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肝细胞增殖     
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  hepatocyte proliferation
     Results KCCM could promote primary hepatocyte proliferation significantly (A=0.746±0.06) compared with control (A=0.536±0.06, P<0.01).
     结果KCCM能明显促进原代肝细胞增殖(A=0·746±0·06),与对照组(A=0·536±0·06)相比有显著性差异(P<0·01);
短句来源
     The Relationship between Hepatocyte Proliferation, Apoptosis and Revision of Liver Fibrosis and Its Mechanisms
     肝细胞增殖、凋亡与肝纤维化逆转的关系及机制探讨
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     Conclusion: Retrorsine can obviously inhibit hepatocyte proliferation after liver injury and is suitable for liver cell transplantation in rats,while it is the contrary in mice.
     结论:应用retrorsine可明显抑制大鼠肝损伤后肝细胞增殖,适用于建立大鼠肝细胞移植模型; retrorsine对小鼠肝损伤后肝细胞增殖无明显抑制作用,不适用于建立小鼠肝细胞移植模型。
短句来源
     At 0(before administration),1,2,3,4,6,15 d after CCl_(4) administration,the animals were sacrificed and their livers were subjected to H-E staining and Ki-67 antibody immunohistochemistry analysis to evaluate the pathological changes and hepatocyte proliferation.
     末次注射4周后,所有的动物均予CCl4注射(0.5 mg/kg),分别在CCl4注射前即刻(记为0时)、注射后第1、2、3、4、6和15天取动物肝组织样本。 H-E染色检查动物肝组织病理学变化,Ki-67染色检测动物肝细胞增殖情况。
短句来源
     The role of MAPK pathway in primary rat hepatocyte proliferation stimulated by FGF1
     MAPK信号通路在FGF1刺激大鼠原代肝细胞增殖中的作用
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  hepatocyte regeneration
     INHIBITORY EFFECT OF FLUORIDE ON HEPATOCYTE REGENERATION AND ACTIVITY OF LDH STIMULATED BY HSS
     HSS对氟中毒肝细胞增殖与乳酸脱氢酶的影响
短句来源
     Objective:To investigate the effect of somatotrophin on hepatocyte proliferative cell nuclear antigen(PCNA)expression in experimental obstructive jaundice(OJ). To comfirmate the role of somatotrophin in OJ hepatocyte regeneration.
     目的:研究重组人生长激素(rhGH)对实验性梗阻性黄疸(OJ)肝细胞增殖细胞核抗原(PCNA)表达的影响,以证实rhGH促OJ肝细胞再生的作用。
短句来源
  hepatic proliferation
     he rabbit anti rat HPI (hepatic proliferation inhibitor, HPI) antiserum was prepared with the titer of 1:32 (this 90% purity of HPI was purified in our laboratory) as the first antibody to examine the expression of HPI in livers.
     用90%纯度的肝细胞增殖抑制因子(HPI)制备了效价为1∶32的兔抗鼠HPI抗血清,并检测了HPI在肝内的原位表达。
短句来源
     The hepatic proliferation inhibitor (HPI) including the samples of crude, partially purified and purified preparation possesses remarkable inhibitory effect on the proliferation of human hepatoma cells in vitro, and With the increas of HPI purity, its inhibitory activitystrengthened gradually.
     肝细胞增殖抑制因子(Hepaticproliferationinhibitor,HPI)粗制品、半纯品和纯品对体外培养的人肝癌细胞具有显著抑增殖作用,随样品纯度提高抑制活性逐渐增强。
短句来源
     These results suggested that TGFβ 1 expression and its changes in the stages of rat embryo, growth and development, adult and regeneration after SH are favorable to regulating the hepatic proliferation and maintaining the stability of hepatic growth and that the expression of TGFβ 1 during hepatocarcinomagenesis can not prevent the hepatoma happening, its reason mighty be the receptor changes of TGFβ 1 in the surface of hepatoma cells and incapability of activating TGFβ 1 precursor.
     结果提示:大鼠肝在胚胎期、生长发育期、成年期和再生期TGFβ1的表达变化,有利于肝细胞增殖活动的调节和相对稳定。 大鼠肝癌诱发期TGFβ1表达未能阻止肝癌的发生发展,可能与肝癌细胞表面TGFβ1受体的改变和TGFβ1前体激活机制的丧失有关。
短句来源
  hepatocellular proliferation
     Role of vitamin D_3 receptor mRNA in hepatocellular proliferation and hepatocarcinoma
     维生素D_3受体mRNA在肝细胞增殖和肝癌发展中的作用
短句来源
     Effect of growth hormone on hepatocellular proliferation dynamics in rats with severe hepatitis
     生长激素对大鼠重症肝炎肝细胞增殖动力学的影响
短句来源
     Objective To investigate the effect of growth hormone on hepatocellular proliferation dynamics in rats with severe hepatitis.
     目的 探讨生长激素对重症肝炎肝细胞增殖动力学的影响。
短句来源
     Transforming growth factor-alpha(TGF-alpha) is a potent mitogen of normal and neoplastic hepatocytes. It could promote the hepatocellular proliferation,differentiation,regeneration and tumor cell growth.
     转化生长因子_α(TGF_α)是一种参与调节正常细胞和肿瘤细胞增殖、分化的细胞因子,是肝细胞增殖分化过程中必不可少的有丝分裂原。
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  hepatocyte proliferation
Hepatocyte proliferation in the liver regenerating after partial hepatectomy ceases when the organ is restored, and the mechanism of this phenomenon is still unclear.
      
