ライフサイエンスコーパス: FDR

1 FDR is related to the proportion of true relationships a

2 = -0.28; 95%CI, -0.43 to -0.13; P = 0.0003; FDR = 0.004).

3 131.7 +/- 17.8 vs 108.7 +/- 19.7, p = 0.0004 FDR-corrected).

4 ge's g = 0.60; 95%CI, 0.26-0.94; P = 0.0006; FDR = 0.004) only in responders, and responders showed s

5 th participants with lower HbA1c (P < 0.001, FDR = 0.00016).

6 ed enrichment score (NES) = 2.01, P = 0.001, FDR P = 0.005], and cholesteryl esters (NES = -1.77, P =

7 cholesteryl esters (NES = -1.77, P = 0.005, FDR P = 0.02), and phosphatidylcholines (NES = -1.72, P

8 rs, 75.8 +/- 7.9 vs 68.8 +/- 12.0, p = 0.043 FDR-corrected) and changes from one meta-state to anothe

9 es, 77.1 +/- 7.3 vs 71.2 +/- 11.0, p = 0.043 FDR-corrected) than beginner chess players.

10 ed genes (>=2.0-fold change, p-value < 0.05, FDR <0.05).

11 ferentially expressed genes (DEG) (p < 0.05, FDR <0.1, fold change >2) between the BRSV challenged an

12 d) and cortical thinning (W-score, p < 0.05, FDR-corrected) than typical CADASIL patients.

13 ificantly differed between groups (P < 0.05; FDR < 0.07), and performed well as CSF biomarkers (ROC >

14 tandardized coefficients = -0.111 to -0.068, FDR corrected P values < 0.039) and were significantly n

15 RAP-MTHFR-NPPA/B gene locus on chromosome 1 (FDR = 1.3E-04), with additional probes on chromosomes 2,

16 ed the number of data points by 30-50% at 1% FDR, and thus decreased missing data.

17 2,052 unique residue pair cross-links at 1% FDR.

18 ing at least one putative aneuploid cell (1% FDR).

19 188 O-glycopeptide spectra reported under 1% FDR.

20 APA quantitative trait loci (apaQTLs) at 10% FDR, of which 152 were nuclear specific.

21 ant druggable genes outside the MHC, and 128 FDR-significant biological pathways related to neurons,

22 sional AD, vs healthy skin (fold-change >=2, FDR <0.05), with 100% sample recovery.

23 oderate-high correlation with ACE2 (r > 0.3, FDR < 0.05) had known interactions with existing drug co

24 he 304 independent variants associated at 5% FDR in this study explain 21.2% of CAD heritability and

25 ng increased the number of residue pairs (5% FDR) by 33% (n = 108 to n = 144).

26 Eleven of them replicate (5% FDR) in five independent longevity studies combined; all

27 on our previous list of loci meeting the 5% FDR threshold, thus providing strong support that the re

28 temporal lobe (beta=0.66-0.76, t=3.90-5.58, FDR-corrected p (p(FDR))=<0.001-0.002) and orbitofrontal

29 of drug response (concordance index > 0.60; FDR < 0.05).

30 qPCR validation rate of 90% for DECs with a FDR of < 5%.

31 the voom transformation in term of accuracy, FDR, and FNR.

32 n was shown between Lachnospira and acetate (FDR-corrected P = 0.002) or butyrate (FDR-corrected P =

33 oduction, and beta oxidation of fatty acids (FDR < 0.1) that differed between diets, with more favora

34 Recently, many covariate-adaptive FDR control methods have been developed, but application

35 e the performance of five covariate-adaptive FDR control methods with EWAS-related covariates using s

36 Covariate-adaptive FDR control methods with informative covariates can sign

37 pregnancy and direct exposure in adulthood (FDR < 10%)-these differences were largely driven by pren

38 For people with 1 affected FDR (92% of those with a family history), screening ever

39 perspective, individuals with more affected FDRs should start screening earlier and at shorter inter

40 For each number of affected FDRs, we used the Microsimulation Screening Analysis mod

41 od not only detected the reported SNPs after FDR adjustment but also discovered a novel BiPN-associat

42 the literature failed to identify SNPs after FDR adjustment.

