@prefix this: . @prefix rdfs: . @prefix xsd: . @prefix sio: . @prefix ncit: . @prefix lld: . @prefix miriam-gene: . @prefix miriam-pubmed: . @prefix eco: . @prefix wi: . @prefix prov: . @prefix pav: . @prefix prv: . @prefix dcterms: . @prefix np: . @prefix dgn-np: . @prefix dgn-gda: . @prefix dgn-void: . dgn-np:NP174789.RATOYvOqYonqKWhYsnAGZwmdB2Vx2xCfQXaAMuvW-DjMQ130_head { this: np:hasAssertion dgn-np:NP174789.RATOYvOqYonqKWhYsnAGZwmdB2Vx2xCfQXaAMuvW-DjMQ130_assertion; np:hasProvenance dgn-np:NP174789.RATOYvOqYonqKWhYsnAGZwmdB2Vx2xCfQXaAMuvW-DjMQ130_provenance; np:hasPublicationInfo dgn-np:NP174789.RATOYvOqYonqKWhYsnAGZwmdB2Vx2xCfQXaAMuvW-DjMQ130_publicationInfo; a np:Nanopublication . dgn-np:NP174789.RATOYvOqYonqKWhYsnAGZwmdB2Vx2xCfQXaAMuvW-DjMQ130_assertion a np:Assertion . dgn-np:NP174789.RATOYvOqYonqKWhYsnAGZwmdB2Vx2xCfQXaAMuvW-DjMQ130_provenance a np:Provenance . dgn-np:NP174789.RATOYvOqYonqKWhYsnAGZwmdB2Vx2xCfQXaAMuvW-DjMQ130_publicationInfo a np:PublicationInfo . } dgn-np:NP174789.RATOYvOqYonqKWhYsnAGZwmdB2Vx2xCfQXaAMuvW-DjMQ130_assertion { miriam-gene:102 a ncit:C16612 . lld:C0010068 a ncit:C7057 . dgn-gda:DGNd72b5177d17cf7b1f4ad56f8160b2fc0 sio:SIO_000628 miriam-gene:102, lld:C0010068; a sio:SIO_001121 . } dgn-np:NP174789.RATOYvOqYonqKWhYsnAGZwmdB2Vx2xCfQXaAMuvW-DjMQ130_provenance { dgn-np:NP174789.RATOYvOqYonqKWhYsnAGZwmdB2Vx2xCfQXaAMuvW-DjMQ130_assertion dcterms:description "[Our main findings were: (i) patients with stable (n = 40) and unstable (n = 40) angina had elevated plasma levels of CXCL16 compared with controls (n = 20); (ii) low-dose simvastatin (20 mg qd, n = 15) and high-dose atorvastatin (80 mg qd, n = 9) down-regulated plasma levels of CXCL16 during 6 months of therapy; (iii) in vitro, atorvastatin significantly decreased the interleukin (IL)-1beta-mediated release of CXCL16 from PBMC and endothelial cells; (iv) attenuating effect of atorvastatin on the IL-1beta-mediated release of CXCL16 in PBMC seems to involve post-transcriptional modulation as well as down-regulation of CXCL16 release through inhibition of the protease a disintegrin and metalloproteinase 10 (ADAM10); (v) soluble CXCL16 increased the release of IL-8, monocyte chemoattractant peptide 1, and matrix metalloproteinases in vascular SMC and increased the release of IL-8 and monocyte chemoattractant peptide 1 in PBMC, with particularly enhancing effects in cells from CAD patients.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine."@en; wi:evidence dgn-void:source_evidence_literature; sio:SIO_000772 miriam-pubmed:18339644; prov:wasDerivedFrom dgn-void:befree-20140225; prov:wasGeneratedBy eco:ECO_0000203 . dgn-void:befree-20140225 pav:importedOn "2014-02-25"^^xsd:date . dgn-void:source_evidence_literature a eco:ECO_0000212; rdfs:comment "Gene-disease associations inferred from text-mining the literature."@en; rdfs:label "DisGeNET evidence - LITERATURE"@en . } dgn-np:NP174789.RATOYvOqYonqKWhYsnAGZwmdB2Vx2xCfQXaAMuvW-DjMQ130_publicationInfo { this: dcterms:created "2014-10-02T12:33:34+02:00"^^xsd:dateTime; dcterms:rights ; dcterms:rightsHolder dgn-void:IBIGroup; dcterms:subject sio:SIO_000983; prv:usedData dgn-void:disgenetrdf; pav:authoredBy , , , , ; pav:createdBy ; pav:version "v2.1.0.0" . dgn-void:disgenetrdf pav:version "v2.1.0" . }