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1 ngle-nucleotide polymorphisms, corrected for multiple testing).
2 equivalent to P > 0.05 after accounting for multiple testing).
3 , 95% CI 0.53-0.84; p=0.0004; unadjusted for multiple testing).
4 ge, sex, and acquisition site (corrected for multiple testing).
5 e body of the corpus callosum (corrected for multiple testing).
6 comparison was positive (Hochberg method for multiple testing).
7 can be reduced by pooling raw test data from multiple tests.
8 s complicated and expensive, often involving multiple tests.
9 and can be used in the presence of single or multiple tests.
10 tional statistical methodologies and require multiple tests.
11 n, followed with a Bonferroni correction for multiple tests.
12 this result did not withstand correction for multiple tests.
13 e no longer significant after correction for multiple tests.
14 ease following a conservative correction for multiple tests.
15 om HIV suppression to death and adjusted for multiple tests.
16 d against the practicality and cost of using multiple tests.
17 dependent SNPs was calculated to correct for multiple testing.
18 sis (Cox regression) with no corrections for multiple testing.
19 significance after Bonferroni correction for multiple testing.
20 ndings may be missed owing to correction for multiple testing.
21 ontrolling procedure was used to account for multiple testing.
22 coronary artery disease after correction for multiple testing.
23 ant analysis and paired t tests adjusted for multiple testing.
24 ere significant for CVD after adjustment for multiple testing.
25 t associations remained after adjustment for multiple testing.
26 cance was based on Bonferroni correction for multiple testing.
27 selectivity, limited external validity, and multiple testing.
28 rank product statistic to adequately address multiple testing.
29 ion was not significant after correction for multiple testing.
30 This leads to a problem of multi-dimensional multiple testing.
31 ; however, none would survive correction for multiple testing.
32 significant after Bonferroni correction for multiple testing.
33 ce was set at less than 0.001 to control for multiple testing.
34 ith 15-PGDH expression, after adjustment for multiple testing.
35 ns were not significant after correction for multiple testing.
36 for correlated tests (P(ACT)) to account for multiple testing.
37 idually, only a few survived adjustments for multiple testing.
38 ansethnic meta-analysis after correction for multiple testing.
39 tatistical significance after correcting for multiple testing.
40 the opposite direction, after adjustment for multiple testing.
41 l SNPs were significant after correction for multiple testing.
42 groups were examined without corrections for multiple testing.
43 ropsychological measures after adjusting for multiple testing.
44 ion was significant following correction for multiple testing.
45 results are reassuring in an era of extreme multiple testing.
46 diabetes, only a few can pass adjustment for multiple testing.
47 ific IgE, respectively, after correction for multiple testing.
48 cant (p = 3.7 x 10(-4)) after correcting for multiple testing.
49 ter adjusting for a range of confounders and multiple testing.
50 atistically significant after correction for multiple testing.
51 tly associated with OAG after correction for multiple testing.
52 the false discovery rate (FDR) to adjust for multiple testing.
53 ry rate (FDR) method was used to correct for multiple testing.
54 Ps achieved significance after adjusting for multiple testing.
55 o overall disease risk, after adjustment for multiple testing.
56 ol, imputation and analysis issues including multiple testing.
57 lse discovery rates were used to account for multiple testing.
58 2x10(-3), respectively) after correction for multiple testing.
59 wo remained significant after adjustment for multiple testing.
60 e-treatment interactions after adjusting for multiple testing.
61 ues; and (4) uses simulations to account for multiple testing.
62 atistically significant after correction for multiple testing.
63 up remained significant after correcting for multiple testing.
64 dietary factor that are likely explained by multiple testing.
65 significance threshold after correction for multiple testing.
66 r SNP-phenotype pairs, after controlling for multiple testing.
67 e, BMI, and sex as covariates, corrected for multiple testing.
68 e proportions, and Bonferroni-correction for multiple testing.
69 oms from Weeks 12 to 36 after correction for multiple testing.
70 ants and the permutation test to correct for multiple testing.
71 s, but none of these survives correction for multiple testing.
72 burdens of interpretation and penalties for multiple testing.
73 the replication cohort after correction for multiple testing.
74 onferroni correction was used to account for multiple testing.
75 ly Parkinson's disease after controlling for multiple testing.
76 ted with UM risk, all passing adjustment for multiple testing.
