血管内皮舒张因子在氧自由基所致慢性缺氧大鼠肺内动脉收缩中的作用

以黄嘌岭(X)-黄嘌呤氧化酶(XO)系统产生氧自由基,应用微量生物测定法观察慢性缺氧(5000m,10d)对大鼠氧自由基所致肺内动脉收缩的影响及内皮舒张因子(EDRF)在其中的作用。慢性缺氧大鼠有内皮的肺内动脉环对氧自由基的收缩反应较正常环境中的对照动物明显增强,加入EDRF灭活剂还原型血红蛋白(RHb)后更加显著;而加入超氧化物歧化酶(铜锌SOD)后则减弱,甚至消除。反之,不论加入RHb或SOD对氧自由基所致去内皮肺内动脉环的收缩反应均无明显影响。上述结果表明慢性缺氧引起肺内动脉收缩增强与EDRF有密切关系:慢性缺氧可能使EDRF的作用减弱,肺内动脉对氧自由基的反应性增强。表示EDRF及其与氧自由基的关系在慢性缺氧性肺动脉高压的形成中可能具有十分重要的意义。     

MPDA: Microarray pooled DNA analyzer

Background  

Microarray-based pooled DNA experiments that combine the merits of DNA pooling and gene chip technology constitute a pivotal advance in biotechnology. This new technique uses pooled DNA, thereby reducing costs associated with the typing of DNA from numerous individuals. Moreover, use of an oligonucleotide gene chip reduces costs related to processing various DNA segments (e.g., primers, reagents). Thus, the technique provides an overall cost-effective solution for large-scale genomic/genetic research. However, few publicly shared tools are available to systematically analyze the rapidly accumulating volume of whole-genome pooled DNA data.     

三苯基锡,二环己基碳二亚胺和寡霉素对叶绿体CF0与CF1功能联系的影响

作用于H~ —ATP酶复合体质子通道的能量传递抑制剂 TPT、DQCD和 OM能明显抑制叶绿体光合磷酸化反应和膜上 ATP酶活性,减小恒态ΛpH值,加速ΛpH和515 nm吸收衰减。这种在正常叶绿体加速H_(in)~ 经CF_0外流与在残缺膜中阻塞质子外流不一致。TPT等物质是干扰了CF_0与CF_1的构象连接,使 CF_0的质子传导失去CF_1的控制,H_(in)~ 无效漏失或质子逆向转移受影响,从而抑制与质子传导紧密相关的光合磷酸化反应和膜上ATP酶活性。     

大菜粉蝶颗粒体病毒的研究:包含体结合的碱性蛋白酶

本文报道从新疆分离的一株大菜粉蝶(Pieris brassicae)颗粒体病毒(PbGV)包含体上结合有碱性蛋白酶.提取含酶的包含体蛋白,以酪蛋白为底物鉴定表明此酶在pH9.4有最大的酶活力,并定位于“包裹”在病毒粒子套膜外的包含体蛋白中.在高pH时分子皿为26,500的包含体蛋白被酶降解为19,500和15,600道尔顿的两个组分.Hg⁺⁺、Cu⁺⁺仅部分抑制酶活力,可被二异丙基氟磷酸(DFP)完全抑制.75℃以上加热处理可使酶失活,并大大降低病毒包含体的解离.推测此酶是影响PbGV对寄主感染率的因子之一.     

β-蝮蛇毒素对蟾蜍交感神经节突触传递的影响

β-蝮蛇毒素(β-agkistrodotoxin简写β-AgTX)对骨胳肌神经肌肉接头的作用已有实验分析,本文则观察了β-AgTX对蟾蜍交感神经节胆碱能性和非胆碱能性突触电位的作用。结果表明,β-AgTX对胆碱能性快兴奋性突触后电位(f-EPSP)和由压力微量注射ACh产生的ACh电位快成分有可逆性抑制作用,且对f-EPSP的幅值抑制率明显大于对ACh电位的抑制率,方差分析显示β-AgTX对f-EPSP和对ACh电位的抑制之间的差异显著(P<0.01)。β-AgTX对非胆碱能性迟慢兴奋性突触后电位(1s-EPSP)无明显作用。本结果提示β-AgTX可能是通过抑制节前神经末梢释放AGh的突触前机制和占据突触后N型胆碱能受体影响ACh的作用之突触后机制,抑制蟾蜍交感神经节的胆碱能性传递过程。     

