Pathogenesis of alcoholic liver disease: newer mechanisms of injury.

Pathogenesis of alcoholic liver disease: newer mechanisms of injury. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Pathogenesis of alcoholic liver disease: newer mechanisms of injury. Abstract Text:

The understanding of how alcohol damages the liver has expanded substantially over the last decade. In particular, the genetics of alcoholism, the genesis of fatty liver, the role of oxidant stress, interactions between endotoxin and the Kupffer cell, and the factors that control activation of the hepatic stellate cell (HSC) have been the focus of a great deal of research. Genetic mechanisms for increasing the risk of alcoholism include alterations in alcohol metabolizing enzymes as well as neurobiological differences between individuals. The development of fatty liver may involve both redox forces, oxidative stress, and alterations in peroxisome proliferator activated receptor function. Oxidative stress is now known to involve both microsomal and mitochondrial systems. Recent studies implicate stimulation of Kupffer cells by portal vein endotoxin as a cause of release of cytokines and chemokines, hepatocyte hyper-metabolism, and activation of HSC. These actions appear to be in part gender-dependent and may explain the susceptibility of women to alcoholic liver disease. Activation of HSC underlies liver fibrosis and cirrhosis of all types; control of this activation might permit control of the progression of fibrosis. These advances suggest a number of new approaches as therapy for alcoholic liver injury.

Pathogenesis of alcoholic liver disease: newer mechanisms of injury. Publishing Authors By Initials

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Pathogenesis of alcoholic liver disease: newer mechanisms of injury. Journal Published:

PUBLICATION TYPE: Review

Journal: The Keio journal of medicine

VOLUME: 48

Page Numbers: 184-8

Journal Abbreviation: Keio J Med

ISSN: 0022-9717

DAY: 7

MONTH: Dec

YEAR: 1999

Pathogenesis of alcoholic liver disease: newer mechanisms of injury. Information

Number of References: 31

LANGUAGE: eng

NlmUniqueID: 376354

Pathogenesis of alcoholic liver disease: newer mechanisms of injury. Keywords Mesh Terms:

KEYWORDS: Sex Characteristics

MESH TERMS: therapy

Chemical & Substance for Abstract: Pathogenesis of alcoholic liver disease: newer mechanisms of injury. Information

Substance Name: Endotoxins

Registry Number: 0

Grant and Affiliation Information for Pathogenesis of alcoholic liver disease: newer mechanisms of injury.

AFFILIATION: Department of Medicine, Biochemistry and Molecular Biology, School of Medicine, Indiana University, Indianapolis 46202-5124, USA.

Country: JAPAN

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Keio J Med

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Pathogenesis of alcoholic liver disease: newer mechanisms of injury Related Publications

• A rapid rosin-celloidin-paraffin method for embedding tissues.
• Alcohol Deranges Hepatic Lipid Metabolism via Altered Transcriptional Regulation.
• Alcohol and lipid metabolism.
• Analysis of visual field progression in glaucoma.
• Antibiotic sensitivity of staphylococci from noses of veterinary surgeons and farmers.
• Association of the aldehyde dehydrogenase 2 promoter polymorphism with alcohol consumption and reactions in an American Jewish population.
• CRALBP ligand and protein interactions.
• Carboxyethylpyrrole adducts, age-related macular degeneration and neovascularization.
• Evidence for a common role for the serine-type Plasmodium falciparum serine repeat antigen proteases: implications for vaccine and drug design.
• Evidence that invasion-inhibitory antibodies specific for the 19-kDa fragment of merozoite surface protein-1 (MSP-1 19) can play a protective role against blood-stage Plasmodium falciparum infection in individuals in a malaria endemic area of Africa.
• Genetic, age and light mediated effects on crystallin protein expression in the retina.
• Loss of sexual differentiation of rat hepatocytes in short-term culture.
• MSP1(19) miniproteins can serve as targets for invasion inhibitory antibodies in Plasmodium falciparum provided they contain the correct domains for cell surface trafficking.
• Metaphen and mercurochrome intravenously for sepsis.
• Metastasis in hamsters implanted with emulsified and with solid pieces of a mixed-cell sarcoma.
• More sensitive assay to detect drug-resistant HIV.
• Pathogenesis of alcoholic liver disease: newer mechanisms of injury.
• Retinal pigment epithelium lipofuscin proteomics.
• Targets of tyrosine nitration in diabetic rat retina.
• The cleansing of root canals.
• Towards a Vaccine against Plasmodium vivax Malaria.
• Truncation of Plasmodium berghei merozoite surface protein 8 does not affect in vivo blood-stage development.
• Will histone deacetylase inhibitors require combination with other agents to fulfil their therapeutic potential?