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P J McAlpine N Van Cong C Boucheix A J Pakstis R C Doute T B Shows 《Cytogenetics and cell genetics》1987,46(1-4):29-101
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Nguyen van Cong G. Uzan M. S. Gross C. Jegou-Foubert P. Frachet C. Boucheix G. Marguerie J. Frézal 《Human genetics》1988,80(4):389-392
Summary The platelet GPIIb-IIIa complex functions as a receptor for fibrinogen, fibronectin, and von Willebrand factor on activated platelets. This glycoprotein is a member of a broadly distributed family of structurally and immunologically related membrane receptors involved in cell-cell contact and cell-matrices interactions. GPIIb-IIIa is a heterodimer complex composed of GPIIb (the subunit), which consists of two disulfide-linked heavy and light chains, and GPIIIa (the subunit), which is a single polypeptide chain. Congenital absence of platelet GPIIb-IIIa in Glanzmann's thrombasthenia results in a severe bleeding disorder characterized by defective platelet aggregation and failure of fibrinogen to bind to platelets. The gene coding for GPIIb was located on 17q21.1-17q21.3 as determined by in situ hybridization with a 2650-pb GP2B (GPIIb) cDNA probe prepared from human megakaryocytes. 相似文献
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The epimerization and dehydration reactions of the 17 beta-hydroxy group of anabolic 17 beta-hydroxy-17 alpha-methyl steroids have been investigated using the pyridinium salts of 17 beta-sulfate derivatives of methandienone 1, methyltestosterone 4, oxandrolone 7, mestanolone 10 and stanozolol 11 as model compounds. Rearrangement of the sulfate conjugates in buffered urine (pH 5.2) afforded the corresponding 17-epimers and 18-nor-17,17-dimethyl-13(14)-enes in a ratio of 0.8:1. These data indicated that both epimerization and dehydration of the 17 beta-sulfate derivatives were not dependent upon the respective chemical features of the steroids studied, but were instead inherent to the chemistry of the tertiary 17 beta-hydroxy group of these steroids. Interestingly, in vivo studies carried out with human male volunteers showed that only methandienone 1, methyltestosterone 4 and oxandrolone 7 yielded the corresponding 17-epimers 2, 5 and 8 and the 18-nor-17,17-dimethyl-13(14)-enes 3, 6 and 9 in ratios of 0.5:1, 2:1 and 2.7:1, respectively. No trace of the corresponding 17-epimers and 18-nor-17,17-dimethyl-13(14)-enes derivatives of mestanolone 10 and stanozolol 11 was detected in urine samples collected after administration of these steroids. These data suggested that the in vivo formation of the 17-epimers and 18-nor-17,17-dimethyl-13(14)-enes derivatives of 17 beta-hydroxy-17 alpha-methyl steroids is also dependent upon phase I and phase II metabolic reactions other than sulfation of the tertiary 17 beta-hydroxyl group, which are probably modulated by the respective chemical features of the steroidal substrates. The data reported in this study demonstrate that the 17-epimers and 18-nor-17,17-dimethyl-13(14)-enes are not artifacts resulting from the acidic or microbial degradation of the parent steroids in the gut as previously suggested by other authors, but arise from the rearrangement of their 17 beta-sulfate derivatives. Unchanged oxandrolone 7 was solely detected in the unconjugated steroid fraction whereas unchanged steroids 1, 4 and 11 were recovered from the glucuronide fraction. These data are indirect evidences suggesting that the glucuronide conjugates of compounds 1 and 4 are probably enol glucuronides and that of compound 11 is excreted in urine as a N-glucuronide involving its pyrazole moiety. The urinary excretion profiles of the epimeric and 18-nor-17,17-dimethyl-13(14)-ene steroids are presented and discussed on the basis of their structural features. 相似文献
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烟草愈伤组织分化和芽原基形成期间呼吸代谢途径的改变 总被引:3,自引:0,他引:3
接种在继代培养基上的柳叶烟草愈伤组织,未观察到组织分化和芽原基形成。在分化培养基上生长的愈伤组织,接种后第6天可见拟分生组织和管胞分化,9—12天有芽原基形成,15—18天可观察到苗端结构。根据碘乙酸、Na_3PO_4和丙二酸抑制试验,以及3-磷酸甘油醛脱氢酶与琥珀酸脱氢酶活性测定结果,初步表明烟草愈伤组织呼吸中存在有EMP、HMP和TCAC代谢途径.在发生输导组织和芽原基分化的愈伤组织中(接种后第6—12天),HMP途径的运行程度较高;而芽原基的继续生长(培养12天以后),则与EMP途径的增加有关;分化培养基上生长的愈伤组织,始终较继代培养愈伤组织具有较高的FCAC活性水平。 相似文献
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ESR检测大鼠肺巨噬细胞释放的活性氧自由基 总被引:4,自引:0,他引:4
用ESR捕捉技术检测大鼠AM释放的活性氧自由基的性质表明:1.PMA和BCG均能刺激AM产生较强的OH·;能刺激人末稍血白细胞释放活性氧自由基的ConA和顺铂在本实验条件下未能使AM产生活性氧自由基信号。2.经膜活性剂PMA刺激的AM所释放活性氧自由基的高峰在刺激后2min,而经颗粒性物质BCG刺激,AM释放自由基的高峰时间明显后移。3.测试体系中的AM数过多或过少都不适合捕捉ESR信号。在本实验条件下,捕捉到最高自由基信号的AM终浓度为5×107AM/ml。4.测试体系中存在DETAPAC或EDTA,可使捕捉到的自由基信号明显增强。 相似文献
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