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人类肺腺癌
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  human lung adenocarcinoma
     The Experimental Study of p73 Gene on Angiogenesis in Human Lung Adenocarcinoma
     p73基因对人类肺腺癌血管生成影响的实验研究
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     In this dissertation, the effect of different fluence LPLI on human lung adenocarcinoma cells (ASTC-a-1) growth was analyzed using Cell Counting Kit-8;
     本论文主要利用Cell CountingKit-8测定细胞存活率的方法研究了不同剂量激光照射对人类肺腺癌细胞(ASTC-a-1)生长的影响;
短句来源
     Effect of Thalidomide on the Expressions of Vascular Endothelial Growth Factor in Human Lung Adenocarcinoma Cell Line
     反应停对人类肺腺癌细胞系血管内皮生长因子表达影响
短句来源
     Objective: To study the effect of p73 gene overexpression on angiogenesis in human lung adenocarcinoma and the difference function between the p73 variants. Then find a new way for NSCLC gene therapy.
     目的:了解高表达p73基因在人类肺腺癌血管生成方面的作用,以及p73基因不同变异体之间功能的差异,并且为非小细胞肺癌的基因治疗提供一种新的方法。
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  “人类肺腺癌”译为未确定词的双语例句
     Objective It is to discuss the role of different concentration and different times benzo(a)pyrene (BaP) on Heat shock proteins 70 (HSP70) expression of lung adenocarcinoma cell in vitro of mankind in chsomosome damage and apoptosis.
     目的 探讨不同浓度苯并[a]芘(BaP)作用不同时间时,体外人类肺腺癌细胞热休克蛋白70 (HSP70 )表达在染色体损伤和细胞凋亡中的作用。
短句来源
     Methods The roles of different concentration and 6 h BaP on HSP70 expression of lung adenocarcinoma cell A549 in vitro of mankind, apoptosis and chromosome damage were respectively studied through Western-blot, Annexin V-FITC apoptosis kit and cytokinesis-blocked micronucleus (CBMN) test.
     方法 用Westernblot和AnnexinV -FITCapoptosis凋亡试剂盒以及松胞素B阻断核质分裂微核法分别研究了BaP不同浓度作用6h体外人类肺腺癌A5 4 9细胞HSP70的表达、细胞凋亡和染色体的损伤。
短句来源
     Conclusion The cytotoxicity resulted by BaP at low concentration and short time mainly shows at inducing cytogenetic matter damage, and apoptosis is mainly induced by BaP at high concentration, high HSP70 expression can protect mankind lung adenocarcinoma cell chromosome damage and apoptosis induced by BaP.
     结论 低浓度、短时间作用BaP的细胞毒性主要表现为对细胞遗传物质的损伤,细胞凋亡主要在高浓度的BaP诱导下发生,高表达的HSP70可以保护BaP致人类肺腺癌细胞染色体的损伤和凋亡。
短句来源
     Methods :The effects of BaP on HSP70 expression and chromosome damage were detected by Western-blot and cytokinesis-blocked micronucleus (CBMN) test respectively and apoptotic cells were assessed by Annexin V-FITC staining and necrotic cells by propidium iodide (PI) staining using flow cytometry on cultured human adenocarcinoma A549 under different concentration (0,1.25,2.5,5.0 and 10μmol/L) BaP.
     方法:用Westernblot和AnnexinV FITCapoptosis凋亡试剂盒以及松胞素B阻断核质分裂微核法分别研究了BaP不同浓度( 0 ,1 2 5 ,2 5 ,5 0 ,10 μmol/L)作用6h体外人类肺腺癌A5 49细胞HSP70的表达、细胞凋亡和染色体的损伤。
短句来源
     Conclusion :BaP resulted in the cytotoxicity such as inducing chromosome damage and stimulating apoptosis,but not apoptosis at low concentration of BaP,BaP inhibited HSP70 expression and the induced expression of HSP70 can protect chromosome damage against BaP.
     结论:低浓度、短时间作用BaP的细胞毒性主要表现为对细胞遗传物质的损伤,细胞凋亡主要在高浓度的BaP诱导下发生,高表达的HSP70可以保护BaP致人类肺腺癌细胞染色体的损伤和凋亡
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  相似匹配句对
     The Experimental Study of p73 Gene on Angiogenesis in Human Lung Adenocarcinoma
     p73基因对人类腺癌血管生成影响的实验研究
短句来源
     Morphometrical Study of CEA in Adenocarcinoma of Lung
     腺癌癌胚抗原计量学的研究
短句来源
     The Risk Factors of Female Lung Adenocarcinoma
     女性腺癌危险因素分析
短句来源
     Effect of Thalidomide on the Expressions of Vascular Endothelial Growth Factor in Human Lung Adenocarcinoma Cell Line
     反应停对人类腺癌细胞系血管内皮生长因子表达影响
短句来源
     The tropical rain-forest is the lungs of our Earth, and is the common wealth of mankind.
     热带雨林是地球的,是人类的共同时富。
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  human lung adenocarcinoma
Arachidonic Acid Metabolism in Growth Control of A549 Human Lung Adenocarcinoma Cells
      