Genome-wide networks of amino acid covariances are common among viruses

Coordinated variation among positions in amino acid sequence alignments can reveal genetic dependencies at noncontiguous positions, but methods to assess these interactions are incompletely developed. Previously, we found genome-wide networks of covarying residue positions in the hepatitis C virus genome (R. Aurora, M. J. Donlin, N. A. Cannon, and J. E. Tavis, J. Clin. Invest. 119:225-236, 2009). Here, we asked whether such networks are present in a diverse set of viruses and, if so, what they may imply about viral biology. Viral sequences were obtained for 16 viruses in 13 species from 9 families. The entire viral coding potential for each virus was aligned, all possible amino acid covariances were identified using the observed-minus-expected-squared algorithm at a false-discovery rate of ≤1%, and networks of covariances were assessed using standard methods. Covariances that spanned the viral coding potential were common in all viruses. In all cases, the covariances formed a single network that contained essentially all of the covariances. The hepatitis C virus networks had hub-and-spoke topologies, but all other networks had random topologies with an unusually large number of highly connected nodes. These results indicate that genome-wide networks of genetic associations and the coordinated evolution they imply are very common in viral genomes, that the networks rarely have the hub-and-spoke topology that dominates other biological networks, and that network topologies can vary substantially even within a given viral group. Five examples with hepatitis B virus and poliovirus are presented to illustrate how covariance network analysis can lead to inferences about viral biology.     

KRE genes are required for β‐1,6‐glucan synthesis,maintenance of capsule architecture and cell wall protein anchoring in Cryptococcus neoformans

The polysaccharide β‐1,6‐glucan is a major component of the cell wall of Cryptococcus neoformans, but its function has not been investigated in this fungal pathogen. We have identified and characterized seven genes, belonging to the KRE family, which are putatively involved in β‐1,6‐glucan synthesis. The H99 deletion mutants kre5Δ and kre6Δskn1Δ contained less cell wall β‐1,6‐glucan, grew slowly with an aberrant morphology, were highly sensitive to environmental and chemical stress and were avirulent in a mouse inhalation model of infection. These two mutants displayed alterations in cell wall chitosan and the exopolysaccharide capsule, a primary cryptococcal virulence determinant. The cell wall content of the GPI‐anchored phospholipase B1 (Plb1) enzyme, which is required for cryptococcal cell wall integrity and virulence, was reduced in kre5Δ and kre6Δskn1Δ. Our results indicate that KRE5, KRE6 and SKN1 are involved in β‐1,6‐glucan synthesis, maintenance of cell wall integrity and retention of mannoproteins and known cryptococcal virulence factors in the cell wall of C. neoformans. This study sets the stage for future investigations into the function of this abundant cell wall polymer.     

Defective thymocyte maturation by transgenic expression of a truncated form of the T lymphocyte adapter molecule and Fyn substrate,Sin

Adapter molecules that promote protein-protein interactions play a central role in T lymphocyte differentiation and activation. In this study, we examined the role of the T lymphocyte-expressed adapter protein and Src kinase substrate, Sin, on thymocyte function using transgenic mice expressing an activated, truncated allele of Sin (SinDeltaC). We found that SinDeltaC expression led to reduced numbers of CD4(+) and CD8(+) single-positive cells and reduced thymic cellularity due to increased thymocyte apoptosis. Because the adapter properties of Sin are mediated by tyrosine-based motifs and given that Sin is a substrate for Src tyrosine kinases, we examined the involvement of these kinases in the inhibitory effects of SinDeltaC. We found that in transgenic thymocytes, SinDeltaC was constitutively phosphorylated by the Src kinase Fyn, but not by the related kinase Lck. Using SinDeltaC and fyn(-/-) animals, we also found that the expression of Fyn was required for the inhibitory effect of SinDeltaC on thymocyte apoptosis but not for SinDeltaC-mediated inhibition of T cell maturation. The inhibitory effect of SinDeltaC on thymocyte maturation correlated with defective activation of the mitogen-activated protein kinase extracellular signal-regulated kinase. Our results suggest that the Sin mutant inhibits thymocyte differentiation through Fyn-dependent and -independent mechanisms and that endogenous Sin may be an important regulator of thymocyte development.