Gender, Media and Leader Emergence: Examining the Impression Management Strategies of Men and Women in Different Settings

This study examined the impact of media (face-to-face versus computer-mediated communication) on the process of leadership emergence by females and males. Specifically, we adapted the literature associated with impression management to investigate whether there are any differences in terms of two key impression management behaviors- self-promotion and supplication- between males and females who emerged as leaders in face-to-face and technology-mediated settings. Our findings challenge conventional gender-related findings. The results indicated that self-promotion plays an important role in influencing leadership emergence while supplication negatively impacts leadership emergence. In a face-to-face context, females who emerged as leaders were found to employ more self-promotion tactics than male leaders while female leaders and male leaders did not differ with respect to the amount of supplication tactics used. Females who emerged as leaders in a face-to-face context were also found to engage in greater self-promotion and more supplication tactics than females who emerged as leaders in a CmC context. Interestingly, there was no significant impact of media on the extent of self-promotion and supplication strategies displayed by male leaders. Future research avenues and implications are discussed

Hospital Outcomes of Spontaneous Coronary Artery Dissection With Concurrent Ventricular Arrhythmias

Background While patients with spontaneous coronary artery dissection (SCAD) occasionally present with concurrent ventricular arrhythmias (VA), the impact of VA on in-hospital outcomes in the United States (US) is not well-established. This study aims to analyze in-hospital outcomes of patients with SCAD and concurrent VA and to determine the factors associated with VA occurrence in this high-risk population in the US. Methods Using the Nationwide Readmissions Database, our study included patients age 18 years or older who had SCAD between 2017 and 2020. We categorized the cohort into 2 groups depending on the presence of VA during hospitalization. In-hospital outcomes were assessed between SCAD patients with VA and those without. Weighted analysis was performed. We analyzed the independent factors associated with VA occurring among SCAD patients through univariable and multivariable analyses. Results Eight hundred seventy-seven SCAD patients were included in the study: 118 (13.5%) with VA and 759 (86.6%) without. SCAD patients with concurrent VA were associated with higher rates of early mortality (10.2% vs 2.0%; P \u3c .01), prolonged index hospital stay (≥7 days) (33.1% vs 11.7%; P \u3c .01), and non-home discharge (21.2% vs 5.9%; P \u3c .01). The length of hospital stay was longer in the SCAD with concurrent VA group (7.39 days vs 3.58 days; P \u3c .01), and the median cumulative cost of hospitalization was also higher in this group ($31,451 vs$13,802; P \u3c .01). SCAD patients with concurrent VA had increased in-hospital adverse events: acute heart failure, cardiac arrest, cardiogenic shock, cerebral infarction, pulmonary edema, and acute kidney injury. In multivariable analysis, the independent factors associated with VA occurrence among SCAD patients were chronic liver disease (aOR, 3.42; 95% CI, 1.43-8.20; P \u3c .01) and heart failure (aOR, 5.63; 95% CI, 3.36-9.42; P \u3c .01). Conclusions Concurrence of VA among SCAD patients was associated with poorer in-hospital outcomes. Heart failure and chronic liver disease were the independent factors associated with VA occurrence in SCAD patients

Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.

Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition

Biological effects of cobalt-chromium nanoparticles and ions on dural fibroblasts and dural epithelial cells.

The introduction of metal-on-metal total disc replacements motivated studies to evaluate the effects of cobalt-chromium (CoCr) nanoparticles on cells of the dura mater. Porcine fibroblasts and epithelial cells isolated from the dura mater were cultured with clinically-relevant CoCr nanoparticles and the ions, generated by the particles over 24 h, at doses up to 121 μm(3)per cell. Cell viability and production of proinflammatory cytokines was assessed over 4 days. The capacity of the particles to induce oxidative stress in the cells was evaluated at 24 h. The CoCr particles and their ions significantly reduced the viability of the dural epithelial cells in a dose-dependent manner but not the fibroblasts. Both cell types secreted IL-8 in response to particle exposure at doses of 60.5 μm(3) (epithelial cells) and 121 μm(3) (fibroblasts, epithelial cells) per cell. No significant release of IL-6 was observed in both cell types at any dose. Reactive oxygen species were induced in both cell types at 50 μm(3) per cell after 24 h exposure. The data suggested novel differences in the resistance of the dural epithelial cells and fibroblasts to CoCr nanoparticle/ion toxicity and demonstrated the inflammatory potential of the particles. The data contributes to a greater understanding of the potential biological consequences of the use of metal-on-metal total disc prostheses

