PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
9607127-6	1998	Mechanisms other than lipoprotein lipase, cholesteryl ester transfer protein activities, and an apolipoprotein B gene polymorphism may be responsible for the resistance to lowering of plasma total and low-density lipoprotein cholesterol levels with bezafibrate treatment in familial combined hyperlipidemic patients with impaired glucose tolerance.	Bezafibrate	249-260	apolipoprotein B	Homo sapiens	96-112	
12048068-5	2002	The cells with steatosis showed increased levels of intracellular triglycerides and apolipoprotein B, which were reduced in the presence of bezafibrate at 100 &mgr;g/ml.	Bezafibrate	140-151	apolipoprotein B	Homo sapiens	84-100	
11426588-6	2000	The CH content in apolipoprotein B100 particles after treatment with either bezafibrate or pravastatin decreased significantly (group A: 24.7%, group B: 26.6%).	Bezafibrate	76-87	apolipoprotein B	Homo sapiens	18-37	
10751747-6	2000	With bezafibrate treatment the LDL-cholesterol/LDL-ApoB ratio showed a tendency to rise, suggesting a change in the LDL particle composition to a less small and dense form, while pravastatin treatment induced a decrease in this ratio suggesting a change in the LDL particle to a more dense form.	Bezafibrate	5-16	apolipoprotein B	Homo sapiens	51-55	
9822092-7	1998	CONCLUSIONS: Our results suggest that the effect of bezafibrate on progression of focal coronary atherosclerosis could be at least partly attributed to a rise in HDL3 cholesterol and a decrease in the total number of apo B-containing lipoproteins.	Bezafibrate	52-63	apolipoprotein B	Homo sapiens	217-222	
1596293-5	1992	Pravastatin and bezafibrate also altered the composition of LDL as evidenced by the reduction of its cholesterol/apo B100 ratio.	Bezafibrate	16-27	apolipoprotein B	Homo sapiens	113-121	
1397477-5	1992	The marked BZF-induced Tg reduction was associated with a proportional decrease in Apo B, while an increase in total HDL-, HDL2 and HDL3-CHOL, together with a significant increase in Apo AI, was observed.	Bezafibrate	11-14	apolipoprotein B	Homo sapiens	83-88	
2360915-2	1990	When bezafibrate therapy was interrupted in patients who had been on continuous treatment for hyperlipoproteinemia for 4-10 years, there were significant increases in the serum cholesterol, triglyceride and apolipoprotein B concentrations corresponding to an increase of the very low density lipoprotein (VLDL) levels by approximately 50%.	Bezafibrate	5-16	apolipoprotein B	Homo sapiens	207-223	
3884023-1	1985	In our study, bezafibrate in short-acting formula and long-acting formula, administered to hyperlipidaemic patients, resulted in a significant lowering of atherogenic lipids and lipoproteins (chol.-T, LDL and VLDL-chol., apolipoprotein B and VDLD-TR), and a marked increase in the levels of HDL, HDL2, HDL3-chol.	Bezafibrate	14-25	apolipoprotein B	Homo sapiens	221-237	
2894548-2	1988	Simvastatin was better than bezafibrate at lowering total and low-density lipoprotein (LDL)-cholesterol and apolipoprotein B concentrations (30.4% [p less than 0.001], 37.3% [p less than 0.001], and 37.8% [p less than 0.001] vs 17.0%, 19.6%, and 24.0%, respectively).	Bezafibrate	28-39	apolipoprotein B	Homo sapiens	108-124