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   肾小管间质 的翻译结果: 查询用时:0.037秒
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肾小管间质     
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  renal tubulointerstitial
     Results There were positive correlations between the expressions of CD4+, CD8+ and CD68+ in the renal interstitium and renal tubulointerstitial pathological changes (r_s=0.570,P=0.029;r_s=0.368,P=0.009, r_s=0.468, P=0.003).
     结果 肾间质中CD4+,CD8+,CD68+细胞浸润密度与肾小管间质病变程度呈正相关(rs=0.570, P=0.029;rs=0.368,P=0.009,rs=0.468,P=0.003)。
短句来源
     The degree of renal tubulointerstitial lesion is positively correlated with renal function (P<0.01).
     IgAN 患者的肾功能与肾小管间质病变程度呈显著的正相关(相关系数r=0.564,P<0.01);
短句来源
     PAI-1,TIMP-1 gene expression in renal tubulointerstitial fibrosis of ureteral obstruction and the interfering effects of HGF treatment
     PAI-1和TIMP-1基因在肾小管间质纤维化中的表达及HGF的干预作用
短句来源
     CD40/CD40L and B7-1/CD28 participate in renal tubular epithelial cell injury, immunocompetent cell infiltration and renal tubulointerstitial fibrosis.
     结论在小鼠叶酸性肾病中,肾组织CD40/CD40L和B7-1/CD28的表达上调并参与了肾小管上皮细胞损伤、免疫活性细胞浸润和肾小管间质纤维化的过程。
短句来源
     Effects of omapatrilat on renal tubulointerstitial fibrosis in 5/6 subtotal nephrectomized rats
     omapatrilat对5/6肾切除大鼠肾小管间质病变的影响
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  renal tubular interstitial
     CONCLUSION: p38MAPK may participate in the renal tubular interstitial fibrosis in UUO rats, and the antifibrotic action may be achieved by restraining the pathway of p38MAPK reacted by Atorvastatin.
     结论:丝裂原活化蛋白激酶p38可能参与单侧输尿管梗阻大鼠肾小管间质纤维化过程,阿托伐他汀可能是通过抑制丝裂原活化蛋白激酶p38活性而达到抗肾小管间质纤维化作用的。
短句来源
     AIM: To observe the changes in expressions of mitogen-activated protein kinase (MAPK) p38 and phosphorylation MAPK p38 in renal tubular interstitium of rats with unilateral ureteral occlusion (UUO), and analyze the effect of atorvastatin on renal tubular interstitial fibrosis of p38MAPK and its possible anti-mechanism on renal tubular interstitial fibrosis.
     目的:观察单侧输尿管梗阻大鼠肾小管间质丝裂原活化蛋白激酶p38、磷酸化丝裂原活化蛋白激酶p38的表达变化,分析丝裂原活化蛋白激酶p38在肾小管间质纤维化发生中的作用及阿托伐他汀抗肾小管间质纤维化的可能机制。
短句来源
     Method Group A(without renal tubular interstitial damage,n=12) and group B(with renal tubular interstitial damage,n=19) were compared and analysed.
     方法 将患者分A组 (无合并肾小管间质损害 ,n =12 )和B组 (合并肾小管间质损害 ,n =19)进行对比分析。
短句来源
     The excretion of 24 hour proteinuria decreased in rheic acid group as compared with diabetic group,renal tubular interstitial damage and fibrosis were alleviated as well. The positive expressions of α-SMA and vimentin(0.1449±0.0447 and 0.822±0.0176 respectively)were down-regulated significantly than those in diabetic group(P<0.01).
     大黄酸组大鼠24h尿蛋白排泄较糖尿病组减少,肾小管间质损伤和间质纤维化程度减轻,其肾小管上皮细胞α-SMA、Vimentin阳性表达面积分别为(0.1449±0.0447)和(0.822±0.0176),表达较糖尿病组显著下调(P<0.01)。
短句来源
     Diagnostic value of the combinative measuring of proteinuria electrophoresis and urinary β_2-microglobulin in renal tubular interstitial damage
     尿蛋白电泳及尿β_2微球蛋白联合检测在肾小管间质损伤中的诊断价值
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  renal tubule interstitial
     Effect of Safflower(honghua) on the expression of TGF-β_1, TGF-β_1 mRNA and c-fos in rats with renal tubule interstitial fibrosis
     红花对肾小管间质纤维化大鼠TGF-β_1、TGF-β_1 mRNA及c-fos表达的影响
短句来源
     Relationship between urine α1-MG, NAG and renal tubule interstitial pathological change
     尿α_1-MG和尿NAG与肾小管间质病理变化的关系
短句来源
     Objective To investigate the relationship between urine alpha 1-microglobulin (α1-MG), N-acetyl-beta-D-glucosamidase (NAG) and renal tubule interstitial pathological change.
