Barely Significant
← all phrases

“nominally significant”

7,733 sentences · 7,733 papers · 10,034 search hits before verification · confirmed specimen

Sighted at

p=0.08

Listed by Hankins (2013) · Otte et al. (2022)

In the literature

Previously reported associations of HCC in the context of ArC with variants of HSD17B13 rs72613567:TA (p=8.95×10 −3 ; OR=0.81 (95% CI 0.69 to 0.95) and APOE rs429358:C (p=5.44×10 −3 ; OR=0.74 (95% CI 0.60 to 0.91) were nominally significant in this study, but did not achieve genome-wide significance in the discovery cohort ( online supplemental tables 5 and 7 ).
39 , 40 The four variables presented are the top performers, and even though the VI ordering is strong, the inclusion proportions are small, suggesting that no one feature is overwhelmingly dominating the prediction, even while the corresponding permutation p ‐values, which ranged from <0.0005 to 0.035, are nominally significant.
Moreover, SNP heritability for schizophrenia, bipolar disorder, and major depressive disorder was enriched at Bonferroni-corrected significance in NeuN+ OCRs overlapping either fetal H3K4me1 sites ( Figure 5 ) or H3K4me3 sites, with nominally significant enrichments observed for ASD in NeuN+ OCRs overlapping H3K4me1 sites and for ADHD in NeuN+ OCRs overlapping H3K4me3 sites ( Table S3 ).
After further applying Bonferroni correction to this set of 2388 nominally significant ACE-associated variants at a p -value threshold of 3 × 10 −7 , which was previously found reasonable for exome-sequencing studies of rare variants [ 62 ], we identified 17 variants in 12 genes that reached exome-wide significance— Table 2 .
However, when analysing family-based and peer-based interpersonal stress separately, few nominally significant associations emerged only for family-based stress with inflammation. 4.1 Interpersonal stress and inflammation Contrary to our pre-registered hypotheses, we did not find evidence supporting that cumulative, interpersonal stress throughout adolescence predicts DNAm indices of inflammation during late adolescence or young adulthood.
Ten out of 13 SNPs were found to achieve nominally significant association in regression tests (Tables 1 and 2 , Supplementary Table 5 ), the remaining 3 SNPs included two SNPs ( SEMA4D rs45483393 and TMEM132C rs1683723) identified with exome sequencing but not replicated in a set of 849 samples and one SNP ( TBC1D22A rs1005241) with suggestive association in Adhikari et al.
The strongest association at the gene level was with reduced expression of COL28A1 ( P corrected = 0.012), encoding a collagen that is predominantly expressed in developing neural tissue 19 .Consistent with this being a primarily early neurodevelopmental risk mechanism, a previous TWAS of ADHD using expression predictors from multiple adult brain regions found only nominally significant evidence for association with COL28A1 expression in two brain areas (amygdala and cerebellum; Supplementary Table 3 ) 20 .
In addition, the analysis involved multiple cytokines, time points and subgroup comparisons; although Bonferroni and false-discovery-rate corrections were applied, some nominally significant associations (notably the borderline 6-month IL-1α difference) did not survive correction and may represent chance findings.
report genetic overlap with inflammatory bowel disease [IBD] by comparing the number of nominally significant single nucleotide polymorphisms [SNPs] in both phenotypes. 3 The most frequently cited environmental risk factors are medications, with non-steroidal anti-inflammatory drugs [NSAIDs], proton-pump inhibitors [PPIs] and selective serotonin reuptake inhibitors [SSRIs] most commonly implicated. 5–7 There have been no reported investigations of potential pharmacogenetic risk factors for microscopic colitis.