Redox modification of caveolar proteins in the cardiovascular system- role in cellular signalling and disease.
Identifieur interne : 000320 ( Main/Exploration ); précédent : 000319; suivant : 000321Redox modification of caveolar proteins in the cardiovascular system- role in cellular signalling and disease.
Auteurs : Kristen J. Bubb [Australie] ; Asa Birna Birgisdottir [Norvège] ; Owen Tang [Australie] ; Thomas Hansen [Australie] ; Gemma A. Figtree [Australie]Source :
- Free radical biology & medicine [ 1873-4596 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Cardiomyopathies (anatomopathologie), Cardiomyopathies (génétique), Cardiomyopathies (métabolisme), Cardiomégalie (anatomopathologie), Cardiomégalie (génétique), Cardiomégalie (métabolisme), Cavéoles (anatomopathologie), Cavéoles (métabolisme), Cavéolines (génétique), Cavéolines (métabolisme), Défaillance cardiaque (anatomopathologie), Défaillance cardiaque (génétique), Défaillance cardiaque (métabolisme), Espèces réactives de l'oxygène (métabolisme), Humains (MeSH), NADPH oxidase (génétique), NADPH oxidase (métabolisme), Nitric oxide synthase type III (génétique), Nitric oxide synthase type III (métabolisme), Oxydoréduction (MeSH), Régulation de l'expression des gènes (MeSH), Souris (MeSH), Souris knockout (MeSH), Système cardiovasculaire (anatomopathologie), Système cardiovasculaire (métabolisme), Transduction du signal (MeSH).
- MESH :
- anatomopathologie : Cardiomyopathies, Cardiomégalie, Cavéoles, Défaillance cardiaque, Système cardiovasculaire.
- génétique : Cardiomyopathies, Cardiomégalie, Cavéolines, Défaillance cardiaque, NADPH oxidase, Nitric oxide synthase type III.
- métabolisme : Cardiomyopathies, Cardiomégalie, Cavéoles, Cavéolines, Défaillance cardiaque, Espèces réactives de l'oxygène, NADPH oxidase, Nitric oxide synthase type III, Système cardiovasculaire.
- Animaux, Humains, Oxydoréduction, Régulation de l'expression des gènes, Souris, Souris knockout, Transduction du signal.
English descriptors
- KwdEn :
- Animals (MeSH), Cardiomegaly (genetics), Cardiomegaly (metabolism), Cardiomegaly (pathology), Cardiomyopathies (genetics), Cardiomyopathies (metabolism), Cardiomyopathies (pathology), Cardiovascular System (metabolism), Cardiovascular System (pathology), Caveolae (metabolism), Caveolae (pathology), Caveolins (genetics), Caveolins (metabolism), Gene Expression Regulation (MeSH), Heart Failure (genetics), Heart Failure (metabolism), Heart Failure (pathology), Humans (MeSH), Mice (MeSH), Mice, Knockout (MeSH), NADPH Oxidases (genetics), NADPH Oxidases (metabolism), Nitric Oxide Synthase Type III (genetics), Nitric Oxide Synthase Type III (metabolism), Oxidation-Reduction (MeSH), Reactive Oxygen Species (metabolism), Signal Transduction (MeSH).
- MESH :
- chemical , genetics : Caveolins, NADPH Oxidases, Nitric Oxide Synthase Type III.
- genetics : Cardiomegaly, Cardiomyopathies, Heart Failure.
- metabolism : Cardiomegaly, Cardiomyopathies, Cardiovascular System, Caveolae, Caveolins, Heart Failure, NADPH Oxidases, Nitric Oxide Synthase Type III, Reactive Oxygen Species.
- pathology : Cardiomegaly, Cardiomyopathies, Cardiovascular System, Caveolae, Heart Failure.
- Animals, Gene Expression Regulation, Humans, Mice, Mice, Knockout, Oxidation-Reduction, Signal Transduction.
