细胞凋亡的基因调节

现普遍认为细胞凋亡是基因介导的细胞死亡,大量的实验结果表明导致细胞凋亡的基因有ｃｅｄ３,ｃｅｄ４,ｐ５３,ｃ－ｍｙｃ,Ｅ１Ａ以及ＩＣＥ基因等。抑制细胞亡的基因有ｃｅｄ９,ｖ－ａｂ１,ｖ－ｒａｆ,Ｅ１Ｂ,Ｐ３５,ｂｃｌ－２及相关基因等。这些基因在不同的生存因子以及在不同的细胞中,作用效果不尽相同。     

大肠杆菌二硫键异构酶DsbA和脯氨酸异构酶PPIaseA双顺反子表达载体的构建及其在大肠杆菌中的表达

用ＰＣＲ方法获得大肠杆菌二硫键异构酶ＤｓｂＡ的编码基因ｄｓｂＡ和大肠杆菌脯氨酸异构酶ＰＰＩａｓｅＡ的编码基因ｒｏｔ,并将ＤｓｂＡ和ｒｏｔ以双顺反子形式克隆至含有Ｐｔａｃ启动子的表达载体ｐＫＫ２３３－２中。在ＩＰＴＧ的诱导下,ＤｓｂＡ和ＰＰＩａｓｅＡ获得了表达。ＳＤＳ－ＰＡＧＥ和薄层扫描分析表明：ＤｓｂＡ、ＰＰＩａｓｅＡ的表达水平分别为占菌体裂解上清液总蛋白质的４．３２％和４．０６％。     

天门冬糖蛋白的分离纯化及其糖肽腱的研究

冷水浸提中西药天门冬，提取物经丙酮分级，得到ＡＧ－ａ，ＡＧ′－ｂ和ＡＧ′－Ｃ三个级份，ＡＧ－ｃ用ＤＥＡＥ－纤维素柱纯化，得到水洗脱级份ＡＧ－Ｗ和０．５ＮＮａＣｌ洗脱级份ＡＧ－ｃ。凝胶柱层和醋酸纤维薄膜电泳，均表明ＡＧ－ｃ为均一性糖蛋白。红外光谱显示，所有的天门科冬糖蛋白级份均含有乙酰基因，β－消去反应检测，ＡＧ－ｃ中糖和蛋白质间的连接键为Ｏ－型糖肽腱。     

金属离子与生物膜脂双层的络合作用研究（Ⅱ）──Eu~（3＋）和Al~（3＋）对DPPC的核磁共振光谱

研究了金属离子Ｅｕ３＋和ＡｌＵ＋对工人膜ＤＰＰＣ脂双层的络合作用及稳定性的核磁共振谱．实验结果表明，Ｅｕ３＋和Ａｌ们＋对ＤＰＰＣ脂双层头部基因的取向产生不同影响，同时一定浓度的金属离子对于ＤＰＰＣ脂双层的稳定性是有益的。     

高级语音开发器ASD

本文推出一种新型的语音开发器ＡＳＤ（ＡｄｖａｎｃｅｄＳｏｕｎｉｃｓＤｅｖｅｌｏｐｍｅｎｔ－ｄｅｖｉｃｅ），可用于留言电话、公共汽车报站等语音系统的开发。     

缺氧对脑星状细胞GAPDH和β—Actin基因表达的影响

目的：样本ＲＮＡ加样量的差异是影响Ｎｏｒｔｈｅｒｎ杂交ＲＮＡ分析和反转录ＰＣＲ（ＲＴ－ＰＣＲ）半定量分析的重要因素。因５－磷酸甘油醛脱氢酶（ＧＡＰＤＨ）和β肌动蛋白（β－ａｃｔｉｎ）ｍＲＮＡ水平一般相对恒定,常用于基因表达研究时样本加样量的校正。但有报道表明某些因素对ＧＡＰＤＨ和β－ａｃｔｉｎ的ｍＲＮＡ水平有一定影响。脑星状细胞（ＡＣ）是近年来神经科学的研究热点之一,有关其基因的研究得到广泛的重视     

—3位碱基对HBVc基因在昆虫细胞中表达的影响

应用ＰＣＲ定点突变技术,分别扩增出－３位碱基是Ａ或Ｔ的乙肝病毒核心抗原基因ｃ１,ｃ２,平端克隆到自行构建便于ＰＣＲ产物克隆的通用载体ｐＢｌｕｅｏＳ中后,利用经ＰＣＲ引物在ｃ１及ｃ２末端引入的酶切位点,切出ｃ１,ｃ２基因,构建出ｐＸ３－ｃ１和ｐＸ３－ｃ２．在Ｓｆ９细胞中瞬时表达ｃ１,ｃ２基因,乙肝核心抗原放免检测结果表明,两种形式的ｃ基因的表达无明显差异．说明－３位是否为Ａ对ｃ基因在昆虫细胞中的表达量没有影响．     

