Tokyo University of Science

About: Tokyo University of Science is a education organization based out in Tokyo, Japan. It is known for research contribution in the topics: Thin film & Enantioselective synthesis. The organization has 15800 authors who have published 24147 publications receiving 438081 citations. The organization is also known as: Tōkyō Rika Daigaku & Science University of Tokyo.

The Cosmic-Ray Energy Spectrum Observed with the Surface Detector of the Telescope Array Experiment

Abstract: The Telescope Array experiment is supported by the Japan Society for the Promotion of Science through Grants-in-Aids for Scientific Research on Specially Promoted Research (21000002) "Extreme Phenomena in the Universe Explored by Highest Energy Cosmic Rays" and for Scientific Research (S) (19104006), and the Inter-University Research Program of the Institute for Cosmic Ray Research; by the U.S. National Science Foundation awards PHY-0307098, PHY-0601915, PHY-0703893, PHY-0758342, and PHY-0848320 (Utah), and PHY-0649681 (Rutgers); by the National Research Foundation of Korea (2006-0050031, 2007-0056005, 2007-0093860, 2010-0011378, 2010-0028071, R32-10130, 2011-0002617); by the Russian Academy of Sciences, RFBR grants 10-02-01406a and 11-02-01528a (INR), IISN project No. 4.4509.10 and Belgian Science Policy under IUAP VI/11 (ULB). The foundations of Dr. Ezekiel R. and Edna Wattis Dumke, Willard L. Eccles and the George S. and Dolores Dore Eccles all helped with generous donations. The State of Utah supported the project through its Economic Development Board, and the University of Utah through the Office of the Vice President for Research. The experimental site became available through the cooperation of the Utah School and Institutional Trust Lands Administration (SITLA), U. S. Bureau of Land Management, and the U. S. Air Force. We also thank the people and the officials of Millard County, Utah for their steadfast and warm support. We gratefully acknowledge the contributions from the technical staffs of our home institutions. An allocation of computer time from the Center for High Performance Computing at the University of Utah is gratefully acknowledged.

Phenylboronic Acid-Installed Polymeric Micelles for Targeting Sialylated Epitopes in Solid Tumors

Abstract: Ligand-mediated targeting of nanocarriers to tumors is an attractive strategy for increasing the efficiency of chemotherapies. Sialylated glycans represent a propitious target as they are broadly overexpressed in tumor cells. Because phenylboronic acid (PBA) can selectively recognize sialic acid (SA), herein, we developed PBA-installed micellar nanocarriers incorporating the parent complex of the anticancer drug oxaliplatin, for targeting sialylated epitopes overexpressed on cancer cells. Following PBA-installation, the micelles showed high affinity for SA, as confirmed by fluorescence spectroscopy even at intratumoral pH conditions, i.e., pH 6.5, improving their cellular recognition and uptake and enhancing their in vitro cytotoxicity against B16F10 murine melanoma cells. In vivo, PBA-installed micelles effectively reduced the growth rate of both orthotopic and lung metastasis models of melanoma, suggesting the potential of PBA-installed nanocarriers for enhanced tumor targeting

Isolation, structure, and stability of a dodecanethiolate-protected Pd1Au24 cluster

Abstract: A dodecanethiolate-protected Pd1Au24(SC12H25)18 cluster, which is a mono-Pd-doped cluster of the well understood magic gold cluster Au25(SR)18, was isolated in high purity using solvent fractionation and high-performance liquid chromatography (HPLC) after the preparation of dodecanethiolate-protected palladium–gold bimetal clusters. The cluster thus isolated was identified as the neutral [Pd1Au24(SC12H25)18]0 from the retention time in reverse phase columns and by elemental analyses. The LDI mass spectrum of [Pd1Au24(SC12H25)18]0 indicates that [Pd1Au24(SC12H25)18]0 adopts a similar framework structure to Au25(SR)18, in which an icosahedral Au13 core is protected by six [–S–Au–S–Au–S–] oligomers. The optical absorption spectrum of [Pd1Au24(SC12H25)18]0 exhibits peaks at ∼690 and ∼620 nm, which is consistent with calculated results on [Pd1@Au24(SC1H3)18]0 in which the central gold atom of Au25(SC1H3)18 is replaced with Pd. These results strongly indicate that the isolated [Pd1Au24(SC12H25)18]0 has a core–shell [Pd1@Au24(SC12H25)18]0 structure in which the central Pd atom is surrounded by a frame of Au24(SC12H25)18. Experiments on the stability of the cluster showed that Pd1@Au24(SC12H25)18 is more stable against degradation in solution and laser dissociation than Au25(SC12H25)18. These results indicate that the doping of a central atom is a powerful method to increase the stability beyond the Au25(SR)18 cluster.

Induction of Apoptosis in Leukemic Cells by Homovanillic Acid Derivative, Capsaicin, through Oxidative Stress: Implication of Phosphorylation of p53 at Ser-15 Residue by Reactive Oxygen Species

Abstract: Capsaicin (N-vanillyl-8-methyl-1-nonenamide) is a homovanillic acid derivative found in pungent fruits. Several investigators have reported the ability of capsaicin to inhibit events associated with the promotion of cancer. However, the effects of capsaicin on human leukemic cells have never been investigated. We investigated the effects of capsaicin on leukemic cells in vitro and in vivo and further examined the molecular mechanisms of capsaicin-induced apoptosis in myeloid leukemic cells. Capsaicin suppressed the growth of leukemic cells, but not normal bone marrow mononuclear cells, via induction of G(0)-G(1) phase cell cycle arrest and apoptosis. Capsaicin-induced apoptosis was in association with the elevation of intracellular reactive oxygen species production. Interestingly, capsaicin-sensitive leukemic cells were possessed of wild-type p53, resulting in the phosphorylation of p53 at the Ser-15 residue by the treatment of capsaicin. Abrogation of p53 expression by the antisense oligonucleotides significantly attenuated capsaicin-induced cell cycle arrest and apoptosis. Pretreatment with the antioxidant N-acetyl-L-cystein and catalase, but not superoxide dismutase, completely inhibited capsaicin-induced apoptosis by inhibiting phosphorylation of Ser-15 residue of p53. Moreover, capsaicin effectively inhibited tumor growth and induced apoptosis in vivo using NOD/SCID mice with no toxic effects. We conclude that capsaicin has potential as a novel therapeutic agent for the treatment of leukemia.