Abstract
Rapid and coordinated release of a variety of reactive oxygen species (ROS) such as superoxide (O2.-), hydrogen peroxide (H2O2) and peroxynitrite, in specific microdomains, play a crucial role in cell signalling in the cardiovascular system. These reactions are mediated by reversible and functional modifications of a wide variety of key proteins. Dysregulation of this oxidative signalling occurs in almost all forms of cardiovascular disease (CVD), including at the very early phases. Despite the heavily publicized failure of "antioxidants" to improve CVD progression, pharmacotherapies such as those targeting the renin-angiotensin system, or statins, exert at least part of their large clinical benefit via modulating cellular redox signalling. Over 250 proteins, including receptors, ion channels and pumps, and signalling proteins are found in the caveolae. An increasing proportion of these are being recognized as redox regulated-proteins, that reside in the immediate vicinity of the two major cellular sources of ROS, nicotinamide adenine dinucleotide phosphate oxidase (Nox) and uncoupled endothelial nitric oxide synthase (eNOS). This review focuses on what is known about redox signalling within the caveolae, as well as endogenous protective mechanisms utilized by the cell, and new approaches to targeting dysregulated redox signalling in the caveolae as a therapeutic strategy in CVD.
DOI: 10.1016/j.freeradbiomed.2017.02.012
PubMed: 28188926
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Figtree</name><affiliation wicri:level="1"><nlm:affiliation>Kolling Institute of Medical Research, University of Sydney and Cardiology Department, Royal North Shore Hospital, St Leonards, NSW 2065, Australia. Electronic address: gemma.figtree@sydney.edu.au.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Kolling Institute of Medical Research, University of Sydney and Cardiology Department, Royal North Shore Hospital, St Leonards, NSW 2065</wicri:regionArea><wicri:noRegion>NSW 2065</wicri:noRegion></affiliation></author></analytic><series><title level="j">Free radical biology & medicine</title><idno type="eISSN">1873-4596</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Cardiomegaly (genetics)</term><term>Cardiomegaly (metabolism)</term><term>Cardiomegaly (pathology)</term><term>Cardiomyopathies (genetics)</term><term>Cardiomyopathies (metabolism)</term><term>Cardiomyopathies (pathology)</term><term>Cardiovascular System (metabolism)</term><term>Cardiovascular System (pathology)</term><term>Caveolae (metabolism)</term><term>Caveolae (pathology)</term><term>Caveolins (genetics)</term><term>Caveolins (metabolism)</term><term>Gene Expression Regulation (MeSH)</term><term>Heart Failure (genetics)</term><term>Heart Failure (metabolism)</term><term>Heart Failure (pathology)</term><term>Humans (MeSH)</term><term>Mice (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>NADPH Oxidases (genetics)</term><term>NADPH Oxidases (metabolism)</term><term>Nitric Oxide Synthase Type III (genetics)</term><term>Nitric Oxide Synthase Type III (metabolism)</term><term>Oxidation-Reduction (MeSH)</term><term>Reactive Oxygen Species (metabolism)</term><term>Signal Transduction (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Cardiomyopathies (anatomopathologie)</term><term>Cardiomyopathies (génétique)</term><term>Cardiomyopathies (métabolisme)</term><term>Cardiomégalie (anatomopathologie)</term><term>Cardiomégalie (génétique)</term><term>Cardiomégalie (métabolisme)</term><term>Cavéoles (anatomopathologie)</term><term>Cavéoles (métabolisme)</term><term>Cavéolines (génétique)</term><term>Cavéolines (métabolisme)</term><term>Défaillance cardiaque (anatomopathologie)</term><term>Défaillance cardiaque (génétique)</term><term>Défaillance cardiaque (métabolisme)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Humains (MeSH)</term><term>NADPH oxidase (génétique)</term><term>NADPH oxidase (métabolisme)</term><term>Nitric oxide synthase type III (génétique)</term><term>Nitric oxide synthase type III (métabolisme)</term><term>Oxydoréduction (MeSH)</term><term>Régulation de l'expression des gènes (MeSH)</term><term>Souris (MeSH)</term><term>Souris knockout (MeSH)</term><term>Système cardiovasculaire (anatomopathologie)</term><term>Système cardiovasculaire (métabolisme)</term><term>Transduction du signal (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Caveolins</term><term>NADPH Oxidases</term><term>Nitric Oxide Synthase Type III</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cardiomyopathies</term><term>Cardiomégalie</term><term>Cavéoles</term><term>Défaillance cardiaque</term><term>Système cardiovasculaire</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cardiomegaly</term><term>Cardiomyopathies</term><term>Heart Failure</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Cardiomyopathies</term><term>Cardiomégalie</term><term>Cavéolines</term><term>Défaillance