4 research outputs found

    Dye Degrading and Fouling-Resistant Membranes Formed by Deposition with Ternary Nanocomposites of N-Doped Graphene/TiO2/Activated Carbon

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    A ternary nanocomposite consisting of N-doped graphene (NGR)/TiO2/activated carbon (NGRT@AC) was prepared, and the components’ synergetic effect on dye degradation was investigated after deposition on the surface of a polysulfone membrane (PSF). As far as we know, this ternary composite catalyst has never previously been used to degrade dyes nor been used as a functional layer for separation membranes. The surface morphology and structure of the as-prepared membranes were analyzed by scanning electron microscopy (SEM) and energy-dispersive X-ray spectroscopy (EDS). The NGRT@AC-modified PSF membrane (NGRT@AC-PSF) presents excellent photodegradation efficiency to methyl orange (MO) under both UV (95.2%) and sunlight (78.1%) irradiation, much higher than those values of PSF, TiO2- modified PSF (TiO2-PSF), and N-doped graphene/TiO2 (NGRT)-modified PSF membranes (NGRT-PSF) under the same conditions. The high flux recovery ratio (95.5%) demonstrates that the NGRT@AC-PSF membrane shows improved antifouling performance. The photocatalytic results prove that surface deposition method (95.2%) was better than the blending method (31.1%) for forming high-performance membranes. Therefore, the NGRT@AC-PSF membrane has the potential for broad applications in dye degradation to treat waste water from textile industries

    Downregulation of Roundabout guidance receptor 2 suppresses hepatocellular carcinoma progression by interacting with Y-box binding protein 1

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    Abstract Roundabout guidance receptor 2 (Robo2) is closely related to malignant tumors such as pancreatic cancer and liver fibrosis, but there is no relevant research on the role of Robo2 in HCC. The study will further explore the function and mechanism of Robo2 and its downstream target genes in HCC. Firstly, Robo2 protein levels in human HCC tissues and paired adjacent normal liver tissues were detected. Then we established HepG2 and Huh7 hepatoma cell lines with knock-down Robo2 by transfection with lentiviral vectors, and examined the occurrence of EMT, proliferation and apoptosis abilities in HCC cells by western blot, flow cytometry, wound healing assay and TUNEL staining. Then we verified the interaction between Robo2 and its target gene by Co-IP and immunofluorescence co-staining, and further explored the mechanism of Robo2 and YB-1 by rescue study. The protein expression level of Robo2 in HCC was considerably higher than that in the normal liver tissues. After successfully constructing hepatoma cells with knock-down Robo2, it was confirmed that down-regulated Robo2 suppressed EMT and proliferation of hepatoma cells, and accelerated the cell apoptosis. High-throughput sequencing and validation experiments verified that YB-1 was the downstream target gene of Robo2, and over-expression of YB-1 could reverse the apoptosis induced by Robo2 down-regulation and its inhibitory effect on EMT and proliferation. Robo2 deficiency inhibits EMT and proliferation of hepatoma cells and augments the cell apoptosis by regulating YB-1, thus inhibits the occurrence of HCC and provides a new strategy for the treatment of HCC

    Molecular modeling of human APOBEC3G to predict the binding modes of the inhibitor compounds IMB26 and IMB35

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    APOBEC3G(A3G) is a host cytidine deaminase that incorporates into HIV-1 virions and efficiently inhibits viral replication. The virally encoded protein Vif binds to A3G and induces its degradation, thereby counteracting the antiviral activity of A3G. Vif-mediated A3G degradation clearly represents a potential target for anti-HIV drug development. Currently, there is an urgent need for understanding the three dimensional structure of full-length A3G. In this work, we use a homology modeling approach to propose a structure for A3G based on the crystal structure of APOBEC2 (APO2) and the catalytic domain structure of A3G. Two compounds, IMB26 and IMB35, which have been shown to bind to A3G and block degradation by Vif, were docked into the A3G model and the binding modes were generated for further analysis. The results may be used to design or optimize molecules targeting Vif–A3G interaction, and lead to the development of novel anti-HIV drugs
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