Increased interstitial protein because of impaired lymph drainage does not induce fibrosis and inflammation in lymphedema.
Identifieur interne : 001D66 ( PubMed/Corpus ); précédent : 001D65; suivant : 001D67Increased interstitial protein because of impaired lymph drainage does not induce fibrosis and inflammation in lymphedema.
Auteurs : C E Markhus ; T V Karlsen ; Marek Wagner ; M. Wagner ; S. Svendsen ; O. Tenstad ; K. Alitalo ; H. WiigSource :
- Arteriosclerosis, thrombosis, and vascular biology [ 1524-4636 ] ; 2013.
English descriptors
- KwdEn :
- Animals, Collagen (metabolism), Dermatitis, Allergic Contact (genetics), Dermatitis, Allergic Contact (immunology), Dermatitis, Allergic Contact (metabolism), Dermatitis, Allergic Contact (pathology), Dermatitis, Allergic Contact (physiopathology), Disease Models, Animal, Extracellular Fluid (metabolism), Female, Fibrosis, Genotype, Inflammation Mediators (metabolism), Interleukin-12 (metabolism), Interleukin-2 (metabolism), Interleukin-6 (metabolism), Lymphatic Vessels (immunology), Lymphatic Vessels (metabolism), Lymphatic Vessels (pathology), Lymphatic Vessels (physiopathology), Lymphedema (genetics), Lymphedema (immunology), Lymphedema (metabolism), Lymphedema (pathology), Lymphedema (physiopathology), Macrophages (immunology), Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Osmotic Pressure, Permeability, Phenotype, Proteins (metabolism), Serum Albumin (metabolism), Skin (immunology), Skin (metabolism), Skin (pathology), Skin (physiopathology), Time Factors, Vascular Endothelial Growth Factor Receptor-3 (genetics), Vascular Endothelial Growth Factor Receptor-3 (metabolism), Water-Electrolyte Imbalance (immunology), Water-Electrolyte Imbalance (metabolism), Water-Electrolyte Imbalance (pathology).
- MESH :
- chemical , genetics : Vascular Endothelial Growth Factor Receptor-3.
- chemical , metabolism : Collagen, Inflammation Mediators, Interleukin-12, Interleukin-2, Interleukin-6, Proteins, Serum Albumin, Vascular Endothelial Growth Factor Receptor-3.
- genetics : Dermatitis, Allergic Contact, Lymphedema.
- immunology : Dermatitis, Allergic Contact, Lymphatic Vessels, Lymphedema, Macrophages, Skin, Water-Electrolyte Imbalance.
- metabolism : Dermatitis, Allergic Contact, Extracellular Fluid, Lymphatic Vessels, Lymphedema, Skin, Water-Electrolyte Imbalance.
- pathology : Dermatitis, Allergic Contact, Lymphatic Vessels, Lymphedema, Skin, Water-Electrolyte Imbalance.
- physiopathology : Dermatitis, Allergic Contact, Lymphatic Vessels, Lymphedema, Skin.
- Animals, Disease Models, Animal, Female, Fibrosis, Genotype, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Osmotic Pressure, Permeability, Phenotype, Time Factors.
Abstract
The pathophysiology of lymphedema is incompletely understood. We asked how transcapillary fluid balance parameters and lymph flow are affected in a transgenic mouse model of primary lymphedema, which due to an inhibition of vascular endothelial growth factor receptor-3 (VEGFR-3) signaling lacks dermal lymphatics, and whether protein accumulation in the interstitium occurring in lymphedema results in inflammation.
