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External temperature change has been shown to modify epigenetic patterns, such as DNA methylation, which regulates gene expression. DNA methylation is heritable, and as such provides a mechanism to convey environmental information to subsequent generations. Studies on epigenetic response to temperature increase are still scarce in wild mammals, even more so studies that compare tissue-specific epigenetic responses. Here, we aim to address differential epigenetic responses on a gene and gene pathway level in two organs, liver and testis. We chose these organs, because the liver is the main metabolic and thermoregulation organ, and epigenetic modifications in testis are potentially transmitted to the F2 generation. We focused on the transmission of DNA methylation changes to naive male offspring after paternal exposure to an ambient temperature increase of 10 degrees C, and investigated differential methylated regions of sons sired before and after the paternal exposure using Reduced Representation Bisulfite Sequencing. We detected both a highly tissue-specific epigenetic response, reflected in genes involved in organ-specific metabolic pathways, and a more general regulation of single genes epigenetically modified in both organs. We conclude that genomes are context-specifically differentially epigenetically regulated in response to temperature increase. These findings emphasize the epigenetic relevance in cell differentiation, which is essential for the specific function(s) of complex organs, and is represented in a diverse molecular regulation of genes and gene pathways. The results also emphasize the paternal contribution to adaptive processes.
External temperature change has been shown to modify epigenetic patterns, such as DNA methylation, which regulates gene expression. DNA methylation is heritable, and as such provides a mechanism to convey environmental information to subsequent generations. Studies on epigenetic response to temperature increase are still scarce in wild mammals, even more so studies that compare tissue-specific epigenetic responses. Here, we aim to address differential epigenetic responses on a gene and gene pathway level in two organs, liver and testis. We chose these organs, because the liver is the main metabolic and thermoregulation organ, and epigenetic modifications in testis are potentially transmitted to the F2 generation. We focused on the transmission of DNA methylation changes to naive male offspring after paternal exposure to an ambient temperature increase of 10 degrees C, and investigated differential methylated regions of sons sired before and after the paternal exposure using Reduced Representation Bisulfite Sequencing. We detected both a highly tissue-specific epigenetic response, reflected in genes involved in organ-specific metabolic pathways, and a more general regulation of single genes epigenetically modified in both organs. We conclude that genomes are context-specifically differentially epigenetically regulated in response to temperature increase. These findings emphasize the epigenetic relevance in cell differentiation, which is essential for the specific function(s) of complex organs, and is represented in a diverse molecular regulation of genes and gene pathways. The results also emphasize the paternal contribution to adaptive processes.
Recent research on proactive work behaviours (PWBs) pointed out that these behaviours can have negative consequences for the proactive individual. We add to this perspective by showing that PWBs may be a source of strain at work and result in elevated time pressure. Challenging the view of time pressure as a challenge stressor, we hypothesize that over the course of work weeks, time pressure will result in less (rather than more) PWB. We investigate these reciprocal effects as within-person, week-level fluctuations of time pressure and PWB based on experience sampling data (N = 52 participants, k = 274 observations). Over the course of three consecutive work weeks, results show a positive lagged effect of PWB in the first week on experiencing time pressure in the second week; in turn, time pressure in the second week had a negative lagged effect on PWB in the third week. Results further suggest that PWB is lowest in work weeks of low time pressure when following a week of high time pressure, indicating a conservation of resources interpretation of the results.
Fluid intelligence (fluid IQ), defined as the capacity for rapid problem solving and behavioral adaptation, is known to be modulated by learning and experience. Both stressful life events (SLES) and neural correlates of learning [specifically, a key mediator of adaptive learning in the brain, namely the ventral striatal representation of prediction errors (PE)] have been shown to be associated with individual differences in fluid IQ. Here, we examine the interaction between adaptive learning signals (using a well-characterized probabilistic reversal learning task in combination with fMRI) and SLES on fluid IQ measures. We find that the correlation between ventral striatal BOLD PE and fluid IQ, which we have previously reported, is quantitatively modulated by the amount of reported SLES. Thus, after experiencing adversity, basic neuronal learning signatures appear to align more closely with a general measure of flexible learning (fluid IQ), a finding complementing studies on the effects of acute stress on learning. The results suggest that an understanding of the neurobiological correlates of trait variables like fluid IQ needs to take socioemotional influences such as chronic stress into account.
