The Model of Neurovisceral Integration suggests that vagally mediated heart rate variability (vmHRV) represents a psychophysiological index of inhibitory control and thus, is associated with emotion regulation capacity. Over the past decade, growing empirical evidence supports this notion, showing that those with higher resting vmHRV can regulate negative emotions more adequately. However, to our knowledge, no study has previously examined how resting vmHRV may relate to everyday perceived difficulties in emotion regulation. The present study attempts to examine such relationship in 183 undergraduate students (98 female, 60 minority, mean Age = 19.34). Resting vmHRV was collected during a 5-min resting baseline period, and everyday difficulties in emotion regulation were assessed using the Difficulties in Emotion Regulation Scale (DERS). Controlling for potential covariates (including both trait anxiety and rumination), results revealed a negative relationship between resting vmHRV and DERS such that lower resting vmHRV was associated with greater difficulties in emotional regulation, especially a lack of emotional clarity and impulse control, as indicated by the respective subscales of the DERS. These findings provide further evidence for the Neurovisceral Integration Model, suggesting that emotion regulation and autonomic regulation share neural networks within the brain. Moreover, the present study extends prior research by highlighting two distinct facets of emotion regulation (impulse control and emotional clarity) that should be of particular interest when investigating the link between emotion regulation, resting vmHRV, and related health outcomes including morbidity and mortality.

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Objective: Relapsing polychondritis (RP) is a systemic inflammatory disease of unknown etiology. The study objective was to examine the contribution of rare genetic variations in RP. Methods: We performed a case-control exome-wide rare variant association analysis including 66 unrelated European American RP cases and 2923 healthy controls. Gene-level collapsing analysis was performed using Firth's logistics regression. Pathway analysis was performed on an exploratory basis with three different methods: Gene Set Enrichment Analysis (GSEA), sequence kernel association test (SKAT) and higher criticism test. Plasma DCBLD2 levels were measured in patients with RP and healthy controls using enzyme-linked immunosorbent assay (ELISA). Results: In the collapsing analysis, RP was associated with higher burden of ultra-rare damaging variants in the DCBLD2 gene (7.6% vs 0.1%, unadjusted odds ratio = 79.8, p = 2.93 x 10-7). Patients with RP and ultra-rare damaging variants in DCBLD2 had a higher prevalence of cardiovascular manifestations. Plasma DCBLD2 protein levels were significantly higher in RP than healthy controls (5.9 vs 2.3, p < 0.001). Pathway analysis showed statistically significant enrichment of genes in the tumor necrosis factor (TNF) signaling pathway driven by rare damaging variants in RELB, RELA and REL using higher criticism test weighted by degree and eigenvector centrality. Conclusions: This study identified specific rare variants in DCBLD2 as putative genetic risk factors for RP. Genetic variation within the TNF pathway is also potentially associated with development of RP. These findings should be validated in additional patients with RP and supported by future functional experiments.