The Mechanisms of Endogenous Control of Hepatocyte Proliferation Are Different in Mice of Two Inbred Strains (BALB/c and AKR)
      
Hepatocyte proliferation was measured 24 h after partial hepatectomy.
      
In the group given d-GaIN, apoptotic cells with TUNEL assays and caspase-3 activity, which are liver injury markers induced by d-GaIN, the hepatocyte proliferation with cell proliferation assay increased.
      
The cascade of molecular events leading to liver cancer in rodents involves hepatocyte proliferation and oxidative stress, but the PPARα target genes that mediate this response are unknown.
      
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  hepatocyte regeneration
One possibility is that, similar to models of hepatocyte regeneration, β-cells can arise either by neogenesis or replication, depending on the particular stimulus.
      
Hepatocyte growth factor (HGF), a potent hepatocyte mitogen in vitro, triggers hepatocyte regeneration after partial hepatectomy and acute liver cell necrosis induced by chemicals.
      
Hepatocyte regeneration in chronic hepatitis C and interferon treatment: Analysis of immunohistological identification of prolif
      
Hepatocyte regeneration has been widely investigated, with the mitotic index and the incorporation of [3H]thymidine being used as regeneration markers.
      
PE induces atrophy of the ipsilateral lobe and hypertrophy or hyperplasia of the contralateral lobe by hepatocyte regeneration.
      
更多          
  hepatic proliferation
Peroxisome proliferators (PPs) are a diverse group of chemicals that cause hepatic proliferation, suppression of apoptosis, peroxisome proliferation and liver tumours in rodents.
      
At 36 and 48?h after microsurgical hepatic resection, markers of hepatic proliferation (Ki67, BrdU) were elevated in G-CSF-treated mice compared to sham injected control animals (P?>amp;lt;?0.0001) and dry liver weight was increased (P?>amp;lt;?0.05).
      
During the last decade, hepatic proliferation inhibitors of varying degrees of purity have been isolated using regenerating rat liver or hepatoma cell cultures as test systems.
      
The results of the present study suggests that liver cell proliferation is influencing the hypothalamic GABAergic neurotransmission and these changes regulate the hepatic proliferation through the sympathetic stimulation.
      
The results of the present study indicate that liver cell proliferation is influencing the brain stem GABAergic neurotransmission and these changes regulate the hepatic proliferation through the sympathetic stimulation.
      
更多          
  hepatocellular proliferation
Neonatal (5-day) rats have ongoing hepatocellular proliferation in contrast to adult (5-month) rats, and should be therefore resilient to GalN toxicity.
      
Diethylnitrosamine exposure-responses for DNA ethylation, hepatocellular proliferation, and initiation of carcinogenesis in rat
      
Effect of cytochrome P-450 inhibition on tetrahydrofuran-induced hepatocellular proliferation in female mice
      
The studies presented were designed to investigate the effects of cytochrome P450 inhibition on tetrahydrofuran-induced hepatocellular proliferation in female B6C3F1 mice.
      
There may therefore be a role for gastrin in embryonic hepatocellular proliferation and perhaps also in the proliferation of some hepatocellular tumors.
      