43 e levels of 9 taxa predicted FPG change (all FDR <0.05), among which Stomatobaculum sp oral taxon 097

44 55; 95% CI 0.37-0.83) lower risk of GDM (all FDR-corrected P values < 0.05).

45 10%, 25%, 50%, and 70%, respectively, of all FDR, SDR, and TDR were tested for familial mutations.

46 mated to be causal (gamma = 0.005) giving an FDR in preclinical research of 92.6%, which likely makes

47 dges, which consisted of 50 clusters with an FDR threshold at 0.05.

48 evotella (FDR p-value = 0.03), Anaerococcus (FDR p-value = 0.07), and Dialister (FDR p-value = 0.09)

49 FDR < 0.05) and Regions (DMRs; >= 5-CpGs and FDR < 0.05) for asthma (285-CpGs), FeNO (8,372-CpGs; 191

50 HIV was also associated (FDR corrected p < 0.05) with higher plasma levels of inf

51 ine-guanine dinucleotide regions associated (FDR-P < 0.05) with the Matsuda index, S(I), and BMI, res

52 We found a significant association (FDR p < 0.05) of the CTD subset with 62 common variants

53 At FDR adjusted p-value < 0.05, 29 genes were differentiall

54 nt, revealed 473 DEG at p < 0.05 but none at FDR < 0.05, suggesting that DKK1 did not strongly modify

55 classes were associated with risk overall at FDR <= 0.20.

56 associated with perfluorooctanoate (PFOA) at FDR < 0.05.

57 ciated with the LV mass genetic predictor at FDR q < 0.05.

58 ith high tumor (18)F-fluorocholine uptake at FDR q < 0.05, including those from three different clini

59 ites differently-methylated in BCVY vs. BCO (FDR < 0.05; beta-value difference +/- 0.1).

60 FC > 1.5) in CD patients and controls before FDR correction and 4 after.

61 q-value procedure and also result in better FDR control and higher stability than Storey's q-value p

62 prostate cancer and show that the bootstrap FDRs are highly useful in selecting the most robust patt

63 etate (FDR-corrected P = 0.002) or butyrate (FDR-corrected P = 0.005).

64 Significant gene sets were enumerated by FDR based on phenotype permutation.

65 upport that the remaining loci identified by FDR represent genuine signals.

66 s associated with different types of cancer (FDR < 0.05).

67 enes were associated with smoking-cessation (FDR < 0.05, FC >=1.7) with a majority of the changes occ

68 ed transcripts with at least twofold change (FDR corrected p < 0.05) in needle tissues in response to

69 ve covariate provide advantages over classic FDR-controlling procedures, with the relative gain depen

70 While classic FDR methods use only p values as input, more modern FDR

71 h using a combination of RES and conditional FDR improved power of traditional GWAS for gene discover

72 evaluate genetic pleiotropy and conditional FDR to identify novel FTD-associated SNPs.

73 sk loci and 1 novel SCZ locus at conditional FDR < .01.

74 the five SNPs, all identified by conditional FDR, were replicated (P < 0.05) in an independent sample

75 notably four additional SNPs by conditional FDR.

76 ignificant SNPs were identified (conditional FDR < 0.05).

77 ndependent ADHD-associated loci (conditional FDR < 0.01), of which 30 were shared between ADHD and ed

78 Here, SNP's conditional FDR was estimated given its RES based on SNP prior infor

79 his cross-trait enrichment using conditional FDR analysis and identified 9 novel PD risk loci and 1 n

80 associated with PD and SCZ at conjunctional FDR < .05.

81 th both BD and intelligence at conjunctional FDR < 0.01.

82 nment or general intelligence (conjunctional FDR < 0.01) and 46 were novel risk loci for ADHD.

