Prevention of de novo hepatitis B with adefovir dipivoxil in recipients of liver grafts from hepatitis B core antibody–positive donors

Matthew S. Chang, Sonja K. Olsen, Elsa M. Pichardo, Scott Heese, Jessica B. Stiles, Rita Abdelmessih, Elizabeth C. Verna, James V. Guarrera, Jean C. Emond, Robert S. Brown – 16 March 2012 – Lamivudine has been shown to prevent de novo hepatitis B virus (HBV) infections in liver transplantation (LT) patients receiving hepatitis B core antibody–positive (HBcAb+) grafts, but it may produce long‐term resistance. Adefovir dipivoxil (ADV) might be effective in preventing de novo hepatitis and resistance.

Clinical cofactors and hepatic fibrosis in hereditary hemochromatosis: The role of diabetes mellitus

Marnie J. Wood, Lawrie W. Powell, Jeannette L. Dixon, Grant A. Ramm – 15 March 2012 – The risk of hepatic fibrosis and cirrhosis in hereditary hemochromatosis relates to the degree of iron loading, but iron alone does not explain the variability in disease penetrance. This study sought to identify clinical cofactors that increase the risk of progressive liver disease. We identified 291 patients from our database who were homozygous for the C282Y mutation in HFE and had undergone a liver biopsy with quantification of hepatic iron concentration (HIC) and fibrosis staging.

A large case‐control study on the predictability of hepatitis B surface antigen levels three years before hepatitis B surface antigen seroclearance

Wai‐Kay Seto, Danny Ka‐Ho Wong, James Fung, Ivan Fan‐Ngai Hung, Daniel Yee‐Tak Fong, John Chi‐Hang Yuen, Teresa Tong, Ching‐Lung Lai, Man‐Fung Yuen – 15 March 2012 – The kinetics of hepatitis B surface antigen (HBsAg) levels preceding spontaneous HBsAg seroclearance has not been fully investigated. The kinetics of HBsAg and hepatitis B virus (HBV) DNA of 203 treatment‐naïve, hepatitis B e antigen (HBeAg)‐negative patients with spontaneous HBsAg seroclearance were compared with 203 age‐ and sex‐matched HBeAg‐negative controls.

Prevention of hepatocellular adenoma and correction of metabolic abnormalities in murine glycogen storage disease type Ia by gene therapy

Young Mok Lee, Hyun Sik Jun, Chi‐Jiunn Pan, Su Ru Lin, Lane H. Wilson, Brian C. Mansfield, Janice Y. Chou – 15 March 2012 – Glycogen storage disease type Ia (GSD‐Ia), which is characterized by impaired glucose homeostasis and chronic risk of hepatocellular adenoma (HCA), is caused by deficiencies in the endoplasmic reticulum (ER)‐associated glucose‐6‐phosphatase‐α (G6Pase‐α or G6PC) that hydrolyzes glucose‐6‐phosphate (G6P) to glucose. G6Pase‐α activity depends on the G6P transporter (G6PT) that translocates G6P from the cytoplasm into the ER lumen.

Structural analysis of oval‐cell–mediated liver regeneration in rats

Katalin Dezső, Veronika Papp, Edina Bugyik, Hargita Hegyesi, Géza Sáfrány, Csaba Bödör, Péter Nagy, Sándor Paku – 15 March 2012 – We have analyzed the architectural aspects of progenitor‐cell–driven regenerative growth in rat liver by applying the 2‐acetaminofluorene/partial hepatectomy experimental model. The regeneration is initiated by the proliferation of so‐called oval cells. The oval cells at the proximal tips of the ductules have a more differentiated phenotype and higher proliferative rate.

Human mesenchymal stem cells are recruited to injured liver in a β1‐integrin and CD44 dependent manner

Victoria Aldridge, Abhilok Garg, Nicholas Davies, David C. Bartlett, Janine Youster, Heather Beard, Dean P. Kavanagh, Neena Kalia, Jon Frampton, Patricia F. Lalor, Philip N. Newsome – 15 March 2012 – Human bone marrow mesenchymal stem cells (hMSCs) have shown benefit in clinical trials of patients with liver disease. Efficient delivery of cells to target organs is critical to improving their effectiveness. This requires an understanding of the mechanisms governing cellular engraftment into the liver.

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