PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
2498455-0	1989	Rise of plasma t-PA fibrinolytic activity in a group of maturity onset diabetic patients shifted from a first generation (tolbutamide) to a second generation sulphonylurea (gliclazide).	Gliclazide	173-183	plasminogen activator, tissue type	Homo sapiens	15-19	
2498455-2	1989	All 10 patients responded on the change in treatment to gliclazide with an increase in activity of t-PA.	Gliclazide	56-66	plasminogen activator, tissue type	Homo sapiens	99-103	
2498455-4	1989	The concentration in plasma of t-PA antigen under basal conditions and after stimulation (venous occlusion) increased significantly during the period of treatment with gliclazide.	Gliclazide	168-178	plasminogen activator, tissue type	Homo sapiens	31-35	
2498455-6	1989	In contrast to these findings seven patients with marked activities of t-PA during treatment with tolbutamide retained unchanged levels of the variables reported above after a change in treatment to gliclazide.	Gliclazide	199-209	plasminogen activator, tissue type	Homo sapiens	71-75	
3050364-8	1988	It is concluded that gliclazide induces small, but significant, non-insulin-dependent extrametabolic effects on the extrinsic (t-PA) and intrinsic (prekallikrein) system of fibrinolysis.	Gliclazide	21-31	plasminogen activator, tissue type	Homo sapiens	127-131	
1908183-1	1991	This study examined the effect of gliclazide on tissue-type plasminogen activator (t-PA)-related fibrinolysis in 23 Type I diabetic patients without residual beta-cell function and 17 Type II diabetic patients initially treated with tolbutamide.	Gliclazide	34-44	plasminogen activator, tissue type	Homo sapiens	48-81	
1908183-1	1991	This study examined the effect of gliclazide on tissue-type plasminogen activator (t-PA)-related fibrinolysis in 23 Type I diabetic patients without residual beta-cell function and 17 Type II diabetic patients initially treated with tolbutamide.	Gliclazide	34-44	plasminogen activator, tissue type	Homo sapiens	83-87	
1908183-3	1991	In Type I diabetic patients, after 2-3 months of treatment with gliclazide, we observed a significant increase in plasma concentrations of total t-PA antigen that remained stable until discontinuation of the drug (p less than 0.0002), whereas the plasma concentrations of plasminogen activator inhibitor (PAI) did not change significantly during the study.	Gliclazide	64-74	plasminogen activator, tissue type	Homo sapiens	145-149	
1908183-4	1991	Next, we investigated the possibility of gliclazide inducing t-PA-related fibrinolysis in a subset of Type II diabetics without detectable concentrations of t-PA during treatment with tolbutamide.	Gliclazide	41-51	plasminogen activator, tissue type	Homo sapiens	61-65	
1908183-5	1991	The concentrations of active t-PA increased significantly 3 months after a change in treatment to gliclazide, and active t-PA again decreased in one patient to undetectable levels after 12 months with gliclazide.	Gliclazide	201-211	plasminogen activator, tissue type	Homo sapiens	121-125	
1908183-8	1991	We conclude that gliclazide has the potential to exert extrametabolic non-insulin-mediated effects on t-PA-related fibrinolysis in diabetic patients.	Gliclazide	17-27	plasminogen activator, tissue type	Homo sapiens	102-106