BackgroundChildhood obesity has been a serious public health problem. An effective school-based physical activity (PA) intervention is still lacking in China. This study aimed to assess the effectiveness of a school-based physical activity intervention during 12 weeks on obesity and related health outcomes in school children.MethodsIt was a non-randomized controlled trial. Altogether 921 children aged 7 to 15 years were recruited at baseline survey. Children in the intervention group (n = 388) participated in a multi-component physical activity intervention during 12 weeks that included improvement of physical education, extracurricular physical activities for overweight/obese students, physical activities at home, and health education lectures for students and parents. Children (n = 533) in the control group participated in usual practice.ResultsParticipants had mean age of 10.4 years, mean body mass index (BMI) of 19.59 kg/m2, and 36.8 % of them were overweight or obese at baseline survey. The change in BMI in intervention group (−0.02 ± 0.06 kg/m2) was significantly different from that in control group (0.41 ± 0.08 kg/m2). The adjusted mean difference was −0.43 kg/m2 (95% CI: −0.63 to −0.23 kg/m2, P < 0.001). The effects on triceps, subscapular, abdominal skinfold thickness and fasting glucose were also significant in intervention group compared with control group (all P < 0.05). The change in duration of moderate to vigorous physical activity (MVPA) in intervention group (8.9 ± 4.3 min/day) was significantly different from that in control group (−13.8 ± 3.3 min/day). The adjusted mean difference was 22.7 min/day (95% CI: 12.2 to 33.2 min/day, P < 0.001).ConclusionsThe school-based, multi-component physical activity intervention was effective to decreasing levels of BMI, skinfold thickness, fasting glucose and increasing duration of MVPA. These findings provided evidence for the development of effective and feasible school-based obesity interventions.Trial registrationClinicaltrials.gov Identifier: NCT02074332 (2014-02-26)

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The contribution of CXCL12/CXCR4/CXCR7 axis to cancer progression has been increasingly recognized. However, its role in thyroid cancer development remains unclear. The present study aimed to examine the expression and function of CXCL12 and its receptors in thyroid cancer. The expression of CXCL12/CXCR4/CXCR7 in human tissue specimens of papillary, follicular, medullary, and anaplastic thyroid carcinoma, follicular adenoma, Hashimoto's thyroiditis and nodular goiter were examined by immunohistochemistry using a tissue microarray. CXCR4 and CXCR7 were over-expressed in human thyroid cancer cells K1 by transduction of recombinant lentivirus. The effect of overexpression of CXCR4 and CXCR7 on K1 cell proliferation and invasion and the molecular mechanism underlying the effect were investigated. CXCL12 was exclusively expressed in papillary thyroid carcinoma tissue but absent in other types of thyroid malignancies and benign lesions. CXCR7 was widely expressed in the endothelial cells of all types of malignancy but only occasionally detected in benign lesions. CXCR4 was expressed in 62.5% of papillary thyroid carcinoma tissue specimens and in 30–40% of other types of malignancy, and it was either absent or weakly expressed in benign lesions. CXCL12 stimulated the invasion and migration of K1 cells overexpressing CXCR4, but did not affect K1 cells overexpressing CXCR7. K1 cell proliferation was not affected by overexpression of CXCR4 or CXCR7. Overexpression of CXCR4 in K1 cells significantly increased AKT and ERK phosphorylation and markedly induced the expression and activity of matrix metalloproteinase-2 (MMP-2). Thus, CXCL12 may be an effective diagnostic marker for papillary thyroid carcinoma, and CXCL12/CXCR4/CXCR7 axis may contribute to thyroid cancer development by regulating cancer cell migration and invasion via AKT and ERK signaling and MMP-2 activation.

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Aims The protein expression of programmed death‐ligand 1 (PD‐L1) has been recognised as being a biomarker for poor prognosis in diffuse large B‐cell lymphoma (DLBCL). The aims of this study were to determine PD‐L1 DNA status and mRNA status, and to explore whether they contribute to protein expression and their clinicopathological correlation in DLBCL. Methods and results In this study, we used fluorescence in‐situ hybridisation, RNA in‐situ hybridisation and immunohistochemistry to determine PD‐L1 status at three different levels in 287 DLBCL samples with follow‐up. Their correlation and clinical pathological relevance were also analysed. Our results showed that 1.7% (3/175) of patients had PD‐L1 DNA amplification, 19.9% (57/287) had high PD‐L1 mRNA expression, and 11.8% (34/287) had high PD‐L1 protein expression. Both mRNA and protein expression of PD‐L1 were significantly higher in non‐germinal centre B‐cell‐like (GCB) DLBCL than in GCB DLBCL (P < 0.05). In addition, the patients with high PD‐L1 mRNA or high PD‐L1 protein expression but no PD‐L1 DNA amplification had significantly poorer overall survival (OS) than those with low PD‐L1 expression (P < 0.05). Furthermore, we found that PD‐L1 mRNA and PD‐L1 protein expression were highly correlated (P = 0.012), which was observed in all three samples with DNA amplification. Conclusions PD‐L1 DNA amplification is a rare event, PD‐L1 mRNA is the main contributor to the high PD‐L1 protein expression, and the latter two will serve as important biomarkers for predicting the prognosis of DLBCL patients and selecting them for immunotherapy.