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cirrhosis
相关语句
  肝硬化
    THE STUDY OF EXPERIMENTAL CIRRHOSIS OF LIVER
    实验性肝硬化的研究
短句来源
    HISTOCHEMISTRY OF LIVER CIRRHOSIS IN SCHISTOSOMIASIS OF RABBITS
    兔血吸虫性肝硬化过程组织化学研究
短句来源
    Changes of collagen and glycosaminoglycans in liver at different stages of experimental cirrhosis
    实验性肝硬化形成过程中肝脏糖胺多糖和胶原含量的变化
短句来源
    The dynamic changes of glucagon and sodium retention in experimental liver cirrhosis in rats
    实验性肝硬化鼠血浆胰高血糖素的动态变化与钠潴留
短句来源
    The mechanism for splenic promoting effects on liver cirrhosis
    脾脏在大鼠肝硬化形成过程中免疫调控机制的探讨
短句来源
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  肝硬变
    Histopathological study on inspection of tongue vessels of rats with liver cirrhosis and venous congestion
    大鼠肝硬变瘀证舌脉诊的病理组织学研究
短句来源
    EXPRESSION OF PROTEIN KINASE SUBSTRATE P36 IN LIVER CIRRHOSIS AND HEPATOCELLULAR CARCINOMA AND ITS RELATIONSHIP WITH HBV AND HCV INFECTIONS
    蛋白激酶底物p36在肝硬变、肝细胞肝癌中的表达及与HBV、HCV感染的关系
短句来源
    Study on the Relationship between Ascites and Tumour Necrosis Factor α of the Experimental Rat Liver Cirrhosis
    大鼠实验性肝硬变腹水形成及其与肿瘤坏死因子α关系的研究
短句来源
    The relationships between expression of P21~(WAF1) and p53 and between P21~(WAF1) and PCNA in tissues of hepatocellular carcinoma and liver cirrhosis
    肝细胞肝癌和肝硬变组织中P21~(WAF1)与P53,PCNA表达之间的关系
短句来源
    Regulation of p53 and bcl 2 proteins to apoptosis and cell proliferation in liver cirrhosis and hepatocellular carcinoma
    Bcl-2 和p53 蛋白表达对肝硬变和肝细胞癌中细胞增殖和凋亡的调节
短句来源
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  “cirrhosis”译为未确定词的双语例句
    Exprcssion of c-erbB-2 protein and EGF reccptor in hepatitis B,cirrhosis and hepatocellular carcinoma
    c-erbB-2蛋白和表皮生长因子受体在肝脏病变中的表达
短句来源
    Distribution and significance of HBV DNA and HBAg in human primary hepatocellular carcinoma and liver cirrhosis
    Distribution and significance of HBV DNA and HBAg in human primary hepatocellular carcinoma and liver cirrhosis
短句来源
    The Relationship between the Morphology of Nucleus of Liver Cells and the Liver Functions and Prognosis of Portal Hypertension due to Hepatic Cirrhosis
    The Relationship between the Morphology of Nucleus of Liver Cells and the Liver Functions and Prognosis of Portal Hypertensio
短句来源
    Expression of endothelin1 and nitric oxide synthase mRNA in gastric mucosa of rats with cirrhosis and portal hyptensive gastropathy after disconnective opertations.
    门静脉高压症大鼠断流术后胃粘膜内皮素-1及一氧化氮合酶mRNA的表达
短句来源
    Study of expression of matrixmetalloproteinases in liver cirrhosis
    基质金属蛋白酶在肝纤维化组织中的表达
短句来源
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  cirrhosis
In treating hepatocellular carcinoma (HCC) patients with advanced cirrhosis, one of the most difficult problems is concomitant esophageal varices and hypersplenism.
      
The surgical treatment methods for cirrhosis patients complicated with portal hypertension are complicated.
      
From 1979 to 2005, 274 cirrhosis patients with portal hypertension who underwent the new treatment strategy were followed up to observe different clinical indexes, which were then compared with those of the traditional surgery treatment.
      
Postoperative hepatic insulin-like growth factor-1 (IGF-1) production may be severely disturbed in patients with liver cirrhosis.
      