DOI: 10.1161/ATVBAHA.112.300384
PubMed: 23288156
Links to Exploration step
pubmed:23288156Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Increased interstitial protein because of impaired lymph drainage does not induce fibrosis and inflammation in lymphedema.</title><author><name sortKey="Markhus, C E" sort="Markhus, C E" uniqKey="Markhus C" first="C E" last="Markhus">C E Markhus</name><affiliation><nlm:affiliation>Department of Biomedicine, University of Bergen, Norway.</nlm:affiliation></affiliation></author><author><name sortKey="Karlsen, T V" sort="Karlsen, T V" uniqKey="Karlsen T" first="T V" last="Karlsen">T V Karlsen</name></author><author><name sortKey="Wagner, Marek" sort="Wagner, Marek" uniqKey="Wagner M" first="Marek" last="Wagner">Marek Wagner</name></author><author><name sortKey="Wagner, M" sort="Wagner, M" uniqKey="Wagner M" first="M" last="Wagner">M. Wagner</name></author><author><name sortKey="Svendsen, S" sort="Svendsen, S" uniqKey="Svendsen " first=" S" last="Svendsen"> S. Svendsen</name></author><author><name sortKey="Tenstad, O" sort="Tenstad, O" uniqKey="Tenstad O" first="O" last="Tenstad">O. Tenstad</name></author><author><name sortKey="Alitalo, K" sort="Alitalo, K" uniqKey="Alitalo K" first="K" last="Alitalo">K. Alitalo</name></author><author><name sortKey="Wiig, H" sort="Wiig, H" uniqKey="Wiig H" first="H" last="Wiig">H. Wiig</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:23288156</idno><idno type="pmid">23288156</idno><idno type="doi">10.1161/ATVBAHA.112.300384</idno><idno type="wicri:Area/PubMed/Corpus">001D66</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001D66</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Increased interstitial protein because of impaired lymph drainage does not induce fibrosis and inflammation in lymphedema.</title><author><name sortKey="Markhus, C E" sort="Markhus, C E" uniqKey="Markhus C" first="C E" last="Markhus">C E Markhus</name><affiliation><nlm:affiliation>Department of Biomedicine, University of Bergen, Norway.</nlm:affiliation></affiliation></author><author><name sortKey="Karlsen, T V" sort="Karlsen, T V" uniqKey="Karlsen T" first="T V" last="Karlsen">T V Karlsen</name></author><author><name sortKey="Wagner, Marek" sort="Wagner, Marek" uniqKey="Wagner M" first="Marek" last="Wagner">Marek Wagner</name></author><author><name sortKey="Wagner, M" sort="Wagner, M" uniqKey="Wagner M" first="M" last="Wagner">M. Wagner</name></author><author><name sortKey="Svendsen, S" sort="Svendsen, S" uniqKey="Svendsen " first=" S" last="Svendsen"> S. Svendsen</name></author><author><name sortKey="Tenstad, O" sort="Tenstad, O" uniqKey="Tenstad O" first="O" last="Tenstad">O. Tenstad</name></author><author><name sortKey="Alitalo, K" sort="Alitalo, K" uniqKey="Alitalo K" first="K" last="Alitalo">K. Alitalo</name></author><author><name sortKey="Wiig, H" sort="Wiig, H" uniqKey="Wiig H" first="H" last="Wiig">H. Wiig</name></author></analytic><series><title level="j">Arteriosclerosis, thrombosis, and vascular biology</title><idno type="eISSN">1524-4636</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Collagen (metabolism)</term><term>Dermatitis, Allergic Contact (genetics)</term><term>Dermatitis, Allergic Contact (immunology)</term><term>Dermatitis, Allergic Contact (metabolism)</term><term>Dermatitis, Allergic Contact (pathology)</term><term>Dermatitis, Allergic Contact (physiopathology)</term><term>Disease Models, Animal</term><term>Extracellular Fluid (metabolism)</term><term>Female</term><term>Fibrosis</term><term>Genotype</term><term>Inflammation Mediators (metabolism)</term><term>Interleukin-12 (metabolism)</term><term>Interleukin-2 (metabolism)</term><term>Interleukin-6 (metabolism)</term><term>Lymphatic Vessels (immunology)</term><term>Lymphatic Vessels (metabolism)</term><term>Lymphatic Vessels (pathology)</term><term>Lymphatic Vessels (physiopathology)</term><term>Lymphedema (genetics)</term><term>Lymphedema (immunology)</term><term>Lymphedema (metabolism)</term><term>Lymphedema (pathology)</term><term>Lymphedema (physiopathology)</term><term>Macrophages (immunology)</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Osmotic Pressure</term><term>Permeability</term><term>Phenotype</term><term>Proteins (metabolism)</term><term>Serum Albumin (metabolism)</term><term>Skin (immunology)</term><term>Skin (metabolism)</term><term>Skin (pathology)</term><term>Skin (physiopathology)</term><term>Time