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人腺病毒41型(Ad41)难养研究进展
人肠腺病毒41(Human Adenovirus Type 41,Ad41)属于人腺病毒F组,是引起胃肠炎的病原之一,因而被称为肠腺病毒.由于在体外难于培养,又被称为难养性腺病毒.6%~80%的4岁以下婴幼儿腹泻由该病毒引起~([1]).Flewett等首次在电镜下观察得到Ad41~([2]),De Jung首次成功分离Ad41的病毒株,并将其命名为Tak株~([3]).
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苏州地区急性呼吸道感染儿童中腺病毒感染特点
腺病毒(Adenovims,ADV)是儿童急性呼吸道感染重要病毒病原之一,其明确诊断依赖于实验室的病原学检测.我们运用直接免疫荧光法,对2001年1月-2007年12月苏州地区儿童急性呼吸道感染进行ADV病原学监测,了解近7年来苏州地区儿科急性呼吸道感染中ADV的感染状况.同时2006年起对部分确诊ADV患儿进行人类偏肺病毒(hMPV)混合感染的监测,探讨其病原学特点.
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Our previous study showed that when glutamate receptor (GluR)6 C terminus-containing pep-tide conjugated with the human immunodeficiency virus Tat protein (GluR6)-9c is delivered into hippocampal neurons in a brain ischemic model, the activation of mixed lineage kinase 3 (MLK3) and c-Jun NH2-terminal kinase (JNK) is inhibited via GluR6-postsynaptic density pro-tein 95 (PSD95). In the present study, we investigated whether the recombinant adenovirus (Ad) carrying GluR6c could suppress the assembly of the GluR6-PSD95-MLK3 signaling module and decrease neuronal cell death induced by kainate in hippocampal CA1 subregion. A seizure model in Sprague-Dawley rats was induced by intraperitoneal injections of kainate. The effect of Ad-Glur6-9c on the phosphorylation of JNK, MLK3 and mitogen-activated kinase kinase 7 (MKK7) was observed with western immunoblots and immunohistochemistry. Our findings revealed that overexpression of GluR6c inhibited the interaction of GluR6 with PSD95 and prevented the kainate-induced activation of JNK, MLK3 and MKK7. Furthermore, kainate-mediated neuronal cell death was signiifcantly suppressed by GluR6c. Taken together, GluR6 may play a pivotal role in neuronal cell death.
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1例重组人p53腺病毒注射液联合顺伯、替加氟治疗舌癌的护理
肿瘤是一个全身性疾病,综合治疗已成为共识.继手术、放疗、化疗等治疗方法之后,肿瘤的基因治疗逐步应用并且显示了一定的疗效.2007年3月,我院应用重组人p53腺病毒注射液联合顺伯、替加氟治疗舌癌1例,疗效显著.现报告如下.
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1例重组人p53腺病毒联合化疗治疗复发鼻咽癌病人的护理
p53基因与头颈肿瘤的发生发展关系极为密切[1].重组人p53腺病毒注射剂由腺病毒载体DNA和p53基因两部分组成,可以有效地将p53基因转入肿瘤组织内,刺激机体产生特异性抗肿瘤免疫反应,上调多种抗癌基因和下调多种癌基因的活性,从而瀑布性增强抑癌效应,特异地引起肿瘤细胞程序性死亡,或使肿瘤细胞处于冬眠状态.重组人p53腺病毒注射液瘤内注射结合放疗、化疗治疗头颈部恶性肿瘤,疗效显著[2],但如何对注射部位及周围皮肤进行观察和护理的报道较少.我们使用重组人p53腺病毒联合PF方案治疗复发性鼻咽癌伴颈部淋巴结转移1例,经精心护理,毒副反应轻微,疗效良好.现报道如下.
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急性腺病毒上呼吸道感染患儿血清白细胞介素-6和α1-酸性糖蛋白的测定
腺病毒(adenovirus,ADV)为DNA病毒,是我国儿童呼吸道感染的一种常见病原体,交叉感染发生率达60%-85%,短接触20 min即可致病[1-2],不同地区感染情况存在差异,在北方地区冬春季节有着较高的感染阳性检出率[3-4];白细胞介素-6(Interleukin-6,IL-6)是在炎症反应中具有重要作用的细胞因子,在感染性疾病中发挥着重要作用,α1-酸性糖蛋白(α1-acid glycoprotein,AAG)作为急性时相反应蛋白,已在临床中得到广泛应用.对我院46例急性上呼吸道腺病毒感染患儿进行血清IL-6和AAG的测定,以了解急性上呼吸道腺病毒感染患儿血清IL-6和AAG的改变及评价儿童急性上呼吸道腺病毒感染的特征.
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荷载白介素24的溶瘤腺病毒联合达卡巴嗪对裸鼠黑素瘤的抑制作用
目的 研究荷载白介素24(IL-24)的溶瘤腺病毒ZD55-IL-24联合达卡巴嗪抑制裸鼠黑素瘤的作用.方法 建立裸鼠恶性黑素瘤A375细胞移植瘤模型后,分别给予ZD55-IL-24联合达卡巴嗪、ZD55-IL-24、达卡巴嗪、磷酸盐缓冲液(PBS)干预.Western印迹法检测A375细胞移植瘤组织IL-24、E1A蛋白表达.测量裸鼠肿瘤生长体积.结果 Western印迹结果表明,ZD55-IL-24联合达卡巴嗪作用的裸鼠黑素瘤高效表达IL -24、E1A蛋白.接种30 d后,ZD55-IL-24联合达卡巴嗪组肿瘤平均体积为(2346.5±576.0) mm3,ZD55-IL-24组为(4141.6±1348.2) mm3,达卡巴嗪组为(5230.1±922.8) mm3,PBS组为(7135.1±1002.3)mm3,ZD55-IL-24联合达卡巴嗪组与各组之间差异均有统计学意义(P<0.05).结论 荷载IL-24基因的溶瘤腺病毒ZD55-IL-24联合达卡巴嗪有抑制黑素瘤增殖的作用.
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Objective: To provide a highly efficient adenoviralvector Ad-CMV-hTGFβ1 for the study of gene therapy forreversion of the intervertebral disc degeneration.Methods: A newly developed recombinant adenoviralvector construction system was used in the study. ThecDNA of hTGFβ1 was first subcloned into a shuttle plasmidpShuttle-CMV. The resultant plasmid was linearized bydigesting with restriction endonuclease PmeI, andsubsequently transformed into E.coll. BJ5183 cells with anadenoviral backbone plasmid pAdEasy-1. Recombinantswere selected by kanamycin resistance and confirmed byrestriction endonuclease analysis. Finally, the recombinantplasmid linearized by PmeI was transfected into 293 cells.Recombinant adenoviruses were generated within 2 weeks.Results: The recombinant adenoviral plasmids werecut by BamHI and PacI respectively, and the diagnosticfragments appeared in 0.8% agarose electrophoresis. Theinfected 293 cells showed evident cytopathlc effect (CPE).The productions of PCR confirmed the presence ofrecombinant adenovirus. The expression of hTGFβ1 wasverified by immunohistochemical staining.Conclusions: The successful generation of theadenoviral vector Ad-CMV-hTGFβ1 and the confirmationof the interest gene expression make it possible for theexperimental study of the reversion of the intervertebraldisc degeneration by gene therapy.