Addressing Childhood Obesity Through Multisector Collaborations: Evaluation of a National Quality Improvement Effort.

The Healthy Weight Collaborative (HWC) represents a national quality improvement effort to increase uptake of evidence-based community-based interventions to address obesity among children. Implemented from 2011 to 2013, the HWC built the capacity of 49 community-based multisector teams (10 teams in the Phase 1 pilot, 39 teams in Phase 2), delivered services to support health behavior changes in children and families, and implemented sustainable social and environmental policy change at the organizational and community levels. Phase 2 teams participated in three virtual collaborative learning sessions interspersed with three "action periods" during which teams implemented the HWC "change package" while receiving tailored coaching and peer-support. All of the teams participating in Phase 2 adopted a healthy weight message, 59% implemented community-wide healthy weight assessments and healthy weight plans, and 31% made progress toward developing and implementing policies to promote healthy weight. By the end of the project, one-third of teams had developed sustainability plans to continue working with this approach. The HWC offers a collaborative team model with the potential to effectively address other public health challenges.

The Healthy Weight Collaborative: using learning collaboratives to enhance community-based prevention initiatives addressing childhood obesity.

This report from the field describes the design, implementation, and early evaluation results of the Healthy Weight Collaborative, a federally-supported learning collaborative to develop, test, and disseminate an integrated change package of six promising, evidence-based clinical and community-based strategies to prevent and treat obesity for children and families.

Expanding the role of primary care in the prevention and treatment of childhood obesity: a review of clinic- and community-based recommendations and interventions.

Although pediatric providers have traditionally assessed and treated childhood obesity and associated health-related conditions in the clinic setting, there is a recognized need to expand the provider role. We reviewed the literature published from 2005 to 2012 to (1) provide examples of the spectrum of roles that primary care providers can play in the successful treatment and prevention of childhood obesity in both clinic and community settings and (2) synthesize the evidence of important characteristics, factors, or strategies in successful community-based models. The review identified 96 articles that provide evidence of how primary care providers can successfully prevent and treat childhood obesity by coordinating efforts within the primary care setting and through linkages to obesity prevention and treatment resources within the community. By aligning the most promising interventions with recommendations published over the past decade by the Institute of Medicine, the American Academy of Pediatrics, and other health organizations, we present nine areas in which providers can promote the prevention and treatment of childhood obesity through efforts in clinical and community settings: weight status assessment and monitoring, healthy lifestyle promotion, treatment, clinician skill development, clinic infrastructure development, community program referrals, community health education, multisector community initiatives, and policy advocacy.

Associations between household and neighborhood income and anxiety symptoms in young adolescents.

BACKGROUND: A better understanding of the role of both family- and neighborhood-level socioeconomic characteristics in the development of anxiety disorders is important for identifying salient target populations for intervention efforts. Little research has examined the question of whether associations between anxiety and socioeconomic status (SES) differ depending upon the level at which SES is measured or way in which anxiety manifests. We studied associations between both household- and neighborhood-level income and four different manifestations of anxiety in a community sample of young adolescents. METHODS: We conducted a cross-sectional analysis of data on 498 subjects aged 11-13 from a cohort study of Seattle-area middle school students. Generalized estimating equations were used to examine the association between both annual household income and neighborhood median income and each of four anxiety subscale scores from the multidimensional anxiety scale for children (MASC): physical symptoms, harm avoidance, social anxiety, and separation/panic anxiety. RESULTS: A negative association was found between household income and scores on two of the four MASC subscales--physical symptoms and separation/panic anxiety. In contrast, at equivalent levels of household income, adolescents living in higher income neighborhoods reported higher physical and harm avoidance symptom scores. CONCLUSION: The role that SES plays in the development of childhood anxiety appears to be complex and to differ depending on the specific type of anxiety that is manifest and whether income is evaluated at the household or neighborhood level.

Effects of small molecules on chaperone-mediated autophagy.

Autophagy, including macroautophagy (MA), chaperone-mediated autophagy (CMA), crinophagy, pexophagy and microautophagy, are processes by which cells select internal components such as proteins, secretory vesicles, organelles, or foreign bodies, and deliver them to lysosomes for degradation. MA and CMA are activated during conditions of serum withdrawal in cell culture and during short-term and prolonged starvation in organisms, respectively. Although MA and CMA are activated under similar conditions, they are regulated by different mechanisms. We used pulse/chase analysis under conditions in which most intracellular proteolysis is due to CMA to test a variety of compounds for effects on this process. We show that inhibitors of MA such as 3-methyladenine, wortmannin, and LY294002 have no effect on CMA. Protein degradation by MA is sensitive to microtubule inhibitors such as colcemide and vinblastine, but protein degradation by CMA is not. Activators of MA such as rapamycin also have no effect on CMA. We demonstrate that CMA, like MA, is inhibited by protein synthesis inhibitors anisomycin and cycloheximide. CMA is also partially inhibited when the p38 mitogen activated protein kinase is blocked. Finally we demonstrate that the glucose-6-phophate dehydrogenase inhibitor, 6-aminonicotinamide, and heat shock protein of 90 kilodaltons inhibitor, geldanamycin, have the ability to activate CMA.