83 mple sizes while PairedFB is able to control FDR close to the nominal levels.

84 iologically significant DEGs with controlled FDR.

85 m-onset preHD cohort compared with controls (FDR<0.0001, =0.01, and =0.03, respectively).

86 after false discovery rate (FDR) correction (FDR < 0.05).

87 t hoc false-discovery rate (FDR) correction (FDR-corrected P values > 0.05).

88 ind multiple differentially methylated CpGs (FDR < 0.05) and Regions (DMRs; >= 5-CpGs and FDR < 0.05)

89 G sites (22,272 out of studied 437,022 CpGs, FDR < 0.05).

90 coprotein (FDR = 3.08 x 10(-13)) and hs-CRP (FDR = 2.44 x 10(-3))), and an increase in functionally i

91 re identified within the T1 + T2-FLAIR data (FDR corrected, p < 0.05).

92 bolite-signal match score and a target-decoy FDR estimate for spatial metabolomics.

93 st-degree family history of type 1 diabetes (FDR children) than in children in the general population

94 ococcus (FDR p-value = 0.07), and Dialister (FDR p-value = 0.09) were detected at higher relative abu

95 .14 x 10-5), aminoacylase-1 (ACY1, Discovery FDR-corrected p = 1.86 x 10-3, Replication FDR-corrected

96 and growth hormone receptor (GHR, Discovery FDR-corrected p = 3.49 x 10-4, Replication FDR-corrected

97 = 1.03 x 10-4), osteomodulin (OMD, Discovery FDR-corrected p = 2.14 x 10-2, Replication FDR-corrected

98 We identify 90 genes enriched for DNMs (FDR 5%; e.g., GABRG2 and UIMC1); of which, 61 reach FWER

99 cantly associated with response to 51 drugs (FDR < 0.05).

100 At an empirical FDR of 5%, 48 genes were associated with asthma risk.

101 creased pro-inflammatory Enterobacteriaceae (FDR-corrected P = 0.25).

102 erentially expressed between these entities (FDR < 0.05).

103 hes (DFAs) have been widely used to estimate FDR.

104 chromosome 8p was excluded before estimating FDR due to long-range LD structure.

105 trols the FDR through the posterior expected FDR.

106 ssociation with parental Holocaust exposure (FDR-adjusted p < 0.05); most of these genes were downreg

107 showed significant differential expression (FDR < 10%).

108 The test data set validated these findings (FDR < 0.05).

109 We introduce a new decoy-free framework for FDR estimation that generalizes present DFAs while explo

110 locations, pre-selected via traditional FWER/FDR methods in a 2-stage analysis.

111 late the 748 differentially expressed genes (FDR < 0.01) that were mainly enriched into mitochondrial

112 dentified 16 differentially expressed genes (FDR < 0.05) and numerous genes that co-varied with behav

113 23 oxidative phosphorylation-related genes (FDR <10%).

114 sal impact on gene expression (~ 2300 genes; FDR < 0.05, logFC > 1.5), but only modestly impacted PPA

115 test to select oscillatory genes at a given FDR threshold.

116 mation (e.g., as alpha(1)-acid glycoprotein (FDR = 3.08 x 10(-13)) and hs-CRP (FDR = 2.44 x 10(-3))),

117 ing, and metabolism for 10 mg/L LCO at 48 h (FDR-adjusted, p < 0.1).

118 Imbalance) test(1) to call out 1680 haQTLs (FDR, 10%).

119 in patients with MDD and suicidal ideation (FDR-adjusted p < 0.05).

120 ed upon sequence reversal for identification FDR estimation and further multiplied by performing in s

121 and PARD3B), 3 novel genes were identified (FDR q < 0.05), including the non-coding RNAs ENTPD3-AS1,

122 ple sizes, the Bon-EV procedure has improved FDR control and stability compared with the Storey's q-v

123 ociated with an average increase of 0.020 in FDR (p = 2.545E-04).

124 a novel risk gene, BTNL2, was identified in FDR children compared with GP children.

