Investigation of the knowledge of South African high school rugby coaches on concussion and the return-to-play protocol

Background: Coaches are pivotal in the management of concussed players. Assessing the knowledge of high school rugby coaches with regard to concussion management will enable relevant future education on this topic to be covered. Objectives: To investigate the knowledge of South African high school rugby coaches on concussion symptom recognition, knowledge and stepwise return-to-play (RTP) protocols. Methods: A cross-sectional descriptive study involving 143 first team, high school rugby coaches was completed via an electronic questionnaire. Independent variables included coach demographics, qualifications, experience, BokSmart accreditation, and school size. Dependent variables included knowledge scores on concussion symptoms, general concussion knowledge, stepwise RTP and Maddocks questions. Relationships between total scores for different demographic groupings were established using non-parametric techniques. Results: The coaches had high general, symptom and overall concussion knowledge scores (77% - 80%) in contrast with low RTP scores (62%) and very low Maddocks questions knowledge scores (26%). The 35-44-year age group received top scores for symptom recognition (p=0.034) and total concussion knowledge (p=0.041). Larger category school coaches (p=0.008) and BokSmart accredited coaches (p=0.041) outperformed all other coaches in general concussion knowledge and total knowledge, respectively. However, respondents were not familiar with emotional symptoms or the importance of cognitive rest after a concussion. Educational programmes were the most popular knowledge source for coaches. Conclusion: In general, coaches presented with good general concussion knowledge but lesser expertise on emotional symptoms, cognitive rest and RTP management. Modifiable predictors of knowledge included the expansion of BokSmart accreditation, focussing information sessions on smaller rugby size schools and the education of coaches younger than 35 years or older than 45 years of age.

Can diverse herbivore communities increase landscape heterogeneity? Comparing wild and domestic herbivore assemblages in a South African savanna

This research article published by Elsevier, 2015The structure and composition of woody and grassy vegetation in savannas is strongly influenced by herbivores. In recent decades, the proportion of browsers has declined across African savannas in favour of more grazers, triggered by large-scale human-induced cattle grazing. This has led to overgrazing and an imbalance of woody and grassy vegetation. Our study investigated mono-specific and multi-species herbivore assemblages of varying density and assessed similarities in vegetation patterns under wildlife and livestock herbivory in and around Kruger National Park, South Africa. Under mono-specific herbivory, overall tree cover was more than twice as high compared to multi-species herbivory while the branching height of small and tall trees was lowest. Small tree and bush densities were strongly elevated at mono-specific compared to multi-species herbivore sites. Tall trees were dominated by Acacia nigrescens under multi-species herbivory at low wildlife density but not at high density sites. Grass leaf nitrogen contents were almost twice as high at multi compared to mono herbivory sites, particularly beneath tree canopies. Livestock and wildlife herbivore sites showed similar patterns in their woody plant structure and grass nutrients. We conclude that a characteristic herbaceous and woody vegetation structure as well as species composition can be matched with mammalian herbivore communities, which has implications for landscape heterogeneity and grazing management in savanna systems

A comparison between heart rate and heart rate variability as indicators of cardiac health and fitness

Quantification of cardiac autonomic activity and control via heart rate (HR) and heart rate variability (HRV) is known to provide prognostic information in clinical populations. Issues with regard to standardisation and interpretation of HRV data make the use of the more easily accessible HR on its own as an indicator of autonomic cardiac control very appealing. The aim of this study was to investigate the strength of associations between an important cardio vascular health metric such as VO2max and the following: HR, HRV indicators and normalised HRV indicators (divided by mean RR interval). A cross sectional descriptive study was done including 145 healthy volunteers aged between 18 and 22 years. HRV was quantified by time domain, frequency domain and Poincaré plot analysis. Indirect VO2max was determined using the Multistage Coopers test. The Pearson correlation coefficient was calculated to quantify the strength of the associations. Both simple linear and multiple stepwise regressions were performed to be able to discriminate between the role of the individual indicators as well as their combined association with VO2max. Only HR, RR interval and pNN50 showed significant (p<0.01, p<0.01 and p=0.03) correlations with VO2max. Stepwise multiple regression indicated that, when combining all HRV indicators the most important predictor of cardio vascular fitness as represented by VO2max, is HR. HR explains 17% of the variation, while the inclusion of HF (high frequency HRV indicator) added only an additional 3.1% to the coefficient of determination. Results also showed when testing the normalised indicators, HR explained of the largest percentage of the changes in VO2max (16.5%). Thus HR on its own is the most important predictor of changes in an important cardiac health metric such as VO2max. These results may indicate that during investigation of exercise ability (VO2max) phenomena, quantification of HRV may not add significant value.http://www.frontiersin.org/Physiologyhb2014ay201

