Further studies of canine von Willebrand's disease.
Identifieur interne : 007356 ( PubMed/Corpus ); précédent : 007355; suivant : 007357Further studies of canine von Willebrand's disease.
Auteurs : W J DoddsSource :
- Blood [ 0006-4971 ] ; 1975.
English descriptors
- KwdEn :
- Acute Kidney Injury (etiology), Age Factors, Animals, Blood Coagulation Tests, Blood Platelets (analysis), Colitis (complications), Dog Diseases (genetics), Dogs, Eosinophilia (etiology), Factor VIII (analysis), Female, Fibrinogen (analysis), Glomerulonephritis (complications), Intestinal Obstruction (etiology), Lymphedema (congenital), Lymphoma (complications), Male, Melena (etiology), Methionine (metabolism), Osteitis (etiology), Pregnancy, Rabbits, von Willebrand Diseases (immunology), von Willebrand Diseases (veterinary).
- MESH :
- chemical , analysis : Factor VIII, Fibrinogen.
- analysis : Blood Platelets.
- complications : Colitis, Glomerulonephritis, Lymphoma.
- congenital : Lymphedema.
- etiology : Acute Kidney Injury, Eosinophilia, Intestinal Obstruction, Melena, Osteitis.
- genetics : Dog Diseases.
- immunology : von Willebrand Diseases.
- chemical , metabolism : Methionine.
- veterinary : von Willebrand Diseases.
- Age Factors, Animals, Blood Coagulation Tests, Dogs, Female, Male, Pregnancy, Rabbits.
Abstract
Additional characterization of von Willebrand's disease (VWD) in a family of German shepherd dogs is presented. Genetic studies of three generations of affected dogs indicate that about 50% of the progeny are affected if one parent has VWD and about 60% if both parents have the defect. Some of these progeny manifested an incomplete form of VWD, suggesting autosomal dominant inheritance with variable expressivity. The disease become progressively less severe with advancing age and repeated pregnancies. Ristocetin-induced platelet aggregation was significantly reduced in VWD dogs as compared with normal, thrombopathic, and hemophilic carrier dogs. Immunodiffusion and electroimmunodiffusion studies with rabbit anticanine factor VII showed the level of factor VII-related antigen to be low in VWD dogs but present in increased amounts in hemophilic dogs. VWD affected dogs had markedly delayed hemostatic plug formation, but their plugs appeared normal by light and electron microscopy. Their platelet nucleotides, ATP/ADP ration, and platelet protein content were normal. Platelet and fibrinogen survival times with [75Se] selenomethionine were also normal, although platelets from VWD dogs incorporated more radioactivity than did those from normal dogs or from dogs with incomplete VWD.
PubMed: 1078981
Links to Exploration step
pubmed:1078981Le document en format XML
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Genetic studies of three generations of affected dogs indicate that about 50% of the progeny are affected if one parent has VWD and about 60% if both parents have the defect. Some of these progeny manifested an incomplete form of VWD, suggesting autosomal dominant inheritance with variable expressivity. The disease become progressively less severe with advancing age and repeated pregnancies. Ristocetin-induced platelet aggregation was significantly reduced in VWD dogs as compared with normal, thrombopathic, and hemophilic carrier dogs. Immunodiffusion and electroimmunodiffusion studies with rabbit anticanine factor VII showed the level of factor VII-related antigen to be low in VWD dogs but present in increased amounts in hemophilic dogs. VWD affected dogs had markedly delayed hemostatic plug formation, but their plugs appeared normal by light and electron microscopy. Their platelet nucleotides, ATP/ADP ration, and platelet protein content were normal. Platelet and fibrinogen survival times with [75Se] selenomethionine were also normal, although platelets from VWD dogs incorporated more radioactivity than did those from normal dogs or from dogs with incomplete VWD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">1078981</PMID><DateCreated><Year>1975</Year><Month>06</Month><Day>18</Day></DateCreated><DateCompleted><Year>1975</Year><Month>06</Month><Day>18</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0006-4971</ISSN><JournalIssue CitedMedium="Print"><Volume>45</Volume><Issue>2</Issue><PubDate><Year>1975</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Blood</Title><ISOAbbreviation>Blood</ISOAbbreviation></Journal><ArticleTitle>Further studies of canine von Willebrand's disease.</ArticleTitle><Pagination><MedlinePgn>221-30</MedlinePgn></Pagination><Abstract><AbstractText>Additional characterization of von Willebrand's disease (VWD) in a family of German shepherd dogs is presented. Genetic studies of three generations of affected dogs indicate that about 50% of the progeny are affected if one parent has VWD and about 60% if both parents have the defect. Some of these progeny manifested an incomplete form of VWD, suggesting autosomal dominant inheritance with variable expressivity. The disease become progressively less severe with advancing age and repeated pregnancies. Ristocetin-induced platelet aggregation was significantly reduced in VWD dogs as compared with normal, thrombopathic, and hemophilic carrier dogs. Immunodiffusion and electroimmunodiffusion studies with rabbit anticanine factor VII showed the level of factor VII-related antigen to be low in VWD dogs but present in increased amounts in hemophilic dogs. VWD affected dogs had markedly delayed hemostatic plug formation, but their plugs appeared normal by light and electron microscopy. Their platelet nucleotides, ATP/ADP ration, and platelet protein content were normal. Platelet and fibrinogen survival times with [75Se] selenomethionine were also normal, although platelets from VWD dogs incorporated more radioactivity than did those from normal dogs or from dogs with incomplete VWD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dodds</LastName><ForeName>W J</ForeName><Initials>WJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Blood</MedlineTA><NlmUniqueID>7603509</NlmUniqueID><ISSNLinking>0006-4971</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9001-27-8</RegistryNumber><NameOfSubstance UI="D005169">Factor VIII</NameOfSubstance></Chemical><Chemical><RegistryNumber>9001-32-5</RegistryNumber><NameOfSubstance UI="D005340">Fibrinogen</NameOfSubstance></Chemical><Chemical><RegistryNumber>AE28F7PNPL</RegistryNumber><NameOfSubstance UI="D008715">Methionine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D058186" MajorTopicYN="N">Acute Kidney Injury</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000367" MajorTopicYN="N">Age Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001780" MajorTopicYN="N">Blood Coagulation Tests</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001792" MajorTopicYN="N">Blood Platelets</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003092" MajorTopicYN="N">Colitis</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004283" MajorTopicYN="N">Dog Diseases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004285" MajorTopicYN="N">Dogs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004802" MajorTopicYN="N">Eosinophilia</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005169" MajorTopicYN="N">Factor VIII</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005340" MajorTopicYN="N">Fibrinogen</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005921" MajorTopicYN="N">Glomerulonephritis</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007415" MajorTopicYN="N">Intestinal Obstruction</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName><QualifierName UI="Q000151" MajorTopicYN="N">congenital</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008223" MajorTopicYN="N">Lymphoma</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008551" MajorTopicYN="N">Melena</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008715" MajorTopicYN="N">Methionine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010000" MajorTopicYN="N">Osteitis</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011247" MajorTopicYN="N">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011817" MajorTopicYN="N">Rabbits</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014842" MajorTopicYN="N">von Willebrand Diseases</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000662" MajorTopicYN="Y">veterinary</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1975</Year><Month>2</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1975</Year><Month>2</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1975</Year><Month>2</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">1078981</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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