杉木,火力楠纯林及混交林细根周转的研究

系统研究了杉木、火力楠纯林及混交林细根生物量、生产力及年周转率。结果表明,杉木、火力楠纯林及混交林活细根生物量分别为８８０、３０３５和１５６０ｋｇ．ｈａ＾－１;死细根生物量为２３５、３９８和５６５ｋｇ．ｈａ＾－１;细根年周转率为１．２９、１．４２和１．４０;年生产量为１１３７、４３１８和２１７９ｋｇ．ｈａ＾－１;年死亡量为４９７．５９５和１１４９ｋｇ．ｈａ＾－１,分别相当于林分枯枝落叶年凋落量为３     

银杏外种皮的双黄酮成分

从银杏外种皮的乙酸乙酯提取中分离得到６个化合物,其中５个经物理常数及光谱分析鉴定为金松双黄酮、银杏素、奶杏素、１－５’－甲氧基白果素及白果素。这些化合物均首次从银杏外种皮分离。     

流行性出血热循环免疫复合物组分分析

应用ＳＤＳ－聚丙烯酰胺凝胶电泳及免疫转印技术对流行性出血热患才血清中免疫合物组分进行了分析。流行性出血热循环免疫复合物经ＳＤＳ－ＰＡＧＥ分离,考马斯亮兰染色,显色主要有７条带,分子量分别为２３ｋＤ,５０ｋＤ,５２ｋＤ,６５ｋＤ,７２ｋＤ,８０ｋＤ及１００ｋＤ。采用该病毒特异性抗血清、单克隆抗体以及人免疫球蛋白、补体成分抗血清识别,在其特环免疫复合物中可检出特异性病毒抗在及相应的免疫球状蛋白和补体成     

戊肝病毒活性肽的选择,合成与应用

对戊型肝炎病毒（ＨＥＶ）编码蛋白序列进行了亲水性分析及二级结构预测,选择亲水性强、具有β－转角与β－折叠的区段,采用多肽固相合成法合成了ＨＥＶ基因组３个开读框架（ＯＲＦ１,ＯＲＦ２和ＯＲＦ３）中可能的抗原表位,以免疫学方法进行鉴定并选出了分别来自ＨＥＶ３个ＯＲＦ的、具有重要生物活性与应用前景的３段肽（ＥＨ１７４、ＥＨ２６５、ＥＨ３６２）。在此基础上,进行了抗ＨＥＶＥＬＩＳＡ新型检测试剂盒的实验室研究及临床试用。结果表明,所研究的戊肝抗体检测试剂盒特异性高、临床符合性好、具有可重复性,在戊肝辅助诊断及流行病学调查中具有重要意义。     

草鱼出血病病毒多肽的免疫原性

采用中和试验比较了草鱼出血病病毒ＧＣＨＶ８７３的１１个多肽的免疫原性,确定了主要中和抗原。纯化的单个病毒多肽免疫家兔获得抗血清,多太ＶＰ１、ＶＰ５、ＶＰ６和ＶＰ９的抗血清具有中和效价,而ＶＰ２、ＶＰ３、ＶＰ４、ＶＰ８、ＶＰ１０和ＶＰ１１则不能诱生中和抗体。其中ＶＰ５的抗血清中和效价最高,因此,ＶＰ６极可能是病毒多肽中的主要中和抗原。     

不同月龄婴儿接种DTP后血清中百日咳抗体水平的观测

本文对比观察了２１３例２月龄、３月龄婴儿接种ＤＴＰ后百日咳抗体水平的变化,探讨了母传抗体对免后抗体增长的影响。结果表明２月龄、３月龄婴儿ＤＴＰ免疫后１个月和３个月血清中百日咳抗体达保护水平的百分率无显著性差异（ｘ￣２＝０．０３６,ｐ＞０．９;ｘ￣２＝０．３２７,ｐ＞０．５）,免后１个月抗体ＧＭＴ无显著性差异（ｔ＝０．１７,ｐ＞０．５）,免后３个月抗体ＧＭＴ３月龄组高于２月龄组（ｔ＝２．２２,ｐ＜０．０５）。我们还发现免前抗体水平与免后１个月ＧＭＴ虽有负相关（ｒ＝—０,７５４）的倾向,但总体上对抑制免后抗体应答不明显,因而建议将儿童ＤＴＰ基础免疫的起始月龄提前至２月龄进行。     

