Intestinal flora induces the expression of Cyp3a in the mouse liver.
Identifieur interne : 001F52 ( Main/Exploration ); précédent : 001F51; suivant : 001F53Intestinal flora induces the expression of Cyp3a in the mouse liver.
Auteurs : T. Toda [Japon] ; N. Saito ; N. Ikarashi ; K. Ito ; M. Yamamoto ; A. Ishige ; K. Watanabe ; K. SugiyamaSource :
- Xenobiotica; the fate of foreign compounds in biological systems [ 1366-5928 ] ; 2009.
Descripteurs français
- KwdFr :
- ARN messager (métabolisme), Acide lithocholique (pharmacologie), Amorces ADN (génétique), Animaux (MeSH), Axénie (MeSH), Bactéries (composition chimique), Chromatographie en phase liquide à haute performance (MeSH), Cinétique (MeSH), Cytochrome P-450 enzyme system (métabolisme), Facteurs de transcription (métabolisme), Foie (métabolisme), Intestins (microbiologie), Isoenzymes (métabolisme), Mâle (MeSH), Organismes exempts d'organismes pathogènes spécifiques (MeSH), RT-PCR (MeSH), Récepteur du prégnane X (MeSH), Récepteurs aux stéroïdes (métabolisme), Récepteurs cytoplasmiques et nucléaires (métabolisme), Régulation de l'expression des gènes codant pour des enzymes (effets des médicaments et des substances chimiques), Souris (MeSH), Séquençage par oligonucléotides en batterie (MeSH), Technique de Western (MeSH).
- MESH :
- composition chimique : Bactéries.
- effets des médicaments et des substances chimiques : Régulation de l'expression des gènes codant pour des enzymes.
- génétique : Amorces ADN.
- microbiologie : Intestins.
- métabolisme : ARN messager, Cytochrome P-450 enzyme system, Facteurs de transcription, Foie, Isoenzymes, Récepteurs aux stéroïdes, Récepteurs cytoplasmiques et nucléaires.
- pharmacologie : Acide lithocholique.
- Animaux, Axénie, Chromatographie en phase liquide à haute performance, Cinétique, Mâle, Organismes exempts d'organismes pathogènes spécifiques, RT-PCR, Récepteur du prégnane X, Souris, Séquençage par oligonucléotides en batterie, Technique de Western.
English descriptors
- KwdEn :
- Animals (MeSH), Bacteria (chemistry), Blotting, Western (MeSH), Chromatography, High Pressure Liquid (MeSH), Cytochrome P-450 Enzyme System (metabolism), DNA Primers (genetics), Gene Expression Regulation, Enzymologic (drug effects), Germ-Free Life (MeSH), Intestines (microbiology), Isoenzymes (metabolism), Kinetics (MeSH), Lithocholic Acid (pharmacology), Liver (metabolism), Male (MeSH), Mice (MeSH), Oligonucleotide Array Sequence Analysis (MeSH), Pregnane X Receptor (MeSH), RNA, Messenger (metabolism), Receptors, Cytoplasmic and Nuclear (metabolism), Receptors, Steroid (metabolism), Reverse Transcriptase Polymerase Chain Reaction (MeSH), Specific Pathogen-Free Organisms (MeSH), Transcription Factors (metabolism).
- MESH :
- chemical , genetics : DNA Primers.
- chemical , metabolism : Cytochrome P-450 Enzyme System, Isoenzymes, RNA, Messenger, Receptors, Cytoplasmic and Nuclear, Receptors, Steroid, Transcription Factors.
- chemistry : Bacteria.
- drug effects : Gene Expression Regulation, Enzymologic.
- metabolism : Liver.
- microbiology : Intestines.
- chemical , pharmacology : Lithocholic Acid.
- Animals, Blotting, Western, Chromatography, High Pressure Liquid, Germ-Free Life, Kinetics, Male, Mice, Oligonucleotide Array Sequence Analysis, Pregnane X Receptor, Reverse Transcriptase Polymerase Chain Reaction, Specific Pathogen-Free Organisms.
