Animal models for the study of lymphatic insufficiency.
Identifieur interne : 003E16 ( PubMed/Corpus ); précédent : 003E15; suivant : 003E17Animal models for the study of lymphatic insufficiency.
Auteurs : William S. Shin ; Andrzej Szuba ; Stanley G. RocksonSource :
- Lymphatic research and biology [ 1539-6851 ] ; 2003.
English descriptors
- KwdEn :
- MESH :
Abstract
Lymphedema is the term commonly employed to describe the spectrum of pathological states that arise as a consequence of functional lymphatic insufficiency. These human disease entities currently lack an effective cure. Satisfactory therapeutic strategies for both primary and secondary lymphedema will require additional insight into the complex cellular mechanisms and responses that comprise both normal lymphatic function and its regional derangement in states of pathologic dysfunction. Such insights must, initially, be derived from suitable animal models of the chronic human disease process. Historically, efforts to replicate the untreated disease of human lymphedema in animals, through surgery, irradiation, and toxicology, have been fraught with difficulty. The major impediments to the creation of satisfactory animal models have included an inability to reproduce the chronic disease in a stable, reproducible format. Recently, with the promise of potentially successful growth factor-mediated therapeutic lymphangiogenesis, and with the enhanced availability of investigative tools to assess therapeutic responses to molecular therapies, there has been a resurgence of interest in the development of viable animal models of lymphatic insufficiency. Current research has led to the development of genetic and postsurgical models of lymphedema that closely simulate the human conditions of primary and secondary lymphatic insufficiency, respectively. Such models will help to refine the assessment of various therapeutic approaches and their potential applicability to human disease interventions.
DOI: 10.1089/153968503321642642
PubMed: 15624423
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Rockson</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2003">2003</date><idno type="RBID">pubmed:15624423</idno><idno type="pmid">15624423</idno><idno type="doi">10.1089/153968503321642642</idno><idno type="wicri:Area/PubMed/Corpus">003E16</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">003E16</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Animal models for the study of lymphatic insufficiency.</title><author><name sortKey="Shin, William S" sort="Shin, William S" uniqKey="Shin W" first="William S" last="Shin">William S. Shin</name><affiliation><nlm:affiliation>Stanford Center for Lymphatic and Venous Disorders, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Szuba, Andrzej" sort="Szuba, Andrzej" uniqKey="Szuba A" first="Andrzej" last="Szuba">Andrzej Szuba</name></author><author><name sortKey="Rockson, Stanley G" sort="Rockson, Stanley G" uniqKey="Rockson S" first="Stanley G" last="Rockson">Stanley G. Rockson</name></author></analytic><series><title level="j">Lymphatic research and biology</title><idno type="ISSN">1539-6851</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Lymph Nodes (pathology)</term><term>Lymphangiogenesis</term><term>Lymphatic Diseases (pathology)</term><term>Lymphatic System (pathology)</term><term>Lymphatic Vessels (pathology)</term><term>Lymphedema (pathology)</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lymph Nodes</term><term>Lymphatic Diseases</term><term>Lymphatic System</term><term>Lymphatic Vessels</term><term>Lymphedema</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Lymphangiogenesis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lymphedema is the term commonly employed to describe the spectrum of pathological states that arise as a consequence of functional lymphatic insufficiency. These human disease entities currently lack an effective cure. Satisfactory therapeutic strategies for both primary and secondary lymphedema will require additional insight into the complex cellular mechanisms and responses that comprise both normal lymphatic function and its regional derangement in states of pathologic dysfunction. Such insights must, initially, be derived from suitable animal models of the chronic human disease process. Historically, efforts to replicate the untreated disease of human lymphedema in animals, through surgery, irradiation, and toxicology, have been fraught with difficulty. The major impediments to the creation of satisfactory animal models have included an inability to reproduce the chronic disease in a stable, reproducible format. Recently, with the promise of potentially successful growth factor-mediated therapeutic lymphangiogenesis, and with the enhanced availability of investigative tools to assess therapeutic responses to molecular therapies, there has been a resurgence of interest in the development of viable animal models of lymphatic insufficiency. Current research has led to the development of genetic and postsurgical models of lymphedema that closely simulate the human conditions of primary and secondary lymphatic insufficiency, respectively. Such models will help to refine the assessment of various therapeutic approaches and their potential applicability to human disease interventions.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15624423</PMID><DateCreated><Year>2004</Year><Month>12</Month><Day>30</Day></DateCreated><DateCompleted><Year>2005</Year><Month>02</Month><Day>01</Day></DateCompleted><DateRevised><Year>2005</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1539-6851</ISSN><JournalIssue CitedMedium="Print"><Volume>1</Volume><Issue>2</Issue><PubDate><Year>2003</Year></PubDate></JournalIssue><Title>Lymphatic research and biology</Title><ISOAbbreviation>Lymphat Res Biol</ISOAbbreviation></Journal><ArticleTitle>Animal models for the study of lymphatic insufficiency.</ArticleTitle><Pagination><MedlinePgn>159-69</MedlinePgn></Pagination><Abstract><AbstractText>Lymphedema is the term commonly employed to describe the spectrum of pathological states that arise as a consequence of functional lymphatic insufficiency. These human disease entities currently lack an effective cure. Satisfactory therapeutic strategies for both primary and secondary lymphedema will require additional insight into the complex cellular mechanisms and responses that comprise both normal lymphatic function and its regional derangement in states of pathologic dysfunction. Such insights must, initially, be derived from suitable animal models of the chronic human disease process. Historically, efforts to replicate the untreated disease of human lymphedema in animals, through surgery, irradiation, and toxicology, have been fraught with difficulty. The major impediments to the creation of satisfactory animal models have included an inability to reproduce the chronic disease in a stable, reproducible format. Recently, with the promise of potentially successful growth factor-mediated therapeutic lymphangiogenesis, and with the enhanced availability of investigative tools to assess therapeutic responses to molecular therapies, there has been a resurgence of interest in the development of viable animal models of lymphatic insufficiency. Current research has led to the development of genetic and postsurgical models of lymphedema that closely simulate the human conditions of primary and secondary lymphatic insufficiency, respectively. Such models will help to refine the assessment of various therapeutic approaches and their potential applicability to human disease interventions.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shin</LastName><ForeName>William S</ForeName><Initials>WS</Initials><AffiliationInfo><Affiliation>Stanford Center for Lymphatic and Venous Disorders, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Szuba</LastName><ForeName>Andrzej</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Rockson</LastName><ForeName>Stanley G</ForeName><Initials>SG</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Lymphat Res Biol</MedlineTA><NlmUniqueID>101163587</NlmUniqueID><ISSNLinking>1539-6851</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="Y">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008198" MajorTopicYN="N">Lymph Nodes</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042583" MajorTopicYN="N">Lymphangiogenesis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008206" MajorTopicYN="N">Lymphatic Diseases</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008208" MajorTopicYN="N">Lymphatic System</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042601" MajorTopicYN="N">Lymphatic Vessels</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>56</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2004</Year><Month>12</Month><Day>31</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>2</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2004</Year><Month>12</Month><Day>31</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15624423</ArticleId><ArticleId IdType="doi">10.1089/153968503321642642</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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