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纤维化
相关语句
  fibrosis
    TGF-β/Smad Signaling Pathway and Renal Tubulointerstitial Fibrosis
    TGF-β/Smad信号通路在肾小管间质纤维化中的作用及机制的实验研究
短句来源
    Studies on Molecular Pathogenetic Mechanism of Renal Fibrosis
    肾纤维化分子病理机制的研究
短句来源
    The Protective Effects and Mechanisms of PPARγ and TZDs on Renal Tubulointerstitial Inflammation and Fibrosis
    PPARγ和TZDs对肾小管间质炎症和纤维化的保护作用及其机制
短句来源
    The Effect of TNF-α on TEMT of Renal Interstitial Fibrosis and Inhibition Effect of Chinese Herbs Nourishing Kidney and Activing Blood on Transdifferentiation of Tubular Epithelium
    TNF-α对肾间质纤维化细胞表型变化的作用及补肾活血法中药对肾小管上皮细胞转分化的抑制作用
短句来源
    Clinical Study on the Relationship between Transforming Growth Factor Beta-1 and Tubulointerstitial Fibrosis in Obstructive Nephropathy
    转化生长因子β_1与梗阻性肾病肾小管间质纤维化关系的研究
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  “纤维化”译为未确定词的双语例句
    Conclusion RA reduced interstitial inflammation and tubular lesion of UUO rat,this role might be through reducing the expression of RANTES,CCR5 and TGF-β1.
    结论维甲酸能减少UUO大鼠肾间质炎性细胞浸润、减轻肾小管损害,抑制RANTES、CCR5和TGF-β1表达,从而减轻肾脏炎症反应和纤维化
短句来源
    The density of PTC was 14.52±4.85/5285.5m2, and the percentage of endothelial chimerism was 0.16±0.04. There was no correlation between the density of CD31 positive peritubular capillaries and the ratio of microvessels in which endothelial cells were replaced by recipients(r=0.13, P>0.05).
    PTC密度与间质纤维化程度有关,CD31阳性的PTC每单位面积密度14.52±4.85个,微血管内皮细胞嵌合出现比例为0.16±0.04,两者无明显相关性(r=0.13,P>0.05)。
短句来源
    The renal interstitial inflammation may promote the apoptosis in the remnant kidney.
    结论:细胞凋亡参与肾小球硬化、肾小管萎缩及间质纤维化的过程,肾间质炎细胞的浸润更促进残肾凋亡的发生。
短句来源
    The antagonistic effect of adrenomedullin on extracellular matrix accumulation stimulated by transforming growth factor β_1 and the cellular mechanism
    肾上腺髓质素拮抗转化生长因子β_1的促纤维化作用及其机制
短句来源
    Expression of decorin and TGF-β_1 correlate with tubulointerstitial damage in renal biopsy
    肾组织核心蛋白聚糖和转化生长因子-β_1的表达与肾间质纤维化的关系
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  fibrosis
Hepatic steatosis, lobular inflammation, hepatocytic ballooning and fibrosis were presented widespread in NAFLD liver tissues.
      
Mild perisinusoidal fibrosis and periportal fibrosis were often observed in stage 1 cases.
      
According to the statistic analysis, hepatic steatosis was positively correlated with lobular inflammation, hepatocytic ballooning and fibrosis (r = 0.587, 0.488, 0.374, respectively, all P value >amp;lt; 0.01).
      
The number of microgranulomas, lipogranulomas and apoptotic bodies increased following severity of steatosis, lobular inflammation and fibrosis.
      
We suggest that the role of portal inflammation should be emphasized besides hepatic steatosis, lobular inflammation, hepatocyte ballooning and fibrosis in diagnosis and evaluation of NAFLD.
      
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Testicular dysfunction is one of the primary causes of male infertility.Ultrastruc-tural observation of testicular biopsies provides useful approach to the diagnosis of male in-fertiaity.This paper presents an ultrastructural study on tesicular biopsies from 25 caseswith oligospermia or azoospermia.Five kinds of changes were noted in the limiting mem-brane of the seminiferous tubule:(1)thickening and layering of the basal lamina or fold-ing into the seminiferous tubule;(2)thickening of the peritubular tissue...

