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    膀胱癌患者体液和肿瘤组织内TGFβ1水平及其对肿瘤局部和全身细胞免疫功能影响的研究
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    1.Screening Down-regulated Genes and Cloning Down-Regulated Novel Genes in Gastric Cancer 2.Cloning, Cellular Location and Functional Study of Down-Regulated Novel Gene CA11 in Gastric Cancer
    1.胃癌下调功能基因组的筛选与下调新基因的克隆 2.胃癌下调新基因CA11的克隆、细胞定位和功能研究
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    Identification of Metastasis-associated Proteins by Proteomic Analysis and Functional Characterization of IL-18 in Metastasis of Lung Cancer
    肺癌转移相关蛋白的比较蛋白质组分析,鉴定及候选蛋白IL-18促进肺癌细胞转移的功能鉴定
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(1) A comparative study has been made on the induction of tryptophan pyrrolase by substrate and corticoids in liver tumor and the precancerous liver induced by 3'-MeDAB.(2) The liver tumor, contrary to normal liver, was inactive in response to both tryptophan and hydrocortisone for the induction of tryptophan pyrrolase, while the tissue adjacent to the tumor was active with respect to both substrate and hormonal induction.(3) A decrease in both substrate and hormonal induction was observed in the precancerous...

(1) A comparative study has been made on the induction of tryptophan pyrrolase by substrate and corticoids in liver tumor and the precancerous liver induced by 3'-MeDAB.(2) The liver tumor, contrary to normal liver, was inactive in response to both tryptophan and hydrocortisone for the induction of tryptophan pyrrolase, while the tissue adjacent to the tumor was active with respect to both substrate and hormonal induction.(3) A decrease in both substrate and hormonal induction was observed in the precancerous liver developed by feeding 3'-MeDAB for different time intervals. In experiments by injecting intraperitoneally the carcinogen into animals,for 25 hours, similar results were obtained as in the feeding experiments.(4) 2-MeDAB, a non-carcinogenic substance, caused the same effect on the induction of tryptophan pyrrolase in every case as did 3'-MeDAB. It thus appears that the effect of 3'-MeDAB on the enzyme induction may not be specific.(5) No inhibitors of tryptophan pyrrolase or activators of kynureninase were found in the cell sap of liver tumor and the liver of rats fed 3'-MeDAB or 2-MeDAB in the course of induction.(6) The cell sap from liver tumor (non-induced) contained only a small amount of enzyme protein, as shown by the fact that the enzyme activity being only slightly increased by the addition of either normal microsome or hematin, of which the level has not elevated by the administration of tryptophan or hydrocortisone.(7) Similar experiments have shown that the cell sap from the substrate and hormonal induced liver in the precancerous stage contained a decreased amount of enzyme protein as compared to that of the control. The same was true of the rats fed 2-MeDAB.(8) Microsomes from liver tumor have lost almost completely the ability of activating tryptophan pyrrolase in the cell sap. The ability of activation due to microsomes from the precancerous liver was remarkably reduced, though not yet completely lost, while the microsomes from the liver of rats fed 2-MeDAB were normal. It was in this respect that the effect of non-carcinogen (2-MeDAB) was found to be different from that of the carcinogen (3'-MeDAB).(9) From the results presented, it was concluded that the default of tryptophan pyrrolase induction observed in the liver tumor and the precancerous liver was mainly due to an inadequate amount of apoenzyme, rather than a deficiency of co-factor (hematin) or an increment of protein other than the enzyme. The possible cause of these effects was briefly discussed.

本文对大鼠肝癌及癌前期肝内TP的底物诱导和激素诱导作了比较研究。在3′-MeDAB诱发的肝癌中,TP活性很低,且不因注射色氨酸或氢可地松而升高,而癌周组织则仍保留对底物和激素诱导的能力。喂3′-MeDAB 13天、28天、90天大鼠肝内TP的底物诱导效应都较对照组为低。急性注射3′-MeDAB25小时,以100毫克/100克体重的L-色氨酸进行诱导,TP的诱导效应亦较对照组为低。氢可地松诱导的结果与底物诱导的相似,无论在喂或急性注射3′-MeDAB的情况下,TP的诱导效应都受到抑制。但在相同条件下,非致癌物,2-MeDAB,对TP的底物诱导和激素诱导(慢性的或急性的实验)也有相似的作用。诱导后肝癌组织或喂偶氮染料的肝组织中都未发现有TP的抑制物或狗尿酸酶的激活物。微粒体及正铁血红素与上清液的加合实验表明:(1)肝癌微粒体几乎完全不具有激活TP的活力;癌前期(3′-MeDAB组)肝微粒体已部分失去此种生化功能,但2-MeDAB组微粒体则否。3′-MeDAB对肝微粒体中辅助因子(正铁血红素)的结构并无破坏,而可能使辅助因子的含量减少。(2)微粒体对激活上清液TP的效果较自由的正铁血红素差,即使加入过量...

