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mfc细胞
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  mfc cell
     RESULTS: 1)Over a concentration ranged from 0.1 to 100 mmol/L,AG had inhibited the growth of MFC cell significantly.
     结果 :1)在 0 1~ 10 0mmol/L浓度下 ,AG对MFC细胞生长抑制率与 0 0 0 1mmol/LAG比较 ,P <0 0 1;
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     Methods After the MFC cell line was established by transfection for tumor vaccine, the immune inoculate, the therapeutic of SE effects of the cells being used as vaccine on gastric cancer were investigated in mice.
     方法 将经SE处理的MFC细胞作为异构瘤苗,进行免疫接种及实验治疗观察。
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     METHODS: MTT method was used to examine the effects of AG on the proliferation of MFC cell lines. Nitrite levels in MFC cells supernatants were tested by using the Greiss assay.
     方法 :采用MTT法观察AG在不同时间点对MFC细胞增殖的影响 ,Greiss反应法检测对细胞培养上清液中一氧化氮 (NO)含量的影响。
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  “mfc细胞”译为未确定词的双语例句
     The in vitroinhibiting rate by 100μg/ml, 30μg/ml, 10μg/ml, 3μg/ml and 1μg/ml doses of resveratrol to MFC cells is 100.00%, 71.50%, 50.00%,
     100μg/ml、30μg/ml、10μg/ml、3μg/ml、1μg/ml 的白藜芦醇分别作用于 MFC 细胞,抑瘤率分别为 100.00%、71.50%、50.00%、31.75%、1.33%;
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     The oncogenicity of MFC/4-1BBL cells was obviously lower than that of MFC/ pMKITneo cells and wild-type MFC cells in vivo.
     MFC/4-1BBL细胞在小鼠体内的致瘤性较MFC/pMKITneo细胞和野生型MFC细胞明显降低。
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     Results After 4-1BBL gene transferred MFC cells were injected into 615 mice,it was found that the tumor grew slowly.
     结果4-1BBL基因转染后的胃癌MFC细胞在615小鼠体内成瘤所需的时间长、瘤体的重量轻;
短句来源
     METHODS: P.acnes mobilized F4/80"B220"CDllc+DC precursors werematured in vitro , loaded with MFC cells lysate to create vaccine;
     方法 在体外,将P. acnes动员的F4/80~-B220~-CD11c~+DC前体细胞培养诱导成DC,荷载MFC细胞冻溶抗原,制成DC疫苗;
短句来源
     Conclusion 4-1BBL gene transferred MFC cells can increase immunopotency of the mice bearing tumor,inhabit tumor development and promote tumor cell's apoptosis.
     结论4-1BBL基因导入胃癌MFC细胞后能够提高荷瘤机体的免疫能力、延缓肿瘤的发生、抑制肿瘤的发展、促进肿瘤细胞的凋亡。
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  相似匹配句对
     Cellular Spectro-Analysis
     细胞光谱分析
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     2. basal cell;
     基细胞;
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     RESULTS:The proliferation of MFCs transfercted by B7 1 was suppressed, P <0 05.CONCLUSIONS:The transfer of B7 1 gene can effectively suppress the proliferation of MFC cells.
     结论 :B7 1基因对MFC细胞增殖活性有抑制作用。
短句来源
     The result was compared with the resuilt of MFC trans ferred by blank-carrier NDA3.Results The proliferation of MFC that were transferred by B7-1 was inhibited.
     结果 转染B7- 1基因的MFC细胞增殖活性受到抑制。
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     5 only inhibited spores germination rate of P. expansum, but it could not kill them.
     expansum的MIC和MFC
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hydroxycarbophenyl retiamide(RⅡ)is a new synthetic analogue of retinol,but with lower toxicity than retinoic acid.We studied its induction effects and its effects on some malignant phenotypes of the MFC cell line. The mechanism of these effects was also explored.MFC cells were grown in complete RPMI 1640 medium supplemented with 10-5mol/L R Ⅱ for five passages. By then the cell growth rate slowed down;the rate of 3H-TdR incorporation and the colony-forming capacity of MFC cells decreased;morphologically,the...

