水生观赏植物的调查和研究

水生绿化观赏植物是美化园林水景的重要植物材料,作者通过几年的调查研究和引种栽培,提出了28种(其中荷花含18个品种,睡莲含20个品种)水生绿化观赏植物,同时介绍了20种(其中荷花含6个品种)观赏价值较高的水生绿化观赏植物。     

欺骗,契约,合作的ESS

动物竞争中的欺骗、契约、合作现象是极为常见的。本文就论述与此有关的ESS。一、欺骗某些动物竞争时信号a后跟随发生行为A,如一个体不出现A则为欺骗。欺骗是相对真实     

活性氧对巨噬细胞呼吸爆发影响及云芝多糖的保护作用

用化学发光法观察到叔丁基氢过氧化物对培养的小鼠腹腔巨噬细胞呼吸爆发有强烈的抑制作用。云芝多糖经腹腔注射后,能增强巨噬细胞呼吸爆发功能对叔丁基氢过氧化物损伤的抵抗力。云芝多糖处理的巨噬细胞谷胱甘肽过氧化物酶基础活力显著提高,在叔丁基氢过氧化物作用下,云芝多糖处理的巨噬细胞仍有较高的谷胱甘肽过氧化物酶活力。说明巨噬细胞的免疫功能与谷胱甘肽过氧化物酶活力有关,非特异性免疫多糖可提高细胞抗氧化能力,减轻活性氧损伤作用。     

人肌肌酸激酶胍变性时的失活与构象变化的比较研究

应用二阶导数光谱、紫外差吸收光谱和荧光光谱等监测手段,研究了人肌肌酸激酶在盐酸胍溶液中的构象变化。二阶导数光谱结果表明,若以6M盐酸胍中肌酸激酶酪氨酸残基的暴露程度为100％,则天然酶酪氨酸残基的暴露程度只有2％。而紫外差吸收光谱和荧光光谱的变化与兔肌肌酸激酶的结果相似。比较不同胍浓度下人肌肌酸激酶的失活与构象变化,表明酶的失活先于构象变化。同时还测定了不同浓度胍溶液中人肌酶的失活与构象变化的速度常数。结果表明以几种方法测定的构象变化均为单相的一级过程,而酶的失活却呈现了由快慢两相组成的一级反应过程。比较同浓度胍溶液中的失活速度与构象变化速度,发现酶失活的快相反应速度常数比构象变化的速度常数大1—2个数量级,慢相速度常数与构象变化速度常数相近。上述结果进一步支持了酶的活性部位构象柔性的观点。     

人酸性成纤维细胞生长因子神经营养作用的初步研究

本实验研究了人酸性成纤维细胞生长因子(haFGF)的体外神经营养作用。结果表明,haFGF在体外能明显促进鸡胚(E-8)脊髓组织神经突起的生长,并能明显改变新生大鼠脑星形胶质细胞的形态,使扁平、多角形紧密联接的细胞转化为具有纤维样突起的胶质细胞,同时对胶质细胞DNA合成也有一定促进作用。实验还证明,haFGF可增加体外培养新生大鼠海马神经元的存活,且大大增加神经元胞体体积及突起长度。     

人α1/158Ⅴ型(α1c型)干扰素基因在大肠杆菌中的表达及其产物的初步纯化

采用DNA聚合酶链反应(PCR)技术,将本实验室从中国人胎肝细胞染色体DNA中发现和分离的IFN-α1/158V基因的原始克隆,改造成适于进行非融合蛋白原核表达的结构形式,并在大肠杆菌中获得高效表达。测得重组IFN-α1/158V的抗病毒活性为1.9×10~7单位/升菌液。随后又采用以单克隆抗体亲和层析为主的纯化流程对表达产物进行初步纯化,获得了在SDS-聚丙烯酰胺凝胶电泳上呈现单一条带的纯化产物。     

酸性水和投加铝、钙对鲢鱼早期发育和鳃超微结构的影响

在实验室条件下,研究了酸性水和投加铝、钙对鲢鱼胚胎孵化和鱼苗存活以及幼鱼鳃超微结构的影响。pH4.0引起所有胚胎在24小时内死亡,暴露于pH4.5—6.0的胚胎孵化率和暴露于pH4.0—6.0的5—15日龄鱼苗存活率随pH值上升而增高。投加0.5mg Al~(3+)/L使在酸性pH暴露条件下的胚胎孵化率和鱼苗存活率进一步降低。投加3.0mg Ca~(2+)/L可显著提高暴露于pH4.5和5.0的胚胎孵化率;投加2.0mg Ca~(2+)/L可在一定程度上提高暴露于pH4.5和5.0的鱼苗存活率。幼苗经pH4.5暴露8小时后出现严重的鳃超微结构损害;投加1.0mg Al~(3+)/L使鳃结构损害加剧;投加5.0mg Ca~(2+)/L可明显缓解酸性水对鳃的损害。     

