Ursodeoxycholic acid administration in patients with cholestasis of pregnancy: Effects on primary bile acids in babies and mothers

Giuseppe Mazzella, Rizzo Nicola, Azzaroli Francesco, Simoni Patrizia, Bovicelli Luciano, Miracolo Anna, Simonazzi Giuliana, Colecchia Antonio, Nigro Giovanni, Mwangemi Constance, Festi Davide, Roda Enrico – 30 December 2003 – Little is known about the effects on the fetus of ursodeoxycholic acid (UDCA) treatment for intrahepatic cholestasis of pregnancy (ICP). Twenty ICP patients were given UDCA at 1.5 to 2 g/d, to our knowledge the highest dosage yet reported.

Sinusoidal ultrastructure evaluated during the revascularization of regenerating rat liver

Kathryn E. Wack, Mark A. Ross, Vasthy Zegarra, Laura R. Sysko, Simon C. Watkins, Donna Beer Stolz – 30 December 2003 – Sinusoidal endothelial cell (SEC) porosities were compared between the periportal (zone 1) and pericentral (zone 3) regions of the rat liver during regeneration following partial hepatectomy (PHx). SEC porosities and fenestration diameters were measured in control livers, as well as at 5 minutes, 24, 48, 72, 96, 120 hours, and 14 days following PHx.

RECK gene expression in hepatocellular carcinoma: Correlation with invasion‐related clinicopathological factors and its clinical significance

Katsuyoshi Furumoto, Shigeki Arii, Akira Mori, Hiroaki Furuyama, Manuel J. Gorrin Rivas, Teizou Nakao, Naoki Isobe, Toru Murata, Chiaki Takahashi, Makoto Noda, Masayuki Imamura – 30 December 2003 – The RECK (reversion‐inducing‐cysteine‐rich protein with Kazal motifs) gene was initially isolated as a transformation suppressor gene. It encodes a membrane‐anchored glycoprotein with multiple serine protease inhibitor‐like domains. The RECK gene is expressed widely in normal organs but is undetectable in many tumor‐derived cell lines.

Outcome of hospital care of liver disease associated with hepatitis C in the United States

W. Ray Kim, John B. Gross, John J. Poterucha, G. Richard Locke, E. Rolland Dickson – 30 December 2003 – We describe mortality and resource utilization for inpatient care of hepatitis C (HCV) in comparison to alcohol‐induced liver disease (ALD) in the United States and identify factors that affect outcomes. The Healthcare Cost and Utilization Project database, a national inpatient sample was used to identify hospitalization records with diagnoses related to liver disease from HCV and ALD.

HLA class II genes determine the natural variance of hepatitis C viral load

Liam J. Fanning, John Levis, Elizabeth Kenny‐Walsh, Michael Whelton, Kathleen O'Sullivan, Fergus Shanahan – 30 December 2003 – The aim of this study was to investigate the relationship between human leukocyte antigen (HLA) class II genes and the natural fluctuations in hepatitis C viral load in a homogeneous patient population. The study group consisted of 57 viremic (hepatitis C virus [HCV] 1b) women for whom HLA class II DRB1 and DQB1 haplotyping, virologic, histologic, and biochemical markers of disease activity were available.

Preconditioning protects against systemic disorders associated with hepatic ischemia‐reperfusion through blockade of tumor necrosis factor–induced P‐selectin up‐regulation in the rat

Carmen Peralta, Leticia Fernández, Julià Panés, Neus Prats, Miquel Sans, Josep Maria Piqué, Emilio Gelpí, Joan Roselló‐Catafau – 30 December 2003 – Previous studies indicate that ischemic preconditioning protects against lung injury resulting from hepatic ischemia‐reperfusion (I/R) through inhibition of tumor necrosis factor (TNF) release from Kupffer cells. The present study investigated whether this effect is limited to the lung or is a generalized systemic response and explores the molecular mechanisms involved.

The hepatitis B virus X protein (HBx) induces a migratory phenotype in a CD44‐dependent manner: Possible role of HBx in invasion and metastasis

Enrique Lara‐Pezzi, Juan M. Serrador, María C. Montoya, David Zamora, María Yáñez‐Mó, Marta Carretero, Heinz Furthmayr, Francisco Sánchez‐Madrid, Manuel López‐Cabrera – 30 December 2003 – The hepatitis B virus X protein (HBx) of the hepatitis B virus (HBV) has been involved in the development of hepatocellular carcinoma (HCC). However, its possible contribution to the metastatic spreading of liver tumors has not been explored so far.

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