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肾小管损伤指数
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  “肾小管损伤指数”译为未确定词的双语例句
     Results The expression of CTGF,LRP,Collagen I and a-SMA in UUO group was obviously higher than those in sham group (P<0.01),but significantly higher than those in atorvastatin treatment group (P<0.01).
     结果UUO模型组平滑肌肌动蛋白、Ⅰ型胶原、结缔组织生长因子、低密度脂蛋白受体相关蛋白的表达及肾小管损伤指数均明显高于假手术组(P<0.01),而阿托伐他汀治疗组明显低于模型组(P<0.01)。
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     (2) The expression of TGF-β_(1) in renal tubules obviously increased in all rats with tubulointerstitial injury.
     肾小管TGP-β_1阳性表达率与肾小管损伤指数(TI)呈高度正相关(r=0.971,p<0.01);
短句来源
     ②In the adenine model group, the TBM of the mouse becomes thicker and the amount of matrix in the tubuloinertitiumincrease, the amount of the HGB decreases, and the difference is clear compared with the normal group.
     ②腺嘌呤模型组大鼠TBM增厚,间质基质增多,肾小球损伤指数和肾小管损伤指数评分增加,大鼠尿蛋白和血清肌酐升高,血红蛋白减少,与正常对照组比较,差异具有显著性;
短句来源
     The expression of HSP27 significantly increased in the tubules of the cortex regions in rats with UUO and come to the peak at day 3. Through day 3 to day 14 the positive rates of HSP27 of tubules had a converse correlation with the tubular injury indexes in experimental rats.
     模型组梗阻肾皮质HSP27的表达明显上调,分布于扩张的肾小管,肾小管HSP27阳性表达率于实验第3天达高峰,以后随着肾小管间质损伤程度的加重逐渐下降,并与肾小管损伤指数呈负相关。
短句来源
     ①After 12 weeks, the result of light microscope showed the renal tubules of DM rats atrophied lightly or tube cavity expanded, the epithelial cells presented edema, small fat vacuoles were found in plasma, the injured index of renal tubules increased;
     ①糖尿病组大鼠12周时光镜下可见部分肾小管轻度萎缩或管腔扩张,上皮细胞水肿,胞浆内可见小脂肪空泡,肾小管损伤指数增高;
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     CTGF had positive correlation with the indexes of tubulointerstitial damage and α-SMA.
     CTGF与小管间质损伤指数、α-SMA为正相关关系。
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     Apolipoprotein H gene expression in renal tubule lesion
     小管损伤中载脂蛋白H表达的研究
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     The degree of tubulointerstitial damage was scored by HE and Masson staining.
     并常规行HE和Masson染色观察小管间质损伤指数
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     It also could alleviate the pathological damage of kidney tissue, especially in decreasing renal tubular mesenchymal damage index.
     同时组织病理损伤减轻 ,尤其是小管间质损伤指数明显降低 ;
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     Conclusion:Cadmium may induce non-reversible renal tubular damage.
     结论:镉能引起小管的不可逆损伤;
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Objective: To investigate the expression of heat shock protein 27(HSP27) and its possible role in progression of tubu-lointerstitial lesions in rats. Methods: The time course of the injurious process in rats with unilatral ureteral obstruction (UUO) was examined by histopathology and the expression of HSP27 was observed by immunochemistry. Results: The weak positive signals of HSP27 were located in glomeruli and a few of tubules and collecting ducts in the control rats. The expression of HSP27 significantly...

Objective: To investigate the expression of heat shock protein 27(HSP27) and its possible role in progression of tubu-lointerstitial lesions in rats. Methods: The time course of the injurious process in rats with unilatral ureteral obstruction (UUO) was examined by histopathology and the expression of HSP27 was observed by immunochemistry. Results: The weak positive signals of HSP27 were located in glomeruli and a few of tubules and collecting ducts in the control rats. The expression of HSP27 significantly increased in the tubules of the cortex regions in rats with UUO and come to the peak at day 3. Through day 3 to day 14 the positive rates of HSP27 of tubules had a converse correlation with the tubular injury indexes in experimental rats. Conclusion: The expression of HSP27 inceased in the tubules in rats with tubulointerstitial injury and it may be a protective response for the injurious tubular epithelial cells.

