Apoptosis induced by Fas signaling does not alter hepatic hepcidin expression.

Aim: To determine the regulation of human hepcidin (HAMP) and mouse hepcidin (hepcidin-1 and hepcidin-2) gene expression in the liver by apoptosis using in vivo and in vitro experimental models.

Methods: For the induction of the extrinsic apoptotic pathway, HepG2 cells were treated with various concentrations of CH11, an activating antibody for human Fas receptor, for 12 h. Male C57BL/6NCR and C57BL/6J strains of mice were injected intraperitoneally with sublethal doses of an activating antibody for mouse Fas receptor, Jo2.

Assessing the distribution and protection status of two types of cool environment to facilitate their conservation under climate change.

Strategies to mitigate climate change can protect different types of cool environments. Two are receiving much attention: protection of ephemeral refuges (i.e.

Can volunteers collect data that are comparable to professional scientists? A study of variables used in monitoring the outcomes of ecosystem rehabilitation.

Having volunteers collect data can be a cost-effective strategy to complement or replace those collected by scientists. The quality of these data is essential where field-collected data are used to monitor progress against predetermined standards because they provide decision makers with confidence that choices they make will not cause more harm than good. The integrity of volunteer-collected data is often doubted.

Regulation of liver hepcidin expression by alcohol in vivo does not involve Kupffer cell activation or TNF-alpha signaling.

Alcohol downregulates hepcidin expression in the liver leading to an increase in intestinal iron transport and liver iron storage. We have previously demonstrated that alcohol-mediated oxidative stress is involved in the inhibition of hepcidin transcription by alcohol in vivo. Kupffer cells and TNF-alpha play a key role in alcohol-induced liver injury.

Iron-mediated regulation of liver hepcidin expression in rats and mice is abolished by alcohol.

Unlabelled: Alcohol reduces and iron increases liver hepcidin synthesis. This study investigates the interaction of alcohol and iron in the regulation of hepcidin messenger RNA (mRNA) expression in animal models. Mice were administered 10% ethanol for 7 days after an iron-overloaded diet.

Alcohol metabolism-mediated oxidative stress down-regulates hepcidin transcription and leads to increased duodenal iron transporter expression.

Patients with alcoholic liver disease frequently exhibit iron overload in association with increased hepatic fibrosis. Even moderate alcohol consumption elevates body iron stores; however, the underlying molecular mechanisms are unknown. Hepcidin, a circulatory peptide synthesized in the liver, is a key mediator of iron metabolism.

Emerging therapeutics for chronic hepatitis B.

Hepatitis B is a global health problem. Patients with chronic hepatitis B (CHB) carry a significant risk to eventually develop cirrhotic liver disease. Recent therapeutic advances against CHB offer excellent potential for long-term suppression of hepatitis B virus (HBV) replication during antiviral therapy, and occasionally a durable remission off medication.

Recent developments in the pathophysiology of cholestasis.

The past decade has brought tremendous growth in the under-standing of the pathophysiologic mechanisms involved in cholestasis, both at the genetic and acquired levels. The discovery and characterization of an array of hepatobiliary transport proteins, the nuclear receptors that regulate them, and the potential clinical implications of these defective, altered, or variably expressed proteins are the key elements of our current understanding of cholestasis. It is hoped that future studies will enhance therapeutic options and the ability to care for patients with cholestatic disorders.

Gastrointestinal disorders of the critically ill. Cholestasis of sepsis.

Cholestasis of sepsis is a form of hepatocellular cholestasis that occurs as a result of sepsis. Usually, prior to the development of cholestasis, the manifestations of sepsis dominate the clinical picture. The occurrence of cholestasis is without direct bacterial involvement of the biliary system and appears to be mediated systemically by pro-inflammatory cytokines.

Metabolic liver disease in the young adult.

This chapter describes the gene mutations, phenotypes, diagnosis and therapy of the common metabolic liver diseases in young adulthood: haemochromatosis, Wilson disease, alpha(1)-anti-trypsin deficiency and cystic fibrosis. The remarkable variability of the phenotypical expression of the mutated genotypes makes screening recommendations and the establishment of prognosis for these liver disorders in young adults problematical. The diagnosis and therapy of the young adult with metabolic liver disease is discussed, with an emphasis on maintaining quality-of-life and balancing the importance of early intervention with the stigmatization of the diagnosis of potentially life-threatening liver disease.