PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
22735429-1	2012	CONTEXT: Intravenous tissue plasminogen activator (tPA) is known to improve outcomes in ischemic stroke; however, patients receiving long-term chronic warfarin therapy may face an increased risk for intracranial hemorrhage when treated with tPA.	Warfarin	151-159	chromosome 20 open reading frame 181	Homo sapiens	21-49	
26731441-2	2016	The observation that five psychotic patients on chronic warfarin therapy for deep-vein thrombosis showed long-term remission of psychotic symptoms made us suspect that abnormalities in the coagulation pathway, specifically low tissue plasminogen activator (tPA) activity, could be one of the missing links.	Warfarin	56-64	chromosome 20 open reading frame 181	Homo sapiens	227-255	
26731441-2	2016	The observation that five psychotic patients on chronic warfarin therapy for deep-vein thrombosis showed long-term remission of psychotic symptoms made us suspect that abnormalities in the coagulation pathway, specifically low tissue plasminogen activator (tPA) activity, could be one of the missing links.	Warfarin	56-64	chromosome 20 open reading frame 181	Homo sapiens	257-260	
22735429-1	2012	CONTEXT: Intravenous tissue plasminogen activator (tPA) is known to improve outcomes in ischemic stroke; however, patients receiving long-term chronic warfarin therapy may face an increased risk for intracranial hemorrhage when treated with tPA.	Warfarin	151-159	chromosome 20 open reading frame 181	Homo sapiens	51-54	
22735429-1	2012	CONTEXT: Intravenous tissue plasminogen activator (tPA) is known to improve outcomes in ischemic stroke; however, patients receiving long-term chronic warfarin therapy may face an increased risk for intracranial hemorrhage when treated with tPA.	Warfarin	151-159	chromosome 20 open reading frame 181	Homo sapiens	241-244	
22735429-2	2012	Although current guidelines endorse administering intravenous tPA to warfarin-treated patients if their international normalized ratio (INR) is 1.7 or lower, there are few data on safety of intravenous tPA in warfarin-treated patients in clinical practice.	Warfarin	209-217	chromosome 20 open reading frame 181	Homo sapiens	202-205	
22735429-3	2012	OBJECTIVES: To determine the risk of symptomatic intracranial hemorrhage (sICH) among patients with ischemic stroke treated with intravenous tPA who were receiving warfarin vs those who were not and to determine this risk as a function of INR.	Warfarin	164-172	chromosome 20 open reading frame 181	Homo sapiens	141-144	
22735429-7	2012	RESULTS: Overall, 1802 (7.7%) patients with stroke treated with tPA were receiving warfarin (median INR, 1.20; interquartile range [IQR], 1.07-1.40).	Warfarin	83-91	chromosome 20 open reading frame 181	Homo sapiens	64-67	
22735429-12	2012	CONCLUSION: Among patients with ischemic stroke, the use of intravenous tPA among warfarin-treated patients (INR <=1.7) was not associated with increased sICH risk compared with non-warfarin-treated patients.	Warfarin	82-90	chromosome 20 open reading frame 181	Homo sapiens	72-75	
21350204-1	2011	BACKGROUND AND PURPOSE: Concern exists that preadmission warfarin use may be associated with an increased risk of intracerebral hemorrhage in patients with ischemic stroke receiving intravenous tissue plasminogen activator, even in those with an international normalized ratio <1.7.	Warfarin	57-65	chromosome 20 open reading frame 181	Homo sapiens	194-222	
21350204-11	2011	CONCLUSIONS: The results from the present study suggest that tissue plasminogen activator treatment appears to be safe in patients with acute ischemic stroke taking warfarin with an international normalized ratio <1.7 and may reduce the risk of poor functional outcome.	Warfarin	165-173	chromosome 20 open reading frame 181	Homo sapiens	61-89