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Mobile health interventions (i.e., “apps”) are used to address mental health and are an increasingly popular method available to both individuals and organizations to manage workplace stress. However, at present, there is a lack of research on the effectiveness of mobile health interventions in counteracting or improving stress-related health problems, particularly in naturalistic, non-clinical settings. This project aimed at validating a mobile health intervention (which is theoretically grounded in the Job Demands-Resources Model) in preventing and managing stress at work. Within the mobile health intervention, employees make an evidence-based, personalized, psycho-educational journey to build further resources, and thus, reduce stress. A large-scale longitudinal randomized control trial, conducted with six European companies over 6 weeks using four measurement points, examined indicators of mental health via measures of stress, wellbeing, resilience, and sleep. The data were analyzed by means of hierarchical multilevel models for repeated measures, including both self-report measures and user behavior metrics from the app. The results (n = 532) suggest that using the mobile health intervention (vs. waitlist control group) significantly improved stress and wellbeing over time. Higher engagement in the intervention increased the beneficial effects. Additionally, use of the sleep tracking function led to an improvement in sleeping troubles. The intervention had no effects on measures of physical health or social community at work. Theoretical and practical implications of these findings are discussed, focusing on benefits and challenges of using technological solutions for organizations to support individuals’ mental health in the workplace.
Multiple lines of evidence implicate brain serotonin (5-hydroxytryptamine; 5-HT) system dysfunction in the pathophysiology of stressor-related and anxiety disorders. Here we investigate the influence of constitutively deficient 5-HT synthesis on stressor-related anxiety-like behaviors using Tryptophan hydroxylase 2 (Tph2) mutant mice. Functional assessment of c-Fos after associated foot shock, electrophysiological recordings of GABAergic synaptic transmission, differential expression of the Slc6a4 gene in serotonergic neurons were combined with locomotor and anxiety-like measurements in different contextual settings. Our findings indicate that constitutive Tph2 inactivation and consequential lack of 5-HT synthesis in Tph2 null mutant mice (Tph2\(^{-/-}\)) results in increased freezing to associated foot shock and a differential c-Fos activity pattern in the basolateral complex of the amygdala. This is accompanied by altered GABAergic transmission as observed by recordings of inhibitory postsynaptic currents on principal neurons in the basolateral nucleus, which may explain increased fear associated with hyperlocomotion and escape-like responses in aversive inescapable contexts. In contrast, lifelong 5-HT deficiency as observed in Tph2 heterozygous mice (Tph\(^{+/-}\)) is able to be compensated through reduced GABAergic transmission in the basolateral nucleus of the amygdala based on Slc6a4 mRNA upregulation in subdivisions of dorsal raphe neurons. This results in increased activity of the basolateral nucleus of the amygdala due to associated foot shock. In conclusion, our results reflect characteristic syndromal dimensions of panic disorder and agoraphobia. Thus, constitutive lack of 5-HT synthesis influence the risk for anxiety- and stressor-related disorders including panic disorder and comorbid agoraphobia through the absence of GABAergic-dependent compensatory mechanisms in the basolateral nucleus of the amygdala.
Stress impacts negatively on plant growth and crop productivity, causing extensive losses to agricultural production worldwide. Throughout their life, plants are often confronted with multiple types of stress that affect overall cellular energy status and activate energy-saving responses. The resulting low energy syndrome (LES) includes transcriptional, translational, and metabolic reprogramming and is essential for stress adaptation. The conserved kinases sucrose-non-fermenting-1-related protein kinase-1 (SnRK1) and target of rapamycin (TOR) play central roles in the regulation of LES in response to stress conditions, affecting cellular processes and leading to growth arrest and metabolic reprogramming. We review the current understanding of how TOR and SnRK1 are involved in regulating the response of plants to low energy conditions. The central role in the regulation of cellular processes, the reprogramming of metabolism, and the phenotypic consequences of these two kinases will be discussed in light of current knowledge and potential future developments.
