Individual Differences and Ecological Validity of Emotion Regulation in Response to Sadness

The majority of research on emotion regulation processes has been restricted to controlled laboratory settingsthat use experimental paradigms to investigate short-term outcomes (Berking & Wupperman, 2012). A true understanding of emotion regulation requires an unobtrusive, ecologically valid assessment of the construct as it naturally unfolds in the environment. Digital phenotyping, or moment-by-moment quantification of individual-level human behavior using data from smartphone sensors (Torous & Onnela, 2016), is a novel method for evaluating human behavior in naturalistic settings. The present project is the first to implement digital phenotyping in the investigation of emotion regulation. The central aim of the study was to evaluate whether smartphone-based digital phenotyping data predicted individual differences in emotion regulation in both in-lab and naturalistic settings. During an in-lab session, unselected adult participants (N = 69) completed self-report questionnaires measuring trait emotion regulation as well as state affect/emotion regulation following a neutral mood induction, negative mood induction, and recovery period. Smartphone-based digital phenotyping data were collected during a 7-day follow-up period using the Beiwe Research Platform (Onnela & Rauch, 2016), an open-access mobile- and cloud-based research tool for collecting digital data via smartphones. Results showed that variation in mobile power state level and GPS distance were significantly associated with variation in negative state affect and state cognitive reappraisal over time. Clustering and classification analyses showed power state level and GPS distance over time to accurately, and with high sensitivity and specificity, classify two trait emotion clusters. Variation in power state level and GPS distance together with trait and state emotion regulation was not associated with current depressive symptoms. Overall, the findings provide initial data on the use of digital phenotyping data in predicting individual differences in state and trait emotion regulation in both in-lab and naturalistic settings. The results suggest that operationalizations of digital phenotyping data and modeling approaches are particularly important factors to consider when implementing digital phenotyping methodology in the study of mental health processes such as emotion regulation

Symptom changes in multiple sclerosis following psychological interventions: a systematic review

Background: Multiple Sclerosis is a disease of the central nervous system involving a variety of debilitating physical, sensory, cognitive and emotional symptoms. This literature review evaluated the impact of psychological interventions on the physiological symptoms associated with the illness. Methods: A systematic literature search was conducted using Medline, PsycINFO, Scopus, and the Cochrane Library databases, as well as reference lists. Relevant studies were selected and assessed according to a preset protocol. Results: The search produced 220 articles, with 22 meeting inclusion criteria for the review. A total of 5,705 subjects with Multiple Sclerosis were analyzed. Results from the included studies indicate a general improvement in both psychological and physiological outcomes following psychological treatment. The most highly influenced physical symptoms include fatigue, sleep disturbances, pain, and physical vitality. Conclusions: Findings from the review suggest a positive relationship between psychological interventions and physiological Multiple Sclerosis symptoms. Implications for future research are discussed

Dynamics of Barred Galaxies

Some 30% of disc galaxies have a pronounced central bar feature in the disc plane and many more have weaker features of a similar kind. Kinematic data indicate that the bar constitutes a major non-axisymmetric component of the mass distribution and that the bar pattern tumbles rapidly about the axis normal to the disc plane. The observed motions are consistent with material within the bar streaming along highly elongated orbits aligned with the rotating major axis. A barred galaxy may also contain a spheroidal bulge at its centre, spirals in the outer disc and, less commonly, other features such as a ring or lens. Mild asymmetries in both the light and kinematics are quite common. We review the main problems presented by these complicated dynamical systems and summarize the effort so far made towards their solution, emphasizing results which appear secure. (Truncated)Comment: This old review appeared in 1993. Plain tex with macro file. 82 pages 18 figures. A pdf version with figures at full resolution (3.24MB) is available at http://www.physics.rutgers.edu/~sellwood/bar_review.pd

Stellar polytropes and Navarro-Frenk-White halo models: comparison with observations

