BackgroundThe rate, prognostic impacts, and predisposing factors of major vascular complications (MVCs) in patients underwent venoarterial extracorporeal membrane oxygenation (VA-ECMO) by surgical cut-down are poorly understood. The purpose of this study was to identify these parameters in adult VA-ECMO patients.MethodsAdult postcardiotomy cardiogenic shock (PCS) patients receiving VA-ECMO by femoral surgical cut-down cannulation from January 2004 to December 2015 were enrolled in this study. Patients were separated into two groups depending on the presence of MVCs. Multivariate logistic regression was performed to identify factors independently associated with MVCs.ResultsOf 432 patients with PCS treated with VA-ECMO, 252 patients (58.3%) were weaned off VA-ECMO and 153 patients (35.4%) survived to discharge. MVCs were seen in 72 patients (16.7%), including bleeding or hematoma in the cannulation site (8.6%), limb ischemia requiring fasciotomy (8.6%), femoral artery embolism (0.7%), and retroperitoneal bleeding (0.7%). The rate of survival to discharge was 16.7 and 39.2% in patients with or without MVCs, respectively (p < 0.001). Obesity, concomitant with intra-aortic balloon pump (IABP), Sequential Organ Failure Assessment (SOFA) score at 24 h post-ECMO, and hemostasis disorder were shown to be associated with MVCs. MVCs were an independent risk factor for in-hospital mortality by multivariate analysis (odds ratio 3.91; 95% confidence interval, 1.67–9.14; p = 0.013).ConclusionsMVCs are common and associated with higher in-hospital mortality among adult PCS patients receiving peripheral VA-ECMO support. The obesity, concomitant with IABP, SOFA score at 24 h post-ECMO, and hemostasis disorder were independent risk factor of MVCs.

IntroductionDifferential hypoxia is a pivotal problem in patients with femoral veno-arterial (VA) extracorporeal membrane oxygenation (ECMO) support. Despite recognition of differential hypoxia and attempts to deliver more oxygenated blood to the upper body, the mechanism of differential hypoxia as well as prevention strategies have not been well investigated.MethodsWe used a sheep model of acute respiratory failure that was supported with femoral VA ECMO from the inferior vena cava to the femoral artery (IVC-FA), ECMO from the superior vena cava to the FA (SVC-FA), ECMO from the IVC to the carotid artery (IVC-CA) and ECMO with an additional return cannula to the internal jugular vein based on the femoral VA ECMO (FA-IJV). Angiography and blood gas analyses were performed.ResultsWith IVC-FA, blood oxygen saturation (SO2) of the IVC (83.6 ± 0.8%) was higher than that of the SVC (40.3 ± 1.0%). Oxygen-rich blood was drained back to the ECMO circuit and poorly oxygenated blood in the SVC entered the right atrium (RA). SVC-FA achieved oxygen-rich blood return from the IVC to the RA without shifting the arterial cannulation. Subsequently, SO2 of the SVC and the pulmonary artery increased (70.4 ± 1.0% and 73.4 ± 1.1%, respectively). Compared with IVC-FA, a lesser difference in venous oxygen return and attenuated differential hypoxia were observed with IVC-CA and FA-IJV.ConclusionsDifferential venous oxygen return is a key factor in the etiology of differential hypoxia in VA ECMO. With knowledge of this mechanism, we can apply better cannula configurations in clinical practice.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-015-0791-2) contains supplementary material, which is available to authorized users.