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  其他


In connection with the study of the mechanism of carcinogenesis,we have underta-ken an investigation on the relative changes in activities of the proliferating enzymesuch as aspartate carbamyl transferase(ACT)and the tissue-specific enzymes such asornithine carbamyl transferase(OCT)and carbamyl phosphate synthetase(CPS_1)in amodel system of hepatocarcinogenesis of rats induced by diethylnitrosamine(DENA).Similar observations have also been made during development of rat liver.(1)Based on the pathological study...

In connection with the study of the mechanism of carcinogenesis,we have underta-ken an investigation on the relative changes in activities of the proliferating enzymesuch as aspartate carbamyl transferase(ACT)and the tissue-specific enzymes such asornithine carbamyl transferase(OCT)and carbamyl phosphate synthetase(CPS_1)in amodel system of hepatocarcinogenesis of rats induced by diethylnitrosamine(DENA).Similar observations have also been made during development of rat liver.(1)Based on the pathological study and enzymatic changes of liver in the presentexperiment,the process of carcinogenesis may be tentatively divided into three stages:(1)stage of simple hyperplasia—the early 6 weeks of DENA feeding.Changes in therelative ratio of ACT,OCT,and CPS_1 activities in this stage are reversible,similar tothose observed in the regenerating liver.(2)stage of malignant transformation—fromthe 6th to the 16th week of feeding the carcinogen.In this stage there appears anaplastichyperplasia of liver cells characterized by an irreversible change of the relative ratioof enzyme activities and (3)stage of the development of hepatocellular carcinoma—fromthe 16th to the 30th week of carcinogenesis.(2)During carcinogenesis of rat liver(after the 6th week of feeding DENA),activities of OCT and CPS_1 decreased while those of ACT increased gradually till theformation of cancer.In hepatocellular carcinoma the activities of OCT and CPS_1 areabout 10~20% of the normal liver,while those of ACT being about 2~3 times higher than the normal liver.The pattern of relative changes in activities of both groups ofenzyme during carcinogenesis was found to be the reverse of those observed in thedevelopment of rat liver.(3)The above enzymes in hepatocellular carcinoma and normal liver are probablyidentical entities,as shown by the similarities of pH optima and distribution patternsof enzyme activity in polyacrylamide gel electrophoresis.Similar K_m values anddifferent V_m values of OCT and ACT in hepatocellular carcinoma and normal liverpreparations suggested that changes in enzyme activities during carcinogenesis maypossibly be the result of an alteration in the amount of enzyme proteins.Furthermore,the specific activities of OCT and CPS_1 in the mitochondria of hepatocellular carcinomahave been found to be much lower than those of normal liver,although the proteincontent in the mitochondria of hepatocellular carcinoma decreased to an extent of about40% of that of normal liver.(4)The possible correlation between cell proliferation and differentiation to themechanism of carcinogenesis is discussed.As seen from Fig.3,the process of carcinogenesisseems to be a reversal of that of normal differentiation(development).Changes in enzymeactivities during carcinogenesis may be explained as a result of repression andderepression of the tissue-specific operons and mitotic operons,which are closelylinked and mutually repressed.It appears likely that cell proliferation may provide afundamental condition for the malignant transformation of the hepatocytes,while lossor decrease in the activities of tissue-specific function may be of primary importance tothe initiation of carcinogenesis.It is thus concluded that carcinogenesis would be dueto a random impairment of the control mechanism for gene activities of certain tissue-specific operons,leading to irreversible changes in nucleic acid biosynthesis and intissue-specific metabolism and their key enzyme activities which in turn give rise to anirreversible disturbance of the normal balance between cell proliferation and tissue-specific function,resulting in an abnormal growth and finally the formation of cancer.

