Hepatic Kupffer cells: The portal that permits infection of hepatocytes by malarial sporozoites?
John W. Barnwell – 30 December 2003
John W. Barnwell – 30 December 2003
Marius C. Van Den Heuvel, Maarten J. H. Slooff, Lydia Visser, Michael Muller, Koert P. De Jong, Sibrand Poppema, Annette S. H. Gouw – 30 December 2003 – Following hepatic injury, proliferation of anastomosing ductules can be observed. The origin of this ductular reaction is not completely clear, although there is considerable evidence for proliferation of a putative hepatic progenitor cell, reported to be located in the canals of Hering (CoH) and showing morphologic similarities with rat oval cells.
Carol J. Soroka, John M. Lee, Francesco Azzaroli, James L. Boyer – 30 December 2003 – The hepatic expression of the ATP‐dependent conjugate export pump multidrug resistance–associated protein 2 (Mrp2) is diminished in experimentally induced models of cholestasis. In this study we have examined the localization and expression of Mrp3, another member of the multidrug resistance–associated protein family, in normal liver and after obstructive cholestasis in the rat.
Yoshimichi Haruna, Tsutomu Kanda, Masaharu Honda, Tetsuto Takao, Norio Hayashi – 30 December 2003 – The pathobiology of hepatitis C virus (HCV) in the biliary system has not been clarified yet, although bile duct damage is a histological finding characteristic of chronic hepatitis C. In this study, we examined whether HCV infects bile ducts and is released into the bile. Twelve patients positive for serum HCV antibody were examined in this study, and eight were seropositive for HCV RNA by polymerase chain reaction (PCR).
Hisashi Taniai, Makoto Suematsu, Tsuneharu Suzuki, Shinji Norimizu, Rio Hori, Yuzuru Ishimura, Yuji Nimura – 30 December 2003 – This study aimed to investigate the roles of endothelin (ET) receptors in biliary dysfunction and cell injury in postischemic livers. Rat livers perfused with oxygenated Krebs‐Henseleit solution were exposed to reoxygenation following 20‐minute hypoxia. The anoxic perfusion decreased bile output and reduced cyclic guanosine monophosphate (cGMP) contents, an index of nitric oxide (NO) generation.
Lichuan Liu, Ming Zhang, Bao Luo, Gary A. Abrams, Michael B. Fallon – 30 December 2003 – The hepatopulmonary syndrome (HPS) results from pulmonary microvascular dilatation in cirrhosis and is associated with increased pulmonary endothelial nitric oxide synthase (eNOS) levels. In the common bile duct ligation (CBDL) model, endothelin‐1 (ET‐1) released from the liver contributes to the rise in pulmonary eNOS and intrapulmonary vasodilatation.
Marcus Schmitt, Ralf Kubitz, Sabine Lizun, Matthias Wettstein, Dieter Häussinger – 30 December 2003 – Canalicular transport via the bile salt export pump (Bsep) represents the rate‐controlling step in taurocholate excretion, whose capacity is under osmotic control. The short‐term effects of anisoosmolarity and Ca2+‐withdrawal on the localization of Bsep and the tight junction proteins Zo‐1 and occludin were studied in perfused rat liver by immunohistochemistry, confocal microscopy, and densitometry.
Gernot Zollner, Peter Fickert, Rainer Zenz, Andrea Fuchsbichler, Conny Stumptner, Lukas Kenner, Peter Ferenci, Rudolf E. Stauber, Guenter J. Krejs, Helmut Denk, Kurt Zatloukal, Michael Trauner – 30 December 2003 – Reduced hepatobiliary transporter expression could explain impaired hepatic uptake and excretion of bile salts and other biliary constituents resulting in cholestasis and jaundice. Because little is known about alterations of hepatobiliary transport systems in human cholestatic liver diseases, it was the aim of this study to investigate such potential changes.
Germana V. Gregorio, Bernard Portmann, John Karani, Phil Harrison, Peter T. Donaldson, Diego Vergani, Giorgina Mieli‐Vergani – 30 December 2003 – To investigate whether sclerosing cholangitis with an autoimmune serology characteristic of autoimmune hepatitis (AIH) and AIH are distinct entities, we studied 55 consecutive children with clinical and/or biochemical evidence of liver disease and circulating antinuclear (ANA), anti‐smooth muscle (SMA), and/or liver‐kidney‐microsomal type 1 (LKM1) autoantibodies.
Michael T. Milliano, Bruce A. Luxon – 30 December 2003 – The role of cytosolic fatty acid binding protein (FABP) in cellular fatty acid metabolism remains poorly defined. The intracellular movement of fatty acids is thought to be facilitated through codiffusion with FABP. Peroxisomal proliferators like clofibrate induce FABP and may stimulate fatty acid use by increasing cytoplasmic diffusion rates. Our aim was to determine if induction of FABP by clofibrate increases the cytoplasmic transport of a fluorescent fatty acid NBD‐stearate.