Objectively measured patterns of sedentary time and physical activity in young adults of the Raine study cohort

Background: To provide a detailed description of young adults' sedentary time and physical activity. Methods: 384 young women and 389 young men aged 22.1±0.6 years, all participants in the 22 year old follow-up of the Raine Study pregnancy cohort, wore Actigraph GT3X+ monitors on the hip for 24 h/day over a one-week period for at least one 'valid' day (=10 h of waking wear time). Each minute epoch was classified as sedentary, light, moderate or vigorous intensity using 100 count and Freedson cut-points. Mixed models assessed hourly and daily variation; t-tests assessed gender differences. Results: The average (mean±SD) waking wear time was 15.0±1.6 h/day, of which 61.4±10.1 % was spent sedentary, 34.6±9.1 % in light-, 3.7±5.3 % in moderate- and, 0.3±0.6 % in vigorous-intensity activity. Average time spent in moderate to vigorous activity (MVPA) was 36.2±27.5 min/day. Relative to men, women had higher sedentary time, but also higher vigorous activity time. The 'usual' bout duration of sedentary time was 11.8±4.5 min in women and 11.7±5.2 min in men. By contrast, other activities were accumulated in shorter bout durations. There was large variation by hour of the day and by day of the week in both sedentary time and MVPA. Evenings and Sundays through Wednesdays tended to be particularly sedentary and/or inactive. Conclusion: For these young adults, much of the waking day was spent sedentary and many participants were physically inactive (low levels of MVPA). We provide novel evidence on the time for which activities were performed and on the time periods when young adults were more sedentary and/or less active. With high sedentary time and low MVPA, young adults may be at risk for the life-course sequelae of these behaviours

The genetic architecture of type 2 diabetes

The genetic architecture of common traits, including the number, frequency, and effect sizes of inherited variants that contribute to individual risk, has been long debated. Genome-wide association studies have identified scores of common variants associated with type 2 diabetes, but in aggregate, these explain only a fraction of heritability. To test the hypothesis that lower-frequency variants explain much of the remainder, the GoT2D and T2D-GENES consortia performed whole genome sequencing in 2,657 Europeans with and without diabetes, and exome sequencing in a total of 12,940 subjects from five ancestral groups. To increase statistical power, we expanded sample size via genotyping and imputation in a further 111,548 subjects. Variants associated with type 2 diabetes after sequencing were overwhelmingly common and most fell within regions previously identified by genome-wide association studies. Comprehensive enumeration of sequence variation is necessary to identify functional alleles that provide important clues to disease pathophysiology, but large-scale sequencing does not support a major role for lower-frequency variants in predisposition to type 2 diabetes

Genome-wide Analyses Identify KIF5A as a Novel ALS Gene

To identify novel genes associated with ALS, we undertook two lines of investigation. We carried out a genome-wide association study comparing 20,806 ALS cases and 59,804 controls. Independently, we performed a rare variant burden analysis comparing 1,138 index familial ALS cases and 19,494 controls. Through both approaches, we identified kinesin family member 5A (KIF5A) as a novel gene associated with ALS. Interestingly, mutations predominantly in the N-terminal motor domain of KIF5A are causative for two neurodegenerative diseases: hereditary spastic paraplegia (SPG10) and Charcot-Marie-Tooth type 2 (CMT2). In contrast, ALS-associated mutations are primarily located at the C-terminal cargo-binding tail domain and patients harboring loss-of-function mutations displayed an extended survival relative to typical ALS cases. Taken together, these results broaden the phenotype spectrum resulting from mutations in KIF5A and strengthen the role of cytoskeletal defects in the pathogenesis of ALS.Peer reviewe