Fast Reconstruction of Cracks Using Boundary Measurements

This paper develops a fast algorithm for locating one or more perfectly insulating, pair-wise disjoint, linear cracks in a homogeneous two-dimensional electrical conductor, using boundary measurements

Ambient air pollution exposure and full-term birth weight in California

<p>Abstract</p> <p>Background</p> <p>Studies have identified relationships between air pollution and birth weight, but have been inconsistent in identifying individual pollutants inversely associated with birth weight or elucidating susceptibility of the fetus by trimester of exposure. We examined effects of prenatal ambient pollution exposure on average birth weight and risk of low birth weight in full-term births.</p> <p>Methods</p> <p>We estimated average ambient air pollutant concentrations throughout pregnancy in the neighborhoods of women who delivered term singleton live births between 1996 and 2006 in California. We adjusted effect estimates of air pollutants on birth weight for infant characteristics, maternal characteristics, neighborhood socioeconomic factors, and year and season of birth.</p> <p>Results</p> <p>3,545,177 singleton births had monitoring for at least one air pollutant within a 10 km radius of the tract or ZIP Code of the mother's residence. In multivariate models, pollutants were associated with decreased birth weight; -5.4 grams (95% confidence interval -6.8 g, -4.1 g) per ppm carbon monoxide, -9.0 g (-9.6 g, -8.4 g) per pphm nitrogen dioxide, -5.7 g (-6.6 g, -4.9 g) per pphm ozone, -7.7 g (-7.9 g, -6.6 g) per 10 <it>μ</it>g/m³particulate matter under 10 μm, -12.8 g (-14.3 g, -11.3 g) per 10 <it>μ</it>g/m³particulate matter under 2.5 μm, and -9.3 g (-10.7 g, -7.9 g) per 10 <it>μ</it>g/m³of coarse particulate matter. With the exception of carbon monoxide, estimates were largely unchanged after controlling for co-pollutants. Effect estimates for the third trimester largely reflect the results seen from full pregnancy exposure estimates; greater variation in results is seen in effect estimates specific to the first and second trimesters.</p> <p>Conclusions</p> <p>This study indicates that maternal exposure to ambient air pollution results in modestly lower infant birth weight. A small decline in birth weight is unlikely to have clinical relevance for individual infants, and there is debate about whether a small shift in the population distribution of birth weight has broader health implications. However, the ubiquity of air pollution exposures, the responsiveness of pollutant levels to regulation, and the fact that the highest pollution levels in California are lower than those regularly experienced in other countries suggest that precautionary efforts to reduce pollutants may be beneficial for infant health from a population perspective.</p

Air Pollution, Urgent Asthma Medical Visits and the Modifying Effect of Neighborhood Asthma Prevalence

Background: Social and environmental stressors, may modify associations between environmental pollutants and asthma symptoms. We examined if neighborhood asthma prevalence (higher: HAPN vs. lower: LAPN), a surrogate for underlying risk factors for asthma, modified the relationship between pollutants and urgent asthma visits. Methods: Through zip code, home addresses were linked to New York City Community Air Survey’s land use regression model for street-level, annual average nitrogen dioxide (NO2), particulate matter (PM2.5), elemental carbon (EC); summer average ozone (O3); winter average sulfur dioxide (SO2) concentrations. Poisson regression models were fit to estimate the association (prevalence ratio, PR) between pollutant exposures and seeking urgent asthma care. Results: All pollutants, except O3 were higher in HAPN than LAPN (P0.05). Conclusions: Relationships between modeled street-level pollutants and urgent asthma were stronger in LAPN compared to HAPN. Social stressors that may be more prevalent in HAPN than LAPN, could play a greater role in asthma exacerbations in HAPN versus pollutant exposure alone

Cars, corporations, and commodities: Consequences for the social determinants of health