Based on recent findings that show that depletion of factor XII (FXII) leads to better posttraumatic neurological recovery, we studied the effect of FXII-deficiency on post-traumatic cognitive and behavioral outcomes in female and male mice. In agreement with our previous findings, neurological deficits on day 7 after weight-drop traumatic brain injury (TBI) were significantly reduced in FXII\(^{−/−}\) mice compared to wild type (WT) mice. Also, glycoprotein Ib (GPIb)-positive platelet aggregates were more frequent in brain microvasculature of WT than FXII\(^{−/−}\) mice 3 months after TBI. Six weeks after TBI, memory for novel object was significantly reduced in both female and male WT but not in FXII\(^{−/−}\) mice compared to sham-operated mice. In the setting of automated home-cage monitoring of socially housed mice in IntelliCages, female WT mice but not FXII\(^{−/−}\) mice showed decreased exploration and reacted negatively to reward extinction one month after TBI. Since neuroendocrine stress after TBI might contribute to trauma-induced cognitive dysfunction and negative emotional contrast reactions, we measured peripheral corticosterone levels and the ration of heart, lung, and spleen weight to bodyweight. Three months after TBI, plasma corticosterone levels were significantly suppressed in both female and male WT but not in FXII\(^{−/−}\) mice, while the relative heart weight increased in males but not in females of both phenotypes when compared to sham-operated mice. Our results indicate that FXII deficiency is associated with efficient post-traumatic behavioral and neuroendocrine recovery.
The presented work shows the analysis of the correlation between the spatial and temporal expression pattern of NtAQP1 and its function in water relation in planta. In situ immunological studies indicated NtAQP1-protein accumulation in the root exodermis and endodermis, in the cortex, close to vascular bundles, in the xylem parenchyma and in cells of the stomatal cavities. The aquaporin was also found to be abundant in longitudinal cell-rows in the petioles. Expression studies with generated transgenic plants (Ntaqp1-promoter::gus or luc) confirmed the Ntaqp1 accumulation in the root, stem and petioles but also revealed further localization in pollen grains, adventitious roots and leaf glandular hairs. Ntaqp1-expression was induced during growth processes, like stem bending after gravistimulation or photostimulation, seed germination and hypocotyl elongation as well as during the comparatively fast circadian leaf movement. The expression was further stimulated by phytohormones, especially gibberellic acid (GA) and osmotic stress. Further analysis displayed a diurnal and even circadian expression of Ntaqp1 in roots and petioles. The functional analysis of the aquaporin was accomplished by reverse genetics and biophysical studies. The antisense technique was used to reduce NtAQP1-expression in tobacco plants. The antisense (AS) plants exhibited a severe reduction of Ntaqp1-mRNA, less reduction of the highly homologous NtPIP1a RNA and no effect on expression of other aquaporin family genes (PIP2, TIP). The function of NtAQP1 at the cellular level was investigated by a newly developed experimental setup to record the osmotically induced increase in protoplast volume. The reduction of NtAQP1 by the antisense expression decreased the overall cellular waterpermeability Pos for more than 50 %. Function of NtAQP1 at the whole plant level was e.g. measured by the “high-pressure flow meter method”. Those measurements revealed that the root hydraulic conductivity per unit root surface area (KRA) of roots from the AS-lines was reduced by more than 50 %. KRA displayed a strong diurnal and circadian variation with a maximum in the middle of the light period, similar to the expression pattern of Ntaqp1 in roots. Gas exchange-, stem (Ystem) and leaf (Yleaf) water potential measurement gave dissimilar values in AS and control plants under well-watered conditions. Under a water-limiting environment the Y of AS-plants remained at more negative water values, even though a further decrease in transpiration of AS-plants was detected. Quantitative analysis displayed a much stronger wilting reaction in the AS than in the control plants. Quantitative studies of the leaf movement in AS compared to control plants exhibited a dramatic reduction in velocity and also in the extent of the process. The following conclusions can be drawn. NtAQP1 was expressed at sites of anticipated high water fluxes from and to the apoplast or symplast. Additionally, the specific distribution pattern and temporal expression of NtAQP1 in petioles and the bending stem strongly indicate a role in transcellular movement of water. The reduction of NtAQP1 by the antisense expression decreased the overall cellular Pos. Conclusively, NtAQP1-function increases membrane water permeability of tobacco root protoplasts. The decrease of the specific root hydraulic conductivity (KRA) was in the same order of magnitude as the mean cellular water permeability reduction, indicating that aquaporin expression is essential in maintaining a natural root hydraulic conductance. Reduction of KRA in AS plants might be the first definitive proof that the pathway of water uptake from the root surface to the xylem involves passage across membranes. The absence of NtAQP1 resulted in a water stress signal, causing a certain stomatal closure. NtAQP1 seems to contribute to water stress avoidance in tobacco. NtAQP1 plays an essential role in fast plant movements and transcellular water shift.
