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慢性特發(fā)性軸索性多神經病的病理及免疫組化研究

發(fā)布時間:2018-03-01 00:04

  本文關鍵詞: 慢性特發(fā)性軸索性多神經病 腓腸神經 血栓調節(jié)蛋白 內皮源性一氧化氮合酶 出處:《中風與神經疾病雜志》2017年01期  論文類型:期刊論文


【摘要】:目的 研究慢性特發(fā)性軸索性多神經病(chronic idiopathic axonal polyneuropathy,CIAP)病理改變特點,并探索腓腸神經炎細胞CD3、CD20、CD68抗體及其微小血管內皮細胞膜結合性血栓調節(jié)蛋白(thrombomodulin,TM)、內皮源性一氧化氮合酶(endothelial-nitricoxide synthase,e NOS)的表達規(guī)律。方法 10例經過臨床、電生理、腓腸神經活檢病理檢查證實的CIAP患者,均進行腓腸神經活檢標本的常規(guī)病理組織學染色以及以抗CD3、CD20、CD68、TM、e NOS、v WF(von Willebrand factor,v WF)抗體作為第一抗體的免疫組織化學染色。結果 10例患者腓腸神經病理檢查顯示有髓神經纖維輕-中度減少,伴隨軸索變性和再生,部分可見輕微脫髓鞘改變,4例患者出現毛細血管基底膜肥厚。4例患者腓腸神經神經束衣間小血管周圍有散在分布的CD68陽性單核細胞浸潤。所有患者血管內皮細胞v WF、e NOS、TM均正常表達。結論 CIAP病理特點為軸索損害為主,發(fā)病可能和體液免疫異常有關,部分患者毛細血管基底膜肥厚提示血管內皮細胞可能受損,但內皮細胞功能相關蛋白表達初步提示正常。
[Abstract]:Objective to study the pathological changes of chronic idiopathic axonal polyneuropathy in chronic idiopathic axonal polyneuropathy (CIP). To investigate the expression of CD3 + CD20 + CD68 antibody and thrombomodular thrombomodulin (TMN) and endothelial-derived nitric oxide synthase (NOS) in sural neuritis cells, 10 patients with sural neuritis were enrolled in this study. Sural nerve biopsy confirmed by pathological examination in patients with CIAP, All the specimens of sural nerve biopsy were stained by routine histopathology and immunohistochemical staining of anti CD3 + CD20 WF(von Willebrand factor v WF.Results the pathological examination of sural nerve showed myelinated nerve in 10 patients. Mild to moderate fiber reduction, With axonal degeneration and regeneration, Some slight demyelinating changes were observed in 4 patients with capillary basement membrane hypertrophy. 4 patients had scattered CD68 positive monocyte infiltration around the small vessels between the sural nerve bundles. Vascular endothelial cells were found in all patients. Conclusion the pathological features of CIAP are axonal damage. The pathogenesis may be related to the abnormal humoral immunity. The hypertrophy of capillary basement membrane suggests that vascular endothelial cells may be damaged, but the expression of function-related proteins of endothelial cells may be normal.
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