A scalable, reproducible method of synthesizing UiO-66- and UiO-67-type MOFs, entailing the addition of HCl to the reaction mixture, has been investigated. The new protocol requires a fraction of the time of previously reported procedures, yields exceptional porosities, and works with a range of linkers.

The present work is a critical review of metal exchange (transmetalation) involving metal nodes and metalated struts in metal-organic frameworks. Particular emphasis is given to drawing parallels between different examples of transmetalation in order to understand the influence of coordination environment, solvents, nature of the metals and other variables on the process. We hope that the present review will be of use to those involved in the incorporation of various metal centers to create isostructural MOFs and study their properties.

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Gold recovery using environmentally benign chemistry is imperative from an environmental perspective. Here we report the spontaneous assembly of a one-dimensional supramolecular complex with an extended {[K(OH2)6][AuBr4](α-cyclodextrin)2}n chain superstructure formed during the rapid co-precipitation of α-cyclodextrin and KAuBr4 in water. This phase change is selective for this gold salt, even in the presence of other square-planar palladium and platinum complexes. From single-crystal X-ray analyses of six inclusion complexes between α-, β- and γ-cyclodextrins with KAuBr4 and KAuCl4, we hypothesize that a perfect match in molecular recognition between α-cyclodextrin and [AuBr4]− leads to a near-axial orientation of the ion with respect to the α-cyclodextrin channel, which facilitates a highly specific second-sphere coordination involving [AuBr4]− and [K(OH2)6]+ and drives the co-precipitation of the 1:2 adduct. This discovery heralds a green host–guest procedure for gold recovery from gold-bearing raw materials making use of α-cyclodextrin—an inexpensive and environmentally benign carbohydrate.

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ARTICLE This journal isA comparative study of the support effect in three different UiO-66-based MOFs with Ti IV supported as part of the node (UiO-66-Tiex), attached to the node (Ti-UiO-66), and on a catecholate organic linker (UiO-66-Cat-Ti) is reported. The three MOFs were evaluated for their catalytic activity and selectivity for cyclohexene oxidation. Ti-UiO-66 exhibited greater catalytic turnover numbers than UiO-66-Cat-Ti and UiO-66-Tiex.

Gut dysbiosis is commonly observed in patients with cirrhosis and chronic gastrointestinal disorders, however, its effect on anti-tumor immunity in the liver is largely unknown. Here we studied how the gut microbiome affects anti-tumor immunity in cholangiocarcinoma. Primary sclerosing cholangitis (PSC) or colitis, two known risk factors for cholangiocarcinoma, which promote tumor development in mice caused an accumulation of CXCR2 + polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC). A decrease in gut barrier function observed in mice with PSC and colitis allowed gut derived bacteria and lipopolysaccharide (LPS) to appear in the liver and induced CXCL1 expression in hepatocytes through a TLR4-dependent mechanism and an accumulation of CXCR2 + PMN-MDSC. On the contrary, neomycin treatment blocked CXCL1 expression, PMN-MDSC accumulation and inhibited tumor growth even in the absence of liver disease or colitis. Our study demonstrates that the gut microbiome controls hepatocytes to form an immunosuppressive environment by increasing PMN-MDSC to promote liver cancer.

Background: Cytokine-induced killer (CIK) cell-based immunotherapy is effective as adjuvant therapy in early stage hepatocellular carcinoma (HCC) but lacks efficacy in advanced HCC. We investigated immune suppressor mechanisms focuing on CIKs and myeloid-derived suppressor cells (MDSCs).Methods: MDSCs were quantified by flow cytometry and quantitative real-time PCR. Cytokines were detected by cytokine array. An LDH cytotoxicity assay was performed in the presence or absence of MDSCs to study CIK function against HCC cells in vitro. An FDA approved PDE5 inhibitor, tadalafil, was used to target MDSCs in vitro and in vivo. Two different murine HCC cell lines were tested in subcutaneous and orthotopic tumor models in C57BL/6 and BALB/c mice. The anti-tumor effects of human CIKs and MDSCs were also tested in vitro.Results: Adoptive cell transfer of CIKs into tumor bearing mice induced inflammatory mediators (e.g., CX3CL1, IL-13) in the tumor microenvironment and an increase of tumor infiltrating MDSCs leading to impaired anti-tumor activity in two different HCC tumor models. MDSCs efficiently suppressed the cytotoxic activity of CIKs in vitro. In contrast, treatment with a PDE5 inhibitor reversed the MDSC suppressor function via ARG1 and iNOS blockade and systemic treatment with a PDE5 inhibitor prevented MDSC accumulation in the tumor microenvironment