ライフサイエンスコーパス: simvastatin

1 atients using atorvastatin, pravastatin, and simvastatin.

2 ein in vitro, and this could be prevented by simvastatin.

3 oronary syndrome to simvastatin or ezetimibe/simvastatin.

4 nofibrate plus simvastatin with placebo plus simvastatin.

5 jury and then treated either with or without simvastatin.

6 wo other hydrophobic statins, lovastatin and simvastatin.

7 ezetimibe/simvastatin (E/S) or 40 mg placebo/simvastatin.

8 eatment with the HMG-CoA reductase inhibitor simvastatin.

9 ed with sepsis was assessed with and without simvastatin.

10 coronary syndrome (ACS) compared to placebo/simvastatin.

11 ular protection of calpastatin induction and simvastatin.

12 CR3 ligand-binding I domain in complex with simvastatin.

13 Of note, administration of simvastatin (0.2 mg/kg) did not significantly up-regulat

14 41-0.64), pravastatin (0.40; 0.28-0.58), and simvastatin (0.33; 0.21-0.52) were all significantly ass

15 red mRNA profiles after 24 h incubation with simvastatin (2 microm) or sham buffer.

16 Participants were randomly assigned to simvastatin 20 mg tablets twice-daily plus vitamin D3 1,

17 (not on dialysis) were randomly assigned to simvastatin (20 mg) plus ezetimibe (10 mg) daily or matc

18 d-Pugh class of A or B vs C, to groups given simvastatin (20 mg/d the first 15 days, 40 mg/d thereaft

19 treated with placebo; (2) rats treated with simvastatin (25 mg/kg, orally), given at 3 and 23 hours

20 LPS/saline challenge; (3) rats treated with simvastatin (25 mg/kg/24 h, orally) from 3 days before L

21 roups of six animals received oral saline or simvastatin (3, 10, and 30 mg/kg/day) until sacrifice on

22 Simvastatin (30 mg/kg) increased TAP activity on day 11

23 nts were randomly assigned to receive either simvastatin 40 mg (n=391) or placebo (n=412).

24 Simvastatin 40 mg and atorvastatin 40 mg accounted for 2

25 years of randomized treatment with combined simvastatin 40 mg and ezetimibe 10 mg daily or placebo.

26 We aimed to determine whether simvastatin 40 mg could improve the long-term outcome in

27 e randomly allocated (1:1) to receive either simvastatin 40 mg or placebo once a day for up to 21 day

28 ct of a polypill (containing aspirin 100 mg, simvastatin 40 mg, and ramipril 2.5, 5, or 10 mg) compar

29 rvastatin 20-<40 mg, rosuvastatin 10-<20 mg, simvastatin 40-<80 mg), and 12.9% low-dose statins (ator

30 The combination of simvastatin (40 mg) and ezetimibe (10 mg) (simvastatin-e

31 g) (simvastatin-ezetimibe) was compared with simvastatin (40 mg) and placebo (simvastatin monotherapy

32 training or to exercise in combination with simvastatin (40 mg/day).

33 y, moderate-intensity (atorvastatin [10 mg], simvastatin [40 mg], or rosuvastatin [5 mg]) or high-int

34 Participants were randomized to receive simvastatin (60 mg) or placebo, started on the same day

35 igned patients (1:1 ratio) to receive either simvastatin 80 mg or placebo daily for up to a maximum o

36 Patients received simvastatin 80 mg or placebo enterally for 4 days preope

37 torvastatin 40-80 mg, rosuvastatin 20-40 mg, simvastatin 80 mg), 28.6% moderate-dose statins (atorvas

38 n 40 to 80 mg, rosuvastatin 20 to 40 mg, and simvastatin 80 mg.

39 nth were more likely randomized to ezetimibe/simvastatin (85%), had lower baseline LDL-C values, and

40 Simvastatin after LPS challenge did not prevent the incr

41 tin met dual targets than those treated with simvastatin alone (50% versus 29%, P<0.001).