新疆呼图壁盐化草甸群落的DCA, CCA及DCCA分析

 本文应用DCA、CCA及DCCA排序技术对新疆呼图壁盐化草甸群落进行了分析。分析中选取了地下水位、粘土层出现深度、粘土层厚度、地下水pH值及地下水矿化度5个环境因子;同时为了分析空间格局对植被分异影响的大小,建立了样地空间坐标矩阵。结果表明：地下水位和地下水的pH值是引起植被分异的两个主要因素,空间格局对植被分异的影响大于环境因子对植被分异的影响。     

无花果蛋白酶在阴离子交换树脂上的固定化

无花果蛋白酶通过８％戊二醛活化载体,共价结合到聚苯乙烯阴离子交换树脂ＧＭ２０１上,固定化作用在ｐＨ７．７,酶浓度０．８ｍｇ／ｇ树脂,４℃下进行６ｈ。得到的固定化酶表观Ｋ_ｍ值（酪蛋白,１．１１×１０~（－４）ｍｏｌ／Ｌ）小于溶液酶Ｋ_ｍ值（１．９６×１０~（－４）ｍｏｌ／Ｌ）;固定化酶活性在ｐＨ６～８保持稳定,溶液酶最适ｐＨ为７．２;固定化酶最适温度由溶液酶的５０～６０℃移至３７℃;固定化酶２５℃保持７ｄ,重复水解酪蛋白７次后,保留８３．３％活性。固定化酶对酪蛋白水解度达４７．５％,对大豆球蛋白达１１．６％。     

Differential effects of corticotropin-releasing hormone on central dopaminergic and noradrenergic neurons

Corticotropin-releasing hormone (CRH) has been shown to be a central mediator for most, if not all, stress-induced responses. Since stressful stimuli may decrease hypothalamic tuberoinfundibular and tuberohypophysial dopaminergic neuronal activities, we aimed to determine whether CRH is involved. Using central administration of various doses of ovine CRH (oCRH; 1, 3 and 10 µg/rat) into the lateral cerebroventricle of either male or female rats, the neurochemical changes in various parts of the central nervous system, including the hypothalamus, were determined by high-performance liquid chromatography at various times after the injection (30, 60, 120 and 240 min). The concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxy-4-hydroxy-phenylethyleneglycol (MHPG), two major metabolites of dopamine and norepinephrine, respectively, in discrete brain regions were used as indices for catecholaminergic neuron activity. Plasma corticosterone levels increased significantly after all doses of oCRH and at all time points studied. oCRH also exerted significant stimulatory effects on noradrenergic neuron terminals in the frontal cortex, and on dopaminergic neuron terminals in the nucleus accumbens, hypothalamic paraventricular and periventricular nuclei, and intermediate pituitary lobe. Dopaminergic neuron terminals in the median eminence and the neural lobe of the pituitary, however, were not affected. There was no major difference in the responses between male and female rats. We conclude that CRH has a differential effect on central catecholaminergic neurons.     

A novel inhibitor of cyclin-Cdk activity detected in transforming growth factor beta-arrested epithelial cells.

Transforming growth factor beta (TGF-beta) is a potent inhibitor of epithelial cell growth. Cyclins E and A in association with Cdk2 have been shown to play a role in the G1-to-S phase transition in mammalian cells. We have studied the effects of TGF-beta-mediated growth arrest on G1/S cyclins E and A. Inhibition of cyclin A-associated kinase by TGF-beta is primarily due to a decrease in cyclin A mRNA and protein. By contrast, while TGF-beta inhibits accumulation of cyclin E mRNA, the reduction in cyclin E protein is minimal. Instead, we find that the activation of cyclin E-associated kinase that normally accompanies the G1-to-S phase transition is inhibited. A novel inhibitor of cyclin-Cdk complexes was detected in TGF-beta-treated cell lysates. Inhibition is mediated by a heat-stable protein that targets both Cdk2 and Cdc2 kinases. In G0-arrested cells, a similar inhibitor of Cdk2 kinase was detected. These data suggest the existence of an inhibitor of cyclin-dependent kinases induced under different conditions to mediate antiproliferative responses.