{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1361699996237437696.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1161/01.cir.0000015700.27754.6f"}},{"identifier":{"@type":"URI","@value":"https://www.ahajournals.org/doi/full/10.1161/01.CIR.0000015700.27754.6F"}}],"dc:title":[{"@value":"Increased Platelet Binding to Circulating Monocytes in Acute Coronary Syndromes"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Background</jats:italic>\n                </jats:bold>\n                —\n              </jats:italic>\n            </jats:bold>\n            Present therapies for acute coronary syndromes aim toward limiting platelet–platelet adhesion and aggregation processes. However, platelet–leukocyte interactions may contribute importantly to disease progression in the arterial wall. Recent studies suggest that prevention of platelet–leukocyte binding via P-selectin glycoprotein ligand-1 (PSGL-1) may be beneficial in animal models of vascular injury.\n          </jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Methods and Results</jats:italic>\n                </jats:bold>\n                —\n              </jats:italic>\n            </jats:bold>\n            P-selectin–PSGL-1 interactions were found to account for most platelet–monocyte binding observed in peripheral blood samples from healthy donors. However, a significant component of observed adhesion was calcium independent, involving neither PSGL-1 nor P-selectin. Platelet–monocyte interactions were examined in 52 patients admitted within 14 hours of symptom onset, with acute coronary syndromes defined as unstable angina (n=12) and acute myocardial infarction (n=13) or noncardiac chest pain (n=27). When compared with patients with noncardiac chest pain, significantly elevated levels of platelet–monocyte binding were found in patients with acute myocardial infarction (70.1±15.4% versus 45.4±23.3%;\n            <jats:italic>P</jats:italic>\n            <0.01) and unstable angina (67.4±12.9% versus 45.4±23.3%;\n            <jats:italic>P</jats:italic>\n            >0.01). Calcium-independent platelet–monocyte binding was significantly elevated in myocardial infarction patients alone (14.7±7.7% versus 6.1±5.96%;\n            <jats:italic>P</jats:italic>\n            <0.001).\n          </jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>\n                <jats:bold>\n                  <jats:italic>Conclusions</jats:italic>\n                </jats:bold>\n                —\n              </jats:italic>\n            </jats:bold>\n            There is evidence for a significant P-selectin–independent molecular component to the platelet–monocyte conjugation observed in peripheral blood. Patients with myocardial infarction and unstable angina demonstrate increased total binding of platelets to monocytes. Additionally, calcium-independent adhesion was significantly elevated in patients with evidence of myocardial infarction. These findings demonstrate that novel cation-independent adhesion mechanisms may mediate platelet–monocyte binding, representing a new therapeutic target after vascular injury associated with myocardial infarction.\n          </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1381699996237437697","@type":"Researcher","foaf:name":[{"@value":"Jaydeep Sarma"}],"jpcoar:affiliationName":[{"@value":"From the Medical Research Council Centre for Inflammation Research, University of Edinburgh Medical School (J.S., K.A.L., I.D.) and Cardiovascular Research Unit, Royal Infirmary (S.A., A.J., K.A.A.F.), Edinburgh, UK."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996237437698","@type":"Researcher","foaf:name":[{"@value":"Caterina A. Laan"}],"jpcoar:affiliationName":[{"@value":"From the Medical Research Council Centre for Inflammation Research, University of Edinburgh Medical School (J.S., K.A.L., I.D.) and Cardiovascular Research Unit, Royal Infirmary (S.A., A.J., K.A.A.F.), Edinburgh, UK."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996237437699","@type":"Researcher","foaf:name":[{"@value":"Shirjel Alam"}],"jpcoar:affiliationName":[{"@value":"From the Medical Research Council Centre for Inflammation Research, University of Edinburgh Medical School (J.S., K.A.L., I.D.) and Cardiovascular Research Unit, Royal Infirmary (S.A., A.J., K.A.A.F.), Edinburgh, UK."