42 ed in greater LDL-C reductions compared with simvastatin alone at 33 weeks (mean, -54.0% [SD, 1.4%] v

43 nd a study of simvastatin + ezetimibe versus simvastatin alone in 6-month cardiovascular outcomes.

44 MPROVE-IT (ezetimibe plus simvastatin versus simvastatin alone in individuals with cardiovascular dis

45 ter reperfusion, donor treatment either with simvastatin alone or with high dose of methylprednisolon

46 apy with ezetimibe/simvastatin compared with simvastatin alone was associated with a significant redu

47 nd hs-CRP targets than patients treated with simvastatin alone.

48 Simvastatin also decreased burn-induced TNF-alpha and ca

49 Simvastatin, an agent for hypercholesterolemia treatment

50 The present study demonstrates that simvastatin, an antihyperlipidemic drug exhibited broad-

51 a signaling and recent studies revealed that simvastatin, an FDA-approved cholesterol-lowering medica

52 Simvastatin, an HMG-coA reductase inhibitor, is known to

53 -year was similar, as well: 0.63 events with simvastatin and 0.62 events with placebo.

54 ber of ventilator-free days (12.6+/-9.9 with simvastatin and 11.5+/-10.4 with placebo, P=0.21) or day

55 lity was 21.5% (95% CI, 15.4% to 29.1%) with simvastatin and 13.8% (95% CI, 8.8% to 21.0%) with place

56 Fifteen patients received simvastatin and 16 received placebo.

57 540 patients, with 259 patients assigned to simvastatin and 281 to placebo.

58 tween the two groups (5.7 days [SD 5.1] with simvastatin and 6.1 days [5.2] with placebo; mean differ

59 onate pathway, by lipophilic statins such as simvastatin and atorvastatin resulted in a specific inhi

60 patients with initial asymptomatic AS in the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) stud

61 ed LDL-C and hs-CRP targets and outcomes for simvastatin and ezetimibe/simvastatin was prespecified i

62 commonly prescribed statin (73%) followed by simvastatin and lovastatin.

63 Our findings identify a novel activity of simvastatin and mechanism of SASP regulation.

64 estigated the effect of donor treatment with simvastatin and methylprednisolone on microvascular dysf

65 hylprednisolone alone or in combination with simvastatin and methylprednisolone significantly reduced

66 erbations per person-year was similar in the simvastatin and placebo groups: 1.36+/-1.61 exacerbation

67 Using simvastatin and sham incubated lymphoblastoid cell lines

68 lipid composition were similar for high-dose simvastatin and simvastatin/ezetimibe combination therap

69 Simvastatin and tBHQ suppress KLF1 and BCL11 gene expres

70 ere exposed to lovastatin, atorvastatin, and simvastatin and the minimum inhibitory concentrations (M

71 Subjects taking simvastatin and/or ezetimibe were randomized to receive

72 eatment with the HMG-CoA reductase inhibitor simvastatin, and 3) shRNA-mediated knockdown of SREBP2.

73 steady-state warfarin dose, myotoxicity with simvastatin, and certain drug-induced arrhythmias.

74 The mice then were treated with or without simvastatin, and the spleen was harvested to measure the

75 ligand binding kinetics as discriminator for simvastatin antagonism.

76 Simvastatin antagonizes I domain binding to the compleme

77 ion for further investigation of repurposing simvastatin as a topical antibacterial agent to treat sk

78 ions, while enabling assessment of potential simvastatin-associated pleiotropic effects.

