PEAK RATE OF TRUNK ENERGY OUTFLOW DIFFERS BETWEEN PITCH TYPES IN SOFTBALL PITCHERS

In softball players, it is unclear how certain pitch types may increase the risk of injury. The purpose of this study was to determine energy flow differences in the trunk and upper-arm segments between pitch types. Twenty-three softball pitchers participated. Absolute values of trunk energy inflow (IF) and outflow (OF), and upper arm IF, as well as segment energy flow when normalized to pitch speed were assessed in three pitch types. Differences between trunk energy OF were found between fastballs compared to curveballs and dropballs. When normalized to pitch speed, trunk energy OF only differed between fastballs and dropballs. For the upper arm, absolute differences were found between the fastball and curveball. Similar rates of humerus IF between the fastball and dropball and less trunk outflow in the dropball may indicate increased upper extremity demands in the dropball

EFFICIENCY INDEX USED TO ASSESS SHOULDER STRESS IN COLLEGE SOFTBALL PITCHERS THROUGHOUT A SIMULATED GAME

Shoulder distraction forces in softball pitching are known to have a positive impact on performance yet a negative impact on musculoskeletal health. The purpose of this study was to assess changes in shoulder stress across innings pitched using Efficiency Arm-Stress Index (EASI) scores. Motion capture was used on collegiate softball pitchers pitching a simulated game. Peak shoulder distraction force was obtained using inverse dynamics procedures and used to calculate an EASI score (fastball velocity divided by peak shoulder distraction force in percent body weight). A RM·ANOVA revealed inning had no effect on EASI score (F[6,7]=1.28, p=0.286). Understanding a pitcher’s efficiency score may help shape individual pitching loads. Future work should investigate clinically meaningful changes in efficiency scores and mechanisms behind low efficiencies

What are we missing? Risk behaviors among Arabâ American adolescents and emerging adults

Background and purposeResearch on Arabâ Americans as a distinct ethnic group is limited, especially when considering the health of Arabâ American youth. This study describes health risk (substance use, violence); health promotive behaviors (hope, spirituality); and sexual activity (oral, vaginal, anal sex) of Arabâ American adolescents and emerging adults (aged 15â 23) within their life context, as well as the association between these behaviors.MethodsA secondary analysis of data on a subset of Arabâ American participants obtained from a randomizedâ control trial was utilized to conduct mixed methods analyses. Qualitative analyses completed on the openâ ended questions used the constant comparative method for a subsample (n = 24) of participants. Descriptive quantitative analyses of survey data utilized bivariate analyses and stepwise logistic regression to explore the relation between risk behaviors and sexual activity among the full sample (n = 57).ConclusionsQualitative analyses revealed two groups of participants: (a) multiple risk behaviors and negative lifeâ events, and (b) minimal risk behaviors and positive lifeâ events. Quantitative analyses indicated older youth, smokers, and those with higher hope pathways were more likely to report vaginal sex.Implications for practiceThe unique cultural and social contexts of Arabâ American youth provide a framework for recommendations for the prevention of risk behaviors.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/134166/1/jaan12352.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/134166/2/jaan12352_am.pd

Exome-wide association study to identify rare variants influencing COVID-19 outcomes : Results from the Host Genetics Initiative

Publisher Copyright: Copyright: © 2022 Butler-Laporte et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Host genetics is a key determinant of COVID-19 outcomes. Previously, the COVID-19 Host Genetics Initiative genome-wide association study used common variants to identify multiple loci associated with COVID-19 outcomes. However, variants with the largest impact on COVID-19 outcomes are expected to be rare in the population. Hence, studying rare variants may provide additional insights into disease susceptibility and pathogenesis, thereby informing therapeutics development. Here, we combined whole-exome and whole-genome sequencing from 21 cohorts across 12 countries and performed rare variant exome-wide burden analyses for COVID-19 outcomes. In an analysis of 5,085 severe disease cases and 571,737 controls, we observed that carrying a rare deleterious variant in the SARS-CoV-2 sensor toll-like receptor TLR7 (on chromosome X) was associated with a 5.3-fold increase in severe disease (95% CI: 2.75–10.05, p = 5.41x10-7). This association was consistent across sexes. These results further support TLR7 as a genetic determinant of severe disease and suggest that larger studies on rare variants influencing COVID-19 outcomes could provide additional insights.Peer reviewe

Trans-ancestry meta-analyses identify rare and common variants associated with blood pressure and hypertension

High blood pressure is a major risk factor for cardiovascular disease and premature death. However, there is limited knowledge on specific causal genes and pathways. To better understand the genetics of blood pressure, we genotyped 242,296 rare, low-frequency and common genetic variants in up to ~192,000 individuals, and used ~155,063 samples for independent replication. We identified 31 novel blood pressure or hypertension associated genetic regions in the general population, including three rare missense variants in RBM47, COL21A1 and RRAS with larger effects (>1.5mmHg/allele) than common variants. Multiple rare, nonsense and missense variant associations were found in A2ML1 and a low-frequency nonsense variant in ENPEP was identified. Our data extend the spectrum of allelic variation underlying blood pressure traits and hypertension, provide new insights into the pathophysiology of hypertension and indicate new targets for clinical intervention

Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk.

Blood pressure is a heritable trait influenced by several biological pathways and responsive to environmental stimuli. Over one billion people worldwide have hypertension (≥140 mm Hg systolic blood pressure or  ≥90 mm Hg diastolic blood pressure). Even small increments in blood pressure are associated with an increased risk of cardiovascular events. This genome-wide association study of systolic and diastolic blood pressure, which used a multi-stage design in 200,000 individuals of European descent, identified sixteen novel loci: six of these loci contain genes previously known or suspected to regulate blood pressure (GUCY1A3-GUCY1B3, NPR3-C5orf23, ADM, FURIN-FES, GOSR2, GNAS-EDN3); the other ten provide new clues to blood pressure physiology. A genetic risk score based on 29 genome-wide significant variants was associated with hypertension, left ventricular wall thickness, stroke and coronary artery disease, but not kidney disease or kidney function. We also observed associations with blood pressure in East Asian, South Asian and African ancestry individuals. Our findings provide new insights into the genetics and biology of blood pressure, and suggest potential novel therapeutic pathways for cardiovascular disease prevention

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

Causal effect of plasminogen activator inhibitor type 1 on coronary heart disease

Background--Plasminogen activator inhibitor type 1 (PAI-1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI-1 levels are associated with increased risk of coronary heart disease (CHD). However, it is unclear whether the association reflects a causal influence of PAI-1 on CHD risk. Methods and Results--To evaluate the association between PAI-1 and CHD, we applied a 3-step strategy. First, we investigated the observational association between PAI-1 and CHD incidence using a systematic review based on a literature search for PAI-1 and CHD studies. Second, we explored the causal association between PAI-1 and CHD using a Mendelian randomization approach using summary statistics from large genome-wide association studies. Finally, we explored the causal effect of PAI-1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta-analysis, the highest quantile of blood PAI-1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age- and sex-adjusted model. The effect size was reduced in studies using a multivariable-adjusted model (odds ratio=1.46; 95% CI: 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI-1 level on CHD risk (odds ratio=1.22 per unit increase of log-transformed PAI-1; 95% CI: 1.01, 1.47). In addition, we also detected a causal effect of PAI-1 on elevating blood glucose and high-density lipoprotein cholesterol. Conclusions--Our study indicates a causal effect of elevated PAI-1 level on CHD risk, which may be mediated by glucose dysfunction