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  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
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We are analyzing https://link.springer.com/article/10.1186/1479-7364-3-2-121.

Title:
Effect of the allelic variants of aldehyde dehydrogenase ALDH2*2 and alcohol dehydrogenase ADH1B*2on blood acetaldehyde concentrations | Human Genomics
Description:
Alcoholism is a complex behavioural disorder. Molecular genetics studies have identified numerous candidate genes associated with alcoholism. It is crucial to verify the disease susceptibility genes by correlating the pinpointed allelic variations to the causal phenotypes. Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are the principal enzymes responsible for ethanol metabolism in humans. Both ADH and ALDH exhibit functional polymorphisms among racial populations; these polymorphisms have been shown to be the important genetic determinants in ethanol metabolism and alcoholism. Here, we briefly review recent advances in genomic studies of human ADH/ALDH families and alcoholism, with an emphasis on the pharmacogenetic consequences of venous blood acetaldehyde in the different ALDH2 genotypes following the intake of various doses of ethanol. This paper illustrates a paradigmatic example of phenotypic verifications in a protective disease gene for substance abuse.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Science
  • Health & Fitness
  • Education

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {πŸ’Έ}

We don't see any clear sign of profit-making.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {πŸ”}

aldh, alcohol, acetaldehyde, pubmed, google, scholar, article, ethanol, alcoholism, cas, adhb, dehydrogenase, metabolism, blood, human, adh, genes, variant, aldehyde, functional, concentrations, yin, gene, hepatic, protection, studies, polymorphisms, polymorphism, homozygotes, heterozygotes, table, activity, allozymes, allele, disease, oxidation, adhc, peng, genetic, family, cent, aldha, genotypes, liver, allelic, molecular, pharmacogenetics, risk, dependence, class,

Topics {βœ’οΈ}

shih-jiun yin tri-service general hospital glutamic acid/lysine exchange single nucleotide polymorphism x-ray crystallographic studies alcohol-induced organ damage complex behavioural disorder human adh/aldh families alcoholic liver disease single amino acid mitochondrial aldehyde dehydrogenase article peng single nucleotide significantly faster elimination alcoholic patient homozygous eukaryotic aldehyde dehydrogenase privacy choices/manage cookies hepatic high-km adh1a steady-state concentrations adh/aldh isozymes blood acetaldehyde concentrations alcohol dehydrogenase genes blood acetaldehyde concentration extrahepatic low-km aldhs venous blood acetaldehyde aldehyde dehydrogenase aldh22 antecubital venous blood adh1c isozymes/allozymes aldehyde dehydrogenase genotypes adh gene cluster homozygous aldh22/2 genotype normal aldh21/1 genotype blood acetaldehyde levels aldh gene superfamily protective disease gene alcohol metabolism gene hepatic venous blood higher alcohol concentrations gene-environment interactions [5 multiple significant associations alcohol related pathology alcohol-related pathology amino acid exchanges lee s divergently related enzymes yin s adh/aldh families national science council strongest genetic modifier human liver tissues

