ABSTRACT
This study aimed to develop a Chinese Healthy Eating Index for School-age Children (CHEI-SC), apply it in the 2011 China Health and Nutrition Survey (CHNS) to assess dietary quality, and compared it with our former developed index named CHEI. Data of 3-day 24-hour diet recalls and household food inventory survey from 1600 school-age children in CHNS-2011 were used to develop the CHEI-SC, using the methods of standard portion size, energy-density-based approach, and least restrictive approach. The CHEI-SC included 19 components with a total score (T-score) ranging from 0 to 100. The investigated children had a median score of 49.6. Children with a higher T-score were more likely to have higher social economic status (SES), higher level of urbanisation, fewer family size, and regularly attending school. The CHEI-SC was able to assess dietary quality of Chinese school-age children, was sensitive to demographics, and more comprehensive and accurate than the CHEI.
Subject(s)
Diet, Healthy , Nutrition Surveys , Adolescent , Child , China , Humans , Portion Size , Socioeconomic FactorsABSTRACT
The constitutive activation of signal transducer and activator of transcription 3 (STAT3) contributes to resistance to temozolomide (TMZ) in glioblastoma multiforme (GBM). The aim of this study was to explore the biological role of microRNA-31 (miR-31) in GBM, particularly its role in the regulation of TMZ chemosensitivity. For this purpose, the human GBM cell lines, U251 and U87, were transfected with a miR-31 precursor (pre-miR-31), and cell proliferation, apoptosis and STAT3 phosphorylation were then assessed. To evaluate the effects of miR-31 on TMZ cytotoxicity, the cells were transfected with pre-miR-31 and exposed to 100 µM TMZ for 72 h prior to cell proliferation and apoptosis analysis. A constitutively active STAT3 mutant was co-transfected with pre-miR-31 into the cells to confirm the mediating role of STAT3 signaling. The enforced expression of miR-31 significantly reduced cell proliferation and induced mitochondrial apoptosis, as manifested by the loss of mitochondrial membrane potential and the increase in caspase-9 and caspase-3 activity. The phosphorylation level of STAT3 was significantly decreased by the overexpression of miR-31. The co-delivery of the constitutively active STAT3 mutant blocked the tumor suppressive effects of miR-31. In addition, miR-31 overexpression significantly enhanced the cytotoxic effects of TMZ on the GBM cells, as evidenced by the accelerated suppression of cell proliferation and the induction of apoptosis. The chemosensitizing effects of miR-31 were significantly impaired by the expression of the constitutively active STAT3 mutant. Taken together, our results indicate that miR-31 triggers mitochondrial apoptosis and potentiates TMZ cytotoxicity in GBM cells largely through the suppression of STAT3 activation. Thus, the restoration of miR-31 expression may be of therapeutic beenefit in the treatment of GBM.