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To investigate the relationship between depression in early pregnancy and sleep quality in mid-pregnancy, and explore whether sleep disorders independently predicts depression across the perinatal period within women with or without depression in early pregnancy. Data were collected at 7 time points from 12 weeks of pregnancy to 6 weeks postpartum. Multiple logistic regression and survival analysis were used to explore the relationship between sleep quality in mid-pregnancy and perinatal depression within women with or without depression in early pregnancy. 390 women were included. Women with depression in early pregnancy were more likely to have sleep disorders and perinatal depression. Women with sleep disorders had a higher risk of perinatal depression compared to women without sleep disorders in mid-pregnancy. Stratified analysis based on whether depressed at 12 weeks of pregnancy found that among women without depression, those with sleep disorders in mid-pregnancy were more likely to have subsequent perinatal depression and appeared earlier; whereas, among women with depression, mid-pregnancy sleep disorders was not a predictor of subsequent perinatal depression. High rates of missed visits may lead to sample bias, with depression and sleep quality being assessed by self-report. Women with depression in early pregnancy are more likely to have sleep disorders in mid-pregnancy. There is a strong correlation between sleep quality in mid-pregnancy and perinatal depression among women without depression in early pregnancy. Routine screening and intervention for sleep disorders should be a priority in perinatal care to reduce the incidence of perinatal depression. • Women with depression were more likely to have sleep disorders in mid-pregnancy. • Depression in early pregnancy predicted the presence of depression from mid-pregnancy to 6 weeks postpartum. • Among non-depressed in early pregnancy, women with mid-pregnancy sleep disorders had a higher risk of perinatal depression. [ABSTRACT FROM AUTHOR]

There have been reports of association between psoriasis and psychological illnesses. Nevertheless, it is not easy to draw conclusions with high quality causality from conventional observational studies. The objective of this study was to evaluate the causality of psoriasis and psychological illnesses. All summary-level data from genome-wide association studies for psoriasis and psychological illnesses were collected from Neale Lab and MRC Integrative Epidemiology Unit. Bidirectional Mendelian randomization analysis was performed to determine the random orientation with an independent genetic variation. The main estimated effects are derived using Inverse-Variance Weighted, weighted median, and MR Egger methods. Multiple data sets were validated against each other, and a series of sensitivity studies were conducted to ensure the reliability of the results. Mendelian randomization analysis revealed a causal effect of psoriasis [odds ratio (OR) 1·34, 95% confidence interval (CI) 1·21–1·46, P < 0.001; and OR 1.28, CI 1.17–1.39, P < 0.001] on psychological illnesses, and vice versa (OR 1.23, CI 1.14–1.31, P < 0.001; and OR 1.21, CI 1.11–1.31, P < 0.001). The results were supported by a series of sensitivity analyses. The findings of this Mendelian randomization study support a causal effect between psoriasis and psychological illnesses, and vice versa. [ABSTRACT FROM AUTHOR]

It was reported that within the head and neck cancer (HNC) cell line CAL21 the epithelial-mesenchymal transition (EMT) and cell proliferation were promoted by Urokinase-Type Plasminogen Activator (PLAU) proteinase through TNFRSF12A. Additionally, in this paper HNC cell lines refer to Fadu and Tu686. A novel PLAU-STAT3 axis was found to be involved in HNC cell line proliferation and metastasis. PLAU expression in HNC samples was upregulated, besides, the elevated expression of PLAU was linked to the lower overall survival (OS) and disease-free survival (DFS). Ectopic PLAU expression promoted cell proliferation and migration, while PLAU knockdown exhibited opposite results. RNA-seq data identified the JAK-STAT signaling pathway, confirmed by western blotting. A recovery assay using S3I-201, a selective inhibitor of signal transducer and activator of transcription 3 (STAT3), indicated that PLAU promoted HNC cell line progression via STAT3 signaling in vitro. The oncogenic role of PLAU in HNC tumor growth in vivo was confirmed using xenograft models. In summary, we identified the tumorigenic PLAU function in the HNC progress. PLAU may represent a potential prognostic biomarker of HNC and the PLAU-STAT3 pathway might be considered a therapeutic target of HNC. • High PLAU expression indicates poor overall and disease-free survival of HNC. • PLAU promotes HNC cell proliferation and migration via JAK-STAT signaling pathway. • PLAU suppresses HNC tumor growth in vivo. [ABSTRACT FROM AUTHOR]