Abstract
In order to determine the effects of intestinal flora on the expression of cytochrome P450 (CYP), the mRNA expression of CYP was compared between specific pathogen-free (SPF) and germ-free (GF) mice. Most of the major CYP isozymes showed higher expression in the livers of SPF mice compared with GF mice. Nuclear factors such as pregnane X receptor (PXR) and constitutive androstane receptor (CAR), as well as transporters and conjugation enzymes involved in the detoxification of lithocholic acid (LCA), also showed higher expression in SPF mice. The findings suggest that in the livers of SPF mice, LCA produced by intestinal flora increases the expression of CYPs via activation of PXR and CAR. Drugs such as antibiotics, some diseases and ageing, etc. are known to alter intestinal flora. The present findings suggest that such changes also affect CYP and are one of the factors responsible for individual differences in pharmacokinetics.
DOI: 10.1080/00498250802651984
PubMed: 19350455
Affiliations:
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Ikarashi</name></author><author><name sortKey="Ito, K" sort="Ito, K" uniqKey="Ito K" first="K" last="Ito">K. Ito</name></author><author><name sortKey="Yamamoto, M" sort="Yamamoto, M" uniqKey="Yamamoto M" first="M" last="Yamamoto">M. Yamamoto</name></author><author><name sortKey="Ishige, A" sort="Ishige, A" uniqKey="Ishige A" first="A" last="Ishige">A. Ishige</name></author><author><name sortKey="Watanabe, K" sort="Watanabe, K" uniqKey="Watanabe K" first="K" last="Watanabe">K. Watanabe</name></author><author><name sortKey="Sugiyama, K" sort="Sugiyama, K" uniqKey="Sugiyama K" first="K" last="Sugiyama">K. Sugiyama</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="RBID">pubmed:19350455</idno><idno type="pmid">19350455</idno><idno type="doi">10.1080/00498250802651984</idno><idno type="wicri:Area/Main/Corpus">001F70</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">001F70</idno><idno type="wicri:Area/Main/Curation">001F70</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">001F70</idno><idno type="wicri:Area/Main/Exploration">001F70</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Intestinal flora induces the expression of Cyp3a in the mouse liver.</title><author><name sortKey="Toda, T" sort="Toda, T" uniqKey="Toda T" first="T" last="Toda">T. Toda</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Pharmacokinetics, Hoshi University, Ebara, Shinagawa-ku, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Clinical Pharmacokinetics, Hoshi University, Ebara, Shinagawa-ku, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Saito, N" sort="Saito, N" uniqKey="Saito N" first="N" last="Saito">N. Saito</name></author><author><name sortKey="Ikarashi, N" sort="Ikarashi, N" uniqKey="Ikarashi N" first="N" last="Ikarashi">N. Ikarashi</name></author><author><name sortKey="Ito, K" sort="Ito, K" uniqKey="Ito K" first="K" last="Ito">K. Ito</name></author><author><name sortKey="Yamamoto, M" sort="Yamamoto, M" uniqKey="Yamamoto M" first="M" last="Yamamoto">M. 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Sugiyama</name></author></analytic><series><title level="j">Xenobiotica; the fate of foreign compounds in biological systems</title><idno type="eISSN">1366-5928</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Bacteria (chemistry)</term><term>Blotting, Western (MeSH)</term><term>Chromatography, High Pressure Liquid (MeSH)</term><term>Cytochrome P-450 Enzyme System (metabolism)</term><term>DNA Primers (genetics)</term><term>Gene Expression Regulation, Enzymologic (drug effects)</term><term>Germ-Free Life (MeSH)</term><term>Intestines (microbiology)</term><term>Isoenzymes (metabolism)</term><term>Kinetics (MeSH)</term><term>Lithocholic Acid (pharmacology)</term><term>Liver (metabolism)</term><term>Male (MeSH)</term><term>Mice (MeSH)</term><term>Oligonucleotide Array Sequence Analysis (MeSH)</term><term>Pregnane X Receptor (MeSH)</term><term>RNA, Messenger (metabolism)</term><term>Receptors, Cytoplasmic and Nuclear (metabolism)</term><term>Receptors, Steroid (metabolism)</term><term>Reverse Transcriptase Polymerase Chain Reaction (MeSH)</term><term>Specific Pathogen-Free Organisms (MeSH)</term><term>Transcription Factors (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (métabolisme)</term><term>Acide lithocholique (pharmacologie)</term><term>Amorces ADN (génétique)</term><term>Animaux (MeSH)</term><term>Axénie (MeSH)</term><term>Bactéries (composition chimique)</term><term>Chromatographie en phase liquide à haute performance (MeSH)</term><term>Cinétique (MeSH)</term><term>Cytochrome P-450 enzyme system (métabolisme)</term><term>Facteurs de transcription (métabolisme)</term><term>Foie (métabolisme)</term><term>Intestins (microbiologie)</term><term>Isoenzymes (métabolisme)</term><term>Mâle (MeSH)</term><term>Organismes exempts