RESUMEN
INTRODUCTION: To counteract the recently observed increase in forearm fractures in children worldwide, an educational programme to improve fall skills was developed. In this 8-week programme children learned basic martial arts falling techniques in their physical education classes. In this study, the effectiveness of this educational programme to improve fall skills was evaluated. METHODS: A cluster randomised controlled trial was conducted in 33 primary schools. The intervention group received the educational programme to improve falling skills during their physical education (PE) classes whereas the control group received their regular PE curriculum. At baseline (October 2009) and follow-up (May 2010), a questionnaire was completed by the children about their physical activity behaviours. Furthermore, fall-related injuries were registered continuously during an entire school-year. RESULTS: A total of 36 incident injuries was reported in the intervention group, equalling an injury incidence density (IID) of 0.14 fall-related injuries per 1000 h of physical activity (95% CI 0.09 to 0.18). In contrast, 96 injuries were reported by the control group corresponding to an IID of 0.26 (95% CI 0.21 to 0.32). However, because intracluster correlation was high (ICC=0.46), differences in injury incidence were not statistically significant. When activity level was taken into account, a trend was shown suggesting that the 'falling is a sport' programme was effective in decreasing falling-related injury risk, but only in the least active children. DISCUSSION AND CONCLUSION: Although results did not reach significance because of strong clustering effects, a trend was found suggesting that a school-based educational programme to improve falling skills may be more beneficial for the prevention of falling-related injuries in children with low levels of habitual physical activity.
Asunto(s)
Accidentes por Caídas/prevención & control , Traumatismos del Antebrazo/prevención & control , Fracturas Óseas/prevención & control , Educación del Paciente como Asunto/métodos , Traumatismos en Atletas/prevención & control , Niño , Análisis por Conglomerados , Ejercicio Físico , Terapia por Ejercicio/métodos , Femenino , Humanos , Masculino , Artes Marciales , Educación y Entrenamiento Físico/métodos , Servicios de Salud Escolar , Encuestas y Cuestionarios , Índices de Gravedad del TraumaRESUMEN
The disaccharide galactose(alpha)1,3 galactose (the alphaGal epitope) is the major xenoantigen responsible for the hyperacute vascular rejection occurring in pig-to-primates organ transplantation. The synthesis of the alphaGal epitope is catalyzed by the enzyme alpha1,3-galactosyltransferase (alpha1,3GalT). To be able to control porcine alpha1,3GalT gene expression specifically, we have analyzed the upstream portion of the alpha1,3GalT gene, and identified the regulatory sequences. Porcine alpha1,3GalT transcripts were detected by 5' RACE analysis, and the corresponding genomic sequences were isolated from a phage library. The porcine alpha1,3GalT gene consists of at least 10 different exons, four of which contain 5' untranslated sequence. Four distinct promoters, termed A-D, drive alpha1,3GalT gene transcription in porcine cells. A combination of alternative promoter usage and alternative splicing produces a series of transcripts that differ in their 5' portion, but encode the same protein. Promoters A-C have been isolated, and functionally characterized using luciferase reporter gene assays in transfected porcine endothelial cells (PEC-A). Promoter preference in porcine endothelial cells was estimated on the basis of relative transcript levels as determined by real-time quantitative PCR. More than 90% of the alpha1,3GalT transcripts in PEC-A cells originate from promoter B, which has characteristics of a housekeeping gene promoter. While promoter preference remains unchanged, alpha1,3GalT mRNA levels increase by 50% in 12 h upon tumour necrosis factor alpha-activation of PEC-A cells. However, the magnitude of this change induced by inflammatory conditions could be insufficient to affect cell surface alpha1,3-galactosylation.