Motivated by the possible conflict between the Navarro-Frenk-White(NFW) model predictions for the dark matter contents of galactic systems and its correlation with baryonic surface density, we will explore an alternative paradigm for the description of dark matter halos. Such an alternative emerges from Tsallis' non-extensive thermodynamics applied to self-gravitating systems and leads to the so-called ``stellar polytrope'' (SP) model. We consider that this could be a better approach to real structures rather than the isothermal model, given the fact that the first one takes into account the non-extensivity of energy and entropy present in these type of systems characterized by long-range interactions. We compare a halo based on the Navarro-Frenk-White (NFW) and one which follows the SP description. Analyzing the dark matter contents estimated by means of global physical parameters of galactic disks, obtained from a sample of actual galaxies, with the ones of the unobserved dark matter halos, we conclude that the SP model is favored over the NFW model in such a comparison.Comment: 21 pages, 4 figures. Accepted for publication in the Journal of Cosmology and Astroparticle Physic

A novel mouse model for pyridoxine-dependent epilepsy due to antiquitin deficiency

Pyridoxine-dependent epilepsy (PDE) is a rare autosomal recessive disease caused by mutations in the ALDH7A1 gene leading to blockade of the lysine catabolism pathway. PDE is characterized by recurrent seizures that are resistant to conventional anticonvulsant treatment but are well-controlled by pyridoxine (PN). Most PDE patients also suffer from neurodevelopmental deficits despite adequate seizure control with PN. To investigate potential pathophysiological mechanisms associated with ALDH7A1 deficiency, we generated a transgenic mouse strain with constitutive genetic ablation of Aldh7a1. We undertook extensive biochemical characterization of Aldh7a1-KO mice consuming a low lysine/high PN diet. Results showed that KO mice accumulated high concentrations of upstream lysine metabolites including δ1-piperideine-6-carboxylic acid (P6C), α-aminoadipic semialdehyde (α-AASA) and pipecolic acid both in brain and liver tissues, similar to the biochemical picture in ALDH7A1-deficient patients. We also observed preliminary evidence of a widely deranged amino acid profile and increased levels of methionine sulfoxide, an oxidative stress biomarker, in the brains of KO mice, suggesting that increased oxidative stress may be a novel pathobiochemical mechanism in ALDH7A1 deficiency. KO mice lacked epileptic seizures when fed a low lysine/high PN diet. Switching mice to a high lysine/low PN diet led to vigorous seizures and a quick death in KO mice. Treatment with PN controlled seizures and improved survival of high-lysine/low PN fed KO mice. This study expands the spectrum of biochemical abnormalities that may be associated with ALDH7A1 deficiency and provides a proof-of-concept for the utility of the model to study PDE pathophysiology and to test new therapeutics

A novel mouse model for pyridoxine-dependent epilepsy due to antiquitin deficiency

Pyridoxine-dependent epilepsy (PDE) is a rare autosomal recessive disease caused by mutations in the ALDH7A1 gene leading to blockade of the lysine catabolism pathway. PDE is characterized by recurrent seizures that are resistant to conventional anticonvulsant treatment but are well-controlled by pyridoxine (PN). Most PDE patients also suffer from neurodevelopmental deficits despite adequate seizure control with PN. To investigate potential pathophysiological mechanisms associated with ALDH7A1 deficiency, we generated a transgenic mouse strain with constitutive genetic ablation of Aldh7a1. We undertook extensive biochemical characterization of Aldh7a1-KO mice consuming a low lysine/high PN diet. Results showed that KO mice accumulated high concentrations of upstream lysine metabolites including ∆1-piperideine-6-carboxylic acid (P6C), α-aminoadipic semialdehyde (α-AASA) and pipecolic acid both in brain and liver tissues, similar to the biochemical picture in ALDH7A1-deficient patients. We also observed preliminary evidence of a widely deranged amino acid profile and increased levels of methionine sulfoxide, an oxidative stress biomarker, in the brains of KO mice, suggesting that increased oxidative stress may be a novel pathobiochemical mechanism in ALDH7A1 deficiency. KO mice lacked epileptic seizures when fed a low lysine/high PN diet. Switching mice to a high lysine/low PN diet led to vigorous seizures and a quick death in KO mice. Treatment with PN controlled seizures and improved survival of high-lysine/low PN fed KO mice. This study expands the spectrum of biochemical abnormalities that may be associated with ALDH7A1 deficiency and provides a proof-of-concept for the utility of the model to study PDE pathophysiology and to test new therapeutics