We analyze the moduli space of the low-energy limit of 3-dimensional N = 3 Maxwell-Chern-Simons theories described by circular quiver diagrams, as for 4-dimensional elliptic models. We define the theories by using D3-NS5-(k,1)5-brane systems with an arbitrary number of fivebranes. The supersymmetry is expected to be enhanced to N = 4 in the low-energy limit. We show that the Higgs branch, in which all bifundamental scalar fields develop vacuum expectation values, is an abelian orbifold of C 4 . We confirm that the same geometry is obtained as an M-theory dual of the brane system. We also consider theories realized by introducing more than two kinds of fivebranes, and obtain nontoric fourfolds as moduli spaces. * ) typeset using PTPT E X.cls Ver.0.9 * ) The possibility that the existence of magnetic monopoles causes a discrete indentification in the orbifold is also mentioned.

Among various metal oxide-supported Au nanoparticles, Au/rutile TiO2 exhibits a particularly high level of visible-light activity for aerobic oxidation of amines to yield the corresponding imines on a synthetic scale with high selectivity (>99%) at 298 K. Experimental results have suggested that the reaction proceeds via the localized surface plasmon resonance-excited electron transfer from the Au nanoparticle to the TiO2.

The photocatalytic activities of Au nanoparticle-loaded anatase (Au/anatase) and rutile (Au/rutile) for green organic synthesis are compared under illumination of UV and visible light. Whereas Au/anatase shows a higher UV-light activity for the reduction of nitrobenzene than Au/rutile, the replacement of anatase by rutile greatly increases the visible-light activity of Au/TiO2 for the oxidation of alcohols to carbonyl compounds. The quantum efficiencies (molecules produced/incident photons) for the Au/rutile and Au/anatase systems for the selective oxidation of cinnamyl alcohol to cinnamaldehyde were calculated to be 1.4 × 10–3 at λ = 585 ± 15 nm and 0.33 × 10–3 at λ = 555 ± 15 nm, respectively. This superiority of rutile over anatase as the support of Au nanoparticle (NP) plasmon photocatalyst is also confirmed in the heterosupramolecular system consisting of Au/TiO2 and a cationic surfactant. In the system using Au/rutile, a quantum efficiency of 6.8 × 10–3 at λ = 585 ± 15 nm has been achieved for the cinnamyl alcohol oxidation. Also, the plot of the visible-light activity versus Au particle size (d) for the Au/rutile system shows a volcano-shaped curve with a maximum at d ≈ 5 nm, while the activity of the Au/anatase system weakly depends on d. Photoelectrochemical measurements indicate that the Au/rutile system favors the localized surface plasmon resonance (LSPR) induced interfacial electron transfer from Au to TiO2. Further, intrinsic Fano analysis for the absorption spectra of Au/TiO2 suggests that the elongation of the LSPR lifetime with the Au NP loading on rutile is primarily responsible for the enhancement of the alcohol oxidation. We concluded that the optimum d value is determined by the factors of the LSPR absorption intensity, the interfacial electron transfer efficiency, and the surface area.

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Tumor necrosis factor-α (TNF-α) is a cytokine produced by monocytes, macrophages, and T cells and is induced by pathogens, endotoxins, or related substances. TNF-α may play a key role in bone metabolism and is important in inflammatory bone diseases such as rheumatoid arthritis. Cells directly involved in osteoclastogenesis include macrophages, which are osteoclast precursor cells, osteoblasts, or stromal cells. These cells express receptor activator of NF-κB ligand (RANKL) to induce osteoclastogenesis, and T cells, which secrete RANKL, promote osteoclastogenesis during inflammation. Elucidating the detailed effects of TNF-α on bone metabolism may enable the identification of therapeutic targets that can efficiently suppress bone destruction in inflammatory bone diseases. TNF-α is considered to act by directly increasing RANK expression in macrophages and by increasing RANKL in stromal cells. Inflammatory cytokines such as interleukin- (IL-) 12, IL-18, and interferon-γ (IFN-γ) strongly inhibit osteoclast formation. IL-12, IL-18, and IFN-γ induce apoptosis in bone marrow cells treated with TNF-α   in vitro, and osteoclastogenesis is inhibited by the interactions of TNF-α-induced Fas and Fas ligand induced by IL-12, IL-18, and IFN-γ. This review describes and discusses the role of cells concerned with osteoclast formation and immunological reactions in TNF-α-mediated osteoclastogenesis in vitro and in vivo.