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   fulminant hepatitis 在 内分泌腺及全身性疾病 分类中 的翻译结果: 查询用时:0.183秒
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fulminant hepatitis
相关语句
  暴发性肝炎
    TRANSGENIC RESCUE FROM FULMINANT HEPATITIS IN LEC RAT BY INTRODUCING HUMAN ATP7B cDNA
    人ATP7B基因对Wilson病动物模型LEC大鼠暴发性肝炎的治疗
短句来源
    These data showed that the LEC rats were successfully rescued from fulminant hepatitis after introducing of human ATP7B gene.
    说明人ATP7B的导入 ,成功地抑制了Wilson病动物模型LEC大鼠的暴发性肝炎的发生。
短句来源
  “fulminant hepatitis”译为未确定词的双语例句
    Results The morbidity and mortality of fulminant hepatitis was both higher in group 1(31% and 22%) than that in group 2(20% and 17%).
    结果HRZ联合化疗组暴发型肝炎的发生率为31%(16/51),死亡率为22%(11/51);
短句来源
    Methods The HBsAg positive rates of 81 cases caused by antituberculotics and 14 cases of a-cute or subacute fulminant hepatitis among them were analyzed,and the clinical features of hepatitis caused by antituberculotics were compared between HBsAg postive group and HBsAg negative group.
    方法观察81例抗结核药物性肝炎及其中14例急性、亚急性暴发型肝炎患者中HBsAg阳性率,比较HBsAg阳性和HBsAg阴性两组抗结核药物性肝炎患者的临床特点。
短句来源
    Results HBsAg positive rates in patients with liver function damage and acute or subacute fulminant hepatitis due to the antituberculotics were 48% (39/81) and 64% (9/14) respectively.
    结果在结核病化学治疗过程中出现肝功能损害的患者,HBsAg阳性者占48%(39/81); 急性、亚急性暴发型肝炎患者中,HBsAg阳性者占64%(9/14)。
短句来源
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  fulminant hepatitis
Fulminant hepatitis is fatal in most cases and timely liver transplantation is the only effective treatment.
      
In general, it is extremely difficult to treat fulminant hepatitis by conservative regimen, particularly, in cases with rapid progression.
      
Emergency adult living-donor liver transplantation is an effective treatment for fulminant hepatitis patients and is relatively safe for donors.
      
Construction of shRNA of fulminant hepatitis related gene mfgl2 and investigation of its biological effects in vitro
      
He developed fulminant hepatitis with acute liver failure and an acute respiratory distress syndrom (ARDS).
      
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Blood sugar, insulin and C-peptide were detected in 11 cases of fulminant heratitis confirmed by liver biopsy before G-I treatment and 15, 30, 90, 120, 180 minutes after instillation.The restults showed that blood sugars were normal or less before instillation, ard elevated slightly then dropped to normal level afler instillation.Insulin C-peptide and glucagon were bigger than normal before instillation and reached peak value 15 minutes after instillation,C-peptide and glucagon recovered to pre-instillation...

Blood sugar, insulin and C-peptide were detected in 11 cases of fulminant heratitis confirmed by liver biopsy before G-I treatment and 15, 30, 90, 120, 180 minutes after instillation.The restults showed that blood sugars were normal or less before instillation, ard elevated slightly then dropped to normal level afler instillation.Insulin C-peptide and glucagon were bigger than normal before instillation and reached peak value 15 minutes after instillation,C-peptide and glucagon recovered to pre-instillation level 3 hours after instilla tion. But insulin persisted in peak value. Therefore in the patients with fulminant hepatitis,function to intake and to degrade insulin decreased, and the function to intake and to degrade glucagon was present.

