Effect of Copper-Modification of g-C3N4 on the Visible-Light-Driven Photocatalytic Oxidation of Nitrophenols.

Graphitic carbon nitride (g-C3N4) has proved to be a promising heterogeneous photocatalyst in the visible range. It can be used, among others, for the oxidative conversion of environmentally harmful nitrophenols occurring in wastewater. However, its photocatalytic activity needs to be enhanced, which can be achieved by modification with various dopants. In our work, copper-modified g-C3N4 was prepared by ultrasonic impregnation of the pristine g-C3N4 synthesized from thiourea. The morphology, microstructure, and optical properties of the photocatalysts were characterized by XRD, FT-IR, DRS, SEM, XPS, and TEM. DRS analysis indicated a slight change in both the CB and the VB energies of Cu/g-C3N4 compared to those of g-C3N4. The efficiency of the photocatalysts prepared was tested by the degradation of nitrophenols. Copper modification caused a sevenfold increase in the rate of 4-nitrophenol degradation in the presence of H2O2 at pH = 3. This dramatic enhancement can be attributed to the synergistic effect of copper and H2O2 in this photocatalytic system. A minor Fenton reaction role was also detected. The reusability of the Cu/g-C3N4 catalyst was demonstrated through five cycles. Copper-modified g-C3N4 with H2O2 proved to be applicable for efficient visible-light-driven photocatalytic oxidative degradation of nitrophenols.

Pyridinedicarboxylate-Tb(III) Complex-Based Luminescent Probes for ATP Monitoring.

The pyridinedicarboxylate-Tb(III) complexes, TbPDC and Tb(PDC)3, as luminescent probes for ATP monitoring have been conveniently prepared and characterized by FT-IR, 1H-NMR, ESI-MS, UV-Vis, excitation, and emission spectroscopy. Interestingly, these two Tb(III) complexes were quenched by ATP by a similar mechanism via π-π stacking interaction between the chelating ligand and adenine moiety. The ability of luminescent probes applied for the determination of ATP in aqueous solution has been investigated. The dynamic ranges for the quantification of ATP are within 10-90 µM and 10-100 µM with detection limits of 7.62 and 11.20 µM for TbPDC and Tb(PDC)3, respectively. The results demonstrated that these luminescent probes would be a potential candidate assay for ATP monitoring in hygiene assessment.

Interface Engineering of Graphene-Supported Cu Nanoparticles Encapsulated by Mesoporous Silica for Size-Dependent Catalytic Oxidative Coupling of Aromatic Amines.

In this study, graphene nanosheet-supported ultrafine Cu nanoparticles (NPs) encapsulated with thin mesoporous silica (Cu-GO@m-SiO2) materials are fabricated with particle sizes ranging from 60 to 7.8 nm and are systematically investigated for the oxidative coupling of amines to produce biologically and pharmaceutically important imine derivatives. Catalytic activity remarkably increased from 76.5% conversion of benzyl amine for 60 nm NPs to 99.3% conversion and exclusive selectivity of N-benzylidene-1-phenylmethanamine for 7.8 nm NPs. The superior catalytic performance along with the outstanding catalyst stability of newly designed catalysts are attributed to the easy diffusion of organic molecules through the porous channel of mesoporous SiO2 layers, which not only restricts the restacking of the graphene nanosheets but also prevents the sintering and leaching of metal NPs to an extreme extent through the nanoconfinement effect. Density functional theory calculations were performed to shed light on the reaction mechanism and to give insight into the trend of catalytic activity observed. The computed activation barriers of all elementary steps are very high on terrace Cu(111) sites, which dominate the large-sized Cu NPs, but are significantly lower on step sites, which are presented in higher density on smaller-sized Cu NPs and could explain the higher activity of smaller Cu-GO@m-SiO2 samples. In particular, the activation barrier for the elementary coupling reaction is reduced from 139 kJ/mol on flat terrace Cu(111) sites to the feasible value of 94 kJ/mol at step sites, demonstrating the crucial role of the step site in facilitating the formation of secondary imine products.

CD34(+) Liver Cancer Stem Cells Were Formed by Fusion of Hepatobiliary Stem/Progenitor Cells with Hematopoietic Precursor-Derived Myeloid Intermediates.