hydroxycarbophenyl retiamide(RⅡ)is a new synthetic analogue of retinol,but with lower toxicity than retinoic acid.We studied its induction effects and its effects on some malignant phenotypes of the MFC cell line. The mechanism of these effects was also explored.MFC cells were grown in complete RPMI 1640 medium supplemented with 10-5mol/L R Ⅱ for five passages. By then the cell growth rate slowed down;the rate of 3H-TdR incorporation and the colony-forming capacity of MFC cells decreased;morphologically,the cells became epithelial rather than fibroblastic with various degrees of polarization. Further investigation about the mechanism of these changes was also undergone. First by flow cytometry,it was shown that the R Ⅱ-treated cells were retained in G1 phase. Second,dot blot hybridization showed a decrease of more than 61% of c+myc mRNA and an increase of more than 52% of v-fos mRNA. The major chromosome distribution changed from 54-56 to 46-54 with an increase in diploid.Scanning microscopic examination showed that the R Ⅱ-treated cells were covered by numerous microvilli and pseudopodia with round terminal expansion in contrast to the ruffle protrusions and leaf-like pseudopodia of control cells. All the results suggested that R Ⅱ could reverse some malignant phenotypes of MFC Cells.

采用较其母体维甲酸低毒的维胺酸(RⅡ)诱导小鼠前胃癌(MFC)细胞系分化和细胞恶性表型逆转并分析其可能的机制。实验用10~(-5)mol/LRⅡ 且连续用药5代结果表明,经RⅡ处理后瘤细胞生长受到明显抑制,~3H-TdR的掺入率显著降低,几乎丧失在软琼脂中形成集落的能力。流式细胞仪检测显示,瘤细胞由G1期向S期移行受阻断。此外,药物处理后的前胃癌细胞染色体主流范围下降,并开始出现二倍体细胞,且其形态发生了显著变化。培养中的细胞由上皮细胞型转变为成纤维细胞型。组织学观察发现,瘤细胞密度降低,可见到胞浆丰富区,局部瘤细胞出现极性;扫描电镜观察到RⅡ处理后的MFC细胞微绒毛丰富,丝状伪足的末端常见圆形膨大结构,而对照细胞表面多为折皱状结构,尚可见多量叶状伪足,但未见末端膨大结构。斑点杂交验证RⅡ能降低小鼠MFC细胞c-myc癌基因的表达,诱导v-fos癌基因的高表达。

Newly synthesized retinoic acid derivative-retinamide (RII) was employed as differentiation inducing agent. Cultured tumor cells of epithelial origin were exposed to 10-5mol/L RII for 5 passages. These cells included mouse fore stomach carcinoma (MFC, lung metastatic rate 85%), human nasopharyngeal carcinoma (CNE-2Z, 56%), and clonal variants from CNE-2Z, CNE2L2 (100%) and CNE2L4 (13%) . The results of serial observation were as follows. The growth, clone-forming ability, motility, invasiveness of these tumor...

Newly synthesized retinoic acid derivative-retinamide (RII) was employed as differentiation inducing agent. Cultured tumor cells of epithelial origin were exposed to 10-5mol/L RII for 5 passages. These cells included mouse fore stomach carcinoma (MFC, lung metastatic rate 85%), human nasopharyngeal carcinoma (CNE-2Z, 56%), and clonal variants from CNE-2Z, CNE2L2 (100%) and CNE2L4 (13%) . The results of serial observation were as follows. The growth, clone-forming ability, motility, invasiveness of these tumor cells were obviously inhibted. Their adhesion to fibronectin and laminin was increased. Morphological ultrastructure changes, mainly of surface structure, were also observed. These changes suggested that RII made metastatic cells less aggressive and showed a tendency toward differentiation. After exposured to RII, different changes of oncogene and antioncogene expression of these tumor cells were detected. For example, RE caused expression of nm23in MFC cells, but down regulated (decreased) its expression in CNE2L2 cells and similar changes of rasH, fos, nm23, Rb. Expression were observed for CNE-2Z cells and its clonal variants CNE2L2 CNE2ZL2. RII down regulated both these oncogene and antioncogenes in both CNE-2Z and CNE2L2, but up regulated all of them in CNE2L4. The results indicated that oncogene and antioncogene may play different roles in different tumor cells, the same factor (RII) may lead to different changes of gene-expression in different metastatic tumor cells. So the function of oncogene and antioncogene may be of relativity and may be influenced by multifactors. Our data were mostly from in vitro experiments. It could not be deduced completely to a level as a whole in vivo.

