Research opportunities on alcohol and liver damage

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Alcohol and liver damage

Chronic heavy drinking can cause the liver to become fatty. Fat deposits in the liver block the liver cells from their blood supply, depriving them of oxygen and other nutrients, eventually killing them. As the name implies, the liver performs so many vital functions that we cannot live without it. The liver filters all of the blood in our bodies, breaking down and eliminating toxins, convertin...

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Alcohol and liver damage.

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Dental students’ opinions on the challenges and research opportunities: A qualitative research

BACKGROUND AND AIM: The first step to improve research in a society is a true understanding of abilities, available possibilities, and also the strengths and weakness of research projects. The purpose of this study was to survey the students’ ideas about research challenges and opportunities among dental students of Kerman, Iran.METHODS: In this qualitative action research, personal and group d...

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Mechanisms of alcohol liver damage: aldehydes, scavenger receptors, and autoimmunity.

While most of the investigations into the causative events in the development of alcoholic liver disease (ALD) have been focused on multiple factors, increasing interest has centered around the possible role of immune mechanisms in the pathogenesis and perpetuation of ALD. This is because many of the clinical features of ALD suggest that immune effector mechanisms may be contributing to liver t...

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Peroxisome Proliferator-Activated Receptor Protects Against Alcohol-Induced Liver Damage

The mechanisms underlying alcoholic liver disease are not completely understood, but lipid accumulation seems to be central to the cause of this disease. The peroxisome proliferatoractivated receptor (PPAR ) plays an important role in the control of lipid homeostasis, metabolism of bioactive molecules, and modulation of inflammatory responses. To investigate the roles of PPAR in alcoholic liver...

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ژورنال

عنوان ژورنال: Hepatology

سال: 2005

ISSN: 0270-9139,1527-3350

DOI: 10.1002/hep.20972