82 these towards zero while, on P-value scale, multiple testing adjustment (MTA) shrinks P-values towar
85 dantly and significantly (when corrected for multiple testing) altered in tissue and serum, and cyste
86 ose an efficient approach for correcting for multiple testing and assess eGene p values by utilizing
87 t achieves significance after correction for multiple testing and we do not detect any alleles of mod
88 tion (r > 0.3, P < 0.01 after correction for multiple testing) and discriminant [pcorr (1) > 0.3, VIP
89 ; p values are Sidak adjusted to account for multiple testing) and less likely to have normalising (p
90 tion analysis with rare variants, (2) severe multiple testing, and (3) time-consuming computations.
91 uires association thresholds consistent with multiple testing, and finally evaluates novel candidates
92 t stringent significance thresholds to allow multiple testing, and it is useful only when studies hav
93 r by using a strict threshold accounting for multiple tests, and no SNP overlapped among the analyses
95 ere significantly associated (correcting for multiple testing): ANKK1 SNP rs877138 (most strongly ass
98 the procedures available for accounting for multiple tests are either too conservative or fail to me
99 riate individual gene analysis corrected for multiple testing as well as a standard a Gene Set Enrich
100 association with BMI survived correction for multiple testing at rs4140535 (beta = -0.04, 95% confide
101 significance after Bonferroni adjustment for multiple testing at the level of P0.0012 (0.05/42) excep
103 cted for demographics, cell composition, and multiple testing (Benjamini-Hochberg) and verified hits
104 s were greater than .05 after correction for multiple testing) between MBL2 genotypes and any of our
108 ncy in collinear NMR data sets to reduce the multiple testing burden, (ii) carry out robust and accur
110 its of gene-based approaches such as reduced multiple-testing burden and a principled approach to the
111 ysis Workshop 19 (GAW19) sought reduction of multiple-testing burden through various approaches to ag
112 the replication sample after correcting for multiple testing, but the combined analysis of the two s
113 was associated with EFS after correction for multiple testing, but this analysis was underpowered.
114 sing linear regression models, corrected for multiple testing by using Bonferroni correction and eval
116 P2, PLEKHA1, SLC3A2 and SLC7A6 genes meeting multiple-testing corrected significance for replication
117 3.6 x 10(-5) and 6.1 x 10(-5), which met the multiple-testing corrected threshold of 7.3 x 10(-5)).
120 -based association method, which reached the multiple testing-corrected threshold of 10(-4); P = .003
121 2 x 10(-5) for rs12122228, which reached the multiple testing-corrected threshold) in EGEA using FBAT
126 omosome 17p that were also significant after multiple testing correction (best P = 3.1 x 10(-6) for m
129 est is considered to be the gold standard in multiple testing correction as it accurately takes into
130 ted with cIMT at significance levels passing multiple testing correction at both stages (array-wide s
131 hese associations remained significant after multiple testing correction but were not significant in
132 e propose a novel algorithm, rapid and exact multiple testing correction by resampling (REM), to addr
134 es in the IL33-IL1RL1 pathway after applying multiple testing correction in the meta-analysis: 2 IL33
137 ted using supervised learning methods, and a multiple testing correction technique is used to control
138 or longitudinal associations, respectively; multiple testing correction was based on false discovery
148 on markers was based on HapMap II-CEU, and a multiple-test correction was applied (genome-wide thresh
151 be applied to a variety of resampling-based multiple-testing correction methods including permutatio
153 ovides a simpler, more efficient approach to multiple-testing correction than existing methods and fi
155 these differences were nonsignificant after multiple-testing correction, suggesting genetic heteroge
162 fied 1 significant locus, GRM7, which passed multiple test corrections for 2 hypertension-derived tra
163 nd rs11918967, was associated with BMI after multiple testing corrections (combined P = 2.20 x 10(-4)
165 ease imposes a statistical cost owing to the multiple testing corrections needed to avoid large numbe
171 ols, statistical group comparisons (P < .01; multiple-test corrections) identified 3376 differentiall
176 s as a simple and efficient means to isolate multiple test domains on a single test strip, which faci
177 ore effective compared with strategies using multiple tests, due to avoidance of false positives.
