Functional magnetic resonance imaging monitoring of pathological changes in rodent livers during hyperoxia and hypercapnia

Hila Barash, Eitan Gross, Yifat Edrei, Orit Pappo, Gadi Spira, Israel Vlodavsky, Eithan Galun, Idit Matot, Rinat Abramovitch – 26 September 2008 – Liver diseases and regeneration are associated with hemodynamic changes denoting pathological alterations. Determining and monitoring physiological and pathological liver changes is essential for diagnostic and therapeutic objectives. Our aim was to determine the feasibility of functional magnetic resonance imaging (fMRI) during hypercapnia and hyperoxia for monitoring liver pathology.

The hepatic apelin system: A new therapeutic target for liver disease

Alessandro Principe, Pedro Melgar‐Lesmes, Guillermo Fernández‐Varo, Luis Ruiz del Arbol, Josefa Ros, Manuel Morales‐Ruiz, Mauro Bernardi, Vicente Arroyo, Wladimiro Jiménez – 26 September 2008 – Apelin is a peptide that plays an important role in heart physiology and pathophysiology, inflammation, and angiogenesis. We evaluated whether the endogenous apelin system is involved in the pathogenesis of the hepatic remodeling and cardiovascular and renal complications occurring in advanced liver disease.

Reliability of the Roussel Uclaf Causality Assessment Method for assessing causality in drug‐induced liver injury

James Rochon, Petr Protiva, Leonard B. Seeff, Robert J. Fontana, Suthat Liangpunsakul, Paul B. Watkins, Timothy Davern, John G. McHutchison, Drug‐Induced Liver Injury Network (DILIN) – 26 September 2008 – The Roussel Uclaf Causality Assessment Method (RUCAM) was developed to quantify the strength of association between a liver injury and the medication implicated as causing the injury. However, its reliability in a research setting has never been fully explored.

Mitochondrial dysfunction contributes to the increased vulnerabilities of adiponectin knockout mice to liver injury

Mingyan Zhou, Aimin Xu, Paul K. H. Tam, Karen S. L. Lam, Lawrence Chan, Ruby L. C. Hoo, Jing Liu, Kim H. M. Chow, Yu Wang – 26 September 2008 – Adiponectin is an adipocyte‐derived hormone with a wide range of beneficial effects on obesity‐related medical complications. Numerous epidemiological investigations in diverse ethnic groups have identified a lower adiponectin level as an independent risk factor for nonalcoholic fatty liver diseases and liver dysfunctions.

A randomized trial of combination hepatitis B therapy in HIV/HBV coinfected antiretroviral naïve individuals in Thailand

Gail V. Matthews, Anchalee Avihingsanon, Sharon R. Lewin, Janaki Amin, Rungsun Rerknimitr, Panusit Petcharapirat, Pip Marks, Joe Sasadeusz, David A. Cooper, Scott Bowden, Stephen Locarnini, Kiat Ruxrungtham, Gregory J. Dore – 26 September 2008 – Coinfection with human immunodeficiency virus (HIV) and hepatitis B virus (HBV) is associated with considerable liver disease morbidity and mortality. Emerging HIV epidemics in areas of high HBV endemicity such as Asia are expanding the population with HIV/HBV coinfection.

Induction of incomplete autophagic response by hepatitis C virus via the unfolded protein response

Donna Sir, Wen‐ling Chen, Jinah Choi, Takaji Wakita, T.S. Benedict Yen, Jing‐hsiung James Ou – 26 September 2008 – Autophagy is important for cellular homeostasis and can serve as innate immunity to remove intracellular pathogens. Here, we demonstrate by a battery of morphological and biochemical assays that hepatitis C virus (HCV) induces the accumulation of autophagosomes in cells without enhancing autophagic protein degradation.

Hepatocyte signaling through CXC chemokine receptor‐2 is detrimental to liver recovery after ischemia/reperfusion in mice

Satoshi Kuboki, Thomas Shin, Nadine Huber, Thorsten Eismann, Elizabeth Galloway, Rebecca Schuster, John Blanchard, Michael J. Edwards, Alex B. Lentsch – 26 September 2008 – CXC chemokines and their receptor, CXC chemokine receptor‐2 (CXCR2), are important components of the hepatic inflammatory response to ischemia/reperfusion (I/R). However, direct effects of CXC chemokines on hepatocytes during this response have not been studied. Wild‐type and CXCR2−/− mice were subjected to 90 minutes of partial hepatic ischemia followed by up to 96 hours of reperfusion.

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