ライフサイエンスコーパス: randomization

1 ng both observational analysis and Mendelian randomization.

2 A total of 378 patients underwent randomization.

3 A total of 171 patients underwent randomization.

4 atients per group withdrew immediately after randomization.

5 t the patients were receiving at the time of randomization.

6 nd RP-S6K circulating levels using Mendelian Randomization.

7 , were included in a simple sequence without randomization.

8 ortium) type 3 to 5 bleeding at 1 year after randomization.

9 men available for analysis at 6 months after randomization.

10 A total of 240 patients underwent randomization.

11 usally related to depression using Mendelian randomization.

12 trasound was repeated at 6 and 12 weeks post randomization.

13 A total of 61 patients underwent randomization.

14 6 (n = 1,113) and 48 weeks (n = 1,016) after randomization.

15 ian time since diagnosis, 36 days) underwent randomization.

16 A total of 195 participants underwent randomization.

17 was discontinued for a 2-week period before randomization.

18 emoval from the trial, and at 6 months after randomization.

19 l among the first 480 patients who underwent randomization.

20 primary endpoint was PVR at 12 months after randomization.

21 l CT at a mean (+/-SD) of 90+/-15 days after randomization.

22 n the dapagliflozin and placebo groups after randomization.

23 lycaemic traits), using two-sample Mendelian randomization.

24 enterally over the initial 7 days following randomization.

25 semiannually during the first 3 years after randomization.

26 ardial infarction, or stroke at 1 year after randomization.

27 or bias that would have been produced under randomization.

28 t between treatment groups at 6 months after randomization.

29 intensive part B score was 37 (+/-10) before randomization.

30 mean gestational age, 25.9 weeks) underwent randomization.

31 d up at 3, 6, 9, 12, 15, and 18 months after randomization.

32 ndia, Kenya, Nigeria, and Pakistan underwent randomization.

33 tionally and with validation using Mendelian Randomization.

34 %) had had no angina during the month before randomization.

35 as death from any cause within 30 days after randomization.

36 167 infants in the same trial 7 months after randomization.

37 ed statistical significance at 12 days after randomization.

38 zed trial where the hospital was the unit of randomization.

39 l relationships with multivariable Mendelian randomization.

40 an evaluable computed tomography scan after randomization.

41 total motile sperm count) at 6 months after randomization.

42 drugs or atrial fibrillation ablation after randomization.

43 erall survival (OS) from the first or second randomizations.

44 Randomization (1:1) was stratified by site, surgeon, and

45 Among 331 patients who underwent randomization, 109 were assigned to roflumilast 0.3% cre

46 221 of a planned 690 patients had undergone randomization (111 to the thrombectomy group and 110 to

47 1, 2019, a total of 3000 children underwent randomization: 1497 children were assigned to the 3-day

48 A total of 228 women underwent randomization: 152 to the Lactin-V group and 76 to the p

49 A total of 316 patients underwent randomization (154 patients to the intervention group an

50 A total of 309 patients underwent randomization; 154 patients were assigned to the ruxolit

51 ses were based on 328 patients who underwent randomization (164 patients per group); 85.7% of the pat

52 who were receiving no respiratory support at randomization (17.8% vs. 14.0%; rate ratio, 1.19; 95% CI

53 A total of 3604 patients underwent randomization; 1809 patients were assigned to receive ri

54 30, 2017, a total of 4002 children underwent randomization (1999 in the placebo group and 2003 in the

55 rquartile range) of 185 (182-193) days after randomization, 2,492 survivors were surveyed and reporte

56 At 28 days after randomization, 25 of 241 patients (10.4%) in the hydroxy

57 als in 30 countries, 11,330 adults underwent randomization; 2750 were assigned to receive remdesivir,

58 A total of 5522 patients underwent randomization; 2762 were assigned to the colchicine grou

59 one-sample two stage least squares Mendelian randomization (2SLS MR) to show a causal relationship fo

60 A total of 6564 patients underwent randomization; 3286 were assigned to the rivaroxaban gro

61 48 patients were included in the trial after randomization - 375 were assigned to the dexamethasone g

62 After randomization, 411 of 635 (64.7%) patients allocated to

63 Of the 65 patients who underwent randomization, 43 were assigned to receive AK002 and 22

64 f 495 patients with no detectable CMV DNA at randomization, 437 had vital-status data available throu