     目的 探讨尿α1-微球蛋白(α1-MG)、尿N-乙酰-β-D-葡萄糖苷酶(NAG)与肾小管间质病理变化的关系。
短句来源
     Conclusion TGF-β1 promoted the renal tubule interstitial fibrosis in rats with UUO.
     结论TGFβ1促使梗阻性肾病大鼠肾小管间质进行性纤维化。
短句来源
     The rats were sacrificed at 1,4,7,10,and 14 day. Smooth muscle actin(a-SMA),and collagen I,connective tissue growth factor(CTGF),low density lipoprotein receptor-related protein and renal tubule interstitial damage index were detected by HE staining,PAS staining,immunohistochemistry and Western blot respectively.
     手术后第1、4、7、10、14天处死大鼠,经HE染色、PAS染色、天狼星红染色,免疫组化、West-ern蛋白印迹分析方法,观察各组α-平滑肌肌动蛋白、Ⅰ型胶原、结缔组织生长因子、低密度脂蛋白受体相关蛋白及肾小管间质损伤指数。
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  tubular interstitial
     Males were predominant in most renal diseases,females were predominant in lupus nephritis(LN),and tubular interstitial disease.
     大多数肾脏疾病男性占优势,而狼疮性肾炎(LN)、原发性小血管炎肾损害、肾小管间质疾病(TID)女性占优势。
短句来源
     CONCLUSION: p38MAPK may participate in the renal tubular interstitial fibrosis in UUO rats, and the antifibrotic action may be achieved by restraining the pathway of p38MAPK reacted by Atorvastatin.
     结论:丝裂原活化蛋白激酶p38可能参与单侧输尿管梗阻大鼠肾小管间质纤维化过程,阿托伐他汀可能是通过抑制丝裂原活化蛋白激酶p38活性而达到抗肾小管间质纤维化作用的。
短句来源
     Objective Early dignosis of the tubular interstitial damage in elderly diabetic nephropathy with urinary α 1 microglobulin(α 1 MG) were investigated.
     目的 探讨应用尿 α1 -微球蛋白 (α1 - MG)早期诊断老年糖尿病肾病肾小管间质损害。
短句来源
     AIM: To observe the changes in expressions of mitogen-activated protein kinase (MAPK) p38 and phosphorylation MAPK p38 in renal tubular interstitium of rats with unilateral ureteral occlusion (UUO), and analyze the effect of atorvastatin on renal tubular interstitial fibrosis of p38MAPK and its possible anti-mechanism on renal tubular interstitial fibrosis.
     目的:观察单侧输尿管梗阻大鼠肾小管间质丝裂原活化蛋白激酶p38、磷酸化丝裂原活化蛋白激酶p38的表达变化,分析丝裂原活化蛋白激酶p38在肾小管间质纤维化发生中的作用及阿托伐他汀抗肾小管间质纤维化的可能机制。
短句来源
     Method Group A(without renal tubular interstitial damage,n=12) and group B(with renal tubular interstitial damage,n=19) were compared and analysed.
     方法 将患者分A组 (无合并肾小管间质损害 ,n =12 )和B组 (合并肾小管间质损害 ,n =19)进行对比分析。
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  renal tubulointerstitial
Expression of connective tissue growth factor in renal tubulointerstitial fibrosis in rats and its pathogenic role
      
In order to explore the role of connective tissue growth factor (CTGF) in the pathogenesis of renal tubulointerstitial fibrosis, 48 Wistar rats were randomly divided into sham-operated and unilateral ureteral obstruction (UUO) group.
      
The renal tubulointerstitial injury index was evaluated according to the MASSON staining.
      
On the post-UUO day 7, the protein level of CTGF was positively related to the renal tubulointerstitial injury index (r=0.62,P>amp;lt;0.01), the expression of TGF-β1 (r=0.85,P>amp;lt;0.01), col I (r=0.78,P>amp;lt;0.01), and PAI-1 (r=0.76,P>amp;lt;0.01).
      
The role of protease activated receptor-2 (PAR-2) in the renal tubulointerstitial lesion induced by unilateral ureteral obstruction (UUO) was explored.
      
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  tubular interstitial
A patient with myoglobininduced acute tubular interstitial nephritis was found to have initially an asymmetric renal affection as evidenced by renography.
      
Tubular interstitial alterations in these disorders other than cast nephropathy were firmly documented when careful ultrastructural studies were conducted experimentally and using clinical material.
      
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