目的:研究肾小管间质损伤大鼠肾组织中热休克蛋白27(HSP27)的表达及其可能的作用。方法:建立单侧输尿管梗阻(UUO)肾小管间质损伤大鼠模型,应用组织病理学和免疫组织化学SP法观察模型组和对照组大鼠肾小管间质损伤情况,以及HSP27的表达。结果:对照组肾小球、少数肾小管和集合管HSP27弱阳性。模型组梗阻肾皮质HSP27的表达明显上调,分布于扩张的肾小管,肾小管HSP27阳性表达率于实验第3天达高峰,以后随着肾小管间质损伤程度的加重逐渐下降,并与肾小管损伤指数呈负相关。结论:肾小管间质损伤过程中,皮质肾小管HSP27表达明显上调;HSP27的表达可能是损伤肾小管上皮细胞的自身保护反应。

AIM: To observe the expression changes of marked proteins: α-smooth muscle actin α-SMA, cyte-keratin CK18 and transforming growth factor-β1 TGF-β1 in renal tubular epithelial myofibroblast transdifferentiation TEMT in rats with Type-2 diabetes mellitus DM, and analyze the possible pathologic mechanisms for occurrence and development of renal tubular lesion and renal interstitial fibrosis in diabetic nephropathy DN. METHODS: The experiment was conducted at the Second Hospital of Hebei Medical University between...

AIM: To observe the expression changes of marked proteins: α-smooth muscle actin α-SMA, cyte-keratin CK18 and transforming growth factor-β1 TGF-β1 in renal tubular epithelial myofibroblast transdifferentiation TEMT in rats with Type-2 diabetes mellitus DM, and analyze the possible pathologic mechanisms for occurrence and development of renal tubular lesion and renal interstitial fibrosis in diabetic nephropathy DN. METHODS: The experiment was conducted at the Second Hospital of Hebei Medical University between October 2002 and May 2003. Totally 40 female SD rats of 8-week old and Grade 2 were divided into 2 groups: control group and DM group, with 20 in each. Type-2 DM rat models were established by a combination of high-sugar and high-fat diets and small dose of streptozotocin intraperitoneal injection. The pathological and functional changes of DN rats were observed after 12, 24 weeks in both groups. The expressions of α-SMA, CK18, TGF-β1 in renal tubular epithelial cells were detected by immunohistochemical method and flow cytometry in the transforming process. RESULTS: Totally 16 rats in DM group and 20 rats in the control group were involved in the result analysis, with other 4 rats were excluded because the blood sugar did not increase.①After 12 weeks, the result of light microscope showed the renal tubules of DM rats atrophied lightly or tube cavity expanded, the epithelial cells presented edema, small fat vacuoles were found in plasma, the injured index of renal tubules increased; After 24 weeks, the above changes became more severer, the deciduous cells were found in the tubules. The result of electron microscope showed the mitochondrion presented edema partly, the cristae disappeared mostly, the microvilli reduced remarkably, part of renal tubular basement membrane thickened obviously, mass collagen fibres were seen between the tubules.②Immunohistochemical result: In the plasma of renal tubular epithelial cell of DM rats, the expressions of α-SMA, TGF-β1 enhanced and the expression of CK18 decreased, which all aggravated with the disease course. ③The detected results of α-SMA and TGF-β1 by flow cytometry were coincided with those by immunohistochemical method. Furthermore, the injured index of renal tubules had significantly positive correlation with triacylglycerol, cholesterol, urine albumin excretory rate, and negative correlation with creatinine clearance rate. CONCLUSION: TEMT indeed exists in the process of DN in Type-2 DM, and TGF-β1 is a key cytokine of it. TEMT is also paralleled with the decreased level of the renal function.

目的:观察2型糖尿病大鼠肾小管上皮细胞转分化过程中的标志蛋白α-平滑肌肌动蛋白、角蛋白18及转化生长因子β1表达变化,分析糖尿病肾病时肾小管病变、肾间质纤维化可能的发生、发展机制。方法:实验于2002-10/2003-05在河北医科大学第二医院完成。纳入二级8周龄雌性SD大鼠40只。随机分为正常对照组和糖尿病组,各20只。通过高糖、高脂饮食加腹腔注射小剂量链脲佐菌素的方法,制作2型糖尿病大鼠模型。分别动态观察12,24周时对照组,糖尿病组大鼠糖尿病肾病时,肾脏的病理改变及功能变化,并同时应用免疫组化技术及流式细胞学技术检测肾小管上皮细胞转分化过程中的标志蛋白:α-平滑肌肌动蛋白、角蛋白18及转化生长因子β1在肾小管上皮细胞中的表达。结果:糖尿病组共成模16只,血糖没有升高的大鼠未纳入结果分析,两组共纳入结果分析36只。①糖尿病组大鼠12周时光镜下可见部分肾小管轻度萎缩或管腔扩张,上皮细胞水肿,胞浆内可见小脂肪空泡,肾小管损伤指数增高;24周时上述变化程度加深,管腔内可见破碎脱落的细胞。24周电镜下可见线粒体部分水肿,嵴大部分消失,微绒毛显著减少,部分肾小管基底膜明显增厚,小管间可见大量胶原纤维。②...