Twenty-four patients with HCC with cirrhosis who underwent hepatectomy were randomly divided into two groups: a PN group (n = 12) and an rhGH + PN group (n = 12).
      
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Fifty-one male rats (body weights:200—350gm) were raised with laboratory diet, 39 of them were injected once a week with CCl_4 (0.015cc/100gm body weight) in li- quid paraffin through the mesenteric veins and 12 rats without treatment as controls. Rats with 1,2,3,and 4 injections were killed 7 days afterwards.Pieces of liver tissue were taken from the left anterior lobe of the rats from both experimental and control groups.Paraffin sections were prepared from materials fixed in:(1)Susa or Stieve's for Heidenhain's...

Fifty-one male rats (body weights:200—350gm) were raised with laboratory diet, 39 of them were injected once a week with CCl_4 (0.015cc/100gm body weight) in li- quid paraffin through the mesenteric veins and 12 rats without treatment as controls. Rats with 1,2,3,and 4 injections were killed 7 days afterwards.Pieces of liver tissue were taken from the left anterior lobe of the rats from both experimental and control groups.Paraffin sections were prepared from materials fixed in:(1)Susa or Stieve's for Heidenhain's Azan staining;(2)Regaud's for Bensley's acid fuchsin-methyl green staining of mitochondria;(3)cold Carnoy's for methyl green-pyronin staining of ribo- nucleic acid (RNA),with control sections extracted with 20% perchloric acid or 0.17 M NaCl at 56℃ for 2 hrs.;(4)Carnoy's for Yakovlev's ((?)) and Barrnett- Seligman's methods for protein-bound SH-group,with control sections blocked with 0.1M monoiodoacetic acid;(5)Formol-alcohol for Hotchkiss's periodic acid-Schiff's (PAS) reaction of glycogen,with control sections treated with salivary digestion;(6)cold ace- tone for alkaline phosphatase (ALP);and (7) 10% neutral formalin for frozen sections and Sudan Ⅲ testing for fats. After CCl_4-intoxication,during the development of cirrhosis,most of the parenchymal cells degenerated and finally became necrotic.Free fat droplets and hyperplastic fibrous tissues accumulated in the necrotic regions.The liver lobules thus were destroyed and blood sinuses were engorged with blood cells.Surviving cells showed compensative hyperplasia and were isolated into nodules by the developing fibrous tissues.Cirrhosis developed in all the rats treated with CCl_4. The parenchymal cells showed a progressive changes during the development of cirrhosis.There was an increase of fat droplets and a decrease of the number of mito- chondria in the cytoplasm.The mitochondria fragmented into granules or fused in a mass.There was a progressive decline in the content of RNA and glycogen,but an increase of the ALP activity.Those cells showing compensative hyperplasia enlarged in size,and their number of mitochondria,RNA and glycogen content progressively in- creased. Small-sized cells appeared in the necrotic regions among the fat droplets,necrotic cells and fibrous tissues.They decreased in number as the fibrous tissue developed. These cells contained mitochondria and showed positive reactions of PAS,RNA and ALP.Their origin was discussed and their relation to the formation of collagen fibers needs further investigation.

大白鼠肝在CCl_4中毒所引起肝硬化过程中,肝小叶结构被破坏。肝细胞中毒,坏死,脂肪游离增多。血窦因血流受阻而涨大。大部分肝细胞退变或坏死;部分残存而代偿性增生。结缔组织在坏变部分增生并包围肝小结而形成肝硬化。在肝硬化过程中,退变的肝细胞内脂滴增多。线粒体减少,成粒状或溶成一团。核糖核酸,糖元含量也随病变进展而减少。碱性磷酸酶反应增强。代偿性增生的肝细胞体积增大;肝细胞内线粒体增多,核糖核酸,糖元含量逐渐增多。在病变过程中出现冼多小型细胞。小型细胞出现在坏变的肝细胞区域,脂肪空泡附近及结缔组织内并随纤维的增加而减少。小型细胞含线粒体,核糖核酸,PAS反应及碱性磷酸酶反应均为阳性。文中讨论了肝细胞内细胞学和组织化学变化的意义;小型细胞的来源,与纤维形成的关系及纤维增生机制等问题。

An evaluation of praziquantel on rabbit liver cirrhosis due to schistoso-miasis according to pathological changes was reported. Rabbits were treated 18 weeks after infection with praziquantel 100mg/kg/day for 2 days. All cured rabbits showed an excellent recovery 20-36 weeks after treatment with favorable pathological changes: i.e. ,(1)disappearance of vasodilatation, with decrease of hepatic arterioles and increase of portal branches; (2) disappearance of black-brown color, nodular appearance and hard...

