The Historic Role of Boards of Health in Local Innovation: New York City’s Soda Portion Case

Childhood and adult obesity pose major risks for cancer, diabetes, and cardiovascular disease, with the poor and racial minorities suffering from disproportionately high burdens of obesity and chronic disease. With current policies failing, cities and states have moved forward with creative prevention measures–-with boards of health driving policy innovation in many local jurisdictions. The New York City Board of Board of Health’s (NYCBH) soda portion limit pushed the boundaries of innovation, but was struck down on June 26, 2014 by New York State’s highest court, which held that the Board trespassed on the City Council’s authority. The Court’s decision ignored the critical role of local health agencies in responding to 21st century public health threats, including epidemics of obesity and chronic disease. The Court narrowly construed the NYCBH’s authority, characterizing its powers as administrative, and thus potentially stifling local innovation. The decision also obscured the fundamental truth that public health policymaking requires complex trade-offs and incremental action, as well as a multifaceted approach to reducing population weight gain. Policymaking often relies upon limited evidence, and agencies experiment with novel ideas while also transforming social norms and pushing the boundaries of public opinion. Although the portion rule would disproportionately affect disadvantaged individuals who drink the largest amount of soda, government’s failure to act represents a greater injustice. Enhancing opportunities to choose a healthy life path better serves the interests of justice, but the Court’s judgment takes us further away from realizing this social aspiration

Haplotype Analysis Reveals a Possible Founder Effect of RET Mutation R114H for Hirschsprung's Disease in the Chinese Population

Background Hirschsprung's disease (HSCR) is a congenital disorder associated with the lack of intramural ganglion cells in the myenteric and sub-mucosal plexuses along varying segments of the gastrointestinal tract. The RET gene is the major gene implicated in this gastrointestinal disease. A highly recurrent mutation in RET (RETR114H) has recently been identified in ~6-7% of the Chinese HSCR patients which, to date, has not been found in Caucasian patients or controls nor in Chinese controls. Due to the high frequency of RETR114H in this population, we sought to investigate whether this mutation may be a founder HSCR mutation in the Chinese population. Methodology and Principal Findings To test whether all RETR114H were originated from a single mutational event, we predicted the approximate age of RETR114H by applying a Bayesian method to RET SNPs genotyped in 430 Chinese HSCR patients (of whom 25 individuals had the mutation) to be between 4-23 generations old depending on growth rate. We reasoned that if RETR114H was a founder mutation then those with the mutation would share a haplotype on which the mutation resides. Including SNPs spanning 509.31 kb across RET from a recently obtained 500 K genome-wide dataset for a subset of 181 patients (14 RETR114H patients), we applied haplotype estimation methods to determine whether there were any segments shared between patients with RETR114H that are not present in those without the mutation or controls. Analysis yielded a 250.2 kb (51 SNP) shared segment over the RET gene (and downstream) in only those patients with the mutation with no similar segments found among other patients. Conclusions This suggests that RETR114H is a founder mutation for HSCR in the Chinese population. © 2010 Cornes et al.published_or_final_versio

Regulation, Managerial Discretion and Family-Friendliness in Australia's Changing Industrial Relations Environment

This article examines how managers grant employees access to family-friendly work conditions and the institutional, organization and individual-level factors affecting their decision-making processes. This research question is addressed by comparing family-friendly conditions in collective agreements in the Australian retail and public service sectors. An analysis of interviews with management staff in the two sectors then explores how access to these family-friendly conditions works in practice. We found that at an institutional level, the different collective agreement conditions in each sector enabled or constrained managers' ability to create family-friendly working arrangements for employees. Industry-specific pressures and workplace 'cultures' also shaped the ease with which managers could grant employees access to conditions. Most importantly, managers' discretion operated on the basis of a cost-benefit analysis, where managers weighed up the benefits of retaining an employee's skills and knowledge against the costs of implementing a particular family-friendly arrangement. The article concludes by considering managerial discretion in relation to recent reforms to Australia's industrial relations laws

Annexin A1 expression in a pooled breast cancer series : Association with tumor subtypes and prognosis

Background: Annexin A1 (ANXA1) is a protein related with the carcinogenesis process and metastasis formation in many tumors. However, little is known about the prognostic value of ANXA1 in breast cancer. The purpose of this study is to evaluate the association between ANXA1 expression, BRCA1/2 germline carriership, specific tumor subtypes and survival in breast cancer patients. Methods: Clinical-pathological information and follow-up data were collected from nine breast cancer studies from the Breast Cancer Association Consortium (BCAC) (n = 5,752) and from one study of familial breast cancer patients with BRCA1/

RAD51B in familial breast cancer

Common variation on 14q24.1, close to RAD51B, has been associated with breast cancer: rs999737 and rs2588809 with the risk of female breast cancer and rs1314913 with the risk of male breast cancer. The aim of this study was to investigate the role of RAD51B variants in breast cancer predisposition, particularly in the context of familial breast cancer in Finland. We sequenced the coding region of RAD51B in 168 Finnish breast cancer patients from the Helsinki region for identification of possible recurrent founder mutations. In addition, we studied the known rs999737, rs2588809, and rs1314913 SNPs and RAD51B haplotypes in 44,791 breast cancer cases and 43,583 controls from 40 studies participating in the Breast Cancer Association Consortium (BCAC) that were genotyped on a custom chip (iCOGS). We identified one putatively pathogenic missense mutation c.541C>T among the Finnish cancer patients and subsequently genotyped the mutation in additional breast cancer cases (n = 5259) and population controls (n = 3586) from Finland and Belarus. No significant association with breast cancer risk was seen in the meta-analysis of the Finnish datasets or in the large BCAC dataset. The association with previously identified risk variants rs999737, rs2588809, and rs1314913 was replicated among all breast cancer cases and also among familial cases in the BCAC dataset. The most significant association was observed for the haplotype carrying the risk-alleles of all the three SNPs both among all cases (odds ratio (OR): 1.15, 95% confidence interval (CI): 1.11-1.19, P = 8.88 × 10-16) and among familial cases (OR: 1.24, 95% CI: 1.16-1.32, P = 6.19 × 10-11), compared to the haplotype with the respective protective alleles. Our results suggest that loss-of-function mutations in RAD51B are rare, but common variation at the RAD51B region is significantly associated with familial breast cancer risk.</p