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   induced rat hepatocarcinoma 的翻译结果: 查询用时:0.133秒
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induced rat hepatocarcinoma
相关语句
  诱发大鼠肝癌
     STUDY ON GLUTATHIONE S—TRANSFERASE IN EARLY LESION OF INDUCED RAT HEPATOCARCINOMA
     诱发大鼠肝癌早期病变中谷胱甘肽S-转移酶的研究
短句来源
     Changhges of Protein Kinases and Phospholipids in the Early Lesion of Induced Rat Hepatocarcinoma
     诱发大鼠肝癌早期病变中蛋白激酶和磷脂的变化
短句来源
     CHANGES IN THREE KINDS OF PROTEIN KINASE IN DIFFERENT SUBCELLULAR FRACTIONS OF INDUCED RAT HEPATOCARCINOMA
     亚硝胺诱发大鼠肝癌不同细胞组分中三类蛋白激酶的变化
短句来源
     Activities of tyrosine protein kinase(TPK),protein kinase A(PKA)and protein kinase C(PKC) in three different subcellular fractions of the normal rat liver and N-nitrosodiethylamine(DEN)induced rat hepatocarcinoma cells were studied. It was found that in normal rat liver.
     作者研究了正常大鼠肝三个亚细胞组分中酪氨酸蛋白激酶(TPK)、蛋白檄酶A(PKA)和蛋白激酶C(PKC)的活力和亚硝胺诱发大鼠肝癌后这些蛋白激酶的变化。
短句来源
     In human hepatocellular carcinoma,and the late stage of N-nitrosoamine induced rat hepatocarcinoma ,or in human hepatocarcinoma cells after treatment with phorbol ester (PMA), the activities of αl, 6 FuT were increased. Whereas, after the treatment of hepatocarcinoma cells with retinoic acid or dibutyryl cyclic AMP (dbcAMP), the activity of αl, 6FuT was decreased.
     此法在较宽的范围内,产物量与酶量和反应时间成正比.人肝细胞癌、亚硝胺诱发大鼠肝癌后期或用佛波酯(PMA)处理人肝癌细胞后,α1,6FuT增高,而用视黄酸或db-cAMP处理人肝癌细胞后,则该酶活力降低。
短句来源
  “induced rat hepatocarcinoma”译为未确定词的双语例句
     High Performance Liquid Chromatographic Determination of N-acetylglucosam inyltransferase Ⅴ during N-nitrosodiethylamine Induced Rat Hepatocarcinoma
     大鼠诱发肝癌过程中N乙酰氨基葡萄糖转移酶V的高效液相层析测定
短句来源
     Methods Immunohistochemistry was applied for MMP 2 and MMP 9 proprotein during the development of diethylnitrosamine induced rat hepatocarcinoma. The expression of MMP2 and MMP 9 was analyzed with the method of imaging analyzing.
     方法 通过免疫组化 SABC法 ,检测 32只大鼠的肝细胞癌模型标本肝癌及癌旁肝组织 MMP- 2、MMP- 9的表达 ,应用图像分析法进行定量分析 MMP- 2、MMP- 9的变化。
短句来源
  相似匹配句对
     Induced into E.
     将表达载体转化E.
短句来源
     The rat model was induced by alloxan.
     动物模型用四氧嘧啶塑造。
短句来源
     Rat
     鼠(美国电影故事)
短句来源
     Dexamethasone-Induced Insulin-Resistance of Rat
     地塞米松诱导大鼠胰岛素抵抗
短句来源
     with Chemical Hepatocarcinoma
     肝郁脾虚因素刺激对大鼠实验性肝癌发生和鸟氨酸脱羧酶表达的影响
短句来源
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Human transferrin (Tf) was purified from plasms, successively subjected to pronase digestion and hydrazinolysis to release its N-linked sugar chans, which were labeled with fluoresence at the reducing ends by using 2-aminopyridine (PA). followed by removing the sialic acids and galactoses of the outer chains.The prepared fluorescence labeled sugar chain, Gn_2Man_3Gn_2-PA, formed a single peak on high performance liquid chromatography(HPLC)with a BONDAPAK C18 column and its retention time was equal to the standard...

Human transferrin (Tf) was purified from plasms, successively subjected to pronase digestion and hydrazinolysis to release its N-linked sugar chans, which were labeled with fluoresence at the reducing ends by using 2-aminopyridine (PA). followed by removing the sialic acids and galactoses of the outer chains.The prepared fluorescence labeled sugar chain, Gn_2Man_3Gn_2-PA, formed a single peak on high performance liquid chromatography(HPLC)with a BONDAPAK C18 column and its retention time was equal to the standard sugar chain identified by ~1H-NMR. Using this sugar chain as the acceptor, substrste and UDP-GIcNAc as the donor substrate, an assay for the determination of N-acetylglucosaminyltransferase V(GnTV) was established by means of reverse phase HPLC method to separate substrata and product, which was also identified by the standard sugar chain. GnT-V catalyses the addition of N-acetylglucosamine (GIcNAc) through a β 1-6 bond to α 1-6 linked mannose of the pentasaccharide core and to increase the number of antennary of acceptor N-linked sugar chain. In the course of N nitro-sodiethylamine induced rat hepatocarcinoma, the liver GnT-V activity was slightly increased in 4th week from the beginning of induced carcinogenesis,compatible with the proliferative change in morphology,then decreased to normal level in 6tb week. After 10th week, GnT-V was progressively elevated, reached a level which was higher than 20 times above normal in 18-th week and was consistant with the cancerous change of pathological appearance.

