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损伤应答
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  damage response
     Which indicated the interaction between CGB and MT2 was related with the oxidation damage to the DNA damage response.
     以上研究我们得出如下结论:首次发现胞红蛋白与金属蛋白Ⅱ存在相互作用; 胞红蛋白与金属蛋白Ⅱ相互作用与机体氧化损伤应答密切相关。
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     Over 11 known Fanconi anemia gene products are involved in DNA damage response pathway.
     目前已发现11种FA蛋白参与形成了一种DNA损伤应答途径。
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  “损伤应答”译为未确定词的双语例句
     Three different morphological characteristics of hepatic cells were observed during the acute (0-3 h after reperfusion), subacute (3-24 h after reperfusion) and earlier repair phase (24-96 h after reperfusion) of liver responses to I/R: severe cell degeneration, cell atrophy and cell proliferation.
     结论 肝缺血 3 0min再灌注期机体可能通过下述基因调控途径影响细胞损伤应答反应 :①Fas死亡基因与bcl- 2存活基因的双重调控 ;
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     Results Of 63 differentially expressed genes in quadrangle C including DNA damage respon se, repair & recombination related genes, 6 DNA repair related genes were up regulated, 12 were down regulated.
     在有DNA损伤应答、修复、重组相关基因的C区中 ,表达上调的基因有 2 1个 ,与修复相关的有 6个 ; 表达下调的有 4 4个 ,与修复相关的则有 12个。
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     Objective To establish a model of injury to primarily cultured spinal cord neurons,mimicking the neuronal injury after complete transactional spinal cord trauma,for the sake of exploring changes in expression of an immediately-early gene,c-jun,in central nervous system injury.
     目的 建立一个模拟脊髓全横断损伤后脊髓组分———原代培养的脊髓神经元损伤的模型。 探讨中枢神经损伤后损伤应答基因c jun的表达及变化。
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     TRF2 not only functions on modeling telomere morphology, controlling telomere length and protecting 3' G-rich overhang, but also regulates the stability of genome.
     此外,TRF2在细胞DNA损伤应答过程中可能发挥重要作用。
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  相似匹配句对
     Duodenal injuries
     十二指肠损伤
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     Role of Immune Response in the Secondary Injury after Brain Trauma in Rats
     免疫应答在大鼠脑组织创伤后继发性损伤中的作用
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     The Damage Effects Due to Lightning
     雷电的损伤效应
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     Biological Response Modifier, BRM
     生物应答调节剂
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     The effect on ovarian function of mice immunized with PZP and 17D 3mAb ZP was more obvious than that with Ab 2.Conclusion:The results suggested that TH1type immune response was related to the autoimmune ovarian oophoritis.
     结论 :自身免疫性卵巢功能损伤与TH1型免疫应答有关。
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  damage response
HeLa cells were irradiated to drive a DNA damage response, and subjected to sequential chromosomal immunoprecipitation with antibodies against the large subunit of RNA polymerase II and against p53.
      
DNA-damage response network at the crossroads of cell-cycle checkpoints, cellular senescence and apoptosis
      
Our studies suggest that regulation of apoptosis in the breast tumor cell may require modulation of signaling events other than or in addition to the p53-dependent DNA damage response.
      
Inhibitors of poly (ADP-ribose) polymerase and p53 protected oligodendrocytes against cell death induced by homocysteine and amyloid β-peptide, consistent with a role for a DNA-damage response in the cell death process.
      
This implies that other aspects of the damage response are being induced by the jasmonic acid treatment and having a negative effect on subsequent herbivory.
      
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Objective To investigate characteristics of time and areas of liver cell apoptosis and features of gene expression during ischemia/reperfusion and explore their significance. Methods Based on determination of survival rate and pathomorphological changes in 40 SD rats reperfused for 3, 6 and 24 h after hepatic ischemia for 0, 30, 45 and 60 min, we observed pattern of TUNEL cells, indices of G 0-G 1 phase, proliferated and apoptotic cells with flow cytometry, the cell morphological changes with electron microscopy,...

