ライフサイエンスコーパス: gemfibrozil

1 red only 22% with cholystyramine, niacin and gemfibrozil.

2 l as a glucuronidated hydroxyl-metabolite of gemfibrozil.

3 partially explained the beneficial effect of gemfibrozil.

4 en fed diets supplemented with clofibrate or gemfibrozil.

5 ACO mRNA were strongly stimulated by WY and gemfibrozil.

6 2) for rosuvastatin to 2.16 (0.06, 75.0) for gemfibrozil.

7 st identified bacterium capable of degrading gemfibrozil.

8 ibrozil through food chow than those without gemfibrozil.

9 e mutants abrogated the inhibitory effect of gemfibrozil.

10 mol/liter (39.7 +/- 7.1 mg/dl), while taking gemfibrozil (1,200 mg/day); by 35%, to 1.20 +/- 0.21 mmo

11 l 2.9 mmol/L (111 mg/dL), were randomized to gemfibrozil 1200 mg/d or placebo and were followed up fo

12 We conducted a double-blind trial comparing gemfibrozil (1200 mg per day) with placebo in 2531 men w

13 rticipants were randomly assigned to receive gemfibrozil, 1200 mg/d (n = 1264), or matching placebo (

14 and in 219 of the 1264 patients assigned to gemfibrozil (17.3 percent).

15 astewater matrices, and to measure levels of gemfibrozil (254 +/- 20 ng/L), chlorogemfibrozil (166 +/

16 Gemfibrozil (30 mg/kg) for 7 days before and after strok

17 Pretreatment with gemfibrozil (30 mg/kg) for 7 days moderately but signifi

18 SOD levels were also elevated by gemfibrozil (30 mg/kg).

19 Treatment with gemfibrozil, a drug that specifically reduces triglyceri

20 Although therapy with gemfibrozil, a fibric acid derivative, showed reduced oc

21 This study underlines the importance of gemfibrozil, a Food and Drug Administration-approved lip

22 e present study underlines the importance of gemfibrozil, a lipid-lowering drug and an activator of p

23 Earlier studies have shown that gemfibrozil, a lipid-lowering drug, has anti-inflammator

24 Gemfibrozil, a lipid-lowering drug, inhibited cytokine-i

25 ssion of myelin genes via PPAR-beta and that gemfibrozil, a prescribed drug for humans, may find furt

26 n of NF-kappaB, AP-1, and C/EBPbeta and that gemfibrozil, a prescribed drug for humans, may further f

27 in mediating the anti-inflammatory effect of gemfibrozil, a prescribed lipid-lowering drug for humans

28 A selective CFTR channel blocker, gemfibrozil, abrogated the protective effect of IPC.

29 Gemfibrozil administration resulted in a similar inducti

30 ous to examine whether prophylactic usage of gemfibrozil against stroke is beneficial.

31 mfibrozil; p < 0.001 combination therapy vs. gemfibrozil alone; p = 0.088 combination therapy vs. NA

32 In non-stroke animals gemfibrozil also altered gene expression levels of PPARs

33 Gemfibrozil also did not up-regulate myelin genes in oli

34 Gemfibrozil also induced the recruitment of KLF4 to the

35 Similarly, gemfibrozil also inhibited fibrillar amyloid beta (Abeta

36 Gemfibrozil also inhibited the encephalitogenicity of MB

37 Medications such as the fibrate gemfibrozil alter statin metabolism and increase statin

38 This study demonstrates that gemfibrozil, an agonist of peroxisome proliferator-activ

39 Gemfibrozil, an agonist of PPARalpha, induced the recrui

40 Taken together, our results suggest gemfibrozil, an approved drug for hyperlipidemia in huma

41 sodium hypochlorite yielded a 4'-chlorinated gemfibrozil analog (chlorogemfibrozil).

42 ted on the use of the older fibrates such as gemfibrozil and clofibrate.