提纯人血浆运铁蛋白(Tf),经链霉蛋白酶水解,再经肼解法制备Tf中的二天线N糖链,后者经还原末端的氨基吡啶(PA)化进行荧光标记,再切除外链的唾液酸和半乳糖残基,获得Gn_2Man_3Gn_2-PA荧光标记糖链,以此制备的糖链为受体底物,UDP-GlcNAc为供体底物,用反相HPLC分离底物和产物,建立了N乙耽氨基葡萄糖转移酶V(GnT-V)的测定法。用GnT-V作为肿瘤生化标志物,观察到在二乙基亚硝胺诱发大鼠肝癌的过程中,此酶在诱癌第4周轻度上升,第6周恢复,第10周后持续升高,至18周达正常鼠肝的20倍以上,与病理学上的癌变期相一致。

The effect of two differentiation inducers,retinoic acid(RA) and dibutyrycyclic AMP (db-cAMP),and one proliferation stimulator,phorbol myriacetate(PMA) on the N-acetylglucosaminyltransferase(GnT) V and Ⅲ in SMMC-7721 hepatocarcinoma cell line were studied by using the HPLO methods established in our laboratory.It was found that the untreated conlrol cell showed a slight elevation of GuT-V on the sib day of culture.Afler the treatment with RA or db-cAMP,the activities of GuT-V were decreased day by day,but the...

The effect of two differentiation inducers,retinoic acid(RA) and dibutyrycyclic AMP (db-cAMP),and one proliferation stimulator,phorbol myriacetate(PMA) on the N-acetylglucosaminyltransferase(GnT) V and Ⅲ in SMMC-7721 hepatocarcinoma cell line were studied by using the HPLO methods established in our laboratory.It was found that the untreated conlrol cell showed a slight elevation of GuT-V on the sib day of culture.Afler the treatment with RA or db-cAMP,the activities of GuT-V were decreased day by day,but the GuT-Ⅲ activity was undetectable either in control or treated cells.In contrast,the GuT-V and GuT-Ⅲ activities were both increased after PMA treatment,and the increase of GuT-Ⅲ was earlier and more significant than that of GnT-V.The above results are consistent with our results that RA or db-cAMP decreased and PMA increased the antennary number of N-glycans on SMMC-7721 cell Surface,also coincident with our previous results that GuT-Ⅲ and GnT-V activities were increaed during the course of chemical induced rat hepatocarcinoma.

用我室建立的HPLC法测定分化诱导剂,视黄酸(RA)和双丁酰环磷酸腺苷(db-cAMP),及增殖促进剂,佛波醇肉桂酸乙酸酯(PMA)对SMMC-7721人肝癌细胞N-乙酰氨基葡萄糖转移酶V和III(GnT-V,GnT-III)的影响,发现对照细胞在培养5天后GnT-V略见升高。经RA和db-cAMP处理后,可通天降低GnT-V的活力,但不论对照或处理细胞均未测出GnT-III的活力。PMA可增高GnT-V和GnT-III的活力,对GnT-III的增加较GuT-V发生较早亦较强。以上结果和我室报道的RA或db-cAMP减少而PMA增加SMMC-7721细胞表面N-糖链的天线数相符,也和大鼠化学诱发肝癌中GnT-III和V的增高相一致。

Activities of tyrosine protein kinase(TPK),protein kinase A(PKA)and protein kinase C(PKC) in three different subcellular fractions of the normal rat liver and N-nitrosodiethylamine(DEN)induced rat hepatocarcinoma cells were studied.It was found that in normal rat liver.the activity of TPK was nuelear>membranous>cytosolic;the activity of PKA was cytosolic>membranous>nuclear;and for PKC,membranous>cytosolic>nuclear.In the cytosolic fraction,the activity gradient of the protein kinases were PKC>PKA>TPK.In...

Activities of tyrosine protein kinase(TPK),protein kinase A(PKA)and protein kinase C(PKC) in three different subcellular fractions of the normal rat liver and N-nitrosodiethylamine(DEN)induced rat hepatocarcinoma cells were studied.It was found that in normal rat liver.the activity of TPK was nuelear>membranous>cytosolic;the activity of PKA was cytosolic>membranous>nuclear;and for PKC,membranous>cytosolic>nuclear.In the cytosolic fraction,the activity gradient of the protein kinases were PKC>PKA>TPK.In the membranous fraetion,PKC>TPK>PKA.However,in the nuclear fraction.only TPK activity was high, that of PKA and PKC were very low.After 18 weeks following the date of hepatocarcinogenic induction,the membranous and nuclear TPK,especially the former,markedly elevated. The membranous PKA decreased and nuclear PKA increased.The cytosolie TPK and PKA were not significantly changed.PKC was increased only in the cytosolic fraction but not in the membranous or nuclear.The changes of protein kinases mentioned above were probably due to changes of gene expression, but not the results of intracellular translocation of the enzymes,nor increases of the activators or their precursors as for PKC.

作者研究了正常大鼠肝三个亚细胞组分中酪氨酸蛋白激酶(TPK)、蛋白檄酶A(PKA)和蛋白激酶C(PKC)的活力和亚硝胺诱发大鼠肝癌后这些蛋白激酶的变化。发现正常鼠肝中的TPK的活力为胞核>膜性结构>胞液,PKA为胞液>膜结构>胞核,而PKC则为膜结构>胞液>胞核。在胞液的三类蛋白激酶中,PKC>PKA>TPK;膜结构为PKC>TPK>PKA;而胞核却以TPK特别高,PKA和PKC的含量甚微。DEN诱发大鼠肝癌18周后,膜性和胞核TPK升高,尤以膜性TPK升高明显。但膜性PKA则降低而胞核PKA升高,胞液中TPK和PKA均无明显变化;而PKC和TPK相反,胞液中显著升高,膜性及胞核变化不大。其中PKC的增高不是激活剂含量上升的结果。

 
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