125 sing incrementally in GP children but not in FDR children.

126 ore, projectors attenuated heroin seeking in FDR rats.

127 found 30 CRMs with enriched SNVs and indels (FDR < 0.05).

128 In contrast, DESeq2 often had inflated FDR; MetagenomeSeq generally had the lowest sensitivity.

129 t competing methods can have highly inflated FDR for small to moderate sample sizes while PairedFB is

130 boost in power with the annotation-informed FDR method, and provide insight into the genetic archite

131 nymous variants associated with QT interval (FDR 5%), 22 of which were in TTN.

132 taining G-protein coupled receptor 6 (LGR6) (FDR = 0.0002).

133 At the end of our follow-up, by limiting FDR-corrected p < 0.05, regression analyses revealed 180

134 ROCker typically showed 60-fold lower FDR when compared to the common practice of using fixed

135 power, marginal type I error rate, marginal FDR, and false discovery cost (FDC).

136 differences in other brain imaging measures (FDR >0.16).

137 density lipoprotein -associated metabolites (FDR < 0.05).

138 Modern FDR methods that use an informative covariate provide ad

139 hods use only p values as input, more modern FDR methods have been shown to increase power by incorpo

140 nd ease of use of two classic and six modern FDR-controlling methods by performing a systematic bench

141 , we find that the improvement of the modern FDR methods over the classic methods increases with the

142 are (MAF < 0.01%) gene-disruptive mutations (FDR 5%), six of which reach family-wise error rate (FWER

143 relatives (FDRs) from autoantibody-negative FDRs and persisted through clinical diagnosis; late feat

144 We propose a new FDR control procedure that incorporates the prior struct

145 h Ghanaian RVV responders and nonresponders (FDR, 0.008 vs 0.003) and Dutch infants and Ghanaian nonr

146 nt between RVV responders and nonresponders (FDR, 0.12), and Ghanaian responders were more similar to

147 nd Dutch infants and Ghanaian nonresponders (FDR, 0.002 vs 0.009).

148 dividuals closer to expected clinical onset (FDR <0.0001).

149 ts 23.6 years (SD 5.8) from predicted onset (FDR 0.22-0.87 for cognitive measures, 0.31-0.91 for neur

150 closely related to predicted years to onset (FDR=0.54).

151 with depression-PRS (beta: 0.014 to 0.180, p(FDR): 0.049 to 1.28 x 10(-14)) and we find a significant

152 ontal cortex (beta=0.51-0.57, t=3.53-4.30, p(FDR)=0.001-0.004).

153 tter microstructure (beta: 0.125 to 0.868, p(FDR) < 0.043).

154 ing features (sCCA r range: 0.30-0.65, all P(FDR) < 0.001).

155 Twenty associations P(FDR) < 0.05 were detected between lipidomic features and

156 < 0.05, SBC = -0.32), left fusiform gyrus (P(FDR) < 0.01, SBC = -0.51).

157 a=0.66-0.76, t=3.90-5.58, FDR-corrected p (p(FDR))=<0.001-0.002) and orbitofrontal cortex (beta=0.51-

158 One CpG passed FDR <5% in the Indian cohort, but overall effect sizes w

159 significantly enriched biological pathways (FDR corrected p-value < 0.05), of which 38 pathways were

160 ninety-seven differential acetylation peaks (FDR [false discovery rate], 5%) pointed to pathways alte

161 group testing and regression, Porphyromonas (FDR p-value = 0.02), Prevotella (FDR p-value = 0.03), An

162 nsitivity, specificity, accuracy, precision, FDR, and F(1).

163 thematical relationships between preclinical FDR and drug development success rates, and estimated im

164 phyromonas (FDR p-value = 0.02), Prevotella (FDR p-value = 0.03), Anaerococcus (FDR p-value = 0.07),

165 nitric oxide synthase and IL-17C) products (FDR < 0.05).

166 ompared to trypsin (8363 vs 6807; 1% protein FDR).

167 ntly downregulated in both AD and psoriasis (FDR < 0.05).

