中药凌霄花的研究进展

本文对中药凌霄花的研究进展进行了综述,包括生药学研究、化学成分研究、药理学研究及临床应用。     

我国盖蛛属1新纪录种（蜘蛛目：皿蛛科）

记述采自我国云南省勐腊的盖蛛属１新纪录种－鹤嘴盖蛛Ｎｅｒｉｅｎｅｍａｃｅｌｌａ（Ｔｈｏｒｅｌｌ．１８９８）。     

犬囊状动脉瘤模型的制作

本文报道用“静脉囊镶嵌技术·制成犬的囊状动脉瘤模型。18个模型(6个单侧型,6个分叉型,6个末梢型)造型后2周经IA DSA检查。本模型在分型、血流动力学改变方面与人类囊状脑动脉瘤类似。不同类型的动脉瘤模型既有相同的血流动力学特征,又有各自的特点,这与动脉瘤与载瘤动脉的角度有关。我们认为该模型可应用于研究动脉瘤的血流动力学与血管内栓塞治疗。     

用中性红标记酵母原生质体初探

用２％蜗牛酶处理酵母细胞６０分钟,啤酒酵母Ｙ２９的原生质体形成率为９０％,再生率为９．５％;糖化酵母ＩＢ的原生质体形成率为８６％,再生率为１２％。用５００ｐｐｍ中性红染液对Ｙ２９菌株的整细胞和原生质体染色１５分钟,细胞的着色率为８４％,存活率为１２％,而原生质体的着色率为７５％,再生率为６．４％,经染色后的原生质体体积缩小,在交变电场中排队所需的场强电降低。     

Effect of physostigmine on relative acetylcholine output induced by systemic treatment with scopolamine in in vivo microdialysis of rat frontal cortex

By means of an in vivo brain microdialysis, the effect of different concentrations of physostigmine on the acetylcholine level in the dialysate of rat frontal cortex was studied. Perfusion of the various degrees of physostigmine (eserine) concentration (10 nM−10 μM) into the cortex through the dialysis membrane increased the basal acetylcholine level in a dose-dependent manner. In the presence of 10 nM, 0.1 μM and 10 μM physostigmine in the perfusate, systemic treatment with scopolamine (0.5 mg/kg, i.p.) increased 200, 270 and 510%, respectively, the relative acetylcholine level in the dialysates in comparison with the corresponding basal levels, while in the absence of physostigmine the treatment increased it only 40%. From these results, it appears that perfusion of physostigmine at a variety of concentrations, changes not only the basal level of acetylcholine induced by the inhibition of acetylcholinesterase but also the relative acetylcholine output induced by systemic treatment with scopolamine.     

简便、快速提取高质量的RNA分子

MethodsforHandy,RapidIsolationofHighQualityRNAbyGuanadiumThioeyauateDuJianYuanYanhuaMaShenglinDongZhiwei(BeijingInstituteforCancerResearchBeijing100034)硫氰胍是一种有效的蛋白变性剂。早在1979年,Chirgwin等就利用氯化铯／硫氰胍超离心技术成功地从RNA酶富集的胰脏组织中提取出未降解的RNA分子[2],从而使它成为抑制RNA酶的首选药物并得到广泛使用,但受到超速离心设备的限制。1983年,Cathala报道了氯化锂／硫氰胍RNA提取法[1]。该方法操作简便,获得的RNA质量很高,但所需时间较长。为了能在短时间内更快…     

Molecular Cloning and Characterization of Protein Kinase C from the Sea Urchin Lytechinus pictus

Protein kinase C (PKC) has been shown to play a role in events involved in fertilization such as activation of the Na⁺/H⁺antiporter and an NADPH dependent oxidase. In addition, it is involved in cell fate programming later in development of the sea urchin embryo. In order to further address the role of PKC in sea urchin development, we have screened a Lytechinus pictus ovary tissue cDNA library and identified one clone for sea urchin protein kinase C (suPKC1). This clone encodes a deduced protein with a molecular mass of 72.4 kDa, which shows strong homology to invertebrate and mammalian protein kinase C (PKC) sequences. PKC has been partially purified from eggs of L. pictus. This kinase activity has been shown to be dependent upon phosphatidylserine, diacylglycerol and Ca²⁺. In agreement with this biochemical data, suPKC1 has a C2 or Ca²⁺-binding domain suggesting its activity would be Ca²⁺-dependent. Polyclonal antibodies raised against peptides of the suPKC1 sequence recognize an antigen of approximately 71 kDa in DE52 fractions that contain PKC activity; this reactivity is not observed in fractions that lack PKC activity. Using a ribonuclease protection assay, we have demonstrated the presence of suPKC1 message throughout developmental stages of the sea urchin embryo.     

Chronic Nicotine Administration Differentially Affects Neurotransmitter Release from Rat Striatal Slices

Abstract: The objective of these experiments was to determine whether the chronic administration of nicotine, at a dose regimen that increases the density of nicotine binding sites, alters the nicotine-induced release of [³H]dopamine ([³H]DA), [³H]norepinephrine ([³H]NE), [³H]serotonin ([³H]5-HT), or [³H]acetylcholine ([³H]ACh) from rat striatal slices. For these experiments, rats received subcutaneous injections of either saline or nicotine bitartrate [1.76 mg (3.6 µmol)/kg, dissolved in saline] twice daily for 10 days, and neurotransmitter release was measured following preloading of the tissues with [³H]DA, [³H]NE, [³H]5-HT, or [³H]choline. Chronic nicotine administration did not affect the accumulation of tritium by striatal slices, the basal release of radioactivity, or the 25 mM KCl-evoked release of neurotransmitter. Superfusion of striatal slices with 1, 10, and 100 µM nicotine increased [³H]DA release in a concentration-dependent manner, and release from slices from nicotine-injected animals was significantly (p < 0.05) greater than release from saline-injected controls; release from the former increased to 132, 191, and 172% of release from the controls following superfusion with 1, 10, and 100 µM nicotine, respectively. Similarly, [³H]5-HT release increased in a concentration-related manner following superfusion with nicotine, and release from slices from nicotine-injected rats was significantly (p < 0.05) greater than that from controls. [³H]5-HT release from slices from nicotine-injected rats evoked by superfusion with 1 and 10 µM nicotine increased to 453 and 217%, respectively, of release from slices from saline-injected animals. The nicotine-induced release of [³H]NE from striatal slices was also concentration dependent but was unaffected by chronic nicotine administration. [³H]ACh release from striatal slices could not be detected when samples were superfused with nicotine but was measurable when tissues were incubated with nicotine. The release of [³H]ACh from slices from nicotine-injected rats was significantly (p < 0.05) less than release from controls and decreased to 36, 83, and 77% of control values following incubation with 1, 10, or 100 µM nicotine, respectively. This decreased [³H]ACh release could not be attributed to methodological differences because slices from nicotine-injected rats incubated with nicotine exhibited an increased [³H]DA release, similar to results from superfusion studies. In addition, it is unlikely that the decreased release of [³H]ACh from striatal slices from nicotine-injected rats was secondary to increased DA release because [³H]ACh release from slices from hippocampus, which is not tonically inhibited by DA, also decreased significantly (p < 0.05) in response to nicotine; hippocampal slices from nicotine-injected rats incubated with 1 and 10 µM nicotine decreased to 42 and 70%, respectively, of release from slices from saline-injected animals. Results indicate that the chronic administration of nicotine increases the ability of nicotine to induce the release of [³H]DA and [³H]5-HT and decreases the ability of nicotine to evoke the release of [³H]ACh but does not alter the nicotine-induced release of [³H]NE from brain slices.