用新研制的维甲酸的衍生物维胺酸作为分化诱导剂。以上皮细胞来源的癌细胞,如小鼠前胃癌细胞MFC(转移率为85%)、人鼻咽癌细胞系CNE-2Z(转移率为56%)、CNE-2Z的亚系克隆株L2(高转移细胞株,转移率100%)以及L4(低转移细胞株,转移率为13%)作为研究对象,用体外培养的癌细胞,以10~(-5)mol/LRⅡ作用5代后,进行了系列观察。实验结果显示,RⅡ作用于MFC细胞和CNE-2Z及其克隆株后,在生长曲线、集落形成、运动性及侵袭性均查见有明显抑制作用,但对FN和LN基质的粘附性均有升高;在形态下也出现明显的微细结构的改变,主要为细胞表面的改变。这些改变说明RⅡ有一定分化诱导作用,使癌细胞有向正常分化的趋向性。对癌基因表达的影响,动物癌细胞及人癌细胞受RⅡ作用后,与转移的相关性有明显矛盾现象。如高转移的MFC细胞对nm~(23)不表达,RⅡ作用后出现表达而CNE-2Z克隆株中高转移细胞中的nm~(23)表达,在RⅡ作用后受到抑制。在CNE-2Z及其克隆株中发现fos,ras~H,nm和Rb4个基因的表达,具有共同特点。RⅡ作用后在母系及高转移的L2细胞株中的表达受抑制,而在...

用新研制的维甲酸的衍生物维胺酸作为分化诱导剂。以上皮细胞来源的癌细胞,如小鼠前胃癌细胞MFC(转移率为85%)、人鼻咽癌细胞系CNE-2Z(转移率为56%)、CNE-2Z的亚系克隆株L2(高转移细胞株,转移率100%)以及L4(低转移细胞株,转移率为13%)作为研究对象,用体外培养的癌细胞,以10~(-5)mol/LRⅡ作用5代后,进行了系列观察。实验结果显示,RⅡ作用于MFC细胞和CNE-2Z及其克隆株后,在生长曲线、集落形成、运动性及侵袭性均查见有明显抑制作用,但对FN和LN基质的粘附性均有升高;在形态下也出现明显的微细结构的改变,主要为细胞表面的改变。这些改变说明RⅡ有一定分化诱导作用,使癌细胞有向正常分化的趋向性。对癌基因表达的影响,动物癌细胞及人癌细胞受RⅡ作用后,与转移的相关性有明显矛盾现象。如高转移的MFC细胞对nm~(23)不表达,RⅡ作用后出现表达而CNE-2Z克隆株中高转移细胞中的nm~(23)表达,在RⅡ作用后受到抑制。在CNE-2Z及其克隆株中发现fos,ras~H,nm和Rb4个基因的表达,具有共同特点。RⅡ作用后在母系及高转移的L2细胞株中的表达受抑制,而在低转移L4细胞株中均呈高表达。提示癌基因、抑癌基因在不同侵袭转移性癌细胞中引起的作用可能不尽相同,同时对RⅡ作用后不同癌细胞中其基因表达也不尽相同。因此我们认为

To investigate the effect of retinoic acid (RA) on immunogenicity of cultured tumor cells,the cultured mouse forestomach carcinoma (MFC) cells treaed by RA were used as an active vaccine to immunize naive or tumorbearing syngeneic mice. The results showed that the naive mice immunized with treated MFC cells,when challenged by se injection of untreated MFC cells,were tumor free and accompanied by increased cell-mediated immunity. Vaccine treatment in the tumorbearing mice could also induce antitumor immunity...

To investigate the effect of retinoic acid (RA) on immunogenicity of cultured tumor cells,the cultured mouse forestomach carcinoma (MFC) cells treaed by RA were used as an active vaccine to immunize naive or tumorbearing syngeneic mice. The results showed that the naive mice immunized with treated MFC cells,when challenged by se injection of untreated MFC cells,were tumor free and accompanied by increased cell-mediated immunity. Vaccine treatment in the tumorbearing mice could also induce antitumor immunity significantly as demonstrated by diminished tumor growth and increased duration of survival after challenge. These data suggest that RA can induce antitumor immunity by modulating the immunogenicity of tceated-cells.

为观察维甲酸对体外培养的肿瘤细胞免疫原性的影响,本实验将经维甲酸处理的小鼠前胃癌(MFC)细胞作为活瘤苗,进行了免疫接种及免疫治疗的实验观察。结果表明免疫接种小鼠可完全排斥再次接种未经药物处理瘤细胞的生长,同时伴有体内细胞免疫反应增强。将该瘤苗用于荷瘤小鼠的免疫治疗,可使肿瘤生长速度减慢,荷瘤生存期明显延长,提示维甲酸可通过改变肿瘤细胞的免疫原性介导机体抗瘤反应。

 
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