43 on perpetrators with CYP2C8, glucuronides of gemfibrozil and clopidogrel showed marked clinical drug-

44 ferent treatment times and concentrations of gemfibrozil and di-n-butyl phthalate were almost identic

45 Because gemfibrozil and fenofibrate are known to activate peroxi

46 Oral administration of gemfibrozil and fenofibrate inhibited clinical signs of

47 Both gemfibrozil and fenofibrate up-regulated mRNA, protein,

48 This study reveals a novel use of gemfibrozil and fenofibrate, Food and Drug Administratio

49 lts suggest that PPAR alpha agonists such as gemfibrozil and fenofibrate, may be attractive candidate

50 l of the anionic micropollutants diclofenac, gemfibrozil and ibuprofen from EfOM.

51 rent compounds ranged from <10 to 3830 ng/L (gemfibrozil), and those of chloro/bromo byproducts range

52 on the uptake of cimetidine, fluoxetine, and gemfibrozil, and other ionizable PPCPs, to confirm the u

53 -alpha (PPARalpha), the role of PPARalpha in gemfibrozil- and fenofibrate-mediated up-regulation of T

54 l percentage of cerivastatin users also took gemfibrozil, approximately half of the case reports of r

55 tin with nicotinic acid and pravastatin with gemfibrozil are well-tolerated combinations that can mai

56 The drugs diclofenac, fluoxetine, and gemfibrozil belong to different pharmaceutical classes w

57 Events were reduced even further with gemfibrozil beyond that explained by increases in HDL-C

58 rhabdomyolysis, of which 25% were related to gemfibrozil-cerivastatin combination therapy, has focuse

59 The PPAR alpha agonists, gemfibrozil, ciprofibrate, and fenofibrate, have an exce

60 Similar to gemfibrozil, clofibrate, another fibrate drug, also inhi

61 Gemfibrozil consistently inhibited the expression and DN

62 , between serum triglyceride (TG) levels and gemfibrozil consumption with periodontal parameters.

63 e of several enzymes potentially involved in gemfibrozil degradation as well as resulted in the produ

64 e of several enzymes potentially involved in gemfibrozil degradation as well as resulted in the produ

65 Gemfibrozil degradation by Bacillus sp. GeD10 was here s

66 Gemfibrozil degradation by Bacillus sp.　GeD10 was here

67 Bacillus sp. GeD10, a gemfibrozil-degrader, was previously isolated from activ

68 study represents the first omics study on a gemfibrozil-degrading bacterium.

69 genes may allow for monitoring of potential gemfibrozil-degrading organisms in situ and increase the

70 ts with hypertriglyceridemia who were taking gemfibrozil did not show significant differences in CAL

71 0 mg/day, n=53), 2) simvastatin placebo plus gemfibrozil (dose adjusted for renal function, n=36), an

72 queous exposure to halogenated degradates of gemfibrozil enhanced the antiandrogenicity of the parent

73 Overall, gemfibrozil exposure in Bacillus sp. GeD10 increased the

74 Overall, gemfibrozil exposure in Bacillus sp.�GeD10 increased the

75 32, fold change (log2) >/= 1) in response to gemfibrozil exposure.

76 32, fold change (log2) >/= 1) in response to gemfibrozil exposure.

77 ce that had been treated with fenofibrate or gemfibrozil for 7 days.

78 wed that CHD events were reduced by 11% with gemfibrozil for every 5-mg/dL (0.13-mmol/L) increase in

79 sent study underlines a novel application of gemfibrozil (gem), a Food and Drug Administration-approv

80 We report here that gemfibrozil (GFZ) inhibits axenic and intracellular grow

81 in the placebo group (9 fatal) and 58 in the gemfibrozil group (3 fatal), for a relative risk reducti

82 cholesterol level was 4 percent lower in the gemfibrozil group than in the placebo group.

83 was 72% in the simvastatin group, 72% in the gemfibrozil group, and 77% in the placebo control group

84 iving NNRTI-based antiretroviral therapy and gemfibrozil had triglyceride responses similar to those

85 icillin, tetracycline, erythromycin-H2O, and gemfibrozil have significant pollution risk quotients (R

86 ol, bezafibrate, clofibric acid, diclofenac, gemfibrozil, ibuprofen, ketoprofen, naproxen, sulfametho

87 thesized that prophylactic administration of gemfibrozil improves outcome after ischemic stroke.