Objective To investigate characteristics of time and areas of liver cell apoptosis and features of gene expression during ischemia/reperfusion and explore their significance. Methods Based on determination of survival rate and pathomorphological changes in 40 SD rats reperfused for 3, 6 and 24 h after hepatic ischemia for 0, 30, 45 and 60 min, we observed pattern of TUNEL cells, indices of G 0-G 1 phase, proliferated and apoptotic cells with flow cytometry, the cell morphological changes with electron microscopy, expression of p53, bcl-2 mRNA with in situ hybridization and Fas protein and PCNA with immunohistochemistry in 100 rats reperfused for 0, 0.5, 1, 3, 6, 12, 24, 48, 72 and 96 h after hepatic ischemia for 30 min. Results Apoptotic phenomenon was mainly found in the group of hepatic ischemia for 30 min. In this group, TUNEL cells appeared near the vascular system at 6 h and developed for all hepatic labor 12 h after the reperfusion. Subsequently, the increase of index of apoptotic hepatocytes was firstly seen 3 h after reperfusion. The expression pattern of Fas was the earliest and strongest. Fas protein and p53 mRNA also expressed firstly near the vascular system between 1 to 3 h and expressed widely from 3 to 72 h. The expression pattern of PCNA appeared from 3 to 96 h. The index of proliferated cells was significantly increased at the 12 h. bcl-2 mRNA also expressed from 3 to 96 h after reperfusion and but it was weaker. Three different morphological characteristics of hepatic cells were observed during the acute (0-3 h after reperfusion), subacute (3-24 h after reperfusion) and earlier repair phase (24-96 h after reperfusion) of liver responses to I/R: severe cell degeneration, cell atrophy and cell proliferation. Conclusion Apoptosis and proliferation are early events after hepatic ischemia/reperfusion and the specific features of this injury. They are probably related to regulating balances of cell death/survival, apoptosis/proliferation and cell cycle transition after hepatic ischemia/reperfusion injury.

目的 探讨肝缺血再灌注肝细胞凋亡发生的时空分布、基因表达特点及意义。方法 在观察SD大鼠 (n =4 0 )肝缺血 0 ,3 0 ,4 5 ,60min再灌注 3 ,6,2 4h存活率及病理形态基础上 ,重点观察大鼠 (n =10 0 )全肝血流阻断 3 0min再灌注 0 ,0 5 ,1,3 ,6,12 ,2 4 ,4 8,72 ,96h凋亡细胞分布 (原位末端标记术 ,TUNEL) ,G0 ~G1期细胞、凋亡细胞、增殖细胞指数分布 (流式细胞术 ) ,肝细胞显微及超微结构(光镜、电镜技术 ) ,Fas蛋白、PCNA蛋白 (免疫组化 )及p5 3、bcl- 2基因mRNA表达 (原位杂交 )。结果 缺血 3 0min组多见细胞凋亡 ,细胞应答反应主要为三期 :①急性期 :再灌注 0 .5hFas蛋白首先在血管周围高表达 ;②亚急期 ( 3~ 2 4h) :TUNEL阳性细胞在血管周围高分布 ,并向周围扩展 ;病理形态可见严重变性、细胞皱缩、细胞增殖三种变化 ;G1期细胞数大量减少 ,凋亡峰逐渐升高 ,12h后出现增殖峰 ,相关基因表达增强 ;③恢复早期 ( 2 4~ 96h) :G1期细胞指数回升 ,凋亡...

目的 探讨肝缺血再灌注肝细胞凋亡发生的时空分布、基因表达特点及意义。方法 在观察SD大鼠 (n =4 0 )肝缺血 0 ,3 0 ,4 5 ,60min再灌注 3 ,6,2 4h存活率及病理形态基础上 ,重点观察大鼠 (n =10 0 )全肝血流阻断 3 0min再灌注 0 ,0 5 ,1,3 ,6,12 ,2 4 ,4 8,72 ,96h凋亡细胞分布 (原位末端标记术 ,TUNEL) ,G0 ~G1期细胞、凋亡细胞、增殖细胞指数分布 (流式细胞术 ) ,肝细胞显微及超微结构(光镜、电镜技术 ) ,Fas蛋白、PCNA蛋白 (免疫组化 )及p5 3、bcl- 2基因mRNA表达 (原位杂交 )。结果 缺血 3 0min组多见细胞凋亡 ,细胞应答反应主要为三期 :①急性期 :再灌注 0 .5hFas蛋白首先在血管周围高表达 ;②亚急期 ( 3~ 2 4h) :TUNEL阳性细胞在血管周围高分布 ,并向周围扩展 ;病理形态可见严重变性、细胞皱缩、细胞增殖三种变化 ;G1期细胞数大量减少 ,凋亡峰逐渐升高 ,12h后出现增殖峰 ,相关基因表达增强 ;③恢复早期 ( 2 4~ 96h) :G1期细胞指数回升 ,凋亡峰和增殖峰持续并缓慢下降 ;相关基因表达陆续减弱。结论 肝缺血 3 0min再灌注期机体可能通过下述基因调控途径影响细胞损伤应答反应 :①Fas死亡基因与bcl- 2存活基因的双重调控 ;②细胞凋亡与增殖双重调控 ;③经p5 3基因实现的细胞周期调控。

Objective To compare gene expression gene profilie of nasopharyngeal c arcinoma(NPC) tissue with that of normal nasopharyngeal tissues by cDNA array a nd to discuss possible functions of DNA repair related genes in NPC tissue. Methods After hybridization of atlas human cancer cDNA expression array 7742 1 , atlas hybridization results were analyzed by Atlas Image 1.01a software package. Using RT PCR was used to confirm the results. Results Of 63 differentially expressed genes in quadrangle C...