168 In doing so, quantitative trait loci (QTL) (FDR<0.01) increased by an average of 1.62-fold.

169 49 genomic regions at a false dicovery rate (FDR) < 0.05 threshold and prioritize genes at 31, with f

170 y controls and LC at a False Discovery Rate (FDR) < 0.01.

171 s) were evaluated at a false discovery rate (FDR) < 0.05 and differentially methylated regions (DMRs)

172 cant pathways for BMD [false discovery rate (FDR) < 0.05], such as KEGG FOCAL ADHESION and KEGG AXON

173 tween diets at day 28 [false discovery rate (FDR) < 0.05].

174 1801133 x tHcy levels [false-discovery rate (FDR) < 0.05].

175 ed in CRC metagenomes (false discovery rate (FDR) < 1 x 10(-5)).

176 rgets (eGenes), with a false discovery rate (FDR) < 5%.

177 t cis-regulated genes (false discovery rate (FDR) </= 0.05), 2,743 (12%) showed context-dependent eQT

178 significant SNPs with false discovery rate (FDR) </=0.05 were mapped to one novel gene PRPF6 and two

179 ntervention group, all false discovery rate (FDR) <5%], the majority mapping to ESM1, which also repr

180 guanine (dmCpG) sites (false discovery rate (FDR) <= 0.05), respectively, in the infant's cord blood

181 erythritol [P < 0.001, false discovery rate (FDR) = 0.0435], and the targeted assay revealed 15-fold

182 nificantly associated [false discovery rate (FDR) [Formula: see text]] with prenatal [Formula: see te

183 od for controlling the false discovery rate (FDR) [Formula: see text]].

184 adjustment and (iii) a false discovery rate (FDR) adjustment which is widely used in transcriptome st

185 ROC) curve to minimize false discovery rate (FDR) and calculate the best thresholds based on how simu

186 ing better controls of false discovery rate (FDR) and higher sensitivity.

187 (Delta(beta)), target false discovery rate (FDR) and the number of simulated data sets, and have the

188 ditional/conjunctional false discovery rate (FDR) approach to evaluate overlap in common genetic vari

189 med Bon-EV, to control false discovery rate (FDR) based on Bonferroni's approach.

190 False discovery rate (FDR) control has been widely used for multiple testing c

191 in literature that the false discovery rate (FDR) control of some popular methods has been problemati

192 ing procedures such as false discovery rate (FDR) control, methods that take into account the phyloge

193 network structure with false discovery rate (FDR) control.

194 ost popular method for false discovery rate (FDR) control.

195 (n = 54) had evidence (false discovery rate (FDR) corrected p < 0.05) of metabolic stress, including

196 with urinary As after false discovery rate (FDR) correction (FDR < 0.05).

197 persist after post hoc false-discovery rate (FDR) correction (FDR-corrected P values > 0.05).

198 ethods to estimate the false discovery rate (FDR) for 70 public metabolomics data sets.

199 The false discovery rate (FDR) from the target-decoy database search is typically

200 thods that control the false discovery rate (FDR) have emerged as popular and powerful tools for erro

201 ries while controlling false discovery rate (FDR) in extensive experiments.

202 n disease and the high false discovery rate (FDR) in preclinical science.

203 me with spectrum-level false discovery rate (FDR) less than 1%.

204 nsitivity of 90% and a false discovery rate (FDR) of 3%, surpassing the performance of expression-bas

205 of putative loci at a false discovery rate (FDR) of 5% (refs.

206 Accurate estimation of false discovery rate (FDR) of spectral identification is a central problem in

207 The false discovery rate (FDR) of the identification results was controlled and va

208 compared with the PD [false discovery rate (FDR) P < 0.05].

209 (2.0-fold or higher) (false discovery rate (FDR) p <= 0.05), multiple CpGs were p < 5 x 10(-8) with

210 ditional/conjunctional false discovery rate (FDR) statistical framework that increases power of disco

211 ants selected at a 20% false discovery rate (FDR) threshold, the minor allele of rs10508884, which is

212 phenotypes using a 5% false discovery rate (FDR) threshold.