本文对大鼠肝癌及癌前期肝内TP的底物诱导和激素诱导作了比较研究。在3′-MeDAB诱发的肝癌中,TP活性很低,且不因注射色氨酸或氢可地松而升高,而癌周组织则仍保留对底物和激素诱导的能力。喂3′-MeDAB 13天、28天、90天大鼠肝内TP的底物诱导效应都较对照组为低。急性注射3′-MeDAB25小时,以100毫克/100克体重的L-色氨酸进行诱导,TP的诱导效应亦较对照组为低。氢可地松诱导的结果与底物诱导的相似,无论在喂或急性注射3′-MeDAB的情况下,TP的诱导效应都受到抑制。但在相同条件下,非致癌物,2-MeDAB,对TP的底物诱导和激素诱导(慢性的或急性的实验)也有相似的作用。诱导后肝癌组织或喂偶氮染料的肝组织中都未发现有TP的抑制物或狗尿酸酶的激活物。微粒体及正铁血红素与上清液的加合实验表明:(1)肝癌微粒体几乎完全不具有激活TP的活力;癌前期(3′-MeDAB组)肝微粒体已部分失去此种生化功能,但2-MeDAB组微粒体则否。3′-MeDAB对肝微粒体中辅助因子(正铁血红素)的结构并无破坏,而可能使辅助因子的含量减少。(2)微粒体对激活上清液TP的效果较自由的正铁血红素差,即使加入过量微粒体亦不能使TP活性增高到加入正铁血红素的水平;微粒体对3′-MeDAB组上清液的激活不如对2-MeDAB组及对照组上清液(底物或激素诱导)的激活显著,而正铁血红素对三组上清液都有显著激活。(3)肝癌细胞上清液只合有极少量的TP蛋白,且不因注射色氨酸或氢可地松而增加;癌前期肝细胞上清液的TP蛋白因底物或激素诱导而增加的量都较对照粗低。2-MeDAB组也有相似现象。以上结果表明,肝癌及癌前期肝内TP诱导的受损,主要是由于诱导后TP蛋白的缺少,而不是由于辅助因子(如正铁血红素)的不足,或非酶蛋白的增多。

The chemical composition and the enzymatic activities of normal and silicotic alveolar macrophages were compared in order to investigate the changes occurring after the introduction of quartz into the lung. As shown from the SDS-PAGE results, the protein composition of the silicotic alveolar macrophages was different from the normal in three places. Two protein lines showed increased intensity and one protein line was absent from the gel of the silica containing cells.The lecithin and lysolecithin contents were...

The chemical composition and the enzymatic activities of normal and silicotic alveolar macrophages were compared in order to investigate the changes occurring after the introduction of quartz into the lung. As shown from the SDS-PAGE results, the protein composition of the silicotic alveolar macrophages was different from the normal in three places. Two protein lines showed increased intensity and one protein line was absent from the gel of the silica containing cells.The lecithin and lysolecithin contents were both increased in the silicotic macrophages. The presence of an increased amount of lysolecithin may indicate that the cells were destroyed by the quartz.The acid phosphatase actvity and the oxygen consumption of the silica containing cells were both lower than normal cells.After treatment of the silicotic rats with PVNO, the composition and the enzymatic activities of the macrophages were all returned to the normal level. This shows that PVNO protects the alveolar macrophages from destruction by the quartz particles. Other drugs tested also showed some protective effect on the cells.

文中比较了正常大鼠与矽肺大鼠肺泡巨噬细胞中蛋白质与磷脂的组成,以及酸性磷酸酶活性与耗氧量的差别。根据SDS-PAG电泳的结果看到矽肺大鼠肺泡巨噬细胞的蛋白质区带比正常者多两条,但缺少了一条分子量较小的区带。矽肺大鼠肺泡巨噬细胞中含有大量卵磷脂,说明石英能引起肺表面活性物增多。同时,溶血卵磷脂也比正常者明显地增多,酸性磷酸酶活性与耗氧量均比正常者低,这些都说明石英改变了细胞的组成,破坏了细胞的功能。用克矽平(PVNO)治疗过的大鼠肺泡巨噬细胞的化学组成及酶活性都与正常者近似,证明此药能保护巨噬细胞防止被石英破坏。津_5、山梨醇铝等药物对细胞也表现有不同程度的保护作用。

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。

 
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