Cholesteryl esters from oxidized low‐density lipoproteins are in vivo rapidly hydrolyzed in rat kupffer cells and transported to liver parenchymal cells and bile

Moniek N. Pieters, Sebastiaan Esbach, Donald Schouten, Adriaan Brouwer, Dick L. Knook, Theo J. C. Van Berkel – 1 June 1994 – Human low‐density lipoprotein was labeled in its cholesteryl ester moiety with [3H]cholesteryl oleate or [3H]cholesteryl oleoyl ether and oxidized by exposure to 10 μmol/L of cupric sulfate. The in vivo metabolism of cholesteryl esters of oxidized low‐density lipoprotein was determined after injection into rats.

Collagenase pretreatment and the mitogenic effects of hepatocyte growth factor and transforming growth factor‐α in adult rat liver

Meng‐Lun Liu, Wendy M. Mars, Reza Zarnegar, George K. Michalopoulos – 1 June 1994 – Hepatocyte growth factor and transforming growth factor‐α are two well‐known hepatomitogens for primary hepatocyte cultures. Here we report that these two growth factors also stimulate in vivo DNA syntheses in normal, unoperated, adult rat liver after 24‐hr continuous intraportal infusion. As determined by an immunohistochemical staining technique, 5‐bromo‐2′‐deoxyuridine incorporation was increased in a dose‐dependent fashion after infusion of up to 10 μg of growth factor/100 gm body weight in the rat.

Transport of lactoferrin from blood to bile in the rat

Erwin Regoeczi, Paul A. Chindemi, Wei‐Li Hu – 1 June 1994 – The bile contains small quantities of lactoferrin, the origin of which is uncertain. For this reason, we studied the liver's capability of transferring lactoferrin from the plasma to the bile by injecting a dose (10 to 20 μg/100 gm) of labeled bovine lactoferrin intravenously and following its appearance in bile over 3 hr. Whether diferric or iron free, lactoferrin peaked in the bile 35 min after administration (i.e., the same time as bovine lactoperoxidase and diferric rat transferrin).

Ammonia‐induced brain edema and intracranial hypertension in rats after portacaval anastomosis

Andres T. Blei, Sigurdur Olafsson, Guy Therrien, Roger F. Butterworth – 1 June 1994 – Brain edema, leading to intracranial hypertension and brain herniation, is a major cause of death in fulminant liver failure. Astrocyte swelling is a prominent neuropathological feature in experimental fulminant liver failure. It has been postulated that the osmotic effects of glutamine, generated in astrocytes from ammonia and glutamate in a reaction catalyzed by glutamine synthetase, could mediate brain swelling.

Quantitative detection of hepatitis C virus RNA with a solid‐phase signal amplification method: Definition of optimal conditions for specimen collection and clinical application in interferon‐treated patients

Gary L. Davis, Johnson Y.‐N. Lau, Mickie S. Urdea, Paul D. Neuwald, Judith C. Wilber, Karen Lindsay, Robert P. Perrillo, Janice Albrecht – 1 June 1994 – To determine the optimal conditions for preparation of serum specimens for quantitative hepatitis C virus RNA determination, patient samples were processed such that differences in time from clot formation to centrifugation, centrifugation to separation of serum and collection of serum until freezing could be independently assessed. The effects of multiple cycles of freezing and thawing were also determined.

Nonsuppurative cholangitis is induced in neonatally thymectomized mice: A possible animal model for primary biliary cirrhosis

Haruhiko Kobashi, Kazuhide Yamamoto, Toshifumi Yoshioka, Minoru Tomita, Takao Tsuji – 1 June 1994 – Neonatally thymectomized mice are unique in that they are prone to organ‐specific autoimmune diseases. We investigated whether autoimmune cholangitis could be induced in these mice when they were immunized with biliary antigens. Neonatally thymectomized A/J mice were immunized with porcine intrahepatic bile duct epithelial cells (group 1), porcine gallbladder epithelial cells (group 2), porcine splenocytes (group 3) or Freund's adjuvant (group 4).

Lipopolysaccharide‐neutralizing antibody reduces hepatocyte injury from acute hepatotoxin administration

Mark J. Czaja, Jun Xu, Yue Ju, Elaine Alt, Phyllis Schmiedeberg – 1 May 1994 – Endogenous lipopolysaccharide has been implicated as a cofactor in the hepatocellular injury and death resulting from toxic liver injury. To prevent this lipopolysaccharide‐induced injury and to further understand the mechanism of this effect, an anti‐lipopolysaccharide antibody was administered to rats in which toxic hepatocellular injury was induced. Rats were given the hepatotoxin galactosamine together with an isotypic control antibody B55 or the anti‐lipopolysaccharide antibody E5.

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