中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/30708
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    CMUR > China Medical University Hospital > Jurnal articles >  Item 310903500/30708
    Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/30708


    Title: Detection of severe acute respiratory syndrome-associated coronavirus in pneumocytes of the lung
    Authors: Chow, KC;Hsiao, CH;Lin, TY;Chen, CL;Chiou, SH
    Contributors: 附設醫院醫研部;Natl Chung Hsing Univ, Inst Biomed Sci, Taichung 40227, Taiwan;Natl Chung Hsing Univ, Grad Inst Vet Microbiol, Taichung 40227, Taiwan;Natl Taiwan Univ Hosp, Dept Pathol, Taipei 100, Taiwan;China Med Univ Hosp, Dept Pathol, Taichung, Taiwan;China Med Univ Hosp, Dept Med Res, Taichung, Taiwan
    Date: 2004
    Issue Date: 2010-09-24 15:00:22 (UTC+8)
    Publisher: AMER SOC CLINICAL PATHOLOGY
    Abstract: The pharmacological mechanisms of a synthetic compound 1-benzyl-3-(5'-hydroxymethyl-2'-furyl) indazole (YC-1) in preventing smooth muscle cell proliferation remains to be elucidated. The present study was aimed to explore the effects of YC-1 on certain molecules responsible for cell proliferation, including transforming growth factor (TGF)-beta1, soluble guanylyl cyclase (sGC) and focal adhesion kinase (FAK). The in vivo assay was correlated to the in vitro results of YC-1 on vascular stenosis. YC-1 was applied topically via a pluronic gel onto the balloon-injured rat carotid arteries, which were then harvested two weeks later for histological analysis. Our in vitro results showed that TGF-beta1 was suppressed by YC-1 by 50%. The translational level of sGC was threefold activated by YC-1 while the transcription level of sGC was increased up to 24-fold. FAK, the molecule responsible for cell proliferation and migration, was suppressed by YC-1 on the translational levels for 72%. These in vitro results were in consistent with the in vivo observation that the area ratio of neointima to media was reduced by YC-1. This study provides insights into the pharmacological mechanisms of YC-1 in preventing abnormal smooth muscle cell proliferation and thus supports the use of YC-1 as an adjuvant therapy for balloon injury-induced restenosis.
    Relation: AMERICAN JOURNAL OF CLINICAL PATHOLOGY 121(4):574-580
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