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All rights reserved." } ], "http://purl.org/dc/elements/1.1/title" : [ { "@value" : "BEL Framework Large Corpus Document" } ], "http://purl.org/pav/authoredBy" : [ { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAaTPMSTLoSXUrujhTs3MrxDmwuU3m1fuInGZ0I_sFKqg#_5" } ], "http://purl.org/pav/version" : [ { "@value" : "20131211" } ] }, { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAaTPMSTLoSXUrujhTs3MrxDmwuU3m1fuInGZ0I_sFKqg#_4", "http://www.w3.org/ns/prov#value" : [ { "@value" : "Hyperhomocysteinemia (HH) constitutes a risk marker for thrombosis, but the pathophysiological mechanisms in thrombus formation are still unresolved. We investigated the influence of HH on single coagulation factor functions and evaluated the platelet GpIIb/IIIa receptor function in HH-induced changes in whole-blood coagulation profiles (WBCP). Three groups of 12 rats were investigated: control rats, folate deficient-HH (FD-HH) rats, and treated rats. 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