甘薯储藏蛋白(sporamin)A基因在大肠杆菌中的表达研究

利用基因重组技术,将ＰＣＲ扩增获得的甘薯储藏蛋白Ａ基因的成熟肽编码区序列,插入到高效表达载体ｐＴｒｃＨｉｓＢ中,构建成重组表达质粒ｐＴＨＳＰＯ－Ａ,用限制酶切和ＰＣＲ分析均表明重组质粒与预期结果相符,用ＩＰＴＧ诱导重组质粒转化的大肠杆菌ＴＯＰ１０。菌体总蛋白经１２％ＳＤＳ－ＰＡＧＥ分析,可观察到一个大小为１０ｋＤ的蛋白质带,其分子量比预期值小。     

Bc1-2 基因加强表达对 OA 诱发的细胞编程死亡的效应

ＯＡ能诱发人神经母细胞瘤ＳＫ细胞进行编程死亡．死亡细胞缩小变圆，细胞质凝聚，ＤＮＡ有控降解成约２００ｂｐ左右的片段，且这一过程可由蛋白质合成抑制剂亚胺环己酮（ＣＨＸ）抑制．将编码Ｂｃ１－２全长蛋白质的ｃＤＮＡ植入ｐＸＪ４１ｎｅｏ载体中，使其表达由ＨＣＭＶ病毒启动子控制．形成的顺义（ｐＢｃｌ－２－Ｓ）及反义（ｐＢｃｌ－２－ＡＳ）表达质粒经转染导入ＳＫ细胞中获得稳定转染子，Ｗｅｓｔ－ｅｒｎ印迹表明顺义转染子表达较大量的２６ｋｄＢｃ１－２蛋白，而反义转染子则不表达．增强表达的Ｂｃ１－２基因产物对ＯＡ引ＳＫ细胞编程死亡无抑制效应．     

Ac_2O-PCl_3-S_2Cl_2催化乙酸制备高纯度氯乙酸

以乙酸为原料,采用Ａｃ２Ｏ－ＰＣｌ３－Ｓ２Ｃｌ２为催化剂,进行催化氯化制备高纯度氯乙酸,产品含量≥９８．５％。同时讨论了反应温度,催化剂用量等工艺条件对氯化反应及产品质量的影响。     

Phagocytosis promotes programmed cell death in C. elegans.

In the nematode Caenorhabditis elegans programmed cell death requires the killer genes egl-1, ced-4 and ced-3 (refs 1 and 2), and the engulfment of dying cells requires the genes ced-1, ced-2, ced-5, ced-6, ced-7, ced-10 and ced-12 (refs 3,4,5). Here we show that engulfment promotes programmed cell death. Mutations that cause partial loss of function of killer genes allow the survival of some cells that are programmed to die, and mutations in engulfment genes enhance the frequency of this cell survival. Furthermore, mutations in engulfment genes alone allow the survival and differentiation of some cells that would normally die. Engulfment genes probably act in engulfing cells to promote death, as the expression in engulfing cells of ced-1, which encodes a receptor that recognizes cell corpses, rescues the cell-killing defects of ced-1 mutants. We propose that engulfing cells act to ensure that cells triggered to undergo programmed cell death by the CED-3 caspase die rather than recover after the initial stages of death.     

Caenorhabditis elegans gene ced-9 protects cells from programmed cell death.

The gene ced-9 of the nematode Caenorhabditis elegans acts to protect cells from programmed cell death. A mutation that abnormally activates ced-9 prevents the cell deaths that occur during normal C. elegans development. Conversely, mutations that inactivate ced-9 cause cells that normally live to undergo programmed cell death; these mutations result in embryonic lethality, indicating that ced-9 function is essential for development. The ced-9 gene functions by negatively regulating the activities of other genes that are required for the process of programmed cell death.     

细胞编程性死亡及其生物学意义

细胞编程性死亡(英文编写为PCD)是多细胞生物的自然属性,它按照一定的基因编码在时空上顺次表达使死亡细胞呈现一定的表观现象及生理生化特征。PCD受来自机体内其它细胞信号等内源性因素和药物、物理等外源性因素的调节。PCD是一种主动死亡方式且表现为单细胞性,与病理因素作用下的坏死不同,但又有一定联系。PCD在动、植物体的生长发育和成体新陈代谢中有重要的调节作用,PCD异常是某些疾病发病的重要原因     

Programmed cell death, mitochondria and the plant hypersensitive response.

The plant response to attempted infection by microbial pathogens is often accompanied by rapid cell death in and around the initial infection site, a reaction known as the hypersensitive response. This response is associated with restricted pathogen growth and represents a form of programmed cell death (PCD). Recent pharmacological and molecular studies have provided functional evidence for the conservation of some of the basic regulatory mechanisms underlying the response to pathogens and the activation of PCD in animal and plant systems. In animals, the mitochondrion integrates diverse cellular stress signals and initiates the death execution pathway, and studies indicate a similar involvement for mitochondria in regulating PCD in plants. But many of the cell-death regulators that have been characterized in humans, worms and flies are absent from the Arabidopsis genome, indicating that plants probably use other regulators to control this process.     

Structure of the CED-4-CED-9 complex provides insights into programmed cell death in Caenorhabditis elegans

Interplay among four genes--egl-1, ced-9, ced-4 and ced-3--controls the onset of programmed cell death in the nematode Caenorhabditis elegans. Activation of the cell-killing protease CED-3 requires CED-4. However, CED-4 is constitutively inhibited by CED-9 until its release by EGL-1. Here we report the crystal structure of the CED-4-CED-9 complex at 2.6 A resolution, and a complete reconstitution of the CED-3 activation pathway using homogeneous proteins of CED-4, CED-9 and EGL-1. One molecule of CED-9 binds to an asymmetric dimer of CED-4, but specifically recognizes only one of the two CED-4 molecules. This specific interaction prevents CED-4 from activating CED-3. EGL-1 binding induces pronounced conformational changes in CED-9 that result in the dissociation of the CED-4 dimer from CED-9. The released CED-4 dimer further dimerizes to form a tetramer, which facilitates the autoactivation of CED-3. Together, our studies provide important insights into the regulation of cell death activation in C. elegans.     

植物细胞程序性死亡研究进展

植物细胞程序性死亡普遍存在于植物生长发育及环境相互作用过程中,是由基因调控的、主动的细胞死亡过程。植物PCD已成为当前生物学研究的热点之一。本文概述了植物细胞程序性死亡的形态学、分子生物学特征以及植物PCD在植物发育、环境胁迫、超敏反应中的存在,并就植物PCD的细胞形态学、分子生物学等检测方法以及植物PCD的基因、酶和信号分子的调控进行了综述。     

Timing of plant immune responses by a central circadian regulator

The principal immune mechanism against biotrophic pathogens in plants is the resistance (R)-gene-mediated defence. It was proposed to share components with the broad-spectrum basal defence machinery. However, the underlying molecular mechanism is largely unknown. Here we report the identification of novel genes involved in R-gene-mediated resistance against downy mildew in Arabidopsis and their regulatory control by the circadian regulator, CIRCADIAN CLOCK-ASSOCIATED 1 (CCA1). Numerical clustering based on phenotypes of these gene mutants revealed that programmed cell death (PCD) is the major contributor to resistance. Mutants compromised in the R-gene-mediated PCD were also defective in basal resistance, establishing an interconnection between these two distinct defence mechanisms. Surprisingly, we found that these new defence genes are under circadian control by CCA1, allowing plants to 'anticipate' infection at dawn when the pathogen normally disperses the spores and time immune responses according to the perception of different pathogenic signals upon infection. Temporal control of the defence genes by CCA1 differentiates their involvement in basal and R-gene-mediated defence. Our study has revealed a key functional link between the circadian clock and plant immunity.     

1951—2012年中国降水集中度和 集中期的时空格局

以1978年为分界点,对1978年前后的以周为单位的降水集中度和集中期的时空格局和变化趋势进行研究.结果表明:1)中国的降水集中度首先具有明显南北分异规律,其次在中国北部具有明显东西差异;最后,中国整体降水集中度波动呈现减小趋势,且1978年之前波动较大,1978年之后趋于平稳.2)中国的降水集中期主要集中在一年中的第26—30周左右,并在1978年前后有1~3周不同幅度的滞后和提前,且南方以推迟为主,北方以提前为主;中国整体降水集中期波动呈现微弱减少趋势,且1978年前显著减少,但1978年后显著增加.     

高速光纤通信系统中高阶偏振模色散对NRZ码和RZ码的偏振度的影响

用数值模拟方法研究了高速光纤通信系统中高阶偏振模色散对二种常用的码型的偏振度的影响,并分别考察了去偏振项和偏振相关色散对这二种码型的偏振度的影响,结果表明二阶PMD的二项均对RZ码的DOP的影响较为严重,而对NRZ码而言,影响不明显。模拟结果对高阶PMD补偿起一定的指导作用。     

聚晶金刚石刀具低温冷却铣削Cf/SiC磨损机理

采用聚晶金刚石(PCD)刀具对C_f/SiC陶瓷基复合材料进行干式和低温冷却铣削试验,获得了PCD刀具在干式和低温冷却铣削条件下的前刀面和后刀面磨损形貌,测得了不同铣削长度所对应的主切削力和后刀面磨损量,分析了PCD刀具在不同铣削条件下的磨损机理及寿命可靠性。研究表明:在低温冷却条件下,PCD刀具以磨粒磨损为主要磨损机理,失效表面存在明显沟槽磨损和大量长条状划痕;而在干式铣削条件下,PCD刀具以磨粒磨损和局部氧化磨损为主要磨损机理,失效表面呈现均匀的磨损带;低温冷却使PCD刀具有效使用寿命提高约100%。