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

An Analysis of Two Genome-wide Association Meta-analyses Identifies a New Locus for Broad Depression Phenotype

AbstractBackgroundThe genetics of depression has been explored in genome-wide association studies that focused on either major depressive disorder or depressive symptoms with mostly negative findings. A broad depression phenotype including both phenotypes has not been tested previously using a genome-wide association approach. We aimed to identify genetic polymorphisms significantly associated with a broad phenotype from depressive symptoms to major depressive disorder.MethodsWe analyzed two prior studies of 70,017 participants of European ancestry from general and clinical populations in the discovery stage. We performed a replication meta-analysis of 28,328 participants. Single nucleotide polymorphism (SNP)-based heritability and genetic correlations were calculated using linkage disequilibrium score regression. Discovery and replication analyses were performed using a p-value-based meta-analysis. Lifetime major depressive disorder and depressive symptom scores were used as the outcome measures.ResultsThe SNP-based heritability of major depressive disorder was 0.21 (SE = 0.02), the SNP-based heritability of depressive symptoms was 0.04 (SE = 0.01), and their genetic correlation was 1.001 (SE = 0.2). We found one genome-wide significant locus related to the broad depression phenotype (rs9825823, chromosome 3: 61,082,153, p = 8.2 × 10–9) located in an intron of the FHIT gene. We replicated this SNP in independent samples (p = .02) and the overall meta-analysis of the discovery and replication cohorts (1.0 × 10–9).ConclusionsThis large study identified a new locus for depression. Our results support a continuum between depressive symptoms and major depressive disorder. A phenotypically more inclusive approach may help to achieve the large sample sizes needed to detect susceptibility loci for depression

Genetic and environmental variation in educational attainment : an individual-based analysis of 28 twin cohorts

We investigated the heritability of educational attainment and how it differed between birth cohorts and cultural-geographic regions. A classical twin design was applied to pooled data from 28 cohorts representing 16 countries and including 193,518 twins with information on educational attainment at 25 years of age or older. Genetic factors explained the major part of individual differences in educational attainment (heritability: a(2)=0.43; 0.41-0.44), but also environmental variation shared by co-twins was substantial (c(2)=0.31; 0.30-0.33). The proportions of educational variation explained by genetic and shared environmental factors did not differ between Europe, North America and Australia, and East Asia. When restricted to twins 30 years or older to confirm finalized education, the heritability was higher in the older cohorts born in 1900-1949 (a(2)=0.44; 0.41-0.46) than in the later cohorts born in 1950-1989 (a(2)=0.38; 0.36-0.40), with a corresponding lower influence of common environmental factors (c(2)=0.31; 0.29-0.33 and c(2)=0.34; 0.32-0.36, respectively). In conclusion, both genetic and environmental factors shared by co-twins have an important influence on individual differences in educational attainment. The effect of genetic factors on educational attainment has decreased from the cohorts born before to those born after the 1950s.Peer reviewe

Novel loci for childhood body mass index and shared heritability with adult cardiometabolic traits

