increases cellular resistance to ER stress-induced dysfunction. Two distinctly different potential mechanisms for this protective effect were investigated. We show that exposure to valproate increases the expression of chaperones that assist in the folding of proteins in the ER including GRP78/BiP, GRP94, PDI and calreticulin as well as the cytosolic chaperone, HSP70. However, exposure of HepG2 cells to valproate does not decrease the apparent ER stress response in cells challenged with tunicamycin, A23187 or glucosamine, suggesting that valproate-conferred protection occurs downstream of ER dysfunction. Finally, we demonstrate that valproate directly inhibits the glycogen synthase kinases (GSK)-3alpha/beta. The ability of lithium, another inhibitor of GSK3alpha/beta to protect cells from ER stress-induced lipid accumulation suggests that GSK3 plays a central role in signaling downstream effects of ER stress. Strategies to protect cells from agents/conditions that induce ER stress may have potential in the treatment of the growing number of diseases and disorders linked to ER dysfunction.

Examining the correlations between GSK-3 inhibitory properties and anti-convulsant efficacy of valproate and valproate-related compounds.

A family of compounds based upon the chemical structure of valproate were synthesized and assayed for their ability to inhibit glycogen synthase kinase (GSK)-3 alpha and beta activity in vitro. This data is correlated to the known anti-convulsant properties of these compounds in order to determine the potential role of GSK-3 inhibition in the therapeutic efficacy of these drugs.