65 A total of 8851 children underwent randomization: 4418 were assigned to the vitamin D group

66 May 2018, a total of 1049 children underwent randomization; 524 were assigned to the chemoprevention

67 A total of 11,016 patients underwent randomization (5523 in the ticagrelor-aspirin group and

68 A total of 84 participants underwent randomization - 56 were assigned to the golimumab group

69 A total of 1222 patients underwent randomization (608 to the sotagliflozin group and 614 to

70 adults (414 with an appendicolith) underwent randomization; 776 were assigned to receive antibiotics

71 A total of 101 children underwent randomization (78 to the closed-loop group and 23 to the

72 After randomization, 83 participants were assigned to receive

73 Of 140 patients who underwent randomization (85% men; mean [+/-SD] age, 62+/-9 years),

74 e usual care group died within 28 days after randomization (age-adjusted rate ratio, 0.83; 95% confid

75 Here we use Mendelian randomization, an instrumental variables technique, with

76 describe methods for within-family Mendelian randomization analyses and use simulation studies to sho

77 The Mendelian randomization analyses confirmed strong evidence of prev

78 Mendelian randomization analyses demonstrate that reduced FEV(1) i

79 Mendelian randomization analyses did not provide evidence for resi

80 sed as an instrumental variable in Mendelian randomization analyses for homeostatic modeling-derived

81 Mendelian randomization analyses in independent samples support a

82 a imprinted genes, including KCNQ1 Mendelian randomization analyses revealed five loci where placenta

83 everal adverse health outcomes and Mendelian randomization analyses show a genetic association betwee

84 Mendelian randomization analyses show that genetic estimates of de

85 Multivariable Mendelian randomization analyses showed that BMI accounted for nea

86 One-sample Mendelian randomization analyses suggested that the association be

87 Mendelian randomization analyses suggested that triglycerides, int

88 -adjusted regressions and 2-sample Mendelian randomization analyses to assess observational and causa

89 We conducted Mendelian randomization analyses using variants in genes that enco

90 Mendelian randomization analyses were performed to infer phenome-w

91 We conducted Mendelian randomization analyses where genetic variants indexed ex

92 d carried out linear and nonlinear Mendelian randomization analyses.

93 rait locus, and summary data-based mendelian randomization analyses.

94 rongly attenuated in within-family Mendelian randomization analyses.

95 Mendelian randomization analysis did not support a causal effect o

96 Mendelian randomization analysis has recently suggested smoking ma

97 A bidirectional two-sample Mendelian randomization analysis indicated that serum changes of a

98 Mendelian randomization analysis was able to estimate associations

99 expression variations through the Mendelian randomization analysis.

100 tic resonance imaging was completed prior to randomization and 1 month following cessation of treatme

101 Lipoprotein(a) was measured at randomization and 4 and 12 months thereafter.

102 reatic drainage surgery within 6 weeks after randomization and 44 patients randomized to the endoscop

103 patient was already receiving ventilation at randomization and 9.5% otherwise).

104 metabolite (PGIM) excretion were measured at randomization and after 2 weeks, as primary surrogate en

105 Patients and physicians were blinded between randomization and antibiotic discontinuation.

106 he Seattle Angina Questionnaire (SAQ) before randomization and at 1.5, 3, and 6 months and every 6 mo

107 y utilized integrative analysis of Mendelian randomization and colocalization to uncover causal relat

108 isease on peritoneal dialysis (PD) underwent randomization and crossover to either a 2-hour dwell wit

109 and 151 in the placebo group) had undergone randomization and infusion.

110 ant effects that were apparent 28 days after randomization and maintained during long-term follow-up.

111 epidemiological approaches (e.g., mendelian randomization and negative control studies) should be ob

112 ed progression-free survival from the second randomization and overall survival (OS) from the first o

113 Ticagrelor was started immediately after randomization and prasugrel after coronary angiography.

114 A total of 157 patients underwent randomization and received evolocumab (104 patients) or

115 Of the 203 participants who underwent randomization and received treatment, 104 underwent abla

116 riety of trial designs, including individual randomization and several types of cluster randomization

117 cs data analysis approach based on Mendelian randomization and utilized it to search for molecular bi

118 on was the change of the MDS-UPDRS-I between randomization and week 4.

119 A total of 8246 patients underwent randomization and were followed for a mean of 3.5 years.

120 A total of 50 participants underwent randomization and were included in the analyses; 48 part

121 ation class were assessed at baseline (after randomization) and at each follow-up visit.

122 rom pregnancies occurring within 9 months of randomization) and semen quality parameters (sperm conce

123 A total of 710 patients underwent randomization, and 700 were included in the modified int

124 received antibacterial drug therapy prior to randomization, and have severe chest pain at baseline.

