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http://purl.uniprot.org/citations/31978406http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31978406http://www.w3.org/2000/01/rdf-schema#comment"

Objectives

Although a single nucleotide polymorphism in a specific receptor for lysophosphatidylserine, a lysophospholipid mediator involved in the immune system, is reportedly associated with Graves' disease, the association between lysophosphatidylserine and thyroid disorders remains to be elucidated. Therefore, we aimed to investigate the association between the level of phosphatidylserine-specific phospholipase A1 (PS-PLA1), which produces lysophosphatidylserine, and thyroid disorders.

Methods

We measured serum PS-PLA1 levels in the patients with various thyroid disorders (n = 120) and normal subjects (n = 58).

Results

We observed that the serum PS-PLA1 levels were higher in the subjects with Graves' disease, subacute thyroiditis, or silent thyroiditis, while they were not modulated in the patients with hypothyroidism. The serum PS-PLA1 levels were strongly correlated with the levels of thyroid hormones, especially in the subjects with Graves' disease. Moreover, we found that the serum PS-PLA1 levels were lowered by treatment with anti-thyroid reagents in subjects with Graves' disease and that the changes in PS-PLA1 were strongly correlated with those in thyroid hormones.

Conclusion

These results suggest that PS-PLA1 might be a novel target in the treatment of hyperthyroidism, especially Graves' disease, and that its measurement might be useful as a supplementary diagnostic test for thyroid function."xsd:string
http://purl.uniprot.org/citations/31978406http://purl.org/dc/terms/identifier"doi:10.1016/j.cca.2020.01.011"xsd:string
http://purl.uniprot.org/citations/31978406http://purl.uniprot.org/core/author"Aoki J."xsd:string
http://purl.uniprot.org/citations/31978406http://purl.uniprot.org/core/author"Igarashi K."xsd:string
http://purl.uniprot.org/citations/31978406http://purl.uniprot.org/core/author"Murakami M."xsd:string
http://purl.uniprot.org/citations/31978406http://purl.uniprot.org/core/author"Shimamoto S."xsd:string
http://purl.uniprot.org/citations/31978406http://purl.uniprot.org/core/author"Yatomi Y."xsd:string
http://purl.uniprot.org/citations/31978406http://purl.uniprot.org/core/author"Nishikawa M."xsd:string
http://purl.uniprot.org/citations/31978406http://purl.uniprot.org/core/author"Araki O."xsd:string
http://purl.uniprot.org/citations/31978406http://purl.uniprot.org/core/author"Kurano M."xsd:string
http://purl.uniprot.org/citations/31978406http://purl.uniprot.org/core/author"Nakawatari K."xsd:string
http://purl.uniprot.org/citations/31978406http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/31978406http://purl.uniprot.org/core/name"Clin Chim Acta"xsd:string
http://purl.uniprot.org/citations/31978406http://purl.uniprot.org/core/pages"99-106"xsd:string
http://purl.uniprot.org/citations/31978406http://purl.uniprot.org/core/title"Elevated phosphatidylserine-specific phospholipase A1 level in hyperthyroidism."xsd:string
http://purl.uniprot.org/citations/31978406http://purl.uniprot.org/core/volume"503"xsd:string
http://purl.uniprot.org/citations/31978406http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31978406
http://purl.uniprot.org/citations/31978406http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31978406
http://purl.uniprot.org/uniprot/#_G5E9W0-mappedCitation-31978406http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31978406
http://purl.uniprot.org/uniprot/#_Q53H76-mappedCitation-31978406http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31978406
http://purl.uniprot.org/uniprot/Q53H76http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31978406
http://purl.uniprot.org/uniprot/G5E9W0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31978406