排序方式: 共有46条查询结果,搜索用时 8 毫秒
1.
Zhao P Cao J Zhao LJ Qin ZL Ke JS Pan W Ren H Yu JG Qi ZT 《第二军医大学学报》2006,27(5):506-506
The nucleocapsid (N) protein of SARS-coronavirus (SARS-CoV) is the key protein for the formation of the helical nucleocapsid during virion assembly. This protein is believed to be more conserved than other proteins of the virus, such as spike and membrane glycoprotein. In this study, the N protein of SARS-CoV was expressed in Escherichia coli DHSalpha and identified with pooled sera from patients in the convalescence phase of SARS. A plasmid pCI-N, encoding the full-length N gene of SARS-CoV, was constructed. Expression of the N protein was observed in COS1 cells following transfection with pCI-N. The immune responses induced by intramuscular immunization with pCI-N were evaluated in a murine model. Serum anti-N immunoglobutins and splenocytes proliferative responses against N protein were observed in immunized BALB/c mice. The major immunoglobulin G subclass recognizing N protein was immunoglobulin G2a, and stimulated splenocytes secreted high levels of gamma interferon and IL-2 in response to N protein. More importantly, the immunized mice produced strong delayed-type hypersensitivity (DTH) and CD^8+ CTL responses to N protein. 相似文献
2.
TÜTÜNCÜOGLU SARENUR KANTAR MEHMET ÖZTÜRK VESILE YÜNTEN NILGÜN DUMAN YUSUF KULA SABAHATTIN ÖZGÜR TUGRUL 《Pediatrics international》1994,36(6):705-708
Moyamoya disease is a progressive disease which involves the internal carotid arteries and its branches bilaterally. The disease is reported both in adults and in children. Moyamoya disease is frequently seen in Japanese patients having certain human leucocyte antigen (HLA) haplotypes including HLA-Aw24, Bw46 and Bw54. Twin cases are rarely reported in the literature. We hereby present the first Turkish monozygotic twins with moyamoya disease whose HLA haplotypes are A2, A9, B21, Bw22, Bw4, Bw6, Cw3, and DR2, DR4, DRw52, DRw53, Dq7. The patients with advanced disease were given nifedipine and intravenous immunoglobulin (400mg/kg/d for 5 days). During the 11 months of follow-up, the patients were attack free. 相似文献
3.
4.
计算机程序化的初均速法测定双黄连注射液的稳定性 总被引:2,自引:0,他引:2
用计算机程序化的初均速法,测定了双黄连溶液中3种主要成分——绿原酸、黄苓甙、连翘甙的活化能及室温贮存期。该方法简便、快速、结果准确。对临床应用有一定价值。 相似文献
5.
Zhao P Qin ZL Ke JS Lu Y Liu M Pan W Zhao LJ Cao J Qi ZT 《第二军医大学学报》2005,26(10):1167-1167
SARS-CoV isa newly identified coronavirus that causes severe acute respiratory syndrome (SARS). Currently, there is no effective method available for prophylaxis and treatment of SARS-CoVinfections. In the present study, the influence of small interfering RNA (siRNA) on SARS-CoV nucleocapsid (N) protein expression was detected in cultured cells and mouse muscles. Four siRNA expression cassettes driven by mouse U6 promoter targeting SARS-CoV N gene were prepared, and their inhibitory effects on expression of N and enhanced green fluorescence protein (EGFP) fusion protein were observed. 相似文献
6.
目的:观察依达拉奉对深低温保存大鼠断肢再植后出现缺血再灌注损伤时的保护作用。方法:实验于2006-04/11在山东省立医院手足外科低温医学实验室完成。①选取健康成年Wistar大鼠36只,随机分为对照组、冷冻组和依达拉奉组3组,每组12只。②对照组只显露股动静脉而不结扎,其他2组大鼠截断右后肢,对断肢进行深低温冷冻保存处理(自结扎股动静脉至深低温保存约2h)。③1个月后,将冷冻保存的断肢复温、灌洗液洗脱,依达拉奉组所用灌洗液中含依达拉奉0.5mg/kg,行自体肢体回植(自液氮中取出肢体至恢复血供约2h),恢复肢体血供4h后取材,骨骼肌丙二醛含量,超氧化物歧化酶活性以及线粒体ATP酶活性,测定胫前肌含水量,光镜观察各组骨骼肌肌组织的结构改变。结果:36只全部进入结果分析。①骨骼肌丙二醛含量:依达拉奉组低于冷冻组[(10.37±1.25),(15.36±1.28)μmol/g,P<0.01]。②骨骼肌ATP酶和超氧化物歧化酶活性:依达拉奉组高于冷冻组[(206.2±45.2),(72.7±32.5)μkat/g;(83.9±5.2),(70.5±8.0)mkat/g;P均<0.01]。③胫前肌湿/干质量比值:依达拉奉组低于冷冻组(4.89±0.82,6.38±0.63,P<0.01)。④光镜结果显示依达拉奉组骨骼肌损伤程度明显轻于冷冻组。结论:依达拉奉可以降低肢体再灌注后肌肉组织中的氧自由基水平,减轻缺血再灌注对骨骼肌造成的损伤,对缺血再灌注骨骼肌具有保护作用。 相似文献
7.
目的:回顾骨骼肌萎缩细胞分子机制的研究进展,抗萎缩运动模式和药物干预对骨骼肌萎缩的疗效及机制。资料来源:应用计算机检索PubMed数据库1988-03/2007-03相关骨骼肌萎缩的文献,检索词"skeletal muscle,atrophy,exercise,ubiquitin-proteasome,apoptosis",限定文献语言种类为英文。同时计算机检索万方数据库2002-03/2005-05相关骨骼肌萎缩的文献,检索词"骨骼肌,细胞凋亡,运动",限定文章语言种类为中文。资料选择:对资料进行初审,选取包括骨骼肌萎缩的文献,开始查找全文。纳入标准:涉及骨骼肌萎缩的蛋白质泛化、细胞凋亡、抗萎缩运动、药物干预的文章。排除标准:不涉及上述项目。资料提炼:共检索到61篇关于骨骼肌萎缩的文献,最终纳入33篇符合标准的文献。资料综合:骨骼肌萎缩有衰老性、废用性和病理性3种。去神经支配的动物模型有助于从细胞分子水平认识骨骼肌萎缩,蛋白质同化/泛化研究、细胞增殖/凋亡研究从不同角度揭示了骨骼肌萎缩的机制。废用性模型为开发抗萎缩药物和验证抗萎缩运动模式提供了研究平台,但尚缺少一致性结论,运动抵抗/延缓肌肉萎缩的效应体现于结构蛋白基因表达、细胞信号转导、激素、细胞因子等各个层面。在运动抗萎缩治疗中,药物与物理疗法的辅助作用也不可忽略。结论:骨骼肌萎缩的细胞分子机制与蛋白质泛化和细胞凋亡过甚密切相关,运动抵抗/延缓肌肉萎缩的效应体现于相应的细胞分子水平,药物和理疗对骨骼肌萎缩有一定疗效,但机制不明。 相似文献
8.
9.
10.