Increased interstitial protein because of impaired lymph drainage does not induce fibrosis and inflammation in lymphedema.
Identifieur interne : 001D66 ( PubMed/Curation ); précédent : 001D65; suivant : 001D67Increased interstitial protein because of impaired lymph drainage does not induce fibrosis and inflammation in lymphedema.
Auteurs : C E Markhus [Norvège] ; T V Karlsen ; Marek Wagner ; M. Wagner ; S. Svendsen ; O. Tenstad ; K. Alitalo ; H. WiigSource :
- Arteriosclerosis, thrombosis, and vascular biology [ 1524-4636 ] ; 2013.
Descripteurs français
- KwdFr :
- Animaux, Collagène (métabolisme), Eczéma de contact allergique (anatomopathologie), Eczéma de contact allergique (génétique), Eczéma de contact allergique (immunologie), Eczéma de contact allergique (métabolisme), Eczéma de contact allergique (physiopathologie), Facteurs temps, Femelle, Fibrose, Génotype, Interleukine-12 (métabolisme), Interleukine-2 (métabolisme), Interleukine-6 (métabolisme), Liquide extracellulaire (métabolisme), Lymphoedème (anatomopathologie), Lymphoedème (génétique), Lymphoedème (immunologie), Lymphoedème (métabolisme), Lymphoedème (physiopathologie), Macrophages (immunologie), Modèles animaux de maladie humaine, Mâle, Médiateurs de l'inflammation (métabolisme), Peau (anatomopathologie), Peau (immunologie), Peau (métabolisme), Peau (physiopathologie), Perméabilité, Phénotype, Pression osmotique, Protéines (métabolisme), Récepteur-3 au facteur croissance endothéliale vasculaire (génétique), Récepteur-3 au facteur croissance endothéliale vasculaire (métabolisme), Souris, Souris de lignée C57BL, Souris transgéniques, Sérumalbumine (métabolisme), Troubles de l'équilibre hydroélectrolytique (anatomopathologie), Troubles de l'équilibre hydroélectrolytique (immunologie), Troubles de l'équilibre hydroélectrolytique (métabolisme), Vaisseaux lymphatiques (anatomopathologie), Vaisseaux lymphatiques (immunologie), Vaisseaux lymphatiques (métabolisme), Vaisseaux lymphatiques (physiopathologie).
- MESH :
- anatomopathologie : Eczéma de contact allergique, Lymphoedème, Peau, Troubles de l'équilibre hydroélectrolytique, Vaisseaux lymphatiques.
- génétique : Eczéma de contact allergique, Lymphoedème, Récepteur-3 au facteur croissance endothéliale vasculaire.
- immunologie : Eczéma de contact allergique, Lymphoedème, Macrophages, Peau, Troubles de l'équilibre hydroélectrolytique, Vaisseaux lymphatiques.
- métabolisme : Collagène, Eczéma de contact allergique, Interleukine-12, Interleukine-2, Interleukine-6, Liquide extracellulaire, Lymphoedème, Médiateurs de l'inflammation, Peau, Protéines, Récepteur-3 au facteur croissance endothéliale vasculaire, Sérumalbumine, Troubles de l'équilibre hydroélectrolytique, Vaisseaux lymphatiques.
- physiopathologie : Eczéma de contact allergique, Lymphoedème, Peau, Vaisseaux lymphatiques.
- Animaux, Facteurs temps, Femelle, Fibrose, Génotype, Modèles animaux de maladie humaine, Mâle, Perméabilité, Phénotype, Pression osmotique, Souris, Souris de lignée C57BL, Souris transgéniques.
