ABSTRACT
The extent to which sports injuries contribute to the burden of injury among adolescents in low- and middle-income countries (LMICs) is unknown. The goal of this study was to estimate the incidence of sports injuries among adolescents in Africa. Data from the World Health Organization Global School-Based Student Health surveys were used to estimate the annual number of African adolescents sustaining sports injuries. Gender-stratified injury rates were calculated and applied to every African country's adolescent population to estimate country-specific and continent-wide injury totals. A total of 21,858 males and 24,691 females from 14 countries were included in the analysis. Country-specific annual sports injury rates ranged from 13.5% to 38.1% in males and 5.2% to 20.2% in females. Weighted average sports injury rates for males and females were 23.7% (95% CI 23.1%-24.2%) and 12.5% (95% CI 12.1%-12.9%), respectively. When these rates were extrapolated to the adolescent populations of the African continent, an estimated 15,477,798 (95% CI 15,085,955-15,804,333) males and 7,943,625 (95% CI 7,689,429-8,197,821) females sustained sports injuries. Our findings suggest that over 23 million African adolescents sustained sports injuries annually. Further work will help to more precisely define the burden of sports injuries in LMICs and the role that surgery can play in mitigating this burden.
Subject(s)
Athletic Injuries , School Health Services/statistics & numerical data , Adolescent , Africa/epidemiology , Athletic Injuries/diagnosis , Athletic Injuries/epidemiology , Athletic Injuries/prevention & control , Cost of Illness , Female , Humans , Incidence , Male , Needs AssessmentABSTRACT
BACKGROUND: The amino acid response (AAR) is an evolutionarily conserved protective mechanism activated by amino acid deficiency through a key kinase, general control nonderepressible 2. In addition to mobilizing amino acids, the AAR broadly affects gene and protein expression in a variety of pathways and elicits antifibrotic, autophagic, and anti-inflammatory activities. However, little is known regarding its role in cardiac stress. Our aim was to investigate the effects of halofuginone, a prolyl-tRNA synthetase inhibitor, on the AAR pathway in cardiac fibroblasts, cardiomyocytes, and in mouse models of cardiac stress and failure. METHODS AND RESULTS: Consistent with its ability to inhibit prolyl-tRNA synthetase, halofuginone elicited a general control nonderepressible 2-dependent activation of the AAR pathway in cardiac fibroblasts as evidenced by activation of known AAR target genes, broad regulation of the transcriptome and proteome, and reversal by l-proline supplementation. Halofuginone was examined in 3 mouse models of cardiac stress: angiotensin II/phenylephrine, transverse aortic constriction, and acute ischemia reperfusion injury. It activated the AAR pathway in the heart, improved survival, pulmonary congestion, left ventricle remodeling/fibrosis, and left ventricular function, and rescued ischemic myocardium. In human cardiac fibroblasts, halofuginone profoundly reduced collagen deposition in a general control nonderepressible 2-dependent manner and suppressed the extracellular matrix proteome. In human induced pluripotent stem cell-derived cardiomyocytes, halofuginone blocked gene expression associated with endothelin-1-mediated activation of pathologic hypertrophy and restored autophagy in a general control nonderepressible 2/eIF2α-dependent manner. CONCLUSIONS: Halofuginone activated the AAR pathway in the heart and attenuated the structural and functional effects of cardiac stress.