125 A total of 5713 participants underwent randomization, and the mean follow-up was 4.6 years.

126 A total of 389 patients underwent randomization, and the modified intention-to-treat popul

127 hole-exome analysis, fine mapping, Mendelian randomization, and transcriptomic data analyses.

128 ss responses to study interventions prior to randomization; and appropriate use of statistics to moni

129 Applying two-sample Mendelian randomization approaches we investigated associations wi

130 thods such as FLAPS should be preferred over randomization approaches.

131 oth common carotid arteries blinded from the randomization arm.

132 plex traits and the suitability of Mendelian randomization as a causal inference strategy for transcr

133 weighted method and multivariable Mendelian randomization as our main analytical approaches.

134 patients, of a projected 600, had undergone randomization at 28 centers.

135 d a cluster randomized controlled trial with randomization at the level of general practices (73 in e

136 Patients were 9-16 months post randomization at the time of interview.

137 th the Seattle Angina Questionnaire (SAQ) at randomization, at months 1.5, 3, and 6, and every 6 mont

138 Substudy participants were enrolled after randomization, at which time ex vivo assays to quantify

139 efit was examined as a function of time from randomization, attenuation of the ICD benefit was observ

140 29) or UT-DSAEK (n = 25) using minimization randomization based on preoperative BSCVA, recipient cen

141 ve mechanical ventilation or oxygen alone at randomization but not among those receiving no respirato

142 of 4 groups according to stratified blocked randomization by age and sperm concentration.

143 ll-balanced, making it unclear whether as-if randomization can be assumed for the instrument.

144 Response-adaptive randomization can eliminate the benefits that randomizat

145 Mendelian randomization confirmed a direct positive effect of incr

146 Despite randomization, demographic differences were apparent bet

147 A Mendelian randomization design was used to investigate genetic and

148 l randomization and several types of cluster randomization designs: parallel-arm, ring vaccination, a

149 At randomization, eGFR was 63+/-19 mL.min(-1).1.73 m(-)2.

150 This unbiased Mendelian Randomization estimate is consistent with a protective c

151 We meta-analyzed Mendelian randomization estimates for regional variants weighted b

152 However, while Mendelian randomization estimates from samples of unrelated indivi

153 ined into multi-allelic models and mendelian randomization estimates representing lifelong inhibition

154 Both Mendelian randomization estimates using unrelated individuals and

155 days for all-cause infections measured from randomization for up to 1 year.

156 s, one should carefully consider the unit of randomization (for example, patient, encounter, clinicia

157 ue imputation (JTI) approach and a Mendelian randomization framework for causal inference, MR-JTI.

158 (99.0%) completed the trial (n = 735 in both randomization groups) and were included in the analysis.

159 We performed a generalized summary Mendelian randomization (GSMR) analysis using summary statistics o

160 of miscarriage with biobank-scale Mendelian randomization, heritability, and genetic correlation ana

161 Mendelian randomization identified a causal relationship between p

162 Randomization in a 1:1:1 ratio to an individualized CRP-

163 Although underpowered, this second randomization in MINDACT did not show any improvement in

164 that only 1 subgroup is randomized) or after randomization (including all subgroups).

165 nally concordant with observed and Mendelian randomization-inferred associations for GP-5, GRN, and M

166 t of BMI on diabetes by using four Mendelian randomization methods, where a total of 76 independent B

167 aintenance medication to study medication at randomization.Methods: Exacerbations and change from bas

168 causal associations with 2-sample Mendelian randomization (MR) accounting for genetic covariation be

169 Mendelian randomization (MR) allows the evaluation of the causal r

170 the UK Biobank population and used Mendelian randomization (MR) analyses using the ~750 000 UK-Bioban

171 and food intake is now possible in Mendelian randomization (MR) analyses.

172 We used these estimates to conduct Mendelian Randomization (MR) analyses.

173 Two-sample Mendelian randomization (MR) analysis estimates a causal effect be

174 Mendelian randomization (MR) analysis identified several metabolit

175 genome-wide analyses, we conducted Mendelian randomization (MR) analysis to examine their relations t

176 performed two-sample bidirectional Mendelian randomization (MR) analysis to prioritize our results.

177 In Mendelian randomization (MR) analysis, variants that exert horizon

178 disease development, we performed Mendelian randomization (MR) analysis.Methods: RNA sequencing was

179 on 225 phenotypes using two-sample Mendelian randomization (MR) and colocalization.

