Reliability and validity of a semi-quantitative food frequency questionnaire: dietary intake assessment among multi-ethnic populations in Northwest China.

BACKGROUND: Few multi-ethnic dietary culture-sensitive food frequency questionnaires (FFQ) have been developed due to the complexity and diversity of cooking methods and styles. This study aimed to develop and validate a specific FFQ among multi-ethnic groups in Northwest China. METHODS: In the reliability study, 139 participants aged 20-65 completed two identical FFQs separated by 3 months. The relative validation of the FFQ was assessed by three 24-h recalls (24HR) employed in the interval of two FFQs, as a reference. Stratified analyses were also conducted by the major ethnic groups (Han nationality or Ethnic minority). RESULTS: For reproducibility, the median (range) of Spearman's correlation coefficients (SCC) was 0.71 (0.43-0.84) for nutrients. The intra-class correlation coefficients (ICC) covered a spectrum from 0.39 to 0.78 (median: 0.64). Meanwhile, the weighted kappa values ranged from 0.11 to 0.64. For validity, the median (range) of Pearson's correlation coefficients derived from the energy unadjusted and the adjusted values between FFQ and 24HR were 0.61 (0.12-0.79) and 0.56 (0.12-0.77), respectively. The results of correlation coefficients were similar between the two ethnic groups. Moreover, the Bland-Altman plots likewise demonstrated a satisfactory level of agreement between the two methods. CONCLUSIONS: The FFQ showed acceptable reproducibility and moderate relative validity for evaluating dietary intake among multi-ethnic groups in northwest China. It could be a credible nutritional screening tool for forthcoming epidemiological surveys of these populations.

Long non-coding RNA CDKN2B-AS1 promotes osteosarcoma by increasing the expression of MAP3K3 via sponging miR-4458.

Osteosarcoma (OS) is the most common primary malignant bone tumor worldwide. Recently, several studies have shown that the long non-coding RNA (lncRNA) CDKN2B-AS1 plays a critical role in several cancers. However, the function and underlying mechanism of CDKN2B-AS1 in OS development remains elusive. In this study, we firstly assessed the expression of CDKN2B-AS1 in OS tissues and cells, showing that CDKN2B-AS1 expression were remarkably upregulated in OS tissues and cells. Moreover, CDKN2B-AS1 knockdown suppressed cell proliferation, migration, and EMT progress in OS. Interestingly, we found and proved that CDKN2B-AS1 could sponge miR-4458 in OS cells. Moreover, MAP3K3 was certified as a downstream target of miR-4458 in OS. Besides, MAP3K3 was negatively regulated by miR-4458 and positively regulated by CDKN2B-AS1. More importantly, overexpression of MAP3K3 could partly counteract the effect of CDKN2B-AS1 suppression on the biological behavior of OS cells. Also, the in vivo experiments further testified that CDKN2B-AS1 accelerated tumor growth in OS. Our results suggested that CDKN2B-AS1 facilitated OS progression by sponging miR-4458 to enhance MAP3K3 expression, which provides a novel insight into improving diagnostic and therapeutic strategies for patients with OS.