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Investigation on Etiology of Hepatic Venous Obstruction Budd-Chiari Syndrome

机译:肝静脉阻塞性布加综合征的病因学调查

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摘要

Budd-Chiari syndrome (BCS) is an uncommon clinical condition with a complex etiology. Pathogenesis of BCS is still poorly understood. We included hepatic veno-occlusive lesion tissues of 20 patients (patients group) with hepatic venous obstruction BCS and compared with 20 similar tissues with other etiologies (control group). Morphological changes in hepatic veno-occlusive lesion tissues and the positive expression of proliferating cell nuclear antigen (PCNA), C-myc, and P-53 were observed by the pathological examination (H&E staining) and immunohistochemistry assay. Our results showed that PCNA and C-myc positive cell densities were significantly higher in patient group than control group. P-53 positive cell density showed increasing trends in patients than control group. Moreover, we observed irregular hyperplasia in intimal tissue, fibrous connective tissue, and smooth muscle cell, accompanied by tissue degeneration (hyaloid degeneration and fibrinoid degeneration) and a large quantity of inflammatory cell infiltration. In conclusion, an overexpression of PCNA, C-myc, and a weak positive expression of P53 might launch the extremely irregular hepatic venous intimal hyperplasia, which is probably one of the etiologies of hepatic venous obstruction BCS.
机译:Budd-Chiari综合征(BCS)是一种罕见的临床病因,病因复杂。 BCS的发病机理仍知之甚少。我们纳入了20例肝静脉阻塞BCS患者(患者组)的肝静脉闭塞病变组织,并与20例其他病因相似的组织(对照组)进行了比较。通过病理检查(H&E染色)和免疫组织化学分析观察到肝静脉闭塞病变组织的形态变化以及增殖细胞核抗原(PCNA),C-myc和P-53的阳性表达。我们的结果表明,患者组的PCNA和C-myc阳性细胞密度显着高于对照组。患者的P-53阳性细胞密度比对照组增加。此外,我们在内膜组织,纤维结缔组织和平滑肌细胞中观察到不规则增生,并伴有组织变性(透明质样变性和纤维蛋白样变性)和大量炎性细胞浸润。总之,PCNA,C-myc的过表达和P53的弱阳性表达可能导致极不规则的肝静脉内膜增生,这可能是肝静脉阻塞BCS的病因之一。

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