scholarly journals Ductal or Ductular Proliferation

2020 ◽  
Author(s):  
Keyword(s):  
Ductular Proliferation

scholarly journals Ultrastructural Changes in the Pancreata of Selenium-Vitamin E-Deficient Chicks

1977 ◽  
Vol 14 (6) ◽  
pp. 629-642 ◽  
Author(s):  
A. H. Rebar ◽  
J. F. Van Vleet
Keyword(s):  
Endoplasmic Reticulum ◽  
Vitamin E ◽  
Acinar Cell ◽  
Interstitial Fibrosis ◽  
Ultrastructural Changes ◽  
Zymogen Granules ◽  
Cell Cytoplasm ◽  
Torula Yeast ◽  
Cell Changes ◽  
Ductular Proliferation

Three hundred and seventy 1-day-old male, white Leghorn chicks were divided into seven groups and fed a series of semipurified torula yeast diets either deficient in or supplemented with selenium and vitamin E. Chicks in each group were necropsied sequentially and the pancreata examined by light microscopy. Selected pancreata of selenium deficient chicks in various stages of the deficiency disease were examined by electron microscopy. Supplements of either selenium (0.2 mg/kg) or vitamin E (100 IU/kg diet) resulted in protection against pancreatic lesions. Changes in pancreata of selenium deficient chicks progressed from cytoplasmic vacuolation of acinar cell cytoplasm to focal disseminated acinar necrosis. There was ductular proliferation and interstitial fibrosis in advanced lesions. Acini around islets were less frequently affected than acini further away. Ultrastructurally, the mildest lesions were focal dilation of the endoplasmic reticulum and autophagic vacuoles in acinar cell cytoplasm. Necrotic areas contained both membranous and granular debris and fragments of intact endoplasmic reticulum. In fibrotic pancreata the main acinar cell changes were uniform dilation of endoplasmic reticulum and reduction in number of zymogen granules.

New monoclonal antibodies reacting with bile ducts: Further insights into the pathogenesis of bile ductular proliferation in biliary diseases

1991 ◽  
Vol 165 (2) ◽  
pp. 153-161 ◽  
Author(s):  
Reuben C. S. Ayres ◽  
Stefan G. Hübscher ◽  
Jean Shaw ◽  
Chris Garner ◽  
Ruth Joplin ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Bile Ducts ◽  
Biliary Diseases ◽  
Ductular Proliferation

Copper deposition in focal nodular hyperplasia and inflammatory hepatocellular adenoma

2017 ◽  
Vol 71 (6) ◽  
pp. 504-507 ◽  
Author(s):  
Vishal S Chandan ◽  
Sejal S Shah ◽  
Taofic Mounajjed ◽  
Michael S Torbenson ◽  
Tsung-Teh Wu
Keyword(s):  
Focal Nodular Hyperplasia ◽  
Hepatocellular Adenoma ◽  
Copper Deposition ◽  
Histological Features ◽  
Nodular Hyperplasia ◽  
Portal Tracts ◽  
Ductular Proliferation

AimsTo examine copper deposition in focal nodular hyperplasia (FNH) and inflammatory hepatocellular adenoma (IHA) and to determine if it can play a role in their differentiation.Methods28 FNHs and 19 IHAs from surgical resections showing typical morphological and immunohistochemical features were stained with rhodanine to evaluate for copper deposition. Histological features such as nodularity, fibrous bands, ductular proliferation, steatosis, ballooned hepatocytes and lymphocytic inflammation were also scored.ResultsCopper deposition was detected in 96% (27/28) of FNHs and 37% (7/19) of IHAs, P<0.001. In all cases, copper was seen within the hepatocytes only around the pseudo-portal tracts or areas of fibrosis. Copper deposition in IHA was significantly associated with presence of lymphocytic inflammation (P=0.04) but not associated with features like nodularity, fibrous bands, ductular proliferation, ballooned hepatocytes and steatosis (P>0.05, for all). In FNH, the presence and degree of copper deposition was not significantly associated with any histological features (P>0.05, for all).ConclusionsCopper deposition occurs more frequently in FNH (96%) than IHA (37%), P<0.001. However, the presence of copper alone cannot be used as a feature to differentiate between FNH and IHA.

