Parental Influence on Child and Adolescent Physical Activity Level: A Meta-Analysis

Parents are often regarded as one of the significant social agents who are important to the participation of physical activity (PA) among children and adolescents. However, within the literature, the relationships between parental influences and child and adolescent PA have been inconclusive and discordant. The purpose of this meta-analysis was to quantify and synthesize the associations between parental social influences (positive parental influence, punishment, and discouragement) and the PA level of children and adolescents. Through a systematic literature search using PsycINFO, Web of Science, PubMed, ProQuest, and SPORTDiscus databases, we identified 112 eligible studies and subsequently extracted 741 effect sizes for our analysis. Multilevel meta-analysis showed that the corrected zero-order correlation of positive parental influence was positive and statistically significant, r = 0.202, SE = 0.014, t = 14.975, p \u3c 0.001, 95% confidence interval (CI) = [0.176, 0.228]. Further moderation analysis also found that this was significantly moderated by parental gender (maternal vs. paternal), respondent of influence measure (parent-reported vs. child-reported), and type of PA measure (subjective vs. objective). The corrected zero-order correlations of negative parental influences (i.e., punishment and discouragement) were not statistically significant, and no significant moderation effects were observed. The findings of our meta-analysis showed that children and adolescents had higher PA levels when their parents supported PA participation by exerting positive social influence. Punishment and discouragement against PA by parents did not appear to be significantly associated with the PA level of children and adolescents. The findings of negative parental social influence were mixed and required further investigations

Significant others and students’ leisure-time physical activity intention: A prospective test of the social influence in sport model

This two-wave prospective study applied the Social Influence in Sport Model to investigate whether the social influences of parents, physical education (PE) teachers, and peers were predictive of students' intention to engage in leisure-time physical activity (PA). Participants were 2,484 secondary school students (11–18 years old) who completed a questionnaire assessing positive influence, punishment, and dysfunction from the three social agents (parents, PE teachers, and peers) at baseline, and PA intention at a 1-month follow-up. Structural equation modelling (SEM) yielded excellent goodness-of-fit and consistent pathways between the three social agents. Students' leisure-time PA intention (R2 = .103 to 0.112) was positively associated with positive influence (β = .223 to 0.236, p < .001) and punishment (β = .214 to 0.256, p < .01), and negatively associated with dysfunction (β = - 0.281 to -.335, p < .001). Multi-group SEM showed that the predictions were invariant between parents, PE teachers, and peers. Furthermore, no significant differences in students' gender were found between perceived social influence and PA intention. The findings supported the application of the Social Influence in Sport Model in explaining the role of significant others on students’ intention to take part in leisure-time PA

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease