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The key to breaking through the capacity limitation imposed by intercalation chemistry lies in the ability to harness more active sites that can reversibly accommodate more ions (e.g., Li

A method of ultrasound-assisted reduction of a nickel-ammonia complex with borohydride in aqueous solution was used to prepare NiMoB/MCM-41 and NiMoB/SBA-15 supported amorphous alloy catalysts. These catalysts were used to upgrade bio-oil at mild temperatures ranging from 100 to 160 °C and recycling of these two supported catalysts and of unsupported NiMoB was carried out. Then, fresh and third time used catalysts were characterized by X-ray diffraction, X-ray photoelectron spectra, and transmission electron microscopy. Quantitative results were obtained from the analysis of gas chromatography/mass spectrometry. Through mild upgrading, 1-hydroxy-2-propanone, furfural, and 2-methoxy-4-vinylphenol in the bio-oil were converted to relevant alcohols and saturated phenols. The conversion rates were 45.7, 71.5, and 57.1 %, respectively, when crude bio-oil was upgraded using NiMoB/MCM-41 at 160 °C. The two supported catalysts, especially NiMoB/MCM-41, had smaller amorphous NiMoB particles and exhibited more uniform dispersion on mesoporous silica, leading to higher reaction activity and stability than unsupported NiMoB. Deactivation of these catalysts resulted from the reduction of Ni0, B0, and Mo4+ species on the surface, the transition from the amorphous to the crystalline state, particle agglomeration, and coke deposition on the surface.

Dendritic cells (DCs) are the most powerful of all antigen-presenting cells and play a critical role in the induction of primary immune responses. DC-based vaccination represents a potentially powerful strategy for cancer immunotherapy. In this study, a new approach for a DC-based melanoma vaccine was described. Splenic DCs from C57BL/6 mice were fused with B16 melanoma cells, and the resultant B16/DC hybrid cells expressed major histocompatibility complex (MHC) molecules – B7 as well as the B16 tumour marker M562 – which were enriched by Ia-mediated positive selection with a MiniMACS column. The fusion rates were 12·7–26·8%. To generate hybrid tumour vaccines with potentially greater potent therapeutic efficacy, we genetically engineered DCs with granulocyte–macrophage colony-stimulating factor (GM-CSF) prior to cell fusion. Recombinant adenovirus vector was used to mediate gene transfer into DCs with high efficiency and DCs expressed GM-CSF at 96–138 ng/105 cells/ml 24 hr after GM-CSF gene transfer. GM-CSF gene-modified DCs (DC.GM) exhibited higher expression of B7 and co-stimulatory capacity in mixed lymphocyte reaction (MLR). Fusion of DC.GM with B16 cells generated B16/DC.GM hybrid cells secreting GM-CSF at 59–63 ng/105 cells/ml. Immunization of C57BL/6 mice with the B16/DC hybrid vaccine elicited a specific cytotoxic T-lymphocyte (CTL) response and protected the immunized mice from B16 tumour challenge, reduced pulmonary metastases and extended the survival of B16 tumour-bearing mice. The B16/DC.GM hybrid vaccine was able to induce a CTL response and protective immunity more potently and tended to be therapeutically more efficacious than the B16/DC vaccine. In vivo depletion of T-cell subsets demonstrated that both CD8+ and CD4+ T cells were essential for the therapeutic effects of B16/DC and B16/DC.GM hybrid vaccines. Additionally, other non-specific effector cells may also contribute to tumour rejection induced by the B16/DC.GM hybrid vaccine. These data indicate that a DC-based hybrid tumour vaccine may be an attractive strategy for cancer immunotherapy, and that GM-CSF gene-modified DCs may lead to the generation of hybrid vaccines with potentially increased therapeutic efficacy.

Dendritic cells (DC) are professional antigen-presenting cells (APC) within the immune system and antigen-pulsed DC can be used as an effective vaccine for active immunotherapy of cancer. Granulocyte-macrophage colony-stimulating factor (GM-CSF) plays an important role in the generation of DC. We previously showed that GM-CSF can induce murine erythroleukaemia cells (FBL-3) to differentiate into monocyte-like cells. To develop a new vaccinating method to stimulate the host immune response to leukaemia, we further investigate whether FBL-3 cells induced by GM-CSF can differentiate into DC in the present study. After being treated with GM-CSF, FBL-3 cells expressed high levels of 33D1 and NLDC-145, which are the specific markers of DC. The expression of MHC-II, B7-1, B7-2 and vascular cell adhesion molecule-1 (VCAM-1) was up-regulated markedly; the typical morphology of DC were also observed by electron microscopy. Functionally, the GM-CSF-induced FBL-3 cells could apparently stimulate the proliferation of naive allogeneic and autologous T lymphocytes and induce the generation of specific CTL more efficiently than the wild-type FBL-3 cells. Mice immunized with GM-CSF-induced FBL-3 cells could resist the subsequent challenge with the wild-type FBL-3 cells. Collectively, these data indicate that GM-CSF differentiates murine erythroleukaemia cells into DC phenotypically, morphologically and functionally. FBL-3-derived DC can be used as a new type of vaccine. Our results may have important implications for the immunotherapy of leukaemia.