ライフサイエンスコーパス: lipid-lowering drug

1 ipidemia, nearly half of whom were receiving lipid-lowering drugs.

2 ein cholesterol (LDL-c) >/=130 mg/dL, and no lipid-lowering drugs.

3 isk factors, and use of antihypertensive and lipid-lowering drugs.

4 ed as proxies to study the efficacy of these lipid-lowering drugs.

5 ia and often require treatment with multiple lipid-lowering drugs.

6 d by risk and recommendations for the use of lipid-lowering drugs.

7 ght, weight, and use of antihypertensive and lipid-lowering drugs.

8 y revascularization and 70 percent receiving lipid-lowering drugs.

9 ng enzyme inhibitors, and 53% were receiving lipid-lowering drugs.

10 nfluences the lipid and clinical response to lipid-lowering drugs.

11 chronic disease score, and use of non-statin lipid-lowering drugs.

12 osis of hyperlipidaemia or exposure to other lipid-lowering drugs.

13 between fracture risk and use of non-statin lipid-lowering drugs.

14 be a potential target for the development of lipid-lowering drugs.

15 The lipid-lowering drugs, 3-hydroxy-3-methylgulutaryl-coenzy

16 ents: 49% (7,836/16,028) were not prescribed lipid-lowering drugs, 52% (1,647/3,194) were not prescri

17 sin II receptor blockers, beta-blockers, and lipid-lowering drugs also increased among both sexes.

18 cell DNA from 991 Whites in the Genetics of Lipid Lowering Drugs and Diet Network Study was followed

19 nondiabetic participants in the Genetics of Lipid Lowering Drugs and Diet Network study, divided int

20 In the GOLDN (Genetics of Lipid Lowering Drugs and Diet Network) study, higher ABC

21 dchip in 991 participants of the Genetics of Lipid Lowering Drugs and Diet Network.

22 Fibrates are lipid lowering drugs and found as ligands for peroxisome

23 Fenofibrate (FF) is a common lipid-lowering drug and a potent agonist of the peroxiso

24 underlines the importance of gemfibrozil, a lipid-lowering drug and an activator of peroxisome proli

25 ngiotensin-converting enzyme inhibitors, and lipid-lowering drugs, and smoking cessation counseling f

26 ity assessment of conduit and target vessel, lipid-lowering drugs, antithrombotic therapy, and cessat

27 Lipid-lowering drugs are associated with myotoxicity, wh

28 Prescription of a lipid-lowering drug at hospital discharge was independen

29 luation of risk factors prior to prescribing lipid-lowering drugs, attention to muscle symptoms, and

30 substantial increase in antihypertensive and lipid-lowering drugs, blood pressure management remained

31 S1P is a potential target for lipid-lowering drugs, but the effect of S1P blockade in

32 Consequently, the total dosage of lipid-lowering drug consumed, the concomitant use of oth

33 Recommendations for the prescription of lipid-lowering drugs emphasise the importance of an asse

34 By activating PPARalpha, the lipid-lowering drug fenofibrate reverses dyslipidemia an

35 Also, lipid-lowering drugs fenofibrate and niacin reduced live

36 ammatory effect of gemfibrozil, a prescribed lipid-lowering drug for humans, in mouse microglia.

37 s, patients failed to fill prescriptions for lipid-lowering drugs for about 40% of the study year.

38 inhibitors) are the most prescribed class of lipid-lowering drugs for the treatment and prevention of

39 ward, and a prospective analysis for general lipid-lowering drugs from 1994 to 2004.

40 Evidence of carcinogenicity of lipid-lowering drugs from clinical trials in humans is i

41 led and nondetailed drugs in 8 drug classes (lipid-lowering drugs, gastroesophageal reflux disease dr

42 of 8 study drug classes for detailed drugs (lipid-lowering drugs, gastroesophageal reflux disease dr

43 rlier studies have shown that gemfibrozil, a lipid-lowering drug, has anti-inflammatory properties.

44 rated PPARalpha agonists beyond their use as lipid-lowering drugs in anticancer therapy.

