The role of disorder in the motion of chiral swimmers in the presence of obstacles

The presence of obstacles is intuitively expected to hinder the diffusive transport of micro-swimmers. However, for chiral micro-swimmers, a low density of obstacles near a surface can enhance their diffusive behavior, due to the rectification of the chiral motion by the obstacles. Here, we study numerically the role that disorder plays in determining the transport dynamics of chiral micro-swimmers on surfaces with obstacles. We consider different densities of regularly spaced obstacles and distinct types of disorder: noise in the dynamics of the micro-swimmer, quenched noise in the positions of the obstacles as well as obstacle size polydispersity. We show that, depending on the type and strength of the disorder, the presence of obstacles can either enhance or hinder transport, and discuss implications for the control of active transport in disordered media

The role of disorder in the motion of chiral active particles in the presence of obstacles

The presence of obstacles is intuitively expected to hinder the diffusive transport of active particles. However, for chiral active particles, a low density of obstacles near a surface can enhance their diffusive behavior. Here, we study numerically the role that disorder plays in determining the transport dynamics of chiral active particles on surfaces with obstacles. We consider different densities of regularly spaced obstacles and distinct types of disorder: noise in the dynamics of the particle, quenched noise in the positions of the obstacles as well as obstacle size polydispersity. We show that, depending on the type and strength of the disorder, the presence of obstacles can either enhance or hinder transport, and discuss implications for the control of active transport in disordered media

Predicting recurrence of depression using cardiac complexity in individuals tapering antidepressants

It is currently unknown whether the complexity and variability of cardiac dynamics predicts future depression and whether within-subject change herein precedes the recurrence of depression. We tested this in an innovative repeated single-subject study in individuals who had a history of depression and were tapering their antidepressants. In 50 individuals, electrocardiogram (ECG) derived Interbeat-interval (IBI) time-series data were collected for 5 min every morning and evening, for 4 months. Usable data were obtained from 14 participants who experienced a transition (i.e., a clinically significant increase in depressive symptoms) and 14 who did not. The mean, standard deviation, Higuchi dimension and multiscale entropy, calculated from IBIs, were examined for time trends. These quantifiers were also averaged over a baseline period and compared between the groups. No consistent trends were observed in any quantifier before increases in depressive symptoms within individuals. The entropy baseline levels significantly differed between the two groups (morning: P value < 0.001, Cohen’s d = −2.185; evening: P value < 0.001, Cohen’s d = −1.797) and predicted the recurrence of depressive symptoms, in the current sample. Moreover, higher mean IBIs and Higuchi dimensions were observed in individuals who experienced transitions. While we found little evidence to support the existence of within- individual warning signals in IBI time-series data preceding an upcoming depressive transition, our results indicate that individuals who taper antidepressants and showed lower entropy of cardiac dynamics exhibited a higher chance of recurrence of depression. Hence, entropy could be a potential digital phenotype for assessing the risk of recurrence of depression in the short term while tapering antidepressants

Risk Ahead: Actigraphy-Based Early-Warning Signals of Increases in Depressive Symptoms During Antidepressant Discontinuation

Antidepressant discontinuation increases the risk of experiencing depressive symptoms. In a repeated single-subject design, we tested whether transitions in depression were preceded by increases in actigraphy-based critical-slowing-down-based early-warning signals (EWSs; variance, kurtosis, autocorrelation), circadian-rhythm-based indicators, and decreases in mean activity levels. Four months of data from 16 individuals with a transition in depression and nine without a transition in depression were analyzed using a moving-window method. As expected, more participants with a transition showed at least one EWS (50% true positives; 22.2% false positives). Increases in circadian rhythm variables (25.0% true positives vs. 44.4% false positives) and decreases in activity levels (37.5% true positives vs. 44.4% false positives) were more common in participants without a transition. None of the tested risk indicators could confidently predict upcoming transitions in depression, but some evidence was found that critical-slowing-down-based EWSs were more common in participants with a transition

Actors and Factors in European Foreign Policy Making: Insights from the Mediterranean Case

http://www.iue.it/RSCAS/WP-Texts/02_47.pd

Huntingtin gene repeat size variations affect risk of lifetime depression

Huntington disease (HD) is a severe neuropsychiatric disorder caused by a cytosine-adenine-guanine (CAG) repeat expansion in the HTT gene. Although HD is frequently complicated by depression, it is still unknown to what extent common HTT CAG repeat size variations in the normal range could affect depression risk in the general population. Using binary logistic regression, we assessed the association between HTT CAG repeat size and depression risk in two well-characterized Dutch cohorts─the Netherlands Study of Depression and Anxiety and the Netherlands Study of Depression in Older Persons─including 2165 depressed and 1058 non-depressed persons. In both cohorts, separately as well as combined, there was a significant non-linear association between the risk of lifetime depression and HTT CAG repeat size in which both relatively short and relatively large alleles were associated with an increased risk of depression (β = −0.292 and β = 0.006 for the linear and the quadratic term, respectively; both P < 0.01 after adjustment for the effects of sex, age, and education level). The odds of lifetime depression were lowest in persons with a HTT CAG repeat size of 21 (odds ratio: 0.71, 95% confidence interval: 0.52 to 0.98) compared to the average odds in the total cohort. In conclusion, lifetime depression risk was higher with both relatively short and relatively large HTT CAG repeat sizes in the normal range. Our study provides important proof-of-principle that repeat polymorphisms can act as hitherto unappreciated but complex genetic modifiers of depression