79 Simvastatin at a daily dose of 40 mg did not affect exac

80 hin the previous 48 hours to receive enteral simvastatin at a dose of 80 mg or placebo once daily for

81 Simvastatin at its highest doses was associated with cre

82 ATCOPE) as a randomized, controlled trial of simvastatin (at a daily dose of 40 mg) versus placebo, w

83 We found that simvastatin both prevented and reversed depigmentation i

84 compounds including 7-deacetylazadiradione, simvastatin, camptothecin, andrographolide, cinchonine,

85 We confirmed that simvastatin caused the translocation of the small Rho GT

86 f the Cholesterol and Pharmacogenetics (CAP) simvastatin clinical trial, we found that statin-induced

87 ro and in vivo experiments demonstrated that simvastatin combined with tamoxifen increased TamR cell

88 se in day-28 mortality of at least 2.7% with simvastatin compared with placebo after enrollment of th

89 erol (LDL-C)-reducing therapy with ezetimibe/simvastatin compared with simvastatin alone was associat

90 ective of this study is to determine whether simvastatin consumption and hyperlipidemia are associate

91 rations of CDK4/6 and Cyclin D1 triggered by simvastatin could be recovered by PPARgamma-antagonist (

92 Simvastatin decreased burn-induced TNF-alpha and NF-kapp

93 The lipid-lowering drug simvastatin decreases portal pressure, improves hepatoce

94 Here, we show that simvastatin decreases the SASP of senescent human fibrob

95 In contrast, simvastatin did not change Rho-GTP loading in A549 and M

96 Simvastatin did not further decrease burn-caused apoptos

97 optotic hepatocytes in response to burn, and simvastatin did not further decrease hepatocyte apoptosi

98 Simvastatin did not increase survival of patients with C

99 We observed simvastatin did not trigger BCa cell apoptosis, but redu

100 production, suggesting additional effects of simvastatin directly on T cells.

101 the magnitude of the reduction was linked to simvastatin dosage.

102 igher simvastatin doses (by 0.44 mm(2)/10 mg simvastatin dose equivalent; P = .02).

103 .01 mm(2); P = .03) and in those with higher simvastatin doses (by 0.44 mm(2)/10 mg simvastatin dose

104 Simvastatin dramatically reduced damage and enhanced mus

105 2) with ezetimibe/simvastatin versus placebo/simvastatin, driven by a significant 21% reduction in is

106 orrhage should not be treated routinely with simvastatin during the acute stages.

107 125 mg/dL were randomized to 40 mg ezetimibe/simvastatin (E/S) or 40 mg placebo/simvastatin.

108 Simvastatin effectively alleviated bone loss in both ZFR

109 ld mdx mice with severe muscle degeneration, simvastatin enhanced diaphragm force and halved fibrosis

110 Additionally, simvastatin exhibits excellent anti-biofilm activity aga

111 tive trait loci (eQTLs) that interacted with simvastatin exposure, including rs9806699, a cis-eQTL fo

112 tomatic aortic stenosis participating in the Simvastatin Ezetimibe in Aortic Stenosis (SEAS) study.

113 mean of 4.3 years of follow-up in the SEAS (Simvastatin Ezetimibe in Aortic Stenosis) study.

114 We used data from the SEAS trial (Simvastatin Ezetimibe in Aortic Stenosis) to assess what

115 th gastrointestinal bleeding, and a study of simvastatin + ezetimibe versus simvastatin alone in 6-mo

116 rimary end point at 7 years was 32.7% in the simvastatin-ezetimibe group, as compared with 34.7% in t

117 mg per deciliter (1.4 mmol per liter) in the simvastatin-ezetimibe group, as compared with 69.5 mg pe

118 nternational Trial) to examine the impact of simvastatin-ezetimibe versus simvastatin-placebo on card

119 f simvastatin (40 mg) and ezetimibe (10 mg) (simvastatin-ezetimibe) was compared with simvastatin (40

120 n were similar for high-dose simvastatin and simvastatin/ezetimibe combination therapy, but the magni

121 ients in every centre by blocks of ten (five simvastatin, five placebo).

122 ial did not detect any benefit in the use of simvastatin for long-term or short-term outcome in patie

123 the efficacy of the addition of ezetimibe to simvastatin for the prevention of stroke and other adver

124 Treatment with simvastatin from 3 days before LPS prevented the increas

125 e was significantly lower in patients in the simvastatin group (0.288% per year [SD 0.521]) than in t

126 Day-28 mortality was not lower in the simvastatin group (21.2% [95% CI, 15.4% to 28.6%) than i

127 lacebo group died (22%) vs 6 patients in the simvastatin group (9%) (hazard ratio for adding simvasta

128 nts in the placebo group and 22 of 69 in the simvastatin group (P = .423).

