Effects of auditory-motor synchronization on 400-m sprint performance: An applied study

There is a conspicuous dearth of empirical research regarding the ergogenic and psychological effects of synchronous music when applied in a sports training context. The main purpose of this longitudinal intervention study was to investigate the ergogenic and psychological effects of synchronous music applied over a one-month period of speed endurance training. Twelve participants (six women and six men; 21.1 ± 1.7 years) were randomly assigned to either an experimental group (sprint training coordinated with synchronous music) or a control group (conventional sprint training). Immediately after each training session and each time trial, the Feeling Scale, CR-10 Rating of Perceived Exertion Scale, and Physical Activity Enjoyment Scale were administered to each participant. No significant interaction effect of Group × Time for Rating of Perceived Exertion ( p = .898) or Physical Activity Enjoyment Scale ( p = .411) was identified during the training sessions. A significant Group × Time interaction was identified for Feeling Scale scores ( p = .007). Nonetheless, following Bonferroni adjustment for pairwise comparisons, the between-group differences in Feeling Scale scores did not reach significance. No significant interaction effect of Group × Time or main effect of group was identified for sprint performance, although the latter effect was associated with a large effect size (ηp2 = 0.35). Experimental group participants executed the 400-m time trials 5.07% faster than control group participants. This finding is noteworthy from an applied perspective, given the potential ergogenic effects associated with auditory-motor synchronization. </jats:p

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

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 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

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Psychosocial impact of undergoing prostate cancer screening for men with BRCA1 or BRCA2 mutations.

OBJECTIVES: To report the baseline results of a longitudinal psychosocial study that forms part of the IMPACT study, a multi-national investigation of targeted prostate cancer (PCa) screening among men with a known pathogenic germline mutation in the BRCA1 or BRCA2 genes. PARTICPANTS AND METHODS: Men enrolled in the IMPACT study were invited to complete a questionnaire at collaborating sites prior to each annual screening visit. The questionnaire included sociodemographic characteristics and the following measures: the Hospital Anxiety and Depression Scale (HADS), Impact of Event Scale (IES), 36-item short-form health survey (SF-36), Memorial Anxiety Scale for Prostate Cancer, Cancer Worry Scale-Revised, risk perception and knowledge. The results of the baseline questionnaire are presented. RESULTS: A total of 432 men completed questionnaires: 98 and 160 had mutations in BRCA1 and BRCA2 genes, respectively, and 174 were controls (familial mutation negative). Participants' perception of PCa risk was influenced by genetic status. Knowledge levels were high and unrelated to genetic status. Mean scores for the HADS and SF-36 were within reported general population norms and mean IES scores were within normal range. IES mean intrusion and avoidance scores were significantly higher in BRCA1/BRCA2 carriers than in controls and were higher in men with increased PCa risk perception. At the multivariate level, risk perception contributed more significantly to variance in IES scores than genetic status. CONCLUSION: This is the first study to report the psychosocial profile of men with BRCA1/BRCA2 mutations undergoing PCa screening. No clinically concerning levels of general or cancer-specific distress or poor quality of life were detected in the cohort as a whole. A small subset of participants reported higher levels of distress, suggesting the need for healthcare professionals offering PCa screening to identify these risk factors and offer additional information and support to men seeking PCa screening

The dynamics of expanding mangroves in New Zealand

In contrast to the global trend of mangrove decline, New Zealand mangroves are rapidly expanding, facilitated by elevated sediment inputs in coastal waters as a consequence of large-scale land use changes following European settlement. New Zealand mangroves are at the southern limit of the global mangrove extent, which limits the tree height of Avicennia marina var. australasica, the only mangrove species present. Mangroves in New Zealand thrive in the sheltered environments of infilling drowned river valleys with abundant supply of fine terrigenous sediments, showing various stages of mangrove succession and expansion dynamics. Bio-physical interactions and carbon dynamics in these expanding temperate mangrove systems show similarities to, but also differ from those in tropical mangrove forests, for instance due to the limited height and complexity of the mangrove communities. Likewise, ecosystem services provided by New Zealand mangroves deviate from those offered by tropical mangroves. In particular, the association of mangrove expansion with the accumulation of (the increased supply of) fine sediments and the consequent change of estuarine ecosystems, has provoked a negative perception of mangrove expansion and subsequently led to mangrove clearance. Over recent decades, a body of knowledge has been developed regarding the planning and decision making relating to mangrove removal, yet there are still effects that are unknown, for example with respect to the post-clearance recovery of the original sandflat ecosystems. In this chapter we discuss the dynamics of New Zealand’s expanding mangroves from a range of viewpoints, with the aim of elucidating the possible contributions of expanding mangroves to coastal ecosystem services, now and in the future. This chapter also reviews current policies and practice regarding mangrove removal in New Zealand and addresses the (un)known effects of mangrove clearance. These combined insights may contribute to the development of integrated coastal management strategies that recognise the full potential of expanding mangrove ecosystems

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

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 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

Thigh-length compression stockings and DVT after stroke

Controversy exists as to whether neoadjuvant chemotherapy improves survival in patients with invasive bladder cancer, despite randomised controlled trials of more than 3000 patients. We undertook a systematic review and meta-analysis to assess the effect of such treatment on survival in patients with this disease