Objective: To compare concussion rates (CRs) over one academic year in high school athletes with and without a COVID-19 infection prior to concussion.
Methods: Illness and concussion were prospectively reported for male and female high school athletes across six states over one academic year in the Players Health Rehab surveillance system. Concussion was truncated to 60 days following recovery and return to sport from COVID-19.
Context: Youth sport specialization may place young athletes at increased risk for negative impacts to their physical and/or psychological health. In response to these health concerns, several health organizations have created guidelines and position statements to guide parents and practitioners toward best practices for management of the young athlete.
Objective: To systematically review and synthesize current organizations' recommendations and guidelines regarding youth sport specialization.
Sports Health
December 2021
Context: Youth athletes may be at elevated risk for adverse health due to sport specialization. Sport organizations have developed guidelines for participation during growth and development.
Objective: To assess youth sport development guidelines using a 15-item framework across sport organizations and governing bodies in soccer, basketball, ice hockey, and swimming.
Objective: To determine the association between the physical activity vital sign (PAVS) and markers of cardiometabolic disease.
Design: Patients were assessed through the PAVS, a validated tool self-reporting the frequency and duration of physical activity. Patients were categorized into 3 groups: inactive (0 minutes per week), underactive (1-149 minutes per week), and active (>150 minutes per week).
Background: The physical activity vital sign (PAVS) is a simple, validated tool for assessing physical activity in adults that has not been previously studied in pediatrics.
Hypothesis: Reported physical activity utilizing the PAVS in pediatric patients should vary according to known associations with physical activity, such as age, sex, blood pressure, and body mass index (BMI).
Study Design: Cross-sectional study.
Environmental agents and genetic variants can induce heritable epigenetic changes that affect phenotypic variation and disease risk in many species. These transgenerational effects challenge conventional understanding about the modes and mechanisms of inheritance, but their molecular basis is poorly understood. The Deadend1 (Dnd1) gene enhances susceptibility to testicular germ cell tumors (TGCTs) in mice, in part by interacting epigenetically with other TGCT modifier genes in previous generations.
View Article and Find Full Text PDFSince Mendel, studies of phenotypic variation and disease risk have emphasized associations between genotype and phenotype among affected individuals in families and populations. Although this paradigm has led to important insights into the molecular basis for many traits and diseases, most of the genetic variants that control the inheritance of these conditions continue to elude detection. Recent studies suggest an alternative mode of inheritance where genetic variants that are present in one generation affect phenotypes in subsequent generations, thereby decoupling the conventional relations between genotype and phenotype, and perhaps, contributing to 'missing heritability'.
View Article and Find Full Text PDFAims: Recent evidence suggests that transgenerational genetic effects contribute to phenotypic variation in complex traits. To test for the general occurrence of these effects and to estimate their strength, we took advantage of chromosome substitution strains (CSSs) of mice where the Y chromosome of the host strain has been replaced with the Y chromosome of the donor strain. Daughters of these CSS-Y males and host strain females are genetically identical and should be phenotypically indistinguishable in the absence of transgenerational genetic effects of the fathers' Y chromosome on daughters' phenotypes.
View Article and Find Full Text PDFDespite strong heritability, little is known about the genetic control of susceptibility to testicular germ cell tumors (TGCT) in humans or mice. Although the mouse model of spontaneous TGCTs has been extensively studied, conventional linkage analysis has failed to locate the factors that control teratocarcinogenesis in the susceptible 129 family of inbred strains. As an alternative approach, we used both chromosome substitution strains (CSS) to identify individual chromosomes that harbor susceptibility genes and a panel of congenic strains derived from a selected CSS to determine the number and location of susceptibility variants on the substituted chromosome.
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