Alcoholism Thesis Paper

Alcoholism Thesis Paper-42
Human genetic studies on alcohol-related phenotypes have used family-based linkage and population-based association analyses to identify quantitative trait loci (QTLs).Linkage studies are based on co-segregation between genetic markers and alcohol dependence in families with several affected members.This can be done by considering the effects of molecular polymorphisms on phenotypes mediated via complex networks of transcriptional, protein, metabolic and neurogenetic endophenotypes.

Human genetic studies on alcohol-related phenotypes have used family-based linkage and population-based association analyses to identify quantitative trait loci (QTLs).Linkage studies are based on co-segregation between genetic markers and alcohol dependence in families with several affected members.This can be done by considering the effects of molecular polymorphisms on phenotypes mediated via complex networks of transcriptional, protein, metabolic and neurogenetic endophenotypes.

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Alcohol-related phenotypes are typical quantitative traits, with population variation attributable to multiple segregating loci with effects that are sensitive to environmental exposures.

Given that many loci are likely to affect alcohol drinking behavior and the development of dependence, we need to shift our focus from a 'one gene at a time' approach to genetic networks.

The risk of upper gastrointestinal cancer is increased by a missense variant in the gene encoding aldehyde dehydrogenase (ALDH), which is found in some 500 million East Asians [2].

Depression, epilepsy, hypertension and hemorrhagic stroke occur secondary to alcohol consumption [3].

The main pathway of ethanol metabolism involves its conversion to acetaldehyde by alcohol dehydrogenase (ADH; Figure 1).

Acetaldehyde is oxidized to acetate by aldehyde dehydrogenase (ALDH).

In addition, a small fraction of ethanol is metabolized by cytochrome P450 2E1 (CYP2E1) and in the brain by catalase.

The diagram presents only those members of the ADH and ALDH families referred to in the text.

The first stage of liver damage following chronic alcohol consumption is the development of fatty liver, which may be followed by inflammation, apoptosis, fibrosis and cirrhosis.

Alcohol and its metabolite acetaldehyde are carcinogens, and excessive alcohol consumption is associated with increased risk for mouth and oropharyngeal cancer, breast cancer and liver cancer.

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