From Roots to Results: A Qualitative Case Study of the Evolution of a Public Health Leadership Institute Building Capacity in Collaborating for Equity and Justice.

Policy, systems, and environmental change are now widely accepted as critical to sustaining improvements in community health. Evidence suggests that such systems-level change is most effective when driven by community-based partnerships. Yet, after more than three decades of building community-based partnership work, health inequities have continued to deepen. To address health inequities, current and historical distributions of power are increasingly recognized as important considerations in efforts to ensure all individuals have the opportunity to attain their full health potential (i.e., achieving health equity). Building on social determinants of health literature, social injustice and powerlessness are put forth as fundamental causes of health inequities. Focusing on power as a root cause of health and health equity through application of Wolff and colleagues' six principles requires substantial changes in contemporary public health practice. This case study uses document analysis of a single case, the Community Teams Program, to assess the evolution of a statewide public health leadership program's efforts to build the capacity of coalition-based teams to catalyze community change in line with Wolff and colleagues' principles. Deductive, selective coding of the materials surface four themes in the program adaptations: (1) the need to focus on power as a root cause, (2) shifting power through relationship building, (3) storytelling as a way to shift narrative, and (4) building mechanisms into the curriculum that hold coalitions accountable for applying and sustaining learned skills. The themes demonstrate philosophical, pedagogical, and organizational changes to center power building approaches in health promotion. Findings are triangulated by reflections from the program director and recorded reflections of participants captured in existing evaluation data.

Lessons From a Pilot Community-Driven Approach for Obesity Prevention.

INTRODUCTION: The Wisconsin Obesity Prevention Initiative has piloted a novel approach for community action for obesity prevention that incorporates both coalition and community organizing efforts in 2 counties. This article describes lessons learned to date from this experience. METHODS: A description of the progress made in these communities and the support provided by Initiative staff and other partners are drawn from process evaluation of the pilot from November 2014 through December 2015, as well as the reflections of community partners. RESULTS: In Marathon County, building towards coalition action required thoughtful re-engagement and restructuring of an existing obesity-focused coalition. Community organizing surfaced local concerns related to the root causes of obesity, including poverty and transit. In Menominee County, coalition and community organizing efforts both have drawn attention to cultural assets for health promotion, such as traditional food practices, as well as the links between cultural loss and obesity. CONCLUSIONS: Building coalition action and community organizing varies across community contexts and requires addressing various steps and challenges. Both approaches require critical local examination of existing community action and stakeholders, attention to relationship building, and support from outside partners. In coalition action, backbone staff provide important infrastructure, including member recruitment and facilitating group processes towards collaboration. Community organizing involves broad resident engagement to identify shared interests and concerns and build new leadership. A community-driven systems change model offers potential to increase community action for obesity prevention.

State-level differences in breast and cervical cancer screening by disability status: United States, 2008.

INTRODUCTION AND BACKGROUND: Despite reported disparities in the use of preventive services by disability status, there has been no national surveillance of breast and cervical cancer screening among women with disabilities in the United States. To address this, we used state-level surveillance data to identify disparities in breast and cervical cancer screening among women by disability status. METHODS: Data from the 2008 Behavioral Risk Factor Surveillance System were used to estimate disability prevalence and state-level differences in breast and cervical cancer screening among women by disability status. RESULTS: Overall, modest differences in breast cancer screening were found; women with a disability were less likely than those without to report receiving a mammogram during the past 2 years (72.2% vs. 77.8%; p < .001). However, disparities in breast cancer screening were more pronounced at the state level. Furthermore, women with a disability were less likely than those without a disability to report receiving a Pap test during the past 3 years (78.9% vs. 83.4%; p < .001). DISCUSSION: This epidemiologic evidence identifies an opportunity for federal and state programs, as well as other stakeholders, to form partnerships to align disability and women's health policies. Furthermore, it identifies the need for increased public awareness and resource allocation to reduce barriers to breast and cervical cancer screening experienced by women with disabilities.

Do factors related to endogenous and exogenous estrogens modify the relationship between obesity and risk of colorectal adenomas in women?