目的:观察2型糖尿病大鼠肾小管上皮细胞转分化过程中的标志蛋白α-平滑肌肌动蛋白、角蛋白18及转化生长因子β1表达变化,分析糖尿病肾病时肾小管病变、肾间质纤维化可能的发生、发展机制。方法:实验于2002-10/2003-05在河北医科大学第二医院完成。纳入二级8周龄雌性SD大鼠40只。随机分为正常对照组和糖尿病组,各20只。通过高糖、高脂饮食加腹腔注射小剂量链脲佐菌素的方法,制作2型糖尿病大鼠模型。分别动态观察12,24周时对照组,糖尿病组大鼠糖尿病肾病时,肾脏的病理改变及功能变化,并同时应用免疫组化技术及流式细胞学技术检测肾小管上皮细胞转分化过程中的标志蛋白:α-平滑肌肌动蛋白、角蛋白18及转化生长因子β1在肾小管上皮细胞中的表达。结果:糖尿病组共成模16只,血糖没有升高的大鼠未纳入结果分析,两组共纳入结果分析36只。①糖尿病组大鼠12周时光镜下可见部分肾小管轻度萎缩或管腔扩张,上皮细胞水肿,胞浆内可见小脂肪空泡,肾小管损伤指数增高;24周时上述变化程度加深,管腔内可见破碎脱落的细胞。24周电镜下可见线粒体部分水肿,嵴大部分消失,微绒毛显著减少,部分肾小管基底膜明显增厚,小管间可见大量胶原纤维。②免疫组化显示:糖尿病组大鼠肾小管上皮细胞胞浆中α-平滑肌肌动蛋白、转化生长因子β1表达增强,角蛋白18表达则下降,它们均随病程进展而加重。③流式测α-平滑肌肌动蛋白及转化生长因子β1表达与免疫组化结果一致,并且与三酰甘油、胆固醇、24h尿白蛋白排泄率明显正相关,与肌酐清除率负相关。结论:在2型糖尿病肾病的发展过程中确实存在小管上皮-肌成纤维细胞转分化,而且转化生长因子β1是其重要的促进因子。小管上皮-肌成纤维细胞转分化与肾功能下降的程度相平行。

Objective To investigate the effects of atorvastatin on renal interstitial fibrosis of unilateral ureteral obstruction(UUO) in rats and its mechanism.Methods The Rats model of renal interstitial fibrosis was made with unilateral urethral ligation,which were randomly divided into three groups: sham operation group(SOG),model group(UUO),atorvastatin treatment group.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...

Objective To investigate the effects of atorvastatin on renal interstitial fibrosis of unilateral ureteral obstruction(UUO) in rats and its mechanism.Methods The Rats model of renal interstitial fibrosis was made with unilateral urethral ligation,which were randomly divided into three groups: sham operation group(SOG),model group(UUO),atorvastatin treatment group.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.Results The expression of CTGF,LRP,Collagen I and a-SMA in UUO group was obviously higher than those in sham group (P<0.01),but significantly higher than those in atorvastatin treatment group (P<0.01).Conclusion Connective tissue growth factor,low density lipoprotein receptor-related protein and renal interstitial fibrosis developed in the same way.Atorvastatin may decrease the expression of low density lipoprotein receptor-related protein,downregulate the expression of Collagen I and a-smooth muscle actin and delay the development of renal interstitial fibrosis.

目的观察阿托伐他汀对单侧输尿管梗阻(UUO)大鼠模型肾间质纤维化的作用及机制。方法采用单侧输尿管结扎术致肾间质纤维化大鼠模型,将大鼠随机分为3组:假手术组、UUO模型组、阿托伐他汀治疗组。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。结果UUO模型组平滑肌肌动蛋白、Ⅰ型胶原、结缔组织生长因子、低密度脂蛋白受体相关蛋白的表达及肾小管损伤指数均明显高于假手术组(P<0.01),而阿托伐他汀治疗组明显低于模型组(P<0.01)。结论结缔组织生长因子、低密度脂蛋白受体相关蛋白与肾间质纤维化进展相一致;阿托伐他汀减少单侧输尿管梗阻侧大鼠肾脏低密度脂蛋白受体相关蛋白的表达,下调单侧输尿管梗阻侧大鼠肾脏Ⅰ型胶原、平滑肌肌动蛋白的表达,阿托伐他汀通过非降脂途径延缓UUO所致大鼠肾间质纤维化的程度。

 
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