Tinnitus is a phantom sound perception in the ears or head and can arise from many different medical disorders. Currently, there is no standard treatment for tinnitus that reliably reduces tinnitus. Individual patients reported that acupressure at various points around the ear can help to reduce tinnitus, which was investigated here. With this longitudinal observational study, we report a systematic evaluation of auricular acupressure on 39 tinnitus sufferers, combined with a self-help smartphone app. The participants were asked to report on tinnitus, stress, mood, neck, and jaw muscle tensions twice a day using an ecological momentary assessment study design for six weeks. On average, 123.6 questionnaires per person were provided and used for statistical analysis. The treatment responses of the participants were heterogeneous. On average, we observed significant negative trends for tinnitus loudness (Cohen's d effect size: −0.861), tinnitus distress (d = −0.478), stress (d = −0.675), and tensions in the neck muscles (d = −0.356). Comparison with a matched control group revealed significant improvements for tinnitus loudness (p = 0.027) and self-reported stress level (p = 0.003). The positive results of the observational study motivate further research including a randomized clinical trial and long-term assessment of the clinical improvement.
Background
Chronic stress is detrimental to health, and children and young people have had to cope with significantly more stress since the start of the COVID-19 pandemic. In particular, stress at school and in relation to learning is a major problem in this age group. Studies in Germany have indicated that the pandemic has led to a reduced quality of life (QoL) and an increased risk for psychiatric disorders in children and adolescents. Schools are an ideal setting for interventions against stress, which is one of the strongest predictors for the development of psychosocial problems. The present study seeks to address stress by means of a short prevention training programme in schools, including emotion regulation, mindfulness, and self-compassion. In addition to information material for self-study, students should have the opportunity to actively deal with the topic of stress and develop coping strategies within a short space of time. In contrast to very long stress reduction programmes that often last several weeks, the programme is delivered in just 90 min.
Methods
The effectiveness of the short and economical prevention programme LessStress will be examined in a cluster-randomised controlled trial (RCT) encompassing 1894 students. At several measurement time points, students from two groups (intervention and control) will be asked about their subjectively perceived stress levels, among other aspects. Due to the clustered nature of the data, mainly multilevel analyses will be performed.
Discussion
In Germany, there are no nationwide universal prevention programmes for students against stress in schools, and this gap has become more evident since the outbreak of the pandemic. Universal stress prevention in schools may be a starting point to promote resilience. By dealing with stress in a healthy way, mental health can be strengthened and maintained. Moreover, to reach at-risk students at an early stage, we advocate for a stronger networking between child psychiatry and schools.
