Adherence to an Injury Prevention Warm-Up Program in Children’s Soccer—A Secondary Analysis of a Randomized Controlled Trial

This study examined the impact of high adherence to a neuromuscular training (NMT) warm-up on the risk of lower extremity (LE) injuries in children’s soccer. Twenty U11–U14 youth clubs (n = 92 teams, 1409 players) were randomized into intervention (n = 44 teams) and control (n = 48 teams) groups. The intervention group was advised to perform an NMT warm-up 2 to 3 times a week for 20 weeks. Team adherence, injuries, and exposure were registered throughout the follow-up. Primary outcomes were the incidence of soccer-related acute LE injuries and the prevalence of overuse LE injuries. Intervention teams conducted mean 1.7 (SD 1.0) NMT warm-ups weekly through follow-up. The seasonal trend for adherence declined significantly by −1.9% (95% CI −0.8% to −3.1%) a week. There was no difference in the incidence of acute injuries nor the prevalence of overuse LE injuries in high team adherence group (n = 17 teams) compared to controls. However, the risk for acute noncontact LE injuries was 31% lower in the high team adherence group compared to controls (IRR 0.69, 95% CI 0.49 to 0.97). In an efficacy analysis (n = 7 teams), there was a significant reduction of 47% in the rate of noncontact LE injuries (IRR 0.53, 95% CI 0.29 to 0.97). In conclusion, teams conducted NMT warm-up sessions regularly, but with a declining trend. A greater protective effect was seen in teams with the highest adherence to the NMT warm-up

Neuromuscular Training Warm-up Prevents Acute Noncontact Lower Extremity Injuries in Children’s Soccer : A Cluster Randomized Controlled Trial

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Uniting biobank resources reveals novel genetic pathways modulating susceptibility for atopic dermatitis

Publisher Copyright: © 2021 The AuthorsBackground: Atopic dermatitis (AD) is a common chronic inflammatory skin disease with high heritability. Previous genome-wide association studies have identified several loci predisposing to AD. These findings explain approximately 30% of the variance in AD susceptibility, suggesting that further work is required to fully understand the genetic underpinnings. Objective: We sought to gain additional understanding of the genetic contribution to AD risk by using biobank resources. Methods: We completed a genome-wide meta-analysis of AD in 796,661 individuals (Ncases = 22,474) from the FinnGen study, the Estonian Biobank, and the UK Biobank. We further performed downstream in silico analyses to characterize the risk variants at the novel loci. Results: We report 30 loci associating with AD (P < 5 × 10−8), 5 of which are novel. In 2 of the novel loci, we identified missense mutations with deleterious predictions in desmocollin 1 and serpin family B member 7, genes encoding proteins crucial to epidermal strength and integrity. Conclusions: These findings elucidate novel genetic pathways involved in AD pathophysiology. The likely involvement of desmocollin 1 and serpin family B member 7 in AD pathogenesis may offer opportunities for the development of novel treatment strategies for AD in the future.Peer reviewe

Uniting biobank resources reveals novel genetic pathways modulating susceptibility for atopic dermatitis

Publisher Copyright: © 2021 The AuthorsBackground: Atopic dermatitis (AD) is a common chronic inflammatory skin disease with high heritability. Previous genome-wide association studies have identified several loci predisposing to AD. These findings explain approximately 30% of the variance in AD susceptibility, suggesting that further work is required to fully understand the genetic underpinnings. Objective: We sought to gain additional understanding of the genetic contribution to AD risk by using biobank resources. Methods: We completed a genome-wide meta-analysis of AD in 796,661 individuals (Ncases = 22,474) from the FinnGen study, the Estonian Biobank, and the UK Biobank. We further performed downstream in silico analyses to characterize the risk variants at the novel loci. Results: We report 30 loci associating with AD (P < 5 × 10−8), 5 of which are novel. In 2 of the novel loci, we identified missense mutations with deleterious predictions in desmocollin 1 and serpin family B member 7, genes encoding proteins crucial to epidermal strength and integrity. Conclusions: These findings elucidate novel genetic pathways involved in AD pathophysiology. The likely involvement of desmocollin 1 and serpin family B member 7 in AD pathogenesis may offer opportunities for the development of novel treatment strategies for AD in the future.Peer reviewe