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增殖细胞周期
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  “增殖细胞周期”译为未确定词的双语例句
     ③ LXA_4 suppressed the proliferation of Jurkat T cells activated by a-CD3 and a-CD28 antibodies in a dose-dependent manner,as well as the entry of Jurkat T cells from G_1 to S phase and it could decrease the ratio of cells in the S phase,PI values and DNA contents.
     ③LXA4呈剂量依赖性抑制a-CD3和抗CD28单抗(a-CD28)诱导的Jurkat T细胞增殖,细胞周期分析发现LXA4阻止Jurkat T细胞由G1期进入S期,降低S期细胞比例、细胞增殖指数(P I)和DNA含量。
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     Methods We observed the effect of Ang Ⅱ on KFB proliferation,cell cycle and the expression of collagen type Ⅰ on FKB,as well as the inhibiting effect of Emodin with 3H TdR incorporation method,Flowcytometry and immunohistochemical technique respectively.
     方法 用3 H TdR掺入法 ,流式细胞仪及免疫组织化学技术观察了AngⅡ对KFB增殖 ,细胞周期及Ⅰ型胶原表达的影响以及大黄素对AngⅡ作用于KFB的保护效应。
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     Results5-aza-2-deoxycytidine blocks cell cycle at G1 phase increasing apoptosis rate.
     结果 5 氮 2 脱氧胞苷抑制胆管癌细胞QBC939的增殖 ,细胞周期阻滞于G1期 ,凋亡增加。
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     Proliferation of 7721 was inhibited significantly by stable p21 gene transfected and chemotherapeutic drugs in vitro. The progression of cell cycle was arrested from G1 to G2 phase.
     结果经过3~4 w G418筛选得到稳定表达的细胞株,p21基因稳定转染并联合化疗药物应用可明显抑制7721细胞的体外增殖,细胞周期明显改变,细胞从G1期到G2期发生阻滞。
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     RESULTS: 5-Aza-CdR inhibited the proliferation of SW48 cells in a time- and concentration-dependent manner (1-5 d, 0.4-102.4 μmol/L). After 5-Aza-CdR treatment, the number of G0/G1 cells was increased, and 5-Aza-CdR blocked the cell cycle at G1 phase.
     结果:5-氮杂2'-脱氧胞苷在1.6μmol/L就可以明显的抑制SW48结肠腺癌细胞的增殖,细胞周期中处于G0/G1期的细胞明显的增多,阻滞于G1期,凋亡率增高,而且以上作用与药物作用浓度,时间在一定范围内呈正相关.
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     The ALP granul es in the cells stained thicker and th e cells' proliferation cycle shortened.
     细胞增殖周期缩短。
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     The cycle of the adventitions buds multiplication is 35 days every time.
     增殖周期为 35
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     While cell proliferation is carried out through cell cycle.
     细胞增殖是通过细胞周期而实现的 .
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     however,CsA did not influence the proliferation of the MHCC97H cells.
     CsA对细胞周期增殖无影响。
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     rate of S period is rise inproliferation of cell period .
     细胞增殖周期中的S期细胞百分比升高。
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  proliferative cell cycle
Androgen-responsive human prostate cancer cells are able to undergo programmed cell death after androgen ablation (even if the cells are not in the proliferative cell cycle).
      
Abnormalities in the proliferative cell cycle of carcinoma cells and normal cells adjacent to a carcinoma were also found.
      
Therefore, we next examined whether MAPK might also control the proliferative cell cycle in YT cells.
      


The biological features of HL-60 and a11-trans-retinoic acid resistant HL-60 cells(HL-60/RA)were studied in terms of cell proliferation,cyokinetics,chromosome distributionand G-band karyotypes. Results indicated that the two cell lines exhibited similar morpholo-gy and doubling time and similar cytokinetic features,but the cell population in S phase ofHL-60/RA is smaller than that of HL-60 cells. Their chromosome number is around 45 ± 3for HL60 and 45±1for HL-60/RA cells.G-band karyotype analysis showed that...

The biological features of HL-60 and a11-trans-retinoic acid resistant HL-60 cells(HL-60/RA)were studied in terms of cell proliferation,cyokinetics,chromosome distributionand G-band karyotypes. Results indicated that the two cell lines exhibited similar morpholo-gy and doubling time and similar cytokinetic features,but the cell population in S phase ofHL-60/RA is smaller than that of HL-60 cells. Their chromosome number is around 45 ± 3for HL60 and 45±1for HL-60/RA cells.G-band karyotype analysis showed that they haveasimilar diploid karyotype and some abnormal chromosomes.These results demonstratedthat HL-60 and HL-60/RA cell lines were originated from the same source.

对本实验室克隆的人急性早幼粒白血病细胞株HL-60及其抗维甲酸分化亚系HL-60/RA进行细胞增殖、细胞周期、分裂中期细胞染色体分布和G-显带核型分析。发现两者在倍增时间和细胞形态上基本一致。在细胞周期分布上,两者都具有肿瘤细胞的周期分布特征,但HL-60/RA细胞的S期细胞群少于HL-60细胞。两者染色体数量分布比较集中,染色体众数分别为45±3(HL-60)和45±1(HL-60/RA),呈近二倍体核型,G-显带核型分析表明两者都接近正常二倍体核型,都含较多的异常染色体。上述结果说明HL-60和HL-60/RA细胞的遗传学来源一致。

Proliferation, cell cycle, total amount of DNA, area of cell nucleus, as well as epidermal growth factor receptors (EGFR) and expression of oncogene C erbB2 mRNA of Chinese breast cancer cell line (BCaP 37) after being treated with kappa selenocarrageenan were determined by cell culture technique, image cytometry (ICM) and northern blot to explore its anti tumor mechanism. Results revealed 3.0~120 mg/L selenocarrageenan could inhibit proliferation of BCaP 37, with a response of time and dose dependence....

