At rs1477798 in 15q22.31 which showed evidence of linkage in clinic-based, larger families, a nominally significant case-control association was observed (OR 1.16, p = 0.04) which was modestly strengthened for cases with CRC family history (OR 1.24, p = 0.03); however, no significant difference in risk by family history was observed and associations were far from genome-wide significant.
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In the sensitivity analysis accounting for medication use, those who switched medications (mixed use) had 1.81 greater odds of experiencing high negative symptoms compared to those with continued AAP use; however, this was nominally significant ( p = 0.04).
A nominally significant negative association was observed between baseline EPA levels and treatment effect size (slope = −1.05, p = 0.0406; Figure 5 ).
For the post-2020 slope-change term (β 3 ), the arithmetic mean result remained significant after Bonferroni correction (adjusted p = 0.0165), whereas the harmonic mean result, although nominally significant in the unadjusted analysis (raw p = 0.0409), no longer met the corrected significance threshold (Bonferroni-adjusted p = 0.1227; BH-adjusted p = 0.0614).
However, a nominally significant interaction was detected between rs603424 and dietary SFA intake on cardiovascular disease ( β = 0.0073, SE = 0.0036, p = 0.041), suggesting a potential modifying effect of this genotype on the relationship between SFA intake and cardiovascular disease risk.
Differences in the total spine density between control neurons and those overexpressing NISCH were nominally significant (control, 5.57 ± 0.16 spines per 10 μm; overexpression of NISCH , 6.20 ± 0.26 spines per 10 μm, F (19, 19) = 2.72, df = 38, t = 2.11, P = 0.041, two-tailed Student’s t -tests; Fig. 2 A, B).
On analyzing myocardial infarction risk, we detected a nominally significant (P = 0.041) association in type-2 diabetic subjects (HR: 1.86; 95% CI:1.03-3.37 for AA versus G-carriers), although this association did not remain statistically significant following correction for multiple comparisons.
In this study of AMD in East Asians, the evidence of association for VEGFA rs943080 was only nominally significant ( P =0.041 in the discovery stage; Supplementary Table 1 ).
26 Gene-based analysis suggested a nominally significant association between STS (chrX:7 065 298–7 272 682, GRCh37/h19 genome build) and AF in males (4556 cases (2.7%) vs 163 499 controls (97.3%), p=0.041) but not in females (2144 cases (1.1%) vs 193 494 controls (98.9%), p=0.793) ( table 1 and figure 2 ).
The model did show a lower nominally significant ( p < 0.041) specificity for the focus-on-sensitivity cut-off (Fig. 3b and Supplementary Table 1 ).
By contrast, CD8 + T-cell counts did not differ significantly between groups during the treatment period at the cross-sectional level (TwHF-M6 through Post-M12, all P > 0.05; Supplementary Table S1 ), although linear mixed-effects modeling showed a nominally significant group × time interaction for CD8 + T-cell counts ( P = 0.041; Supplementary Table S2 ), suggesting a differential longitudinal trajectory that warrants further investigation.
The prespecified MCI group (MMSE >26, N = 125) showed nominally significant positive effects on ADAS-Cog13 (52%, nominal p = 0.041) and DAD (96%, nominal p = 0.016), positive trend on CDR-SB (102%, nominal p = 0.053), with significant hippocampal atrophy slowing (26%, p = 0.004), and positive grey/white matter effects on MRI-DTI.
However, the physical discomfort subscale showed a nominally significant improvement in the treatment group ( p = 0.041).
There was no association between S100β at age 73 years and visually rated PVS change ( r = −0.034, p = 0.475), and the nominally significant association with longitudinal S100β concentrations ( r = −0.096, p = 0.041) did not survive FDR correction.
In OPPERA, four variants exhibited nominally significant associations with painful TMD: rs33389 (p = 0.041, NR3C1 ), rs143383 (p = 0.030, GDF5 ), rs3918242 (p = 0.023, MMP9 ), and rs60249166 (p = 0.021, RXP2 ).
Although there was a nominally significant p value of L/L with 24CA using the CMH test combining allele counts from the current cohort and the Australian cohort from the previous study ( p = 0.041), this result does not pass the multiple testing correction threshold (α = 0.05/10; p = 0.005).
The nominally significant difference in interaction time when confronted to XX* and X*Y females (V = 56, p = 0.041) did not survive correction for multiple testing.
Results IVW showed a nominally significant effect of HRI on CV events (odds ratio [OR] = 1.0012, P = 4.11 × 10 –2 ) and on CAD and AF.
Results of meta-analysis of all three studies showed only nominally significant association between lower ACE2 expression and higher triglyceride levels (β [95% CI]= -0.13[-0.25, 0.00]; P = 4.15x10 -2 ), but this association was not significant after multiple testing correction (MTC threshold P < 3.33x10 -3 ).
MMSE showed a 76% lower decline from baseline in the active treatment group compared to the sham group that was nominally significant (ΔLS Mean [SE]: 2.10 (1.006), 95% CI of difference: [0.08, 4.12], p = 0.0417, Figure 2B ).
We genotyped the rest of replication 1 (1602 cases and 506 controls residing in Shanghai and Jiangsu Province) and pooled analysis (Replication 1: 2660 cases and 2068 controls) showed a nominally significant association of rs3773159 with T2D ( P = 0.0418, OR = 1.137, Table 1 ).
In the left AF, there was a nominally significant age-by-group interaction for MD that failed to survive correction ( p = 0.0418).
For ‘liking’, there was a nominally significant interaction between group and effort–reward condition [F(1.293, 75.007) = 3.897, p = 0.042, η 2 partial = 0.063], but it did not survive the Holm-adjusted significance threshold, so evidence for group differences in ‘liking’ adaptation should be regarded as tentative.
A similar, nominally significant decrease was also observed in the thalamus ( P =0.042) but not in eight other brain regions.
A global test for differences in heteroplasmy count by haplogroup was nominally significant ( P = 0.042), with 0.007% of the variance of heteroplasmy count explained by haplogroups in the adjusted model.