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Elliot, E.

Publications and source records attributed to Elliot, E..

3 recordsLinked to original sources

The React & Rebound Model: Capturing Emotion Regulation Dynamics from Passive Wearable Data

BackgroundEmotion regulation--the ability to respond to and restore equilibrium after emotional perturbations--is central to mental health. Yet objective measurement remains limited to lab-based studies with group-level results, while consumer wearables focus on physical activity-related metrics rather than emotional dynamics. ObjectiveWe aimed to develop computational models that extract personalized, interpretable emotion regulation parameters from continuous heart rate variability (HRV) data collected via consumer wearables during everyday life, and validate these parameters against self-reported anxiety symptoms. MethodsWe analyzed 4 weeks of continuous HRV data from N = 49 healthy adults wearing Samsung Galaxy Active 2 smartwatches. We derived a continuous autonomic balance signal and developed three computational modeling approaches of increasing sophistication: (1) a static sympathetic load metric, (2) an Ornstein-Uhlenbeck (OU) dynamical systems model capturing continuous restoration dynamics, and (3) a discrete-state Markov transition model--the React & Rebound model-- capturing reactivity and rebound dynamics. All models were estimated using joint hierarchical Bayesian models that simultaneously extract subject-specific parameters from HRV time series and estimate their association with Generalized Anxiety Disorder 7-item scale (GAD-7) scores. The validity of extracted parameters was evaluated against anxiety symptom severity. ResultsStatic sympathetic load correlated modestly with GAD-7 (r = 0.39, R2 = 0.16). The OU model captured 69% of variance (R2 = 0.69), and the React & Rebound model captured 60% (R2 = 0.60) with substantially fewer parameters. Both models revealed that anxiety symptom severity is associated with the interaction between activation and restoration parameters--not either alone. Fast rebound appeared protective even for highly reactive individuals, who scored comparably to low-reactivity groups when restoration was rapid (Cohens d = 1.17 between highest- and lowest-risk quadrants). In the OU model, the interaction effect was specific to GAD-7 scores versus PHQ-9 and ISI scores; in the React & Rebound model, the interaction was credible across all three symptom measures. Both models were unchanged after controlling for physical activity ({Delta}R2 < 0.002). ConclusionsComputational models can extract interpretable emotion regulation parameters from naturalistic wearable data. The React & Rebound model yields two personalized parameters--reactivity and rebound--that are strongly associated with anxiety symptoms and define meaningful autonomic profiles. These parameters bridge autonomic dynamics measurable via consumer devices to neural circuit models of emotion regulation, with implications for characterizing individual autonomic profiles via consumer wearables.

neuroscience↗

The G Protein-Coupled Receptor GPR31 Promotes Pro-inflammatory Responses in Pancreatic Islets and Macrophages

In type 1 diabetes (T1D), the innate and adaptive immune systems attack and eventually destroy the insulin-secreting pancreatic {beta} cells. During this process, {beta} cells activate inflammatory signaling pathways that augment the dysfunction and destruction imposed by cellular autoimmunity. The 12-lipoxygenase (12-LOX) pathway produces the pro-inflammatory eicosanoid 12-HETE, which induces oxidative and endoplasmic reticulum stress and results in diminished insulin secretion and apoptosis. The G protein-coupled receptor GPR31 has been identified as a putative receptor for 12-HETE. In this study, we generated conventional GPR31 knockout (KO) mice on the C57BL/6J background. To interrogate the role of GPR31 in {beta} cells, we treated islets from wildtype and Gpr31b KO mice with pro-inflammatory cytokines and subjected the islets to RNA sequencing. Differentially expressed pathways in Gpr31b KO islets included those pertaining to inflammation and oxidative stress, consistent with functional studies that demonstrated reduced cytokine-induced oxidative stress in Gpr31b KO islets compared to wildtype controls. Bone marrow-derived macrophages from Gpr31b KO mice showed reduced macrophage migration and decreased inflammatory IFN- and IFN-{gamma} signaling by RNA sequencing. To mimic islet and macrophage inflammation as seen in T1D, wildtype and Gpr31b KO mice were treated with the diabetogenic toxin streptozotocin. Compared to wildtype, Gpr31b KO mice had improved glucose tolerance and preserved {beta}-cell mass. siRNA knockdown of Gpr31b in non-obese diabetic (NOD) mice reduced insulitis, macrophage infiltration, and oxidative stress. Collectively, these findings are consistent with previously published data using 12/15-LOX KO mice and suggest that GPR31 mediates the pro-inflammatory responses of 12-HETE in both {beta} cells and macrophages.

molecular biology↗

Fast Low-Input Efficient Hi-C

We developed FLIE (Fast Low-Input Efficient) Hi-C, a highly optimized and simplified version of Hi-C. Our method shortens the duration of Hi-C from five days to two days and decreases key reagent amounts 5-20 fold, while maintaining experimental controls and data quality. Importantly, the method also reduces the required input material by 100-1000 fold, as we demonstrate by generating detailed high complexity interaction maps from low-input sorted mouse frozen neuron nuclei and from 5,000-10,000 human Hap1 cells.

genomics↗