Absence of glutaredoxin1 increases lens susceptibility to oxidative stress induced by UVR-B.
Identifieur interne : 000B53 ( Main/Exploration ); précédent : 000B52; suivant : 000B54Absence of glutaredoxin1 increases lens susceptibility to oxidative stress induced by UVR-B.
Auteurs : Linda M. Meyer [Allemagne] ; Stefan Löfgren ; Ye-Shih Ho ; Marjorie Lou ; Alfred Wegener ; Frank Holz ; Per SöderbergSource :
- Experimental eye research [ 1096-0007 ] ; 2009.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Cataracte (anatomopathologie), Cataracte (enzymologie), Cataracte (étiologie), Cristallin (effets des radiations), Cristallin (métabolisme), Diffusion de rayonnements (MeSH), Femelle (MeSH), Glutarédoxines (déficit), Glutarédoxines (physiologie), Glutathion (métabolisme), Lésions radiques expérimentales (anatomopathologie), Lésions radiques expérimentales (enzymologie), Lésions radiques expérimentales (étiologie), Rayons ultraviolets (effets indésirables), Relation dose-effet des rayonnements (MeSH), Souris (MeSH), Souris knockout (MeSH), Stress oxydatif (effets des radiations).
- MESH :
- anatomopathologie : Cataracte, Lésions radiques expérimentales.
- déficit : Glutarédoxines.
- effets des radiations : Cristallin, Stress oxydatif.
- effets indésirables : Rayons ultraviolets.
- enzymologie : Cataracte, Lésions radiques expérimentales.
- métabolisme : Cristallin, Glutathion.
- physiologie : Glutarédoxines.
- étiologie : Cataracte, Lésions radiques expérimentales.
- Animaux, Diffusion de rayonnements, Femelle, Relation dose-effet des rayonnements, Souris, Souris knockout.
English descriptors
- KwdEn :
- Animals (MeSH), Cataract (enzymology), Cataract (etiology), Cataract (pathology), Dose-Response Relationship, Radiation (MeSH), Female (MeSH), Glutaredoxins (deficiency), Glutaredoxins (physiology), Glutathione (metabolism), Lens, Crystalline (metabolism), Lens, Crystalline (radiation effects), Mice (MeSH), Mice, Knockout (MeSH), Oxidative Stress (radiation effects), Radiation Injuries, Experimental (enzymology), Radiation Injuries, Experimental (etiology), Radiation Injuries, Experimental (pathology), Scattering, Radiation (MeSH), Ultraviolet Rays (adverse effects).
- MESH :
- chemical , deficiency : Glutaredoxins.
- adverse effects : Ultraviolet Rays.
- enzymology : Cataract, Radiation Injuries, Experimental.
- etiology : Cataract, Radiation Injuries, Experimental.
- chemical , metabolism : Glutathione, Lens, Crystalline.
- pathology : Cataract, Radiation Injuries, Experimental.
- chemical , physiology : Glutaredoxins.
- radiation effects : Lens, Crystalline, Oxidative Stress.
- Animals, Dose-Response Relationship, Radiation, Female, Mice, Mice, Knockout, Scattering, Radiation.
Abstract
We investigated if the absence of glutaredoxin1, a critical protein thiol repair enzyme, increases lens susceptibility to oxidative stress caused by in vivo exposure to ultraviolet radiation type B (UVR-B). Glrx(-/-) mice and Glrx(+/+) mice were unilaterally exposed in vivo to UVR-B for 15 min. Groups of 12 animals each received 4.3, 8.7, and 14.5 kJ/m(2) respectively. 48 h post UVR-B exposure, the induced cataract was quantified as forward lens light scattering. Cataract morphology was documented with darkfield illumination photography. Glutathione (GSH/GSSG) content was analyzed in Glrx(-/-) and Glrx(+/+) lenses. UVR-B exposure induced anterior sub-capsular cataract (ASC) in Glrx(-/-) and Glrx(+/+) mice. In Glrx(-/-) lenses the opacities extended further towards the lens equator than in wild type animals (Glrx(+/+)). Lens light scattering in Glrx(-/-) mice was increased in all dose groups compared to lenses with normal glutaredoxin1 function. The difference was more pronounced with increasing exposure dose. Lens sensitivity for UVR-B induced damage was significantly higher in Glrx(-/-) lenses compared to Glrx(+/+) lenses. The Glrx gene provides a 44% increase of protection against close to threshold UVR-B induced oxidative stress compared to the absence of the Glrx gene. In conclusion, the absence of glutaredoxin1 increases lens susceptibility to UVR-B induced oxidative stress in the mouse.