cardiaque</term><term>NADPH oxidase</term><term>Nitric oxide synthase type III</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cardiomegaly</term><term>Cardiomyopathies</term><term>Cardiovascular System</term><term>Caveolae</term><term>Caveolins</term><term>Heart Failure</term><term>NADPH Oxidases</term><term>Nitric Oxide Synthase Type III</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cardiomyopathies</term><term>Cardiomégalie</term><term>Cavéoles</term><term>Cavéolines</term><term>Défaillance cardiaque</term><term>Espèces réactives de l'oxygène</term><term>NADPH oxidase</term><term>Nitric oxide synthase type III</term><term>Système cardiovasculaire</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cardiomegaly</term><term>Cardiomyopathies</term><term>Cardiovascular System</term><term>Caveolae</term><term>Heart Failure</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Gene Expression Regulation</term><term>Humans</term><term>Mice</term><term>Mice, Knockout</term><term>Oxidation-Reduction</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Oxydoréduction</term><term>Régulation de l'expression des gènes</term><term>Souris</term><term>Souris knockout</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Rapid and coordinated release of a variety of reactive oxygen species (ROS) such as superoxide (O<sub>2</sub><sup>.-</sup>), hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) and peroxynitrite, in specific microdomains, play a crucial role in cell signalling in the cardiovascular system. These reactions are mediated by reversible and functional modifications of a wide variety of key proteins. Dysregulation of this oxidative signalling occurs in almost all forms of cardiovascular disease (CVD), including at the very early phases. Despite the heavily publicized failure of "antioxidants" to improve CVD progression, pharmacotherapies such as those targeting the renin-angiotensin system, or statins, exert at least part of their large clinical benefit via modulating cellular redox signalling. Over 250 proteins, including receptors, ion channels and pumps, and signalling proteins are found in the caveolae. An increasing proportion of these are being recognized as redox regulated-proteins, that reside in the immediate vicinity of the two major cellular sources of ROS, nicotinamide adenine dinucleotide phosphate oxidase (Nox) and uncoupled endothelial nitric oxide synthase (eNOS). This review focuses on what is known about redox signalling within the caveolae, as well as endogenous protective mechanisms utilized by the cell, and new approaches to targeting dysregulated redox signalling in the caveolae as a therapeutic strategy in CVD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28188926</PMID><DateCompleted><Year>2018</Year><Month>03</Month><Day>13</Day></DateCompleted><DateRevised><Year>2018</Year><Month>03</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-4596</ISSN><JournalIssue CitedMedium="Internet"><Volume>109</Volume><PubDate><Year>2017</Year><Month>08</Month></PubDate></JournalIssue><Title>Free radical biology & medicine</Title><ISOAbbreviation>Free Radic Biol Med</ISOAbbreviation></Journal><ArticleTitle>Redox modification of caveolar proteins in the cardiovascular system- role in cellular signalling and disease.</ArticleTitle><Pagination><MedlinePgn>61-74</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0891-5849(17)30074-6</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.freeradbiomed.2017.02.012</ELocationID><Abstract><AbstractText>Rapid and coordinated release of a variety of reactive oxygen species (ROS) such as superoxide (O<sub>2</sub><sup>.-</sup>), hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) and peroxynitrite, in specific microdomains, play a crucial role in cell signalling in the cardiovascular system. These reactions are mediated by reversible and functional modifications of a wide variety of key proteins. Dysregulation of this oxidative signalling occurs in almost all forms of cardiovascular disease (CVD), including at the very early phases. Despite the heavily publicized failure of "antioxidants" to improve CVD progression, pharmacotherapies such as those targeting the renin-angiotensin system, or statins, exert at least part of their large clinical benefit via modulating cellular redox signalling. Over 250 proteins, including receptors, ion channels and pumps, and signalling proteins are found in the caveolae. An increasing proportion of these are being recognized as redox regulated-proteins, that reside in the immediate vicinity of the two major cellular sources of ROS, nicotinamide adenine dinucleotide phosphate oxidase (Nox) and uncoupled endothelial nitric oxide synthase (eNOS). This review focuses on what is known about redox signalling within the caveolae, as well as endogenous protective mechanisms utilized by the cell, and new approaches to targeting dysregulated redox signalling in the caveolae as a therapeutic strategy in CVD.