Hensleymeyers2140

Effects of antithrombotic agents on the bleeding risk after transurethral resection of the prostate (TURP) were assessed in patients with benign prostatic hyperplasia (BPH). Controlled clinical trials on the effects of perioperative anticoagulant therapy on postoperative bleeding in BPH patients published during January 1990 and February 2019 were searched in PubMed, Embase and the Cochrane Library. Two independent reviewers screened the studies according to the inclusion and exclusion criteria, extracted the data, evaluated the quality, and conducted a meta-analysis using the RevMan 5.3 software. A total of 20 studies were included. Analysis of these studies found that compared with interrupted use of antithrombotic agents, continuous use of antithrombotic drugs led to more frequent post-TURP bleeding (OR=4.34, 95% CI=2.29-8.23), and higher transfusion rate (2.96, 1.19-7.36). Compared with patients who never used antithrombotic agents, those who used antithrombotic agents continuously had higher bleeding risk (5.52, 1.64-18.66). Those who continued using antithrombotic agents during laser treatment had higher transfusion rate than those who stopped using them before the operation (5.39, 1.49-19.53), but it had no significant difference in clot retention, blood transfusion rate, intraoperative hemoglobin decrease and postoperative catheter-indwelling time compared with those who never used antithrombotic agents (P>0.05). Those who continued using antithrombotic agents during TURP showed less intraoperative hemoglobin decrease (-0.46, -0.58-0.35) than the patients who underwent low molecular weight heparin substitution. Interruption of antithrombotic agents during TURP can prevent the risk of postoperative bleeding; continuous use of antithrombotic agents is safe and feasible during laser treatment of BPH; whether low molecular weight heparin substitution is necessary during the discontinuation of antithrombotic agents is controversial.This aim of the present study was to investigate the expression and function of claudin 3 (CLDN3) in pregnancy-induced hypertension. The mRNA expression levels of CLDN3 in the placental tissue and peripheral blood of patients with pregnancy-induced hypertension were measured using reverse transcription-quantitative PCR. Human trophoblast HTR8/SVneo cells overexpressing CLDN3 were generated using a lentiviral vector. Cell Counting kit-8 (CCK-8) assay, flow cytometry, Transwell chamber assays, confocal laser scanning microscopy and western blot analysis were performed to detect cell proliferation, invasion, migration and apoptosis, in addition to matrix metalloproteinase (MMP) expression and ERK1/2 phosphorylation. The mRNA expression levels of CLDN3 were significantly reduced in the placental tissues and peripheral blood samples of patients with pregnancy-induced hypertension compared with healthy pregnant controls. CLDN3 overexpression significantly increased HTR8/SVneo cell proliferation, invasion and migration whilst reducing apoptosis. HTR8/SVneo cells overexpressing CLDN3 also exhibited increased myofiber levels, increased MMP-2 and MMP-9 expression and increased ERK1/2 signaling activity. CLDN3 downregulation may be associated with the pathogenesis of pregnancy-induced hypertension. In conclusion, CLDN3 promotes the proliferative and invasive capabilities of human trophoblast cells, with the underlying mechanisms possibly involving upregulation of MMP expression via the ERK1/2 signaling pathway.The present study investigated the effect of long non-coding RNA (lncRNA) Dlx6os1 silencing on cell proliferation, apoptosis and fibrosis, and further explored its influence on the mRNA expression profile in mouse mesangial cells (MMCs) of a diabetic nephropathy (DN) cellular model. A DN cellular model was constructed in SV40 MES13 MMCs under high glucose conditions (30 mmol/l glucose culture). lncRNA Dlx6os1 short hairpin (sh)RNA plasmids and negative control (NC) shRNA plasmids were transfected into the MMCs of the DN cellular model as the sh-lncRNA group and sh-NC group respectively. The mRNA expression profile was determined in the sh-lncRNA and sh-NC groups. Inflammation inhibitor Compared with the sh-NC group, the cell proliferation, mRNA and protein expression levels of proliferative markers (cyclin D1 and proliferating cell nuclear antigen) as well as fibrosis markers (fibronectin and collagen I) were suppressed, whereas cell apoptosis was promoted in the sh-lncRNA group. The mRNA expression profile identified 423 upregulated mRNAs and 438 downregulated mRNAs in the sh-lncRNA group compared with the sh-NC group. Additionally, Gene Ontology/Kyoto Encyclopedia of Genes and Genomes enrichment analyses revealed that the differentially expressed mRNAs were enriched in apoptosis and inflammation-related pathways. Further gene-set enrichment analysis of apoptosis and inflammation revealed that lncRNA Dlx6os1 inhibition promoted apoptosis and suppressed inflammation in MMCs of the DN cellular model. In conclusion, lncRNA Dlx6os1 may serve as a potential treatment target for DN via regulation of multiple apoptosis- and inflammation-related pathways.Sepsis is an emergency systemic illness caused by pathogen infection and the combined result of the underactivity and overactivity of a patient's own immune system. However, the molecular mechanism of this illness remains largely unknown. Lipopolysaccharide (LPS) was injected to establish a sepsis model, and heart tissue was used to analyze transcriptome changes in mice. LPS injection was used to develop a sepsis model, which resulted in cardiac tissue rearrangement and inflammatory response activation. An RNA-sequencing-based transcriptome assay using mouse heart tissue with or without LPS injection showed that 3,326 and 1,769 genes were upregulated and downregulated, respectively (>2-fold changes; P less then 0.05). Furthermore, these differentially expressed genes were classified into 20 pathways, including 'Wnt signaling pathway', 'VEGF signaling pathway' and 'TGF-β signaling pathway', and these altered genes were enriched in 41 Gene Ontology terms. The application of Wnt3a inhibited the activation of the LPS-induced inflammatory response and activated Wnt signaling, as well as protecting against LPS-mediated cardiac tissue damage in mice.