213 We used conjunction false discovery rate (FDR) to evaluate genetic pleiotropy and conditional FDR

214 rms of sensitivity and false discovery rate (FDR) using real data and simulated data.

215 de significance level [false discovery rate (FDR)<0.05].

216 axon, (c) controls the False Discovery Rate (FDR), (d) maintains adequate power, and (e) is computati

217 ating stratum-specific false discovery rate (FDR), where strata are classified according to enrichmen

218 method for estimating false discovery rate (FDR), which is a conventional significance measure in th

219 comparisons using the false discovery rate (FDR), with FDR <0.05 deemed a significant result.

220 pySM, a framework for false discovery rate (FDR)-controlled metabolite annotation at the level of th

221 At a false discovery rate (FDR)-corrected level of 0.05, we found 6 differentially

222 producer Lachnospira [false-discovery rate (FDR)-corrected P = 0.25] but decreased pro-inflammatory

223 ly controls the weaker false discovery rate (FDR).

224 (RES) and conditional false discovery rate (FDR).

225 t Bayes factor at a 5% false discovery rate (FDR).

226 significance, such as False Discovery Rate (FDR).

227 g adjustment using the false discovery rate (FDR).

228 ltiple comparisons via false discovery rate (FDR).

229 ts do not preserve the false discovery rate (FDR).

230 cance was based on the false discovery rate (FDR; <0.05) or a Bonferroni-corrected P value of 1 x 10(

231 ferentially expressed (false-discovery rate [FDR] < 0.01).

232 ely (fold change >= 2; false discovery rate [FDR] < 0.05).

233 of 3,857 transcripts (false discovery rate [FDR] <= 0.1 and absolute fold change [FC] expression >=

234 1.06-1.27, P < 0.001, false discovery rate [FDR] = 0.008) but not at 24 or 36 months.

235 provement index (>30%; false discovery rate [FDR] corrected p < 0.0008) and nontrained WM tests after

236 mer and winter births (False Discovery Rate [FDR] q < .05); among these, BHLHE40, MIR210HG, and HILPD

237 the Benjamini-Hochberg false discovery rate [FDR] showed that 18 miRNAs were significantly altered (1

238 nd beta-casein (P<.01, false discovery rate [FDR]<.1).

239 tment for confounders (false-discovery rate [FDR], < 0.10).

240 rotein (BSP, Discovery false discovery rate [FDR]-corrected p = 2.82 x 10-2, Replication FDR-correcte

241 ns for 82 transcripts (false discovery rate [FDR]-P < 0.05).

242 in visceral fat mass (false discovery rate, FDR < 2.0 x 10(-16)), accompanied by anti-atherogenic ef

243 njamini-Hochberg (BH) false discovery rates (FDR) approach was applied to control alpha error due to

244 ds for estimating the false discovery rates (FDR) of these annotations.

245 BA-to-glutamate and GABA-to-glutamine ratio (FDR-p < 0.05).

246 first-, second-, and third-degree relatives (FDR, SDR, TDR, respectively), family size, prevalence of

247 ody-positive at-risk first-degree relatives (FDRs) from autoantibody-negative FDRs and persisted thro

248 d number of affected first-degree relatives (FDRs) using data from publications.

249 [FDR]-corrected p = 2.82 x 10-2, Replication FDR-corrected p = 1.03 x 10-4), osteomodulin (OMD, Disco

250 y FDR-corrected p = 2.14 x 10-2, Replication FDR-corrected p = 9.14 x 10-5), aminoacylase-1 (ACY1, Di

251 y FDR-corrected p = 1.86 x 10-3, Replication FDR-corrected p = 2.18 x 10-2), and growth hormone recep

252 y FDR-corrected p = 3.49 x 10-4, Replication FDR-corrected p = 2.97 x 10-3).

