Glucocorticoid signaling synchronizes the liver circadian transcriptome

Akhilesh B. Reddy, Elizabeth S. Maywood, Natasha A. Karp, Verdun M. King, Yusuke Inoue, Frank J. Gonzalez, Kathryn S. Lilley, Charalambos P. Kyriacou, Michael H. Hastings – 30 May 2007 – Circadian control of physiology is mediated by local, tissue‐based clocks, synchronized to each other and to solar time by signals from the suprachiasmatic nuclei (SCN), the master oscillator in the hypothalamus. These local clocks coordinate the transcription of key pathways to establish tissue‐specific daily metabolic programs.

Induction of cytochrome promotes liver injury in ob/ob mice

Aparajita Dey, Arthur I. Cederbaum – 30 May 2007 – Cytochrome P450 2E1 (CYP2E1) activates several hepatotoxins and contributes to alcoholic liver damage. Obesity is a growing health problem in the United States. The aim of the present study was to evaluate whether acetone‐ or pyrazole‐mediated induction of CYP2E1 can potentiate liver injury in obesity. CYP2E1 protein and activity were elevated in acetone‐ or pyrazole‐treated obese and lean mice.

A new priority policy for patients with hepatocellular carcinoma awaiting liver transplantation within the model for end‐stage liver disease system

Fabio Piscaglia, Valeria Camaggi, Matteo Ravaioli, Gian Luca Grazi, Matteo Zanello, Simona Leoni, Giorgio Ballardini, Giulia Cavrini, Antonio Daniele Pinna, Luigi Bolondi – 30 May 2007 – The best prioritization of patients with hepatocellular carcinoma (HCC) waiting for liver transplantation under the model for end‐stage liver disease (MELD) allocation system is still being debated. We analyzed the impact of a MELD adjustment for HCC, which consisted of the addition of an extra score (based on the HCC stage and waiting time) to the native MELD score.

Engulfment of apoptotic cells expressing HCV proteins leads to differential chemokine expression and STAT signaling in human dendritic cells

Anne M. Wertheimer, Stephen J. Polyak, Rachel Leistikow, Hugo R. Rosen – 30 May 2007 – In the majority of cases, infection with hepatitis C virus (HCV) becomes chronic and is often associated with impaired innate and adaptive immune responses. The mechanisms underlying viral persistence and lack of protective immunity are poorly understood. Considering that dendritic cells (DCs) play critical roles in initiating and modulating immune responses, we explored the effect of HCV proteins on DC gene and protein expression, phenotype, and function.

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