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Background: Enolase 1 (ENO1) is a metabolic enzyme which participates in pyruvate synthesis and ATP production in cells. Previously, differential expression of ENO1 was discovered in villous tissues between recurrent miscarriage and induced abortion. This study was designed to explore whether ENO1 influences the proliferation and invasion of villous trophoblasts and the related molecular mechanisms. Methods: First, ENO1 expression in placental villus tissues collected from recurrent miscarriage (RM) patients and women for induced abortion as well as in trophoblast‐derived cell lines was detected by RT‐qPCR and western blotting. ENO1 localization and expression in villus tissues were further confirmed through immunohistochemistry staining. Then, the effects of ENO1 downregulation on trophoblast Bewo cell proliferation, migration, invasion, and epithelial‐mesenchymal transition (EMT) process were evaluated by CCK‐8 assay, transwell assay, and western blotting. As for the regulatory mechanism of ENO1, the expression of COX‐2, c‐Myc and cyclin D1 in Bewo cells after ENO1 knockdown was finally evaluated by RT‐qPCR and western blotting. Results: ENO1 was mainly localized in the cytoplasm, with very small amounts in the nucleus of trophoblast cells. ENO1 expression in the villi tissues of RM patients was significantly increased, when compared with the villous tissues of healthy controls. Furthermore, Bewo cells, a trophoblast cell line with relatively higher expression of ENO1, was used to downregulate the ENO1 expression by ENO1‐siRNA transfection. ENO1 knockdown significantly facilitated Bewo cell growth, EMT process, migration, and invasion. ENO1 silencing markedly elevated COX‐2, c‐Myc, and cyclin D1 expression. Conclusion: ENO1 may participate in the development of RM via suppressing the growth and invasion of villous trophoblasts via reducing the expression of COX‐2, c‐Myc, and cyclin D1. ENO1 may participate in the development of RM via suppressing the growth and invasion of villous trophoblasts via reducing the expression of COX‐2, c‐Myc, and cyclin D1. [ABSTRACT FROM AUTHOR]

Objective: To investigate the correlation between serum asymmetric dimethylarginine (ADMA) and the risk of ischaemic stroke and carotid atherosclerosis in adults. Methods: We systematically searched PubMed, EMBASE, Web of Science and other databases for relevant studies on serum ADMA and ischaemic stroke or carotid atherosclerosis, which were published from December 1980 to December 2019. The quality of the included studies was evaluated according to the Cochrane system evaluation standard. The difference in serum ADMA level between ischaemic stroke and control group was selected as the effect size (standardized mean difference, SMD). The pooled analysis was performed using Review Manager (V.5.3). Results: According to the selection criteria, thirteen studies were included in the meta‐analysis after screening. Nine studies compared ADMA levels between the ischaemic stroke group and healthy control group, involving a total of 1315 and 880 subjects in the two groups, respectively. Pooled effect sizes were calculated using the random‐effects model due to the high heterogeneity (I2 = 93%, P <.00001). The level of serum ADMA in patients with ischaemic stroke was significantly higher than that in healthy people (SDM = 0.69, 95% CI [0.32, 1.06], P =.0002). Seven of the thirteen articles compared ADMA levels between the carotid arteriosclerosis group and the healthy control group, with 559 and 330 subjects in the two groups, respectively. The random‐effects model was applied due to the high heterogeneity (I2 = 91%, P <.00001). The level of serum ADMA in patients with carotid arteriosclerosis was significantly higher than that in healthy people (SDM = 1.03, 95% CI [0.49, 1.57], P =.0002). Conclusion: The serum ADMA may be related to ischaemic stroke, and it is a risk factor for carotid atherosclerosis. [ABSTRACT FROM AUTHOR]

Abstract: A visible‐light‐induced trifluoromethylation of isonitrile‐substituted indole derivatives has been developed from the reaction of isonitrile‐substituted indoles with Togni II reagent, affording 1‐(trifluoromethyl)‐4,9‐dihydro‐3H‐pyrido[3,4‐b]indoles in moderate to good yields. The further transformations to β‐carboline derivatives and a harmacine derivative have been performed, demonstrating the potential synthetic utility of this method. A preliminary biological study indicated that the CF3‐containing harmine analogue significantly stimulated the secretion of glucagon‐like peptide‐1 (GLP‐1), suggesting an improvement in treating diabetes. [ABSTRACT FROM AUTHOR]