Bone marrow–derived immune cells mediate sensitization to liver injury in a myeloid differentiation factor 88–dependent fashion

Istvan Hritz, Arumugam Velayudham, Angela Dolganiuc, Karen Kodys, Pranoti Mandrekar, Evelyn Kurt‐Jones, Gyongyi Szabo – 26 September 2008 – Toll‐like receptors (TLRs) expressed on both immune cells and hepatocytes recognize microbial danger signals and regulate immune responses. Previous studies showed that TLR9 and TLR2 mediate Propionibacterium acnes–induced sensitization to lipopolysaccharide‐triggered acute liver injury in mice. Ligand‐specific activation of TLR2 and TLR9 are dependent on the common TLR adaptor, myeloid differentiation factor 88 (MyD88).

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.

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