“nominally significant”

A total of 205 risk factor associations were found to be nominally significant ( p < 0.05).

Multi-omics analyses revealed nominally significant associations with specific gut microbes (e.g., Lactobacillus), inflammatory proteins (TNFSF12, CXCL5), immunophenotypes, and plasma metabolites (all P <.05).

In SMR analyses of gene expression and migraine within the Finnish cohort, six genes—EP300, HDAC3, SIRT1, AARS2, SLC16A1, and SMARCA4—showed nominally significant associations ( P < 0.05).

Three out of 11 HbA 1c -associated SNPs had nominally significant ( p < 0.05) associations with HbA 1c levels in at least one of the three race-ethnic groups, but altogether only four of the 33 possible associations (11 SNPs x three race-ethnic groups) were significant ( p < 0.05).

Using a nominally significant cutoff ( p < 0.05), 30 module-trait relationships emerge, with a range from zero to six significantly correlated modules per trait.

Of these 57 lipid species, only 2 showed nominally significant mediation effects ( p <0.05, FDR >0.60, Supplementary Table 10 ) on the reverse association between PFAS mixture exposure and MACCE risk.

For each bootstrap replicate, two statistics were computed: (i) whether the global log-rank test remained nominally significant ( P < 0.05), yielding a bootstrap significance rate; and (ii) whether the same subgroup retained the best and worst survival ordering as in the original data, yielding a direction-consistency measure. “Bootstrap-stable prognostic stratification” was defined as FDR < 0.05 together with a bootstrap significance rate ≥ 80% and direction consistency ≥ 80%.

For any medication with a nominally significant association ( p < .05), the same analysis was repeated in the chemotherapy group to test for nonspecific effects.

Raw P < 0.05 was considered nominally significant, whereas FDR-adjusted P < 0.05 was considered significant after correction for multiple comparisons.

We selectively included 44 diseases (excluding cancer, which is a limitation to be noted) in the first part of phenome-wide association analysis (PheWAS) and identified nominally significant associations ( P < 0.05) between the SES-associated variants and CHD.

In order to eliminate effect of these confounding parameters we residualized our phenotypes using backward multiple regression model (lme function in nlme R package): starting from all variables included into the model we step by step eliminated less significant ones until all variables were nominally significant (p<0.05).

The 36 nominally significant miRNAs ( p < 0.05) identified in the PDN/PDD comparison from LIMMA were used to classify disease state (See Figure 2B ), though with more limited accuracy than the PD-control model (absolute error rate = 13.8%, sensitivity = 81.2%, specificity = 88.9%).

Although findings were nominally significant ( p < .05) for remission, they did not withstand correction for multiple testing.

To ensure a sufficiently large sampling distribution, we restricted our analysis to six nominally significant ( p < 0.05 952 ≈ 5.25 × 10 − 5 ) gene-trait combinations with at least 10 individuals who are either CH variant carriers or with ≥2 pLoF or damaging missense/protein-altering variants on the same haplotype ( STAR Methods ).

Smoothed methylation values over nominally significant ( p < 0.05) DMRs from each comparison were obtained using the “getMeth” function in the bsseq R package v1.36.0.

We retained for downstream analyses all loci with nominally significant binomial p values ( p < 0.05) and at least 2 reads (10%) mapped to any allele.

A total of 19 HLA alleles had nominally significant maternal and/or fetal effects on BW ( P <0.05; Supplementary Table S7 , available as Supplementary data at IJE online); 13 of the 19 alleles had evidence for a maternal effect only, four alleles primarily had evidence for a fetal effect only and two alleles had evidence of both.

Models were run for phenotype pairs that shared at least nominally significant ( p < 0.05) genetic overlap.

Further investigation of BMP8A using the Genotype Tissue Expression Database revealed multiple variants with nominally significant (P < 0.05) interaction P-values in our EA cohort were significant BMP8A eQTLs in tissue types highlight relevant for PAD such as rs755249 (tibial nerve, eQTL P = 3.6x10 -6 ) and rs1180341 (tibial artery, eQTL P = 5.3x10 -6 ).

Of the 629 candidate genes associated with circulating vitamin D in the Phase 1 gene-set, 55 had nominally significant expression change after supplementation ( P < 0.05).

To illustrate the broader applicability of the method, we have applied it to the data from START randomized controlled trial.We showed that theCVRSmethod applied with an additional selection step, identified a sensitive group that conferred a nominally significant interaction effect ( P <.05) between the treatment and the sensitivity status, in the case where there was no overall significant treatment effect.

For all nominally significant associations (P < 0.05), we conducted a Bayesian colocalisation analysis to determine whether GWAS and expression quantitative trait locus (eQTL) signals shared a causal variant [ 40 ].

To confirm whether the nominally significant SNPs ( P < 0.05) from the candidate genes and the top SNPs ( P < 0.0025) in each of the genomic regions with IQ were simply due to chance, we tested these SNPs in the replication samples.

Seventy CpGs (in 41 genes) showed nominally significant associations ( P < 0.05) with AD-ND codependence in both AAs and EAs.

In detail, results were only considered when they met the following criteria: (1) MR results were based on three or more SNPs, as this allowed us to perform the sensitivity analyses listed below; (2) MR results showed a Benjamini-Hochberg-corrected p value < 0.05 using IVW and nominally significant results ( p value < 0.05) using two other MR approaches (weighted median and MR PRESSO test [ 56 , 57 ]); (3) MR results did not show indications of horizontal pleiotropy or heterogeneity, as estimated using MR Egger [ 57 ] (intercept p value > 0.05) and the MR PRESSO [ 56 ] outlier-adjusted test (