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Designing solid electrolyte is deemed as an effective approach to suppress the side reaction of zinc anode and active material dissolution of cathodes in liquid electrolytes for zinc metal batteries (ZMBs). Herein, kaolin is comprehensively investigated as raw material to prepare solid electrolyte (KL−Zn) for ZMBs. As demonstrated, KL−Zn electrolyte is an excellent electronic insulator and zinc ionic conductor, which presents wide voltage window of 2.73 V, high ionic conductivity of 5.08 mS cm−1, and high Zn2+ transference number of 0.79. For the Zn//Zn cells, superior cyclic stability lasting for 2200 h can be achieved at 0.2 mA cm−2. For the Zn//NH4V4O10 batteries, stable capacity of 245.8 mAh g−1 can be maintained at 0.2 A g−1 after 200 cycles along with high retention ratio of 81 %, manifesting KL−Zn electrolyte contributes to stabilize the crystal structure of NH4V4O10 cathode. These satisfying performances can be attributed to the enlarged interlayer spacing, zinc (de)solvation‐free mechanism and fast diffusion kinetics of KL−Zn electrolyte, availably guaranteeing uniform zinc deposition for zinc anode and reversible zinc (de)intercalation for NH4V4O10 cathode. Additionally, this work also verifies the application possibility of KL−Zn electrolyte for Zn//MnO2 batteries and Zn//I2 batteries, suggesting the universality of mineral‐based solid electrolyte. [ABSTRACT FROM AUTHOR]

Simple reaction conditions and recyclable reagents are crucial for environmentally friendly industrial applications. An environment-friendly, recyclable and economic strategy was developed to synthesize diaryl chalcogenides by the CuCl2-catalyzed C–S bond-formation reaction via iodobenzenes and benzenethiols/1,2-diphenyldisulfanes using N , N ′-dimethylethane-1,2-diamine (DMEDA) as ligand, base, and solvent. For these reactions, especially the reactions of diiodobenzenes and aminobenzenethiols/disulfanediyldianilines, a range of substrates are compatible and give the corresponding products in good to excellent yields. Both of the reagents in the catalytic system (CuCl2 /DMEDA) are inexpensive, conveniently separable, and recyclable for more than five cycles. [ABSTRACT FROM AUTHOR]

Abstract Background Perturbation of DNA methylation is frequent in cancers and has emerged as an important mechanism involved in tumorigenesis. To determine how DNA methylation is modified in the genome of primary glioma, we used Methyl-DNA immunoprecipitation (MeDIP) and Nimblegen CpG promoter microarrays to identify differentially DNA methylation sequences between primary glioma and normal brain tissue samples. Methods MeDIP-chip technology was used to investigate the whole-genome differential methylation patterns in glioma and normal brain tissues. Subsequently, the promoter methylation status of eight candidate genes was validated in 40 glioma samples and 4 cell lines by Sequenom's MassARRAY system. Then, the epigenetically regulated expression of these genes and the potential mechanisms were examined by chromatin immunoprecipitation and quantitative real-time PCR. Results A total of 524 hypermethylated and 104 hypomethylated regions were identified in glioma. Among them, 216 hypermethylated and 60 hypomethylated regions were mapped to the promoters of known genes related to a variety of important cellular processes. Eight promoter-hypermethylated genes (ANKDD1A, GAD1, HIST1H3E, PCDHA8, PCDHA13, PHOX2B, SIX3, and SST) were confirmed in primary glioma and cell lines. Aberrant promoter methylation and changed histone modifications were associated with their reduced expression in glioma. In addition, we found loss of heterozygosity (LOH) at the miR-185 locus located in the 22q11.2 in glioma and induction of miR-185 over-expression reduced global DNA methylation and induced the expression of the promoter-hypermethylated genes in glioma cells by directly targeting the DNA methyltransferases 1. Conclusion These comprehensive data may provide new insights into the epigenetic pathogenesis of human gliomas.

Context: The sensitivity and specificity of blood microRNA-421 (miR-421) as a gastric cancer (GC) biomarker has not been determined. Objective: To investigate the diagnostic value of blood miR-421 as GC biomarker. Materials and methods: miR-421 in serum and peripheral blood mononuclear cells (PBMCs) of 90 GC patients and 90 controls was detected by quantitative real-time PCR. The correlation of miR-421 to GC clinicopathological features as well as the diagnostic value of miR-421 comparing to carcinoembryonic antigen (CEA) and cancer antigen 125 (CA-125) were analyzed. Results: miR-421 increased significantly in GC patients than in controls. miR-421 in either serum or PBMCs had higher sensitivity and specificity than CEA and CA-125 in GC diagnosis. The GC positive prediction rates of miR-421 were also significantly higher than those of CEA and CA-125. Discussion and conclusions: miR-421 in serum or PBMCs may be a new potential diagnostic biomarker for GC. [ABSTRACT FROM AUTHOR]