129 patients in the placebo group and 25% in the simvastatin group (P = .583).

130 11% in the placebo group vs 8% in the in the simvastatin group (P = .599).

131 patients in the placebo group and 49% in the simvastatin group (P = .752); the percentages of serious

132 30 deaths in the placebo group and 28 in the simvastatin group (P=0.89).

133 The simvastatin group also had a 2.5 points better mean phys

134 in the placebo group and no patients in the simvastatin group although this difference was not stati

135 6 months, we recorded 37 (10%) deaths in the simvastatin group compared with 35 (9%) in the placebo g

136 serious adverse events were reported in the simvastatin group compared with 74 (18%) in the placebo

137 urable outcome, mRS 0-2 (271 patients in the simvastatin group vs 289 in the placebo group).

138 he upper limit of normal (eight [11%] in the simvastatin group vs three [4%] in the placebo group p=0

139 Two patients in the simvastatin group, each with advanced liver disease, dev

140 with no differences between the placebo and simvastatin groups in proportions of participants who ha

141 Simvastatin had a similar effect, but the combination of

142 Importantly, simvastatin has also been reported to have anti-tumor ef

143 m in the pathogenesis of delirium, and since simvastatin has anti-inflammatory properties it might re

144 Simvastatin has been shown to possess potent anti-inflam

145 This study sought to determine if simvastatin impairs exercise training adaptations.

146 Treatment with simvastatin improved alveolar bone loss within all of th

147 Lipid-lowering therapy with ezetimibe plus simvastatin improved clinical outcomes.

148 nfirming in vitro results, high-dose (80-mg) simvastatin improved neutrophil migratory accuracy witho

149 Moreover, simvastatin improved restenosis indicators by suppressin

150 is proof of concept study, pretreatment with simvastatin in esophagectomy decreased biomarkers of inf

151 ezetimibe and simvastatin or to placebo and simvastatin in IMPROVE-IT (Improved Reduction of Outcome

152 poprotein cholesterol therapy with ezetimibe/simvastatin in IMPROVE-IT (IMProved Reduction of Outcome

153 to receive ezetimibe/simvastatin or placebo/simvastatin in IMPROVE-IT.

154 tified a p53(R270H) -specific sensitivity to simvastatin in lung tumors, and the transcriptional sign

155 The addition of ezetimibe to simvastatin in patients stabilized after acute coronary

156 We prospectively studied the efficacy of simvastatin in preventing exacerbations in a large, mult

157 ctive Randomized Placebo-Controlled Trial of Simvastatin in the Prevention of COPD Exacerbations (STA

158 by 9% with ezetimibe/simvastatin vs placebo/simvastatin (incidence-rate ratio [RR]: 0.91; 95% confid

159 Simvastatin induced apoptotic cell death via the intrins

160 over, flow cytometry analysis indicated that simvastatin induced cell cycle arrest at G0/G1 phase, su

161 fferentiating primary human erythroid cells, simvastatin induced HbF alone and additively with tBHQ,

162 Here we show that the MEV cascade inhibitor simvastatin induced significant cell death in a wide ran

163 ults indicate that MEV cascade inhibition by simvastatin induced the intrinsic apoptosis pathway via

164 In all cancer cell types tested, simvastatin-induced cell death was not rescued by choles

165 plicated in adverse drug reactions including simvastatin-induced myopathy and docetaxel-induced neutr

166 Simvastatin-induced Rho-GTP loading significantly increa

167 Simvastatin inhibited 3-hydroxy-3-methyl-glutaryl-CoA re

168 , our study for the first time revealed that simvastatin inhibited bladder cancer cell proliferation

