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    CMUR > China Medical University Hospital > Jurnal articles >  Item 310903500/29669
    Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/29669


    Title: Technetium-99m tetrofosmin single photon emission computed tomography to detect metastatic papillary thyroid carcinoma in patients with elevated human serum thyroglobulin levels but negative I-131 whole body scan
    Authors: Wu, HS;Liu, FY;Huang, WS;Liu, YC;Chang, CT;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, Div Endocrinol & Metab, Taichung, Taiwan;Tri Serv Gen Hosp, Natl Def Med Ctr, Dept Nucl Med, Taipei, Taiwan;Tri Serv Gen Hosp, Natl Def Med Ctr, Dept Surg, Taipei, Taiwan;Far Eastern Mem Hosp, Dept Nucl Med, Taipei, Taiwan;Show Chwan Mem Hosp, Dept Surg, Changhua, Taiwan
    Date: 2003
    Issue Date: 2010-09-24 14:40:03 (UTC+8)
    Publisher: W B SAUNDERS CO LTD
    Abstract: The inhibition of formyl-methionyl-leucyl-phenylalanine (fMLP)-induced respiratory burst by 2',5'-dihydroxy-2-furfurylchalcone (DHFC) was investigated in rat neutrophils, and the underlying mechanism of this inhibition was assessed. DHFC concentration-dependently inhibited superoxide anion (O-2(-)) generation (IC50 4.2+/-1.2 muM), reaching a plateau within 5-10 min preincubation time, and inhibited oxygen consumption (IC50 6.9+/-1.9 muM) in rat neutrophils. In cell-free systems, DHFC failed to scavenge the (O-2(-)) generated during dihydroxyfumaric acid auto-oxidation. DHFC was less effective in the inhibition of both phorbol 12-myristate 13-acetate-activated neutrophil particulate NADPH oxidase activity and arachidonic acid-induced NADPH oxidase activation. In rat neutrophils, DHFC did not exert a cAMP-elevating effect, nor did it affect fMLP-induced [Ca2+](i) change to a considerable extent. DHFC slightly reduced fMLP-induced phosphatidylinositol 3-kinase (PI3 K) activation but showed moderate inhibition of Akt phosphorylation. fMLP-induced cellular phospholipase D (PLD) activation was markedly inhibited by DHFC (IC50 8.9+/-2.0 muM). In addition, DHFC effectively attenuated the membrane association of protein kinase C (PKC)-alpha, ADP-ribosylation factor (ARF) and Rho A in fMLP-stimulated cells. However, DHFC had no effect on the membrane association of ARF and Rho A caused by guanosine 5'-[gamma-thio]triphosphate (GTPgammaS) in cell lysate. fMLP-stimulated protein tyrosine phosphorylation was weakly attenuated by DHFC. DHFC was more efficient in the inhibition of extracellular signal-regulated kinase (ERK) phosphorylation than p38 mitogen-activated protein kinase (MAPK) phosphorylation. Collectively, these results indicate that the suppression of fMLP-induced respiratory burst by DHFC in rat neutrophils is probably mainly attributable to the inhibition of PLD activation, via the blockade of PKC-alpha, ARF and Rho A membrane association.
    Relation: CLINICAL RADIOLOGY 58(10):787-790
    Appears in Collections:[China Medical University Hospital] Jurnal articles

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