Dysregulation of proteoglycan production by intrahepatic biliary epithelial cells bearing defective (Delta‐f508) cystic fibrosis transmembrane conductance regulator

K. Ramakrishnan Bhaskar, Bradley S. Turner, Shelley A. Grubman, Douglas M. Jefferson, J.Thomas LaMont – 30 December 2003 – Hepatic dysfunction in cystic fibrosis (CF) has been attributed to accumulation of viscous mucoid secretions in intrahepatic bile ducts. The purpose of our study was to compare glycoconjugate secretion by intrahepatic biliary epithelial (IBE) cells derived from normal livers and livers of CF patients with the delta F508 mutation of the cystic fibrosis transmembrane conductance regulator (CFTR).

Stimulation of inducible nitric oxide synthase in rat liver by hyaluronan fragments

Don C. Rockey, John J. Chung, Charlotte M. McKee, Paul W. Noble – 30 December 2003 – Hepatic injury and chronic wounding are characterized by increased synthesis of extracellular matrix proteins including hyaluronan (HA). Recently, it has been recognized that low‐molecular‐weight fragments of HA, but not native HA (e.g., high‐molecular‐weight HA), induce inflammatory gene expression, and activate the transcriptional regulator, nuclear factor κB (NF‐κB).

Mallory body formation by ethanol feeding in drug‐primed mice

Zhi‐Qi Zhang‐Gouillon, Qi‐X. Yuan, Bing Hu, Norman Marceau, Barbara A. French, Karl Gaal, Yasuki Nagao, Y.‐J. Yvonne Wan, Samuel W. French – 30 December 2003 – Drug‐primed mice, created by a 5‐month feeding of diethyl‐1,4‐dihydro‐2,4,6‐trimethyl‐3,5‐pyridinedicarboxylate (DDC), followed by a 1‐month withdrawal, were refed ethanol or isocaloric dextrose (control) diets intragastrically for 7 days. The formation of Mallory bodies (MBs) was monitored by immunofluorescence and immunoperoxidase microscopy using antibodies to cytokeratin and ubiquitin, and also by electron microscopy.

Lipoprotein changes in children after liver transplantation: Mild hypertriglyceridemia and a decrease in HDL/HDL ratio

Esther Granot – 30 December 2003 – Hyperlipidemia is frequently observed in patients who undergo renal, cardiac, bone marrow, or liver transplantation, and its contribution to the long‐term morbidity and survival of patients with organ transplants may be substantial. In the few studies that have focused on the pediatric age group, findings have been inconsistent. The lipoprotein profile of 10 children after liver transplantation was characterized and compared with those in normal population controls and 10 healthy siblings.

High prevalence of the His63Asp HFE mutation in italian patients with porphyria cutanea tarda

Maurizio Sampietro, Alberto Piperno, Loredana Lupica, Cristina Arosio, Anna Vergani, Noemi Corbetta, Ida Malosio, Michela Mattioli, Anna Ludovica Fracanzani, Maria Domenica Cappellini, Gemino Fiorelli, Silvia Fargion – 30 December 2003 – Sporadic porphyria cutanea tarda (PCT) is caused by a reduced activity of uroporphyrinogen decarboxylase (URO‐D) in the liver. Mild to moderate iron overload is common in PCT, as iron is one of the factors which trigger the clinical manifestations of the disease through the inactivation of URO‐D.

Management of adult patients with ascites caused by cirrhosis

Bruce A. Runyon – 30 December 2003 – Ascites is the most common of the major complications of cirrhosis. The development of ascites is an important landmark in the natural history of cirrhosis and has been proposed as an indication for liver transplantation. The initial evaluation of a patient with ascites should include a history, physical evaluation, and abdominal paracentesis with ascitic fluid analysis. Treatment should consist of abstinence from alcohol, sodium restricted diet, and diuretics. This regimen is effective in ≈90% of patients.

Comparison of liver progenitor cells in human atypical ductular reactions with those seen in experimental models of liver injury

Stewart Sell – 30 December 2003 – The ultrastructural characteristics of liver progenitor cell types of human atypical ductular reactions seen in chronic cholestasis, in regenerating human liver after submassive necrosis, in alcoholic liver disease, and in focal nodular hyperplasia are compared with liver progenitor cell types seen during experimental cholangiocarcinogenesis in hamsters; during hepatocarcinogenesis in rats; and in response to periportal liver injury induced by allyl alcohol in rats.

High prevalence of sleep disturbance in cirrhosis

Juan Córdoba, Juan Cabrera, Louis Lataif, Plamen Penev, Phyllis Zee, Andrés T. Blei – 30 December 2003 – Sleep disturbance is a classic sign of hepatic encephalopathy. However, there are limited data regarding its prevalence in cirrhotic patients without overt hepatic encephalopathy. We assessed the characteristics of sleep in cirrhosis using a sleep questionnaire (n = 44) and actigraphy (n = 20). The results were compared with those of subjects with chronic renal failure and those of healthy controls.

Somatosensory evoked potentials in subclinical portosystemic encephalopathy: A comparison with psychometric tests

Sien‐Sing Yang, Chi‐Hwa Wu, Tsuey‐Ru Chiang, Ding‐Shinn Chen – 30 December 2003 – We prospectively studied the role of somatosensory evoked potentials (SEPs) and psychometric tests in the assessment of subclinical portosystemic encephalopathy (PSE) in 61 cirrhotic patients with grade 0 PSE and 20 controls. Six additional uneducated controls underwent only psychometric tests. Median nerve‐evoked cortical responses were recorded for N20‐N65 interpeak latencies (IPLs). Psychometric tests were conducted within 4 hours of SEP testing.

Bile acid synthesis in primary cultures of rat and human hepatocytes

Ewa Ellis, Bryan Goodwin, Anna Abrahamsson, Chris Liddle, Agneta Mode, Mats Rudling, Ingemar Björkhem, Curt Einarsson – 30 December 2003 – The regulation of hepatic bile acid formation is incompletely understood. Primary cultures of mammalian hepatocytes offer an opportunity to examine putative regulatory factors in relative isolation. Using rat and human hepatocytes in primary culture, we examined bile acid composition and the expression of the rate‐limiting enzyme of formation, cholesterol 7α‐hydroxylase.

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