Caspase 1 overexpression in chronic pancreatitis due to ductular proliferation

2000 ◽  
Vol 118 (4) ◽  
pp. A1042
Author(s):  
Marco Ramadani ◽  
Yinmo Yang ◽  
Frank Gansauge ◽  
Hans G. Beger ◽  
Susanne Gansauge
Keyword(s):  
Chronic Pancreatitis ◽  
Caspase 1 ◽  
Ductular Proliferation

Gadolinium chloride, a Kupffer cell inhibitor, attenuates hepatic injury in a rat model of chronic cholestasis

2011 ◽  
Vol 30 (11) ◽  
pp. 1804-1810 ◽  
Author(s):  
Ali Zandieh ◽  
Seyedmehedi Payabvash ◽  
Parvin Pasalar ◽  
Afsaneh Morteza ◽  
Basira Zandieh ◽  
...  
Keyword(s):  
Kupffer Cell ◽  
Kupffer Cells ◽  
Enzyme Activities ◽  
Hepatic Injury ◽  
Morphological Changes ◽  
Gadolinium Chloride ◽  
Sham Operation ◽  
Chronic Cholestasis ◽  
Duct Ligation ◽  
Ductular Proliferation

The aim of the current study was to elucidate the effect of Kupffer cells inhibition on hepatic injury induced by chronic cholestasis. Sprague-Dawley rats underwent bile duct ligation (BDL) or sham operation and were treated with either saline solution or gadolinium chloride (GdCl3, a specific Kupffer cell inhibitor, 20 mg/kg i.p. daily). Serum and liver samples were collected after 28 days. Direct and total bilirubin concentrations and serum enzyme activities of alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and γ-glutamyl transpeptidase (GGT) increased following BDL ( p < 0.01). On the contrary to bilirubin concentrations and AST activity, GdCl3 partially prevented the elevation in ALP, ALT and GGT enzyme activities ( p < 0.05). GdCl3 alleviated lipid peroxidation (reflected by malondialdehyde [MDA] concentration) and increased the activities of antioxidant enzymes (i.e. catalase and glutathione peroxidase) in liver samples after BDL ( p < 0.05). Fibrosis, ductular proliferation and portal inflammation were also scored in liver samples. Among morphological changes appeared following BDL (i.e. marked fibrosis, portal inflammation and ductular proliferation); only ductular proliferation was not alleviated by GdCl3. Therefore, Kupffer cells inhibition has beneficial effects against the development of hepatic injury induced by chronic cholestasis.

scholarly journals Human extrahepatic biliary atresia: portal connective tissue activation related to ductular proliferation

2008 ◽  
Vol 6 (5) ◽  
pp. 253-261 ◽  
Author(s):  
L. A. R. Freitas ◽  
Michèle Chevallier ◽  
Dominique Louis ◽  
Jean-Alexis Grimaud
Keyword(s):  
Connective Tissue ◽  
Biliary Atresia ◽  
Extrahepatic Biliary Atresia ◽  
Ductular Proliferation

scholarly journals Steatohepatitis in laboratory opossums exhibiting a high lipemic response to dietary cholesterol and fat

2012 ◽  
Vol 303 (1) ◽  
pp. G12-G19 ◽  
Author(s):  
Jeannie Chan ◽  
Francis E. Sharkey ◽  
Rampratap S. Kushwaha ◽  
Jane F. VandeBerg ◽  
John L. VandeBerg
Keyword(s):  
Gene Expression ◽  
Expression Patterns ◽  
Dietary Cholesterol ◽  
Inflammatory Cells ◽  
Low Responders ◽  
Fatty Livers ◽  
Histological Characteristics ◽  
Collagen Genes ◽  
High Responders ◽  
Ductular Proliferation

Plasma VLDL and LDL cholesterol were markedly elevated (>40-fold) in high-responding opossums, but moderately elevated (6-fold) in low-responding opossums after they had consumed a high-cholesterol and high-fat diet for 24 wk. In both high- and low-responding opossums, plasma triglycerides were slightly elevated, threefold and twofold, respectively. Dietary challenge also induced fatty livers in high responders, but not in low responders. We studied the lipid composition, histopathological features, and gene expression patterns of the fatty livers. Free cholesterol (2-fold), esterified cholesterol (11-fold), and triglycerides (2-fold) were higher in the livers of high responders than those in low responders, whereas free fatty acid levels were similar. The fatty livers of high responders showed extensive lobular disarray by histology. Inflammatory cells and ballooned hepatocytes were also present, as were perisinusoidal fibrosis and ductular proliferation. In contrast, liver histology was normal in low responders. Hepatic gene expression revealed differences associated with the development of steatohepatitis in high responders. The accumulation of hepatic cholesterol was concomitant with upregulation of the HMGCR gene and downregulation of the CYP27A1, ABCG8, and ABCB4 genes. Genes involved in inflammation ( TNF, NFKB1, and COX2) and in oxidative stress ( CYBA and NCF1) were upregulated. Upregulation of the growth factor genes ( PDGF and TGFB1) and collagen genes ( Col1A1, Col3A1, and Col4A1) was consistent with fibrosis. Some of the histological characteristics of the fatty livers of high-responding opossums imitate those in the livers of humans with nonalcoholic steatohepatitis.

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