253 riglycerides and birth weight, respectively (FDR < 0.1).

254 154 and 2863 genes that were TH-responsive (FDR < 0.05) in the tilapia cerebellum, thalamus-pituitar

255 d access to food) or mildly food-restricted (FDR).

256 between CF and healthy control (HC) samples (FDR < 0.05, log2 FC>=2).

257 types are associated with either age or sex (FDR < 0.1).

258 hway analysis, we identified 39 significant (FDR < 0.05) genes and 127 significantly (FDR < 0.05) enr

259 plasma glycome map revealed 796 significant (FDR < 0.05) site-specific inter-protein and intra-protei

260 RNA sequencing identified five significant (FDR<0.01) and seven trending (0.01FDR<0.02) gene sets re

261 were identified using the genes significant (FDR < 0.05) in at least one comparison of each patient r

262 ; miR-511-5p, miR-483-5p showed significant (FDR corrected; p < 0.05) differential regulation in the

263 se enrichment was statistically significant (FDR < 5%) after conditioning on all genes and 75 known f

264 nt (FDR < 0.05) genes and 127 significantly (FDR < 0.05) enriched gene sets, which were missed by our

265 1646 genes changed expression significantly (FDR > 0.05) in the resistant strain, the majority of whi

266 ad differential methylation at 29 CpG sites (FDR < 10%).

267 airway epithelial cells to cigarette smoke (FDR < 0.05).

268 ane were significantly associated with sPTB (FDR < 0.05) in the Cork subset.

269 although these associations did not survive FDR adjustment.

270 o the T1-only data where no regions survived FDR correction.

271 significantly enriched for microRNA targets (FDR < 5%).

272 nt AF after correction for multiple testing (FDR < 0.05).

273 The FDR estimation methods presented will enable a user to a

274 eases power of discovery by conditioning the FDR on overlapping associations.

275 by a totally different method to control the FDR at the spectrum, peptide, and protein levels, while

276 oposed the first procedures that control the FDR for online hypothesis testing.

277 simulations indicate the LDM controlled the FDR well.

278 ated bacterial species while controlling the FDR at desired levels.

279 ting for multiple testing by controlling the FDR, and a connection to distance-based ordination.

280 of methods are successful at controlling the FDR, with the exception of two modern methods under cert

281 eatment effects among pairs and controls the FDR through the posterior expected FDR.

282 We estimated the FDR in preclinical science, its effect on drug developme

283 ion for genetic enrichment, the risks in the FDR and GP children converged but were not identical for

284 l validation is not possible, minimising the FDR and improving specificity may be a preferable trade-

285 (UKBB) data to evaluate the validity of the FDR approach.

286 An alternative approach to the FDR can be useful for further evaluating the confidence

287 It has been demonstrated that the FDRs in top-down proteomics can be drastically underesti

288 However, traditional FDR control methods do not use auxiliary covariates, and

289 vements after adaptive WMT (Global: training FDR corrected, p = 0.004), and only HIV participants imp

290 antitative trait loci (eQTL; <1 Mb from TSS, FDR < 1%).

291 NP was detected by analyses of unconditional FDR and traditional GWAS in the discovery sample (N = 59

292 s a random variable and it may underestimate FDR in practice.

293 An underestimated FDR can lead to unexpected false discoveries in the foll

294 nd 10 nutrients independently linked to VFM (FDR < 5%).

295 cohort had slightly smaller putamen volumes (FDR=0.03), but this did not appear to be closely related

296 predicting glucocorticoid dose of >0.9 with FDR adjusted P values in the range 3.3 E-04 -1.9 E-10.

297 cific analyses, we identified more CpGs with FDR<0.05 among female infants (n=38) than among male inf

298 s using the false discovery rate (FDR), with FDR <0.05 deemed a significant result.

299 groups at 1 and 6 months after adaptive WMT (FDR corrected, p < 0.0001), with normalization of brain

300 and nontrained WM tests after adaptive WMT (FDR corrected, p </= 0.001), but not after nonadaptive W