An evaluation of praziquantel on rabbit liver cirrhosis due to schistoso-miasis according to pathological changes was reported. Rabbits were treated 18 weeks after infection with praziquantel 100mg/kg/day for 2 days. All cured rabbits showed an excellent recovery 20-36 weeks after treatment with favorable pathological changes: i.e. ,(1)disappearance of vasodilatation, with decrease of hepatic arterioles and increase of portal branches; (2) disappearance of black-brown color, nodular appearance and hard feeling; and (3) disappearance of ova in portal areas, surrounded by collagen fibers and newly delevoped arterioles. Results indicated that praziquantel was a drug of choice in treatment for liver cirrhosis due to schistosomiasis.( Acknowledgmemt of support from the UNDP/World Bank/WHO Special Program for Research and Training in Tropical Diseases )

用肝脏血管造型和病理组织学方法观察吡喹酮对家兔日本血吸虫病肝硬化的影响。感染尾蚴后18周,用吡喹酮100mg/kg/日进行两天治疗,所有治愈家兔肝脏血管模型、病理形态及组织学的异常变化均在停药后20~36周得到很好恢复,提示吡喹酮是一个治愈血吸虫病肝硬化较为理想的药物。

Using 125I-UdR labelled K 562 cells as target cell for assaying NK activity in peripheral blood from 29 cases of viral hepatitis B, acute hepatitis 17, chronic persistent hepatitis 9, asymptomatic HBsAg carriers 3 and cirrhosis of liver 2, together with 40 healthyadults as controls. The following results were obtained:mean ± SD of NK activity of the control group was 35.24 ±12.24%; found to be markedly elevated in 5 early acute hepatitis cases (P< 0.001), significantly depressed in 7 chronic persistent...

Using 125I-UdR labelled K 562 cells as target cell for assaying NK activity in peripheral blood from 29 cases of viral hepatitis B, acute hepatitis 17, chronic persistent hepatitis 9, asymptomatic HBsAg carriers 3 and cirrhosis of liver 2, together with 40 healthyadults as controls. The following results were obtained:mean ± SD of NK activity of the control group was 35.24 ±12.24%; found to be markedly elevated in 5 early acute hepatitis cases (P< 0.001), significantly depressed in 7 chronic persistent hepatitis and 2 cirrhosis of liver patients (P<0.05), while that of 3 carriers and of 9 convalescents were within normal range. The above results consistent well with the reports of some authors, but not with some of the others. According to our observation the early rise of NK activity in acute infection and the declination in chronic stage was in accordance with the blood interferon level as was observed in some other viral diseases, (e. g. CMV, LCM et al), and also it was in parallel with SGPT level in early stage of acute hepatitis B.

本文用~(125)IUdR 标记的K 562细胞作为靶细胞,检测 29例病毒性乙型肝炎患者(急性期17例、慢迁肝7例、无症状 HBsAg 携带者3例和肝硬化2例)外周血中自然杀伤(NK)细胞的活性。结果发现40例正常对照组的NK活性平均值±SD 为35.24±12.24%;5例急性早期患者显著升高(P<0.001);7例慢迁肝患者明显降低(P<0.05);9例恢复期和 3例无症状 HBsAg携带者均在正常范围内。以上结果与中岛悦朗和Serdengerti的报道相符,但与另些作者的资料有差异。我们认为NK活性在病程初期升高和在慢性期降低与干扰素的生成和乙肝病人早期肝损害有关,与若干种其他病毒性疾病中所见的规律相仿。

 
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