87 research outputs found

    Rosiglitazone Suppresses the Growth and Invasiveness of SGC-7901 Gastric Cancer Cells and Angiogenesis In Vitro via PPARĪ³ Dependent and Independent Mechanisms

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    Although thiazolidinediones (TZDs) were found to be ligands for peroxisome proliferators-activated receptorĪ³ (PPARĪ³), the mechanism by which TZDs exert their anticancer effect remains unclear. Furthermore, the effect of TZDs on metastatic and angiogenesis potential of cancer cells is unknown. Our results in this paper show that rosiglitazone inhibited SGC-7901 gastric cancer cells growth, caused G1 cell cycle arrest and induced apoptosis in a dose-dependent manner. The effects of rosiglitazone on SGC-7901 cancer cells were completely reversed by treatment with PPARĪ³ antagonist GW9662. Rosiglitazone inhibited SGC-7901 cell migration, invasiveness, and the expression of MMP-2 in dose-dependent manner via PPARĪ³-independent manner. Rosiglitazone reduced the VEGF induced angiogenesis of HUVEC in dose-dependent manner through PPARĪ³-dependent pathway. Moreover, rosiglitazone did not affect the expression of VEGF by SGC-7901 cells. Our results demonstrated that by PPARĪ³ ligand, rosiglitazone inhibited growth and invasiveness of SGC-7901 gastric cancer cells and angiogenesis in vitro via PPARĪ³-dependent or -independent pathway

    Proteaseā€Activatable Hybrid Nanoprobe for Tumor Imaging

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/108698/1/adfm201400419.pd

    Treatment to Prevent HIV Transmission in Serodiscordant Couples in Henan, China, 2006 to 2012

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    Background. Antiretroviral therapy (ART) administered in clinical trial settings virtually eliminates the sexual transmission of human immunodeficiency virus (HIV) in serodiscordant couples, but effectiveness of treatment as prevention in the community is debated. Conflicting results from previous analyses in a Chinese cohort underscore the importance of determining effectiveness of ART delivered in resource limited settings

    Transient behavior and reaction mechanism of CO catalytic ignition over a CuOā€“CeO2 mixed oxide

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    As a key heterogeneous process, the catalytic oxidation of CO is essential not only for practical applications such as automotive exhaust purification and fuel cells but also as a model reaction to study the reaction mechanism and structure-reactivity correlation of catalysts. In this study, the variation in activity-controlling factors during CO catalytic ignition over a CuO-CeO 2 catalyst was investigated. The activity for CO combustion follows the decreasing order of CuO-CeO 2 > CuO > CeO 2. Except for inactive CeO 2, increasing temperature induces CO ignition to achieve self-sustained combustion over CuO and CuO-CeO 2. However, CuO provides enough copper sites to adsorb CO, and abundant active lattice oxygen, thus obtaining a higher hot zone temperature (208.3 Ā°C) than that of CuO-CeO 2 (197.3 Ā°C). Catalytic ignition triggers a kinetic transition from the low-rate steady-state regime to a high-rate steady-state regime. During the induction process, Raman, X-ray photoelectron spectroscopy, CO temperature-programmed desorption and IR spectroscopy results indicated that CO is preferentially adsorbed on oxygen vacancies (Cu +-[Ov]-Ce 3+) to yield Cu +-[Cā‰”O]-Ce 3+ complexes. Because of the self-poisoning of CO, the adsorbed CO and traces of adsorbed oxygen react at a relative rate, which is entirely governed by the kinetics on the CO-covered surface and the heat transport until the pre-ignition regime. The Cu +-[Cā‰”O]-Ce 3+ complex is a major contributor to CO ignition. The step-response runs and kinetic models showed that after ignition, a kinetic phase transition occurs from a CO-covered surface to an active lattice oxygen-covered surface. During CO self-sustained combustion, the rapid gas diffusivity and mass transfer is beneficial for handling the low coverage of CO. The active lattice oxygen of CuO takes part in CO oxidation
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