d'organismes pathogènes spécifiques (MeSH)</term><term>RT-PCR (MeSH)</term><term>Récepteur du prégnane X (MeSH)</term><term>Récepteurs aux stéroïdes (métabolisme)</term><term>Récepteurs cytoplasmiques et nucléaires (métabolisme)</term><term>Régulation de l'expression des gènes codant pour des enzymes (effets des médicaments et des substances chimiques)</term><term>Souris (MeSH)</term><term>Séquençage par oligonucléotides en batterie (MeSH)</term><term>Technique de Western (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA Primers</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytochrome P-450 Enzyme System</term><term>Isoenzymes</term><term>RNA, Messenger</term><term>Receptors, Cytoplasmic and Nuclear</term><term>Receptors, Steroid</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Bacteria</term></keywords><keywords scheme="MESH" 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stéroïdes</term><term>Récepteurs cytoplasmiques et nucléaires</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acide lithocholique</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Lithocholic Acid</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Blotting, Western</term><term>Chromatography, High Pressure Liquid</term><term>Germ-Free Life</term><term>Kinetics</term><term>Male</term><term>Mice</term><term>Oligonucleotide Array Sequence Analysis</term><term>Pregnane X Receptor</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Specific Pathogen-Free Organisms</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Axénie</term><term>Chromatographie en phase liquide à haute performance</term><term>Cinétique</term><term>Mâle</term><term>Organismes exempts d'organismes pathogènes spécifiques</term><term>RT-PCR</term><term>Récepteur du prégnane X</term><term>Souris</term><term>Séquençage par oligonucléotides en batterie</term><term>Technique de Western</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In order to determine the effects of intestinal flora on the expression of cytochrome P450 (CYP), the mRNA expression of CYP was compared between specific pathogen-free (SPF) and germ-free (GF) mice. Most of the major CYP isozymes showed higher expression in the livers of SPF mice compared with GF mice. Nuclear factors such as pregnane X receptor (PXR) and constitutive androstane receptor (CAR), as well as transporters and conjugation enzymes involved in the detoxification of lithocholic acid (LCA), also showed higher expression in SPF mice. The findings suggest that in the livers of SPF mice, LCA produced by intestinal flora increases the expression of CYPs via activation of PXR and CAR. Drugs such as antibiotics, some diseases and ageing, etc. are known to alter intestinal flora. The present findings suggest that such changes also affect CYP and are one of the factors responsible for individual differences in pharmacokinetics.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19350455</PMID><DateCompleted><Year>2009</Year><Month>06</Month><Day>01</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>01</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1366-5928</ISSN><JournalIssue CitedMedium="Internet"><Volume>39</Volume><Issue>4</Issue><PubDate><Year>2009</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Xenobiotica; the fate of foreign compounds in biological systems</Title><ISOAbbreviation>Xenobiotica</ISOAbbreviation></Journal><ArticleTitle>Intestinal flora induces the expression of Cyp3a in the mouse liver.</ArticleTitle><Pagination><MedlinePgn>323-34</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/00498250802651984</ELocationID><Abstract><AbstractText>In order to determine the effects of intestinal flora on the expression of cytochrome P450 (CYP), the mRNA expression of CYP was compared between specific pathogen-free (SPF) and germ-free (GF) mice. Most of the major CYP isozymes showed higher expression in the livers of SPF mice compared with GF mice. Nuclear factors such as pregnane X receptor (PXR) and constitutive androstane receptor (CAR), as well as transporters and conjugation enzymes involved in the detoxification of lithocholic acid (LCA), also showed higher expression in SPF mice. The findings suggest that in the livers of SPF mice, LCA produced by intestinal flora increases the expression of CYPs via activation of PXR and CAR. Drugs such as antibiotics, some diseases and ageing, etc. are known to alter intestinal flora. The present findings suggest that such changes also affect CYP and are one of the factors responsible for individual differences in pharmacokinetics.