Identifying variables associated with lower QOL in obese children and adolescents offers new perspectives for prevention and care. Further research is needed to better elucidate these findings. Better understanding QOL is a key element essential for the treatment for childhood and adolescent obesity.

Background and aimsDespite many positive benefits, mobile phone use can be associated with harmful and detrimental behaviors. The aim of this study was twofold: to examine (a) cross-cultural patterns of perceived dependence on mobile phones in ten European countries, first, grouped in four different regions (North: Finland and UK; South: Spain and Italy; East: Hungary and Poland; West: France, Belgium, Germany, and Switzerland), and second by country, and (b) how socio-demographics, geographic differences, mobile phone usage patterns, and associated activities predicted this perceived dependence.MethodsA sample of 2,775 young adults (aged 18–29 years) were recruited in different European Universities who participated in an online survey. Measures included socio-demographic variables, patterns of mobile phone use, and the dependence subscale of a short version of the Problematic Mobile Phone Use Questionnaire (PMPUQ; Billieux, Van der Linden, & Rochat, 2008).ResultsThe young adults from the Northern and Southern regions reported the heaviest use of mobile phones, whereas perceived dependence was less prevalent in the Eastern region. However, the proportion of highly dependent mobile phone users was more elevated in Belgium, UK, and France. Regression analysis identified several risk factors for increased scores on the PMPUQ dependence subscale, namely using mobile phones daily, being female, engaging in social networking, playing video games, shopping and viewing TV shows through the Internet, chatting and messaging, and using mobile phones for downloading-related activities.Discussion and conclusionsSelf-reported dependence on mobile phone use is influenced by frequency and specific application usage.

Abstract-Cardiotrophin 1 (CT-1), a cytokine belonging to the interleukin 6 family, is increased in hypertension and in heart failure. We aimed to study the precise role of CT-1 on cardiac, vascular, and renal function; morphology; and remodeling in early stages without hypertension. CT-1 (20 g/kg per day) or vehicle was administrated to Wistar rats for 6 weeks. Cardiac and vascular functions were analyzed in vivo using M-mode echocardiography, Doppler, and echo tracking device and ex vivo using a scanning acoustic microscopy method. Cardiovascular and renal histomorphology were measured by immunohistochemistry, RT-PCR, and Western blot. Kidney functional properties were assessed by serum creatinine and neutrophile gelatinase-associated lipocalin and microalbuminuria/creatininuria ratio. Without alterations in blood pressure levels, CT-1 treatment increased left ventricular volumes, reduced fractional shortening and ejection fraction, and induced myocardial dilatation and myocardial fibrosis. In the carotid artery of CT-1-treated rats, the circumferential wall stress-incremental elastic modulus curve was shifted leftward, and the acoustic speed of sound in the aorta was augmented, indicating increased arterial stiffness. Vascular media thickness, collagen, and fibronectin content were increased by CT-1 treatment. CT-1-treated rats presented unaltered serum creatinine concentrations but increased urinary and serum neutrophile gelatinase-associated lipocalin and microalbuminuria/creatininuria ratio. This paralleled a glomerular and tubulointerstitial fibrosis accompanied by renal epithelial-mesenchymal transition. CT-1 is a new potent fibrotic agent in heart, vessels, and kidney able to induce cardiovascular-renal dysfunction independent from blood pressure. Thus, CT-1 could be a new target simultaneously integrating alterations of heart, vessels, and kidney in early stages of heart failure. 1-3 Cardiac hypertrophy is attributable to cardiomyocyte hypertrophy, the proliferation of interstitial fibroblasts, and increased depositions of extracellular matrix (ECM) components.4 Arterial stiffening is associated with decreased distensibility and modified wall structure mainly characterized by increased ECM. 5,6 Chronic kidney disease progression is generally associated with tubulointerstitial fibrosis. 7,8 Therefore, it is of paramount importance to identify common pathways able to trigger cardiovascular and renal fibrosis.Cardiotrophin 1 (CT-1) is an interleukin 6 superfamily member.9 Elevated CT-1 levels have been reported in HF and in hypertensive patients.10-12 Moreover, CT-1 positively correlates with left ventricular (LV) mass index and the serum concentration of carboxy-terminal propeptide of procollagen type I, a biomarker of collagen synthesis, 10 suggesting that CT-1 may contribute to the development of cardiomyocyte hypertrophy and fibrosis. Accordingly, CT-1 administration increases heart weight in mice. 13 Our group has characterized CT-1-induced cardiomyocyte survival and hypertrophy, 10,14 as well as CT-1...