Zhang‐Xu Liu, Derick Han, Basuki Gunawan, Neil Kaplowitz – 25 May 2006 – We previously reported that liver natural killer (NK) and NKT cells play a critical role in mouse model of acetaminophen (APAP)‐induced liver injury by producing interferon gamma (IFN‐γ) and modulating chemokine production and subsequent recruitment of neutrophils into the liver. In this report, we examined the role of neutrophils in the progression of APAP hepatotoxicity.

25 May 2006

25 May 2006

Mei‐Shu Lai, Meng‐Shu Hsieh, Yueh‐Hsia Chiu, Tony Hsiu‐Hsi Chen – 25 May 2006 – This study aimed to elucidate the relationship of type 2 diabetes, other known risk factors, and primary hepatocellular carcinoma (HCC) in countries with a high prevalence of hepatitis infection. We followed a prospective cohort of 54,979 subjects who participated in the Keelung Community‐Based Integrated Screening program between 1999 and 2002.

Soohyun Lee, Paul A. Dawson, Amitha K. Hewavitharana, P. Nicholas Shaw, Daniel Markovich – 25 May 2006 – Sulfate is required for detoxification of xenobiotics such as acetaminophen (APAP), a leading cause of liver failure in humans. The NaS1 sulfate transporter maintains blood sulfate levels sufficiently high for sulfonation reactions to work effectively for drug detoxification. In the present study, we identified two loss‐of‐function polymorphisms in the human NaS1 gene and showed the Nas1‐null mouse to be hypersensitive to APAP hepatotoxicity.

Tiangang Li, Asmeen Jahan, John Y. L. Chiang – 25 May 2006 – Cholesterol 7α‐hydroxylase (CYP7A1) of the bile acid biosynthesis pathway is suppressed by bile acids and inflammatory cytokines. Bile acids are known to induce inflammatory cytokines to activate the mitogen‐activated protein kinase/c‐Jun N‐terminal kinase (JNK) signaling pathway that inhibits CYP7A1 gene transcription. c‐Jun has been postulated to mediate bile acid inhibition of CYP7A1. However, the c‐Jun target involved in the regulation of CYP7A1 is unknown.

Yoon‐Seon Lee, Dong Jin Suh, Young‐Suk Lim, Suk Won Jung, Kang Mo Kim, Han Chu Lee, Young‐Hwa Chung, Yung Sang Lee, Wangdon Yoo, Soo‐Ok Kim – 25 May 2006 – Although adefovir dipivoxil (ADV) has a unique profile of delayed and infrequent resistance in treatment‐naïve chronic hepatitis B patients, the association of ADV resistance with previous lamivudine (LAM) resistance is not well understood. We compared the emergence of the ADV‐resistant mutations rtA181V/T and rtN236T between LAM‐resistant patients and treatment‐naïve patients at 48 weeks of ADV monotherapy.

David Saadoun, Tarik Asselah, Mathieu Resche‐Rigon, Frédéric Charlotte, Pierre Bedossa, Dominique Valla, Jean‐Charles Piette, Patrick Marcellin, Patrice Cacoub – 25 May 2006 – The relationship between cryoglobulin and severity of liver lesions is debated. No study has focused on the relationship between cryoglobulin, liver steatosis, and fibrosis. The aim of this study was to determine the relationship between cryoglobulins and liver lesions (necroinflammation, fibrosis, and steatosis) in patients with hepatitis C virus (HCV) infection.

Xandra Volkmann, Markus Cornberg, Heiner Wedemeyer, Frank Lehner, Michael P. Manns, Klaus Schulze‐Osthoff, Heike Bantel – 25 May 2006 – Only half of patients with chronic hepatitis C virus (HCV) infection and genotype‐1 show a sustained antiviral response to the current antiviral therapy. The reason this treatment fails is unclear, and no reliable marker exists that predicts the treatment outcome. In the present study, we investigated the apoptotic activation of caspases in HCV patients undergoing antiviral therapy with regard to the treatment outcome.

Pavel Strnad, Tim C. Lienau, Guo‐Zhong Tao, Laura C. Lazzeroni, Felix Stickel, Detlef Schuppan, M. Bishr Omary – 25 May 2006 – Keratins 8 and 18 (K8/K18) protect the liver from various forms of injury. Studies of liver explants from a large cohort of U.S. patients showed that K8/K18 mutations confer a risk to developing end‐stage liver diseases, though which diseases are preferentially involved is unknown. We tested the hypothesis that K8/K18 variants are associated with chronic hepatitis C (CHC) and that their presence correlates with progression of fibrosis.