A large number of cancer stem cells (CSCs) were identified and characterized; however, the origins and formation of CSCs remain elusive. In this study, we examined the origination of the newly identified CD34(+) liver CSC (LCSC). We found that CD34(+) LCSC coexpressed liver stem cell and myelomonocytic cell markers, showing a mixed phenotype, a combination of hepatobiliary stem/progenitor cells (HSPCs) and myelomonocytic cells. Moreover, human xenografts produced by CD34(+) LCSCs and the parental cells, which CD34(+) LCSC was isolated from, coexpressed liver cancer and myelomonocytic markers, also demonstrating mixed phenotypes. The xenografts and the parental cells secreted albumin demonstrating their hepatocyte origin and also expressed cytokines [interleukin (IL)-1b, IL-6, IL-12A, IL-18, tumor necrosis factor-alpha (TNF-α), and CSF1] and chemokines (IL-8, CCL2, and CCL5). Expression of these cytokines and chemokines responded to the stimuli [interferon-γ (INF-γ), IL-4, and lipopolysaccharide (LPS)]. Furthermore, human xenografts and the parental cells phagocytized Escherichia coli. CD34(+) LCSC coexpressed CD45, demonstrating that its origin appears to be from a hematopoietic precursor. The percentage of cells positive for OV6, CD34, and CD31, presenting the markers of HSPC, hematopoietic, and myelomonocytic cells, increased under treatment of CD34(+) LCSC with a drug. Cytogenetic analysis showed that CD34(+) LCSC contained a greater number of chromosomes. HBV DNA integrations and mutations in CD34(+) LCSC and the parental cells were identical to those in the literature or the database. Thus, these results demonstrated that CD34(+) LCSCs were formed by fusion of HSPC with CD34(+) hematopoietic precursor-derived myeloid intermediates; it appears that this is the first report that human CSCs have been formed by the fusion. Therefore, it represents a significant step toward better understanding of the formation of human CSC and the diverse origins of liver cancers.

Clonogenically Culturing and Expanding CD34+ Liver Cancer Stem Cells in Vitro.

A large number of cancer stem cells (CSCs) have been isolated and identified; however, none has been cultured in an unlimited manner in vitro without losing tumorigenicity and multipotency. In this study, we successfully clonogenically cultured a newly identified CD34+ liver CSC (LCSC) on feeder cells up to 22 passages (to date) without losing CSC property. Cloned CD34+ LCSC formed a round packed morphology and it could also be cryopreserved and recultured. Stem cell markers, CD34, CD117, and SOX2; normal liver stem cell markers, alpha fetoprotein, CK19, CK18, and OV6; putative CSC markers, CD44, CD133, EpCAM, and CD90; as well as CD31 were expressed in cloned CD34+ LCSC. SOX2 was the major factor in maintaining this LCSC before colonization, and interestingly, OCT4, SOX2, NAONG, Klf4, c-Myc, and Lin28 were upregulated in association with symmetric self-renewal for colony growth of CD34+ LCSC on feeder cells. Gene expression patterns of in vitro differentiation were consistent with our in vivo finding; furthermore, the tumorigenicity of cloned CD34+ LCSC was not different from uncloned CD34+ LCSC sorted from parental PLC. These results show that our cloned CD34+ LCSC maintained CSC property, including self-renewal, bipotency, and tumorigenicity after long-term culture, demonstrating that this LCSC can be cultured in an unlimited manner in vitro. Thus, establishing pure population of CSCs isolated from the patients will provide an opportunity to explore the mechanisms of tumorigenesis and cancer development, and to identify unique biomarkers presenting potential indicators of drug efficacy against CSCs for establishment of a novel strategy for cancer therapy.

Identification of cancer stem cell subpopulations of CD34(+) PLC/PRF/5 that result in three types of human liver carcinomas.

CD34(+) stem cells play an important role during liver development and regeneration. Thus, we hypothesized that some human liver carcinomas (HLCs) might be derived from transformed CD34(+) stem cells. Here, we determined that a population of CD34(+) cells isolated from PLC/PRF/5 hepatoma cells (PLC) appears to function as liver cancer stem cells (LCSCs) by forming HLCs in immunodeficient mice with as few as 100 cells. Moreover, the CD34(+) PLC subpopulation cells had an advantage over CD34(-) PLCs at initiating tumors. Three types of HLCs were generated from CD34(+) PLC: hepatocellular carcinomas (HCCs); cholangiocarcinomas (CC); and combined hepatocellular cholangiocarcinomas (CHCs). Tumors formed in mice transplanted with 12 subpopulations and 6 progeny subpopulations of CD34(+) PLC cells. Interestingly, progenies with certain surface antigens (CD133, CD44, CD90, or EPCAM) predominantly yielded HCCs. CD34(+) PLCs that also expressed OV6 and their progeny OV6(+) cells primarily produced CHC and CC. This represents the first experiment to demonstrate that the OV6(+) antigen is associated with human CHC and CC. CD34(+) PLCs that also expressed CD31 and their progeny CD31(+) cells formed CHCs. Gene expression patterns and tumor cell populations from all xenografts exhibited diverse patterns, indicating that tumor-initiating cells (TICs) with distinct antigenic profiles contribute to cancer cell heterogeneity. Therefore, we identified CD34(+) PLC cells functioning as LCSCs generating three types of HLCs. Eighteen subpopulations from one origin had the capacity independently to initiate tumors, thus functioning as TICs. This finding has broad implications for better understanding of the multistep model of tumor initiation and progression. Our finding also indicates that CD34(+) PLCs that also express OV6 or CD31 result in types of HLCs. This is the first report that PLC/PRF/5 subpopulations expressing CD34 in combination with particular antigens defines categories of HLCs, implicating a diversity of origins for HLC.