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http://purl.uniprot.org/citations/12064834http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/12064834http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Impaired fibrinolytical outcomes may be one of the pathogenic factors for thrombotic events in patients with antiphospholipid antibodies (aPL). We investigated the consequences of the gene polymorphisms of tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) in patients positive for aPL.

Methods

Seventy-seven Japanese and 82 British patients with aPL were examined for Alu-repeat insertion (I)/deletion (D) polymorphism of the tPA gene by polymerase chain reaction (PCR), and 4G/5G polymorphism in the PAI-1 promoter gene by site-directed mutagenesis-PCR and restriction fragment length polymorphism analysis. Correlations between these polymorphisms and clinical symptoms of antiphospholipid syndrome (APS) (arterial thrombosis, venous thrombosis, miscarriage) were analyzed.

Results

Significant differences in the allele frequencies of these genes did not exist between patients and controls. There was no significant correlation between these gene polymorphisms and clinical symptoms of APS in patients with aPL.

Conclusion

Polymorphisms of the tPA or PAI-1 genes probably do not significantly influence the risk of anerial thrombosis, venous thrombosis, or pregnancy morbidity in patients with aPL."xsd:string
http://purl.uniprot.org/citations/12064834http://purl.uniprot.org/core/author"Atsumi T."xsd:string
http://purl.uniprot.org/citations/12064834http://purl.uniprot.org/core/author"Koike T."xsd:string
http://purl.uniprot.org/citations/12064834http://purl.uniprot.org/core/author"Yasuda S."xsd:string
http://purl.uniprot.org/citations/12064834http://purl.uniprot.org/core/author"Tsutsumi A."xsd:string
http://purl.uniprot.org/citations/12064834http://purl.uniprot.org/core/author"Ichikawa K."xsd:string
http://purl.uniprot.org/citations/12064834http://purl.uniprot.org/core/author"Hughes G.R."xsd:string
http://purl.uniprot.org/citations/12064834http://purl.uniprot.org/core/author"Khamashta M.A."xsd:string
http://purl.uniprot.org/citations/12064834http://purl.uniprot.org/core/author"Bertolaccini M.L."xsd:string
http://purl.uniprot.org/citations/12064834http://purl.uniprot.org/core/date"2002"xsd:gYear
http://purl.uniprot.org/citations/12064834http://purl.uniprot.org/core/name"J Rheumatol"xsd:string
http://purl.uniprot.org/citations/12064834http://purl.uniprot.org/core/pages"1192-1197"xsd:string
http://purl.uniprot.org/citations/12064834http://purl.uniprot.org/core/title"Gene polymorphisms of tissue plasminogen activator and plasminogen activator inhibitor-1 in patients with antiphospholipid antibodies."xsd:string
http://purl.uniprot.org/citations/12064834http://purl.uniprot.org/core/volume"29"xsd:string
http://purl.uniprot.org/citations/12064834http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/12064834
http://purl.uniprot.org/citations/12064834http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/12064834
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