Neointimal proliferation after vascular injury is a key mechanism of restenosis, a major cause of percutaneous transluminal angioplasty failure and artery bypass occlusion. Emodin, an anthraquinone with multiple physiological activities, has been reported to inhibit proliferation of vascular smooth muscle cells (VSMCs) that might cause intimal arterial thickening. Thus, in this study, we established a rat model of balloon-injured carotid artery and investigated the therapeutic effect of emodin and its underlying mechanism. Intimal thickness was analyzed by hematoxylin and eosin staining. Expression of Wnt4, dvl-1, β-catenin and collagen was determined by immunohistochemistry and/or western blotting. The proliferation of VSMC was evaluated by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and electron microscopy. MicroRNA levels were quantified by real-time quantitative PCR. Emodin relieved injury-induced artery intimal thickness. Results of western blots and immunohistochemistry showed that emodin suppressed expression of signaling molecules Wnt4/Dvl-1/β-catenin as well as collagen protein in the injured artery. In addition, emodin enhanced expression of an artery injury-related microRNA, miR-126. In vitro, MTT assay showed that emodin suppressed angiotensin II (AngII)-induced proliferation of VSMCs. Emodin reversed AngII-induced activation of Wnt4/Dvl-1/β-catenin signaling by increasing expression of miR-126 that was strongly supported by transfection of mimic or inhibitor for miR-126. Emodin prevents intimal thickening via Wnt4/Dvl-1/β-catenin signaling pathway mediated by miR-126 in balloon-injured carotid artery of rats.
This study showed that impaired kidney function at discharge was shown to be an important risk factor affecting the long-term renal survival rates of critically ill patients with AKI. An eGFR <45 mL/min/1.73 m was an independent risk factor for decreased overall survival and renal survival.
Background: Central venous catheters are used extensively as temporary or permanent vascular access for haemodialysis patients. Catheter-related bloodstream infections are the main complication of central venous catheters and increase morbidity and mortality in haemodialysis patients. Objectives: The aim was to assess the most appropriate lock solution for central venous catheters to prevent catheter-related bloodstream infections and other complications. Data sources: Medline, Embase and the Cochrane Central Register of Controlled Trials from the date of their inception to August 2018 were used as data sources. The reference lists of eligible studies and relevant reviews were also checked. Study eligibility criteria and participants: Randomized controlled trials (RCTs) comparing different lock solutions for the prevention of central venous catheter-related infectious and bleeding complications for adult dialysis patients were included. Interventions: Interventions were lock solutions for haemodialysis catheters. Methods: The primary outcomes were catheter-related bloodstream infections and bleeding events. The secondary outcomes were catheter malfunction, exit-site infection, and all-cause mortality. We estimated summary risk ratios (RRs) using pairwise and network meta-analysis. We assessed the risk of bias of individual studies with the Cochrane risk of bias tool. Results: Forty-nine trials (7020 patients) were included for this study. Compared with heparin 5000 U/ mL, antibiotic locks (antibiotics with trisodium citrate (TSC), ethylenediamine tetraacetic acid (EDTA), heparin 5000 U/mL, low-dose heparin or urokinase) and ethanol locks were more effective in preventing catheter-related bloodstream infections. Antimicrobial agents plus low-dose heparin (500e2500 U/mL), TSC and low-dose heparin locks had lower risk of bleeding events than heparin 5000 U/mL. None of the lock solutions reduced rates of catheter malfunction and all-cause mortality compared with heparin 5000 U/mL. In summary, antibiotics plus low-dose heparin was ranked as the best lock solution. The overall results were not materially changed in sensitivity analyses. Conclusions: Taking into account both efficacy and safety, antibiotics plus low-dose heparin (500e2500 U/mL) may be the preferred lock solution.
The above article, published online on 13 October 2014 in Wiley Online Library (http://onlinelibrary.wiley.com/doi/10.1002/cbin.10388/abstract), has been retracted by agreement between the authors, the journal Editor, Sergio Schenkman, and John Wiley & Sons Ltd. The retraction has been agreed because the authors discovered after publication that one of the cell lines described in the article had been unintentionally misidentified. The experiments described in the article as being conducted on Human Oral Squamous Cell Carcinoma cell line KB were in fact conducted on a Human Oral Epidermal-like Cancer cell line. The authors and publisher apologise for any inconvenience. References He Y, Chen F, Cai Y and Chen S (2015) Knockdown of tumor protein D52-like 2 induces cell growth inhibition and apoptosis in oral squamous cell carcinoma. Cell Biology International 39: 264-271. doi: 10.1002/cbin.10388.
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