黏附分子T-cadherin表达对C6细胞恶性特性的影响

目的 探讨T-cadherin分子表达对胶质母细胞瘤C6细胞的恶性生物学特征的影响。方法 C6细胞分别转染pcDNA3．T-cadherin和pcDNA3表达质粒后。筛选3个表达不同水平T．cadherin的C6克隆和2个不表达T．cadherin的C6克隆，研究T-cadherin分子表达水平对C6细胞的细胞黏附、迁移及聚集能力的影响。结果 与不表达T-cadherin的C6细胞相比．表达T-cadherin的C6细胞在附着后1h和4h时的细胞黏附能力均显著增强，分别增强61．2％和25．1％（P〈0．01），而其细胞迁移能力平均下降72．6％（P〈0．010）。同时，T-cadherin表达诱导显著的同源细胞聚集，聚集指数平均下降52．4％（P〈0．01）。结论 T-cadherin分子表达显著抑制胶质母细胞瘤C6细胞的恶性生物学特性。     

游离植皮的生物学治愈过程

本文重点阐述了游离植皮的皮肤色泽变化。如果移植皮片与受区周围的正常皮肤相似,术后两者间不会出现明显的色泽差异;而从非暴露部移植到暴露部的皮肤,其色泽有明显的差异,但多有随季节性变动的倾向,而脚掌部皮肤移植到手掌时色泽不会发生变化。经电镜观察,移植皮肤的黑色素细胞亦呈规律性变化。同时对移植皮肤的收缩及挛缩、硬化、感觉恢复和皮肤器官的功能重建也进行了讨论。     

ATP and other nucleoside triphosphates inhibit the binding of insulin to its receptor

ATP, in a dose-dependent manner, inhibited the binding of 125I-insulin to its receptor in rat liver and human placental membranes. With rat liver plasma membranes an effect of ATP was detected at concentrations between 1.0 and 2.5 mmol/L, and maximal effects were seen at 10.0 mmol/L where binding was decreased by approximately 40%. The effect of ATP was one half-maximal within 10 minutes and maximal within 60 minutes. Scatchard analysis indicated that ATP was acting primarily to change the binding affinity of the insulin receptor. The effect of ATP was mimicked by CTP, GTP, and UTP, but not by ADP, 5'-AMP, 3'-AMP, 3'5'-cyclic AMP and adenosine. The ATP analog AMP-PNP had a potency approximately 10% that of ATP. The effect of ATP was not significantly influenced by inhibitors of phosphoprotein kinases and phosphoprotein phosphatases. In human placental membranes, ATP had a similar effect in inhibiting 125I-insulin binding to its receptor. Moreover, ATP was active in inhibiting insulin binding to purified human placental insulin receptors at 0.01 mmol/L, a concentration 1/100 of that needed for inhibiting binding to intact membranes. These studies indicate, therefore, that ATP and other nucleoside triphosphates influence the ability of the insulin receptor to bind insulin.     

系统药理学原理、方法及在中医药中的应用

目的:建立科学有效的现代中药研究体系,是中医药现代化进程中亟待解决的关键问题之一,然而目前从系统和整体水平研究中药的理论和方法均不成熟。方法:本文将综述当前系统药理学的最新进展,阐明如何整合药效学、药动学以及基因、蛋白、药物网络分析等技术,形成一个完整的可供中药药理学、药效学预测和验证的技术体系。结果:重点从中药基础理论、复方解析、注射液的研究、老方优化和新药开发方面介绍系统药理学在中医药中的应用。结论:本文提出的系统药理学研究体系为中药的现代研究提供了新方法学,将有助于系统、深刻地从系统水平和分子水平揭示中药和机体的相互作用机制,从而指导中药新药研发。     

Catecholamine and divalent cation effects on frog liver adenylate cyclase

Frog liver adenylate cyclase was characterized with respect to divalent cation interaction and hormonally stimulated activities. The enzyme catalyzed the synthesis of cyclic [³²P]3′,5′-AMP from α-³²P-labeled ATP. The activity of the enzyme was linear with time and00 protein concentration. The K_m for ATP was 0.5 mM, in the presence or absence of stimulators. The temperature optimum was 25°. GTP (10^?4M) increased the stimulation of adenylate cyclase by epinephrine. Similar activities were obtained using 5 mM Mg²⁺ or Mn²⁺. At higher concentrations, both ions inhibited epinephrine-stimulated, but not basal or fluoride-stimulated activities. Approximately equivalent hormonal stimulation was obtained with maximal stimulating concentrations of epinephrine, isoproterenol, glucagon, and prostaglandin E₁. Norepinephrine was less stimulatory. Only catecholamine-stimulated activities were inhibited by propranolol (10^?5M). The data suggest that catecholamines stimulate frog liver adenylate cyclase through interactions with β adrenergic receptors. The adenylate cyclase in frog liver differs from its mammalian counterpart in its response to temperature and maximally stimulatory concentrations of hormones.