88 However, it remains unknown whether gemfibrozil improves outcome after stroke.

89 First, we tested gemfibrozil in a filamentous MCAO model.

90 iNOS promoter-driven luciferase activity by gemfibrozil in cytokine-stimulated U373MG astroglial cel

91 follow the in situ halogenation reaction of gemfibrozil in deionized water and wastewater matrices,

92 t study identified another novel property of gemfibrozil in stimulating the expression of myelin-spec

93 red by laser speckle imaging was improved by gemfibrozil in the ischemic hemisphere.

94 In this study, we measured the impact of gemfibrozil in two permanent middle cerebral artery occl

95 This study delineates a novel property of gemfibrozil in up-regulating SOCS3 in glial cells via PI

96 hould investigate whether discontinuation of gemfibrozil in warfarin users results in serious underan

97 ted or untreated human oligodendrocytes, and gemfibrozil increased the expression of myelin genes in

98 Gemfibrozil increased the expression of Socs3 mRNA and p

99 We demonstrated that treatment with gemfibrozil increases expression of the Th2 transcriptio

100 Gemfibrozil induced peroxisome proliferator-responsive e

101 Furthermore, we demonstrated that gemfibrozil induced the activation of Kruppel-like facto

102 Interestingly, gemfibrozil induced the activation of p85alpha-associate

103 Interestingly, gemfibrozil induced the activation of type IA phosphatid

104 tin immunoprecipitation analysis showed that gemfibrozil induced the recruitment of PPAR-beta to the

105 the mechanism by which the PPARalpha agonist gemfibrozil induces immune deviation and protects mice f

106 Gemfibrozil inhibited LPS-induced expression of inducibl

107 -mediated inhibition of iNOS suggesting that gemfibrozil inhibits iNOS independent of PPAR-alpha.

108 PAR-alpha-/- mice, we have demonstrated that gemfibrozil inhibits the activation of microglia indepen

109 mfibrozil via the PI3K pathway suggests that gemfibrozil inhibits the activation of NF-kappaB and the

110 These results suggest that gemfibrozil inhibits the induction of iNOS probably by i

111 this combination therapy, and a cerivastatin-gemfibrozil interaction was supported by the results of

112 Although gemfibrozil is a known activator of peroxisome prolifera

113 The cholesterol-lowering pharmaceutical gemfibrozil is a relevant environmental contaminant beca

114 Gemfibrozil is a widely used hypolipidemic and triglycer

115 Since gemfibrozil is known to activate peroxisome proliferator

116 On the other hand, gemfibrozil markedly increased the expression of PPAR-be

117 Furthermore, gemfibrozil may be of therapeutic value in the treatment

118 ediated activation of KLF4 and suggests that gemfibrozil may find therapeutic application in neuroinf

119 ver, DeltahPPAR-alpha was unable to abrogate gemfibrozil-mediated inhibition of iNOS suggesting that

120 ), we investigated the role of PPAR-alpha in gemfibrozil-mediated inhibition of iNOS.

121 y and that siRNA knockdown of KLF4 abrogated gemfibrozil-mediated up-regulation of SOCS3.

122 ase and AKT by chemical inhibitors abrogated gemfibrozil-mediated up-regulation of SOCS3.

123 t not PPARbeta and PPARgamma, is involved in gemfibrozil-mediated up-regulation of TFEB.

124 ell as resulted in the production of several gemfibrozil metabolites.

125 ell as resulted in the production of several gemfibrozil metabolites.

