中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/29676
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 29490/55136 (53%)
Visitors : 1999308      Online Users : 431
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    CMUR > China Medical University Hospital > Jurnal articles >  Item 310903500/29676
    Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/29676


    Title: Compare FDG-PET and Tc-99m tetrofosmin SPECT to detect metastatic thyroid carcinoma
    Authors: Chen, YK;Liu, FY;Yen, RF;Kao, CH
    Contributors: 附設醫院核子醫學部;China Med Univ Hosp, Dept Nucl Med, Taichung 404, Taiwan;China Med Univ Hosp, PET Ctr, Taichung 404, Taiwan;Shin Kong Wu Ho Su Mem Hosp, Dept Nucl Med, Taipei, Taiwan;Shin Kong Wu Ho Su Mem Hosp, PET Ctr, Taipei, Taiwan;Natl Taiwan Univ Hosp, Dept Nucl Med, Taipei, Taiwan;Natl Taiwan Univ Hosp, PET Ctr, Taipei, Taiwan;Taichung Healthcare & Management Univ, Grad Inst Bioinformat, Taichung, Taiwan
    Date: 2003
    Issue Date: 2010-09-24 14:40:14 (UTC+8)
    Publisher: ASSOC UNIV RADIOLOGISTS
    Abstract: There are two protease-activated receptors (PARS), PAR I and PAR4, in human platelets. It has been suggested that PAR I mediates platelet responses to low concentrations of thrombin, whereas PAR4 mediates signaling only at high concentrations. In the present study, we used a selective PAR4 blocker, YD-3, to investigate the role of PAR4 in thrombin-induced thromboxane formation in human platelets. YD-3 completely prevented thromboxane production by either a low concentration of thrombin (0.1 U/ml) or the PAR4 agonist peptide GYPGKF In contrast,YD-3 did not affect thromboxane production caused by the PAR I agonist peptide SFLLRN, collagen or arachidonic acid. YD-3 also decreased [H-3]arachidonic acid release from thrombin-stimulated platelets. Moreover, desensitization' of platelets with GYPGKF prevented low thrombin-induced thromboxane formation. The decreased thromboxane production by YD-3 is linked to inhibition of calcium influx in thrombin-stimulated platelets. These results suggest that PAR4 plays an important role in the regulation of thromboxane formation in platelets responding to thrombin through prolonged elevation of [Ca2+](i) and activation of phospholipase A(2). These data also indicate that PAR4 can be activated by relatively low concentrations of thrombin in human platelets. The selective inhibition of thrombin-induced thromboxane production by YD-3 may be of therapeutic benefit for thrombotic diseases.
    Relation: ACADEMIC RADIOLOGY 10(8):835-839
    Appears in Collections:[China Medical University Hospital] Jurnal articles

    Files in This Item:

    There are no files associated with this item.



    All items in CMUR are protected by copyright, with all rights reserved.

     


    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback