909 research outputs found

    Cosmic R-string, R-tube and Vacuum Instability

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    We show that a cosmic string associated with spontaneous U(1)RU(1)_R symmetry breaking gives a constraint for supersymmetric model building. In some models, the string can be viewed as a tube-like domain wall with a winding number interpolating a false vacuum and a true vacuum. Such string causes inhomogeneous decay of the false vacuum to the true vacuum via rapid expansion of the radius of the tube and hence its formation would be inconsistent with the present Universe. However, we demonstrate that there exist metastable solutions which do not expand rapidly. Furthermore, when the true vacua are degenerate, the structure inside the tube becomes involved. As an example, we show a "bamboo"-like solution, which suggests a possibility observing an information of true vacua from outside of the tube through the shape and the tension of the tube.Comment: 28 pages, 17 figures, v2: references added, improved arguments in sec 3.5.

    Role of Sulfated O-Glycans Expressed by High Endothelial Venule-Like Vessels in Pathogenesis of Chronic Inflammatory Gastrointestinal Diseases

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    Lymphocyte homing is mediated by a cascade of adhesive interactions between circulating lymphocytes and specialized endothelial cells comprising high endothelial venules (HEVs). Sulfated O-glycans expressed on HEVs, collectively called peripheral lymph node addressin (PNAd), interact with L-selectin expressed on lymphocytes, contributing to the initial step of the lymphocyte homing. In chronic inflammatory states, PNAd is induced on HEV-like vessels but absent in non-lymphoid tissues under normal conditions. Such HEV-like vessels have been observed in various chronic inflammatory diseases including rheumatoid arthritis, lymphocytic thyroiditis, Helicobacter pylori-associated chronic gastritis, and inflammatory bowel disease (IBD), and implicated in lymphocyte recruitment in those diseases. In H. pylori-associated chronic gastritis, PNAd-expressing HEV-like vessels are induced, and the progression of chronic inflammation is highly correlated with appearance of these vessels. Furthermore, eradication of H. pylori by antibiotics resulted in disappearance of PNAd. These results indicate that inhibition of PNAd formation could have therapeutic effect by attenuating lymphocyte recruitment. In ulcerative colitis (UC), PNAd-expressing HEV-like vessels are induced, preferentially in the active phase, and T cells, particularly CD4(+) T cells, are closely associated with these vessels, suggesting that T cell recruitment via PNAd-expressing HEV-like vessels plays at least a partial role in UC pathogenesis. Additionally, N-acetylglucosamine-6-O-sulfotransferase I (GlcNAc6ST-1) is suggested to be a candidate to regulate PNAd induction on HEV-like vessels in UC. These results provide a potential therapeutic strategy to treat UC by blocking T cell adhesion to PNAd-expressing HEV-like vessels. Inhibition or down-regulation of GlcNAc6ST-1 may be an alternative.ArticleBIOLOGICAL & PHARMACEUTICAL BULLETIN. 32(5):774-779 (2009)journal articl

    Design of dynamic soundscape : mapping time to space for audio browsing with simultaneous listening

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    Thesis (M.S.)--Massachusetts Institute of Technology, Program in Media Arts & Sciences, 1996.Includes bibliographical references (p. 58-61).by Minoru Kobayashi.M.S

    PLK1 blockade enhances therapeutic effects of radiation by inducing cell cycle arrest at the mitotic phase

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    The cytotoxicity of ionizing radiation depends on the cell cycle phase; therefore, its pharmacological manipulation, especially the induction of cell cycle arrest at the radiosensitive mitotic-phase (M-phase), has been attempted for effective radiation therapy. Polo-like kinase 1 (PLK1) is a serine/threonine kinase that functions in mitotic progression, and is now recognized as a potential target for radiosensitization. We herein investigated whether PLK1 blockade enhanced the cytotoxic effects of radiation by modulating cell cycle phases of cancer cells using the novel small molecule inhibitor of PLK1, TAK-960. The TAK-960 treatment exhibited radiosensitizing effects in vitro, especially when it increased the proportion of M-phase cells. TAK-960 did not sensitize cancer cells to radiation when an insufficient amount of time was provided to induce mitotic arrest. The overexpression of a PLK1 mutant, PLK1-R136G&T210D, which was confirmed to cancel the TAK-960-mediated increase in the proportion of mitotic cells, abrogated the radiosensitizing effects of TAK-960. A tumor growth delay assay also demonstrated that the radiosensitizing effects of TAK-960 depended on an increase in the proportion of M-phase cells. These results provide a rational basis for targeting PLK1 for radiosensitization when considering the therapeutic time window for M-phase arrest as the best timing for radiation treatments
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