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과량의 구리를 지속적으로 투여한 쥐에서 시간적 변화에 따른 간 손상의 전자현미경적 소견
한남익 ( Nam Ik Han ),최상덕 ( Sang Duk Choi ),정규원 ( Kyu Won Chung ),남순우 ( Soon Woo Nam ),한준열 ( Joon Yeol Han ),최상욱 ( Sang Wook Choi ),이영석 ( Young Sok Lee ),선희식 ( Hee Sik Sun ) 대한소화기학회 2003 대한소화기학회지 Vol.41 No.5
Background/Aims: This study was designed to clarify the sequential morphologic changes of copper overloaded-rat liver. Methods: The Sprague-Dawley rats were divided into three groups according to copper and penicillamine administration: Group I. normal control injected with lipiodol; Group II, treated with copper only; Group III, treated with copper plus D-penicillamine. Liver tissues were stained with hematoxylin-eosin and rubeanic acid. In order to elucidate the ultrastructural changes of the liver, transmission electron microscopic examination was also performed. Results: Electron microscopic findings in copper-treated group were characterized by a number of copper-containing lysosomes at pericanalicular ectoplasm, normal sized and bizarre mitochondria with small vacuoles (at 2 weeks), dilated bile canaliculi with decreased microvilli (at 3 weeks), disruption of sinusoidal border (at 4 weeks), microsteatosis (at 5 weeks), a Councilman body-like inclusion in sinusoid and round hepatocytes undergone coagulation necrosis in sinusoid (at 7 weeks), increased collagen bundles in Disse space and loss of microvilli (at 12 weeks). There were increased copper containing granules in hepatocytes of copper plus D-penicillamine treated group, but normal ultrastructural findings were observed. Conclusions: These findings indicate that hepatic injury induced by copper overload is caused by deranged copper metabolism in the lysosome of the hepatocytes and administration of D-penicillamine in copper stressed rats seems to be effective for the restoration of hepatocyte function and morphologic changes. (Korean J Gastroenterol 2003;41:374-381)
만성 바이러스성 간염 환자의 간조직에서 Fas 항원의 면역조직화학적 관찰
최상욱,양진모,김병욱,정규원,최황,선희식,한남익,이창돈,차상복,김성수,남순우 대한소화기학회 1999 대한소화기학회지 Vol.34 No.5
Background/Aims: Fas was proposed as a protein that triggers or mediates apoptosis combining with Fas ligand on cytotoxic T lymphocytes. The mechanism of hepatic injury in chronic viral hepatitis may also include Fas-mediated apoptosis. We evaluated the expression patterns of Fas in liver tissues of patients with chronic viral hepatitis. Methods: Eighty-six liver biopsy samples from patients with chronic viral hepatitis (64 HBsAg positive, 22 anti-HCV positive) were immunohistochemically stained for Fas. Histological findings were evaluated according to the Knodell's Histologic Activity Index (HAI). Results: Incidence of Fas-positive hepatocytes in chronic viral hepatitis was 75.5% (75% in type B and 77.2% in type C). Hepatocellular localization of Fas expression in hepatitis B was the membrane in 89.5% of the patients and the cytoplasm in 87.5% of them. In hepatitis C, it was the membrane in all cases and the cytoplasm in 76.4%. Fas positive hepatocytes were the most frequently detected in periportal area. The prevalence of Fas expression was 100% in chronic active hepatitis of both type B and type C, while in chronic persistent hapatitis, it was 68.8% in type B and 73.3% in type C. There was a positive relationship between the grade of Fas expression and HAI score. Conclusions: Hepatocytic apoptosis associated with Fas expression may play a role in the pathological mechanism of the hepatic injury in chronic viral hepatitis.