The role of individual eicosanoids of the arachidonic acid (AA) cascade in the growth control of A549 human lung adenocarcinoma cells has been studied.
      
They exhibit similar phototoxicities on the cells of A549 human lung adenocarcinoma, which are 40- and 100-fold higher than those of chlorin p6 and the clinically used Photogem, respectively, and are not toxic in the absence of light irradiation.
      
Selective gene therapy for human lung adenocarcinoma by tumor-specific expression of herpes simplex virus thymidine kinase gene
      
Alteration of membrane lipid biophysical properties and resistance of human lung adenocarcinoma A549 cells to cisplatin
      
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In order to establish a better animalmodel of pulmonary adenocarcinoma for la-boratory study, 30 Kunming mice were in-jected with 0.6% MNNG solution subcuta-neously(1.2mg/once, total amount 14.4mg/mouse) weekly for 12 times (20 mice wereinjected with distilled water for controls).Within 4-6 weeks after the beginning ofthe experiment, 4 tested mice (13.3%) and4 in controls (20%) died spontaneously, notumor was found. In the 12th week, all 26tested mice were sacrificed; the incidence oflung tumor was 92.3% (24/26);...

In order to establish a better animalmodel of pulmonary adenocarcinoma for la-boratory study, 30 Kunming mice were in-jected with 0.6% MNNG solution subcuta-neously(1.2mg/once, total amount 14.4mg/mouse) weekly for 12 times (20 mice wereinjected with distilled water for controls).Within 4-6 weeks after the beginning ofthe experiment, 4 tested mice (13.3%) and4 in controls (20%) died spontaneously, notumor was found. In the 12th week, all 26tested mice were sacrificed; the incidence oflung tumor was 92.3% (24/26); and notumor in other organs was found. Whenthe controls were examined at the end ofthe 20th week, no tumor was found. Under microscopy, the incidence of pul-monary adenoma was 92.3% (24/26); ade-noma with malignant change 53.8% (14/26);pulmonary adenocarcinoma 53.8% (14/26)and malignant lung tumor 69.2% (18/26).One hundred and four tumor nodules werestudied, the percentage of adenoma, ade-noma with malignant change and adenocar-cinoma was 41.3%, 30.8%, 27.9% respec-tively.Three histologic types of adenocarci-noma were observed, no squamous cellcarcinoma was found. By AB/PAS staining,acid mucopolysaccharide was found in thecells of the normal bronchiolar epitheliumand papillary adenocarcinoma, which wassimilar to human pulmonary adenocarcinomaderived from bronchiolo-alveolar epithelialcells. The result showed that MNNG couldinduce lung tumor in Kunming mice, andthe incidence of tumor and the organotropywere high. The inductive period of tumorwas short, the spontaneous death rate ofanimals was low. This mathod might pro-vide a better animal model for the study ofhuman lung adenocarcinoma.

用0.6%甲基硝基亚硝基胍(MNNG)0.2ml皮下注射雌性昆明种小鼠,每周1次,共12次,总用药量为14.4mg/只。结果:肉眼下肺肿瘤发生率为92.3%(24/26);镜下腺瘤发生率为92.3%(24/26),腺瘤恶变率为53.8%(14/26),腺癌发生率为53.8%(14/26),肺恶性肿瘤发生率为69.2%(18/26),未见其它器官肿瘤。表明MNNG具有诱发昆明种小鼠肺肿瘤的作用;应用本法可为人类肺腺癌的研究提供一种较好的动物模型。

To explore the effects of thalidomide on the expressions of vasc ular growth factors in parental and cisplatin_resistant human lung adenocarcinom a cell line A549 and A549 .Methods:RT_PCR and Immunohistochemistry were used to detect mRNA and protein expression of VEGF in A549 and A549 .Results:From t he 1st to 5 th day after treatment with physiological concentration of thalidomi de(6 mg/L),VEGF mRNA expression levels in A549 were significant higher than that before treatment.VEGF mRNA expression levels...