Questions {❓}

  • Eriksson CJP: Measurement of acetaldehyde: What levels occur naturally and in response to alcohol?
  • Zintzaras E, Stefanidis I, Santos M, et al: Do alcohol-metabolizing enzyme gene polymorphisms increase the risk of alcoholism and alcoholic liver disease?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Effect of the allelic variants of aldehyde dehydrogenase ALDH2*2 and alcohol dehydrogenase ADH1B*2on blood acetaldehyde concentrations
         description:Alcoholism is a complex behavioural disorder. Molecular genetics studies have identified numerous candidate genes associated with alcoholism. It is crucial to verify the disease susceptibility genes by correlating the pinpointed allelic variations to the causal phenotypes. Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are the principal enzymes responsible for ethanol metabolism in humans. Both ADH and ALDH exhibit functional polymorphisms among racial populations; these polymorphisms have been shown to be the important genetic determinants in ethanol metabolism and alcoholism. Here, we briefly review recent advances in genomic studies of human ADH/ALDH families and alcoholism, with an emphasis on the pharmacogenetic consequences of venous blood acetaldehyde in the different ALDH2 genotypes following the intake of various doses of ethanol. This paper illustrates a paradigmatic example of phenotypic verifications in a protective disease gene for substance abuse.
         datePublished:2009-01-01T00:00:00Z
         dateModified:2009-01-01T00:00:00Z
         pageStart:1
         pageEnd:7
         sameAs:https://doi.org/10.1186/1479-7364-3-2-121
         keywords:
            alcohol dehydrogenase
            aldehyde dehydrogenase
            single nucleotide polymorphism
            alcoholism
            ethanol metabolism
            blood acetaldehyde
            Human Genetics
            Proteomics
            Bioinformatics
         image:
         isPartOf:
            name:Human Genomics
            issn:
               1479-7364
            volumeNumber:3
            type:
               Periodical
               PublicationVolume
         publisher:
            name:BioMed Central
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Giia-Sheun Peng
               affiliation:
                     name:Tri-Service General Hospital
                     address:
                        name:Department of Neurology, Tri-Service General Hospital, Taipei 114, Taiwan
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Shih-Jiun Yin
               affiliation:
                     name:National Defense Medical Center
                     address:
                        name:Department of Biochemistry, National Defense Medical Center, Taipei 114, Taiwan
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Effect of the allelic variants of aldehyde dehydrogenase ALDH2*2 and alcohol dehydrogenase ADH1B*2on blood acetaldehyde concentrations
      description:Alcoholism is a complex behavioural disorder. Molecular genetics studies have identified numerous candidate genes associated with alcoholism. It is crucial to verify the disease susceptibility genes by correlating the pinpointed allelic variations to the causal phenotypes. Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are the principal enzymes responsible for ethanol metabolism in humans. Both ADH and ALDH exhibit functional polymorphisms among racial populations; these polymorphisms have been shown to be the important genetic determinants in ethanol metabolism and alcoholism. Here, we briefly review recent advances in genomic studies of human ADH/ALDH families and alcoholism, with an emphasis on the pharmacogenetic consequences of venous blood acetaldehyde in the different ALDH2 genotypes following the intake of various doses of ethanol. This paper illustrates a paradigmatic example of phenotypic verifications in a protective disease gene for substance abuse.
      datePublished:2009-01-01T00:00:00Z
      dateModified:2009-01-01T00:00:00Z
      pageStart:1
      pageEnd:7
      sameAs:https://doi.org/10.1186/1479-7364-3-2-121
      keywords:
         alcohol dehydrogenase
         aldehyde dehydrogenase
         single nucleotide polymorphism
         alcoholism
         ethanol metabolism
         blood acetaldehyde
         Human Genetics
         Proteomics
         Bioinformatics
      image:
      isPartOf:
         name:Human Genomics
         issn:
            1479-7364
         volumeNumber:3
         type:
            Periodical
            PublicationVolume
      publisher:
         name:BioMed Central
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Giia-Sheun Peng
            affiliation:
                  name:Tri-Service General Hospital
                  address:
                     name:Department of Neurology, Tri-Service General Hospital, Taipei 114, Taiwan
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Shih-Jiun Yin
            affiliation:
                  name:National Defense Medical Center
                  address:
                     name:Department of Biochemistry, National Defense Medical Center, Taipei 114, Taiwan
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Human Genomics
      issn:
         1479-7364
      volumeNumber:3
Organization:
      name:BioMed Central
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Tri-Service General Hospital
      address:
         name:Department of Neurology, Tri-Service General Hospital, Taipei 114, Taiwan
         type:PostalAddress
      name:National Defense Medical Center
      address:
         name:Department of Biochemistry, National Defense Medical Center, Taipei 114, Taiwan
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Giia-Sheun Peng
      affiliation:
            name:Tri-Service General Hospital
            address:
               name:Department of Neurology, Tri-Service General Hospital, Taipei 114, Taiwan
               type:PostalAddress
            type:Organization
      name:Shih-Jiun Yin
      affiliation:
            name:National Defense Medical Center
            address:
               name:Department of Biochemistry, National Defense Medical Center, Taipei 114, Taiwan
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Neurology, Tri-Service General Hospital, Taipei 114, Taiwan
      name:Department of Biochemistry, National Defense Medical Center, Taipei 114, Taiwan

External Links {πŸ”—}(135)

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