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Toda</LastName><ForeName>T</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Clinical Pharmacokinetics, Hoshi University, Ebara, Shinagawa-ku, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Saito</LastName><ForeName>N</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Ikarashi</LastName><ForeName>N</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Ito</LastName><ForeName>K</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Yamamoto</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Ishige</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Watanabe</LastName><ForeName>K</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Sugiyama</LastName><ForeName>K</ForeName><Initials>K</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Xenobiotica</MedlineTA><NlmUniqueID>1306665</NlmUniqueID><ISSNLinking>0049-8254</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017931">DNA Primers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007527">Isoenzymes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000077297">Pregnane X Receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018160">Receptors, Cytoplasmic and Nuclear</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011987">Receptors, Steroid</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>438XLITDI3</RegistryNumber><NameOfSubstance UI="C409467">constitutive androstane receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>5QU0I8393U</RegistryNumber><NameOfSubstance UI="D008095">Lithocholic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>9035-51-2</RegistryNumber><NameOfSubstance UI="D003577">Cytochrome P-450 Enzyme System</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.14.1</RegistryNumber><NameOfSubstance UI="C500811">CYP3A protein, mouse</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001419" MajorTopicYN="N">Bacteria</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015153" MajorTopicYN="N">Blotting, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002851" MajorTopicYN="N">Chromatography, High Pressure Liquid</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003577" MajorTopicYN="N">Cytochrome P-450 Enzyme System</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017931" MajorTopicYN="N">DNA Primers</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015971" MajorTopicYN="N">Gene Expression Regulation, Enzymologic</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005856" MajorTopicYN="N">Germ-Free Life</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007422" MajorTopicYN="N">Intestines</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007527" MajorTopicYN="N">Isoenzymes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007700" MajorTopicYN="N">Kinetics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008095" MajorTopicYN="N">Lithocholic Acid</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008099" MajorTopicYN="N">Liver</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020411" MajorTopicYN="N">Oligonucleotide Array Sequence Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077297" MajorTopicYN="N">Pregnane X Receptor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018160" MajorTopicYN="N">Receptors, Cytoplasmic and Nuclear</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011987" MajorTopicYN="N">Receptors, Steroid</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020133" MajorTopicYN="N">Reverse Transcriptase Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013047" MajorTopicYN="N">Specific Pathogen-Free Organisms</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>4</Month><Day>8</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>4</Month><Day>8</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>6</Month><Day>2</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19350455</ArticleId><ArticleId IdType="pii">909819882</ArticleId><ArticleId IdType="doi">10.1080/00498250802651984</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Japon</li></country><region><li>Région de Kantō</li></region><settlement><li>Tokyo</li></settlement></list><tree><noCountry><name sortKey="Ikarashi, N" sort="Ikarashi, N" uniqKey="Ikarashi N" first="N" last="Ikarashi">N. Ikarashi</name><name sortKey="Ishige, A" sort="Ishige, A" uniqKey="Ishige A" first="A" last="Ishige">A. Ishige</name><name sortKey="Ito, K" sort="Ito, K" uniqKey="Ito K" first="K" last="Ito">K. Ito</name><name sortKey="Saito, N" sort="Saito, N" uniqKey="Saito N" first="N" last="Saito">N. Saito</name><name sortKey="Sugiyama, K" sort="Sugiyama, K" uniqKey="Sugiyama K" first="K" last="Sugiyama">K. Sugiyama</name><name sortKey="Watanabe, K" sort="Watanabe, K" uniqKey="Watanabe K" first="K" last="Watanabe">K. Watanabe</name><name sortKey="Yamamoto, M" sort="Yamamoto, M" uniqKey="Yamamoto M" first="M" last="Yamamoto">M. Yamamoto</name></noCountry><country name="Japon"><region name="Région de Kantō"><name sortKey="Toda, T" sort="Toda, T" uniqKey="Toda T" first="T" last="Toda">T. Toda</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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