Social epidemiologists have drawn attention to health inequalities as avoidable and inequitable, encouraging thinking beyond proximal risk factors to the causes of the causes. However, key debates remain unresolved including the contribution of material and psychosocial pathways to health inequalities. Tools to operationalise social factors have not developed in tandem with conceptual frameworks, and research has often remained focused on the disadvantaged rather than on forces shaping population health across the distribution. Using the example of transport, we argue that closer attention to social processes (capital accumulation and motorisation) and social forms (commodity, corporation, and car) offers a way forward. Corporations tied to the car, primarily oil and vehicle manufacturers, are central to the world economy. Key drivers in establishing this hegemony are the threat of violence from motor vehicles and the creation of distance through the restructuring of place. Transport matters for epidemiology because the growth of mass car ownership is environmentally unsustainable and affects population health through a myriad of pathways. Starting from social forms and processes, rather than their embodiment as individual health outcomes and inequalities, makes visible connections between road traffic injuries, obesity, climate change, underdevelopment of oil producing countries, and the huge opportunity cost of the car economy. Methodological implications include a movement-based understanding of how place affects health and a process-orientated integration of material and psychosocial explanations that, while materially based, contests assumptions of automatic benefits from economic growth. Finally, we identify car and oil corporations as anti-health forces and suggest collaboration with them creates conflicts of interest

A pilot study of Aboriginal health promotion from an ecological perspective

<p>Abstract</p> <p>Background</p> <p>For health promotion to be effective in Aboriginal and Torres Strait Islander Communities, interventions (and their evaluation) need to work within a complex social environment and respect Indigenous knowledge, culture and social systems. At present, there is a lack of culturally appropriate evaluation methods available to practitioners that are capable of capturing this complexity. As an initial response to this problem, we used two non-invasive methods to evaluate a community-directed health promotion program, which aimed to improve nutrition and physical activity for members of the Aboriginal community of the Goulburn-Murray region of northern Victoria, Australia. The study addressed two main questions. First, for members of an Aboriginal sporting club, what changes were made to the nutrition environment in which they meet and how is this related to national guidelines for minimising the risk of chronic disease? Second, to what degree was the overall health promotion program aligned with an ecological model of health promotion that addresses physical, social and policy environments as well as individual knowledge and behaviour?</p> <p>Methods</p> <p>Rather than monitoring individual outcomes, evaluation methods reported on here assessed change in the nutrition environment (sports club food supply) as a facilitator of dietary change and the 'ecological' nature of the overall program (that is, its complexity with respect to numbers of targets, settings and strategies).</p> <p>Results</p> <p>There were favourable changes towards the provision of a food supply consistent with Australian guidelines at the sports club. The ecological analysis indicated that the design and implementation of the program were consistent with an ecological model of health promotion.</p> <p>Conclusions</p> <p>The evaluation was useful for assessing the impact of the program on the nutrition environment and for understanding the ecological nature of program activities.</p

Design, baseline characteristics, and retention of African American light smokers into a randomized trial involving biological data

