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   chang肝细胞 的翻译结果: 查询用时:0.024秒
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chang肝细胞
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  chang liver cells
     Methods The experiment was divided into negative control、empty vector PCXN2 and PCXN2-NS4B.The recombinant plasmid (PCXN2-NS4B) and the empty vector were transfected into Chang liver cells with liposome.
     方法通过脂质体介导法,将空白载体PXCN2及丙型肝炎病毒NS4B重组质粒PCXN2-NS4B引入Chang肝细胞内,并G418筛选作稳定传代,RT-PCR法鉴定质粒成功转染入肝细胞内,免疫细胞化学方法观察细胞内c-myc和ras表达情况。
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  chang cell
     Results Recombinant vector expressing LS, LS 276 and LS-splice repectively could cause the cytoplasm vacuolization both in HepG2 and Chang cell.
     结果 表达LS、LS splice、LS2 76的重组载体转染后均可引起HepG2及Chang肝细胞发生空泡样病变。
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  “chang肝细胞”译为未确定词的双语例句
     Methods The recombinant plasmids of hepatits C virus non--structural protein (PCXN2--NS4B) and mutant-type p52 were detected using immunocytoehemistry.
     方法使用脂质体介导法 ,转染丙型肝炎病毒非结构蛋白重组质粒PCXN2 NS4B及突变型p5 3基因重组质粒P5 3 CX2 2AN3进入Chang肝细胞内 ,并用G4 18筛选获得稳定表达细胞 ,分别采用细胞化学法检测p5 3表达率。
短句来源
     Screening was performed with G418.HCV NS4B mRNA was detected by reversetranscription PCR.
     结果获得具有G418抗性的Chang肝细胞;
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  相似匹配句对
     tubiflorum H.T.Chang & S.Z.
     T. Chang&S.
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     Of late years,steady performance of two sensor hierarchical fusion algorithm with nonfullrate communication was evaluated by Chang K.
     Chang K.
短句来源
     Screening was performed with G418.HCV NS4B mRNA was detected by reversetranscription PCR.
     结果获得具有G418抗性的Chang肝细胞;
短句来源
     Liver Cell Adenoma
     肝细胞腺瘤
短句来源
     The Isolation of Peroxisomes from rat liver
     大鼠肝细胞过氧化物酶体的提取
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  chang liver cells
A normal human liver cell line (Chang liver cells) was selected as the candidate cell line for induction of GST (liver tissues are abundant in GST) by a known chemopreventive agent, oltipraz.
      
A normal human liver cell line (Chang liver cells) or a rodent rat liver cell line (buffalo rat liver cells) was selected as the candidate cell line for induction of QR by a known chemopreventive agent, genistein.
      
Antigenic relationship between Chang liver cells and human hepatocytes
      
It was demonstrated that Chang liver cells (derived from human liver) were more sensitive to the cytotoxic effects of MBZ than the other two cell lines.
      
Inhibition of the proliferation of Chang liver cells by MBZ was detected at a concentration of 0.008 mg/l, a lower concentration than that having a cytotoxic effect.
      
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  chang cell
In addition, when Chang cell cultures were supplemented with soluble MD2, LPS was able to stimulate IL-6 production.
      
Chang cell pellets were solubilized in the two-dimensional lysis buffer described above to a final protein concentration of 1.5 mg/ml.
      
These experiments were repeated on the Chang cell line and we observed identical results.
      


Objective Investigate the effects of non--structural protein NS4B of hepatitis C ivirus on the expression of p53 in the hepatocyte. Methods The recombinant plasmids of hepatits C virus non--structural protein (PCXN2--NS4B) and mutant-type p52 were detected using immunocytoehemistry. Results Compared with controls, the expression of p53 was slightly positive in the vector group and NS4B-transiected group, and significantly positive in the p53-transfected group and both NS4B and p53 -transfected group. Conclusion...

Objective Investigate the effects of non--structural protein NS4B of hepatitis C ivirus on the expression of p53 in the hepatocyte. Methods The recombinant plasmids of hepatits C virus non--structural protein (PCXN2--NS4B) and mutant-type p52 were detected using immunocytoehemistry. Results Compared with controls, the expression of p53 was slightly positive in the vector group and NS4B-transiected group, and significantly positive in the p53-transfected group and both NS4B and p53 -transfected group. Conclusion NS4B might inhibit the expression of the mutant--type p53, or prevent it from entering the nucleus.

