Long‐term risk of recurrent peptic ulcer bleeding in patients with liver cirrhosis: A 10‐year nationwide cohort study

Yao‐Chun Hsu, Jaw‐Town Lin, Tzu‐Ting Chen, Ming‐Shiang Wu, Chun‐Ying Wu – 1 March 2012 – Peptic ulcer bleeding leads to substantial morbidity and mortality in patients with liver cirrhosis, but their long‐term risk of recurrent bleeding remains elusive. This nationwide cohort study aimed to elucidate the association between cirrhosis and recurrent peptic ulcer bleeding by analyzing the Taiwan National Health Insurance Research Database.

Chronic inflammation, immune escape, and oncogenesis in the liver: A unique neighborhood for novel intersections

Jimmy K. Stauffer, Anthony J. Scarzello, Qun Jiang, Robert H. Wiltrout – 1 March 2012 – Sustained hepatic inflammation, driven by alcohol consumption, nonalcoholic fatty liver disease, and/or chronic viral hepatitis (hepatitis B and C), results in damage to parenchyma, oxidative stress, and compensatory regeneration/proliferation. There is substantial evidence linking these inflammation‐associated events with the increased incidence of hepatocellular carcinogenesis.

Fibrosis‐dependent mechanisms of hepatocarcinogenesis

David Y. Zhang, Scott L. Friedman – 1 March 2012 – Hepatocellular carcinoma (HCC) is a rising worldwide cause of cancer mortality, making the elucidation of its underlying mechanisms an urgent priority. The liver is unique in its response to injury, simultaneously undergoing regeneration and fibrosis. HCC occurs in the context of these two divergent responses, leading to distinctive pathways of carcinogenesis. In this review we highlight pathways of liver tumorigenesis that depend on, or are enhanced by, fibrosis.

Long‐term follow‐up of hemodynamic responders to pharmacological therapy after variceal bleeding

Salvador Augustin, Antonio González, Laia Badia, Laura Millán, Aranzazu Gelabert, Alejandro Romero, Antoni Segarra, María Martell, Rafael Esteban, Jaime Guardia, Joan Genescà – 1 March 2012 – Although it is assumed that hemodynamic responders to pharmacological therapy after a variceal hemorrhage are adequately protected from rebleeding, there is no evidence that either this response or its protective effect extend beyond the usual 2‐year follow‐up featured in available studies.

A human claudin‐1–derived peptide inhibits hepatitis C virus entry

Youhui Si, Shufeng Liu, Xiuying Liu, Jana L. Jacobs, Min Cheng, Yuqiang Niu, Qi Jin, Tianyi Wang, Wei Yang – 1 March 2012 – Hepatitis C virus (HCV) entry is a complicated process that requires multiple host factors, such as CD81, scavenger receptor BI, claudin‐1 (CLDN1), and occludin. The interaction of virus and cellular entry factors represents a promising target for novel anti‐HCV drug development. In this study, we sought to identify peptide inhibitors for HCV entry by screening a library of overlapping peptides covering the four above‐mentioned entry factors.

Histopathology of de novo autoimmune hepatitis

Ananya Pongpaibul, Robert S. Venick, Sue V. McDiarmid, Charles R. Lassman – 29 February 2012 – De novo autoimmune hepatitis (DAIH) is a well‐recognized complication of pediatric liver transplantation (LT). The diagnosis is largely based on elevated liver function test results and the development of autoimmune antibodies. The histology of DAIH was first described in 1998. We present detailed histological data from the largest series to date of pretreatment and posttreatment biopsy samples from pediatric LT patients with DAIH.

15‐deoxy‐Δ12,14‐prostaglandin J2 reduces recruitment of bone marrow–derived monocyte/macrophages in chronic liver injury in mice

Zhen Han, Tieping Zhu, Xihong Liu, Changyong Li, Shi Yue, Xin Liu, Le Yang, Lin Yang, Liying Li – 28 February 2012 – 15‐Deoxy‐Δ12,14‐Prostaglandin J2 (15d‐PGJ2), a natural peroxisome proliferator‐activated receptor gamma (PPAR‐γ) ligand, has been implicated as a new antiinflammatory compound with possible clinical applications. Based on this concept, this study was designed to evaluate the effects of 15d‐PGJ2 on bone marrow–derived monocyte/macrophage (BMM) migration, phagocytosis, and cytokine expression after liver injury using mouse models induced by cholestasis or carbon tetrachloride.

Enhancer of zeste homolog 2 epigenetically silences multiple tumor suppressor microRNAs to promote liver cancer metastasis

Sandy Leung‐Kuen Au, Carmen Chak‐Lui Wong, Joyce Man‐Fong Lee, Dorothy Ngo‐Yin Fan, Felice Hoching Tsang, Irene Oi‐Lin Ng, Chun‐Ming Wong – 28 February 2012 – Epigenetic alterations and microRNA (miRNA) deregulation are common in hepatocellular carcinoma (HCC). The histone H3 lysine 27 (H3K27) tri‐methylating enzyme, enhancer of zeste homolog 2 (EZH2) mediates epigenetic silencing of gene expression and is frequently up‐regulated in human cancers. In this study we aimed to delineate the implications of EZH2 up‐regulation in miRNA deregulation and HCC metastasis.

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