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ELMO3 is a member of the engulfment and cell motility (ELMO) protein family, which plays a vital role in the process of chemotaxis and metastasis of tumor cells. However, remarkably little is known about the role of ELMO3 in cancer. The present study was conducted to investigate the function and role of ELMO3 in gastric cancer (GC) progression. The expression level of ELMO3 in gastric cancer tissues and cell lines was measured by means of real-time quantitative PCR (qPCR) and Western blot analysis. RNA interference was used to inhibit ELMO3 expression in gastric cancer cells. Then, wound-healing assays, Transwell assays, MTS assays, flow cytometry, and fluorescence microscopy were applied to detect cancer cell migration, cell invasion, cell proliferation, the cell cycle, and F-actin polymerization, respectively. The results revealed that ELMO3 expression in GC tumor tissues was significantly higher than in the paired adjacent tissues. Moreover, knockdown of ELMO3 by a specific siRNA significantly inhibited the processes of cell proliferation, invasion, metastasis, regulation of the cell cycle, and F-actin polymerization. Collectively, the results indicate that ELMO3 participates in the processes of cell growth, invasion, and migration, and ELMO3 is expected to be a potential diagnostic and prognostic marker for GC. [ABSTRACT FROM AUTHOR]

Background The aim of this study was to explore the prognostic value of copeptin for predicting all-cause mortality in heart failure (HF). Methods PubMed, Embase and Cochrane databases were systematically searched to identify if a 2 × 2 contingency table could be constructed based on both the copeptin level and the all-cause mortality in patients diagnosed with HF. The characteristics of test performance were summarized using forest plots and summary receiver operating characteristic curves (SROC). Q-test and I 2 index were used to evaluate heterogeneity. Results Ten prospective cohort studies comprising 4473 patients were eligible in this meta-analysis. An elevated copeptin level was associated with an increased risk of all-cause mortality in HF patients (Relative risk (RR) was 2.64 (95% CI, 2.09–3.32)). The pooled sensitivity (SEN) and specificity (SPE) of copeptin were 0.57 (95% CI, 0.50–0.63) and 0.74 (95% CI, 0.69–0.79), respectively. The positive likelihood ratio was 2.2 (95% CI, 1.90–2.60) and the negative likelihood ratio was 0.58 (95% CI, 0.52–0.66). Furthermore, the summary Diagnostic Odds Ratio (DOR) was 4.00 (95% CI, 3.00–5.00) and the AUC was 0.70 (95% CI, 0.66–0.74) similar to the AUC of NT-proBNP 0.71 (95% CI, 0.67–0.75). Conclusions Elevated levels of copeptin are associated with all-cause mortality in HF patients. The predictive value of copeptin is comparable with NT-proBNP for all-cause mortality in HF patients. Further studies are warranted to explore the prognostic value of copeptin in conjunction with other biomarkers and to determine an optimal cut-off level. [ABSTRACT FROM AUTHOR]

OBJECTIVES Conventional surgical closure has been considered the gold standard for the treatment of perimembranous ventricular septal defects (PVSDs) in infants for many years, but it requires a cardiopulmonary bypass and midline sternotomy which can lead to both physical and psychological trauma in the future. An intraoperative device closure can be performed with the advantages of reduced invasion, faster recovery and so on. We evaluate the safety and feasibility of intraoperative device closure of PVSDs in infants in comparison with surgical closure. METHODS One hundred eighty-six infants with a PVSD were enrolled in our study. Among them, 97 patients were treated by surgical closure and 89 were treated by intraoperative device closure. The success rates, complications, length of hospital stay and costs were measured. RESULTS The success rate was similar (P = 0.228) in the two groups: 87/89 patients (97.8%) in the device group versus 97/97 patients (100%) in the surgical group. Complication needs management was required in one patient of the device group (1.1%) and in two patients of the surgical group (2.0%) (P = 1.000). Minor complications were observed in 7/87 patients (8.0%) of the device group versus 15/99 patients (15.2%) of the surgical group (P < 0.001). Both groups were similarly effective in reducing the left ventricular end-diastolic dimension, pulmonary arterial pressure and cardiothoracic rate. The procedure time, inpatient stay and intensive care unit stay are shorter in the device group; the total cost was similar for both groups. CONCLUSIONS Intraoperative device closure of PVSDs under real-time transoesophageal echocardiography guidance is safe and feasible without CPB. Under the right conditions, intraoperative device closure can be a good alternative to surgical closure for the treatment of PVSDs in infants. [ABSTRACT FROM PUBLISHER]