利用普通怯寄蝇防治菜粉蝶初探

1 前言 从外地引进寄蝇或人工助长当地寄蝇种类防治农林害虫,是有效的生防手段之一,国外已有很多成功的报道。King等(1981)在路易斯安娜州蔗田中人工大量释放螟利索寄蝇(Lixophaga diatraeae)成虫防治第1代小蔗杆草螟(Diatraea saccharalis),不同地区的寄生率分别达到4.1、8.7和35.7％;由于降低了农药的使用量,奇痣窄径茧蜂(Agathis stigmatera)的自然寄生率也相应提高,很好地控制了蔗田害虫的发生。在寄蝇的田间释放技术方面,国外还没有详细的报道。在我国,利用寄蝇防治害虫的工作也是刚刚起步,很多具体问题有待于进一步研究。     

Functional levels of mitochondrial anion transport proteins in non-insulin-dependent diabetes mellitus

The effect of non-insulin-dependent diabetes mellitus (i.e., NIDDM; type 2 diabetes) on the levels of functional mitochondrial anion transport proteins has been determined utilizing a chemically-induced neonatal model of NIDDM. We hypothesized that moderate insulin deficiency exacerbated by the insulin resistance, which is characteristic of NIDDM, would cause changes in mitochondrial anion transporter function that were similar to those we have previously shown to occur in insulin-dependent diabetes mellitus (i.e., IDDM; type 1 diabetes) (Arch. Biochem. Biophys. 280: 181–191, 1990). Our experimental approach consisted of the extraction of the pyruvate, dicarboxylate and citrate transport proteins from the mitochondrial inner membrane with Triton X-114 using rat liver mitoplasts (prepared from diabetic and control animals) as the starting material, followed by the functional reconstitution of each transporter in a proteoliposomal system. This strategy permitted the quantification of the functional levels of these three transporters in the absence of the complications that arise when such measurements are carried out with intact mitochondria (or mitoplasts). We found that experimental NIDDM did not cause significant changes in the extractable and reconstitutable specific (and total) transport activities of the pyruvate, dicarboxylate, and citrate transporters. These results are in marked contrast to our previous findings obtained using rats with IDDM and negated our hypothesis. The present results, in combination with our earlier findings, allow us to conclude that insulin plays an important role in the regulation of mitochondrial anion transporter function. Accordingly, in this model of NIDDM, where the level of insulin is not profoundly deficient, transporter function is unaltered, whereas in IDDM, where a profound insulinopenia exists, transporter function is altered. Furthermore, the present studies suggest that in the neonatal model of NIDDM the three mitochondrial transporters investigated are neither affected by, nor are they the sites of the well documented hepatic post-receptor insulin resistance which is characteristic of this disease.     

Interleukin—1β对促卵泡生成素（FSH）诱导大鼠...

Interleukin-1 beta (IL-1 beta), one of the polypeptide lymphokines released in response to antigen, toxins, injury or inflammation by nearly all cell types, has multiple systemic effects. In the present study the effect of IL-1 beta on follicle stimulating hormone (FSH)-induced estrogen production in primary culture was investigated. Granulosa cells obtained from immature estrogen-treated female rats were cultured for 3 days with increasing doses of FSH (1-30 ng/ml) with or without increasing doses of IL-1 beta (2-20 U/ml). The FSH stimulated estrogen production is dose-dependent, whereas IL-1 beta alone did not affect estrogen biosynthesis. In contrast, simultaneous treatment with IL-1 beta caused a dose-dependent inhibition of FSH action. This inhibitory effect of IL-1 beta was evident 48 h after the treatment. Furthermore, IL-1 beta inhibited forskolin (10(-5) mmol/L) and (Bu)2 cAMP (10(-2) mmol/L)-stimulated estrogen production, indicating a post-cyclic AMP site of action. The present study suggests that IL-1 beta is a potent modulator of granulosa cell steroidogenesis. Decreased estrogen formation may contribute to the follicle atresia and the impaired reproductive functions during injury and inflammation.