@prefix this: . @prefix sub: . @prefix beldoc: . @prefix rdfs: . @prefix rdf: . @prefix xsd: . @prefix dct: . @prefix dce: . @prefix pav: . @prefix np: . @prefix belv: . @prefix prov: . @prefix chebi: . @prefix go: . @prefix species: . @prefix occursIn: . @prefix mesh: . @prefix pubmed: . @prefix orcid: . sub:Head { this: np:hasAssertion sub:assertion; np:hasProvenance sub:provenance; np:hasPublicationInfo sub:pubinfo; a np:Nanopublication . } sub:assertion { sub:_1 occursIn: mesh:D009420, species:10116; rdf:object go:0008219; rdf:predicate belv:increases; rdf:subject chebi:7583; a rdf:Statement . sub:assertion rdfs:label "a(CHEBI:\"nitric oxide\") -> bp(GO:\"cell death\")" . } sub:provenance { beldoc: dce:description "Approximately 61,000 statements."; dce:rights "Copyright (c) 2011-2012, Selventa. All rights reserved."; dce:title "BEL Framework Large Corpus Document"; pav:authoredBy sub:_3; pav:version "1.4" . sub:_2 prov:value "Reactive nitrogen species are thought to be involved in both hypoxic-ischemic and cytokine-induced brain injury, including periventricular leukomalacia (PVL), the major pathological substrate of cerebral palsy in premature infants. PVL appears to be the result of perinatal inflammatory events and hypoxic-ischemic injury to the cerebral white matter. The chronic disturbance of myelination resulting from PVL suggests that developing oligodendrocytes (OLs) are involved in its pathogenesis. We hypothesized that nitric oxide (NO) could participate in the pathogenesis of PVL through a toxic effect on developing OLs. Using primary cultures of highly enriched OLs we found that NO is toxic to developing OLs (O4+, O1-, MBP-), with an EC50 value of 236 +/- 125 microm of DETANOnoate."; prov:wasQuotedFrom pubmed:15379992 . sub:_3 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:15379992; prov:wasDerivedFrom beldoc:, sub:_2 . } sub:pubinfo { this: dct:created "2014-07-03T14:30:27.992+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }