Eric Lévesque, Hugo Girard, Kim Journault, Johanie Lépine, Chantal Guillemette – 22 December 2006 – UDP‐glucuronosyltransferase 1A1 (UGT1A1) is involved in a wide range of biological and pharmacological processes because of its critical role in the conjugation of a diverse array of endogenous and exogenous compounds. We now describe a new UGT1A1 isoform, referred to as isoform 2 (UGT1A1_i2), encoded by a 1495‐bp complementary DNA isolated from human liver and generated by an alternative splicing event involving an additional exon found at the 3′ end of the UGT1A locus.

Tomohide Tatsumi, Tetsuo Takehara, Shinjiro Yamaguchi, Akira Sasakawa, Ryotaro Sakamori, Kazuyoshi Ohkawa, Keisuke Kohga, Akio Uemura, Norio Hayashi – 22 December 2006 – Alpha‐galactosylceramide, a glycosphingolipid, mediates interaction of dendritic cells (DCs) and NKT cells, leading to activation of both innate and acquired immunity. For cancer treatment, conventional DC‐based vaccine has been tried, but its clinical efficacy is limited against liver cancer.

Hao Yin, Linling Cheng, Robert Langenbach, Cynthia Ju – 22 December 2006 – Studies of the molecular and cellular mechanisms of concanavalin A (ConA)‐induced liver injury have provided important knowledge on the pathogenesis of many liver diseases involving hepatic inflammation. However, studies identifying hepato‐protective factors based on the mechanistic understanding of this model are lacking. Evidence suggests that certain prostaglandin (PG) products of cyclooxygenase (COX)‐1 and COX‐2 provide important anti‐inflammatory and cytoprotective functions in some pathophysiological states.

M. Kumar, S. Satapathy, R. Monga, K. Das, S. Hissar, C. Pande, B. C. Sharma, S. K. Sarin – 22 December 2006 – The role of antivirals in patients with acute viral hepatitis B (AVH‐B) has not been evaluated in controlled trials. The aim of this study was to evaluate the efficacy of lamivudine in patients with AVH‐B. AVH‐B patients with serum bilirubin of more than 5 mg/dL were randomized to receive either 100 mg of lamivudine daily for 3 months (group 1, n = 31) or placebo (group 2, n = 40).

Nadia Gorman, Adrian Zaharia, Heidi S. Trask, Juliana G. Szakacs, Nicholas J. Jacobs, Judith M. Jacobs, Dominic Balestra, Jacqueline F. Sinclair, Peter R. Sinclair – 22 December 2006 – Excess hepatic iron is known to enhance both porphyria cutanea tarda (PCT) and experimental uroporphyria. Since previous studies have suggested a role for ascorbate (AA) in suppressing uroporphyria in AA‐requiring rats (in the absence of excess iron), the present study investigated whether AA could suppress uroporphyria produced by excess hepatic iron.

Gang Zeng, Farrukh Awan, Wade Otruba, Peggy Muller, Udayan Apte, Xinping Tan, Chandrashekhar Gandhi, Anthony J. Demetris, Satdarshan P. S. Monga – 22 December 2006 – The Wnt signaling pathway is essential for a wide array of developmental and physiological processes. Wnts are extracellular ligands that bind to frizzled (Fz) receptors at the membrane, canonically inducing β‐catenin nuclear translocation and activation. Although β‐catenin has been shown to be critical in liver biology, the expression of the 19 Wnt and 10 Fz genes in liver remains undetermined.

Adam C. Straub, Donna B. Stolz, Mark A. Ross, Araceli Hernández‐Zavala, Nicole V. Soucy, Linda R. Klei, Aaron Barchowsky – 22 December 2006 – Trivalent arsenic [As(III)] is a well‐known environmental toxicant that causes a wide range of organ‐specific diseases and cancers. In the human liver, As(III) promotes vascular remodeling, portal fibrosis, and hypertension, but the pathogenesis of these As(III)‐induced vascular changes is unknown.

Karl E. Anderson – 22 December 2006

Amedeo Lonardo, Paola Loria, Marco Bertolotti, Nicola Carulli – 22 December 2006

Hari S. Conjeevaram, David E. Kleiner, Jay E. Everhart, Jay H. Hoofnagle, Steven Zacks, Nezam H. Afdhal, Abdus S. Wahed – 22 December 2006 – Hepatic steatosis is common in chronic hepatitis C and has been linked to concurrent obesity, insulin resistance, diabetes, disease severity, and poor response to therapy. Racial differences in rates of obesity and diabetes may contribute to racial differences in hepatic steatosis and treatment response.