[Association between speed and endurance performance with sleep duration in children and adolescents].

OBJECTIVE: To analyze the association between sleep duration and athletic performance, and provide scientific basis to improve the 50 m and endurance performance in children and adolescents. METHODS: All the 119 462 subjects aged 9-15 years in both genders were sampled from 2014 National Physical Fitness and Health Surveillance by using stratified random cluster sampling method, to measure the height, weight, 50 meters and endurance performance and investigate sleep duration with questionnaire. Their body mass indexes (BMI) were calculated and the students' 50 m, endurance run scores and sleep durations were assessed. Binary Logistic regression was used to analyze the difference between the different sleep groups, and multifactor Logistic regression was used to analyze the relationship between the sleep condition and athletic performance. RESULTS: The prevalence of insufficient sleep was 94.67% in the total subjects, the prevalence was higher among the girls (95.26%)than the boys (94.09%, χ2=80.99, P<0.001), and higher among the urban (95.41%) than the rural students(93.93%, χ2=128.48, P<0.001).The children with sufficient sleep had better performance in 50 m and endurance run scores( χ250 m=10.10, P50 m＜0.01; χ2endurance run=21.76, P<0.001). Logistic regression analysis after controlling the gender, area, grade and BMI showed that children with adequate sleep showed better results(OR50 m=1.14, 95%CI50 m=1.05-1.23, P50 m<0.01; ORendurance run=1.21, 95%CIendurance run=1.11-1.31, Pendurance run<0.001). As for gender, the excellent rates of 50 m and endurance run scores in the boys with adequate sleep were higher (P<0.001), but there were no significant difference in 50 m and endurance run excellent rates in the girls of different sleep conditions. The excellent rates of 50 m and endurance run in the urban children and the endurance rate in the rural children and adolescents with adequate sleep were higher than those with insufficient sleep (P<0.01) while there were no significant difference in the 50 m excellent rates between the different sleep groups in rural areas. The 50 m and endurance run excellent rates of the children and adolescents with adequate sleep in each grade were higher than those of the children in the same grade with insufficient sleep (Pprimary students' endurance performance<0.001, and the rest P<0.05). Children and adolescents with normal BMI and overweight who slept well had better performance in 50 m (P<0.05). The endurance run excellent rate of children and adolescents with adequate sleep in each BMI group was higher than that in children and adolescents with insufficient sleep in the same BMI group (Pmalnutrition<0.01, Pnormal<0.01, Poverweight<0.05, Pobesity<0.05). The children and adolescents were divided into different groups according to the sleep duration,the one who slept less than 7 hours had lower 50 m excellent rate than the other groups with longer sleeping duration (P<0.01) and the rate in the ones who slept more than 9 hours was the highest (P<0.001).The endurance excellent rate in the children and adolescents who slept more than 9 hours was significantly higher than that in the other groups (P<0.001).There was no significant dose-response relationship in excellent rates and sleep durations. CONCLUSION: The prevalence of insufficient sleep has increased, and the sleep condition in children and adolescents is severe. Children and adolescents with sufficient sleep have better athletic performance, so we should strengthen the prevention and control of the lack of sleep in children and adolescents.

Transcription factor Six2 mediates the protection of GDNF on 6-OHDA lesioned dopaminergic neurons by regulating Smurf1 expression.

Glial cell line-derived neurotrophic factor (GDNF) has strong neuroprotective and neurorestorative effects on dopaminergic (DA) neurons in the substantia nigra (SN); however, the underlying molecular mechanisms remain to be fully elucidated. In this study, we found that the expression level of transcription factor Six2 was increased in damaged DA neurons after GDNF rescue in vivo and in vitro. Knockdown of Six2 resulted in decreased cell viability and increased the apoptosis of damaged DA neurons after GDNF treatment in vitro. In contrast, Six2 overexpression increased cell viability and decreased cell apoptosis. Furthermore, genome-wide chromatin immunoprecipitation sequencing (ChIP-seq) indicated that Six2 directly bound to the promoter CAGCTG sequence of smad ubiquitylation regulatory factor 1 (Smurf1). ChIP-quantitative polymerase chain reaction (qPCR) analysis showed that Smurf1 expression was significantly upregulated after GDNF rescue. Moreover, knockdown of Six2 decreased Smurf1 expression, whereas overexpression of Six2 increased Smurf1 expression in damaged DA neurons after GDNF rescue. Meanwhile, knockdown and overexpression of Smurf1 increased and decreased p53 expression, respectively. Taken together, our results from in vitro and in vivo analysis indicate that Six2 mediates the protective effects of GDNF on damaged DA neurons by regulating Smurf1 expression, which could be useful in identifying potential drug targets for injured DA neurons.

Glial cell line-derived neurotrophic factor promotes proliferation of neuroglioma cells by up-regulation of cyclins PCNA and Ki-67.

OBJECTIVE: We wished to test whether glial cell line-derived neurotrophic factor (GDNF) stimulates proliferation of gliomas by up-regulating expression of nuclear cyclins PCNA and Ki37. MATERIALS AND METHODS: As a model, we tested rat C6 glioma cell line exposed to basal conditions, vehicle control, or exogenous GDNF at different concentrations (0-90 µg/L) or different times (0-72 hours). Cell proliferation was quantified by MTT test, cell cycle by flow cytometry and propidium iodide staining, expression of PCNA and Ki67 by intracellular antibody staining and flow cytometry. RESULTS: We first observed that cell proliferation was most stimulated by GDNF at concentration of 70 µg/L and incubation time of 48 hours. Using this concentration and incubation time, we next documented that GDNF increased the percentage of cells in the S phase (47.98% vs. 32.57% in basal cells; p < 0.05), while not affecting the percentage of cells in G0/G1 or G2/M phases. Finally, we demonstrated that expression of both PCNA and Ki67 was significantly increased in cells exposed to GDNF. CONCLUSIONS: We demonstrate that GDNF stimulates proliferation of glioma cells by up-regulating expression of cyclins PCNA and Ki-67.