How does the built environment affect teenagers (aged 13–14) physical activity and fitness? A cross-sectional analysis of the ACTIVE Project

Built environments have been cited as important facilitators of activity and research using geographic information systems (GIS) has emerged as a novel approach in exploring environmental determinants. The Active Children Through Individual Vouchers Evaluation Project used GIS to conduct a cross-sectional analysis of how teenager's (aged 13-14) environments impacted on their amount of activity and influences fitness. The ACTIVE Project recruited 270 participants aged 13-14 (year 9) from 7 secondary schools in south Wales, UK. Demographic data and objective measures of accelerometery and fitness were collected from each participant between September and December 2016. Objective data was mapped in a GIS alongside datasets relating to activity provision, active travel routes, public transport stops, main roads and natural resources. This study shows that fitness and physical activity are not correlated. Teenagers who had higher levels of activity also had higher levels of sedentary time/inactivity. Teenagers showed higher amounts of moderate-to-vigorous physical activity if their homes were closer to public transport. However, they were also more active if their schools were further away from public transport and natural resources. Teenagers were fitter if schools were closer to natural resources. Sedentary behaviour, fitness and activity do not cluster in the same teenagers. Policymakers/planning committees need to consider this when designing teenage friendly environments. Access to public transport, active travel, green space and activities that teenagers want, and need could make a significant difference to teenage health

Accumulation of Krebs cycle intermediaters and over-expression of HIF1alpha in tumours which result from germline FH and SDH mutations.

The nuclear-encoded Krebs cycle enzymes, fumarate hydratase (FH) and succinate dehydrogenase (SDHB, -C and -D), act as tumour suppressors. Germline mutations in FH predispose individuals to leiomyomas and renal cell cancer (HLRCC), whereas mutations in SDH cause paragangliomas and phaeochromocytomas (HPGL). In this study, we have shown that FH-deficient cells and tumours accumulate fumarate and, to a lesser extent, succinate. SDH-deficient tumours principally accumulate succinate. In situ analyses showed that these tumours also have over-expression of hypoxia-inducible factor 1? (HIF1?), activation of HIF1? targets (such as vascular endothelial growth factor) and high microvessel density. We found no evidence of increased reactive oxygen species in our cells. Our data provide in vivo evidence to support the hypothesis that increased succinate and/or fumarate causes stabilization of HIF1? a plausible mechanism, inhibition of HIF prolyl hydroxylases, has previously been suggested by in vitro studies. The basic mechanism of tumorigenesis in HPGL and HLRCC is likely to be pseudo-hypoxic drive, just as it is in von Hippel–Lindau syndrome