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996237437700","@type":"Researcher","foaf:name":[{"@value":"Ashwani Jha"}],"jpcoar:affiliationName":[{"@value":"From the Medical Research Council Centre for Inflammation Research, University of Edinburgh Medical School (J.S., K.A.L., I.D.) and Cardiovascular Research Unit, Royal Infirmary (S.A., A.J., K.A.A.F.), Edinburgh, UK."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996237437696","@type":"Researcher","foaf:name":[{"@value":"Keith A.A. Fox"}],"jpcoar:affiliationName":[{"@value":"From the Medical Research Council Centre for Inflammation Research, University of Edinburgh Medical School (J.S., K.A.L., I.D.) and Cardiovascular Research Unit, Royal Infirmary (S.A., A.J., K.A.A.F.), Edinburgh, UK."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996237437701","@type":"Researcher","foaf:name":[{"@value":"Ian Dransfield"}],"jpcoar:affiliationName":[{"@value":"From the Medical Research Council Centre for Inflammation Research, University of Edinburgh Medical School (J.S., K.A.L., I.D.) and Cardiovascular Research Unit, Royal Infirmary (S.A., A.J., K.A.A.F.), Edinburgh, UK."}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00097322"},{"@type":"EISSN","@value":"15244539"},{"@type":"PISSN","@value":"http://id.crossref.org/issn/00097322"}],"prism:publicationName":[{"@value":"Circulation"}],"dc:publisher":[{"@value":"Ovid Technologies (Wolters Kluwer Health)"}],"prism:publicationDate":"2002-05-07","prism:volume":"105","prism:number":"18","prism:startingPage":"2166","prism:endingPage":"2171"},"reviewed":"false","url":[{"@id":"https://www.ahajournals.org/doi/full/10.1161/01.CIR.0000015700.27754.6F"}],"createdAt":"2002-07-28","modifiedAt":"2024-05-06","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360848661343124224","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Analysing responses to aspirin and clopidogrel by measuring platelet thrombus formation under arterial flow conditions"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001205103931904","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Serial Changes in Platelet Activation in Patients With Unstable Angina Following Coronary Stenting  Evaluation of the Effect of Clopidogrel Loading Dose in Inhibiting Platelet Activation"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001205105149824","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Baseline Platelet Count and Clinical Outcome in Acute Coronary Syndrome"},{"@value":"Platelet Count as a Prognostic Marker in Patients With Acute Coronary Syndromes"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001205107825536","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Platelets: Small in Size But Essential in the Regulation of Vascular Homeostasis　– Translation From Basic Science to Clinical Medicine –"},{"@value":"Platelets: Small in Size But Essential in the Regulation of Vascular Homeostasis"},{"@value":"Small in size but essential in the regulation of vascular homeostasis - translation from basic science to clinical medicine"}]},{"@id":"https://cir.nii.ac.jp/crid/1390282680082184064","@type":"Article","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Platelet Activity is a Biomarker of Cardiac Necrosis and Predictive of Untoward Clinical Outcomes in Patients With Acute Myocardial Infarction Undergoing Primary Coronary Stenting"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1161/01.cir.0000015700.27754.6f"},{"@type":"CROSSREF","@value":"10.1253/circj.69.1208_references_DOI_Hb4ZFcvYhmw3w1vwYUoa9tobsD0"},{"@type":"CROSSREF","@value":"10.1253/circj.cj-14-1434_references_DOI_Hb4ZFcvYhmw3w1vwYUoa9tobsD0"},{"@type":"CROSSREF","@value":"10.1253/circj.70.31_references_DOI_Hb4ZFcvYhmw3w1vwYUoa9tobsD0"},{"@type":"CROSSREF","@value":"10.1160/th12-06-0441_references_DOI_Hb4ZFcvYhmw3w1vwYUoa9tobsD0"},{"@type":"CROSSREF","@value":"10.1253/circj.cj-11-0707_references_DOI_Hb4ZFcvYhmw3w1vwYUoa9tobsD0"}]}