</AbstractText><CopyrightInformation>Copyright © 2017. Published by Elsevier Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bubb</LastName><ForeName>Kristen J</ForeName><Initials>KJ</Initials><AffiliationInfo><Affiliation>Kolling Institute of Medical Research, University of Sydney and Cardiology Department, Royal North Shore Hospital, St Leonards, NSW 2065, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Birgisdottir</LastName><ForeName>Asa Birna</ForeName><Initials>AB</Initials><AffiliationInfo><Affiliation>Kolling Institute of Medical Research, University of Sydney and Cardiology Department, Royal North Shore Hospital, St Leonards, NSW 2065, Australia; Department of Cardiothoracic and Vascular Surgery, Heart and Lung Clinic, University Hospital of North Norway, Tromsø, Norway.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tang</LastName><ForeName>Owen</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Kolling Institute of Medical Research, University of Sydney and Cardiology Department, Royal North Shore Hospital, St Leonards, NSW 2065, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hansen</LastName><ForeName>Thomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Kolling Institute of Medical Research, University of Sydney and Cardiology Department, Royal North Shore Hospital, St Leonards, NSW 2065, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Figtree</LastName><ForeName>Gemma A</ForeName><Initials>GA</Initials><AffiliationInfo><Affiliation>Kolling Institute of Medical Research, University of Sydney and Cardiology Department, Royal North Shore Hospital, St Leonards, NSW 2065, Australia. Electronic address: gemma.figtree@sydney.edu.au.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>02</Month><Day>07</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Free Radic Biol Med</MedlineTA><NlmUniqueID>8709159</NlmUniqueID><ISSNLinking>0891-5849</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D022461">Caveolins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.13.39</RegistryNumber><NameOfSubstance UI="C496314">NOS3 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.13.39</RegistryNumber><NameOfSubstance UI="D052250">Nitric Oxide Synthase Type III</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.6.3.-</RegistryNumber><NameOfSubstance UI="D019255">NADPH Oxidases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006332" MajorTopicYN="N">Cardiomegaly</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009202" MajorTopicYN="N">Cardiomyopathies</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002319" MajorTopicYN="N">Cardiovascular System</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D021941" MajorTopicYN="N">Caveolae</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D022461" MajorTopicYN="N">Caveolins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="N">Heart Failure</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019255" MajorTopicYN="N">NADPH Oxidases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D052250" MajorTopicYN="N">Nitric Oxide Synthase Type III</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Glutaredoxin</Keyword><Keyword MajorTopicYN="Y">Heart failure</Keyword><Keyword MajorTopicYN="Y">Hydrogen peroxide</Keyword><Keyword MajorTopicYN="Y">NADPH oxidase</Keyword><Keyword MajorTopicYN="Y">S-glutathionylation</Keyword><Keyword MajorTopicYN="Y">Superoxide</Keyword><Keyword MajorTopicYN="Y">eNOS</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>12</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>01</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>02</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>2</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>3</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>2</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28188926</ArticleId><ArticleId IdType="pii">S0891-5849(17)30074-6</ArticleId><ArticleId IdType="doi">10.1016/j.freeradbiomed.2017.02.012</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Australie</li><li>Norvège</li></country></list><tree><country name="Australie"><noRegion><name sortKey="Bubb, Kristen J" sort="Bubb, Kristen J" uniqKey="Bubb K" first="Kristen J" last="Bubb">Kristen J. Bubb</name></noRegion><name sortKey="Figtree, Gemma A" sort="Figtree, Gemma A" uniqKey="Figtree G" first="Gemma A" last="Figtree">Gemma A. Figtree</name><name sortKey="Hansen, Thomas" sort="Hansen, Thomas" uniqKey="Hansen T" first="Thomas" last="Hansen">Thomas Hansen</name><name sortKey="Tang, Owen" sort="Tang, Owen" uniqKey="Tang O" first="Owen" last="Tang">Owen Tang</name></country><country name="Norvège"><noRegion><name sortKey="Birgisdottir, Asa Birna" sort="Birgisdottir, Asa Birna" uniqKey="Birgisdottir A" first="Asa Birna" last="Birgisdottir">Asa Birna Birgisdottir</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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