To explore the effects of thalidomide on the expressions of vasc ular growth factors in parental and cisplatin_resistant human lung adenocarcinom a cell line A549 and A549 .Methods:RT_PCR and Immunohistochemistry were used to detect mRNA and protein expression of VEGF in A549 and A549 .Results:From t he 1st to 5 th day after treatment with physiological concentration of thalidomi de(6 mg/L),VEGF mRNA expression levels in A549 were significant higher than that before treatment.VEGF mRNA expression levels in A549 were significant lower. There were significant differences in A549 and A549 among different concentra tion of thalidomide on the 5 th day.The protein expressions were significant coi ncided with the relative VEGF mRNA expression levels in A549 and A549 .Conclus ion:Physiological concentration of thalidomide up_regulated VEGF mRNA expression significantly in A549.But large dose of thalidomide inhibits VEGF expression si gnificantly.Moreover,thalidomide down_regulated VEGF mRNA expression significant ly in A549 .It is dose_independent.The protein expression is significantly coi ncided with the relative VEGF mRNA.

目的 :探讨反应停对亲代与耐顺铂人类肺腺癌细胞系A549 与A549 血管内皮生长因子 (VEGF)表达的影响 ,及在克服肺腺癌顺铂耐药中的作用。方法 :采用RT_PCR和免疫细胞化学方法 ,分别检测经反应停处理前后A549 与A549 VEGFmRNA与蛋白的表达水平。结果 :生理剂量 (6mg/L)反应停处理后第1~5d ,A549 VEGFmRNA表达较处理前显著增加 ,A549 VEGFmRNA表达较处理前显著降低。不同浓度反应停处理后第5d ,A549 与A549 VEGFmRNA表达水平存在显著性差异 ,且蛋白表达与其相应mRNA呈显著正相关。结论 :生理剂量反应停显著上调A549 VEGFmRNA表达 ,但大剂量则抑制其表达 ,同时显著下调A549 VEGFmRNA表达 ,呈剂量依赖性 ,VEGF蛋白表达与mRNA表达量一致。

Objective To establish a human lung adenocarcinoma A549/615-SCID mouse metastatic model. Methods 1×107 A549 cells were implanted into 615-SCID and SCID mice s.c.in the flank region.The morbidity and the tumor growth activity of 615-SCID and SCID mice were compared.Results Both of the strains developed tumor 100% in the injection region,but 615-SCID had a longer latency period and a slower growth rate than SCID.In 615-SCID mice metastasis occured in lung on day 50.Conclusion The 615-SCID mouse is more suitable...

Objective To establish a human lung adenocarcinoma A549/615-SCID mouse metastatic model. Methods 1×107 A549 cells were implanted into 615-SCID and SCID mice s.c.in the flank region.The morbidity and the tumor growth activity of 615-SCID and SCID mice were compared.Results Both of the strains developed tumor 100% in the injection region,but 615-SCID had a longer latency period and a slower growth rate than SCID.In 615-SCID mice metastasis occured in lung on day 50.Conclusion The 615-SCID mouse is more suitable for establishment of human lung cancer metastatic model than SCID.

目的 通过建立A5 4 9人肺腺癌细胞 6 15 SCID小鼠模型 ,评价重度联合免疫缺陷 6 15 SCID小鼠在建立人类肺癌转移模型方面的应用价值。方法 将 1× 10 7A5 4 9细胞接种到 6 15 SCID及SCID小鼠右上肢背部皮下 ,观察成瘤时间、成瘤率、肿瘤生长速度及转移发生。结果 两品系小鼠接种后的成瘤率均为 10 0 % ,6 15 SCID小鼠移植瘤潜伏期较长、生长较缓慢 ,更容易发生转移。结论  6 15 SCID小鼠比SCID小鼠更易于构建人类肺腺癌转移模型 ,对于肺癌转移特性研究具有较大的意义。

 
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