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急性肾损伤
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  acute kidney injury
    The renal tissue ELAM-1 mRNA expression in acute kidney injury induced by endotoxin and its significance
    内毒素急性肾损伤时肾脏ELAM-1mRNA的表达及其意义
短句来源
    Objective To explore the clinicopathological characteristics of acute kidney injury (AKI) of systemic sclerosis (SSc).
    目的探讨系统性硬化(SSc)急性肾损伤(AKI)患者的临床和病理特点。
短句来源
  acute renal injury
    Objective To illustrate the expressional distribution of heat shock protein 70(HSP 70) in the kidney of acute renal injury rats caused by gentamicin.
    目的探讨庆大霉素诱导急性肾损伤大鼠模型中肾脏热休克蛋白70(HSP70)的分布及表达规律。
短句来源
    Effect of anti-P-selectin lectin-EGF domain monoclonal antibody on rat acute renal injury and immune defensive function in rats
    抗P-选择素功能域单抗对急性肾损伤防治及免疫防御功能的影响
短句来源
    Objective To investigate the effect of anti-P-selectin lection-EGF domain monoclonal antibody ( PsL-EGFmAb) on acute renal injury and immune defensive function in rats.
    目的 探讨抗P-选择素lectin-EGF功能域单抗(PsL-EGFmAb)对大鼠急性肾损伤防治及机体免疫防御功能影响。
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    Acute renal injury induced by cyclosporin A and protective effect of reduced glutathione
    环孢素A致急性肾损伤及还原性谷胱甘肽的保护作用
短句来源
    Objective To observe whether taurine provides the protective effect on gentamicin-induced toxic acute renal injury and approach its possible mechanisms.
    目的 观察牛磺酸对庆大霉素(GM)引起的中毒性急性肾损伤是否具有保护作用并探讨其可能机理。
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  “急性肾损伤”译为未确定词的双语例句
    Expression of Heat-Shock Protein 70 in Kidney of Acute Injury Rats Caused by Gentamicin
    庆大霉素诱导急性肾损伤大鼠肾脏热休克蛋白70的表达
短句来源
    Study of Caveolin-1 Expression during the Recovery Phase of Gentamicin-induced Acute Tubular Necrosis in Rats and Its Mechanism
    庆大霉素致大鼠急性肾损伤Caveolin-1表达及其作用的初步探讨
短句来源
    (2)Gent group (n=14): given GM injection as the Taur group and given the same amount of saline instead of taurine;
    (2)庆大霉素组(Gent组,n=14):上法注射GM,制备成中毒性急性肾损伤模型,并腹腔注射生理盐水替代牛磺酸;
短句来源
    Effect of Anti-adhesive Treatment on Dendritic Cell Immigration and Accumulation in Rat Renal Ischemia-reperfasion Injury
    抗黏附治疗对大鼠急性肾损伤中树突状细胞迁移聚集的影响
短句来源
    The results suggest that acuterenal injury was minimal in the Ⅱ group as compared with the other two groups.
    结果表明,2组动物急性肾损伤程度较其它两组病变轻微。
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  acute kidney injury
Reducing contast media exposure, the use of low-osmolar agents, hydration with isotonic saline and N-acetylcysteine have proven effective in the prevention of contrast media-induced acute kidney injury.
      
An algorithm for assessment of individual patient risk and a summary of current concepts in the prevention of contrast media-induced acute kidney injury is provided.
      
In addition to ischemic acute renal failure, hypoxia can also play a crucial role in the development of nephrotoxic acute kidney injury, radiocontrast nephropathy, and acute glomerulonephritis.
      
Acute kidney injury in septic shock-do not under-treat!
      
Comment on "RIFLE classification in patients with acute kidney injury in need of renal replacement therapy" by Maccariello et al
      
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  acute renal injury
After acute renal injury, renal expression of several growth factors becomes transiently altered.
      
The data indicate thatCCr is not an accurate indicator of GFR in children who have had acute renal injury.
      
It is reported that urinary annexin V concentration may be an indicator of apoptosis and acute renal injury related to the urinary protein level.
      
Reactive oxygen species (ROS) have been postulated to play a major role in postischemic acute renal injury.
      
Insulin-like growth factor-I increases p21 expression and attenuates cisplatin-induced acute renal injury in rats
      
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male rabbits were divided into three groups and were treated with three energy levels (20KV, 750SW; 14kv,1 500kv; 10kv, 3 000kv) of extracorporeal shock wave (ESW) respectively. The results suggest that acuterenal injury was minimal in the Ⅱ group as compared with the other two groups.The biological effects of ESW on kidney caused an increase of γGT in urine,degeneration and or necrosis of tubular cells in ultrastructure, and intrarenal and perirenal bleeding in histology.The biological effects were renovated...

male rabbits were divided into three groups and were treated with three energy levels (20KV, 750SW; 14kv,1 500kv; 10kv, 3 000kv) of extracorporeal shock wave (ESW) respectively. The results suggest that acuterenal injury was minimal in the Ⅱ group as compared with the other two groups.The biological effects of ESW on kidney caused an increase of γGT in urine,degeneration and or necrosis of tubular cells in ultrastructure, and intrarenal and perirenal bleeding in histology.The biological effects were renovated with absorbtion and or fibrosis in 28 days after ESW. There was a noted relationship between the energy level (generator voltage and shock wave number) and the biological effect on kidney.