The genetic background of childhood body mass index (BMI), and the extent to which the well-known associations of childhood BMI with adult diseases are explained by shared genetic factors, are largely unknown. We performed a genome-wide association study meta-analysis of BMI in 61,111 children aged between 2 and 10 years. Twenty-five independent loci reached genome-wide significance in the combined discovery and replication analyses. Two of these, located nearNEDD4LandSLC45A3, have not previously been reported in relation to either childhood or adult BMI. Positive genetic correlations of childhood BMI with birth weight and adult BMI, waist-to-hip ratio, diastolic blood pressure and type 2 diabetes were detected (R(g)ranging from 0.11 to 0.76, P-values Author summary Although twin studies have shown that body mass index (BMI) is highly heritable, many common genetic variants involved in the development of BMI have not yet been identified, especially in children. We studied associations of more than 40 million genetic variants with childhood BMI in 61,111 children aged between 2 and 10 years. We identified 25 genetic variants that were associated with childhood BMI. Two of these have not been implicated for BMI previously, located close to the genesNEDD4LandSLC45A3. We also show that the genetic background of childhood BMI overlaps with that of birth weight, adult BMI, waist-to-hip-ratio, diastolic blood pressure, type 2 diabetes, and age at menarche. Our results suggest that the biological processes underlying childhood BMI largely overlap with those underlying adult BMI. However, the overlap is not complete. Additionally, the genetic backgrounds of childhood BMI and other cardio-metabolic phenotypes are overlapping. This may mean that the associations of childhood BMI and later cardio-metabolic outcomes are partially explained by shared genetics, but it could also be explained by the strong association of childhood BMI with adult BMI.Peer reviewe

Maternal and fetal genetic effects on birth weight and their relevance to cardio-metabolic risk factors.

Birth weight variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes. In expanded genome-wide association analyses of own birth weight (n = 321,223) and offspring birth weight (n = 230,069 mothers), we identified 190 independent association signals (129 of which are novel). We used structural equation modeling to decompose the contributions of direct fetal and indirect maternal genetic effects, then applied Mendelian randomization to illuminate causal pathways. For example, both indirect maternal and direct fetal genetic effects drive the observational relationship between lower birth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring birth weight, but only direct fetal effects of these alleles, once inherited, increase later offspring blood pressure. Using maternal birth weight-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it causally raises offspring blood pressure, indicating that the inverse birth weight-blood pressure association is attributable to genetic effects, and not to intrauterine programming.The Fenland Study is funded by the Medical Research Council (MC_U106179471) and Wellcome Trust

X-chromosome and kidney function:evidence from a multi-trait genetic analysis of 908,697 individuals reveals sex-specific and sex-differential findings in genes regulated by androgen response elements

X-chromosomal genetic variants are understudied but can yield valuable insights into sexually dimorphic human traits and diseases. We performed a sex-stratified cross-ancestry X-chromosome-wide association meta-analysis of seven kidney-related traits (n = 908,697), identifying 23 loci genome-wide significantly associated with two of the traits: 7 for uric acid and 16 for estimated glomerular filtration rate (eGFR), including four novel eGFR loci containing the functionally plausible prioritized genes ACSL4, CLDN2, TSPAN6 and the female-specific DRP2. Further, we identified five novel sex-interactions, comprising male-specific effects at FAM9B and AR/EDA2R, and three sex-differential findings with larger genetic effect sizes in males at DCAF12L1 and MST4 and larger effect sizes in females at HPRT1. All prioritized genes in loci showing significant sex-interactions were located next to androgen response elements (ARE). Five ARE genes showed sex-differential expressions. This study contributes new insights into sex-dimorphisms of kidney traits along with new prioritized gene targets for further molecular research.</p

The Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia : design, results and future prospects

The impact of many unfavorable childhood traits or diseases, such as low birth weight and mental disorders, is not limited to childhood and adolescence, as they are also associated with poor outcomes in adulthood, such as cardiovascular disease. Insight into the genetic etiology of childhood and adolescent traits and disorders may therefore provide new perspectives, not only on how to improve wellbeing during childhood, but also how to prevent later adverse outcomes. To achieve the sample sizes required for genetic research, the Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia were established. The majority of the participating cohorts are longitudinal population-based samples, but other cohorts with data on early childhood phenotypes are also involved. Cohorts often have a broad focus and collect(ed) data on various somatic and psychiatric traits as well as environmental factors. Genetic variants have been successfully identified for multiple traits, for example, birth weight, atopic dermatitis, childhood BMI, allergic sensitization, and pubertal growth. Furthermore, the results have shown that genetic factors also partly underlie the association with adult traits. As sample sizes are still increasing, it is expected that future analyses will identify additional variants. This, in combination with the development of innovative statistical methods, will provide detailed insight on the mechanisms underlying the transition from childhood to adult disorders. Both consortia welcome new collaborations. Policies and contact details are available from the corresponding authors of this manuscript and/or the consortium websites.Peer reviewe