盐泽螺旋藻(Spirulina subsalsa)藻胆体的分离和特性

采用一种简便而快速的方法分离了盐泽螺旋藻的藻胆体。藻胆体的最大吸收波长位于618 nm,室温下荧光反射峰位于677～678 nm。利用7～15％SDS—聚丙烯酸胺梯度凝胶板状电泳,可分出三条有色多肽,其中藻蓝蛋白的α亚单位与别藻蓝蛋白的α亚单位几乎重叠,不易区分;另有分子量为117,99,53,49,27,24.5和14kD的七条无色多肽。117和 99kD多肽可能联结藻胆体和类囊体,并作为末端能量受体,而14kD多肽多为“核”亚结构的组分,其余的可能为“棒”亚结构内和“核”“棒”亚结构间的联结蛋白。     

Interstitial cells associated with the deep muscular plexus of the guinea-pig small intestine,with special reference to the interstitial cells of Cajal

Summary Interstitial cells associated with the deep muscular plexus of the guinea-pig small intestine were studied by electron microscopy, and three-dimensional cell models were reconstructed from serial ultrathin sections with a computer graphic system. Three types of cells were recognized. The first type was similar in shape to smooth muscle cells, but did not contain an organized contractile apparatus. Many large gap junctions comprising about 4% of the cell surface were present; they connected cells of the first type to each other, to the second type of cell and to smooth muscle cells of the outer circular layer. The second type of cell had a welldemarcated cell body with long slender processes and was characterized by a large amount of glycogen comprising about 9% of the cell volume. The third type of cell was similar to fibroblasts, and contained well-developed Golgi apparatus and rough endoplasmic retiulum. Some of these fibroblast-like cells (a possible subtype) formed small gap junctions. All three types of cells showed close relationships with nerve varicosities. This cellular network consisting of gap-junction-rich cells, glycogen-rich cells and smooth muscle cells may be involved in the pacemaking activity of intestinal movement.     

Alport syndrome: a genetic study of 31 families

Thirty one families with Alport syndrome including 3 families with associated syndromes were studied. The location of the COL4A5 gene, responsible for the Alport syndrome, was determined by linkage analysis with eight probes of the Xq arm and by a radiation hybrid panel. Concordant data indicated the localization of the Alport gene between DXS17 and DXS11. Four deletions and one single base mutation of the COL4A5 gene were detected. Homogeneity tests failed to show any evidence of genetic heterogeneity superimposed on clinical heterogeneity for ophthalmic signs and end-stage renal disease age.     

去甲肾上腺素在大鼠缰核引起的心血管效应及其机制

在乌拉坦麻醉的大鼠,研究了去甲肾上腺素(NE)在缰核(Hb)引起的心血管效应及其机制。Hb内微量注射NE使平均动脉压和心率呈剂量依赖性增加。用α受体阻断剂酚妥拉明预处理Hb,可明显减弱NE在Hb引起的心血管效应,但β受体阻断剂心得安或生理盐水不引起任何影响。Hb内微量注射海人酸使平均动脉压和心率明显增加,但Hb内微量注射利多卡因则不能引起明显的心血管效应。上述结果表明,Hb内NE在调节心血管活动中起重要作用,而这种效应可能是通过激活α受体使Hb兴奋的结果。     

NO—样松驰因子在大鼠止血带休克中的作用

为探讨NO-样松驰因子(NO-LRF)在休克中的效应及其病理生理意义,本工作在大鼠止血带休克(ToS)模型上发现离体灌流的主动脉环对去甲肾上腺素的反应性降低,组织cGMP含量增加。用NO前体L-精氨酸(L-Arg)或NO合成阻断剂L-NNA,可溶性乌苷酸环化酶抑制剂亚甲蓝灌流,分别增强或减轻ToS动物主动脉的上述变化,而且这些药物的作用不受血管内皮是否存在的影响。实验结果提示非内皮细胞源的NO-LRF是引起ToS动物血管低反应性的因素之一。体内实验表明 L-Arg治疗缓解,而L-NNA恶化ToS病程,提示NO-LRF可能参与机体的适应保护机制。     

人子宫内膜纤蛋白溶酶元激活因子及其抑制因子的分布与调控

人子宫内膜中存在组织型(tPA)及尿激酶型(uPA)两类纤蛋白溶酶元激活因子,其含量在增殖期高于分泌期。本文应用免疫组织化学定位证实uPA及tPA两类抗原存在于子宫内膜的腺体细胞和间质细胞中。应用SDS-PAGE分高蛋白质,继而应用纤蛋白-琼脂糖铺盖技术测得离体培养下间质细胞仅释放tPA,腺体细胞仅释放uPA,但两种细胞均分泌PA的抑制因子(PAI)。培液中加入孕酮,明显抑制PA和刺激PAI生成。雌二醇作用与孕酮相反。某些肽类激素hCG、PRL、GnRH及cAMP作用基本与雌二醇相同。但福司克林(FK)则刺激间质、腺体两种细胞产生tPA及少量uPA,抑制PAI生成。本工作表明人子宫内膜中存在PA及PAI作用相反的酶,受激素调控,其生理意义尚待进一步探讨。     

下丘脑室旁核加压素能神经元参与电针刺激对实验性内脏痛的抑制

本实验采用内脏痛的实验模型,探讨室旁核中的加压素在针刺抑制内脏痛中的作用。实验结果如下:(1)大鼠在在射酒石酸锑钾(0.1％,10ml/kg,i.p.)后,出现可定量的扭体反应,能作为观察内脏痛的客观指标。(2)电针对内脏痛有抑制效应,即具有镇痛作用。(3)电刺激室旁核,能加强电针对内脏痛的抑制效应,损毁室旁核,则此抑制效应基本消失。(4)脑室注射加压素抗血清(14μl)或加压素拮抗剂[d(CH_2)_5Tyr(Me)-AVP,500ng/5μl]都能明显减弱电针的抑制效应。(5)腹腔注射加压素拮抗剂(10μg/kg),不能翻转电针的抑制效应。上述实验结果表明,下丘脑室旁核的加压素能神经元参与了电针刺激对实验性内脏痛的抑制。     

四氯化碳中毒对大鼠离体再生肝细胞钾离子外漏的影响

本工作用三种剂量四氯化碳(CCl_4,10,15和20mmol/L)损伤正常大鼠离体肝细胞,分别在5,10,15和20min测定细胞内K~+和GPT漏出量。实验观察到细胞内K~+和GPT漏出量与CCl_4染毒的剂量和时间有明显关系,而且K~+漏出量较GPT更能灵敏地反映细胞的损伤程度;用中等剂量CCl_4(15mmol/L)损伤离体再生肝细胞20min后,细胞内K~+漏出的变化百分数明显低于正常肝细胞。这些结果表明,大鼠离体再生肝细胞具有较强的抗CCl_4损伤作用,其机制可能与再生肝细胞膜稳定性较强有关。