126 mia were prospectively randomized to receive gemfibrozil, NA or combination therapy in an open-label,

127 n byproducts of salicylic acid, bisphenol A, gemfibrozil, naproxen, diclofenac, technical 4-nonylphen

128 Gemfibrozil, niacin, and cholestyramine or corresponding

129 sitivity across a suite of analytes studied (gemfibrozil, nonylphenol, triclosan, 2,4,6-trichlorophen

130 PI3K also abolished the inhibitory effect of gemfibrozil on Abeta-, PrP-, poly IC-, Tat-, and MPP+-in

131 etected, and a 2.5% chance that an effect of gemfibrozil on acute rejection (versus placebo) was not

132 nt of p110 enhanced the inhibitory effect of gemfibrozil on LPS-induced expression of proinflammatory

133 R-gamma, abrogated the stimulatory effect of gemfibrozil on myelin genes in human oligodendrocytes.

134 The effects of gemfibrozil on NMR-measured LDL and HDL particle subclas

135 a); therefore, we investigated the effect of gemfibrozil on the activation of these transcription fac

136 demonstrate that the differential effect of gemfibrozil on the expression of T-bet and GATA3 was due

137 es also demonstrate the inhibitory effect of gemfibrozil on the invasion of T-bet-positive T cells in

138 e we describe that after Th2 polarization by gemfibrozil or other drugs, MBP-primed T cells induced t

139 aseline and after 7 months of treatment with gemfibrozil or placebo.

140 atients with hypertriglyceridemia and taking gemfibrozil over a 3-month period (group M).

141 ared with baseline/washout; p < 0.005 NA vs. gemfibrozil; p < 0.001 combination therapy vs. gemfibroz

142 mg/dl), while taking combination therapy of gemfibrozil plus NA (p < 0.001 for all interventions as

143 Fenofibrate and gemfibrozil, previously reported to induce TPP1 activity

144 eaction produced an additional 4'-brominated gemfibrozil product (bromogemfibrozil).

145 Simvastatin, but not gemfibrozil, reduced total and low density lipoprotein c

146 Its activation by the drug gemfibrozil reduces clinical events in humans with estab

147 cal study has shown that one type of fibrate gemfibrozil reduces stroke incidence in men.

148 ow HDL cholesterol, and low LDL cholesterol, gemfibrozil reduces stroke incidence.

149 gs, such as pravastatin, sodium benzoate, or gemfibrozil, restored the expression of Foxp3 in MBP-pri

150 The treatment of gemfibrozil solutions with sodium hypochlorite yielded a

151 These results suggest that gemfibrozil stimulates the expression of myelin genes vi

152 Interestingly, gemfibrozil strongly inhibited the activation of NF-kapp

153 Patients with HIV infection beginning gemfibrozil therapy had substantially smaller reductions

154 Gemfibrozil therapy resulted in a significant reduction

155 icantly lower in SJL/J female mice receiving gemfibrozil through food chow than those without gemfibr

156 bout the concomitant use of cerivastatin and gemfibrozil to the package insert for more than 18 month

157 astatin, nicotinic acid, cholestyramine, and gemfibrozil) to decrease total cholesterol levels to les

158 With gemfibrozil, total cholesterol level was unchanged; the

159 e were unable to detect PPAR-alpha in either gemfibrozil-treated or untreated human oligodendrocytes,

160 Furthermore, gemfibrozil treatment also led to the recruitment of PPA

161 Gemfibrozil treatment decreased the number of T-bet-posi

162 Gemfibrozil treatment increased LDL size and lowered num

163 ial (LOCAT), a trial examining the effect of gemfibrozil treatment on progression of atherosclerosis

164 nges in conventional lipid risk factors with gemfibrozil treatment only partially explain the reducti

165 Concentrations of HDL-C achieved with gemfibrozil treatment predicted a significant reduction

166 e and averaged during the first 18 months of gemfibrozil treatment with the combined incidence of non

167 During gemfibrozil treatment, only the increase in HDL-C signif

168 -trans-retinoic acid, alone or together with gemfibrozil, up-regulated TPP1.

169 % vs. 59.3%; P < 0.001), and reductions with gemfibrozil varied by antiretroviral therapy class (44.0

170 on and inhibition of NF-kappaB activation by gemfibrozil via the PI3K pathway suggests that gemfibroz

171 tment with fat restriction, weight loss, and gemfibrozil was continued after hospitalization.

172 More importantly, gemfibrozil was shown to shift the cytokine secretion of

173 of these LDL and HDL particles achieved with gemfibrozil were significant, independent predictors of

174 ing patients with the fibric acid derivative gemfibrozil when the predominant lipid abnormality was l