CO2 electrolysis is a key step in CO2 conversion into fuels and chemicals as a way of mitigating climate change. We report the synthesis and testing of a series of new anion‐conductive membranes (tradenamed Sustainion™) for use in CO2 electrolysis. These membranes incorporate the functional character of imidazolium‐based ionic liquids as co‐catalysts in CO2 reduction into a solid membrane with a styrene backbone. We find that the addition of an imidazolium group onto the styrene side‐chains increases the selectivity of the reaction from approximately 25 % to approximately 95 %. The current at 3 V is increased by a factor of 14. So far we have been able to tune these parameters to achieve stable cells that provide current densities higher than 100 mA cm−2 at 3 V cell potential with a CO product selectivity over 98 %. Stable performance was observed for 6 months of continuous operation (>150 000 000 turnovers). These results demonstrate that imidazolium polymers are ideal membranes for CO2 electrolysis.

We report a modular construction of a new metal-organic framework (MOF) by strategically incorporating a number of water repellent functional groups in the frameworks. These MOFs demonstrate both open structure for high sorption capability and strong water resistance.

Intercalation of polysulfides into LDHs forms layered composites that can separate Hg2+, Ag+ and Cu2+ from mixed ions with high selectivity and capacity.

BackgroundThe Hepatitis C virus (HCV) core protein has been implicated as a potential oncogene or a cofactor in HCV-related hepatocellular carcinoma (HCC), but the underlying mechanisms are unknown. Overactivation of the Wnt/β-catenin signaling is a major factor in oncogenesis of HCC. However, the pathogenesis of HCV core-associated Wnt/β-catenin activation remains to be further characterized. Therefore, we attempted to determine whether HCV core protein plays an important role in regulating Wnt/β-catenin signaling in HCC cells.MethodologyWnt/β-catenin signaling activity was investigated in core-expressing hepatoma cells. Protein and gene expression were examined by Western blot, immunofluorescence staining, RT-qPCR, and reporter assay.Principal FindingsHCV core protein significantly enhances Tcf-dependent transcriptional activity induced by Wnt3A in HCC cell lines. Additionally, core protein increases and stabilizes β-catenin levels in hepatoma cell line Huh7 through inactivation of GSK-3β, which contributes to the up-regulation of downstream target genes, such as c-Myc, cyclin D1, WISP2 and CTGF. Also, core protein increases cell proliferation rate and promotes Wnt3A-induced tumor growth in the xenograft tumor model of human HCC.Conclusions/SignificanceHCV core protein enhances Wnt/β-catenin signaling activity, hence playing an important role in HCV-associated carcinogenesis.

A B S T R A C TThe electrochemical production of syngas would enable production of chemicals and transportation fuels from carbon dioxide, water and renewable energy, but a suitable process at the moment does not exist. In this paper we consider two options for syngas production: (i) CO 2 electrolysis to produce CO, water electrolysis to produce H 2 and then mixing the CO and H 2 to yield syngas; and (ii) the simultaneous coelectrolysis of CO 2 and H 2 O in a single electrolyzer. The results show that both processes can produce syngas at industrially important rates. In this paper we demonstrate CO 2 electrolysis at 100 mA/cm 2 , i.e., about 20 turnovers/s, and water electrolysis at 8 A/cm 2 at 2.0 V/cell, with about 1,600 turnovers/s. Both systems are stable for a thousand hours or more, i.e., millions of turnovers. We also demonstrate simultaneous CO and H 2 production in a single electrolyzer. These results demonstrate that syngas can be produced at industrially important rates via electrolysis.

Our longitudinal study demonstrated that high serum uric acid levels increase the risk of obesity.

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Secreted frizzled-related proteins (SFRPs) are antagonists of the Wnt signaling pathway whose epigenetic downregulation have been shown to be involved in hepatocarcinogenesis. However, dysregulation of SFRPs induced by hepatitis B virus (HBV) X protein (HBx) has never been studied in HBV-related hepatocellular carcinoma (HBV-HCC). In this study, we sought to determine the clinical significance and underlying mechanism of HBx-induced SFRPs dysregulation in hepatoma cells and HBV-HCC patients. Our results showed that SFRP1 and SFRP5 expression were dramatically decreased by HBx in hepatoma cells. The repressed expression in hepatoma cells was partially rescued by a DNA methylation inhibitor and synergistically increased by a combination treatment with a histone deacetyltransferases inhibitor. In addition, we identified that SFRP1 and SFRP5 promoters were hypermethylated in both HBx-expressing hepatoma cells and HBV-HCC tissues. Downregulation of SFRP1 and SFRP5 in HBV-HCC tissues was significantly correlated with overexpression of DNA methyltransferase 1 (DNMT1) and poor tumor differentiation. HBx facilitated the binding of DNMT1 and DNMT3A to SFRP1 and SFRP5 promoters, and resulted in epigenetic silencing of SFRP1 and SFRP5. Moreover, overexpression of SFRP1, SFRP5 or RNA interference mediated silencing of DNMT1 inactivated the Wnt signaling pathway and decreased the expression levels of Wnt target genes c-Myc and CyclinD1, thus impeding HCC growth in vitro and in vivo, and regressing HBx-induced epithelial-mesenchymal transition (EMT). Our findings strongly suggest that epigenetic silencing of SFRP1 and SFRP5 by HBx allows constitutive activation of Wnt signaling pathway and hence contributes to hepatocarcinogenesis.Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide. One of the high risk factors associated with HCC is chronic hepatitis B virus (HBV) infection.1 HBV X protein (HBx), a pleiotropic protein encoded by HBV, plays a vital role in hepatocellular carcinogenesis.2 As a multifunctional regulator, HBx is capable of trans-regulation of many cellular genes by interacting with nuclear transcription factors, such as CREB, AP-1 and NF- jB.3 Further, HBx is involved in the activation of several oncogenic signal transduction pathways, including the Wnt/ b-catenin, SAPK/JNK, NF-jB, Ras/MAPK and FAK pathways.3-5 Recent studies indicated that HBx is also involved in epigenetic regulation of several tumor suppressor genes in hepatocarcinogenesis. 6,7 The Wnt/b-catenin signaling pathway has been implicated in a wide range of biological processes, including cell