经肝活检证实的重症肝炎11例,在胰高血糖素-胰岛素(G-I)疗法前及滴完后15、30、60、120、180分钟采血,检测血清糖、胰岛素、C肽及血浆胰升血糖素。结果:血糖在滴注前正常或偏低,滴后轻度上升即降至滴前水平;胰岛素、C肽及胰升血糖素滴前均高于正常,滴后15分钟高峰,滴后3小时C肽及胰升血糖素恢复到滴前水平,而胰岛素持续呈高值。可见重症肝炎对胰岛素的摄取和降解功能降低,而对胰升血糖素有摄取和降解功能。

The angiotensin Ⅱ(ⅡAT)les in plasma were measured 68 timesby using radio-immunoassay in 30 patientswith viral hepatitis B(HB)and in 35healthy persons as the control group. Theresults showed that the AT Ⅱ levels ofpatients with HB were much higher thanthose of the control group (P<0.001).They were 219. 25±191.31ng/L and 60.70±10.73 ng/L, respectively. These indicatedthat the renin-angiotensin-aldosteronesystem(RAAS) of the patients was inexciting state. The levels of 8 cases ofsevere chronic aotive hepatitis(SCAH)(ATⅡ=270.40±106.55ng/L,...

The angiotensin Ⅱ(ⅡAT)les in plasma were measured 68 timesby using radio-immunoassay in 30 patientswith viral hepatitis B(HB)and in 35healthy persons as the control group. Theresults showed that the AT Ⅱ levels ofpatients with HB were much higher thanthose of the control group (P<0.001).They were 219. 25±191.31ng/L and 60.70±10.73 ng/L, respectively. These indicatedthat the renin-angiotensin-aldosteronesystem(RAAS) of the patients was inexciting state. The levels of 8 cases ofsevere chronic aotive hepatitis(SCAH)(ATⅡ=270.40±106.55ng/L, 6 cases ofsubacute fulminant hepatitis (SFH) (ATⅡ=332.80 140.12 ng/L), and 4 cases ofhepatocirrhosis (HC) (AT Ⅱ=218.50±97.64pg/ml)were all higher than those of 8cases of chronic active hepetitis (CAH)(100.50±83.81ng/L) and those of 4 casesof acute icteric hepatitis (AIH) (123.33±64.97ng/L).These findings showed thatthe levels of AT Ⅱ were directely relatedwith the severity of the illness. The AT Ⅱlevels of 8 cases of HRS (270.50±66.31ng/L) were higher that those withoutHRS(174.501±78.48ng/L).After treatmentwith captopril(CPT), the renal functionof the patients returned to normal andthe patients got better, while the AT Ⅱlevels decreased greatly. The results sug-gested that high AT Ⅱ levels in plasmamay be one of the causes aggressing theHRS.The CPT may inhibit the produceof AT Ⅱ and there are some therapeuticeffects for the HRS.

作者用放射免疫法测定了30例(68例次)乙型肝炎(乙肝)患者和35名正常人的血浆血管紧张素Ⅱ(AT Ⅱ)水平。结果表明,30例乙肝患者AT Ⅱ明显高于35名正常人;各型乙肝患者AT Ⅱ升高值与病情轻重一致,8例肝肾综合征(HRS)患者ATⅡ显著高于未并发HRS者。用巯甲丙脯酸(CPT)治疗后,ATⅡ明显下降,肾功能改善。提示AT Ⅱ升高可能是HRS发生的原因之一,CPT可能抑制了ATⅡ的产生,对HRS有一定疗效。

Objective To investigate the possibility of affecting transgenic rescue for Wilson disease using the human ATP7B transgenic LEC rat.Methods The 7.1kb transgene constructed with human ATP7B cDNA and chicken β-actin promoter was introduced into the fertilized oocytes of LEC rats, an animal model of Wilson disease, by microinjection. The expressions of human ATP7B protein in the transgenic rats were detected by Western blot. The plasma AST and ALT activities, and the total bilirubin levels in transgenic rats...

