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