布氏田鼠肥满度分析和小型兽类肥满度指标K与KWL（重长指标）的比较

通过对两个肥满度指标的理论和生物学意义分析,以及对布氏田鼠肥满度的研究和实际应用的讨论,认为描述动物的肥满度时,重长指标ＫＷＬ优于指标Ｋ。两指标的最大差别是成体的ＫＷＬ值大于幼体,而成体的Ｋ值小于幼体。布氏田鼠肥满度没有性别差异;有异著的年龄差异,成体鼠的肥满度高于幼鼠;有显著的季节变化,鼠种群春季肥满度最高,夏季降低,秋季回升;有显著的年际变化,高数量年的肥满度高于低数量年。     

促黄体素释放激素类似物(LH-RH-A)对人蜕膜组织核糖核酸和蛋白质合成的抑制作用

高剂量LH-RH-A可明显抑制人蜕膜组织在离体下对~3H-尿嘧啶和~3H-亮氨酸的摄取;低剂量LH-RH-A无明显影响。在人蜕膜组织中也发现有高亲合力(K_?=3.83±1.36×10~?M~(-1))的LH-RH-A特异受体。上述发现表明,高剂量LH-RH-A可通过直接抑制RNA和蛋白质的合成而调节蜕膜组织的功能。     

大鼠白蛋白mRNA3''''端顺序的分子克隆(简报)

白蛋白与甲胎蛋白基因是由同一祖先基因进化而来。在小鼠,它们是一前一后定位在同一条染色体DNA上。在个体发育和肝癌变过程中,这两基因的相互关系也呈现相反的表达水平。因此,研究甲胎蛋白基因表达的调控与白蛋白基因是不可分割的。本文简要报道我们克隆了大鼠白蛋白mRNA 3′端顺序,为研究白蛋白基因结构和表达提供了必要的探针。白蛋白mRNA是从Wistar大鼠肝脏用双抗体免疫沉淀法提取。分子克隆技术基本是按“分子克隆”实验手册进行。     

我国青藏区细蚤属一新亚种记述(蚤目:细蚤科)

在整理采自四川、青海的蚤类标本中,发现一新亚种,现记述如下: 栉头细蚤腹凹亚种Leptopsylla(Pectinoctenus) pectiniceps ventrisinulata新亚种 鉴别特征 本新亚种与指名亚种L.(P.) pectiniceps pectiniceps(Wagner, 1893)的主要区别有:(1)♂可动突后缘的近基2/3段较圆凹,其最宽的位置稍高;(2)抱器不动突     

我国西部地区蚤目四种未知雌性的记述

本文系青海省蚤目研究的第四报。首次记述蚤目的四种未知雌性。雄性根据我国西藏采获的标本已先后有人记述:近缘纤蚤Rhadinopsylla accola Wagner,1930;端圆盖蚤Callopsylla kozlovi(Wagner.1929);卷带倍蚤Amphalius sptrataenius Liu,Wu ＆ Wu,1966;短突角叶蚤Ceratophyllus breviprolectus Liu,Wu ＆ Wu,1966。     

杉梢小卷蛾新种记述(鳞翅目:卷蛾科)

近年来由于杉梢小卷蛾在福建、江西、浙江、江苏、湖南、湖北、安徽、广东、广西等省(区)的为害,严重地影响了杉木的成长。现经研究鉴定为一新种,属鳞翅目、卷蛾科(Tortricidae)、小卷蛾亚科(Olethreutinae)、新小卷蛾族(Olethreutini)、Polychrosis属,订名为 Polychrosis cunninghamiacola。     

蛴螬病原菌(Bacillus sp.)的初步研究

蛴螬是农林生产上的重要地下害虫,由于长期栖居地下,防治较为困难。多年实践证明,采用综合防治措施可以有效地控制为害,利用病原微生物防治蛴螬是综合防治中的一个环节,是值得今后深入研究的课题。 1975年9月,我们在河北省任邱县白洋淀附近玉米地采到数头自然患病的阔胸犀金龟(Pento-don patruelis Frivaldszkz)三龄幼虫。1976年5     

竹大象虫初步观察

水竹(箣竹属)是浙南地区群众普遍种植的篾用丛生竹,种植数量占该地区丛生竹类之首位。历年来由于竹大象虫(Cyctotrachelus longimanus Fabricius)的严重为害,造成大量的死笋、断顶竹和畸形竹。平阳水头地区受害率在34—84％之间。为了解决这个问题,近两年来,我们对此虫陆续作了一些观察,现将材料整理如下,以供进一步研究参考。     

Inhibitors of Urokinase and Thrombin in Cultured Neural Cells

Recent studies have suggested important roles for certain proteases and protease inhibitors in the growth and development of the CNS. In the present studies, inhibitors of urokinase or thrombin in cultured neural cells and serum-free medium from the cells were identified by screening for components that formed sodium dodecyl sulfate-stable complexes with 125I-urokinase or 125I-thrombin. Rinsed glioblastoma possessed two components that complexed 125I-urokinase. One was type 1 plasminogen activator inhibitor (PAI-1), because the 125I-urokinase-containing complexes were immunoprecipitated with anti-PAI-1 antibodies. The other component formed complexes with 125I-urokinase that were not recognized by antibodies to PAI-1 or protease nexin-1 (PN-1). Its identity is unknown. In addition to these cell-bound components, the glioblastoma cells also secreted two inhibitors that formed complexes with 125I-urokinase; one was PAI-1, and the other was PN-1. The secreted PN-1 also formed complexes with 125I-thrombin. It was the only thrombin inhibitor detected in these studies. Human neuroblastoma cells did not contain components that formed detectable complexes with either 125I-urokinase or 125I-thrombin. However, human neuroblastoma cells did contain very low levels of PN-1 mRNA and PN-1 protein. Added PN-1 bound to the surface of both glioblastoma and neuroblastoma cells. This interaction accelerated the inhibition of thrombin by PN-1 and blocked the ability of PN-1 to form complexes with 125I-urokinase. Thus, cell-bound PN-1 was a specific thrombin inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)