Application of PET and PET/CT imaging for cancer screening

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 台中附設醫院 > 期刊論文 > Item 310903500/29738

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题名:	Application of PET and PET/CT imaging for cancer screening
作者:	Chen, YK;Ding, HJ;Su, CT;Shen, YY;Chen, LK;Liao, AC;Hung, TZ;Hu, FL;Kao, CH
贡献者:	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 Med Imaging, Taipei, Taiwan;I Shou Univ, Dept Med Radiat Technol, Kaohsiung, Taiwan;Shin Kong Wu Ho Su Mem Hosp, Dept Nucl Med, Taipei, Taiwan;Shin Kong Wu Ho Su Mem Hosp, PET Ctr, Taipei, Taiwan
日期:	2004
上传时间:	2010-09-24 14:41:34 (UTC+8)
出版者:	INT INST ANTICANCER RESEARCH
摘要:	Kazinol B, a natural isoprenylated flavan, stimulated the [Ca2+](i) elevation in the presence or absence of Ca2+ in the medium. Treatment with chymotrypsin or phorbol 12-myristate 13-acetate to shedding Of L-selectin had no effect on subsequent kazinol B-induced Ca2+ response. Upon initial cyclopiazonic acid (CPA) treatment in the absence of external Ca2+, the subsequent [Ca2+](i) rise followed by challenge with kazinol B was greatly diminished. The ryanodine receptor blockers, 8-bromocyclic ADP-ribose and ruthenium red did not affect kazinol B-evoked Ca2+ release from internal stores. However, the inhibitors of sphingosine kinase, dimethylsphingosine, but not dihydrosphingosine, inhibited kazinol B-induced Ca2+ release. Kazinol B-induced [Ca2+](i) rise was not affected by two nitric oxidase inhibitors, N-(3-aminomethyl)benzylacetamidine (1400W) and 7-nitroindazole, cytochalasin B and Na+-deprivation. This response was slightly attenuated by 2-aminoethyldiphenyl borate (2-APB), a D-myo-inositol 1,4,5-trisphosphate (IP3) receptor blocker, and by genistein, a general tyrosine kinase inhibitor. However, the Ca2+ response was greatly diminished by two actin filament reorganizers, calyculin A and jasplakinolide, 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY 294002), an inhibitor of phosphoinositide 3-kinase, N-(3-aminomethyl)benzylacetamidine (SB 203580), the p38 mitogen-activated protein kinase inhibitor, 1-[6-[17beta-3-methoxyestra-1,3,5(10)-trien-17-yl] amino]hexyl]-1H-pyrrole-2,5-dione (U-73122), the inhibitor of phospholipase C-coupled processes, and by 0.3 mM La3+ or Ni2+. Kazinol B did not evoke any appreciable Ba2+ and Sr2+ entry into cells. The Ca2+ entry blockers, 1-[beta-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole( SKF-96365), but not cis-N-(2-phenylcyclopentyl)azacyclotridec-1-en-2-amine (MDL-12,330A), inhibited a kazinol B-induced [Ca2+](i) rise. Kazinol B had no effect on the pharmacologically isolated plasma membrane Ca2+-ATPase activity. In a Ca2+-free medium, kazinol B inhibited the subsequent Ca2+ addition, resulting in robust entry in CPA- and formyl peptide-activated cells. Kazinol B produced a concentration-dependent reduction in the mitochondrial membrane potential. These results indicate that kazinol B stimulates Ca2+ release from internal Ca2+ store, probably through the sphingosine 1-phosphate and IP3 signaling, and activates external Ca2+ influx mainly through a non-store-operated Ca2+ entry (non-SOCE) pathway. Inhibition of SOCE by kazinol B is probably attributable to a break in the Ca2+ driven force of mitochondria.
關聯:	ANTICANCER RESEARCH 24(6):4103-4108
显示于类别:	[台中附設醫院] 期刊論文

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