Reported and recorded sleepiness in obesity and depression

Civil war, flight, escape and expulsion are extremely stressful and assert a negative impact on refugees’ mental health. However scientific research about resilience and coping of refugees is scarce. Especially in the recent refugee crisis, calls have been made to consider factors contributing to coping and resilience in this vulnerable population. Therefore, the current research sought to investigate individual differences that could serve as antecedents of coping and contextual factors that might moderate these effects. Specifically, it took into account individual’s self-regulatory differences in terms of regulatory focus (i.e., a promotion focus on nurturance needs, ideals and gains vs. a prevention focus on security needs, oughts and losses). It furthermore explored contextual influences by considering Syrian refugees in Turkey (Sample 1, N = 273) and Germany (Sample 2, N = 169). Compared to Syrian refugees in Turkey, those in Germany had a stronger promotion focus. They also reported more problem-focused and less maladaptive coping, as well as less symptoms. Both promotion and prevention focus were positively related to problem-focused coping. Problem-focused coping, in turn, predicted more symptoms in Turkey but not in Germany. Furthermore, a stronger promotion focus was associated with less symptoms and maladaptive coping was associated with more symptoms in both samples. These results contribute to the coping literature in demonstrating that under certain conditions problem-focused coping can be maladaptive and extend the scarce previous work on self-regulation and coping. Most importantly, they highlight a promotion focus as a clear resilience factor and the role of maladaptive coping in increasing vulnerability. As such, they might inform the design of effective interventions among Syrian refugees and beyond

Impact of Serum Cytokine Levels on EEG-Measured Arousal Regulation in Patients with Major Depressive Disorder and Healthy Controls

Background: In major depressive disorder (MDD), findings include hyperstable regulation of brain arousal measured by electroencephalography (EEG) vigilance analysis and alterations in serum levels of cytokines. It is also known that cytokines affect sleep-wake regulation. This study investigated the relationship between cytokines and EEG vigilance in participants with MDD and nondepressed controls, and the influence of cytokines on differences in vigilance between the two groups. Methods: In 60 patients with MDD and 129 controls, 15-min resting-state EEG recordings were performed and vigilance was automatically assessed with the VIGALL 2.0 (Vigilance Algorithm Leipzig). Serum levels of the wakefulness-promoting cytokines interleukin (IL)-4, IL-10, IL-13 and somnogenic cytokines tumor necrosis factor-alpha, interferon-gamma and IL-2 were measured prior to the EEG. Results: Summed wakefulness-promoting cytokines, but not somnogenic cytokines, were significantly associated with the time course of EEG vigilance in the MDD group only. In both groups, IL-13 was significantly associated with the course of EEG vigilance. In MDD compared to controls, a hyperstable EEG vigilance regulation was found, significant for group and group x time course interaction. After controlling for wakefulness-promoting cytokines, differences in vigilance regulation between groups remained significant. Conclusions: The present study demonstrated a relationship between wakefulness-promoting cytokines and objectively measured EEG vigilance as an indicator for brain arousal. Altered brain arousal regulation in MDD gives support for future evaluation of vigilance measures as a biomarker in MDD. Since interactions between cytokines and EEG vigilance only moderately differed between the groups and cytokine levels could not explain the group differences in EEG vigilance regulation, cytokines and brain arousal regulation are likely to be associated with MDD in independent ways. (C) 2016 S. Karger AG, Base

Inflammatory Cytokines in General and Central Obesity and Modulating Effects of Physical Activity

Context Chronic systemic inflammation in obesity originates from local immune responses in visceral adipose tissue. However, assessment of a broad range of inflammation-mediating cytokines and their relationship to physical activity and adipometrics has scarcely been reported to date. Objective To characterize the profile of a broad range of pro-and anti-inflammatory cytokines and the impact of physical activity and energy expenditure in individuals with general obesity, central obesity, and non-obese subjects. Design, Setting, and Participants A cross-sectional study comprising 117 obese patients (body mass index (BMI) >= 30) and 83 non-obese community-based volunteers. Main Outcomes Measures Serum levels of interleukin (IL)-2, IL-4, IL-5, IL-10, IL-12, IL-13, granulocyte-macrophage colony-stimulating factor (GM-CSF),interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha were measured. Physical activity and energy expenditure (MET) were assessed with actigraphy. Adipometrics comprised BMI, weight, abdominal-, waist-and hip-circumference, waist to hip ratio (WHR),and waist-to-height-ratio (WHtR). Results General obesity was associated with significantly elevated levels of IL-5, IL-10, IL-12, IL-13, IFN-gamma and TNF-alpha, central obesity with significantly elevated IL-5, IL-10, IL-12, IL-13 and IFN-gamma-levels. In participants with general obesity, levels of IL-4, IL-10 and IL-13 were significantly elevated in participants with low physical activity, even when controlled for BMI which was negatively associated with physical acitivity. Cytokines significantly correlated with adipometrics, particularly in obese participants. Conclusions Results confirm up-regulation of certain pro-and anti-inflammatory cytokines in obesity. In obese subjects, physical activity may lower levels and thus reduce pro-inflammatory effects of cytokines that may link obesity, insulin resistance and diabetes