169 This study demonstrated that simvastatin inhibited LPS-induced alveolar bone loss and

170 romolecular synthesis analyses revealed that simvastatin inhibits multiple biosynthetic pathways and

171 Here we show that simvastatin inhibits the proliferation of human leiomyom

172 ipoprotein cholesterol compared with placebo/simvastatin, irrespective of DM (DM: 49 versus 67 mg/dL;

173 Simvastatin is a cholesterol-lowering drug whose pleiotr

174 udy, the findings suggest that the intake of simvastatin is associated with increasing serum OPG conc

175 Simvastatin is currently one of the most common drugs fo

176 s (atorvastatin <20 mg, rosuvastatin <10 mg, simvastatin <40 mg).

177 Based on these data, simvastatin may be a safe, targeted treatment option for

178 Therefore, we hypothesized that simvastatin may be an effective treatment for vitiligo.

179 In conclusion, simvastatin may suppress TamR cell growth by inhibiting

180 More patients treated with ezetimibe/simvastatin met dual targets than those treated with sim

181 icantly more patients treated with ezetimibe/simvastatin met prespecified and exploratory dual LDL-C

182 docrine resistance in breast cancer and that simvastatin might suppress this resistance.

183 We also show that simvastatin mitigates the effects of senescent condition

184 Simvastatin modified surface adhesion molecule expressio

185 e results do not support the hypothesis that simvastatin modifies duration of delirium and coma in cr

186 mpared with simvastatin (40 mg) and placebo (simvastatin monotherapy).

187 etimibe group, as compared with 34.7% in the simvastatin-monotherapy group (absolute risk difference,

188 mg per deciliter (1.8 mmol per liter) in the simvastatin-monotherapy group (P<0.001).

189 nine patients were treated with either 80 mg simvastatin (n=20) or 10 mg simvastatin plus 10 mg ezeti

190 nts were randomly assigned to receive either simvastatin (n=70) or placebo (n=70).

191 were randomly assigned (1:1) to either 80 mg simvastatin (n=70) or placebo (n=70).

192 2 patients were randomly assigned to receive simvastatin (n=71) or placebo (n=71), and were included

193 This study examined the effects of simvastatin on changes in cardiorespiratory fitness and

194 We found evidence of a positive effect of simvastatin on frontal lobe function and a physical qual

195 This study evaluates the effect of simvastatin on rats subjected to experimental periodonta

196 Although we found no effect of simvastatin on the other outcome measures, these potenti

197 ying mechanisms, we determined the effect of simvastatin on tissue inflammation and the expression of

198 t a protective effect of statins--especially simvastatin--on breast cancer recurrence.

199 ronary syndrome were randomized to a placebo/simvastatin or ezetimibe/simvastatin regimen and followe

200 stabilized after acute coronary syndrome to simvastatin or ezetimibe/simvastatin.

201 ck size of eight, to receive either 80 mg of simvastatin or placebo.

202 in patients randomized to receive ezetimibe/simvastatin or placebo/simvastatin in IMPROVE-IT.

203 Finally, oral administration of simvastatin or the antioxidant apocynin reduced aneurysm

204 patients randomized either to ezetimibe and simvastatin or to placebo and simvastatin in IMPROVE-IT

205 no benefit with the addition of ezetimibe to simvastatin (Pint =0.034).

206 e the impact of simvastatin-ezetimibe versus simvastatin-placebo on cardiovascular-related hospitaliz

207 ith either 80 mg simvastatin (n=20) or 10 mg simvastatin plus 10 mg ezetimibe (n=19) for 6 weeks.

