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Summary: Purpose: Sleep quality was considered a priority concern facing pregnant women. Conventional wisdom argues that good sleep quality benefits pregnant women and their fetuses. The aim of this study is to assess the effects of a specific exercise program on the sleep quality in pregnant women.Methods: Searches were executed in seven databases since their inceptions until February 28, 2019, for randomized controlled trials evaluating the effects of an exercise program on the sleep quality and insomnia in pregnant women. A random-effects model was applied for meta-analysis, and odds ratio, mean differences (MDs), and 95% confidence intervals (CIs) are shown as parts of outcomes.Results: Seven studies were included for meta-analysis. Compared with their not-exercising counterparts, analyses showed that regularly exercising women had significantly enhanced sleep quality, with an odds ratio of 6.21 (95% CI, 2.02–19.11;p = .001; I2 = 80.2%), with a standardized MD of −0.93 (95% CI, −1.19 to −0.67; p < .001; I2 = 30.0%). However, exercising women showed no significant insomnia improvement, with an standardized MD of −2.85 (95% CI, −7.67 to 1.98; p = .250; I2 = 97.0%), relative to their not-exercising counterparts.Conclusion: This research indicated that exercise has a positive impact on the sleep quality of pregnant women. Despite the aforementioned positive impact on sleep quality, the present study did not find evidence to support that exercise may also improve insomnia for pregnant women. Keywords: exercise, meta-analysis, pregnant women, sleep, sleep initiation and maintenance disorders

Malignancies of alimentary tract include esophageal carcinoma (ESCA), stomach adenocarcinoma (STAD), colon adenocarcinoma (COAD), and rectum adenocarcinoma (READ). Despite of their similarities in cancer development and progression, there are numerous researches concentrating on single tumor but relatively little on their common mechanisms. Our study explored the transcriptomic data of digestive tract cancers from The Cancer Genome Atlas database, yielding their common differentially expressed genes including 1,700 mRNAs, 29 miRNAs, and 362 long non-coding RNAs (lncRNAs). There were 12 mRNAs, 5 miRNAs, and 16 lncRNAs in the core competitive endogenous RNAs network by RNA-RNA interactions, highlighting the prognostic nodes of SERPINE1, hsa-mir-145, and SNHG1. In addition, the weighted gene co-expression network analysis (WGCNA) illustrated 20 gene modules associated with clinical traits. By taking intersections of modules related to the same trait, we got 67 common genes shared by ESCA and READ and screened 5 hub genes, including ADCY6, CXCL3, NPBWR1, TAS2R38, and PTGDR2. In conclusion, the present study found that SERPINE1/has-mir-145/SNHG1 axis acted as promising targets and the hub genes reasoned the similarity between ESCA and READ, which revealed the homogeneous tumorigenicity of digestive tract cancers at the transcriptome level and led to further comprehension and therapeutics for digestive tract cancers.

Resistin is known as an adipocyte-specific hormone that can cause insulin resistance and decrease adipocyte differentiation. It can be regulated by transcriptional factors, but the possible role of forkhead transcription factor FOXO1 in regulating resistin gene expression is still unknown. Using 3T3 fibroblast and C3H10T1/2 and 3T3-L1 adipocytes, we found that transient overexpression of a non-phosphorylatable, constitutively active FOXO1, but not the wild type of FOXO1 or a DNA binding-deficient FOXO1, activated resistin promoter-directed luciferase expression. However, transient overexpression of a dominant-negative FOXO1 inactivated resistin promoter activity and reduced resistin mRNA expression. These observations indicate that the action of FOXO1 on resistin gene expression requires the activation of FOXO1 and that the effect of FOXO1 depends on the phosphorylation and dephosphorylation of FOXO1. The FOXO1 protein target sites on the resistin promoter were localized to the proximal -3545 to -787bp of 5'-flanking region of the resistin promoter. A chromatin immunoprecipitation assay also showed that FOXO1 bound the resistin promoter at nucleotide regions of -1539 to -1366bp and -1016 to -835bp, but not at the regions of -795 to -632bp. Results of this study suggest that FOXO1 transcription factor likely activates the expression of adipocyte resistin gene via direct association with the upstream resistin promoter.