<p>Abstract</p> <p>Background</p> <p>African Americans experience significant tobacco-related health disparities despite the fact that over half of African American smokers are light smokers (use ≤10 cigarettes per day). African Americans have been under-represented in smoking cessation research, and few studies have evaluated treatment for light smokers. This paper describes the study design, measures, and baseline characteristics from <it>Kick It at Swope III </it>(KIS-III), the first treatment study of bupropion for African American light smokers.</p> <p>Methods</p> <p>Five hundred forty African American light smokers were randomly assigned to receive bupropion (150mg bid) (n = 270) or placebo (n = 270) for 7 weeks. All participants received written materials and health education counseling. Participants responded to survey items and provided blood samples for evaluation of phenotype and genotype of CYP2A6 and CYP2B6 enzymes involved in nicotine and bupropion metabolism. Primary outcome was cotinine-verified 7-day point prevalence smoking abstinence at Week 26 follow-up.</p> <p>Results</p> <p>Of 2,628 individuals screened, 540 were eligible, consented, and randomized to treatment. Participants had a mean age of 46.5 years and 66.1% were women. Participants smoked an average of 8.0 cigarettes per day, had a mean exhaled carbon monoxide of 16.4ppm (range 1-55) and a mean serum cotinine of 275.8ng/ml. The mean Fagerström Test for Nicotine Dependence was 3.2, and 72.2% of participants smoked within 30 minutes of waking. The average number of quit attempts in the past year was 3.7 and 24.2% reported using pharmacotherapy in their most recent quit attempt. Motivation and confidence to quit were high.</p> <p>Conclusion</p> <p>KIS-III is the first study designed to examine both nicotine and bupropion metabolism, evaluating CYP2A6 and CYP2B6 phenotype and genotype in conjunction with psychosocial factors, in the context of treatment of African American light smokers. Of 1629 smokers screened for study participation, only 18 (1.1%) were ineligible to participate in the study because they refused blood draws, demonstrating the feasibility of recruiting and enrolling African American light smokers into a clinical treatment trial involving biological data collection and genetic analyses. Future evaluation of individual factors associated with treatment outcome will contribute to advancing tailored tobacco use treatment with the goal of enhancing treatment and reducing health disparities for African American light smokers.</p> <p>Trial Registration</p> <p>ClinicalTrials.gov: <a href="URL">NCT00666978</a></p

Experiences of University Life for Students with Asperger’s Syndrome: a comparative study between Spain and England

Research has consistently shown that young people with Asperger’s Syndrome (AS) are likely to experience increased anxiety during new social situations; yet, studies have been regionally and culturally bound. The aim of this study was to explore how higher education students with AS experienced attending university in two European countries: the UK and Spain. The objective was to find out if experiences differed between the two countries in relation to contrasting support arrangements and what kinds of interventions might aid students’ social well-being at university, an important learning outcome for future practice. This small-scale comparative exploratory study incorporated life-history interviews with nine students with AS. The interviews were transcribed verbatim and subjected to Interpretative Phenomenological Analysis. Four superordinate themes significant to both groups of students in Spain and the UK emerged from the data: social relationships, ‘special interests’, ‘environment’ and ‘support mechanisms’. Students with AS need and want clear, unambiguous and structured information from academics; support to get to know others in ‘small special interest groups’; more designated ‘quiet zones’ across campuses; and above all, a move away from ableist notions of AS. To our knowledge, this is the only Spanish–UK comparative study of university students with AS

Large scale multifactorial likelihood quantitative analysis of BRCA1 and BRCA2 variants: An ENIGMA resource to support clinical variant classification

The multifactorial likelihood analysis method has demonstrated utility for quantitative assessment of variant pathogenicity for multiple cancer syndrome genes. Independent data types currently incorporated in the model for assessing BRCA1 and BRCA2 variants include clinically calibrated prior probability of pathogenicity based on variant location and bioinformatic prediction of variant effect, co-segregation, family cancer history profile, co-occurrence with a pathogenic variant in the same gene, breast tumor pathology, and case-control information. Research and clinical data for multifactorial likelihood analysis were collated for 1,395 BRCA1/2 predominantly intronic and missense variants, enabling classification based on posterior probability of pathogenicity for 734 variants: 447 variants were classified as (likely) benign, and 94 as (likely) pathogenic; and 248 classifications were new or considerably altered relative to ClinVar submissions. Classifications were compared with information not yet included in the likelihood model, and evidence strengths aligned to those recommended for ACMG/AMP classification codes. Altered mRNA splicing or function relative to known nonpathogenic variant controls were moderately to strongly predictive of variant pathogenicity. Variant absence in population datasets provided supporting evidence for variant pathogenicity. These findings have direct relevance for BRCA1 and BRCA2 variant evaluation, and justify the need for gene-specific calibration of evidence types used for variant classification

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice