Preparation of Ni-Doped CeFeO3 by Microwave Process and Its Visible-Light Photocatalytic Activity.

Using Ce(NO3)3· 6H2O, Fe(NO3)3· 9H2O and Ni(NO3)3· 6H2O as the main raw materials, nano Ni-doped CeFeO3 was prepared by the microwave method for the first time. The Ni-doped CeFeO3samples were characterized by XRD, SEM, DRS and EDS. The results show that Ni-doped CeFeO3exhibits a perovskite structure (ABO3), and contains nanosheets less than 10 nm thick. The prepared nanosheets have an optical band gap of 1.93 eV. The effect of different doping amounts on the photocatalytic properties of Ni-doped CeFeO3 was studied under visible light, using methyl-orange. When the concentration of the methyl-orange solution was 10 mg/L, and the illumination time allowed for photocatalysis was 90 min, the degradation rate rose to nearly 98%. Moreover, Ni-doped CeFeO3 has a higher photocatalytic activity than pure CeFeO3 powder, making it suitable for a broad range of applications.

Microwave Synthesis of Nanoparticulate SmFeO3 and Its Characterization.

Single phase perovskite SmFeO3 nanoparticles were synthesized using a simple microwave method using Fe(NO3)3· 9H2O and Sm(NO³)³ · 6H2O. The resulting samples were characterized by powder X-ray diffraction (XRD), scanning electron microscopy (SEM), Brunauer-Emmett-Teller (BET) surface area measurement, UV-visible diffuse reflectance spectroscopy (DRS) and Fourier transform infrared spectroscopy (FTIR). XRD and SEM results demonstrate the successful synthesis of nanocrystalline SmFeO3 and show an average grain size of 50-60 nm. The single phase structure and optical properties of SmFeO3 were maintained after calcination at 1000 °C. The prepared nanocrystalline SmFeO3 displays excellent thermal stability and strong visible-light absorption, with an absorption onset of 540 nm or so. The photocatalytic experiment involving the decomposition of methyl orange under visible-light irradiation shows the high photocatalytic activity of the nanoparticles.

Self-floating graphitic carbon nitride/zinc phthalocyanine nanofibers for photocatalytic degradation of contaminants.

The effective elimination of micropollutants by an environmentally friendly method has received extensive attention recently. In this study, a photocatalyst based on polyacrylonitrile (PAN)-supported graphitic carbon nitride coupled with zinc phthalocyanine nanofibers (g-C3N4/ZnTcPc/PAN nanofibers) was successfully prepared, where g-C3N4/ZnTcPc was introduced as the catalytic entity and the PAN nanofibers were employed as support to overcome the defects of easy aggregation and difficult recycling. Herein, rhodamine B (RhB), 4-chlorophenol and carbamazepine (CBZ) were selected as the model pollutants. Compared with the typical hydroxyl radical-dominated catalytic system, g-C3N4/ZnTcPc/PAN nanofibers displayed the targeted adsorption and degradation of contaminants under visible light or solar irradiation in the presence of high additive concentrations. According to the results of the radical scavenging techniques and the electron paramagnetic resonance technology, the degradation of target substrates was achieved by the attack of active species, including photogenerated hole, singlet oxygen, superoxide radicals and hydroxyl radicals. Based on the results of ultra-performance liquid chromatography and mass spectrometry, the role of free radicals on the photocatalytic degradation intermediates was identified and the final photocatalytic degradation products of both RhB and CBZ were some biodegradable small molecules.

Aberrant ADAM10 expression correlates with osteosarcoma progression.

