Objective:This meta-analysis aimed to evaluate the efficiency and safety of tranexamic acid for reducing blood loss and transfusion requirements in patients undergoing total shoulder arthroplasty.Methods:A systematic search was performed in Embase (1980–2017.04, embase.com), Medline (1966–2017.04, medline.com), PubMed (1966–2017.04, pubmed.com), ScienceDirect (1985–2017.04, sciencedirect.com), and Web of Science (1950–2017.04, webofknowledge.com). Study which assessed the efficiency and safety of tranexamic acid in total shoulder arthroplasty was selected. Meta-analysis was performed using Stata 11.0 software.Results:In all, 484 patients from 2 randomized controlled trials (RCTs) and 2 non-RCTs were subjected to meta-analysis. The present meta-analysis demonstrated that there was less total blood loss (mean difference [MD] −172.16, 95% confidence interval [CI] −35.46 to −308.87, P = .01, d = 0.33) and transfusion rate (odds ratio 0.34, 95% CI 0.13 to 0.91, P = .03, d = 0.29) in tranexamic acid groups compared with the control groups. There were no significant differences in duration of surgery (MD 0.02, 95% CI −0.12 to 0.22, P = .89, d = 0.19), length of stay (MD −0.06, 95% CI −0.26 to 0.14, P = .56, d = 0.20), or incidence of adverse effects such as deep venous thrombosis (odds ratio 1.15, 95% CI 0.33 to 4.00, P = .83, d = 0.53).Conclusion:Clinical application of tranexamic acid seemed to result in significant reductions in total blood loss, hemoglobin decline and transfusion requirements following total shoulder arthroplasty. Moreover, no increased risk of the thrombotic events was identified. Due to the limited quality of the evidence currently available, higher quality RCTs are required.

The objective of the present study was to investigate the anticancer properties of hesperidin against human osteosarcoma MG-63 cells. Its effects on apoptosis, cell migration, cell invasion and cell cycle arrest, and its effects on tumor volume and weight were also evaluated in the present study. MTS assay was used to study the cytotoxic effects of the compound on cell viability. Effects on apoptosis and cell cycle arrest were evaluated by flow cytometry. In vitro wound healing assay and Matrigel assay were performed to study the effects of hesperidin on cell migration and cell invasion, respectively. Hesperidin exerted dose-dependent and time-dependent growth inhibitory effects on cervical cancer cells with IC50 values of 33.5, 23.8 and 17.6 µM, respectively, at 24, 48 and 72 h time intervals. Hesperidin led to early and late apoptosis induction in these cells. Hesperidin-treated cells also led to G2/M phase cell cycle arrest, which exhibited strong dose-dependence. Hesperidin treatment also led to inhibition of cell migration and invasion.

Background: Growing studies have suggested the dysregulation of long non-coding RNAs (lncRNAs) in several tumors, including osteosarcoma (OS). However, limited studies report metastasis-associated lncRNAs in OS. Our present study aimed to explore the roles of lncRNA LINC00514 (LINC00514) in OS. Materials and Methods: The LINC00514 expression was measured using qPCR assays in OS tissues and cell lines. The clinical significance of LINC00514 expression in OS patients was analyzed using chi-square test, Kaplan-Meier assays and multivariate analysis. The possible effects of LINC00514 in tumor cellular progression were determined using a series of functional assays. The mechanisms of LINC00514 action were explored through bioinformatics, luciferase reporter assays and RT-PCR assays. The mechanisms involved the upregulation of LINC00514 expression in OS were determined using luciferase reporter and chromatin immunoprecipitation (ChIP) assays. Results: We showed that LINC00514 expressions were distinctly upregulated in both OS tissues and cell lines, especially in advanced cases. High levels of LINC0051 were positively correlated with advanced tumor stages, distant metastasis, and reduced survival of patients with OS. Functional experiments indicated that silencing of LINC00514 suppressed the ability of cell growth, colony formation and metastasis, whereas promoted cell apoptosis in vitro. Mechanistic investigation revealed that LINC00514 could directly bind to miR-708 and effectively serve as a ceRNA for miR-708. In addition, LINC00514 was upregulated by the transcription factor SP1. Conclusion: Our findings revealed SP1-induced upregulation of LINC00514 as an oncogene in OS through competitively binding to miR-708, suggesting that there are potential diagnostic and treatment values of LINC00514 in OS.