Exploring Emotion Representation to Support Dialogue in Police Training on Child Interviewing

Police officers when dealing with interviewing children have to cope with a complex set of emotions from a vulnerable witness. Triggers for recognising those emotions and how to build rapport are often the basis of learning exercises. However, current training pulls together the full complexity of emotions during role-playing which can be over-whelming and reduce appropriate learning focus. Interestingly a serious game’s interface can provide valuable training not because it represents full complex, multimedia interactions but because it can restrict emotional complexity and increase focus during the interactions on key factors for emotional recognition. The focus of this paper is to report on a specific aspect that was explored during the development of a serious game that aims to address the current police-training needs of child interviewing techniques, where the recognition of emotions plays an important role in understanding how to build rapport with children. The review of literature reveals that emotion recognition, through facial expressions, can contribute significantly to the perceived quality of communication. For this study an ‘emotions map’ was created and tested by 41 participants to be used in the development of a targeted interface design to support the different levels of emotion recognition. The emotions identified were validated with a 70 % agreement across experts and non-experts highlighting the innate role of emotion recognition. A discussion is made around the role of emotions and game-based systems to support their identification for work-based training. As part of the graphical development of the Child Interview Stimulator (CIS) we examined different levels of emotional recognition that can be used to support the in-game graphical representation of a child’s response during a police interview

Dynamics and Regulation of RecA Polymerization and De-Polymerization on Double-Stranded DNA

10.1371/journal.pone.0066712PLoS ONE86

Risk factors for posttraumatic stress reactions among chinese students following exposure to a snowstorm disaster

<p>Abstract</p> <p>Background</p> <p>It is important to understand which factors increase the risk of posttraumatic stress disorder (PTSD) in adolescents. Previous studies have shown that the most important risk factors for PTSD include the type, severity, and duration of exposure to the traumatic events.</p> <p>Methods</p> <p>A cross-sectional survey was used to investigate the psychological symptoms associated with the aftermath of a snowstorm disaster in the Hunan province of China in January 2008. Students living in Hunan were surveyed at a three<b>-</b>month follow-up after the disaster. The questionnaire battery included the Impact of Event Scale-Revised (IES-R, trauma and symptoms associated with PTSD), the Chinese version of the Life Orientation Test-Revised (LOT-R, optimism and pessimism), the Chinese version of the Eysenck Personality Questionnaire (EPQ, neuroticism and extraversion), the Chinese Trait Coping Style Questionnaire (TCSQ, positive and negative coping styles), and a range of questions addressing social demographic characteristics and factors relating to the snowstorm. The survey was administered in school, and 968 students completed and returned the questionnaires.</p> <p>Results</p> <p>The results showed that 14.5% of the students had a total IES-R score ≥20. Students with greater school-to-home distances showed higher levels of posttraumatic stress symptoms than students who lived shorter distances from school. Students with emotional support from their teachers reported higher levels of posttraumatic stress symptoms (21.20%) than students without a teacher's emotional support (11.07%). The IES-R total and subscale scores correlated with all variables except extraversion. The binary logistic regression analysis results showed that the teacher's emotional support [odds ratio (OR) = 1.72, 95% confidence interval (CI) = 1.13-2.62], school-to-home distance (OR = 1.01, 95% CI = 1.00-1.01), negative coping (OR = 1.05; 95% CI = 1.02-1.08), and neuroticism (OR = 1.04, 95% CI = 1.02-1.06) were risk factors that predicted PTSD frequency and severity (percentage correct = 85.5%).</p> <p>Conclusions</p> <p>The risk factors that significantly impacted the onset of posttraumatic stress reactions in students living in Hunan, China following a snowstorm disaster were the school-to-home distance, negative coping, neuroticism, and teacher's emotional support.</p

Cardiac afferent activity modulates the expression of racial stereotypes

Negative racial stereotypes tend to associate Black people with threat. This often leads to the misidentification of harmless objects as weapons held by a Black individual. Yet, little is known about how bodily states impact the expression of racial stereotyping. By tapping into the phasic activation of arterial baroreceptors, known to be associated with changes in the neural processing of fearful stimuli, we show activation of race-threat stereotypes synchronized with the cardiovascular cycle. Across two established tasks, stimuli depicting Black or White individuals were presented to coincide with either the cardiac systole or diastole. Results show increased race-driven misidentification of weapons during systole, when baroreceptor afferent firing is maximal, relative to diastole. Importantly, a third study examining the positive Black-athletic stereotypical association fails to demonstrate similar modulations by cardiac cycle. We identify a body–brain interaction wherein interoceptive cues can modulate threat appraisal and racially biased behaviour in context-dependent ways