Das Ziel der vorliegenden Arbeit war die Untersuchung der Reaktionen von Migränepatientinnen mit episodischer (EM) und häufiger Migräne (HM) auf verschiedene Aspekte des Triggerfaktors „Negativer Affekt“ wie Stress und negative Emotionen. Die Ergebnisse der beiden Gruppen wurden mit denen gesunder Kontrollpersonen verglichen (KG). Zur Ermittlung des Aufmerksamkeitsverhaltens gegenüber emotionalen Reizen wurden zwei Emotionale Stroop Tests (EST) durchgeführt. Erwartet wurde ein Aufmerksamkeitsbias der Patientinnen hinsichtlich negativer emotionaler Reize. Im EST 1 wurden allgemeine affektive Wörter der Valenzen positiv, neutral und negativ verwendet. Die Probandinnen sollten auf die Wortfarbe mit Tastendruck reagieren und den Wortinhalt ignorieren. Im EST 2 wurden emotionale Gesichtsausdrücke (ärgerlich, freundlich, neutral) als Reize verwendet. Dabei sollte die Rahmenfarbe der Bilder per Tastendruck bestimmt werden und der Inhalt ignoriert werden. Zur Auswertung wurden Emotionale Stroop Interferenzen (ESI) zum Vergleich Reaktionszeitdifferenzen negativ-neutral und negativ-positiv berechnet. Der erwartete Aufmerksamkeitsbias der HM für negative emotionale Reize wurde dabei nicht gefunden. Dafür zeigten im EST 2 die KG einen Aufmerksamkeitsbias für ärgerliche Gesichter. Ein signifikanter Gruppenunterschied in EST 2 mit sehr niedrigen, im Vergleich negativ-positiv sogar negativen ESI der HM ließ auf ein Vermeidungsverhalten dieser Gruppe ärgerlichen Gesichtern gegenüber schließen. Dieses wurde als Vermeidung negativer sozialer Reize interpretiert und zum gelernten, möglicherweise dysfunktionalen Vermeidungsverhalten von Migränepatienten potentiellen Triggersituationen gegenüber in Bezug gesetzt. Weiterhin wurden die Probandinnen mit dem „Paradigma der Öffentlichen Rede“ psychosozialem Stress ausgesetzt, indem sie vor einer Videokamera unter Beobachtung eine Rede halten sowie eine Kopfrechenaufgabe lösen sollten. Vorher und nachher wurden insgesamt vier Speichelproben zur Bestimmung des Stresshormons Kortisol genommen. Zudem wurden die Druckschmerzschwellen vor und nach dem Experimentalteil gemessen. Die erwartete Kortisolreaktion als Antwort auf die psychosoziale Stressaufgabe blieb aus. Ursache dafür kann die Stichprobenzusammensetzung mit 98% Frauen sein, deren Kortisolreaktion auf Stress durch hormonelle Schwankungen im Experiment nur unzuverlässig stimulierbar ist. Bei der Berechnung der Gesamtkortisolausschüttung über die Zeit zeigte sich im Gegensatz zu dem erwarteten erhöhten Kortisolspiegel der Migränepatientinnen ein linearer Abfall des Spiegels von KG, über EM zu HM, mit den niedrigsten Werten der HM. Diese Ergebnisse könnten auf Veränderungen der Hypophysen-Nebennieren (HHN)-Achse im Sinne eines Hypokortisolismus bei Migränepatientinnen widerspiegeln, der weiterer Klärung bedarf, z.B. durch die Bestimmung eines Kortisoltagesprofils bei Patientinnen. Eine veränderte Funktion der HHN-Achse könnte außerdem zu einer inadäquaten Reaktion auf Stresssituationen beitragen. Die bei Patientinnen ausbleibende Veränderung der Druckschmerzschwelle in Reaktion auf Stress lässt ebenfalls auf eine ungenügende Stressreaktion der Patientinnen schließen. Am Ende der Untersuchung, nach einer Entspannungsphase von 50 Minuten, wurde den Probandinnen Blut abgenommen, in dem die mRNA- und Proteinkonzentrationen ausgewählter pro- und antiinflammatorischer Zytokine bestimmt wurden. Die Analyse der Zytokinkonzentrationen mit Luminex ergab für die Proteindaten aufgrund zu geringer verwertbarer Daten kein interpretierbares Bild. Die mittels Real Time Quantitativer PCR erhaltenen mRNA-Konzentrationen spiegelten die Schmerzfreiheit der Patienten wieder, mit im Vergleich zu KG verringerten proinflammatorischen Zytokinen (TNF-alpha, IL-1beta, IL-2, IL-6) und dem ebenfalls verringerten antiinflammatorischen Zytokin IL-10, sowie dem deutlich erhöhten antiinflammatorischen IL-4. Die im Vergleich zur KG überregulierten Zytokine im schmerzfreien Intervall weisen auf veränderte Regulierungsmechanismen des Immunsystems für die Schmerzmediatoren Zytokine hin. Weitere Schmerzmediatoren könnten ebenfalls verändert sein, was weiterer Klärung in nachfolgenden Studien bedarf. Alles in allem konnten verschiedene Veränderungen in den psychologischen und endokrinen Reaktionen der Migränepatientinnen auf Bestandteile des Triggers „Negativer Affekt“ sowie in der Schmerzregulierung gefunden werden, wobei die Veränderungen bei Patientinnen mit Häufiger Migräne stärker auftraten. Dies weist auf eine mögliche Rolle der einzelnen untersuchten Komponenten bei der Migränechronifizierung hin, was in weiteren Studien vertiefend untersucht werden sollte.