BackgroundCancer incidence and mortality have been increasing in China, making cancer the leading cause of death since 2010 and a major public health concern in the country. Cancer stem cells have been studied in relation to the treatment of different malignancies, including gastric cancer. Anticancer bioactive peptide-3 (ACBP-3) can induce the apoptosis of gastric cancer stem cells (GCSCs) and reduce their tumorigenicity. In the present study, for the first time, we used a miRNA microarray and bioinformatics analysis to identify differentially expressed miRNAs in ACBP-3-treated GCSCs and GCSC-derived tumors in a xenograft model and functionally verified the identified miRNAs. miR-338-5p was selected based on its significant upregulation by ACBP-3 both in cultured GCSCs and in tumor tissues.ResultsmiR-338-5p was downregulated in GCSCs compared with normal gastric epithelial cells, and the ectopic restoration of miR-338-5p expression in GCSCs inhibited cell proliferation and induced apoptosis, which correlated with the upregulation of the pro-apoptotic Bcl-2 proteins BAK and BIM. We also found that ACBP-3-treated GCSCs could respond to lower effective doses of cisplatin (DDP) or 5-fluorouracil (5-FU), possibly because ACBP-3 induced the expression of miR-338-5p and the BAK and BIM proteins and promoted GCSC apoptosis.ConclusionsOur data indicate that miR-338-5p is part of an important pathway for the inhibition of human gastric cancer stem cell proliferation by ACBP-3 combined with chemotherapeutics. ACBP-3 could suppress GCSC proliferation and lower the required effective dose of cisplatin or 5-fluorouracil. Therefore, this study provides not only further evidence for the remarkable anti-tumor effect of ACBP-3 but also a possible new approach for the development of GCSC-targeting therapies.Electronic supplementary materialThe online version of this article (doi:10.1186/s13578-016-0112-8) contains supplementary material, which is available to authorized users.

The immature CD14CD16 monocytes might contribute to blood-circuit contact-induced acute lung injury by generating TNF-α-producing, mature monocytes. New strategies based on monocyte manipulation could be a promising therapeutic approach for minimising CPB-related lung injury.

Background: This experimental design was based on lncRNA LINC01194 to explore the pathogenesis of NSCLC. Methods: RT-qPCR was used to detect the expression of lncRNA LINC01194 and miR-486-5p in NSCLC tissues and cell lines. CCK-8, colony formation, and transwell assays were used to examine the effects of lncRNA LINC01194 and miR-486-5p on NSCLC cell proliferation and migration invasiveness. For target gene prediction and screening, luciferase reporter assays were used to verify downstream target genes for lncRNA LINC01194 and miR-486-5p. The protein expression of CDK4 was detected using Western blotting. The tumor changes in mice were detected by in vivo experiments in nude mice. Results: LncRNA LINC01194 was highly expressed in NSCLC tissues and NSCLC lines (A549, H1299, H460 cells, H1975), and lncRNA LINC01194 significantly promoted cell proliferation and migration of NSCLC cells. MiR-486-5p was identified as a potential target for LINC01194, and miR-486-5p was expressed at a low level in NSCLC tissues and NSCLC lines (A549, H1299, H460 cells, H1975). CDK4 was identified as a potential target for miR-486-5p. LncRNA LINC01194 was able to inhibit miR-486-5p expression and upregulate the expression level of CDK4. Finally, the results of in vivo animal models confirmed that lncRNA LINC01194 promoted NSCLC progression by modulating the miR-486-5p/CDK4 axis. Conclusion: LncRNA LINC01194 promoted the progression of NSCLC by modulating the miR-486-5p/CDK4 axis.

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The urinary trypsin inhibitor (ulinastatin) is used in the clinic to prevent inflammatory responses in patients undergoing cardiopulmonary bypass (CPB); however, the anti-inflammatory mechanism is unclear. In the current study, we recruited 40 patients undergoing selective cardiac valve replacement surgery; and these patients were randomly divided into two groups (ulinastatin group [UG] and control group [CG]). We collected peripheral blood preoperatively, at the end of CPB, and postoperative days 1 and 3 and analyzed the kinetic changes in regulatory T (Treg) cell subsets. There was no statistically significant difference in the number of CD4(+) T cells between the two groups. The number of CD4(+)CD25(+) Treg cells, especially the suppressive activated Treg (aTreg) subset, was higher in the UG than the CG 1 and 3 days postoperatively. Thus, ulinastatin alleviated the inflammatory response during CPB by inducing the expansion of aTreg cells.

Increasing MAP from <60 mmHg to 60-90 mmHg did not affect microcirculation variables in cardiogenic-shock patients with ECMO support.