足突
- 网络foot process
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其病理特点为:在毛细血管内增生的基础上有细胞新月体形成,可见IgG、C3的颗粒状沉积物沿毛细血管袢连续排列,且发现不典型驼峰和部分足突融合;
The pathological features showed that cell crescent was formed on the basis of endocapillary proliferation ; the granular deposition of IgG and C3 was found along the blood capillary , and nontypical hump and partial foot process fusion were also detected .
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缺血12h再灌注3h后胞饮明显减少,线粒体肿胀也少见,但紧密连接开放增加,足突层空泡化呈(+++ ̄++++)。
Besides , pinocytosis and swelling of mitochondrion decreased , but tight junction opening increased 12 h after ischemia and 3 h reperfusion , with foot process vacuoles of astrocyte ( + + + to + + + + ) .
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方法:建立嘌呤霉素(PAN)大鼠肾病模型,用体视学方法检测足突形态改变;
Methods : Puromycin aminonucleoside ( PAN ) nephrosis was established .
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E2组肾脏电镜下见肾小球足突融合。
Electron microscopy of kidneys in group E 2 revealed a fusion of podocytic foot processes .
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目的:研究抗RAP抗体对肾小球上皮足突细胞RAP基因表达调控。
Objective : To research Antibody-induced rat glomerular podocytes RAP gene expression changes in vitro .
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一个有条件的表达模型用来从足突细胞中删除VEGF基因,在四环素衍生物的出现下靶基因被删除。
A conditional expression model , in which the target gene is deleted in the presence of a tetracycline derivative , was used to delete the VEGF gene from podocytes .
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家族性FSGS也可因为某些不同的足突细胞蛋白改变而发生。
Familial forms of FSGS also exist due to alterations of several different podocyte proteins .
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WT1和EGFR双重免疫组化显示阿霉素肾病组EGFR可在足突细胞上表达,正常组则无。
Double-immunohistochemical staining of WT1 and EGFR showed EGFR was co-expressed with WT1 in podocytes in nephrotic rats , but not in control rats .
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肾脏形态变化:B组6h后表现为肾小球GBM断裂、上皮细胞足突融合,肾小管上皮细胞线粒体空泡变性;C组肾损伤明显减轻。
After 6 hours , under electron microscope the renal glomeruli GBM fractured , epithelial cell foot processe obviously fused , and large quantities of mesangial cell mitochondria vacuole degenerated in group A.
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缺血3h再灌注3h中心区足突层空泡化呈(++),边缘区呈(+++);
Foot process vacuoles of astrocyte was ( + + ) in center to ( + + + ) in margins 3h after ischemia and 3 h reperfusion ;
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13块近视网膜面MP有大量足突细胞,其周围胶原丰富,细胞数量和类型增多,包括典型的成纤维样细胞和神经胶质样细胞。
While cells with foot processes were found in 13 membrane sections near the retina and increasing number of various types of cells rich in collagen around were observed including fibroblast-like cells and glial cells .
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日本学者川口吾曾报道过FK506可降低肾病大鼠的蛋白尿,减轻肾小球足突融合及基底膜负电荷位点丢失的程度。
One Japanese scholar reported FK506 could cut down the amount of 24h urine protein of rats , alleviated the fusion of foot processes , reduced the number of missed anionic sites in glomerular basement membranes .
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4~7d,星形细胞高度肿胀,胞质内充满水肿液,细胞器消失,细胞变性,毛细血管周围细胞足突明显肿胀,血管周围间隙见微小出血灶。
To 7 d after , there was severe swelling of astrocyte , abundant fluids in the cytoplasm , organelles vanishing , neuron degeneration , severe swelling of end plate around the capillary and minor focus of hemorrhage in the Virchow Robin space .
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在69例不同病理类型原发性肾病综合征和血尿患儿的肾组织,应用免疫组化法检测perlecan表达,并分别与尿蛋白肌酐比值及电镜下平均足突宽度(FPW)进行相关分析。
Immunohistochemical staining for perlecan was performed in renal biopsies from children with nephritic syndrome or hematuria , with analysis of the correlation of urine protein and foot process width with glomerular expression of perlecan .
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结果:益气养阴、清利活血中药可减少阿霉素肾病大鼠尿蛋白的排泄量,提高血清ALB含量,降低血清TG、CHOL、IL8、TNFα的含量,修复肾小球上皮细胞足突的结构。
Results : The drugs of Yi-Qi Yang-Yin and Qing-Li Huo-Xue can decrease the amount of protein in urine , promote the level of ALB and lower the CHOL , TG , IL-8 , TNF - α in serum , repair injured foot process of glomerule epithelial cell .
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肾小球上皮足突细胞培养表皮生长因子对肾小球上皮影响的实验研究
The Influence of Epidermal Growth Factor on Glomerular Epithelia Cell
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足突变形、融合。
Deformation and confluence of foot processes were also observed .
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嘌呤霉素肾病鼠足突形态改变的形态计量学研究
Morphometric analysis of glomerular foot process in puromycin aminonucleoside nephropathy in rats
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结果:收获的培养细胞为肾小球上皮足突细胞。
Results : Cultured kidney epithelial cells in defined medium characterized as glomerular phagocyte .
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电镜下观察不同缺血时间点胶质细胞足突层空泡化程度。
The glial cell vacuolization degree in foot process layer at different ischemic time points .
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模型组大鼠基底膜阶段增厚、足突融合。
The basement membrane was thickening , and the foot process was fusion in DKD rats .
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嘌呤霉素肾病鼠尿蛋白量与足突形态改变的关系
Correlation between urinary protein excretion and morphometric changes of glomerular foot process in rats with puromycin aminonucleoside nephropathy
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待适应该剂量吉西他滨后,细胞体积缩小,足突消失。
When the cells adapted the dose of gemcitabine , they turned shrinkage , and foot processes disappeared .
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结论:电子显微镜检查证实,在血管畸形病灶周围的脑组织内可见病理性血管。该血管的基膜发生病变,血管周围的星形细胞足突明显减少或破坏。
Conclusion : Electron microscopy shows a kind of pathological vessel in the brain tissue surround the malformation focus .
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3例上皮细胞足突融合消失,上皮下电子致密物沉积。
Ultrastructural microscopy feature is characterized by subepithelial electron-dense deposits and the loss of epithelial foot processes in 3 cases .
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他们制造了一个实验的鼠模型,只定向于足突细胞,它是肾小球血管内皮生长因子产生的主要来源。
They created an experimental mouse model that only targeted podocytes , which are the major source of glomerular VEGF production .
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电镜结果显示模型组小鼠肾小球系膜区有明显电子致密物沉积,足突融合;
Electron microscope showed that mesangium region enlarged with obvious electron dense deposits , and foot process fusion was seen extensively in model group .
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结果在吉西他滨作用后,细胞会表现出形态学上的改变,细胞体积变大,伸出足突,类似神经细胞样改变。
Results After adding gemcitabine , the cells showed morphological changes , cells became larger , extended foot processes , similar to the nerve cell-like change .
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利用图像分析仪和体视学方法分别对肾小球滤过屏障多价阴离子变化及上皮细胞足突的病变进行形态计量学研究。
The changes of polyanion of the glomerular filtration barrier and the morphological changes of epithelial foot processes were studied using an Image Analyzer and stereological techniques .
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毛细血管基底膜局部增厚,肾小球脏层上皮细胞出现不同程度的足突融合现象并伴有部分线粒体空泡变性。
Capillary basement membrane thickened locally , foot processes fusion of visceral epithelial cells were found in varying degrees , accompanied by vacuolar degeneration of some mitochondrial .