Objective To compare gene expression gene profilie of nasopharyngeal c arcinoma(NPC) tissue with that of normal nasopharyngeal tissues by cDNA array a nd to discuss possible functions of DNA repair related genes in NPC tissue. Methods After hybridization of atlas human cancer cDNA expression array 7742 1 , atlas hybridization results were analyzed by Atlas Image 1.01a software package. Using RT PCR was used to confirm the results. Results Of 63 differentially expressed genes in quadrangle C including DNA damage respon se, repair & recombination related genes, 6 DNA repair related genes were up regulated, 12 were down regulated. Conclusion DNA repair related genes may be involved in patho physiological process of nas opharyngeal carcinoma.

目的 用cDNA阵谱比较鼻咽癌组织及正常组织的基因表达谱 ,研究鼻咽癌组织内修复相关基因的表达差异。方法 AtlashumancancercDNAexpressionarray 774 2 1杂交后 ,用AtlasImage1.0 1a分析滤膜杂交结果 ,RT PCR反应验证滤膜杂交结果。结果 在 5 88个肿瘤相关基因中 ,共有134个基因表达上调 ,88个基因表达下调。在有DNA损伤应答、修复、重组相关基因的C区中 ,表达上调的基因有 2 1个 ,与修复相关的有 6个 ;表达下调的有 4 4个 ,与修复相关的则有 12个。结论DNA修复相关基因的改变可能在鼻咽癌病理生理过程中起一定作用。

Objective To explore the cellular response of human senescent diploid fibroblasts (2BS) to the DNA damage caused by methyl methanesulfonate (MMS). Methods After MMS treatment, the changes of cell morphology, cell proliferation and all phases in cell cycle of the senescent cells (>55 population doubling, PD) were compared with those of the young cells(<30 PD), and the changes at transcriptional level of gadd45, p21 and p53 genes were also measured at different population doubling(PD) by Northern blot. Meanwhile,...

Objective To explore the cellular response of human senescent diploid fibroblasts (2BS) to the DNA damage caused by methyl methanesulfonate (MMS). Methods After MMS treatment, the changes of cell morphology, cell proliferation and all phases in cell cycle of the senescent cells (>55 population doubling, PD) were compared with those of the young cells(<30 PD), and the changes at transcriptional level of gadd45, p21 and p53 genes were also measured at different population doubling(PD) by Northern blot. Meanwhile, the repair competency was examined by the unscheduled DNA synthesis(UDS) and the single cell gel electrophoresis(SCGE). Results After DNA damage induced by MMS, the senescent cells showed less changes in morphology, growth curve and cell cycle than the young cells. The inducible gene expression of gadd45, p21 and p53 in senescent cells declined as compared with that of the young cells. At the same time, the DNA self repair function of senescent 2BS cells significantly declined as compared with that of the young ones ( P <0 01). Conclusions The cellular responsive ability of the senescent 2BS cells to DNA damage caused by MMS declined. The decline of DNA self repair function may also be related to the inducible gene expression by DNA injury.

目的 观察衰老的人胚肺二倍体成纤维细胞 (2BS)对烷化剂甲磺酸甲酯 (MMS)诱导的DNA损伤的应答。 方法 以体外培养的不同代龄的人胚肺 2BS为对象 ,以MMS诱导DNA损伤 ,以年轻细胞 (<30代 )为对照 ,观察衰老细胞 (>5 5代 )经MMS处理后的细胞形态、增殖特性、细胞周期的改变 ,并分别检测 gadd4 5、p2 1和p5 3等基因转录水平的表达变化 ,同时以非程序性DNA合成(UDS)和单细胞凝胶电泳试验测定DNA修复能力。 结果 经MMS诱导DNA损伤后 ,衰老细胞的细胞形态、生长曲线和细胞周期的变化均不及年轻细胞明显 ;gadd4 5、p2 1和 p5 3等基因的可诱导性表达均低于年轻细胞 ;同时 ,衰老细胞总的及单个细胞的修复能力较年轻细胞明显下降。 结论 衰老 2BS细胞对MMS诱导的DNA损伤后的细胞应答变化能力下降 ,且其修复能力的减退可能与基因的可诱导性表达下降有关。

 
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