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Physical exercise requiring oxidative energy transfer increases pulmonary ventilation (VE). In an air polluted environment, the exercise-induced increase in VE increases the volume of toxic gases and number of toxic particles to which the pulmonary system is exposed. Using a respiratory air-filtering device (RAFD) during exercise decreases exposure to inhaled toxic gases and particles. However, a RAFD creates external resistance to inspiration and expiration which could decrease pulmonary muscle function and pulmonary volumes, and creates an external mechanical dead-space which produces fractional rebreathing which could increase pulmonary flowrates. This experiment tested the hypotheses that using a RAFD during exercise would; decrease post-exercise peak inspiratory pressure (PPI) and peak expiratory (PPE) pressure, FVC and FEV1, and increase post-exercise flowrates. Using a repeated-measures, counter-balanced design, six healthy moderately aerobically-trained, men (mean ± SD; age 24.7 ± 1.7 years; peak oxygen utilization [VO2peak] 42.8 ± 5.3 ml kg-1 min-1) completed two 30 min exercise test sessions at a power output equal to 75% VO2peak. One session was performed not using (NORAFD), and one using a RAFD (Moldex 8000) fitted with organic vapor cartridges and combined dust and mist pre-filters (inspiratory resistance = 0.216 kPa, expiratory resistance = 0.094 kPa at 85.0 l min-1). All pulmonary function tests were performed immediately pre-(Pre) and 0 (Post-0), 5 (Post-5), and 15 (Post-15) min post-exercise. There was a significant (p

To assess the effectiveness of weight-loss interventions on pain and disability in people with knee and hip osteoarthritis (OA) and spinal pain.Intervention systematic review.Twelve online databases and clinical trial registries.Randomized controlled trials of any weight-loss intervention (eg, diet, physical activity, surgical, pharmaceutical) that reported pain or disability outcomes in people with knee or hip OA or spinal pain.We calculated mean differences or standardized mean differences (SMDs) and 95% confidence intervals (CIs). We used the Cochrane risk of bias tool to assess risk of bias and the Grading of Recommendations Assessment, Development, and Evaluation tool to judge credibility of evidence.Twenty-two trials with 3602 participants were included. There was very low- to very low-credibility evidence for a moderate effect of weight-loss interventions on pain intensity (10 trials, n = 1806; SMD, -0.54; 95% CI: -0.86, -0.22; IWeight-loss interventions may provide small to moderate improvements in pain and disability for OA compared to minimal care. There was limited and inconclusive evidence for weight-loss interventions targeting spinal pain.

This paper explores the application of ethics in two contrasting approaches to evaluation: one that views evaluation as essentially a research project, and the other that sees evaluation as an extension of project management. We argue that the growth in so-called rigorous impact evaluation, characterised by practitioners as evaluation using experimental or quasi-experimental methods, has seen evaluation treated increasingly as a subset of research. This has entailed greater use of ethical committees, and specifically institutional review boards (IRBs), as many academics promoting the use of experimental methods are based in the USA. Elsewhere, evaluation is treated more as a management activity, with professionalisation initiatives such as membership standards and ethical guidance often used in the place of formal review. In this paper, we question whether the simultaneous growth in usage of IRBs and professionalisation addresses the ethical issues faced by evaluators.

Neighborhood context impacts health. Using an index of geospatial disadvantage measures to predict neighborhood socioeconomic disparities would support area-based allocation of preventative resources, as well as the use of location as a clinical risk factor in care of individual patients. This study tested the association of the Area Deprivation Index (ADI), a neighborhood-based index of socioeconomic contextual disadvantage, with elderly obesity risk. We sampled 5066 Medicare beneficiaries at the University of Missouri between September 1, 2013 and September 1, 2014. We excluded patients with unknown street addresses, excluded body mass index (BMI) lower than 18 or higher than 62 as probable errors, and excluded patients with missing BMI data. We used a plot of simple proportions to examine the association between ADI and prevalence of obesity, defined as BMI of 30 and over. We found that obesity was significantly less prevalent in the least-disadvantaged ADI decile (decile 1) than in all other deciles (p

Williams Syndrome Transcription Factor (WSTF) is one of ∼25 haplodeficient genes in patients with the complex developmental disorder Williams Syndrome (WS). WS results in visual/spatial processing defects, cognitive impairment, unique behavioral phenotypes, characteristic “elfin” facial features, low muscle tone and heart defects. WSTF exists in several chromatin remodeling complexes and has roles in transcription, replication, and repair. Chromatin remodeling is essential during embryogenesis, but WSTF’s role in vertebrate development is poorly characterized. To investigate the developmental role of WSTF, we knocked down WSTF in Xenopus laevis embryos using a morpholino that targets WSTF mRNA. BMP4 shows markedly increased and spatially aberrant expression in WSTF-deficient embryos, while SHH, MRF4, PAX2, EPHA4 and SOX2 expression are severely reduced, coupled with defects in a number of developing embryonic structures and organs. WSTF-deficient embryos display defects in anterior neural development. Induction of the neural crest, measured by expression of the neural crest-specific genes SNAIL and SLUG, is unaffected by WSTF depletion. However, at subsequent stages WSTF knockdown results in a severe defect in neural crest migration and/or maintenance. Consistent with a maintenance defect, WSTF knockdowns display a specific pattern of increased apoptosis at the tailbud stage in regions corresponding to the path of cranial neural crest migration. Our work is the first to describe a role for WSTF in proper neural crest function, and suggests that neural crest defects resulting from WSTF haploinsufficiency may be a major contributor to the pathoembryology of WS.