Effects of PPARγ ligands on TGF-β1-induced epithelial-mesenchymal transition in alveolar epithelial cells

BACKGROUND: Transforming growth factor beta1 (TGF-beta1)-mediated epithelial mesenchymal transition (EMT) of alveolar epithelial cells (AEC) may contribute to lung fibrosis. Since PPAR gamma ligands have been shown to inhibit fibroblast activation by TGF-beta1, we assessed the ability of the thiazolidinediones rosiglitazone (RGZ) and ciglitazone (CGZ) to regulate TGF-beta1-mediated EMT of A549 cells, assessing changes in cell morphology, and expression of cell adhesion molecules E-cadherin (epithelial cell marker) and N-cadherin (mesenchymal cell marker), and collagen 1 alpha 1 (COL1A1), CTGF and MMP-2 mRNA. METHODS: Serum-deprived A549 cells (human AEC cell line) were pre-incubated with RGZ and CGZ (1 - 30 microM) in the absence or presence of the PPAR gamma antagonist GW9662 (10 microM) before TGFbeta-1 (0.075-7.5 ng/ml) treatment for up to 72 hrs. Changes in E-cadherin, N-cadherin and phosphorylated Smad2 and Smad3 levels were analysed by Western blot, and changes in mRNA levels including COL1A1 assessed by RT-PCR. RESULTS: TGFbeta-1 (2.5 ng/ml)-induced reductions in E-cadherin expression were associated with a loss of epithelial morphology and cell-cell contact. Concomitant increases in N-cadherin, MMP-2, CTGF and COL1A1 were evident in predominantly elongated fibroblast-like cells. Neither RGZ nor CGZ prevented TGF beta 1-induced changes in cell morphology, and PPAR gamma-dependent inhibitory effects of both ligands on changes in E-cadherin were only evident at submaximal TGF-beta1 (0.25 ng/ml). However, both RGZ and CGZ inhibited the marked elevation of N-cadherin and COL1A1 induced by TGF-beta1 (2.5 ng/ml), with effects on COL1A1 prevented by GW9662. Phosphorylation of Smad2 and Smad3 by TGF-beta1 was not inhibited by RGZ or CGZ. CONCLUSIONS: RGZ and CGZ inhibited profibrotic changes in TGF-beta1-stimulated A549 cells independently of inhibition of Smad phosphorylation. Their inhibitory effects on changes in collagen I and E-cadherin, but not N-cadherin or CTGF, appeared to be PPAR gamma-dependent. Further studies are required to unravel additional mechanisms of inhibition of TGF-beta1 signalling by thiazolidinediones and their implications for the contribution of EMT to lung fibrosis

The PPAR-gamma agonist pioglitazone protects cortical neurons from inflammatory mediators via improvement in peroxisomal function

<p>Abstract</p> <p>Background</p> <p>Inflammation is known to play a pivotal role in mediating neuronal damage and axonal injury in a variety of neurodegenerative disorders. Among the range of inflammatory mediators, nitric oxide and hydrogen peroxide are potent neurotoxic agents. Recent evidence has suggested that oligodendrocyte peroxisomes may play an important role in protecting neurons from inflammatory damage.</p> <p>Methods</p> <p>To assess the influence of peroxisomal activation on nitric oxide mediated neurotoxicity, we investigated the effects of the peroxisomal proliferator activated receptor (PPAR) gamma agonist, pioglitazone in primary cortical neurons that were either exposed to a nitric oxide donor or co-cultured with activated microglia.</p> <p>Results</p> <p>Pioglitazone protected neurons and axons against both nitric-oxide donor-induced and microglia-derived nitric oxide-induced toxicity. Moreover, cortical neurons treated with this compound showed a significant increase in the protein and gene expression of PPAR-gamma, which was associated with a concomitant increase in the enzymatic activity of catalase. In addition, the protection of neurons and axons against hydrogen peroxide-induced toxicity afforded by pioglitazone appeared to be dependent on catalase.</p> <p>Conclusions</p> <p>Collectively, these observations provide evidence that modulation of PPAR-gamma activity and peroxisomal function by pioglitazone attenuates both NO and hydrogen peroxide-mediated neuronal and axonal damage suggesting a new therapeutic approach to protect against neurodegenerative changes associated with neuroinflammation.</p