Recent human and animal studies suggest that epigenetic mechanisms mediate the impact of environment on development of mental disorders. Therefore, we hypothesized that polymorphisms in epigenetic-regulatory genes impact stress-induced emotional changes. A multi-step, multi-sample gene-environment interaction analysis was conducted to test whether 31 single nucleotide polymorphisms (SNPs) in epigenetic-regulatory genes, i.e. three DNA methyltransferase genes DNMT1, DNMT3A, DNMT3B, and methylenetetrahydrofolate reductase (MTHFR), moderate emotional responses to stressful and pleasant stimuli in daily life as measured by Experience Sampling Methodology (ESM). In the first step, main and interactive effects were tested in a sample of 112 healthy individuals. Significant associations in this discovery sample were then investigated in a population-based sample of 434 individuals for replication. SNPs showing significant effects in both the discovery and replication samples were subsequently tested in three other samples of: (i) 85 unaffected siblings of patients with psychosis, (ii) 110 patients with psychotic disorders, and iii) 126 patients with a history of major depressive disorder. Multilevel linear regression analyses showed no significant association between SNPs and negative affect or positive affect. No SNPs moderated the effect of pleasant stimuli on positive affect. Three SNPs of DNMT3A (rs11683424, rs1465764, rs1465825) and 1 SNP of MTHFR (rs1801131) moderated the effect of stressful events on negative affect. Only rs11683424 of DNMT3A showed consistent directions of effect in the majority of the 5 samples. These data provide the first evidence that emotional responses to daily life stressors may be moderated by genetic variation in the genes involved in the epigenetic machinery.
Chronic stress, even stress of a moderate intensity related to daily life, is widely acknowledged to be a predisposing or precipitating factor in neuropsychiatric diseases. There is a clear relationship between disturbances induced by stressful stimuli, especially long-lasting stimuli, and cognitive deficits in rodent models of affective disorders. Regular physical activity has a positive effect on the central nervous system (CNS) functions, contributes to an improvement in mood and of cognitive abilities (including memory and learning), and is correlated with an increase in the expression of the neurotrophic factors and markers of synaptic plasticity as well as a reduction in the inflammatory factors. Studies published so far show that the energy challenge caused by physical exercise can affect the CNS by improving cellular bioenergetics, stimulating the processes responsible for the removal of damaged organelles and molecules, and attenuating inflammation processes. Regular physical activity brings another important benefit: increased stress robustness. The evidence from animal studies is that a sedentary lifestyle is associated with stress vulnerability, whereas a physically active lifestyle is associated with stress resilience. Here, we have performed a comprehensive PubMed Search Strategy for accomplishing an exhaustive literature review. In this review, we discuss the findings from experimental studies on the molecular and neurobiological mechanisms underlying the impact of exercise on brain resilience. A thorough understanding of the mechanisms underlying the neuroprotective potential of preconditioning exercise and of the role of exercise in stress resilience, among other things, may open further options for prevention and therapy in the treatment of CNS diseases.