Information on the contemporary in-situ stress state of the earth’s crust is essential for geotechnical applications and physics-based seismic hazard assessment. Yet, stress data records for a data point are incomplete and their availability is usually not dense enough to allow conclusive statements. This demands a thorough examination of the in-situ stress field which is achieved by 3D geomechanicalnumerical models. However, the models spatial resolution is limited and the resulting local stress state is subject to large uncertainties that confine the significance of the findings. In addition, temporal variations of the in-situ stress field are naturally or anthropogenically induced. In my thesis I address these challenges in three manuscripts that investigate (1) the current crustal stress field orientation, (2) the 3D geomechanical-numerical modelling of the in-situ stress state, and (3) the phenomenon of injection induced temporal stress tensor rotations. In the first manuscript I present the first comprehensive stress data compilation of Iceland with 495 data records. Therefore, I analysed image logs from 57 boreholes in Iceland for indicators of the orientation of the maximum horizontal stress component. The study is the first stress survey from different kinds of stress indicators in a geologically very young and tectonically active area of an onshore spreading ridge. It reveals a distinct stress field with a depth independent stress orientation even very close to the spreading centre. In the second manuscript I present a calibrated 3D geomechanical-numerical modelling approach of the in-situ stress state of the Bavarian Molasse Basin that investigates the regional (70x70x10km³) and local (10x10x10km³) stress state. To link these two models I develop a multi-stage modelling approach that provides a reliable and efficient method to derive from the larger scale model initial and boundary conditions for the smaller scale model. Furthermore, I quantify the uncertainties in the models results which are inherent to geomechanical-numerical modelling in general and the multi-stage approach in particular. I show that the significance of the models results is mainly reduced due to the uncertainties in the material properties and the low number of available stress magnitude data records for calibration. In the third manuscript I investigate the phenomenon of injection induced temporal stress tensor rotation and its controlling factors. I conduct a sensitivity study with a 3D generic thermo-hydro-mechanical model. I show that the key control factors for the stress tensor rotation are the permeability as the decisive factor, the injection rate, and the initial differential stress. In particular for enhanced geothermal systems with a low permeability large rotations of the stress tensor are indicated. According to these findings the estimation of the initial differential stress in a reservoir is possible provided the permeability is known and the angle of stress rotation is observed. I propose that the stress tensor rotations can be a key factor in terms of the potential for induced seismicity on pre-existing faults due to the reorientation of the stress field that changes the optimal orientation of faults.
Background: The use of psychoactive substances to neuroenhance cognitive performance is prevalent. Neuroenhancement (NE) in everyday life and doping in sport might rest on similar attitudinal representations, and both behaviors can be theoretically modeled by comparable means-to-end relations (substance-performance). A behavioral (not substance-based) definition of NE is proposed, with assumed functionality as its core component. It is empirically tested whether different NE variants (lifestyle drug, prescription drug, and illicit substance) can be regressed to school stressors.
Findings: Participants were 519 students (25.8 +/- 8.4 years old, 73.1% female). Logistic regressions indicate that a modified doping attitude scale can predict all three NE variants. Multiple NE substance abuse was frequent. Overwhelming demands in school were associated with lifestyle and prescription drug NE.
Conclusions: Researchers should be sensitive for probable structural similarities between enhancement in everyday life and sport and systematically explore where findings from one domain can be adapted for the other. Policy makers should be aware that students might misperceive NE as an acceptable means of coping with stress in school, and help to form societal sensitivity for the topic of NE among our younger ones in general.
Purpose: Psychosocial variables are known risk factors for the development and chronification of low back pain (LBP). Psychosocial stress is one of these risk factors. Therefore, this study aims to identify the most important types of stress predicting LBP. Self-efficacy was included as a potential protective factor related to both, stress and pain.
Participants and Methods: This prospective observational study assessed n = 1071 subjects with low back pain over 2 years. Psychosocial stress was evaluated in a broad manner using instruments assessing perceived stress, stress experiences in work and social contexts, vital exhaustion and life-event stress. Further, self-efficacy and pain (characteristic pain intensity and disability) were assessed. Using least absolute shrinkage selection operator regression, important predictors of characteristic pain intensity and pain-related disability at 1-year and 2-years follow-up were analyzed.