Cognitive reactivity mediates the relationship between neuroticism and depression

Although neuroticism has long been established as an important risk factor for depression, the mechanisms through which this temperamental predisposition translates into the occurrence of symptoms are still relatively unclear. This study investigated cognitive reactivity, i.e. the ease with which particular patterns of negative thinking are reactivated in response to mild low mood, as a potential mediator. Individuals with (N = 98) and without a previous history of depression (N = 83) who had provided neuroticism scores six years previously were assessed for cognitive reactivity and current symptoms of depression using self-report questionnaires. Tendencies to respond to mild low mood with ruminative thinking mediated the relation between neuroticism and current symptoms of depression in both groups. Reactivation of hopelessness and suicidal thinking occurred as an additional mediator only in those with a history of previous depression. The results suggest that neuroticism predisposes individuals to depression by generally increasing the likelihood of ruminative responses to low mood. In those with a history of depression in the past, neuroticism additionally increases risk of recurrence by facilitating reactivation of previously associated patterns such as suicidal thinking and hopelessness. These findings suggest potential targets for interventions to help preventing the occurrence, or recurrence of depression in those who due to their temperamental predisposition are at an increased risk

Glomerular expression pattern of long non-coding RNAs in the type 2 diabetes mellitus BTBR mouse model

The prevalence of type 2 diabetes mellitus (T2DM) and by association diabetic nephropathy (DN) will continuously increase in the next decades. Nevertheless, the underlying molecular mechanisms are largely unknown and studies on the role of new actors like long non-coding RNAs (lncRNAs) barely exist. In the present study, the inherently insulin-resistant mouse strain "black and tan, brachyuric" (BTBR) served as T2DM model. While wild-type mice do not exhibit pathological changes, leptin-deficient diabetic animals develop a severe T2DM accompanied by a DN, which closely resembles the human phenotype. We analyzed the glomerular expression of lncRNAs from wild-type and diabetic BTBR mice (four, eight, 16, and 24 weeks) applying the "GeneChip Mouse Whole Transcriptome 1.0 ST" array. This microarray covered more lncRNA gene loci than any other array before. Over the observed time, our data revealed differential expression patterns of 1746 lncRNAs, which markedly differed from mRNAs. We identified protein-coding and non-coding genes, that were not only co-located but also co-expressed, indicating a potentially cis-acting function of these lncRNAs. In vitro-experiments strongly suggested a cell-specific expression of these lncRNA-mRNA-pairs. Additionally, protein-coding genes, being associated with significantly regulated lncRNAs, were enriched in various biological processes and pathways, that were strongly linked to diabetes

Cytokine levels in subjects with high versus low physical activity determined by average number of steps during the wake-phase.

<p>^A all cytokines transformed using formula LN(X+1),</p><p>^B ANOVA with activity group as factor,</p><p>^C ANCOVA with activity group as factor and BMI as covariate,</p><p>^D ANCOVA with activity group as factor and age & BMI as covariates,</p><p>^E ANCOVA with activity group as factor and age as covariate, Bonferroni-correction for Multiple Testing: α(0.05) → p = .0055; α(0.01) → p = .0011.</p><p>Cytokine levels in subjects with high versus low physical activity determined by average number of steps during the wake-phase.</p

Comorbidities and current medication in obese and non-obese participants.

<p>Comorbidities and current medication in obese and non-obese participants.</p

Pearson correlations between LN-transformed cytokine levels and age and adipometrics (correlations ≤ -0.3 and ≥ 0.3 are highlighted in bold font).

<p>BMI = Body Mass Index. AC = Abdominal circumference. WC = waist circumference. HC = hip circumference. WHR = waist-to-hip-ratio. WHtR = Waist-to-height-ratio;</p><p>^A all cytokines transformed using formula LN(X+1).</p><p>Pearson correlations between LN-transformed cytokine levels and age and adipometrics (correlations ≤ -0.3 and ≥ 0.3 are highlighted in bold font).</p