Factors</term><term>Vascular Endothelial Growth Factor Receptor-3 (genetics)</term><term>Vascular Endothelial Growth Factor Receptor-3 (metabolism)</term><term>Water-Electrolyte Imbalance (immunology)</term><term>Water-Electrolyte Imbalance (metabolism)</term><term>Water-Electrolyte Imbalance (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Collagen</term><term>Inflammation Mediators</term><term>Interleukin-12</term><term>Interleukin-2</term><term>Interleukin-6</term><term>Proteins</term><term>Serum Albumin</term><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dermatitis, Allergic Contact</term><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Dermatitis, Allergic Contact</term><term>Lymphatic Vessels</term><term>Lymphedema</term><term>Macrophages</term><term>Skin</term><term>Water-Electrolyte Imbalance</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dermatitis, Allergic Contact</term><term>Extracellular Fluid</term><term>Lymphatic Vessels</term><term>Lymphedema</term><term>Skin</term><term>Water-Electrolyte Imbalance</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dermatitis, Allergic Contact</term><term>Lymphatic Vessels</term><term>Lymphedema</term><term>Skin</term><term>Water-Electrolyte Imbalance</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Dermatitis, Allergic Contact</term><term>Lymphatic Vessels</term><term>Lymphedema</term><term>Skin</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Female</term><term>Fibrosis</term><term>Genotype</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Osmotic Pressure</term><term>Permeability</term><term>Phenotype</term><term>Time Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The pathophysiology of lymphedema is incompletely understood. We asked how transcapillary fluid balance parameters and lymph flow are affected in a transgenic mouse model of primary lymphedema, which due to an inhibition of vascular endothelial growth factor receptor-3 (VEGFR-3) signaling lacks dermal lymphatics, and whether protein accumulation in the interstitium occurring in lymphedema results in inflammation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23288156</PMID><DateCreated><Year>2013</Year><Month>01</Month><Day>17</Day></DateCreated><DateCompleted><Year>2013</Year><Month>03</Month><Day>14</Day></DateCompleted><DateRevised><Year>2013</Year><Month>07</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1524-4636</ISSN><JournalIssue CitedMedium="Internet"><Volume>33</Volume><Issue>2</Issue><PubDate><Year>2013</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Arteriosclerosis, thrombosis, and vascular biology</Title><ISOAbbreviation>Arterioscler. Thromb. Vasc. Biol.</ISOAbbreviation></Journal><ArticleTitle>Increased interstitial protein because of impaired lymph drainage does not induce fibrosis and inflammation in lymphedema.</ArticleTitle><Pagination><MedlinePgn>266-74</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1161/ATVBAHA.112.300384</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">The pathophysiology of lymphedema is incompletely understood. We asked how transcapillary fluid balance parameters and lymph flow are affected in a transgenic mouse model of primary lymphedema, which due to an inhibition of vascular endothelial growth factor receptor-3 (VEGFR-3) signaling lacks dermal lymphatics, and whether protein accumulation in the interstitium occurring in lymphedema results in inflammation.</AbstractText><AbstractText Label="METHODS AND RESULTS" NlmCategory="RESULTS">As estimated using a new optical-imaging technique, we found that this signaling defect resulted in lymph drainage in hind limb skin of K14-VEGFR-3-Ig mice that was 34% of the corresponding value in wild-type. The interstitial fluid pressure and tissue fluid volumes were significantly increased in the areas of visible swelling only, whereas the colloid osmotic pressure in plasma, and thus the colloid osmotic pressure gradient, was reduced compared to wild-type mice. An acute volume load resulted in an exaggerated interstitial fluid pressure response in transgenic mice. There was no accumulation of collagen or lipid in skin, suggesting that chronic edema presented in the K14-VEGFR-3-Ig mouse was not sufficient to induce changes in tissue composition. Proinflammatory cytokines (interleukin-2, interleukin-6, interleukin-12) in subcutaneous interstitial fluid and macrophage infiltration in skin of the paw were lower, whereas the monocyte/macrophage cell fraction in blood and spleen was higher in transgenic compared with wild-type mice.