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凋亡
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  apoptosis
    Relationships between induction of apoptosis by Taxol and CDDP in MCF-7/ADR and Hela cells and apoptosis-related proteins and Ca~(2+)
    紫杉醇及顺铂诱导MCF-7/ADR和Hela细胞调亡及其与凋亡相关蛋白和Ca2+的关系
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    Signal Transduction Mechanisms about the Effects of Simvastatin on Proliferation and Apoptosis in Rat Vascular Smooth Muscle Cell
    Sim vastatin抑制大鼠血管平滑肌细胞增殖诱导凋亡及其相关信号转导机制
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    Role of Voltage-dependent Potassium Channels in Aβ_(25-35)-induced Neuronal Apoptosis and the Relevant Pharmacological Study
    电压依赖性钾通道在Aβ_(25-35)诱导的神经元凋亡中的作用及相关药理学研究
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    Estrogens induce apoptosis in mouse peritoneal macrophages
    雌激素诱导小鼠腹腔巨噬细胞凋亡(英文)
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    Effects of Mifepristone on Proliferation and Apoptosis in Early Pregnant Chorionic Villi
    米非司酮对人早期妊娠绒毛细胞增殖和凋亡的影响
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  “凋亡”译为未确定词的双语例句
    Conclusion Desflurane up-regulates hemeoxygenase-1 through ERK1/2/ P90RSK kinase cel-survival signaling pathway and protects neuron against ischemia-reperfusion injury.
    结论Desflurane通过ERK1/2/P90RSK信号转导通路激活HO-1,在海马神经元缺血/再灌注时抑制了神经元凋亡,保护了神经元。
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    The modulation of propofol on Akt,Bcl-2 and p38MAPK expression is related closely to its cardioprotectice effect.
    结论异丙酚对培养心肌细胞缺氧损伤后的凋亡有显著的保护作用,该作用与其对pAkt、Bcl-2和p38的影响密切相关。
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    The bcl-2 and bax positive cells were counted in the cerebral cortex and corpus striatum.
    凋亡组进行免疫组化染色,分别计数大脑皮质和纹状体区每平方毫米的bcl-2和bax的阳性细胞数。
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    The expression of bcl-2 was promoted and the expression of bax was inhibited by estradiol at 24 h of cerebral ischemia.
    在鼠脑缺血24h雌二醇有效促进了抗凋亡基因bcl-2的表达,抑制了促凋亡基因bax的表达。
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    The relationship between the protective action of caffeine and the level of intracellular calcium
    胞内钙离子浓度与咖啡因抗凋亡作用的关系
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  apoptosis
Prodigiosin also could induce apoptosis of pancreatic cancer cells at low concentration and results in the fragmentation pattern of DNA.
      
All these results demonstrate that prodigiosin can obviously inhibit the proliferation of pancreatic cancer cells H8898 by arresting the cell cycle and inducing apoptosis.
      
Detection of the apoptosis of Jurkat cell using an electrorotation chip
      
The apoptosis of cells is one of the fields that attract increasing attention in biology today.
      
Usually, the cells are treated with chemicals when detecting apoptosis.
      
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sing splenic cells which were obtained from FVA infected BALC/c mice as a model of erythroid cells, we investigated the action of Dex to induce the apoptosis of the cells in the presence of erythropoietin (EPO) an apoptotic inhibitor of developing erythroid cells. The result indicated that the cells were characterized by the occurrences of DNA ladders appeared with the prolonged incubation in a certain range of Dex concentration. Transmissional electron microscopy showed there were karyopyknosis, chromatin...

sing splenic cells which were obtained from FVA infected BALC/c mice as a model of erythroid cells, we investigated the action of Dex to induce the apoptosis of the cells in the presence of erythropoietin (EPO) an apoptotic inhibitor of developing erythroid cells. The result indicated that the cells were characterized by the occurrences of DNA ladders appeared with the prolonged incubation in a certain range of Dex concentration. Transmissional electron microscopy showed there were karyopyknosis, chromatin condensation, dilatation of the perinuclear space, karyorrhexis, cytoplasmic vacuolization and cell fragmentation according to the dose of Dex and the treatment time. These results suggest that Dex could induce apoptosis of developing erythroid cells as in other cells.

以FVA病毒诱导BALB/c小鼠脾细胞形成的红系细胞(erythroidcel)为研究对象,在红系细胞凋亡抑制剂——红细胞生成素(EPO)存在情况下,观察了地塞米松(Dex)对上述细胞凋亡的诱导作用。结果表明,在一定浓度范围内,随着Dex作用时间的延长,细胞逐步凋亡并出现特有的DNA梯形(DNAladder),而且其DNA断裂程度与Dex的作用浓度呈正相关。透射电镜的结果证实,经最适浓度(5×10-5mol/L)Dex处理后,红系细胞出现核固缩,染色质凝聚,核周隙扩大,核破裂,胞浆近膜处出现空泡以及细胞破碎等程度不同的细胞凋亡特征。说明Dex可拮抗EPO的作用,有效地诱导红系细胞凋亡

To further study the relationship between resistance to apoptosis and drugresistance in harringtonine-resistant HL-60 cells(HR20),cyclosporine A(CsA)20,10 μg·ml-1 wasshown to induce the sensitive HL-60 cells to apoptosis,showing a typical DNA“ladder”band.But thesame concentrations of CsA retarded the HR20 cells in G1 phase and could not induce the cells toapoptosis.The cellular daunorubicin accumulation increased when HR20 cells were treated with lowconcentration of CsA and the reversal of drug resistance by...

To further study the relationship between resistance to apoptosis and drugresistance in harringtonine-resistant HL-60 cells(HR20),cyclosporine A(CsA)20,10 μg·ml-1 wasshown to induce the sensitive HL-60 cells to apoptosis,showing a typical DNA“ladder”band.But thesame concentrations of CsA retarded the HR20 cells in G1 phase and could not induce the cells toapoptosis.The cellular daunorubicin accumulation increased when HR20 cells were treated with lowconcentration of CsA and the reversal of drug resistance by CsA was unrelated to the retardation of cellcycle progression,High phosphorylation of about 50 kDa protein occured when HR20 cells weretreated with CsA 10μg·ml-1. The results domonstrate that cyclosporine A retarded theharringtonine resistant HL-60 cells in G1 phase but induced HL-60 cells to apoptosis,and theretardation was unrelated to drug resistance.

进一步研究了抗三尖杉酯碱的HL-60细胞(HR20)抗细胞凋亡的机制及该抗性和抗药性的关系。结果表明,环孢菌素A(CsA)20,10μg·ml ̄(-1)诱导HL-60细胞发生凋亡,而阻断HR20细胞于G_1期,就不能诱导细胞发生凋亡。低浓度的CsA明显增加柔红霉素在HR20细胞内的积聚,其逆转抗药性作用与阻断细胞周期运行无关。CsA10μg·ml ̄(-1)处理HR20细胞,可引起50kDa的蛋白质高度磷酸化。结果提示:环孢菌素A阻断抗三尖杉酯碱的HL-60细胞于G_1期,而诱导敏感的HL-60细胞发生凋亡,其阻断作用与抗药性无关

Dexamethasone(Dex) can effforvely induces apoptosis(or programmed cell death, PCD)in nude mice(NM) spleen cells and inhibits the natural killer oell activity. Our results show that:(1)The chromatin is predomiantly arranged along the nuclear envelope which is entire;(2) Agarose gelelectrophoresis of DNA extracted from NM spleen cells has the typical oligonucleosomal ladder pat-tem ofapoptosis, t3)Dex induas apoptosis ouly when its concentration lies between 10-8 10-6mol/L, (4)Typical apoptosis is induced when...

Dexamethasone(Dex) can effforvely induces apoptosis(or programmed cell death, PCD)in nude mice(NM) spleen cells and inhibits the natural killer oell activity. Our results show that:(1)The chromatin is predomiantly arranged along the nuclear envelope which is entire;(2) Agarose gelelectrophoresis of DNA extracted from NM spleen cells has the typical oligonucleosomal ladder pat-tem ofapoptosis, t3)Dex induas apoptosis ouly when its concentration lies between 10-8 10-6mol/L, (4)Typical apoptosis is induced when the cells were incubated with Dex for 12 hours at37 ℃ ;cell naxosis became predominant after they had been incubated with Dex for 24 hours at37℃ .

本文用地塞米松(DEX)与裸鼠脾细胞共培养,发现DEX能有效地诱导脾细胞(包括NK细胞)发生细胞程序性死亡(programmedcelldeath,PCD)或凋亡(apoptosis)从而明显抑制脾NK细胞活性。结果表明:(1)常规电镜显示细胞收缩但胞膜完整,核凝缩,呈现典型的PCD特征。(2)加入DEX的脾细胞DNA琼脂糖凝胶电泳呈现特征性梯状图谱,片段大小为180bp或其倍数,(3)脾NK细胞活性测定结果表明DEX浓度在10 ̄(-8)~10 ̄(-6)mol/L范围内可诱导出明显的PCD现象发生;而当浓度太低(10 ̄(-10)mol/L)时则PCD现象不明显;当浓度太高(10 ̄(-4)mol/L)时PCD现象也不明显,呈现特有的剂量效应关系。(4)动力学结果显示(根据电镜及电泳图)在DEX作用12h已开始有典型的PCD现象发生,24h后则以坏死现象为主。

 
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