DOI: 10.1016/j.exer.2009.07.020
PubMed: 19664619
Affiliations:
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Meyer</name><affiliation wicri:level="3"><nlm:affiliation>Herzog Carl Theodor Eye Clinic, Nymphenburgerstrasse 43, Munich, Germany. linda.meyer@ste.ki.se</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Herzog Carl Theodor Eye Clinic, Nymphenburgerstrasse 43, Munich</wicri:regionArea><placeName><region type="land" nuts="1">Bavière</region><region type="district" nuts="2">District de Haute-Bavière</region><settlement type="city">Munich</settlement></placeName></affiliation></author><author><name sortKey="Lofgren, Stefan" sort="Lofgren, Stefan" uniqKey="Lofgren S" first="Stefan" last="Löfgren">Stefan Löfgren</name></author><author><name sortKey="Ho, Ye Shih" sort="Ho, Ye Shih" uniqKey="Ho Y" first="Ye-Shih" last="Ho">Ye-Shih Ho</name></author><author><name sortKey="Lou, Marjorie" sort="Lou, Marjorie" uniqKey="Lou M" first="Marjorie" last="Lou">Marjorie Lou</name></author><author><name sortKey="Wegener, Alfred" sort="Wegener, Alfred" uniqKey="Wegener A" first="Alfred" last="Wegener">Alfred Wegener</name></author><author><name sortKey="Holz, Frank" sort="Holz, Frank" uniqKey="Holz F" first="Frank" last="Holz">Frank Holz</name></author><author><name sortKey="Soderberg, Per" sort="Soderberg, Per" uniqKey="Soderberg P" first="Per" last="Söderberg">Per Söderberg</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="RBID">pubmed:19664619</idno><idno type="pmid">19664619</idno><idno type="doi">10.1016/j.exer.2009.07.020</idno><idno type="wicri:Area/Main/Corpus">000A88</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000A88</idno><idno type="wicri:Area/Main/Curation">000A88</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000A88</idno><idno type="wicri:Area/Main/Exploration">000A88</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Absence of glutaredoxin1 increases lens susceptibility to oxidative stress induced by UVR-B.</title><author><name sortKey="Meyer, Linda M" sort="Meyer, Linda M" uniqKey="Meyer L" first="Linda M" last="Meyer">Linda M. Meyer</name><affiliation wicri:level="3"><nlm:affiliation>Herzog Carl Theodor Eye Clinic, Nymphenburgerstrasse 43, Munich, Germany. linda.meyer@ste.ki.se</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Herzog Carl Theodor Eye Clinic, Nymphenburgerstrasse 43, Munich</wicri:regionArea><placeName><region type="land" nuts="1">Bavière</region><region type="district" nuts="2">District de Haute-Bavière</region><settlement type="city">Munich</settlement></placeName></affiliation></author><author><name sortKey="Lofgren, Stefan" sort="Lofgren, Stefan" uniqKey="Lofgren S" first="Stefan" last="Löfgren">Stefan Löfgren</name></author><author><name sortKey="Ho, Ye Shih" sort="Ho, Ye Shih" uniqKey="Ho Y" first="Ye-Shih" last="Ho">Ye-Shih Ho</name></author><author><name sortKey="Lou, Marjorie" sort="Lou, Marjorie" uniqKey="Lou M" first="Marjorie" last="Lou">Marjorie Lou</name></author><author><name sortKey="Wegener, Alfred" sort="Wegener, Alfred" uniqKey="Wegener A" first="Alfred" last="Wegener">Alfred Wegener</name></author><author><name sortKey="Holz, Frank" sort="Holz, Frank" uniqKey="Holz F" first="Frank" last="Holz">Frank Holz</name></author><author><name sortKey="Soderberg, Per" sort="Soderberg, Per" uniqKey="Soderberg P" first="Per" last="Söderberg">Per Söderberg</name></author></analytic><series><title level="j">Experimental eye research</title><idno type="eISSN">1096-0007</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>Cataract (enzymology)</term><term>Cataract (etiology)</term><term>Cataract (pathology)</term><term>Dose-Response Relationship, Radiation (MeSH)</term><term>Female (MeSH)</term><term>Glutaredoxins (deficiency)</term><term>Glutaredoxins (physiology)</term><term>Glutathione (metabolism)</term><term>Lens, Crystalline (metabolism)</term><term>Lens, Crystalline (radiation effects)</term><term>Mice (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Oxidative Stress (radiation effects)</term><term>Radiation Injuries, Experimental (enzymology)</term><term>Radiation Injuries, Experimental (etiology)</term><term>Radiation Injuries, Experimental (pathology)</term><term>Scattering, Radiation (MeSH)</term><term>Ultraviolet Rays (adverse effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Cataracte (anatomopathologie)</term><term>Cataracte (enzymologie)</term><term>Cataracte (étiologie)</term><term>Cristallin (effets des radiations)</term><term>Cristallin (métabolisme)</term><term>Diffusion de rayonnements (MeSH)</term><term>Femelle (MeSH)</term><term>Glutarédoxines (déficit)</term><term>Glutarédoxines (physiologie)</term><term>Glutathion (métabolisme)</term><term>Lésions radiques expérimentales (anatomopathologie)</term><term>Lésions radiques expérimentales (enzymologie)</term><term>Lésions radiques expérimentales (étiologie)</term><term>Rayons ultraviolets (effets indésirables)</term><term>Relation dose-effet des rayonnements (MeSH)</term><term>Souris (MeSH)</term><term>Souris knockout (MeSH)</term><term>Stress oxydatif (effets des radiations)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Glutaredoxins</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Ultraviolet Rays</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cataracte</term><term>Lésions radiques expérimentales</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Glutarédoxines</term></keywords><keywords scheme="MESH" qualifier="effets des radiations" xml:lang="fr"><term>Cristallin</term><term>Stress oxydatif</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Rayons ultraviolets</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Cataracte</term><term>Lésions radiques expérimentales</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Cataract</term><term>Radiation Injuries, Experimental</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cataract</term><term>Radiation Injuries, Experimental</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutathione</term><term>Lens, Crystalline</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cristallin</term><term>Glutathion</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cataract</term><term>Radiation Injuries, Experimental</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Glutarédoxines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Glutaredoxins</term></keywords><keywords scheme="MESH" qualifier="radiation effects" xml:lang="en"><term>Lens, Crystalline</term><term>Oxidative Stress</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Cataracte</term><term>Lésions radiques expérimentales</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Dose-Response Relationship, Radiation</term><term>Female</term><term>Mice</term><term>Mice, Knockout</term><term>Scattering, Radiation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Diffusion de rayonnements</term><term>Femelle</term><term>Relation dose-effet des rayonnements</term><term>Souris</term><term>Souris knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We investigated if the absence of glutaredoxin1, a critical protein thiol repair enzyme, increases lens susceptibility to oxidative stress caused by in vivo exposure to ultraviolet radiation type B (UVR-B). Glrx(-/-) mice and Glrx(+/+) mice were unilaterally exposed in vivo to UVR-B for 15 min. Groups of 12 animals each received 4.3, 8.7, and 14.5 kJ/m(2) respectively. 48 h post UVR-B exposure, the induced cataract was quantified as forward lens light scattering. Cataract morphology was documented with darkfield illumination photography. Glutathione (GSH/GSSG) content was analyzed in Glrx(-/-) and Glrx(+/+) lenses. UVR-B exposure induced anterior sub-capsular cataract (ASC) in Glrx(-/-) and Glrx(+/+) mice. In Glrx(-/-) lenses the opacities extended further towards the lens equator than in wild type animals (Glrx(+/+)). Lens light scattering in Glrx(-/-) mice was increased in all dose groups compared to lenses with normal glutaredoxin1 function. The difference was more pronounced with increasing exposure dose. Lens sensitivity for UVR-B induced damage was significantly higher in Glrx(-/-) lenses compared to Glrx(+/+) lenses. The Glrx gene provides a 44% increase of protection against close to threshold UVR-B induced oxidative stress compared to the absence of the Glrx gene. In conclusion, the absence of glutaredoxin1 increases lens susceptibility to UVR-B induced oxidative stress in the mouse.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19664619</PMID><DateCompleted><Year>2010</Year><Month>02</Month><Day>05</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1096-0007</ISSN><JournalIssue CitedMedium="Internet"><Volume>89</Volume><Issue>6</Issue><PubDate><Year>2009</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Experimental eye research</Title><ISOAbbreviation>Exp Eye Res</ISOAbbreviation></Journal><ArticleTitle>Absence of glutaredoxin1 increases lens susceptibility to oxidative stress induced by UVR-B.</ArticleTitle><Pagination><MedlinePgn>833-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.exer.2009.07.020</ELocationID><Abstract><AbstractText>We investigated if the absence of glutaredoxin1, a critical protein thiol repair enzyme, increases lens susceptibility to oxidative stress caused by in vivo exposure to ultraviolet radiation type B (UVR-B). Glrx(-/-) mice and Glrx(+/+) mice were unilaterally exposed in vivo to UVR-B for 15 min. Groups of 12 animals each received 4.3, 8.7, and 14.5 kJ/m(2) respectively. 