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The electronic structure and optical properties of biaxial ZnO–ZnS heterostructure nanoribbons (NRs) have been investigated using x-ray absorption near-edge structures (XANES) and x-ray excited optical luminescence (XEOL). The XANES were recorded in total electron yield and wavelength-selected photoluminescence yield across the K- and L3,2-edges of zinc and sulfur and the K-edge of oxygen. The XEOL from the NRs exhibit a very weak band-gap emission at 392 nm and two intense defect emissions at 491 and 531 nm. The synchrotron x-ray pulse (∼100 ps, 153 ns repetition rate) was used to track the optical decay dynamics from ZnO–ZnS NR, which can be described by two lifetimes (7.6 and 55 ns). Comparison with similar measurements for ZnO and ZnS nanowires reveals that the luminescence from ZnO–ZnS NRs was dominated by the ZnO component of the NR as the ZnS component contributes little. The implication of this observation is discussed. [ABSTRACT FROM AUTHOR]

X-ray excited optical luminescence (XEOL) and x-ray absorption near-edge structure in total electron, x-ray fluorescence, and photoluminescence yields at Sn M5,4-, O K-, and Sn K-edges have been used to study the luminescence from SnO2 nanoribbons. The effect of the surface on the luminescence from SnO2 nanoribbons was studied by preferential excitation of the ions in the near-surface region and at the normal lattice positions, respectively. No noticeable change of luminescence from SnO2 nanoribbons was observed if the Sn ions in the near-surface region were excited selectively, while the luminescence intensity changes markedly when Sn or O ions at the normal lattice positions were excited across the corresponding edges. Based on the experimental results, we show that the luminescence from SnO2 nanoribbons is dominated by energy transfer from the excitation of the whole SnO2 lattice to the surface states. Surface site specificity is not observable due to its low concentration and weak absorption coefficient although the surface plays an important role in the emission as a luminescence center. The energy transfer and site specificity of the XEOL or the lack of the site specificity from a single-phase sample is discussed. [ABSTRACT FROM AUTHOR]

Summary: Objective: Dysregulated Wnt signaling appears to modulate chondrocyte fate and joint disorders. Dickkopf-1 (DKK1) regulates the pathogenesis of skeletal tissue by inhibiting Wnt actions. This study examined whether DKK1 expression is linked to chondrocyte fate in osteoarthritis (OA). Method: Articular cartilage specimens harvested from nine patients with knee OA and from six controls with femoral neck fracture were assessed for DKK1, interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), Bad, Bax, Bcl2 and caspase-3 expression by real time-polymerase chain reaction (RT-PCR) and immunohistochemistry. Apoptotic chondrocytes were detected by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labelling (TUNEL) and 4′, 6-dianidino-2-phenylindole dihydrochloride (DAPI) staining. Human chondrocyte cultures were treated with recombinant IL-1β and monoclonal DKK1 antibody to determine whether DKK1 impairs chondrocyte survival. Results: Expression of DKK1 correlated with inflammatory cytokine levels (IL-1β and TNF-α expressions), proapoptosis regulators (Bad and caspase-3 expressions) and TUNEL staining in OA cartilage tissues. The IL-1β induced expressions of DKK1, Bax, Bad and caspase-3-dependent apoptosis of chondrocyte cultures. Neutralization of DKK1 by monoclonal DKK1 antibody significantly abrogated IL-1β-mediated caspase-3 cleavage and apoptosis and reversed chondrocyte proliferation. Recombinant DKK1 treatment impaired chondrocyte growth and promoted apoptosis. By suppressing nuclear β-catenin accumulation and Akt phosphorylation, DKK1 mediated IL-1β promotion of chondrocyte apoptosis. Conclusion: Chondrocyte apoptosis correlates with joint OA. Expression of DKK1 contributes to cartilage deterioration and is a potent factor in OA pathogenesis. Attenuating DKK1 may reduce cartilage deterioration in OA. [Copyright &y& Elsevier]