Obesity has consistently been associated with increased colorectal cancer risk in men, but not in women. In the absence of postmenopausal hormone use (PMH), adipose-derived estrogen is the primary determinant of circulating estrogen levels in postmenopausal women, perhaps ameliorating the mitogenic effects of obesity in this group. Using data from a case-control study in the United States, we examined associations among obesity, potential modifying effects of factors related to endogenous and exogenous estrogen levels, and risk of colorectal adenoma. Cases (n = 219) were women of ages 30 to 74 years with colonoscopy proven, incident, sporadic, pathology-confirmed, adenomatous polyps of the colon and rectum. Two control groups were recruited: colonoscopy-confirmed polyp-free women (n = 438) and age- and zip code frequency-matched women randomly selected from the community (n = 247). Multivariate odds ratios and 95% confidence intervals (95% CI) for obese [body mass index (BMI) >or=30.0; compared with nonobese, BMI <25.0] premenopausal women were 2.09 (95% CI, 0.81-5.41) versus colonoscopy controls, and 5.18 (95% CI, 1.40-19.32) versus population controls. For PMH users, the corresponding odds ratios were 0.29 (95% CI, 0.12-0.70) versus colonoscopy controls and 0.64 (95% CI, 0.23-1.83) versus population controls. There was no significant association of BMI with adenoma risk for PMH nonusers. Findings for waist-to-hip ratio were similar to those for BMI. These data support the hypothesis that risk for colorectal adenoma may be increased with obesity among premenopausal women but decreased among postmenopausal women, especially if they also take PMH.

Transcriptional profiling of mefloquine-induced disruption of calcium homeostasis in neurons in vitro.

Mefloquine is associated with adverse neurological effects that are mediated via unknown mechanisms. Recent in vitro studies have shown that mefloquine disrupts neuronal calcium homeostasis via liberation of the endoplasmic reticulum (ER) store and induction of calcium influx across the plasma membrane. In the present study, global changes in gene expression induced in neurons in response to mefloquine-induced disruption of calcium homeostasis and appropriate control agents were investigated in vitro using Affymetrix arrays. The mefloquine transcriptome was found to be enriched for important regulatory sequences of the unfolded protein response and the drug was also found to induce key ER stress proteins, albeit in a manner dissimilar to, and at higher equivalent concentrations than, known ER-tropic agents like thapsigargin. Mefloquine also down-regulated several important functional categories of genes, including transcripts encoding G proteins and ion channels. These effects may be related to intrusion of extracellular calcium since they were also observed after glutamate, but not thapsigargin, hydrogen peroxide, or low-dose mefloquine treatment. Mefloquine could be successfully differentiated from other treatments on the basis of principle component analysis of its "calcium-relevant" transcriptome. These data may aid interpretation of expression of results from future in vivo studies.

The antimalarial potential of 4-quinolinecarbinolamines may be limited due to neurotoxicity and cross-resistance in mefloquine-resistant Plasmodium falciparum strains.

The clinical potential of mefloquine has been compromised by reports of adverse neurological effects. A series of 4-quinolinecarbinolamines were compared in terms of neurotoxicity and antimalarial activity in an attempt to identify replacement drugs. Neurotoxicity (MTT [thiazolyl blue reduction] assay) was assessed by exposure of cultured embryonic rat neurons to graded concentrations of the drugs for 20 min. The 50% inhibitory concentration (IC(50)) of mefloquine was 25 microM, while those of the analogs were 19 to 200 microM. The relative (to mefloquine) therapeutic indices of the analogs were determined after using the tritiated hypoxanthine assay for assessment of the antimalarial activity of the analogs against mefloquine-sensitive (W2) and -resistant (D6 and TM91C235) Plasmodium falciparum strains. Five analogs, WR157801, WR073892, WR007930, WR007333, and WR226253, were less neurotoxic than mefloquine and exhibited higher relative therapeutic indices (RTIs) against TM91C235 (2.9 to 12.2). Conventional quinoline antimalarials were generally less neurotoxic (IC(50)s of 400, 600, and 900 for amodiaquine, chloroquine, and quinine) or had higher RTIs (e.g., 30 for halofantrine against TM91C235). The neurotoxicity data for the 4-quinolinecarbinolamines were used to develop a three-dimensional (3D), function-based pharmacophore. The crucial molecular features correlated with neurotoxicity were a hydrogen bond acceptor (lipid) function, an aliphatic hydrophobic function, and a ring aromatic function specifically distributed in the 3D surface of the molecule. Mapping of the 3D structures of a series of structurally diverse quinolines to the pharmacophore allowed accurate qualitative predictions of neurotoxicity (or not) to be made. Extension of this in silico screening approach may aid in the identification of less-neurotoxic quinoline analogs.