180 Genetic analyses used Mendelian randomization (MR) and data from 394 waist-to-hip ratio

181 rtal maturation and asthma through Mendelian randomization (MR) and explored the joint effect of over

182 (n = 321,047) by using two-sample Mendelian randomization (MR) and then replicated this investigatio

183 sed as instrumental variables in a Mendelian randomization (MR) approach to identify the causal featu

184 tic variation in height within the Mendelian randomization (MR) framework to determine whether height

185 Mendelian randomization (MR) is a valuable tool for detecting caus

186 Mendelian randomization (MR) is an epidemiological technique that

187 Mendelian randomization (MR) is the use of genetic variants as ins

188 yses and 2-sample regression-based Mendelian randomization (MR) mediation analysis were performed to

189 Here, we present a probabilistic Mendelian randomization (MR) method, PMR-Egger, for TWAS applicati

190 analyses, including complementary Mendelian randomization (MR) methods, and secondary alcohol consum

191 One-sample Mendelian randomization (MR) of 17,311 European individuals from t

192 useful tools for causal analyses: Mendelian randomization (MR) studies have provided evidence that e

193 We conducted a Mendelian randomization (MR) study to disentangle the comparative

194 The objective of this two-sample Mendelian randomization (MR) study was to analyze their causal ass

195 d genetic variants is critical for Mendelian randomization (MR) to correctly infer risk factors causi

196 We applied 2-sample Mendelian randomization (MR) to estimate the causal effect of tota

197 We therefore use Mendelian randomization (MR) to evaluate whether obesity and AD ar

198 We used two-sample Mendelian randomization (MR) to examine whether this association i

199 We used Mendelian randomization (MR) to predict the effect of alcohol cons

200 Two-sample Mendelian randomization (MR) was used to infer the causal effects

201 its implemented through two-sample Mendelian randomization (MR), we sought to strengthen the evidence

202 tial of a causal association using Mendelian randomization (MR).

203 Mendelian Randomization (MR-Base) R package was used in the analys

204 omization (SVMR) and multivariable Mendelian randomization (MVMR) to simultaneously assess the indepe

205 The direct randomization (no lead-in) design yielded positive resul

206 Randomization occurred from November 2011 through March

207 Randomization of HPTs was associated with greater cohort

208 this study applies a multivariable Mendelian randomization of intelligence and education.

209 d mouth disease (FMD) outbreaks using simple randomization of locations to premises configurations pr

210 A multivariable Mendelian randomization of schooling years and bipolar disorder re

211 to amorphous coaggregates via entropy-driven randomization of the monomers in the rosette.

212 rative annotation using two-sample Mendelian randomization of these methylation regions highlight pot

213 Of 561 patients who underwent randomization (olanzapine/samidorphan combination, N=280

214 Adults (aged >=18 years) were eligible for randomization on day 5 (+/-1 d) of microbiologically eff

215 When these components are applied after randomization, one must consider expected heterogeneity

216 Measurement generally began at randomization or ICU admission, and lasted from 1 to 30

217 interactions between the MTX and nelarabine randomizations (P = .41).

218 Here we report multivariable Mendelian randomization performed in a two-sample approach using s

219 We used a Mendelian randomization phenome-wide association study (MR-pheWAS)

220 e event rate increased following the 3-month randomization point with biventricular single-site pacin

221 lation, cross-trait meta-analysis, Mendelian randomization, polygenic risk score, and functional anal

222 gs were generally mild and tended to peak at randomization, possibly contributing to the lack of bene

223 tatistically significant improvement in post-randomization progression-free survival compared with in

224 f 4 treatment combinations using an adaptive randomization protocol.

225 Response-adaptive randomization (RAR) has recently gained popularity in cl

226 omen in UF-1 and 378 women in UF-2 underwent randomization, received elagolix or placebo, and were in

227 to -0.02), which in multivariable Mendelian randomization remained stable after adjustments for LDL-

228 ut implementation and ensure that continuing randomization remains justified.

229 Mendelian randomization reveals stronger instrumental estimates of

230 apid recruitment of participants; use of pre-randomization run-in periods to improve participant adhe

231 Sixteen weeks after randomization, sacubitril/valsartan decreased tissue inh

232 the modified Rankin scale at 6 months after randomization; scores range from 0 (no symptoms) to 6 (d

233 The computer-generated randomization sequence was stratified by center on cT an

234 up for decision support, should occur before randomization (so that only 1 subgroup is randomized) or

235 and longer-term benefits based on Mendelian randomization studies (model B).

236 ays for hypertension identified in Mendelian randomization studies and highlight the opportunities fo

237 Mendelian randomization studies and randomized trials have conclus

238 ormal testing of this interaction (Mendelian randomization studies assessing whether T2D is causal fo

239 Estimates from Mendelian randomization studies of unrelated individuals can be bi

240 lifespan was further supported by Mendelian randomization studies.