Results: The final sample for the statistic procedure consisted of 588 subjects (age: 39.2 (± 13.4) years; baseline pain intensity: 27.8 (± 18.4); disability: 14.3 (± 17.9)). In the 1-year follow-up, the stress types “tendency to worry”, “social isolation”, “work discontent” as well as vital exhaustion and negative life events were identified as risk factors for both pain intensity and pain-related disability. Within the 2-years follow-up, Lasso models identified the stress types “tendency to worry”, “social isolation”, “social conflicts”, and “perceived long-term stress” as potential risk factors for both pain intensity and disability. Furthermore, “self-efficacy” (“internality”, “self-concept”) and “social externality” play a role in reducing pain-related disability.
Conclusion: Stress experiences in social and work-related contexts were identified as important risk factors for LBP 1 or 2 years in the future, even in subjects with low initial pain levels. Self-efficacy turned out to be a protective factor for pain development, especially in the long-term follow-up. Results suggest a differentiation of stress types in addressing psychosocial factors in research, prevention and therapy approaches.
Purpose: Psychosocial variables are known risk factors for the development and chronification of low back pain (LBP). Psychosocial stress is one of these risk factors. Therefore, this study aims to identify the most important types of stress predicting LBP. Self-efficacy was included as a potential protective factor related to both, stress and pain.
Participants and Methods: This prospective observational study assessed n = 1071 subjects with low back pain over 2 years. Psychosocial stress was evaluated in a broad manner using instruments assessing perceived stress, stress experiences in work and social contexts, vital exhaustion and life-event stress. Further, self-efficacy and pain (characteristic pain intensity and disability) were assessed. Using least absolute shrinkage selection operator regression, important predictors of characteristic pain intensity and pain-related disability at 1-year and 2-years follow-up were analyzed.
Results: The final sample for the statistic procedure consisted of 588 subjects (age: 39.2 (± 13.4) years; baseline pain intensity: 27.8 (± 18.4); disability: 14.3 (± 17.9)). In the 1-year follow-up, the stress types “tendency to worry”, “social isolation”, “work discontent” as well as vital exhaustion and negative life events were identified as risk factors for both pain intensity and pain-related disability. Within the 2-years follow-up, Lasso models identified the stress types “tendency to worry”, “social isolation”, “social conflicts”, and “perceived long-term stress” as potential risk factors for both pain intensity and disability. Furthermore, “self-efficacy” (“internality”, “self-concept”) and “social externality” play a role in reducing pain-related disability.
Conclusion: Stress experiences in social and work-related contexts were identified as important risk factors for LBP 1 or 2 years in the future, even in subjects with low initial pain levels. Self-efficacy turned out to be a protective factor for pain development, especially in the long-term follow-up. Results suggest a differentiation of stress types in addressing psychosocial factors in research, prevention and therapy approaches.
The genesis of chronic pain is explained by a biopsychosocial model. It hypothesizes an interdependency between environmental and genetic factors provoking aberrant long-term changes in biological and psychological regulatory systems. Physiological effects of psychological and physical stressors may play a crucial role in these maladaptive processes. Specifically, long-term demands on the stress response system may moderate central pain processing and influence descending serotonergic and noradrenergic signals from the brainstem, regulating nociceptive processing at the spinal level. However, the underlying mechanisms of this pathophysiological interplay still remain unclear. This paper aims to shed light on possible pathways between physical (exercise) and psychological stress and the potential neurobiological consequences in the genesis and treatment of chronic pain, highlighting evolving concepts and promising research directions in the treatment of chronic pain. Two treatment forms (exercise and mindfulness-based stress reduction as exemplary therapies), their interaction, and the dose-response will be discussed in more detail, which might pave the way to a better understanding of alterations in the pain matrix and help to develop future prevention and therapeutic concepts
The genesis of chronic pain is explained by a biopsychosocial model. It hypothesizes an interdependency between environmental and genetic factors provoking aberrant long-term changes in biological and psychological regulatory systems. Physiological effects of psychological and physical stressors may play a crucial role in these maladaptive processes. Specifically, long-term demands on the stress response system may moderate central pain processing and influence descending serotonergic and noradrenergic signals from the brainstem, regulating nociceptive processing at the spinal level. However, the underlying mechanisms of this pathophysiological interplay still remain unclear. This paper aims to shed light on possible pathways between physical (exercise) and psychological stress and the potential neurobiological consequences in the genesis and treatment of chronic pain, highlighting evolving concepts and promising research directions in the treatment of chronic pain. Two treatment forms (exercise and mindfulness-based stress reduction as exemplary therapies), their interaction, and the dose-response will be discussed in more detail, which might pave the way to a better understanding of alterations in the pain matrix and help to develop future prevention and therapeutic concepts