Exploring choking experiences in elite sport: The role of self- presentation

Objectives The aims of this study were twofold: first, to examine the role of self-presentation within the lived-experience of choking in sport; and second, to explore whether the 2 × 2 framework of self-presentation (Howle, Jackson, Conroy, & Dimmock, 2015) holds the potential to further our understanding of acute sporting failure under pressurized conditions. Design and Method An empirical phenomenological research design was adopted to address the research aims. Purposefully selected participants completed phenomenological interviews, which explored in detail their experiences of choking and clutch performance under pressure. The sample consisted of 9 elite athletes (6 male and 3 female) (Mage = 27.14; SD = 5.27) from a range of sports (netball, rugby union, golf, tennis, and cricket). Results Participants reported a tendency to hold protective-agentic self-presentation motives, low self-presentation efficacy, and self-presentational concerns prior to, and during the choke. Conversely, acquisitive-agentic self-presentation motives, and self-presentation efficacy were experienced before and during clutch performances. However, alongside self-presentation, other psychological constructs also preceded and accompanied the choking experience (e.g., unfamiliarity and perceived control). Conclusion This exploratory study is the first to identify the value of examining choking in sport through the lens of the 2 × 2 self-presentation framework, with self-presentation motives appearing to influence the choking experience. Yet, it is also evident that self-presentation may not explain all choking episodes

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