241 structure and familial effects in Mendelian randomization studies.

242 ta-analysis of this and a previous Mendelian randomization study (OR 1.08; 95% CI 1.02, 1.14; P = 0.0

243 We conducted a two-sample Mendelian randomization study to investigate the associations of P

244 We conducted a two-sample Mendelian randomization study to investigate the causal associatio

245 Mendelian randomization suggested causal association of increasing

246 Mendelian randomization suggested causal effects on liability to P

247 Multivariable Mendelian randomization suggested possible inverse effects of elev

248 Mendelian randomization suggests benefits of long-term increased t

249 Mendelian randomization suggests our top healthful dietary pattern

250 Mendelian randomization supports a stronger causal relationship of

251 conducted 2-sample single-variable Mendelian randomization (SVMR) and multivariable Mendelian randomi

252 andomization can eliminate the benefits that randomization, the most powerful tool in clinical trials

253 At 12 months after randomization, the primary endpoint was met in 6 (12%) D

254 comes and 3 composite ischemic outcomes from randomization through 30 days and from 30 days to 6 mont

255 24 months in a phase III clinical trial with randomization to 2 drug dosages (0.5 mg and 2.0 mg ranib

256 risk of bleeding and ischemic outcomes from randomization to 30 days and from 30 days to 6 months.

257 From randomization to 30 days, aspirin caused more severe ble

258 oral capsules providing 1.2 g/d of DHA from randomization to 36 weeks' postmenstrual age and 229 mot

259 ons for any reason or death from the time of randomization to 6 months after discharge.

260 th placebo, did not affect survival, whereas randomization to an ICD significantly decreased all-caus

261 We used cluster randomization to assign, according to school, students i

262 We used 2-sample Mendelian randomization to consider the impact of birthweight on i

263 eatment and change in diuretic therapy after randomization to dapagliflozin or placebo.

264 of age) depressed children before and after randomization to either 18 weeks of Parent-Child Interac

265 We then used mendelian randomization to examine the causal effects of blood pre

266 d with plasma proteins followed by Mendelian randomization to infer causal relations of proteins for

267 We applied summary-data-based Mendelian randomization to integrate ADHD and ASD GWAS data with f

268 Can clinical trials that utilize individual randomization to intervention and comparison be successf

269 bsequently used summary-data-based Mendelian randomization to investigate if the same variant influen

270 The relationship between randomization to liraglutide and WRF was evaluated using

271 58) and weight (0.61 vs 0.82; P = .453) from randomization to month 36 were comparable, whereas growt

272 Randomization to nicotine e-cigarettes (n = 128), nonnic

273 Randomization to once-daily netarsudil 0.02%/latanoprost

274 older patients with cardiovascular disease, randomization to ramipril had no impact on the incidence

275 velopment and promulgation of tools to apply randomization to real-world data are needed to build the

276 The time from randomization to resolution of stromal keratitis and uve

277 ned to undergo surgery, the median time from randomization to surgery was 3.1 weeks; of the 64 patien

278 ystem blockade that had been adjusted before randomization to the maximum dose on the manufacturer's

279 bout contamination of an intervention across randomization units within clusters (for example, patien

280 was the number of ventilator-free days from randomization until day 28.

281 Randomization used minimization to balance age, sex, FEV

282 We also performed Mendelian randomization using 8 genetic variants associated with c

283 Two-sample Mendelian randomization using TSH index variants as instrumental v

284 imary endpoint was thrombus size at the post-randomization visit with platelet reactivity following s

285 es/mL, and median time from symptom onset to randomization was 3 days.

286 The median duration of symptoms prior to randomization was 5 days (interquartile range [IQR], 3 t

287 Average time from PCI to randomization was 5.4 years (SD, 4.4) and follow-up was

288 The median age of the patients at randomization was 67.8 years.

289 Randomization was not required.

290 Randomization was stratified according to disease severi

291 Randomization was stratified by country.

292 Randomization was stratified by site and intended infert

293 Two-sample Mendelian randomization was then used to validate potentially caus

294 Using two-sample Mendelian randomization we analysed the association of genetically

295 ing of licensed medications: using Mendelian randomization, we found evidence that low expression of

296 Using the framework of 2-sample Mendelian randomization, we found that a 1-SD genetic elevation of

297 station, genetic correlations and Mendelian randomization, we show that there is a substantial genet

298 Additionally, using Mendelian randomization, we were able to identify causal relations

299 Summary data for 2-sample Mendelian randomization were obtained from genome-wide association

300 d call for a broader use of outcome-adaptive randomization when designing clinical trials to test mul