119 research outputs found

    The neural basis of self-control

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    How does stress induce headache? An experimental study

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    Psychological stress triggers headaches, but how this happens is unclear. To explore this, 38 episodic migraine sufferers, 28 with tension-type headache (T-TH) and 20 controls rated nausea, negative affect, task-expectancies and headache at 5-minute intervals during an unpredictable and uncontrollable 25-minute mental arithmetic task with a non-contingent failure rate. Blood pressure and pulse rate were measured every 3 minutes and salivary cortisol was sampled before and after the task. Trigeminal activation was measured by nociceptive blink reflex measures during each of the three experimental phases. Multiple regression analyses indicated that negative affect (NA) was the strongest predictor of headache intensity during the task. Increases in stress-headache were unrelated to consistent changes in cardiovascular activity but were related to declines in cortisol and increased post-task trigeminal activity. In repeated measures ANOVAs, participants who developed headache had higher nausea, NA and self-efficacy expectancies than those with no-or-low headache (p <.05 to p <.001). In further multiple regression analyses to identify which aspects of the stress process contributed to the high NA preceding headache, discouragement, anxiety, irritation and tension mediated the relationship between headache intensity during the stressful task and primary and secondary appraisal processes (stressor exposure and stressor reactivity). Avoidant coping, perceived inability to decrease pain, and outcome expectancy independently predicted headache intensity during the stressful task. Anxiety mediated the relationship between headache intensity and the coping tactics of wishful thinking, self-criticism, pain catastrophizing and praying/hoping. Attachment anxiety and the personality traits of openness, agreeableness and conscientiousness moderated the relationship between stress appraisals and headache. Results were discussed using the model of stress-headache as allostatic load. Findings suggest that headache developed when participants overextended themselves during a stressful task, adopting an information processing style which impeded emotional adjustment to changing situational demands. Learning to modify perceptions of threat and adopting a more flexible, less outcome-dependent processing style which avoids response conflict might help to prevent headache from spiralling upward

    Assessing baseline glucocorticoids as conservation biomarkers in a declining aerial insectivore

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    Conservation biologists are increasingly incorporating a diversity of integrative approaches to monitor, manage, and mitigate the growing threats to biodiversity imparted by climate change and other anthropogenic pressures. Over the past 15 years, stress hormones (i.e., glucocorticoids: corticosterone and cortisol) have been gaining considerable attention as sensitive physiological biomarkers of wildlife disturbance. However, despite a substantial accumulation of studies citing glucocorticoids (GCs) as potential indicators of condition, health, or disturbance, comparatively little is known about their actual utility for conservation monitoring. This thesis aims to validate three key characteristics of baseline plasma GCs that are necessary to their employment as sensitive, predictive biomarkers of wildlife disturbance: 1) correlation with environmental quality; 2) consistency across individuals in response to environmental alteration; 3) relationship with fitness metrics at the individual and population level. I complete these validations across two different reproductive stages in female tree swallows (Tachycineta bicolor), a member of the aerial insectivore guild of birds that is in population decline in North America. My results indicate that baseline GCs may not reflect the natural variation in components of the internal and extrinsic environment that are associated with habitat quality or disturbance. In addition, baseline GCs show considerable within-individual variation across the breeding season, and display individually-specific responses to an experimentally-induced change in environmental quality (i.e., a decline in foraging profitability). Further, baseline GC levels do not relate to multiple metrics of fitness (offspring quality, reproductive output, or survival) despite the careful control of potentially confounding contexts such as age, reproductive stage, time of day, and body condition. Finally, at the average level, my results indicate that an environmental perturbation (i.e., a decline in foraging profitability) can have consequences for body condition, behaviour, and current and future baseline GC levels in habitat type-specific ways without concomitant influences on fitness. Collectively, my findings suggest that baseline GCs may not be easily interpretable as individual or population-level indicators of disturbance or fitness. Importantly, these results indicate that GCs cannot be assumed to represent conservation biomarkers across species or time periods without careful validation

    Applying the Free-Energy Principle to Complex Adaptive Systems

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    The free energy principle is a mathematical theory of the behaviour of self-organising systems that originally gained prominence as a unified model of the brain. Since then, the theory has been applied to a plethora of biological phenomena, extending from single-celled and multicellular organisms through to niche construction and human culture, and even the emergence of life itself. The free energy principle tells us that perception and action operate synergistically to minimize an organism’s exposure to surprising biological states, which are more likely to lead to decay. A key corollary of this hypothesis is active inference—the idea that all behavior involves the selective sampling of sensory data so that we experience what we expect to (in order to avoid surprises). Simply put, we act upon the world to fulfill our expectations. It is now widely recognized that the implications of the free energy principle for our understanding of the human mind and behavior are far-reaching and profound. To date, however, its capacity to extend beyond our brain—to more generally explain living and other complex adaptive systems—has only just begun to be explored. The aim of this collection is to showcase the breadth of the free energy principle as a unified theory of complex adaptive systems—conscious, social, living, or not

    Handbook of Life Course Health Development

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    Health development science; Developmental origins of chronic illnesses; Community; Diabetes; Autism; Obesity; Nutrition; Health disparities across the lifespan; Fetal programmin

    Activation of the pro-resolving receptor Fpr2 attenuates inflammatory microglial activation

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    Poster number: P-T099 Theme: Neurodegenerative disorders & ageing Activation of the pro-resolving receptor Fpr2 reverses inflammatory microglial activation Authors: Edward S Wickstead - Life Science & Technology University of Westminster/Queen Mary University of London Inflammation is a major contributor to many neurodegenerative disease (Heneka et al. 2015). Microglia, as the resident immune cells of the brain and spinal cord, provide the first line of immunological defence, but can become deleterious when chronically activated, triggering extensive neuronal damage (Cunningham, 2013). Dampening or even reversing this activation may provide neuronal protection against chronic inflammatory damage. The aim of this study was to determine whether lipopolysaccharide (LPS)-induced inflammation could be abrogated through activation of the receptor Fpr2, known to play an important role in peripheral inflammatory resolution. Immortalised murine microglia (BV2 cell line) were stimulated with LPS (50ng/ml) for 1 hour prior to the treatment with one of two Fpr2 ligands, either Cpd43 or Quin-C1 (both 100nM), and production of nitric oxide (NO), tumour necrosis factor alpha (TNFα) and interleukin-10 (IL-10) were monitored after 24h and 48h. Treatment with either Fpr2 ligand significantly suppressed LPS-induced production of NO or TNFα after both 24h and 48h exposure, moreover Fpr2 ligand treatment significantly enhanced production of IL-10 48h post-LPS treatment. As we have previously shown Fpr2 to be coupled to a number of intracellular signaling pathways (Cooray et al. 2013), we investigated potential signaling responses. Western blot analysis revealed no activation of ERK1/2, but identified a rapid and potent activation of p38 MAP kinase in BV2 microglia following stimulation with Fpr2 ligands. Together, these data indicate the possibility of exploiting immunomodulatory strategies for the treatment of neurological diseases, and highlight in particular the important potential of resolution mechanisms as novel therapeutic targets in neuroinflammation. References Cooray SN et al. (2013). Proc Natl Acad Sci U S A 110: 18232-7. Cunningham C (2013). Glia 61: 71-90. Heneka MT et al. (2015). Lancet Neurol 14: 388-40
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