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Our data suggest that a high interstitial protein concentration and longstanding edema is not sufficient to induce fibrosis and inflammation characteristic for the human condition and may have implications for our understanding of the pathophysiology of this condition.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Markhus</LastName><ForeName>C E</ForeName><Initials>CE</Initials><AffiliationInfo><Affiliation>Department of Biomedicine, University of Bergen, Norway.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Karlsen</LastName><ForeName>T V</ForeName><Initials>TV</Initials></Author><Author ValidYN="Y"><LastName>Wagner</LastName><ForeName>Marek</ForeName><Initials>M</Initials></Author><Author ValidYN="N"><LastName>Wagner</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Svendsen</LastName><ForeName>Ø S</ForeName><Initials>ØS</Initials></Author><Author ValidYN="Y"><LastName>Tenstad</LastName><ForeName>O</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Alitalo</LastName><ForeName>K</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Wiig</LastName><ForeName>H</ForeName><Initials>H</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>2013</Year><Month>01</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Arterioscler Thromb Vasc Biol</MedlineTA><NlmUniqueID>9505803</NlmUniqueID><ISSNLinking>1079-5642</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018836">Inflammation Mediators</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007376">Interleukin-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015850">Interleukin-6</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011506">Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012709">Serum Albumin</NameOfSubstance></Chemical><Chemical><RegistryNumber>187348-17-0</RegistryNumber><NameOfSubstance UI="D018664">Interleukin-12</NameOfSubstance></Chemical><Chemical><RegistryNumber>9007-34-5</RegistryNumber><NameOfSubstance UI="D003094">Collagen</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D040321">Vascular Endothelial Growth Factor Receptor-3</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="ErratumIn"><RefSource>Arterioscler Thromb Vasc Biol. 2013 Jun;33(6):e119</RefSource><Note>Wagner, M [corrected to Wagner, Marek]</Note></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003094" MajorTopicYN="N">Collagen</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017449" MajorTopicYN="N">Dermatitis, Allergic Contact</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045604" MajorTopicYN="N">Extracellular Fluid</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005355" MajorTopicYN="N">Fibrosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018836" MajorTopicYN="N">Inflammation Mediators</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018664" MajorTopicYN="N">Interleukin-12</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007376" MajorTopicYN="N">Interleukin-2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015850" MajorTopicYN="N">Interleukin-6</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042601" MajorTopicYN="N">Lymphatic Vessels</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009997" MajorTopicYN="N">Osmotic Pressure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010539" MajorTopicYN="N">Permeability</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011506" MajorTopicYN="N">Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012709" MajorTopicYN="N">Serum Albumin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012867" MajorTopicYN="N">Skin</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D040321" MajorTopicYN="N">Vascular Endothelial Growth Factor Receptor-3</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014883" MajorTopicYN="N">Water-Electrolyte Imbalance</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>1</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>1</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>3</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23288156</ArticleId><ArticleId IdType="pii">ATVBAHA.112.300384</ArticleId><ArticleId IdType="doi">10.1161/ATVBAHA.112.300384</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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