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信号阻断
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  “信号阻断”译为未确定词的双语例句
     Influence of the inhibitor of c-Met on the growth and motility of hepatocellular carcinoma cells
     C-Met信号阻断对肝癌细胞生长和运动能力的影响
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     Meanwhile,the proliferative rate and the intracellular IFN-γ of γδT cells are obviously decreased after blockage of the costimulatory signal induced by 4-1BB/4-1BBL interaction.
     与未阻断组相比,阻断4-1BB/4-1BBL信号,γδT细胞的增殖效应和细胞内IFN-γ的产生均明显下降(P<0.01),与CD28/B7-1信号阻断组相比,差异无显著性(P>0.05)。
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     A Preliminary Research on Mobile Phone Signal Intelligent Interdiction
     手机信号智能阻断初探
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     Signal transduction pathway and blocking strategies of NF-κB
     NF-κB的信号通路与阻断策略
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     Signal transduction of ataxia-telangiectasia
     AT的信号传导
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     New method to realize remote signal measure
     信号遥测方法
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AIM: To study the relationship of thy mo cyte apoptosis with ERK1/2 MAPK pathway and calcium ion concentration, and to f urther discuss possible apoptosis mechanism METHOD:Based on dexamethasone-induced mouse thymocyte apoptosis model,flow cyto metry and transmission electronic microscope analysis were used to determine the model fea sibility, adopted real-time confocal microscope analysis to measure intracellular i changing trend,and utilized SDS-page as well as Western blot anal ysis to ob serve the total...

AIM: To study the relationship of thy mo cyte apoptosis with ERK1/2 MAPK pathway and calcium ion concentration, and to f urther discuss possible apoptosis mechanism METHOD:Based on dexamethasone-induced mouse thymocyte apoptosis model,flow cyto metry and transmission electronic microscope analysis were used to determine the model fea sibility, adopted real-time confocal microscope analysis to measure intracellular i changing trend,and utilized SDS-page as well as Western blot anal ysis to ob serve the total and phosphorylated ERK1/2 contentRESULT: T he apoptosis percentage of RPMI1640 control group was (290±062)%, while by 2 5×10 - 6 mol/L DEX treatment, it was (1270±244)% (3 h),(5355±459)% (6 h),P<001, r espectively The intracellular fluorescence intensity was also significantly e nhance d No obvious total ERK1/2 content change trend was observed in control group, w hile in DEX group, total ERK1/2 decreased and phosphorylated ERK1/2 was signific antly inhibited following time lapse CONCLUSION: By the stimul atio n of DEX, ERK1/2 pathway was inhibited rapidly,and intracellular i was increased quickly We assumed that they had coherently relations hip

目的 :研究胸腺细胞凋亡和ERK1/ 2途径及钙离子内流之间关系 ,以进一步探讨细胞凋亡可能的信号通路机制。方法 :以地塞米松 (DEX)诱导小鼠胸腺细胞凋亡为模型 ,通过流式细胞术和电镜测定模型的稳定性 ,利用激光扫描共聚焦分析测定细胞内 [Ca2 + ] i、SDS PAGE及Westernblot检测细胞内总量和磷酸化ERK1/ 2MAPK。结果 :仅在完全RMPI 1640培养基培养条件下 ,小鼠胸腺细胞自发凋亡百分率为 (2 90±0 62 ) % ,而在 2 5× 10 -6mol/LDEX诱导下 ,3h培养组 (12 70± 2 44) %、6h培养组 (53 55± 4 59) %发生了细胞凋亡 ,细胞内Fluo 3绿色荧光明显增强 ;正常细胞ERK1/ 2总量随时间变化不明显 ,而DEX刺激下 ,ERK1/ 2总量随时间呈递减趋势。结论 :DEX诱导小鼠胸腺细胞凋亡过程中 ,磷酸化ERK1/ 2信号被迅速抑制 ,细胞内 [Ca2 + ] i迅速上升 ,推论磷酸化ERK1/ 2信号阻断与 [Ca2 + ] i有密切关系

AIM To study the mechanism of cadmium induced apoptosis in HEK293 cells. METHODS By utilizing acridine orange/ethidium bromide double fluorescent dye staining to detect the apoptosis and by using MTT to detect the growth inhibition; fluorescent dye Fluo 3/AM and Fura 2/AM were used to test the change in intracellular free calcium; the effect of cadmium on calcineurin activity was measured by a calcineurin test kit. RESULTS Cadmium caused apoptosis and growth inhibition in a concentration dependent...

AIM To study the mechanism of cadmium induced apoptosis in HEK293 cells. METHODS By utilizing acridine orange/ethidium bromide double fluorescent dye staining to detect the apoptosis and by using MTT to detect the growth inhibition; fluorescent dye Fluo 3/AM and Fura 2/AM were used to test the change in intracellular free calcium; the effect of cadmium on calcineurin activity was measured by a calcineurin test kit. RESULTS Cadmium caused apoptosis and growth inhibition in a concentration dependent manner, and initiated a rapid release of Ca 2+ from Ca 2+ pool followed by the influx of the extracellular Ca 2+ in HEK293 cells. The result also revealed that some blockers of the calcium signal prevented cadmium inducing apoptosis and that the activity of calcineurin was enhanced by cadmium. CONCLUSION The activation of calcineurin by increased [Ca 2+ ] i plays an essential role in the process of cadmium induced apoptosis.