本实验以二乙基亚硝胺诱发大鼠肝癌为动物模型,结合病理形态学研究了细胞增殖与组织特异代谢关键性酶ACT 及OCT,CPS_1活性的相互改变及其与癌变的关系,同时作了鼠肝发育过程中酶活性变化的比较研究。(1)根据DENA 引癌过程中酶活性CPS_Ⅰ/ACT,OCT/ACT 及ACT/CPS_Ⅰ,ACT/OCT 相对比值的变化,以及病理形态观察结果,DENA 引癌过程大致可分为三个阶段:喂DENA6周以内为单纯性增生期。此时期酶活性相对比值的改变是可逆的,与再生肝相似。第6周以后至16周为癌变期。此时期出现肝细胞异型性增生及癌变病灶。酶活性相对比值的改变是不可逆的。16周到30周为癌变细胞发展成为肝细胞癌期。(2)癌变过程中(喂DENA6周以后),OCT 及CPS_Ⅰ活性持续降低,同时ACT 活性持续增高。肝癌结节中OCT 及CPS_Ⅰ活性约为正常肝的10~20%,ACT 活性约为正常肝的2倍。癌变过程中这两类酶活性的相互改变与发育过程中的情况正好相反。在发育过程中,胚胎肝内OCT 及GPS_Ⅰ活性较成年水平低,而ACT 活性则较高。新生后CPS_Ⅰ及OCT 活性升高,同时ACT 活性降低。(3)肝与肝癌上述酶可能...

本实验以二乙基亚硝胺诱发大鼠肝癌为动物模型,结合病理形态学研究了细胞增殖与组织特异代谢关键性酶ACT 及OCT,CPS_1活性的相互改变及其与癌变的关系,同时作了鼠肝发育过程中酶活性变化的比较研究。(1)根据DENA 引癌过程中酶活性CPS_Ⅰ/ACT,OCT/ACT 及ACT/CPS_Ⅰ,ACT/OCT 相对比值的变化,以及病理形态观察结果,DENA 引癌过程大致可分为三个阶段:喂DENA6周以内为单纯性增生期。此时期酶活性相对比值的改变是可逆的,与再生肝相似。第6周以后至16周为癌变期。此时期出现肝细胞异型性增生及癌变病灶。酶活性相对比值的改变是不可逆的。16周到30周为癌变细胞发展成为肝细胞癌期。(2)癌变过程中(喂DENA6周以后),OCT 及CPS_Ⅰ活性持续降低,同时ACT 活性持续增高。肝癌结节中OCT 及CPS_Ⅰ活性约为正常肝的10~20%,ACT 活性约为正常肝的2倍。癌变过程中这两类酶活性的相互改变与发育过程中的情况正好相反。在发育过程中,胚胎肝内OCT 及GPS_Ⅰ活性较成年水平低,而ACT 活性则较高。新生后CPS_Ⅰ及OCT 活性升高,同时ACT 活性降低。(3)肝与肝癌上述酶可能是相同的。因为酶活性的最适pH 和在聚丙烯酰胺凝胶电泳图上的分布都是一致的。肝与肝癌OCT 及ACT 的K_m 相同而V_m 不同,说明癌变过程中酶活性的变化,主要是由于酶蛋白量的改变。此外,肝癌线粒体的蛋白量减少,但OCT 及CPS_Ⅰ的比活性(单位/毫克线粒体蛋白)仍较正常肝线粒体的低。(4)讨论了增生和分化与癌变的关系。初步认为,肝细胞的癌变是反分化(分化逆转)问题,和正常分化一样系由于基因表现的改变,不一定包含基因结构的改变。就与癌变有关的细胞增殖和分化的矛盾而言,细胞增殖及其有关酶活性的增高,可能是癌变发生的基础,而组织特异功能及其关键性酶活性的降低,可能与癌变的关系更为密切。因此癌变的发生,可能是由于在细胞分裂过程中致癌物使肝细胞特异功能基因的调节控制失常,从而引起增生代谢与特异代谢关键性酶活性不可逆的改变,使之失去肝细胞增殖与特异功能的正常平衡,而代之以不受控制的增生,最后形成癌细胞。

It was found in the present study that thyroxine seemed to play an important role in the regulation of activities of the proliferating enzyme,ACT and the tissue-specific enzymes,CPS1 and OCT in the liver of rats-The effects of thyroxine on the activities of these two different functional enzymes were contradictory.During the development of rats,thyroxine caused an increase of the relative activity of ACT in the liver at two weeks after hirth,with a decrease of that of CPS1 and OCT at the same time.A reverse...