45 em), a Food and Drug Administration-approved lipid-lowering drug, in increasing the expression of IL-

46 zil, a Food and Drug Administration-approved lipid-lowering drug, in up-regulating the expression of

47 brate, Food and Drug Administration-approved lipid-lowering drugs, in up-regulating TPP1 in brain cel

48 by factors that elevate tissue levels of the lipid-lowering drug, including the dose, drug-drug inter

49 ention drug clinically indicated: 16,028 had lipid-lowering drugs indicated, 3,194 anticoagulant drug

50 Gemfibrozil, a lipid-lowering drug, inhibited cytokine-induced producti

51 ncomitant treatment of lomitapide with other lipid-lowering drugs is generally safe.

52 Both the lipid-lowering drug lovastatin and the Rac1-specific inh

53 Lipid-lowering drugs may be indicated in this subgroup.

54 A few studies have suggested that lipid-lowering drugs may have anti-arrhythmic effects in

55 tained in analyses excluding subjects taking lipid-lowering drugs or estrogen and in analyses adjuste

56 tment on American Heart Association diet and lipid-lowering drugs or on strict low-fat diet (<10% of

57 re not using an antihypertensive medication, lipid-lowering drugs, or a glucose-lowering treatment.

58 dds ratio [OR], 1.60 [95% CI, 1.50 to 1.71]; lipid-lowering drugs: OR, 1.59 [CI, 1.50 to 1.68]).

59 likely to be taking aspirin (P < 0.001) and lipid-lowering drugs (P = 0.006).

60 0-95 mg/dL)] who were not being treated with lipid-lowering drugs participated.

61 d a decrease in monthly antihypertensive and lipid-lowering drug prescriptions during the coverage ga

62 ations studied, patients who were prescribed lipid-lowering drug regimens remained without filled pre

63 ntihypertensives, antithrombotic agents, and lipid-lowering drugs (relative risk, 0.55 [95% confidenc

64 The lipid-lowering drug simvastatin decreases portal pressur

65 In addition to lipid-lowering drugs - statins, dietary control, and exe

66 eated for 6 weeks with either bezafibrate, a lipid-lowering drug that does not affect plasma glucose

67 Statins are one of the lipid-lowering drugs that help in reducing cholesterol l

68 Among potential agents, the lipid-lowering drugs, the statins, satisfy these prerequ

69 d inflammation and the potential benefits of lipid-lowering drug therapy after heart transplantation.

70 have negative effects on adherence to statin lipid-lowering drug therapy but not on their initiation

71 th advanced atherosclerosis, NCEP recommends lipid-lowering drug therapy if LDL cholesterol remains >

72 e sufficiently frequent during the course of lipid-lowering drug therapy to pose diagnostic challenge

73 .3% (1964/6704) had dyslipidemia, among whom lipid-lowering drug therapy was reported by 54.0% (1060/

74 thin a single family, and more responsive to lipid-lowering drug therapy.

75 rol (LDL-C) levels to assess eligibility for lipid-lowering drug therapy.

76 olesterolemic patients who are refractory to lipid-lowering drug therapy.

77 fication, in particular early and aggressive lipid-lowering drug therapy; and a number of evolving th

78 uals, 19.7% of those who did not qualify for lipid-lowering drug treatment had CAC >400.

79 characterized regarding plasma lipid status, lipid-lowering drug treatment, and variants at the LPA g

80 periments in animals and humans suggest that lipid-lowering drug treatment, especially with the fibra

81 Lipid-lowering drug use rose significantly for both sexe

82 trends in cholesterol, hypercholesterolemia, lipid-lowering drug use, and cholesterol awareness, trea

83 iving patients who were initially prescribed lipid-lowering drugs were still filling prescriptions fo

84 atherosclerosis in subjects not treated with lipid-lowering drugs while the process is still confined

85 nt of glioblastoma cells with fenofibrate, a lipid-lowering drug with multiple anticancer activities.

86 Most studies compared a lipid-lowering drug with placebo but did not evaluate th

87 Statins are widely used lipid-lowering drugs with immunomodulatory properties th