208 ] and on-study HR: 1.21 [p = 0.017]) and the simvastatin plus ERN group (baseline HR: 1.25 [p = 0.001

209 Similarly, allocation to simvastatin plus ezetimibe had no significant effect on

210 During 4.8 years of follow-up, allocation to simvastatin plus ezetimibe resulted in an average LDL ch

211 e incidence of ESRD (1057 [33.9%] cases with simvastatin plus ezetimibe versus 1084 [34.6%] cases wit

212 y Lp(a) were predictive of CV events in both simvastatin plus placebo (baseline HR: 1.24 [p = 0.002]

213 y lipoprotein cholesterol were randomized to simvastatin plus placebo or simvastatin, plus extended-r

214 k was to assess efficacy and tolerability of simvastatin plus vitamin D for migraine prevention in ad

215 The results demonstrate that simvastatin plus vitamin D is effective for prevention o

216 Compared to placebo, participants using simvastatin plus vitamin D3 demonstrated a greater decre

217 re randomized to simvastatin plus placebo or simvastatin, plus extended-release niacin ([ERN], 1,500

218 oup (p < 0.05), but decreased by 4.5% in the simvastatin-plus-exercise group (p < 0.05 for group-by-t

219 Therefore, simvastatin possesses antitumor effects that are depende

220 Simvastatin potently stimulated leiomyoma cell apoptosis

221 not inhibition of cholesterol synthesis with simvastatin prevented podocyte injury observed in vitro

222 The present data suggest that simvastatin prevents inflammatory bone resorption in exp

223 Using MPs loaded with simvastatin (pro or active drug) or BMP-2, we have demon

224 Simvastatin protected the spleen from apoptosis, reduced

225 Thus, we hypothesized that simvastatin protects against burn-induced apoptosis in t

226 In static cellular experiments, 15-25 mum simvastatin reduced adhesion by K562 cells expressing re

227 Cdc42 were activated in senescent cells, and simvastatin reduced both activities.

228 Simvastatin reduced expression of iNOS, MMP-1 and -8, RA

229 e first and all recurrent strokes, ezetimibe/simvastatin reduced stroke of any etiology (HR, 0.83; 95

230 High-dose simvastatin reduced the annualised rate of whole-brain a

231 Only high-dose simvastatin reduced the relative proportion of sphingomy

232 Simvastatin reduces burn-induced splenic apoptosis via d

233 Simvastatin reduces mouse hepatocyte apoptosis by suppre

234 Ezetimibe, when added to simvastatin, reduces cardiovascular events after acute c

235 omized to a placebo/simvastatin or ezetimibe/simvastatin regimen and followed for a median of 6 years

236 Simvastatin rescued neutrophil migration with age and du

237 Simvastatin resulted in a significant decrease in plasma

238 In 1 trial (n = 248), ezetimibe with simvastatin resulted in greater LDL-C reductions compare

239 ng alone, but was blunted by the addition of simvastatin resulting in only a 1.5% increase (p < 0.005

240 loaded with the HMG-CoA reductase inhibitor simvastatin [S], were evaluated in the apolipoprotein E-

241 This property appears to assist in simvastatin's ability to suppress production of key MRSA

242 the combination of angiopoietin-2 siRNA and simvastatin showed no additive benefit.

243 ion of molecules for osteoclastogenesis, but simvastatin significantly modulated the stimulation.

244 STAT phase 2 trial, we showed that high-dose simvastatin significantly reduced the annualised rate of

245 In contrast, rosuvastatin and simvastatin significantly reduced total and ABCA1-specif

246 RSA skin infection experiment confirmed that simvastatin significantly reduces the bacterial burden a

247 This study evaluates the effect of a novel simvastatin (SIM) prodrug (capable of delivering high do

248 Simvastatin (SIM), a widely used anti-lipidemic drug, ha

249 tion and bone grafting with or without local simvastatin (SIM).

250 Simvastatin (SMV) is a specific competitive inhibitor of

251 Together, our findings highlight that simvastatin substantially improves the overall health an

252 elial dysfunction that might be prevented by simvastatin, suggesting that statins might have potentia

253 Furthermore, simvastatin suppressed BCa cell metastasis by inhibiting

254 An in vitro study demonstrated that simvastatin suppresses TNF-alpha and caspase-3 expressio

255 Simvastatin targets the metal ion-dependent adhesion sit

256 In adults with suspected VAP, adjunctive simvastatin therapy compared with placebo did not improv

257 Simvastatin therapy did not affect circulating levels of

258 Simvastatin therapy, although safe and associated with m

259 Ezetimibe, when added to simvastatin therapy, reduces cardiovascular events after

260 eated with niacin as an adjunct to intensive simvastatin therapy.

