PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
21952256-3	2011	However, a recent study has shown that xenon interacts with tissue-type plasminogen activator (tPA), a well-recognized approved therapy of acute ischemic stroke.	Xenon	39-44	plasminogen activator, tissue type	Rattus norvegicus	60-93	
21952256-3	2011	However, a recent study has shown that xenon interacts with tissue-type plasminogen activator (tPA), a well-recognized approved therapy of acute ischemic stroke.	Xenon	39-44	plasminogen activator, tissue type	Rattus norvegicus	95-98	
21952256-4	2011	Although intraischemic xenon inhibits tPA-induced thrombolysis and subsequent reduction of brain damage, postischemic xenon virtually suppresses both ischemic brain damage and tPA-induced brain hemorrhages and disruption of the blood-brain barrier.	Xenon	23-28	plasminogen activator, tissue type	Rattus norvegicus	38-41	
21952256-4	2011	Although intraischemic xenon inhibits tPA-induced thrombolysis and subsequent reduction of brain damage, postischemic xenon virtually suppresses both ischemic brain damage and tPA-induced brain hemorrhages and disruption of the blood-brain barrier.	Xenon	118-123	plasminogen activator, tissue type	Rattus norvegicus	176-179	
20087367-0	2010	Xenon is an inhibitor of tissue-plasminogen activator: adverse and beneficial effects in a rat model of thromboembolic stroke.	Xenon	0-5	plasminogen activator, tissue type	Rattus norvegicus	25-53	
20087367-4	2010	Because the active site of serine proteases is structurally conserved, we have hypothesized and investigated whether xenon may alter the catalytic efficiency of tissue-type plasminogen activator (tPA), a serine protease that is the only approved therapy for acute ischemic stroke today.	Xenon	117-122	plasminogen activator, tissue type	Rattus norvegicus	161-200	
21952256-7	2011	RESULTS: The authors demonstrate nitrous oxide is a tPA inhibitor, intraischemic nitrous oxide dose-dependently inhibits tPA-induced thrombolysis and subsequent reduction of ischemic brain damage, and postischemic nitrous oxide reduces ischemic brain damage, but in contrast with xenon, it increases brain hemorrhages and disruption of the blood-brain barrier.	Xenon	280-285	plasminogen activator, tissue type	Rattus norvegicus	52-55	
21952256-7	2011	RESULTS: The authors demonstrate nitrous oxide is a tPA inhibitor, intraischemic nitrous oxide dose-dependently inhibits tPA-induced thrombolysis and subsequent reduction of ischemic brain damage, and postischemic nitrous oxide reduces ischemic brain damage, but in contrast with xenon, it increases brain hemorrhages and disruption of the blood-brain barrier.	Xenon	280-285	plasminogen activator, tissue type	Rattus norvegicus	121-124