Proliferation, cell cycle, total amount of DNA, area of cell nucleus, as well as epidermal growth factor receptors (EGFR) and expression of oncogene C erbB2 mRNA of Chinese breast cancer cell line (BCaP 37) after being treated with kappa selenocarrageenan were determined by cell culture technique, image cytometry (ICM) and northern blot to explore its anti tumor mechanism. Results revealed 3.0~120 mg/L selenocarrageenan could inhibit proliferation of BCaP 37, with a response of time and dose dependence. The areas of nuclei were significantly lower with ICM in cells treated with 15 or 60 mg/L selenocarrageenan for four days than those in controls ( P <0.01). Levels of EGFR and expression of C erbB2 mRNA were significantly inhibited in cells treated with 60 mg/L selenocarrageenan. It suggests that selenocarrageenan can inhibit proliferation of breast cancer cells through regulation of the levels of EGFR and expresssion of C erbB2 mRNA.

为探讨硒酸酯多糖的抗肿瘤机理,用细胞培养技术、图像细胞分析技术(ICM)和NorthernBlot方法检测,经硒酸酯多糖作用后中国人乳腺癌细胞株(BCaP-37)的增殖、细胞周期、总DNA含量、细胞核面积以及表皮生长因子受体(EGFR)、癌基因C-erbB2mRNA的表达水平。结果发现,硒酸酯多糖(3.0~120mg/L)对BCaP-37增殖有抑制作用,且有时间和剂量依赖效应。经硒酸酯多糖(15mg/L、60mg/L)处理4天的细胞,在图像细胞分析反映细胞增殖能力的指标中,细胞核面积均显著低于对照组。60mg/L硒酸酯多糖处理的细胞其EGFR、C-erbB2mRNA表达水平受到明显抑制。提示硒酸酯多糖能抑制乳腺癌细胞增殖,其机理可能是对EGFR,C-erbB2mRNA表达水平的调节。

It was found in our previous study that oxidative modification LDL(Ox LDL) could stimulate the proliferation of cultured human arterial smooth muscle cells (SMC). Yet, the mechanism responsible for the SMC proliferation induced by Ox LDL is not clear. Proliferating cell nuclear antiger(PCNA), P53 and P27 are the key regulatory factors of cell replication. In order to observe the effects of Ox LDL on cell cycling phase and PCNA, P53,P27 and c erb B 2 expression in SMC, we used the flow cytometric method...

It was found in our previous study that oxidative modification LDL(Ox LDL) could stimulate the proliferation of cultured human arterial smooth muscle cells (SMC). Yet, the mechanism responsible for the SMC proliferation induced by Ox LDL is not clear. Proliferating cell nuclear antiger(PCNA), P53 and P27 are the key regulatory factors of cell replication. In order to observe the effects of Ox LDL on cell cycling phase and PCNA, P53,P27 and c erb B 2 expression in SMC, we used the flow cytometric method in the present study on the proliferation of cultured human SMC induced by Ox LDL. The results showed a relation between the Ox LDL mediated SMC proliferation and the cycling phase shifting. The relative number of S phase cells in the Ox LDL group was higher than that of the control group (22.9% vs 15.7%). Ox LDL mediated SMC proliferation was accompanied with the increasing expression of PCNA. The percentage of specific PCNA positive FITC cells in the Ox LDL group was significantly higher than that of the control group (12 6% vs 6.5%).PMA, an activitor of protein kinase C(PKC), stimulated SMC proliferation and increased the PCNA exression in cultured SMC, while the PKC inhibitor, F109203X, significantly decreased the PCNA expression in SMC(PCNA positive cells 13 4% vs 0.4%).No changes were observed in the expression of P53,P27 and c erb B 2 in the cultured proliferating SMC induced by Ox LDL. In all, the results suggest that the Ox LDL mediated SMC proliferation is related to increasing S Phase Cells and involved in the PCNA expression which might undergo the PKC cellular signal transduction pathway.

应用流式细胞仪对氧化修饰低密度脂蛋白(Ox-LDL)刺激动脉平滑肌细胞(SMC)增殖、细胞周期及增殖细胞核抗原(PCNA)、P53、P27及c-erbB蛋白表达的影响进行了观察。结果发现:Ox-LDL和天然低密度脂蛋白(N-LDL)刺激培养人动脉SMC细胞增殖时其S期细胞百分率增加,且Ox-LDL的作用比N-LDL强,表明Ox-LDL和N-LDL刺激SMC细胞增殖时与S期细胞的增加有关;Ox-LDL刺激SMC增殖的同时PCNA蛋白阳性率增加,而与P53、P27和c-erbB-2蛋白的表达无关。提示PCNA可能参与了Ox-LDL刺激SMC的细胞增殖作用;特异性蛋白激酶C(PKC)抑制剂GF109203X能降低Ox-LDL刺激SMC增殖过程中PCNA的阳性率,表明该细胞增殖过程中PCNA表达的抑制可能与PKC信号传递通路有关。

 
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