目的了解丙型肝炎病毒非结构蛋白NS4B对肝细胞内p5 3表达的影响 ,探讨其在肝癌发生中的作用 ,及其发生机制。方法使用脂质体介导法 ,转染丙型肝炎病毒非结构蛋白重组质粒PCXN2 NS4B及突变型p5 3基因重组质粒P5 3 CX2 2AN3进入Chang肝细胞内 ,并用G4 18筛选获得稳定表达细胞 ,分别采用细胞化学法检测p5 3表达率。设置空白对照组、空白载体组、转染NS4B组 ,转染p5 3组、共转染NS4B及p5 3组。结果空白对照组无p5 3表达 ,空白载体组及转染NS4B组呈弱阳性表达 ,转染p5 3组及共转染组呈阳性表达 ,与空白对照组、空白载体组及转染NS4B组比较有显著差异 ,P <0 .0 1。结论NS4B可能抑制突变型p5 3表达 ,也可能阻止其进入细胞核。

Objective To investigate the pathogenecity of truncated large surface proteingenerated by 458-1308nt spliced variant of HBV genome. Methods Substituted the initial codon of PreS2 and S region from ATG to ACG in full-length (accession number: AY206390, 3215bp) and 458-1308nt spliced variant(accession number AY238972, 2366bp) of HBV DNA by means of site-directed mutagenesis. Amplified the coding region for truncated large surface protein (LS-splice) and amino-terminal 276 amino acids (LS 276 ) using mutated...

Objective To investigate the pathogenecity of truncated large surface proteingenerated by 458-1308nt spliced variant of HBV genome. Methods Substituted the initial codon of PreS2 and S region from ATG to ACG in full-length (accession number: AY206390, 3215bp) and 458-1308nt spliced variant(accession number AY238972, 2366bp) of HBV DNA by means of site-directed mutagenesis. Amplified the coding region for truncated large surface protein (LS-splice) and amino-terminal 276 amino acids (LS 276 ) using mutated 458-1308nt HBV DNA as the template, and amplified the coding region for full-length large surface antigen (LS) using mutated full-length HBV DNA as the template. Cloned the amplified fragment to eukaryotic expression vector pCDNA3.1 /Hyg(-) separately and transfected the recombinant vector to HepG2 cell and Chang cell lines by LipofectAMINE. Detected the cytoplasm vacuolization and apoptosis by routine hematoxylin-eosin staining and FACS respectively. Results Recombinant vector expressing LS, LS 276 and LS-splice repectively could cause the cytoplasm vacuolization both in HepG2 and Chang cell. In addition, LS could induce the apoptosis both in HepG2 and Chang cell, meanwhile, such effects vanished as to LS 276 and LS-splice. Conclusion Truncated large surface protein generated by 458-1308nt spliced variant of HBV genome was liver-pathogenic, and the pathogenesis was correlated with its amino terminal 276 amino acids. This type of spliced variant may be closely related with the pathogenesis of HBV.

目的 研究 4 5 8~ 130 8nt乙型肝炎病毒 (HBV)基因组剪接变异体截短的表面抗原大蛋白 (largesurfaceantigen ,LS)的肝细胞致病性。方法 将 4 5 8~ 130 8nt剪接变异体HBVDNA(基因号为AY2 38972 ,长度为 2 36 6bp)及全长HBVDNA(基因号AY2 0 6 390 ,长度 32 15bp)中PreS2及S起始密码由ATG定点突变为ACG。以突变后的剪接变异体DNA为模板 ,PCR扩增剪接产生的截短LS编码基因(LS splice)及LS氨基端 2 76个氨基酸的编码基因 (LS2 76) ;以突变后的全长HBVDNA为模板 ,PCR扩增全长LS编码基因。将上述DNA片段克隆至pCDNA3.1/Hyg( )真核表达载体。重组载体以脂质体转染HepG2及Chang肝细胞 ,以HE染色观察细胞的空泡病变 ,并以流式细胞仪检测转染细胞的凋亡率。结果 表达LS、LS splice、LS2 76的重组载体转染后均可引起HepG2及Chang肝细胞发生空泡样病变。此外 ,LS可引起HepG2及Chang肝细胞凋亡 ,...