178 associated with AD even after correction for multiple testing (empirical P value 1 [EMP1], .0001; EMP
182 ctional classes and using the consensus from multiple tests, for identifying candidates for selection
184 t implementation, a novel approach to tackle multiple testing from a Bayesian perspective through pos
187 iminate less promising tests and thus reduce multiple testing, have been widely and successfully appl
189 action effect after stringent correction for multiple testing in Hispanic Americans (HA) (rs1514175 (
191 two sources of false discoveries, one due to multiple testing involving several pairwise comparisons
193 including time-dependent variables; (5) how multiple testing is addressed; (6) distinction between s
194 To maximize the power while addressing the multiple testing issue, we implement filters to remove d
198 es and expressed stably over multiple years, multiple test locations, and when the PrMC2-barnaseH102E
199 overcome the limitations of existing genomic multiple testing methods and robustly demonstrate signif
200 4) remained significant after correcting for multiple testing Methods developed in this study can be
206 7 or 17 (using a conservative correction for multiple testing of P < 1.03 x 10(-7)), suggesting resol
209 antly correlate with T2D after adjusting for multiple testing; of these, 22 were previously reported
210 sing infection is determined indirectly from multiple tests on peripheral clinical specimens, which m
211 r, after false discovery rate correction for multiple testing, only the associations of GIMAP4 with a
213 f four were significant after adjustment for multiple testing (P < 0.0012): rs2476601 in PTPN22 (haza
215 nce with false discovery rate correction for multiple testing (P<0.05) identified 26 genes after 12 w
216 ontrol subjects (n=121) after correction for multiple testing (P<7.3e-5) and confounding factors, inc
219 ated with DN after Bonferroni correction for multiple testing (P=0.0001 and 0.00025, respectively), w
224 Here we present a method for constructing multiple testing plasmids which express small hairpin RN
227 sample size, the rare event nature, and the multiple testing problem, as many variables are monitore
228 have the advantage of strongly reducing the multiple testing problem, while increasing the probabili
232 s shortcoming reflects the combinatorics and multiple-testing problem associated with many-body biolo
234 nection, an approach that is aimed at easing multiple testing problems associated with recovering den
237 r in genomic data analysis, we propose a new multiple testing procedure, named Bon-EV, to control fal
241 framework we discuss provides a platform for multiple testing procedures covering situations involvin
242 y's q-value procedures are two commonly used multiple testing procedures for controlling false discov
248 ntly associated with SZ after correction for multiple testing (rate in SZ, 33 [0.16%]; rate in contro
251 D] age, 52 [10] years), after correction for multiple testing, rs2070951 in the NR3C2 gene was signif
252 -coding disease-specific risk variants under multiple testing scenarios; among all the features, hist
259 ormation more comprehensively by integrating multiple test statistics, each of which has relatively l
264 y to happy faces (all P-values corrected for multiple tests) than offspring of non-bipolar parents an
265 d model and algorithms for normalisation and multiple testing that are specifically adapted to CHi-C
266 pathways, which withstood FDR correction for multiple testing that were identified using both the cur
267 ancer samples, however, after correction for multiple testing the difference was significant only for
268 ctors identified in the discovery cohort and multiple testing, the homozygote minor allele of rs31761
270 ndividually significant after correction for multiple testing, this group of genes continued to show
273 variation and (iii) allowing adjustment for multiple testing to control false discovery rate (FDR) o
275 d common variation and, after correction for multiple testing, two gene sets were associated with sch
285 P value of .008 or less, which accounts for multiple testing, was considered to indicate a significa
287 were insignificant following correction for multiple testing, we predict that few of the genetic dif
288 ciations that did not survive correction for multiple testing were observed for NPSR1 rs324891 (T all
289 ignificant associations after correction for multiple testing were observed for three variants, TMEM1
290 Statistical approaches for controlling for multiple testing were used, both with and without prescr
291 l survival and proliferation, and Holm-Sidak multiple tests were used to assess tumor growth and perf
292 were identified that survived correction for multiple testing when current financial hardship was use
293 VWF and PDGFB with VTE after correction for multiple testing, whereas only weak trends were observed
294 se methods require Bonferroni correction for multiple tests, which often is too conservative when the
296 BUA and seven with VOS after correction for multiple testing, with one novel locus for BUA at FAM167
297 te gene studies, such as power, sample size, multiple testing within and between studies, publication
299 oup (n = 54) after Bonferroni correction for multiple testing; within these compounds, the phosphatid
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