牦牛血清蛋白质的标定及应用

采用3种测定方法分析野牦牛、家牦牛和犏牛血清蛋白质的各组分含量、分子量及水解氨基酸、游离氨基酸的含量,比较其异同点,结果发现:野、家牦牛具有基本相似的血清蛋白质组成,而γ-球蛋白占总球蛋白的比值、个别蛋白带分子量和氨基酸组成含量等方面有某些显著的差异,表明青海牦牛血清蛋白质发生了不同于野牦牛的遗传变异,在牦牛品种培育中利用两个参数(γ-球蛋白占总球蛋白的比值和血清中必需氨基酸与非必需氨基酸之比值)作为选种标志有定向育种效果。     

栗黄枯叶蛾核型多角体病毒病毒粒子的拉曼光谱研究

通过对栗黄枯叶蛾核型多角体病毒TvNPV(Trabala vishnou Nuclear Po-lyhedrosis Virus)的病毒粒子的拉曼光谱研究,讨论了它的蛋白质分子空间构象.其蛋白质主要为β折叠结构、α螺旋结构以及少量无规卷曲(其中包括β回折)结构.蛋白质中酪氨酸残基多数暴露于分子表面,少数埋藏在分子内部;色氨酸残基大多埋藏在疏水环境中.蛋白质分子侧链C—C—S—S—C—C构型为反式—扭曲—反式.     

超氧阴离子自由基(O_2~-)导致红细胞膜蛋白交联作用的机理探讨

用邻苯三酚在碱性条件下自氧化产生的超氧阴离子自由基(O_2~-处理人红细胞膜导致膜蛋白交联形成高分子聚合物(HMP).用一定量的超氧化物歧化酶(SOD)预处理红细胞膜,HMP明显减少.用巯基抑制剂N-乙基马来酰胺(NEM)预处理红细胞膜,则HMP几乎消失.用特异性标记巯基的荧光探针N-(3-芘)马来酰胺(N-[3-P]NEM)来研究经不同浓度邻苯三酚处理的红细胞膜的荧光强度.结果表明,随着邻苯三酚浓度增高,荧光强度相应降低.上述结果提示,O_2~-可能主要是通过氧化巯基导致膜蛋白交联并形成HMP.     

蜉蝣稚虫蛋白质和酯酶同工酶的研究

本文报道了南京宽基蜉(Choroterpes nanjingensis You et al.)、扁蜉蝣(Heptaniasp.)和细蜉蝣(Caenis sp.)等三种不同科稚虫的全稚虫匀浆蛋白质等电点聚焦与酯酶同工酶的研究。结果表明:三种蜉蝣稚虫的蛋白质和酯酶同工酶的带型均有一定的差异.蛋白质和酯酶同工酶都以细蜉蝣的带数最多,扁蜉蝣次之,南京宽基蜉最少,而后两者带数较接近。     

一种预测蛋白质二级结构的简便方法

以“广义摆动假说”为理论基础,从基因密码子的第二位碱基入手,把氨基酸——“词”简并成核苷酸——“语言”,可直接预测蛋白质的二级结构,从对一些蛋白质的预测结果可见,准确度与Chou-Fasman法相近。     

小麦籽粒中蛋白质和氨基酸含量的遗传分析

采用6×6完全双列杂交设计,对小麦籽粒中蛋白质及16种氨基酸含量进行了遗传分析。结果表明:所研究的17个性状杂交F_1普遍存在杂种优势,以表现负向超亲优势的比例最大,其次为正、负部分显性。各性状间的遗传力有很大差异,广义遗传力变幅为54.49～86.25％,狭义遗传力变幅为17.77～68.18％。除缬氨酸、蛋氨酸和丙苯氨酸外,其它各性状的杂种F_1与双亲平均值均有显著的正相关。所有性状的一般配合力和特殊配合力都极显著,并且一般配合力的作用大于特殊配合力的作用。蛋白质含量的一般配合力与大多数氨基酸含量的一般配合力有显著的相关。     

东方簇盾吸虫蛋白质和同工酶电泳研究

本文用浓度梯度电泳技术对东方簇盾吸虫(Lophotapis orientalis)的蛋白质进行了分析,测定了成虫糖蛋白、脂蛋白和纯蛋白的相对迁移率、分子量和相对含量;全蛋白共27条区带,分子量范围为10～300千道尔顿。同时,还对该吸虫的20种同工酶进行了电泳分析,根据18种同工酶的25个基因座位资料,计算出其多态性为0.68,群体平均杂合性为0.7209,说明东方簇盾吸虫自然群体中的遗传变异较大,具较大的进化潜力。     

Alzheimer's disease: fundamental and therapeutic aspects

Alzheimer's disease is the most common type of progressive and debilitating dementia affecting aged people. In some early — as well as late-onset familial cases, a genetic linkage with chromosomes 14, 21 (early-onset) or 19 (late-onset) has been indicated. Furthermore, a direct or indirect role has been attributed to normal or structurally altered amyloid -protein (concentrated in senile plaques) and/or excessively phosphorylated tau protein (located in neurofibrillary tangles). Degeneration of cholinergic neurons and concomitant impairment of cortical and hippocampal neurotransmission lead to cognitive and memory deficits. Several compounds are being tested in attempts to prevent and/or cure Alzheimer's disease, including tacrine, which has very modest efficacy in a sub-group of patients, and new acetylcholinesterase inhibitors. Pilot experiments have also been launched using nerve growth factor (NGF) to prevent or stabilize the processes of cholinergic pathway degeneration. Alternatively, antioxidants, free radical scavengers and/or non steroidal anti-inflammatory agents may be screened as potential therapies for neurodegenerative diseases induced by multiple endogenous and/or exogenous factors. The recent use of transgenic mice, in parallel with other genetic, biochemical and neurobiological systems, in vivo and/or in vitro (cell cultures), should accelerate the discovery and development of specific drugs for the treatment of Alzheimer's disease.     

Genetic and molecular approaches to synthesis and action of the yeast killer toxin

Summary The K1 killer toxin ofSaccharomyces cerevisiae is a secreted, virally-coded protein lethal to sensitive yeasts. Killer yeasts are immune to the toxin they produce. This killer system has been extensively examined from genetic and molecular perspectives. Here we review the biology of killer yeasts, and examine the synthesis and action of the protein toxin and the immunity component. We summarise the structure of the toxin precursor gene and its protein products, outline the proteolytic processing of the toxin subunits from the precursor, and their passage through the yeast secretory pathway. We then discuss the mode of action of the toxin, its lectin-like interaction with a cell wall glucan, and its probable role in forming channels in the yeast plasma membrane. In addition we describe models of how a toxin precursor species functions as the immunity component, probably by interfering with channel formation. We conclude with a review of the functional domains of the toxin structural gene as determined by site-directed mutagenesis. This work has identified regions associated with glucan binding, toxin activity, and immunity.