It was found in the present study that thyroxine seemed to play an important role in the regulation of activities of the proliferating enzyme,ACT and the tissue-specific enzymes,CPS1 and OCT in the liver of rats-The effects of thyroxine on the activities of these two different functional enzymes were contradictory.During the development of rats,thyroxine caused an increase of the relative activity of ACT in the liver at two weeks after hirth,with a decrease of that of CPS1 and OCT at the same time.A reverse manner was,however,noted there after till 10 weeks of age.The pattern of changes in the effects of thyroxine on the enzyme activities during hepato-eareinogenesis induced by diethylnitrosamine was somewhat similar to that observed during post-natal development.Based on the results obtained in the current work,the stage of malignant transformation,as defined in our previous report,could be further divided into two substages:the early stage of malignant transformation (i.e.,the stage of hepatocytes undergoingmalignant transformation)......from the 6th to the 12th week of feeding DBNA,andthe late stage of malignant transformation (i.e.,the stage of formation of cells of hepato-cellular carcinoma)......from the 12th to the 16th week of DBNA feeding.In the early stage of malignant transformation,the effect of thyroxine on the relative ratio of activites of CPS1/ACT and OCT/ACT was decreased,while that of ACT/CPS1 and ACT/OCT was increased.But in the late stage of malignant transformation,a reverse situation was observed in which the induction of CPS1 and OCT activities by thyroxine would suggest a possible role of thyroxine on the stimulation of differentiation of cells of hepato-cellular carcinoma.

本实验观察到甲状腺素具有调节肝细胞增殖酶ACT及组织特异酶CPS_1,及OCT活性的功能,当甲状腺素引起新生二周鼠肝ACT的相对活性增高时,CPS_1及OCT的相对活性降低,但对新生二周以后至成年(10周)鼠肝酶活性的影响则相反。对年龄较大如30周的动物几无影响。甲状腺素对DENA诱发大鼠肝癌过程中肝内上述酶活性的相互影响,与发育过程的情况颇为相似。根据甲状腺素对DENA引癌过程中酶活性的影响,似可将前一报告中所划分的癌变期进一步分为癌变早期(即肝细胞进行癌变期)——喂 DENA 6—12周,及癌变后期(即癌细胞形成期)——喂DENA 12—19周。在癌变早期,甲状腺素对肝内CPS_1及OCT活性的诱导效应下降:对CPS_1/ACT及OCT/ACT活性相对比值的影响下降,同时对ACT/CPS_1及ACT/OCT活性相对比值的影响上升。在癌变后期,甲状腺素又使CPS_1及OCT的相对活性增高;使CPS_1/ACT及OCT/ACT活性相对比值上升,同时使ACT/CPS_1及ACT/OCT活性相对比值下降。 癌变后期的影响表明甲状腺素似有促使癌变了的细胞向正常分化的功能。

After partial hepateotomy (68%) of adult rats, the 3H-dT labeled rate and mito tic index of hepatocy tes reached a high peak at the 24 th and 36 th hour respectively-Then, it declined rapidly within the next twenty-four hours. After that the reduced changes became slow. The kinetic curves of labeled rate and mitotio index were very similar, showing a definite regular change between them.The blood of normal adult rats was drawn from artery, and the rats were perfu-eod immediately with equal part of physiological...

After partial hepateotomy (68%) of adult rats, the 3H-dT labeled rate and mito tic index of hepatocy tes reached a high peak at the 24 th and 36 th hour respectively-Then, it declined rapidly within the next twenty-four hours. After that the reduced changes became slow. The kinetic curves of labeled rate and mitotio index were very similar, showing a definite regular change between them.The blood of normal adult rats was drawn from artery, and the rats were perfu-eod immediately with equal part of physiological saline. The results indicated that the smittic index of hepatocytes was shown to be directly proportional to the degree of lbood dilution. The liver regeneration and its relation with control function of humoral factors (hepatic chalone) for hepatocytic proliferation was discussed.

成年大鼠肝大部(68%)切除后,肝细胞摄取氚化脱氧胸苷(~3H-dT)的核标记指数和分裂指数分别于术后24小时和36小时达高峰。高峰后24小时内下降较快,随后继续缓慢下降。肝细胞核标记指数和分裂指数的动态曲线十分相似,二者之间呈现明显的相关。正常成年大鼠于抽取一定量血液后予以注入等量生理盐水,发现其肝细胞分裂指数与血液稀释度呈正比关系。据此,讨论了肝大部切除后肝细胞的增殖规律性及其与体液因子(肝抑素)调节作用的关系。

 
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