Inactivated LRRC4 has been clinically detected in gliomas, and promoter hypermethylation has been implicated as the mechanism of inactivation in some of those tumors. Our previous researches indicated that LRRC4 is a target gene of miR-381, the interaction of miR-381 and LRRC4 is involved in glioma growth. In this study, we demonstrate that LRRC4 is a target gene of the other microRNA, miR-182. We found that the high expression of miR-182 and miR-381 in gliomas are involved in pathological malignant progression. The silencing of miR-182 and miR-381 inhibited the proliferation in vitro and growth of glioma cell with in vivo magnetic resonance imaging by intracranial transplanted tumor model in rats. We also demonstrated that BRD7, a transcriptional cofactor for p53, is highly expressed and negatively correlated with LRRC4 expression in gliomas. Disturbing miR-182 and miR-381 affected transcriptional regulation of the BRD7 gene. This finding was verified by ectopic overexpression of LRRC4 or restoration of endogenous LRRC4 expression by treatment with the DNA demethylating agent 5-Aza-dC. Taken together, miR-182 and miR-381 may be a useful therapeutic target for treatment of glioma. [ABSTRACT FROM AUTHOR]

Inactivated LRRC4 has been clinically detected in gliomas, and promoter hypermethylation has been implicated as the mechanism of inactivation in some of those tumors. Our previous researches indicated that LRRC4 is a target gene of miR-381, the interaction of miR-381 and LRRC4 is involved in glioma growth. In this study, we demonstrate that LRRC4 is a target gene of the other microRNA, miR-182. We found that the high expression of miR-182 and miR-381 in gliomas are involved in pathological malignant progression. The silencing of miR-182 and miR-381 inhibited the proliferation in vitro and growth of glioma cell with in vivo magnetic resonance imaging by intracranial transplanted tumor model in rats. We also demonstrated that BRD7, a transcriptional cofactor for p53, is highly expressed and negatively correlated with LRRC4 expression in gliomas. Disturbing miR-182 and miR-381 affected transcriptional regulation of the BRD7 gene. This finding was verified by ectopic overexpression of LRRC4 or restoration of endogenous LRRC4 expression by treatment with the DNA demethylating agent 5-Aza-dC. Taken together, miR-182 and miR-381 may be a useful therapeutic target for treatment of glioma. [ABSTRACT FROM AUTHOR]

One bonded- and one discreted-Lindqvist hexatungstate-based copper hybrids (Cu-POMs) ([Cu2(O)OH(phen)2]2[W6O19]·6H2O (1) and [Cu2(phen)4Cl] [HW6O19]·2H2O (2) (phen = 1,10-phenanthroline)) were controllably synthesized and routinely characterized. Cu-POMs 1-2 consisted of identical [W6O19] unit and similar copper-phen complexes, the two units are bonded via four Cu-O chemical bonds in compound 1; however, compound 2 is discreted and stabilized by intermolecular electrostatic interactions. Importantly, these Cu-POMs catalysts were first applied in the novel reaction for the preparation of 2-phenylquinoxalines via the one-pot coupling and oxidation reactions of 2-haloanilines with vinyl azides or 3-phenyl-2H-azirines under mild conditions, and Cu-POMs 1 showed higher catalytic performance in good yields (79-84%). The reactions exhibit some functional group tolerance and allow for the preparation of a number of 2-phenylquinoxalines.

Exosomes containing microRNA-155 act as molecule carriers during immune cell-cell communication and play an important role in the inflammatory response of H. pylori infection macrophages. Previous reports have found that miR-155 was over-expressed in H. pylori infection macrophages, but the significance of which is still unknown. In this study, we analyzed the impact of miR-155 loaded in exosomes derived from macrophages to the inflammatory response of H. pylori infection macrophages and possible mechanisms. We found that miR-155 promoted the expression of inflammatory cytokines including TNF-a, IL-6, IL-23, but also increased the expression of CD40, CD63, CD81, and MCH-I. Meanwhile, inflammatory signal pathways proteins, such as MyD88, NF-κB in H. pylori infection macrophages were down-regulated due to the over-expression of miR-155. Experiments in vitro or in vivo revealed that miR-155 promoted macrophages to inhibit or kill H. pylori by regulating the inflammatory response of cells to prevent the gastritis caused by H. pylori infection. These findings contribute to the understanding of miR-155 contained in exosomes in inflammatory responses of H. pylori infection macrophages.

MicroRNA-381 (miR-381) is a highly expressed onco-miRNA that is involved in malignant progression and has been suggested to be a good target for glioblastoma multiforme (GBM) therapy. In this study, we employed two-dimensional fluorescence differential gel electrophoresis (2-D DIGE) and MALDI-TOF/TOF-MS/MS to identify 27 differentially expressed proteins, including the significantly upregulated neurofilament light polypeptide (NEFL), in glioblastoma cells in which miR-381 expression was inhibited. We identified NEFL as a novel target molecule of miR-381 and a tumor suppressor gene. In human astrocytoma clinical specimens, NEFL was downregulated with increased levels of miR-381 expression. Either suppressing miR-381 or enforcing NEFL expression dramatically sensitized glioblastoma cells to temozolomide (TMZ), a promising chemotherapeutic agent for treating GBMs. The mechanism by which these cells were sensitized to TMZ was investigated by inhibiting various multidrug resistance factors (ABCG2, ABCC3, and ABCC5) and stemness factors (ALDH1, CD44, CKIT, KLF4, Nanog, Nestin, and SOX2). Our results further demonstrated that miR-381 overexpression reversed the viability of U251 cells exhibiting NEFL-mediated TMZ sensitivity. In addition, NEFL-siRNA also reversed the proliferation rate of U251 cells exhibiting locked nucleic acid (LNA)-anti-miR-381-mediated TMZ sensitivity. Overall, the miR-381-NEFL axis is important for TMZ resistance in GBM and may potentially serve as a novel therapeutic target for glioma.