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Cubic MnSe2 microcubes are introduced into sulfur cathodes to prevent the shuttle effect of lithium polysulfide through binding with polysulfide via the strong interaction between Se and S, thus alleviate the shuttle effect significantly. Improved cycle performance and rate capability are achieved. This work offers a new strategy to develop high-performance lithium–sulfur batteries.

Chai-Qin-Cheng-Qi decoction (CQCQD) improves intestinal motility in acute pancreatitis (AP), but the mechanism(s) require elucidation. We investigated the effects of CQCQD and carbachol, a prokinetic agent, on colonic smooth muscle cells (SMCs) in L-arginine-induced necrotising AP model in rats. In treatment groups, intragastric CQCQD (20 g/kg, 2 hourly × 3 doses) or intraperitoneal carbachol (60 μg/kg) was given 24 hours after induction of AP. Both CQCQD and carbachol decreased the severity of pancreatic and colonic histopathology (allP<0.05). Both CQCQD and carbachol reduced serum intestinal fatty acid binding protein, vasoactive intestinal peptide, and substance P and increased motility levels. CQCQD upregulated SMC phospholipase C-beta 1 (PLC-β1) mRNA and PLC protein (bothP<0.05), while both treatments upregulated protein kinase C-alpha (PKC-α) mRNA and PKC protein and downregulated adenylate cyclase (AC) mRNA and protein compared with no treatment (allP<0.05). Neither treatment significantly altered L-arginine-induced PKC-β1 and PKC-εmRNA reduction. Both treatments significantly increased fluorescence intensity of SMC intracellular calcium concentration[Ca2+]i(3563.5 and 3046.9 versus 1086.9, bothP<0.01). These data suggest CQCQD and carbachol improve intestinal motility in AP by increasing[Ca2+]iin colonic SMCs via upregulating PLC, PKC and downregulating AC.

To reveal the key molecular mechanisms of Chaiqinchengqi decoction (CQCQD) in alleviating the pulmonary albumin leakage caused by endotoxemia in severe acute pancreatitis (SAP) rats. Rats models of SAP endotoxemia-induced acute lung injury were established, the studies in vivo provided the important evidences that the therapy of CQCQD significantly ameliorated the increases in plasma levels of lipopolysaccharide (LPS), sCd14, and Lbp, the elevation of serum amylase level, the enhancements of systemic and pulmonary albumin leakage, and the depravation of airways indicators, thus improving respiratory dysfunction and also pancreatic and pulmonary histopathological changes. According to the analyses of rats pulmonary tissue microarray and protein-protein interaction network, c-Fos, c-Src, and p85αwere predicted as the target proteins for CQCQD in alleviating pulmonary albumin leakage. To confirm these predictions, human umbilical vein endothelial cells were employed in in vitro studies, which provide the evidences that (1) LPS-induced paracellular leakage and proinflammatory cytokines release were suppressed by pretreatment with inhibitors of c-Src (PP1) or PI3K (LY294002) or by transfection with siRNAs of c-Fos; (2) fortunately, CQCQD imitated the actions of these selective inhibitions agents to inhibit LPS-induced high expressions of p-Src, p-p85α, and c-Fos, therefore attenuating paracellular leakage and proinflammatory cytokines release.

Background and Aims. The aim of this study was to determine the expression of microRNA-127 (miR-127) in both rat models and patients of acute pancreatitis (AP) with lung injury (LI). Methods. Rats were administrated with retrograde cholangiopancreatography injection of 0.5% or 3.5% sodium taurocholate to induce AP with mild or severe LI and were sacrificed at 6, 12, and 24 h. Rats from the control group received a laparotomy only. Plasma from a prospective cohort of AP patients was collected. The levels of miR-127 in the tissues and plasma were detected using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Results. The upregulation of miR-127 in the lungs of rats was detected in the groups of AP with severe LI at 6 h and 24 h, whereas it was scarcely detectable in plasma. In the pilot study that included 18 AP patients and 5 healthy volunteers, the plasma miR-127 level was significantly downregulated in AP patients with respiratory failure compared with the healthy volunteers (P=0.014) and those without respiratory failure (P=0.043). Conclusion. miR-127 might serve as a potential marker for the identification of AP with LI.

BACKGROUND To investigate in-vitro antagonistic effect of low-dose liquiritigenin on gemcitabine-induced capillary leak syndrome (CLS) in pancreatic adenocarcinoma via inhibiting reactive oxygen species (ROS)- mediated signalling pathways. MATERIALS AND METHODS Human pancreatic adenocarcinoma Panc-1 cells and human umbilical vein endothelial cells (HUVECs) were pre-treated using low-dose liquiritigenin for 24 h, then added into gemcitabine and incubated for 48 h. Cell viability, apoptosis rate and ROS levels of Panc-1 cells and HUVECs were respectively detected through methylthiazolyldiphenyl-tetrazoliumbromide (MTT) and flow cytometry. For HUVECs, transendothelial electrical resistance (TEER) and transcellular and paracellular leak were measured using transwell assays, then poly (ADP-ribose) polymerase 1 (PARP-1) and metal matrix proteinase-9 (MMP9) activity were assayed via kits, mRNA expressions of p53 and Rac-1 were determined through quantitative polymerase chain reaction (qPCR); The expressions of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and PARP-1 were measured via western blotting. RESULTS Low-dose liquiritigenin exerted no effect on gemcitabine-induced changes of cell viability, apoptosis rate and ROS levels in Panc-1 cells, but for HUVECs, liquiritigenin (3 μM) could remarkably elevate gemcitabine- induced decrease of cell viability, transepithelial electrical resistance (TEER), pro-MMP9 level and expression of ICAM-1 and VCAM-1 (p

Background: Chronic gastritis (CG), a poorly understood entity, is a very common disease of the digestive tract and is difficult to cure. Chronic non-atrophic gastritis (CNG) is the most common type of CG. Even if treated with current standard chemotherapy, some patients will not be freed from this confusing disease. Many studies have shown traditional Chinese medicine (TCM) is more effective compared to chemotherapy in the treatment of chronic gastritis and no serious side effects have been identified. However, the studies that have been carried out were not scientifically rigorous trials. Our aim is to design a high-quality trial for a new TCM drug, the Jian-Wei-Qu-Tong Pills (JWQTP), to investigate the efficacy and safety of this new drug in treating chronic non-atrophic gastritis patients with spleen and stomach qi deficiency with damp-heat stasis syndrome (SSQDDSS). Methods/Design: This is a phase II, multicenter, parallel-group, double-blind, randomized and placebo-controlled trial. A total of 240 participants will be assigned to a high-dose group, a low-dose group or a placebo control group with a 1:1:1 ratio at five sites. Then, one dose (six 1-g pills), with a variable ratio between real drug and dummy drug according to the intervention protocol, will be taken three times a day before each meal for 8 weeks. The primary outcome is the eradication rate of epigastric pain. The secondary outcome includes the changes of endoscopic examination, histopathological examination, traditional Chinese medicine symptom scores and patient-reported outcome instrument scores for chronic gastrointestinal diseases and the eradication rate of Helicobacter pylori (HP). Discussion: Many CNG patients suffer from frequent, recurrent bouts of dyspeptic symptoms. This is the first clinical trial to evaluate the safety and efficacy of JWQTP in treating CNG with SSQDDSS in a multicenter, parallel-group, double-blind, randomized and placebo-controlled manner. This trial may not only provide evidence for a phase III clinical trial, but also a vision of an alternative option for CNG treatment. Trial registration: The registration number, ChiCTR-TRC-14004088, was assigned by the Chinese Clinical Trial Registry on 7 January 2014.