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阿霉素

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Methods Following exposure to gradual increased concentration of ADM, the cell line HepG2 was induced to form a multidrug resistant subcell line (HepG2/ADM).

通过梯度增加培养液中阿霉素的浓度,长期筛选培养,建立肝癌HepG2/ADM耐药细胞株。

There were five groups in the examination of cellular levelK562 group,K562/A02 group,K562+ADM group,K562/A02+ADM group and K562/A02+TTD+ADM group).The non-cytotoxicity doses to cell lines K562 and K562/A02 of TTD were got by MTT assay.Using flow cytometry (FCM assay to examine the intracellular ADM concentration.There were three groups in the examination of genic,zymologic and protein levelsK562 group,K562/A02 group and K562/A02+TTD group).The mRNA expression of MDR was measured by fluorescent quantitative reverse transcriptase polymerase chain reaction(RT-PCR.The expression levels of glutathione-S-transferase and topoisomerase Ⅱ were determined by immunohistochemical technique.

细胞水平检测实验分5组(K562组、K562/A02组、K562+ADM组、K562/A02+ADM组和K562/A02+TTD+ADM组),采用MTT法检测TTD对K562和K562/A02细胞的非细胞毒性剂量,流式细胞术检测细胞内阿霉素的浓度,基因、酶学、蛋白水平检测实验分3组(K562组、K562/A02组和K562/A02+TTD组),采用RT-PCR法检测mdr1 mRNA的表达,免疫细胞化学方法检测谷胱甘肽S转移酶π和拓扑异构酶Ⅱ的表达水平,Western-blotting法检测P-糖蛋白和bcl-2表达。

The cell cycle and apoptosis and the expression of P-pg, bcl-2, P53 in the MG63 and MG63/R cell lines were analyzed by flow cytometry. Results The resistance index of the MG63/R cells to cisplatin was 83.557±4.841. The cells also had resistance to doxorubicin, vincristin, methotrexate and cyclophosphamide. Disordered structure of the MG63/R cells was observed through microscopy. The cells appeared in triangle, polygon and polynucleation. The increase of granular endoplasmic reticulums and apophyses was observed through transmission electron microscopy. The proliferation ability of MG63/R increased significantly, with a low apoptosis index.

结果 经顺铂186d的诱导,建立了MG63/R,其对顺铂的耐药指数为83.557±4.841,对阿霉素、长春新碱、氨甲基蝶吟、环磷酰氨亦产生不同程度的交叉耐药;光镜观察可见MG63/R细胞排列不规则,形态呈三角形、多角形及多核现象;透射电镜显示MG63/R细胞表面突起增加,粗面内质网丰富;细胞周期分析显示细胞增殖能力明显增加而细胞凋亡明显降低;MG63/R细胞 P-pg、bcl-2阳性表达较MG63细胞明显增加,P53表达则明显降低。

Methods The disorder of myofibrils,swelling of mitochondria with broken cristae and decrease of cytochrome C oxidase activity caused by ADR were prevented by the administration of teapol.

结果 阿霉素所造成的大鼠心肌细胞肌原纤维排列紊乱、线粒体肿胀,嵴断裂及细胞色素C氧化酶活性降低,可明显地被抗氧化剂天力体保所防止。

Methods The neonatal Wistar rats cardiomyocytes cultured for 72 hours were divided into three groups:normal control group,ADR damnified groups and groups of Salviae Miltiorrhizae Injection for little, middle and higher doses.

目的 观察丹参注射液(Salviae Miltiorrhizae injections SMI)对阿霉素(Adriamycin,ADR)诱导大鼠心肌细胞损伤的保护作用并探讨其作用机制。

According to microscopic examination, we found that the pharmorubicin diffuses through the matrix of the bone cement.

对治疗前后骨水泥块切片研究发现,骨水泥中表阿霉素的释放是以弥散方式进行的。

In terms of the ststistical limitation of DNA intercalating acceptors got from experiments, three-pase-pair DNA acceptors suitable for the intercalators of Adriamycin and its derivatives have been built and refined.

根据DNA嵌插受体的统计性实验约束,优化产生了适用于阿霉素类抗癌药的三碱基对DNA片段的理论嵌插受体模型。

Results: To build CHF model with injecting Adriamycin into the rats' abdomen can injure their myocardia. It can decrease MMP-3 expression and increase TIMP-1 expression obviously.

结果:利用阿霉素的心肌毒性可以成功复制CHF的动物模型;利心I号能够显著降低CHF大鼠心肌组织MMP-3表达而升高TIMP-1的表达。

Under pathologicexamination, little tumor cells, obvious fibroses outside, calcifying necroses inside andapoptosis cells were found in the tumor tissue of all treatment groups, especially in I-125seeds combined with ADM group.

体内治疗实验①各实验组裸鼠均成活,阿霉素+~(125)I组肿瘤直径平均缩小至0.36cm(P<0.05);②白血球水平变化不明显;大体标本观察,心、肾、肝脏无明显改变。

FDA a roves doxorubicin, an anti-tumor antibiotic fromStreptomyces bacteria.

1974年, FDA批准一种来源于链球菌的抗肿瘤抗生素-阿霉素

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