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
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pubmed:23288156Le document en format XML
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<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="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Collagène (métabolisme)</term>
<term>Eczéma de contact allergique (anatomopathologie)</term>
<term>Eczéma de contact allergique (génétique)</term>
<term>Eczéma de contact allergique (immunologie)</term>
<term>Eczéma de contact allergique (métabolisme)</term>
<term>Eczéma de contact allergique (physiopathologie)</term>
<term>Facteurs temps</term>
<term>Femelle</term>
<term>Fibrose</term>
<term>Génotype</term>
<term>Interleukine-12 (métabolisme)</term>
<term>Interleukine-2 (métabolisme)</term>
<term>Interleukine-6 (métabolisme)</term>
<term>Liquide extracellulaire (métabolisme)</term>
<term>Lymphoedème (anatomopathologie)</term>
<term>Lymphoedème (génétique)</term>
<term>Lymphoedème (immunologie)</term>
<term>Lymphoedème (métabolisme)</term>
<term>Lymphoedème (physiopathologie)</term>
<term>Macrophages (immunologie)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mâle</term>
<term>Médiateurs de l'inflammation (métabolisme)</term>
<term>Peau (anatomopathologie)</term>
<term>Peau (immunologie)</term>
<term>Peau (métabolisme)</term>
<term>Peau (physiopathologie)</term>
<term>Perméabilité</term>
<term>Phénotype</term>
<term>Pression osmotique</term>
<term>Protéines (métabolisme)</term>
<term>Récepteur-3 au facteur croissance endothéliale vasculaire (génétique)</term>
<term>Récepteur-3 au facteur croissance endothéliale vasculaire (métabolisme)</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris transgéniques</term>
<term>Sérumalbumine (métabolisme)</term>
<term>Troubles de l'équilibre hydroélectrolytique (anatomopathologie)</term>
<term>Troubles de l'équilibre hydroélectrolytique (immunologie)</term>
<term>Troubles de l'équilibre hydroélectrolytique (métabolisme)</term>
<term>Vaisseaux lymphatiques (anatomopathologie)</term>
<term>Vaisseaux lymphatiques (immunologie)</term>
<term>Vaisseaux lymphatiques (métabolisme)</term>
<term>Vaisseaux lymphatiques (physiopathologie)</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="anatomopathologie" xml:lang="fr"><term>Eczéma de contact allergique</term>
<term>Lymphoedème</term>
<term>Peau</term>
<term>Troubles de l'équilibre hydroélectrolytique</term>
<term>Vaisseaux lymphatiques</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dermatitis, Allergic Contact</term>
<term>Lymphedema</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Eczéma de contact allergique</term>
<term>Lymphoedème</term>
<term>Récepteur-3 au facteur croissance endothéliale vasculaire</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Eczéma de contact allergique</term>
<term>Lymphoedème</term>
<term>Macrophages</term>
<term>Peau</term>
<term>Troubles de l'équilibre hydroélectrolytique</term>
<term>Vaisseaux lymphatiques</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="métabolisme" xml:lang="fr"><term>Collagène</term>
<term>Eczéma de contact allergique</term>
<term>Interleukine-12</term>
<term>Interleukine-2</term>
<term>Interleukine-6</term>
<term>Liquide extracellulaire</term>
<term>Lymphoedème</term>
<term>Médiateurs de l'inflammation</term>
<term>Peau</term>
<term>Protéines</term>
<term>Récepteur-3 au facteur croissance endothéliale vasculaire</term>
<term>Sérumalbumine</term>
<term>Troubles de l'équilibre hydroélectrolytique</term>
<term>Vaisseaux lymphatiques</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="physiopathologie" xml:lang="fr"><term>Eczéma de contact allergique</term>
<term>Lymphoedème</term>
<term>Peau</term>
<term>Vaisseaux lymphatiques</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>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Facteurs temps</term>
<term>Femelle</term>
<term>Fibrose</term>
<term>Génotype</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mâle</term>
<term>Perméabilité</term>
<term>Phénotype</term>
<term>Pression osmotique</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris transgéniques</term>
</keywords>
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<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>
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<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2013</Year>
<Month>01</Month>
<Day>03</Day>
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<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Arterioscler Thromb Vasc Biol</MedlineTA>
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<Chemical><RegistryNumber>187348-17-0</RegistryNumber>
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<Chemical><RegistryNumber>9007-34-5</RegistryNumber>
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<CommentsCorrectionsList><CommentsCorrections RefType="ErratumIn"><RefSource>Arterioscler Thromb Vasc Biol. 2013 Jun;33(6):e119</RefSource>
<Note>Wagner, M [corrected to Wagner, Marek]</Note>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
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<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>
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<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>
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<MeshHeading><DescriptorName UI="D018836" MajorTopicYN="N">Inflammation Mediators</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D018664" MajorTopicYN="N">Interleukin-12</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<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>
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<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>
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<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
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<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D012709" MajorTopicYN="N">Serum Albumin</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<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>
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<MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName>
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<MeshHeading><DescriptorName UI="D040321" MajorTopicYN="N">Vascular Endothelial Growth Factor Receptor-3</DescriptorName>
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<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<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>
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