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Background: With over 2 million new cases annually, stroke is associated with the higher amount of disability-adjusted life-years lost than any other disease in China; however, the relationship between sleep time and stroke has not been concluded yet. Aim of this study was to analyze the relationship between sleep duration and stroke history in middle-aged and elderly people in Guiyang, China. Methods: This study was a cross-sectional survey carried out in 40– 99-years-old permanent residents of Guiyang. Yunyan, Wudang, and Baiyun districts and Xiuwen County were selected by stratified multilevel sampling for a face-to-face survey. Demographics, history of stroke, and self-reported sleep behavior data were collected, and multivariable logistic regression models were used to gradually adjust possible confounding factors. Results: A total of 5065 participants were included, of them 126 (2.5%) had a history of stroke. Short sleep (< 7 h) was observed in 11.0%, sufficient sleep (7– 9 h) in 69.4%, and long sleep (> 9 h) in 19.6%. Sleep duration and stroke prevalence showed a U-shaped distribution. When taking the sleep duration of 7– 9 h as a reference, sleep duration > 9 h was associated with stroke (all P < 0.05) in the univariable model (OR = 2.68, 95% CI: 1.83– 3.93) and in the multivariable models 1 (OR = 2.35, 95% CI: 1.59– 3.47), 2 (OR = 2.27, 95% CI: 1.53– 3.37), 3 (OR = 2.25, 95% CI: 1.51– 3.33), and 4 (OR = 2.11, 95% CI: 1.39– 3.19). There were no significant differences between the < 7 and 7– 9 h groups (P > 0.05). Conclusion: Thus, long sleep duration (> 9 h) is independently associated with history of stroke in middle-aged and elderly people in Guiyang. [ABSTRACT FROM AUTHOR]

Purpose: Follistatin-related gene 3 (FSTL3), an established oncogene, can modulate target gene expression via members of the transforming growth factor β (TGF-β) superfamily. The present study was conducted to evaluate the expression of FSTL3 in gastric cancer (GC) and to determine its prognostic significance. We also evaluated the possible mechanisms involved in the oncogenic role of FSTL3 in gastric carcinogenesis and development. Methods: We obtained data from the Human Protein Atlas, MethSurv, cBioPortal, UALCAN, TIMER, GEPIA, STRING, GeneMANIA, ONCOMINE, and MEXPRESS databases and examined it using R software. RNAi was used to establish stable FSTL3-knockdown (shFSTL3) and overexpression (OE) cell strains. Western blot; enzyme-linked immunosorbent (ELISA); and immunohistochemical (ICH), immunofluorescence, and phalloidin staining were used for examining protein expression. Cell invasion and migration were determined using transwell and scratch-wound assays. After tumor-associated macrophage (TAM) generation, co-culturing of cancer cells with TAMs was performed to confirm the relationship between FSTL3 and TAMs. Results: In GC patients, FSTL3 mRNA and protein levels were upregulated. FSTL3 expression was significantly linked to cancer stage as well as to pathological tumor grade in GC. Moreover, a high expression of FSTL3 was associated with a dismal survival duration in patients with GC. Furthermore, functional enrichment analysis demonstrated that FSTL3 overexpression could activate epithelial–mesenchymal transition (EMT) by promoting F-actin expression and BMP/SMAD signaling. Finally, immunofluorescence staining confirmed that the overexpression of FSTL3 promoted the proliferation of M2 TAMs. Conclusion: Taken together, our findings suggest that FSTL3 may be involved in GC progression via the promotion of BMP/SMAD signaling-mediated EMT and M2 macrophage activation. [ABSTRACT FROM AUTHOR]