Objective To investigate the possibility of affecting transgenic rescue for Wilson disease using the human ATP7B transgenic LEC rat.Methods The 7.1kb transgene constructed with human ATP7B cDNA and chicken β-actin promoter was introduced into the fertilized oocytes of LEC rats, an animal model of Wilson disease, by microinjection. The expressions of human ATP7B protein in the transgenic rats were detected by Western blot. The plasma AST and ALT activities, and the total bilirubin levels in transgenic rats were measured continuously from 6 to 16 weeks using non-transgenic rats and LEA rat as controls. The pathological and histochemistry changes in the liver of the transgenic rats at 13 weeks were analyzed. Results The intact and correct product derived from human ATP7B was confirmed in the liver of transgenic rats. At the age around 12 weeks, the plasma AST and ALT activities, and the total bilirubin levels in transgenic rats were significantly decreased, while the inflammatory reation in the liver of transgenic rats was much mild as compared with that of non-transgenic rats, and the granules of stained copper were less in the hepatocytes of transgenic rats. By the age of 16 weeks, the transgenic rats were phenotypically normal, and the survival rate was 100%. These data showed that the LEC rats were successfully rescued from fulminant hepatitis after introducing of human ATP7B gene. Conclusion The hepatitis in Wilson disease is directly related to the toxicity of excessive accumulated copper, which attributed to the functional deficiency of the ATP7B. Gene transfer probably is the effective method for the therapy of Wilson disease.

目的 探讨人ATP7B基因对Wilson病动物模型LEC大鼠暴发性肝炎的治疗效果。 方法 将构建的 7.1kb含有鸡 β肌动蛋白启动子的人正常ATP7BcDNA ,经显微注射法导入人Wilson病动物模型LEC(long EvansCinnamon)大鼠受精卵 ,建立转基因功能恢复大鼠模型。以Westernbolt检测人ATP7B在转基因大鼠肝内的表达 ,用同窝无转基因大鼠及正常野生型LEA大鼠作对照 ,对 6~ 16周龄的转基因大鼠的血清AST、ALT和总胆红素水平进行连续测定 ,同时取 13周龄转基因大鼠的肝组织进行病理学和组织化学分析。 结果 人ATP7B基因在转基因大鼠的肝组织中获得正确和完整的表达 :12周龄前后 ,与同窝无转基因大鼠相比 ,转基因大鼠的血清AST、ALT和总胆红素水平明显降低 ,肝组织的炎性病变显著减轻 ,肝细胞内铜的蓄积减少 ;至 16周龄 ,转基因大鼠的临床表型未见异常 ,存活率达 10 0 %。说明人ATP7B的导入 ,成功地抑制了Wilson病动物模型LEC大鼠的暴发性肝炎的发生。结论 Wilson病肝炎的发生与ATP7B基因功能缺陷引起的铜蓄积有直接关系。基因转移有可能是...

目的 探讨人ATP7B基因对Wilson病动物模型LEC大鼠暴发性肝炎的治疗效果。 方法 将构建的 7.1kb含有鸡 β肌动蛋白启动子的人正常ATP7BcDNA ,经显微注射法导入人Wilson病动物模型LEC(long EvansCinnamon)大鼠受精卵 ,建立转基因功能恢复大鼠模型。以Westernbolt检测人ATP7B在转基因大鼠肝内的表达 ,用同窝无转基因大鼠及正常野生型LEA大鼠作对照 ,对 6~ 16周龄的转基因大鼠的血清AST、ALT和总胆红素水平进行连续测定 ,同时取 13周龄转基因大鼠的肝组织进行病理学和组织化学分析。 结果 人ATP7B基因在转基因大鼠的肝组织中获得正确和完整的表达 :12周龄前后 ,与同窝无转基因大鼠相比 ,转基因大鼠的血清AST、ALT和总胆红素水平明显降低 ,肝组织的炎性病变显著减轻 ,肝细胞内铜的蓄积减少 ;至 16周龄 ,转基因大鼠的临床表型未见异常 ,存活率达 10 0 %。说明人ATP7B的导入 ,成功地抑制了Wilson病动物模型LEC大鼠的暴发性肝炎的发生。结论 Wilson病肝炎的发生与ATP7B基因功能缺陷引起的铜蓄积有直接关系。基因转移有可能是一种有效的治疗Wilson病的方法。

 
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