雄性家兔45只,分为3组,分别接受三个能量级(20kV,750SW;14kV,1500SW;10kV,3000SW)体外冲击波处理。结果表明,2组动物急性肾损伤程度较其它两组病变轻微。体外冲击波对肾脏的生物学效应表现为尿酶γGT升高;超微结构显示肾小管上皮细胞变性坏死;组织学显示肾内和肾周出血。实验第28天的生物学效应表现为吸收和(或)纤维化修复。体外冲击波能量(包括电压和冲击次数)与其对肾脏生物学效应程度相关。

n

随机将174只大鼠分为Ⅰ、Ⅱ、Ⅲ组,每组58只动物。Ⅰ组:用等渗盐水灌胃;Ⅱ组:用毒蕈匀浆液灌胃;Ⅲ组:毒蕈匀浆液灌胃同时腹腔注射山莨菪碱(654-2)注射液,观察肾脏生化和形态学改变。Ⅱ组灌胃后6h肾皮质自由基有关指标出现明显变化,肾近曲和远曲小管出现超微结构病变,24h后出现光镜下病变,尿钠、钾排泄增加,尿渗透压降低。Ⅲ组灌胃后12h肾皮质匀浆自由基有关指标出现异常变化,肾近曲和远曲小管出现超微结构病变,晚于Ⅱ组出现;48h后出现光镜下病变,尿钠、尿钾排泄增加,尿渗透压降低。说明65个2对毒蕈所致大鼠急性肾损伤有一定的保护作用。

Objective To investigate the functional and pathological changes of acute renal failure induced by aristolochic acid- I in rats. Methods Aristolochic acid- I was extracted from Aristolochia manshuriensis Kom(AMK). Experimental model of acute renal injury was established in the Sprague-Dawley rats with oral administration of aristolochic acid- I, in dosages of 200 mg ·kg~(-1)· d~(-1), 100 mg · kg~(-1) d~(-1) and 50 mg · kg~(-1)·d~(-1)for 3 consecutive days. Serum urea and creatinine...

Objective To investigate the functional and pathological changes of acute renal failure induced by aristolochic acid- I in rats. Methods Aristolochic acid- I was extracted from Aristolochia manshuriensis Kom(AMK). Experimental model of acute renal injury was established in the Sprague-Dawley rats with oral administration of aristolochic acid- I, in dosages of 200 mg ·kg~(-1)· d~(-1), 100 mg · kg~(-1) d~(-1) and 50 mg · kg~(-1)·d~(-1)for 3 consecutive days. Serum urea and creatinine levels, urinary activity of N-acetyl-beta-D-Glucosaminidase (NAG), urinary protein, urinary glucose, urinary volume and urnary osmolality were assayed at the day 4 and 8 of the experiment. Renal histological examination was also performed. Above functional and histological changes were compared to those induced by AMK. Results Renal functional changes of acute nephrotoxicity due to aristolochic acid- I included azotemia, proteinuria, glycouria, NAG enzymuria, and hypoosmotic urine. Histopathological changes in the kidneys of the treated animals showed evidences of acute tubular necrosis, predominantly at the corticomedullary junction. Conclusions Aristolochic acid- I has severe renal toxicity and can induce acute renal failure in rats. The functional and pathological changes mimic those induced by AMK. Aristolochic acid- I may be responsible for the acute nephrotoxicity of AMK.

目的 了解马兜铃酸-Ⅰ肾毒性特点及其在关木通肾毒性中的作用。方法 从关木通中提取纯品马兜铃酸-I,用马兜铃酸-1200mg·kg~(-1)·d~(-1)、100mg·kg~(-1)·d~(-1)和50mg·kg~(-1)·d~(-1)给大鼠连续灌胃3d,引起大鼠急性肾功能损伤。分别于实验第4、第8d留取血、尿和肾组织标本,检测相关肾功能指标,进行组织形态学观察,并与关木通所致大鼠急性肾损伤进行比较。结果 马兜铃酸-Ⅰ作用后,大鼠主要肾功能改变为氮质血症、大量蛋白尿、糖尿、低渗尿、尿NAG酶升高。组织形态学病变主要表现为以皮髓质交界为主的急性肾小管坏死。这些病理表现与关木通所致急性肾损伤极为相似。结论 马兜铃酸-Ⅰ所致大鼠急性肾损伤在肾功能和肾组织形态学表现上与关木通所致急性肾损伤非常相似,这提示马兜铃酸-I是关木通中主要的毒性成分。

 
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