BACKGROUND: Osteosarcoma is the most common type of bone cancer and is notorious for its rapid progression. The Notch signaling pathway has recently been shown to be involved in osteosarcoma. As a major sheddase of Notch receptors, ADAM10 has been implicated in many types of cancers, but its role in osteosarcoma has not been investigated. Previous studies have shown that the expression of CD31 was significantly elevated in metastatic osteosarcoma; however, its expression in nonmetastatic groups is not known. In addition, the mysterious multinucleated giant cell in giant cell-rich osteosarcoma was previously regarded as an osteoclast-like cell, but its exact identity is unclear. METHOD: Tissue chip samples from 40 cases of nonmetastatic osteosarcoma were stained for cytoplasmic ADAM10, activated Notch1 and CD31. Osteoclasts in tumor sections were also stained for tartrate-resistant acid phosphatase (TRAP). RESULTS: Immunofluorescence staining revealed that ADAM10 expression significantly increased with the progression of osteosarcoma as well as in osteoblastic osteosarcoma, whereas the expression of the Notch intracellular domain (NICD) and CD31 was not significantly altered between different pathological stages. In addition, multinucleated giant cells in giant cell-rich osteosarcoma were also found to coexpress CD31, ADAM10 and NICD, but were negative for TRAP staining. CONCLUSIONS: Our results highlight the importance of ADAM10 in the progression of osteosarcoma and suggest that the protein might be a potential therapeutic target in osteosarcoma treatment. This study also demonstrates that the multinucleated giant cell is an angiogenic tumor cell, rather than an osteoclast, and involves ADAM10/Notch1 signaling activation.

Telbivudine treatment corrects HBV-induced epigenetic alterations in liver cells of patients with chronic hepatitis B.

UNLABELLED: Hepatitis B virus (HBV) alters the expression of host cellular genes to support its replication and survival and to promote the liver cell injury. However, the underlying mechanism remained incompletely understood. In this study, we investigated HBV-induced epigenetic changes in HepG2 cells by profiling the landscapes of the active histone modification mark H3K4me3 and repressive mark H3K27me3 using chromatin immunoprecipitation-sequencing. HBV caused the altered histone modifications at thousands of genomic loci, which are critically involved in HBV entry, inflammation, fibrosis and carcinogenesis of host cells. Interestingly, treatment of the HBV-transformed HepG2 cells with the anti-HBV drug Telbivudine substantially restored the H3K4me3 level to that of untransformed HepG2 cells. More importantly, our analysis of liver samples from control and chronic hepatitis B patients revealed that treatment of the patients with Telbivudine not only corrected the target gene expression but also the epigenetic modification of critical genes. In addition, the expression of the histone methyltransferases SMYD3 and EZH2 that regulate histone H3-specific methylation showed no difference in HepG2 cell with or without HBV existence. Thus, our data suggest that abnormal histone modifications might critically involved in HBV-mediated liver pathogenesis and Telbivudine therapy might benefit patients with HBV-related chronic infection, liver cirrhosis and even hepatic carcinoma. SUMMARY: Telbivudine substantially restores in vitro and in vivo HBV-caused abnormal expressions and histone H3K4me3 and H3K27me3 modifications at thousands of genomic loci that are involved in the pathogenesis of liver cells, revealing a novel mechanism for HBV-mediated liver damage.

Cross-immunizing potential of tumor MAGE-A epitopes recognized by HLA-A*02:01-restricted cytotoxic T lymphocytes.

Almost all melanoma cells express at least one member of the MAGE-A antigen family, making the cytotoxic T cells (CTLs) epitopes with cross-immunizing potential in this family attractive candidates for the broad spectrum of anti-melanoma immunotherapy. In this study, four highly homologous peptides (P264: FLWGPRALA, P264I9: FLWGPRALI, P264V9: FLWGPRALV, and P264H8: FLWGPRAHA) from the MAGE-A antigens were selected by homologous alignment. All four peptides showed high binding affinity and stability to HLA-A*02:01 molecules, and could prime CTL immune responses in human PBMCs and in HLA-A*02:01/K(b) transgenic mice. CTLs elicited by the four epitope peptides could cross-lyse tumor cells expressing the mutual target antigens, except MAGE-A11 which was not tested. However, CTLs induced by P264V9 and P264I9 showed the strongest target cell lysis capabilities, suggesting both peptides may represent the common CTL epitopes shared by the eight MAGE-A antigens, which could induce more potent and broad-spectrum antitumor responses in immunotherapy.