Social physique anxiety and physical activity in early adolescent girls : the influence of maturation and physical activity motives

This study considered the influence of maturation on social physique anxiety (SPA), the relationship between SPA and current and future physical activity (PA) levels and the influence of motives for physical activity on this relationship in early adolescent girls (n=162; mean age=11.80±0.33 years). Participants completed the Pubertal Development Scale, the modified Social Physique Anxiety Scale and the Motives for Physical Activity Scale at baseline and the Physical Activity Questionnaire for Older Children at baseline and 6 months later. The girls became less active across the 6 months and girls in the early stages of maturation had significantly lower SPA than the girls in the middle and late stages of maturation. SPA was not related to current or future physical activity in the sample as a whole. Cluster analysis identified four groups with different motive profiles and the High Appearance and Fitness group demonstrated a moderate negative relationship between SPA and PA at phase 1, whereas the other groups did not. These findings indicate that SPA may increase with maturation and the relationship between SPA and PA is dependent on reasons for being active. For girls who are motivated to be active primarily by body-related reasons SPA is likely to lead to lower levels of PA

Practitioner compression force variation in mammography : a 6 year study

The application of breast compression in mammography may be more heavily influenced by the practitioner rather than the client. This could affect image quality and will affect client experience. This study builds on previous research to establish if mammography practitioners vary in the compression force they apply over a six year period. This longitudinal study assessed 3 consecutive analogue screens of 500 clients within one screening centre in the UK. Recorded data included: practitioner code, applied pressure (daN), breast thickness (mm), BI-RADS® density category and breast dose. Exclusion criteria included: previous breast surgery, previous/ongoing assessment, breast implants. 344 met inclusion criteria. Data analysis: assessed variation of compression force (daN) and breast thickness (mm) over 3 sequential screens to determine whether compression force and breast thickness were affected by practitioner variations. Compression force over the 3 screens varied significantly; variation was highly dependent upon the practitioner who performed the mammogram. Significant thickness and compression force differences over the 3 screens were noted for the same client (<0.0001). The amount of compression force applied was highly dependent upon the practitioner. Practitioners fell into one of three practitioner compression groups by their compression force mean values; high (mean 12.6daN), intermediate (mean 8.9daN) and low (mean 6.7daN). For the same client, when the same practitioner performed the 3 screens, maximum compression force variations were low and not significantly different (p>0.31). When practitioners from different compression force groups performed 3 screens, maximum compression force variations were higher and significantly different (p<0.0001). The amount of compression force used is highly dependent upon practitioner rather than client. This has implications for radiation dose, patient experience and image quality consistency

Recollections of pressure to eat during childhood, but not picky eating, predict young adult eating behavior

Picky eating is a childhood behavior that vexes many parents and is a symptom in the newer diagnosis of Avoidant/Restrictive Food Intake Disorder (ARFID) in adults. Pressure to eat, a parental controlling feeding practice aimed at encouraging a child to eat more, is associated with picky eating and a number of other childhood eating concerns. Low intuitive eating, an insensitivity to internal hunger and satiety cues, is also associated with a number of problem eating behaviors in adulthood. Whether picky eating and pressure to eat are predictive of young adult eating behavior is relatively unstudied. Current adult intuitive eating and disordered eating behaviors were self-reported by 170 college students, along with childhood picky eating and pressure through retrospective self- and parent reports. Hierarchical regression analyses revealed that childhood parental pressure to eat, but not picky eating, predicted intuitive eating and disordered eating symptoms in college students. These findings suggest that parental pressure in childhood is associated with problematic eating patterns in young adulthood. Additional research is needed to understand the extent to which parental pressure is a reaction to or perhaps compounds the development of problematic eating behavior

The Continuing Use of Problematic Sexual Stereotypes in Judicial Decision-Making

This article examines the continuing use of problematic sexual stereotypes at appellate level in the English and Welsh legal system. Using five cases as illustrations, it argues that, notwithstanding professional training and guidance on sexual equality matters, certain senior judges in this jurisdiction still at least sometimes openly employ crude and problematic sexual stereotypes in their judgments or fail to deal appropriately with the use of these stereotypes by trial judges. The central point is that there is still a significant problem with the open use of crude sexual stereotypes in legal reasoning at a senior level in this jurisdiction, despite the pressure on all members of the legal system to appear to be ‘politically correct’

Germline variation at 8q24 and prostate cancer risk in men of European ancestry

Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and 52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p < 4.28 × 10−15), including three risk variants that have yet to be reported. From a polygenic risk score (PRS) model, derived to assess the cumulative effect of risk variants at 8q24, men in the top 1% of the PRS have a 4-fold (95%CI = 3.62–4.40) greater risk compared to the population average. These 12 variants account for ~25% of what can be currently explained of the familial risk of prostate cancer by known genetic risk factors. These findings highlight the overwhelming contribution of germline variation at 8q24 on prostate cancer risk which has implications for population risk stratification

Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction.

Prostate cancer is a highly heritable disease with large disparities in incidence rates across ancestry populations. We conducted a multiancestry meta-analysis of prostate cancer genome-wide association studies (107,247 cases and 127,006 controls) and identified 86 new genetic risk variants independently associated with prostate cancer risk, bringing the total to 269 known risk variants. The top genetic risk score (GRS) decile was associated with odds ratios that ranged from 5.06 (95% confidence interval (CI), 4.84-5.29) for men of European ancestry to 3.74 (95% CI, 3.36-4.17) for men of African ancestry. Men of African ancestry were estimated to have a mean GRS that was 2.18-times higher (95% CI, 2.14-2.22), and men of East Asian ancestry 0.73-times lower (95% CI, 0.71-0.76), than men of European ancestry. These findings support the role of germline variation contributing to population differences in prostate cancer risk, with the GRS offering an approach for personalized risk prediction

New loci for body fat percentage reveal link between adiposity and cardiometabolic disease risk

To increase our understanding of the genetic basis of adiposity and its links to cardiometabolic disease risk, we conducted a genome-wide association meta-analysis of body fat percentage (BF%) in up to 100,716 individuals. Twelve loci reached genome-wide significance (P<5 × 10−8), of which eight were previously associated with increased overall adiposity (BMI, BF%) and four (in or near COBLL1/GRB14, IGF2BP1, PLA2G6, CRTC1) were novel associations with BF%. Seven loci showed a larger effect on BF% than on BMI, suggestive of a primary association with adiposity, while five loci showed larger effects on BMI than on BF%, suggesting association with both fat and lean mass. In particular, the loci more strongly associated with BF% showed distinct cross-phenotype association signatures with a range of cardiometabolic traits revealing new insights in the link between adiposity and disease risk

A principal component meta-analysis on multiple anthropometric traits identifies novel loci for body shape

Large consortia have revealed hundreds of genetic loci associated with anthropometric traits, one trait at a time. We examined whether genetic variants affect body shape as a composite phenotype that is represented by a combination of anthropometric traits. We developed an approach that calculates averaged PCs (AvPCs) representing body shape derived from six anthropometric traits (body mass index, height, weight, waist and hip circumference, waist-to-hip ratio). The first four AvPCs explain >99% of the variability, are heritable, and associate with cardiometabolic outcomes. We performed genome-wide association analyses for each body shape composite phenotype across 65 studies and meta-analysed summary statistics. We identify six novel loci: LEMD2 and CD47 for AvPC1, RPS6KA5/C14orf159 and GANAB for AvPC3, and ARL15 and ANP32 for AvPC4. Our findings highlight the value of using multiple traits to define complex phenotypes for discovery, which are not captured by single-trait analyses, and may shed light onto new pathways

Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants

Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Peer reviewe