柯萨奇病毒致病毒性心肌炎的细胞凋亡研究

病毒性心肌炎是心血管系统的常见病与多发病。对病毒引起的心肌细胞病理改变及机制的探讨一直是该领域的研究热点。自从科学家报道“凋亡”这种细胞死亡形式以来,为病毒性疾病研究者找到了一条新的研究途径。此后,许多国内外基础医学研究者通过不同方法对细胞受到病毒侵袭后的死亡形式进行研究。目前认为,病毒性心肌炎急性期机体心肌组织的确存在凋亡,     

动物病毒诱导的细胞凋亡及其生理意义

细胞凋亡是指细胞受到内外信号刺激时发生的一种由细胞内部基因控制的主动性死亡行为,是细胞内在的机制,也是决定生物个体发育和组织平衡的一个重要机制,对于抵御外界各种因素干扰起着非常关键的作用。它呈现一系列典型的生化和形态学特征,如染色质凝集、趋边化以及凋亡小体(ap     

铜绿假单胞菌泳动能力相关新基因的筛选及鉴定

从Mu转座突变子文库中经过表型筛选,得到12株泳动(Swimming motility)能力缺陷的突变子,经Mu转座子插入位点的确认、基因克隆及测序分析发现其中10个突变子中Mu转座子分别插入到10个不同的与鞭毛运动和功能相关的基因中,2个突变子中Mu转座子插入到功能未知的新基因(PA2950和PA5022)中,电镜观察结果表明这2个突变株均具有完整的鞭毛,初步推测这2个基因可能是参与鞭毛泳动的能量代谢、趋化作用或信息传递的新基因。     

TUNEL法检测乳酸杆菌对小鼠宫颈鳞癌的凋亡诱导作用

目的应用脱氧核苷酸转移酶介导的dUTP缺口末端标记法———TUNEL法,检测乳酸杆菌(Lactoba-cillus,LB)对小鼠宫颈鳞癌的凋亡诱导作用。方法建立615近交系小鼠U14移植瘤动物模型,并随机分组,TUNEL法检测各组细胞凋亡指数(apoptosis index,AI)。结果乳酸杆菌实验组的AI为(11.25±4.06)%,与对照组的差异有非常显著性(P<0.01),与抗癌药顺铂组的差异有显著性(P<0.05)。结论乳酸杆菌可诱导U14移植瘤细胞凋亡,这可能是其抑癌机制之一。     

Karyotypes in Leucadendron (Proteaceae): evidence of the primitiveness of the genus

Karyotypes of 27 species in Leucadendron are analysed for the first time. New chromosome counts are reported for 15 species, with 2 n  = 26 occurring in all of them. Karyotype analysis indicated that chromosomes of Leucadendron taxa are small in size and have predominantly median to submedian centromeres. The mean sizes of somatic metaphase chromosomes ranged from 1.05 to 2.65 µm. Based on Stebbins' karyotype classification, 1A type was found in L. galpinii , L. muirii , L. orientale , L. platyspermum , L. rubrum , and L. salignum ; 2A type in L. conicum , L. flexuosum , L. laureolum , L. meridianum , L. salicifolium , L. stelligerum , and L. teretifolium ; and 2B type in L. argenteum , L. chamelaea , L. discolor , L. elimense , L. eucalyptifolium , L. floridum , L. gandogeri , L. linifolium , L. loeriense , L. macowanii , L. procerum , L. spissifolium , L. strobilinum , and L. tinctum . These types are the three most symmetrical karyotypes and are considered to be primitive.  © 2006 The Linnean Society of London, Botanical Journal of the Linnean Society , 2006, 151 , 387–394.     

DNAJC10基因在鼻咽癌中的表达及表达下调机制的研究

运用RT-PCR检测候选抑瘤基因DNAJC10在鼻咽癌组织中的表达,运用甲基化特异性PCR(MSPCR)技术、LOH和测序等技术分别检测DNAJC10基因在鼻咽癌组织中的甲基化状况、LOH和启动子突变情况.结果表明,DNAJC10基因在肿瘤组织中较对照慢性鼻咽炎组织表达明显下调(P<0.05).DNAJC10在鼻咽癌中不表现高甲基化,其LOH的缺失率为6.25%,突变率为66.7%.因此,DNAJC10基因的表达下调主要是其遗传改变(LOH和突变)所致.     

重症肌无力小鼠模型的建立

目的建立重症肌无力小鼠模型。方法电鳗乙酰胆碱受体(TnAChR)和完全弗氏佐剂(CFA)混合物免疫C57BL/6J小鼠,经二次加强免疫后,检测肌力、腓肠肌肌电图、膈肌终板电镜、血清抗体水平等指标。结果与对照小鼠相比,发病小鼠表现出肌力减弱的症状,肌电图显示小鼠腓肠肌复合动作电位振幅幅度显著下降,电镜证实神经肌接头处突触后膜变平、皱褶减少、空泡样变性,发病小鼠血清抗体水平明显升高。结论成功建立了重症肌无力小鼠模型,有助于探讨其发病机理及探索治疗自身免疫病新的途径和方法。     

Ribosomal protein S7 regulates arsenite-induced GADD45α expression by attenuating MDM2-mediated GADD45α ubiquitination and degradation

The stress-responding protein, GADD45α, plays important roles in cell cycle checkpoint, DNA repair and apoptosis. In our recent study, we demonstrate that GADD45α undergoes a dynamic ubiquitination and degradation in vivo, which process can be blocked by the cytotoxic reagent, arsenite, resulting in GADD45α accumulation to activate JNKs cell death pathway, thereby revealing a novel mechanism for the cellular GADD45α functional regulation. But the factors involved in GADD45α stability modulations are unidentified. Here, we demonstrated that MDM2 was an E3 ubiquitin ligase for GADD45α. One of MDM2-binding partner, ribosomal protein S7, interacted with and stabilized GADD45α through preventing the ubiquitination and degradation of GADD45α mediated by MDM2. This novel function of S7 is unrelated to p53 but seems to depend on S7/MDM2 interaction, for the S7 mutant lacking MDM2-binding ability lost its function to stabilize GADD45α. Further investigations indicated that arsenite treatment enhanced S7–MDM2 interaction, resulting in attenuation of MDM2-dependent GADD45α ubiquitination and degradation, thereby leading to GADD45α-dependent cell death pathway activation. Silencing S7 expression suppressed GADD45α-dependent cytotoxicity induced by arsenite. Our findings thus identify a novel function of S7 in control of GADD45α stabilization under both basal and stress conditions and its significance in mediating arsenite-induced cellular stress.     

Fatty alcohol production in engineered E. coli expressing Marinobacter fatty acyl-CoA reductases

Although successful production of fatty alcohols in metabolically engineered Escherichia coli with heterologous expression of fatty acyl-CoA reductase has been reported, low biosynthetic efficiency is still a hurdle to be overcome. In this study, we examined the characteristics of two fatty acyl-CoA reductases encoded by Maqu_2220 and Maqu_2507 genes from Marinobacter aquaeolei VT8 on fatty alcohol production in E. coli. Fatty alcohols with diversified carbon chain length were obtained by co-expressing Maqu_2220 with different carbon chain length-specific acyl-ACP thioesterases. Both fatty acyl-CoA reductases displayed broad substrate specificities for C12–C18 fatty acyl chains in vivo. The optimized mutant strain of E. coli carrying the modified tesA gene and fadD gene from E. coli and Maqu_2220 gene from Marinobacter aquaeolei VT8 produced fatty alcohols at a remarkable level of 1.725 g/L under the fermentation condition.