目的 研究镉诱导HEK2 93细胞钙稳态失调及其引发细胞凋亡的机制。方法 通过吖啶橙 /溴乙锭双荧光染色法检测细胞凋亡 ,并通过MTT法检测细胞生长抑制 ;以Fluo 3/AM和Fura 2 /AM为探针检测胞浆内游离钙离子浓度 ([Ca2 +]i)的变化 ;使用钙调磷酸酶试剂盒测定镉对钙调磷酸酶活性的影响。结果 镉诱导HEK2 93细胞的凋亡和生长抑制呈浓度依赖性 ;镉通过引发胞内钙库的释放后引起胞外钙离子内流 ;钙信号阻断剂能显著地抑制镉引起的细胞凋亡 ;镉使胞内钙调磷酸酶的活性显著增加。结论  [Ca2 +]i 升高使钙调磷酸酶活化可能在镉引发细胞凋亡过程中起重要作用。

Objective To explore the effects of MAPK antagonist on TPO stimulated UT7 cell proliferation and differentiation, and to elucidate the mechanism of TPO functioning on UT7 cells. Methods EGFP pMSCV and MEK 1 pMSCV MEK 1 plasmids were transferred into UT7 cells. Phosphorelated MEK1 of UT7 cells was examined by Western blot. The proliferation and CD41 expression of UT7 cells transfected with mutant (ser222A) MEK1 or exposed to PD98059 were examined. Results ① 60.73%EGFP positive cells were obtained in retroviral...

Objective To explore the effects of MAPK antagonist on TPO stimulated UT7 cell proliferation and differentiation, and to elucidate the mechanism of TPO functioning on UT7 cells. Methods EGFP pMSCV and MEK 1 pMSCV MEK 1 plasmids were transferred into UT7 cells. Phosphorelated MEK1 of UT7 cells was examined by Western blot. The proliferation and CD41 expression of UT7 cells transfected with mutant (ser222A) MEK1 or exposed to PD98059 were examined. Results ① 60.73%EGFP positive cells were obtained in retroviral vector MEK1 pMSCV transfected UT7cells. ② In different time of TPO stimulating UT7 cells, the level of phosphorelated MEK1 was lower in experiment group than in control group. In experiment group, the level of phosphorelated MEK1 was decreased after stimulated by TPO for 1 hour,and almost disappeared after stimulated for 3 hours ③ The effect of TPO on UT7 cell proliferation was inhibited by PD98059 and the transfected mutation MEK1 gene. The proliferation rate was 98.58% in DMSO control group, 39.00% in PD98059 group (P<0.05), 102.13% in EGFP pMSCV group, and 48.94% in MEK1pMSCV(P<0.05).④ The CD41 expression on UT7 was inhibited by PD98059 and the transfected mutation MEK1 gene. Conclusion Phosphorelation of MEK1 in UT7 cells can be induced by TPO. There was a relationship between the TPO stimulating time and phosphorelation of MEK1. The effects of TPO on UT7 cell proliferation and CD41 expression is mediated by MAPK signal transduction pathway.

目的探索促分裂原活化蛋白激酶(mitogenactivatedproteinkinase,MAPK)信号阻断剂对巨核细胞生长分化因子(TPO)促进UT7细胞增殖和分化作用,阐明TPO对UT7细胞作用的机制。方法将EGFPpMSCV和MEK1pMSCV质粒转染UT7细胞;转染细胞与TPO共培养,Westernblot法检测UT7细胞MEK1(MAPK/Erkkinase1)磷酸化;观察转染突变(Ser222A)的MEK1和MAPK阻断剂PD98059对UT7细胞增殖的影响;采用流式细胞仪检测转染突变(Ser222A)的MEK1和MAPK阻断剂PD98059对UT7细胞表达CD41的影响。结果①重组逆转录病毒载体MEK1pMSCV和EGFPpMSCV转染UT7细胞,EGFP阳性率为60.73%。②TPO不同的作用时间(1h,3h),实验组磷酸化MEK1均低于对照组(P值均<0.05)。③MAPK阻断剂PD98059和外源突变MEK基因阻断了TPO对UT7细胞的增殖作用,DMSO对照组的细胞增殖率为98.58%,PD98059组的细胞增殖率为39.00%(P<0.05);转染EGFPpMSCV组细胞增殖...

目的探索促分裂原活化蛋白激酶(mitogenactivatedproteinkinase,MAPK)信号阻断剂对巨核细胞生长分化因子(TPO)促进UT7细胞增殖和分化作用,阐明TPO对UT7细胞作用的机制。方法将EGFPpMSCV和MEK1pMSCV质粒转染UT7细胞;转染细胞与TPO共培养,Westernblot法检测UT7细胞MEK1(MAPK/Erkkinase1)磷酸化;观察转染突变(Ser222A)的MEK1和MAPK阻断剂PD98059对UT7细胞增殖的影响;采用流式细胞仪检测转染突变(Ser222A)的MEK1和MAPK阻断剂PD98059对UT7细胞表达CD41的影响。结果①重组逆转录病毒载体MEK1pMSCV和EGFPpMSCV转染UT7细胞,EGFP阳性率为60.73%。②TPO不同的作用时间(1h,3h),实验组磷酸化MEK1均低于对照组(P值均<0.05)。③MAPK阻断剂PD98059和外源突变MEK基因阻断了TPO对UT7细胞的增殖作用,DMSO对照组的细胞增殖率为98.58%,PD98059组的细胞增殖率为39.00%(P<0.05);转染EGFPpMSCV组细胞增殖率为102.12%,转染MEK1pMSCV组细胞增殖率为48.93%(P<0.05)。④MAPK阻断剂PD98059组UT7细胞CD41表达(10.27%)明显低于对照组(36.43%),转染MEK1pMSCV组UT7细胞CD41表达(24.03%)明显低于转染EGFPpMSCV组(40.16%)。结论TPO诱导UT7细胞MEK1磷酸化,TPO作用时间与UT7细胞MEK1的磷酸化有明显的关系,MAPK信号转导通路介导TPO促进UT7细胞

 
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