目的 研究 4 5 8~ 130 8nt乙型肝炎病毒 (HBV)基因组剪接变异体截短的表面抗原大蛋白 (largesurfaceantigen ,LS)的肝细胞致病性。方法 将 4 5 8~ 130 8nt剪接变异体HBVDNA(基因号为AY2 38972 ,长度为 2 36 6bp)及全长HBVDNA(基因号AY2 0 6 390 ,长度 32 15bp)中PreS2及S起始密码由ATG定点突变为ACG。以突变后的剪接变异体DNA为模板 ,PCR扩增剪接产生的截短LS编码基因(LS splice)及LS氨基端 2 76个氨基酸的编码基因 (LS2 76) ;以突变后的全长HBVDNA为模板 ,PCR扩增全长LS编码基因。将上述DNA片段克隆至pCDNA3.1/Hyg( )真核表达载体。重组载体以脂质体转染HepG2及Chang肝细胞 ,以HE染色观察细胞的空泡病变 ,并以流式细胞仪检测转染细胞的凋亡率。结果 表达LS、LS splice、LS2 76的重组载体转染后均可引起HepG2及Chang肝细胞发生空泡样病变。此外 ,LS可引起HepG2及Chang肝细胞凋亡 ,而LS2 76、LS splice致肝细胞凋亡作用消失。结论  4 5 8~130 8ntHBV基因组剪接变异体产生的截短LS可致肝细胞病变 ,其作用与其氨基端 2 76个氨基酸有关。该类型HBV基因组剪接变异体在乙型肝炎发生发展中可能具有一定作用

Aim To develop a novel non-viral gene delivery systems lipid-polycation-DNA complexes (LPD) and investigate their transfection efficiencies in vitro. Methods LPD were prepared as follows by first mixing the plasmid DNA and protamine together, then the resulted polyplexes were incubated for 10 min at room temperature, followed by addition of preformed cationic liposomes. The morphology of LPD was observed by transmission electron microscopy. The diameter and surface charge of LPD were measured by photon correlation...

Aim To develop a novel non-viral gene delivery systems lipid-polycation-DNA complexes (LPD) and investigate their transfection efficiencies in vitro. Methods LPD were prepared as follows by first mixing the plasmid DNA and protamine together, then the resulted polyplexes were incubated for 10 min at room temperature, followed by addition of preformed cationic liposomes. The morphology of LPD was observed by transmission electron microscopy. The diameter and surface charge of LPD were measured by photon correlation spectroscopy ( PCS). The nuclease protection ability of LPD was evaluated by agarose gel electrophoresis. Estimation of transfection efficiency was performed by galactosidase assay in Chang, HepG2 and SMMC-7721 cells. Results The average diameter and the zeta potential of LPD were 143. 5 nm and 32. 6 mV, respectively. LPD could protect the plasmid DNA from nuclease degradation after 2 hours incubation at 37 ℃ while the naked DNA degraded rapidly. The average transfection efficiencies were (69 ±6)% , (43 ±7)% and (96. 2 ±1. 8)% in Chang cells, HepG2 cells and SMMC-7721 cells respectively. Conclusion LPD could be prepared easily with small particle sizes and high transfection activities. LPD may be good non-viral vectors for applications in gene delivery.

目的 研究新型非病毒载体脂质-聚阳离子-DNA(LPD)复合物的制备方法及其对体外细胞的转染率。方法 用薄膜-挤压法制备空白阳离子脂质体,与鱼精蛋白-DNA复合物在室温孵育后,得到LPD;用透射电镜观察其形态,用激光粒度仪测定其粒径和zeta电位;LPD与DNA酶I溶液在37℃下孵育不同时间后,用琼脂糖凝胶电泳观察其降解情况;用荧光法测定其包封率;用X-gal染色法考察了LPD对张氏(Chang)肝细胞,HepG2肝癌细胞和SMMC-7721肝癌细胞的转染率。结果 LPD的形态近似于球体,平均粒径为143.5 nm,平均zeta电位为+32.6 mV;37℃下核酸酶作用2 h后,LPD中的DNA几乎无降解;平均包封率为93.42%;LPD对张氏(Chang)肝细胞、HepG2肝癌细胞和SMMC-7721肝癌细胞的转染率分别为(69±6)%,(43±7)%和(96.2±1.8)%。结论 LPD是一种制备工艺简单、体外稳定性好、转染率高,具有应用潜力的非病毒载体系统。

 
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