Expecting the Unexpected: Predicting Panic Attacks From Mood, Twitter, and Apple Watch Data.

OBJECTIVE: Panic attacks are an impairing mental health problem that affects 11% of adults every year. Current criteria describe them as occurring without warning, despite evidence suggesting individuals can often identify attack triggers. We aimed to prospectively explore qualitative and quantitative factors associated with the onset of panic attacks. RESULTS: Of 87 participants, 95% retrospectively identified a trigger for their panic attacks. Worse individually reported mood and state-level mood, as indicated by Twitter ratings, were related to greater likelihood of next-day panic attack. In a subsample of participants who uploaded their wearable sensor data (n = 32), louder ambient noise and higher resting heart rate were related to greater likelihood of next-day panic attack. CONCLUSIONS: These promising results suggest that individuals who experience panic attacks may be able to anticipate their next attack which could be used to inform future prevention and intervention efforts.

Adolescent girls' intrapersonal and interpersonal parasympathetic regulation during peer support is moderated by trait and state co-rumination.

Effective emotion regulation (ER) is integral to adolescents' mental well-being and socioemotional development. During adolescence, peer interactions have an increasingly salient influence on the development of effective ER, but not all supportive peer interactions support adaptive ER. Co-rumination reflects the tendency to seek ER support by engaging with peers in negatively focused discussion of ongoing problems. We examined associations between co-rumination (state and trait) with measures of individual's autonomic (i.e., respiratory sinus arrhythmia, RSA) and affective regulation (self-report) among 30 female close-friend dyads (ages 11-17; 74% White) while engaged in a support-seeking discussion in the laboratory. We found that trait co-rumination corresponded with RSA withdrawal during peer support, suggesting a potential mechanism by which co-rumination contributes to dysregulated ER. We also examined dyadic patterns of physiological regulation via prospective change actor partner interdependence models (APIM). Partner effects were moderated by behaviorally coded state co-rumination. Dyads with high state co-rumination displayed coupled RSA movement in opposite directions, while dyads with low state co-rumination exhibited coupled RSA movement in the same direction. These findings are consistent with similar physiologic linkages in close relationships observed in other developmental periods. Results highlight the importance of multimodal assessment for characterizing social ER processes across development.

The autonomic correlates of dysphoric rumination and post-rumination savoring.

Trait dysphoric rumination is a transdiagnostic factor associated with depression and anxiety that has also been linked with blunted respiratory sinus arrhythmia (RSA), an index of reduced emotion regulation capacity. However, the autonomic correlates of state dysphoric rumination remain unclear. We examined the physiological correlates of state dysphoric rumination and the potential repairing effects of savoring on autonomic functioning. To provide a comprehensive assessment of autonomic correlates, we examined changes in parasympathetic (RSA) and sympathetic (cardiac pre-ejection period, PEP; and electrodermal activity, EDA) arousal independently, as well as autonomic coordination among indices. Eighty-two women (ages 18-25) completed laboratory physiological assessments, including rumination and savoring tasks, and self-report measures of trait rumination. Dysphoric rumination was associated with sympathetic activation (i.e., decreases in PEP, increases in EDA), and subsequent savoring following a recovery period also corresponded with decreases in PEP. Trait rumination did not predict autonomic changes during state rumination. However, higher trait rumination was associated with greater sympathetic coordination (PEP-EDA correspondence) during savoring. In summary, dysphoric rumination co-occurred with sympathetic activation, and subsequent savoring successfully recruited sympathetic activity (PEP) redirected on positive moods and events. Results also emphasize the utility of examining sympathetic and parasympathetic indices, and coordination among autonomic indices to delineate autonomic activity associated with emotion regulation strategies.

The molecular landscape of glioma in patients with Neurofibromatosis 1.

Neurofibromatosis type 1 (NF1) is a common tumor predisposition syndrome in which glioma is one of the prevalent tumors. Gliomagenesis in NF1 results in a heterogeneous spectrum of low- to high-grade neoplasms occurring during the entire lifespan of patients. The pattern of genetic and epigenetic alterations of glioma that develops in NF1 patients and the similarities with sporadic glioma remain unknown. Here, we present the molecular landscape of low- and high-grade gliomas in patients affected by NF1 (NF1-glioma). We found that the predisposing germline mutation of the NF1 gene was frequently converted to homozygosity and the somatic mutational load of NF1-glioma was influenced by age and grade. High-grade tumors harbored genetic alterations of TP53 and CDKN2A, frequent mutations of ATRX associated with Alternative Lengthening of Telomere, and were enriched in genetic alterations of transcription/chromatin regulation and PI3 kinase pathways. Low-grade tumors exhibited fewer mutations that were over-represented in genes of the MAP kinase pathway. Approximately 50% of low-grade NF1-gliomas displayed an immune signature, T lymphocyte infiltrates, and increased neo-antigen load. DNA methylation assigned NF1-glioma to LGm6, a poorly defined Isocitrate Dehydrogenase 1 wild-type subgroup enriched with ATRX mutations. Thus, the profiling of NF1-glioma defined a distinct landscape that recapitulates a subset of sporadic tumors.

A metabolic function of FGFR3-TACC3 gene fusions in cancer.

Chromosomal translocations that generate in-frame oncogenic gene fusions are notable examples of the success of targeted cancer therapies. We have previously described gene fusions of FGFR3-TACC3 (F3-T3) in 3% of human glioblastoma cases. Subsequent studies have reported similar frequencies of F3-T3 in many other cancers, indicating that F3-T3 is a commonly occuring fusion across all tumour types. F3-T3 fusions are potent oncogenes that confer sensitivity to FGFR inhibitors, but the downstream oncogenic signalling pathways remain unknown. Here we show that human tumours with F3-T3 fusions cluster within transcriptional subgroups that are characterized by the activation of mitochondrial functions. F3-T3 activates oxidative phosphorylation and mitochondrial biogenesis and induces sensitivity to inhibitors of oxidative metabolism. Phosphorylation of the phosphopeptide PIN4 is an intermediate step in the signalling pathway of the activation of mitochondrial metabolism. The F3-T3-PIN4 axis triggers the biogenesis of peroxisomes and the synthesis of new proteins. The anabolic response converges on the PGC1α coactivator through the production of intracellular reactive oxygen species, which enables mitochondrial respiration and tumour growth. These data illustrate the oncogenic circuit engaged by F3-T3 and show that F3-T3-positive tumours rely on mitochondrial respiration, highlighting this pathway as a therapeutic opportunity for the treatment of tumours with F3-T3 fusions. We also provide insights into the genetic alterations that initiate the chain of metabolic responses that drive mitochondrial metabolism in cancer.