Testicular dysfunction is one of the primary causes of male infertility.Ultrastruc-tural observation of testicular biopsies provides useful approach to the diagnosis of male in-fertiaity.This paper presents an ultrastructural study on tesicular biopsies from 25 caseswith oligospermia or azoospermia.Five kinds of changes were noted in the limiting mem-brane of the seminiferous tubule:(1)thickening and layering of the basal lamina or fold-ing into the seminiferous tubule;(2)thickening of the peritubular tissue resulting fromincseased intercellular matenials;(3)degeneration of myoid cells;(4)widening of the limit-ing membrane due to diffuse deposition of basement membranoid substance;(5)mast cellsexisting in the lim(?)ting membrane.The endothelial cells of small blood vessels showed sig-nificant thickening,which led to progressive encroachement upon the lumen.The Ser-toli cells contained large amounts of lipid droplets and two kinds of Sertoli cells could beseen:mature and immature Sertoli cells.The mature sertoli cells were joined by typicalSertoli-Sertoli junctions,while the immature Sertoli cells were connected simply by inter-digitating processes and without any blood-testis barrier.The possible significance of thesechanges was discussed.

本文对25例男性不育症患者的睾丸活检组织进行了超微结构观察。结果表明不育症患者睾丸曲细精管界膜有显著变化,主要为界膜增厚、界膜纤维化、基膜样物质沉积、肌样细胞变性及肥大细胞增多。间质中可见结缔组织增生或小血管内皮细胞肿胀。支持细胞有空泡变性,支持细胞综合症患者的支持细胞呈未成熟型,支持细胞间未形成复合连接,而在其它病例,则有血睾屏障存在。

Histological and ultrastructural changes from lesions of 55 patients with Focal

本文对55例FSGS进行临床、实验室、免疫荧光、光镜及电镜观察,认为该病是肾活检中常见的原发性肾小球疾患之一,其检出率为15.7%。病理特点为局灶性节段性病变,突出表现为节段塌陷、节段硬化(100%)、包囊粘连(96.36%),肾间质炎及纤维化(96.36%)。按肾小球上述病变的严重程度将FSGS 分为轻、中、重3型,并对硬化性病变发生的可能机制进行了重点讨论。

While observing the ultrastructural change of renal tissue of the feeding derivant experimental animal and the patients with urolithiasis incorporate hydronephrosis, it is found that calcareous salt will deposit inside the obstructed renal tubule, once there is urinary tract obstruction and increasing of calcium oxalate in urine, and it is also found that there will be series of ultrastructural changes, such as:epithelial cells of renal tubule forming into vesicular structure; shedding and disappearing of microvilli;...

While observing the ultrastructural change of renal tissue of the feeding derivant experimental animal and the patients with urolithiasis incorporate hydronephrosis, it is found that calcareous salt will deposit inside the obstructed renal tubule, once there is urinary tract obstruction and increasing of calcium oxalate in urine, and it is also found that there will be series of ultrastructural changes, such as:epithelial cells of renal tubule forming into vesicular structure; shedding and disappearing of microvilli; vasculization of mitochondria; high electron dense of lysosome in cytoplasma, and etc. Vesicular structure causes block in renal tubule lumen, it also causes cell fragments and high electron dense of calcareous materials to deposit and form microlith. Long-term observation can also cause connective tissue hyperplasia of tubule periphery and fibrorization.

观察服诱石剂实验动物及尿石合并积水病人肾组织的超微结构改变,发现一旦尿路梗阻和尿内草酸钙增加,将导致钙盐在梗阻的肾小管内沉积,相继发生肾小管上皮细胞形成泡状结构,微绒毛的脱落和消失,线粒体的空泡变,胞浆内出现较多高电子密度的溶酶体等改变。泡状结构引起肾小管腔壅塞,使细胞碎片和含钙高电子密度物质等沉积而形成微石。长期梗阻还可引起管周结缔组织增生和纤维化

 
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