261 event, would also be reduced with ezetimibe/simvastatin therapy.

262 0.31-0.86; P=0.011) with ezetimibe added to simvastatin therapy.

263 n CV death/MI/iCVA at 7 years with ezetimibe/simvastatin, thus translating to a number-needed-to-trea

264 We assessed whether adding simvastatin to standard therapy could reduce rebleeding

265 n a randomized controlled trial, addition of simvastatin to standard therapy did not reduce rebleedin

266 The ability of simvastatin to target CR3 in its ligand binding-activate

267 vastatin group (9%) (hazard ratio for adding simvastatin to therapy = 0.39; 95% confidence interval:

268 , the FAB score was 1.2 points higher in the simvastatin-treated group than in the placebo group (95%

269 end products was significantly lower in the simvastatin-treated group, as was the urine albumin-crea

270 orylation (OXPHOS) capacity were measured in simvastatin-treated patients (n = 10) and in well-matche

271 Simvastatin-treated patients had an impaired glucose tol

272 protein cholesterol levels were lower in the simvastatin-treated patients than in those who received

273 These simvastatin-treated patients were glucose intolerant.

274 es 73 patients divided into three groups: 1) simvastatin-treated patients with hyperlipidemia (n = 29

275 mpared with the normolipidemic patients, the simvastatin-treated patients with hyperlipidemia showed

276 centrations were significantly higher in the simvastatin-treated patients with hyperlipidemia than in

277 y a decreased maximal OXPHOS capacity in the simvastatin-treated patients.

278 Donor simvastatin treatment inhibited allograft microvascular

279 own-regulated in persons taking statins, and simvastatin treatment of C2C12 cells suppressed NEDD4 tr

280 Long-term simvastatin treatment vastly improved overall muscle hea

281 phoblastoid cell lines (LCLs) after in vitro simvastatin treatment, and identified a number of statin

282 from 480 participants of a clinical trial of simvastatin treatment.

283 duals with CKD was shown with ezetimibe plus simvastatin versus placebo.

284 val [CI], 0.73-1.00; P=0.052) with ezetimibe/simvastatin versus placebo/simvastatin, driven by a sign

285 ividuals from the IMPROVE-IT (ezetimibe plus simvastatin versus simvastatin alone in individuals with

286 e significantly reduced by 9% with ezetimibe/simvastatin vs placebo/simvastatin (incidence-rate ratio

287 etemcomitans lipopolysaccharide (LPS), while simvastatin was given to some of the rats via gavage.

288 rhabdomyolysis in patients receiving 40 mg/d simvastatin was higher than expected.

289 9% of statin use); the defined daily dose of simvastatin was lower in cases than in controls (21-40 m

290 s and outcomes for simvastatin and ezetimibe/simvastatin was prespecified in Improved Reduction of Ou

291 Simvastatin was the most commonly prescribed statin (acc

292 Simvastatin was well tolerated, with no differences betw

293 of atorvasatin, fluvastatin, lovastatin, and simvastatin were associated with higher odds of transami

294 dhering monocytes potentiated the effects of simvastatin where only a 50-100 nm concentration of the

295 Synergy with rapamycin was reproduced by simvastatin, whereas combining atorvastatin with cyclosp

296 chemic stroke with E/S compared with placebo/simvastatin, whereas patients without DM at low or moder

297 Simvastatin, which is widely used for treatment of vascu

298 dyslipidemia trial compared fenofibrate plus simvastatin with placebo plus simvastatin.

299 ed to establish whether early treatment with simvastatin would decrease the time that survivors of cr

300 dy tested the hypothesis that treatment with simvastatin would improve clinical outcomes in patients