48 h post UVR-B exposure, the induced cataract was quantified as forward lens light scattering. Cataract morphology was documented with darkfield illumination photography. Glutathione (GSH/GSSG) content was analyzed in Glrx(-/-) and Glrx(+/+) lenses. UVR-B exposure induced anterior sub-capsular cataract (ASC) in Glrx(-/-) and Glrx(+/+) mice. In Glrx(-/-) lenses the opacities extended further towards the lens equator than in wild type animals (Glrx(+/+)). Lens light scattering in Glrx(-/-) mice was increased in all dose groups compared to lenses with normal glutaredoxin1 function. The difference was more pronounced with increasing exposure dose. Lens sensitivity for UVR-B induced damage was significantly higher in Glrx(-/-) lenses compared to Glrx(+/+) lenses. The Glrx gene provides a 44% increase of protection against close to threshold UVR-B induced oxidative stress compared to the absence of the Glrx gene. In conclusion, the absence of glutaredoxin1 increases lens susceptibility to UVR-B induced oxidative stress in the mouse.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Meyer</LastName><ForeName>Linda M</ForeName><Initials>LM</Initials><AffiliationInfo><Affiliation>Herzog Carl Theodor Eye Clinic, Nymphenburgerstrasse 43, Munich, Germany. linda.meyer@ste.ki.se</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Löfgren</LastName><ForeName>Stefan</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Ho</LastName><ForeName>Ye-Shih</ForeName><Initials>YS</Initials></Author><Author ValidYN="Y"><LastName>Lou</LastName><ForeName>Marjorie</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Wegener</LastName><ForeName>Alfred</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Holz</LastName><ForeName>Frank</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Söderberg</LastName><ForeName>Per</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2009</Year><Month>08</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Exp Eye Res</MedlineTA><NlmUniqueID>0370707</NlmUniqueID><ISSNLinking>0014-4835</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002386" MajorTopicYN="N">Cataract</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004307" MajorTopicYN="N">Dose-Response Relationship, Radiation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="Y">deficiency</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007908" MajorTopicYN="N">Lens, Crystalline</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000528" MajorTopicYN="Y">radiation effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName><QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011833" MajorTopicYN="N">Radiation Injuries, Experimental</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012542" MajorTopicYN="N">Scattering, Radiation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014466" MajorTopicYN="N">Ultraviolet Rays</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2008</Year><Month>07</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2009</Year><Month>07</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2009</Year><Month>07</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>8</Month><Day>12</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>8</Month><Day>12</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2010</Year><Month>2</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19664619</ArticleId><ArticleId IdType="pii">S0014-4835(09)00200-0</ArticleId><ArticleId IdType="doi">10.1016/j.exer.2009.07.020</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country><region><li>Bavière</li><li>District de Haute-Bavière</li></region><settlement><li>Munich</li></settlement></list><tree><noCountry><name sortKey="Ho, Ye Shih" sort="Ho, Ye Shih" uniqKey="Ho Y" first="Ye-Shih" last="Ho">Ye-Shih Ho</name><name sortKey="Holz, Frank" sort="Holz, Frank" uniqKey="Holz F" first="Frank" last="Holz">Frank Holz</name><name sortKey="Lofgren, Stefan" sort="Lofgren, Stefan" uniqKey="Lofgren S" first="Stefan" last="Löfgren">Stefan Löfgren</name><name sortKey="Lou, Marjorie" sort="Lou, Marjorie" uniqKey="Lou M" first="Marjorie" last="Lou">Marjorie Lou</name><name sortKey="Soderberg, Per" sort="Soderberg, Per" uniqKey="Soderberg P" first="Per" last="Söderberg">Per Söderberg</name><name sortKey="Wegener, Alfred" sort="Wegener, Alfred" uniqKey="Wegener A" first="Alfred" last="Wegener">Alfred Wegener</name></noCountry><country name="Allemagne"><region name="Bavière"><name sortKey="Meyer, Linda M" sort="Meyer, Linda M" uniqKey="Meyer L" first="Linda M" last="Meyer">Linda M. 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