Thinking about feeling: using trait emotional intelligence in understanding the associations between early maladaptive schemas and coping styles

Objectives: Maladaptive interpersonal schemas can trigger distressing emotions and drive dysfunctional behaviour that leads to difficulties in interpersonal relationships and perpetuates the original maladaptive schemas. This study sought to identify patterns of association between trait emotional intelligence (TEI), early maladaptive schemas (EMS), and coping styles in a non‐clinical sample. Emotionality profiles were hypothesized to be associated with EMS severity and poorer coping, as early experiences can shape an individual's self‐perceptions through reinforcement by maladaptive responses. Design: Cross‐sectional study with 142 undergraduate students. Methods: We obtained self‐reports of TEI, coping styles, and EMS. Results: Disengagement coping was strongly correlated with EMS severity (r = .565, p < .01). TEI was negatively correlated with EMS (r = −.660, p < .01) and Disengagement (r = −.405, p < .01). Emotionality, Impaired Autonomy, and Overvigilance partially mediated the relationship between Disconnection and Emotion‐Focused Disengagement. Self‐Control fully mediated the relationship between Impaired Limits and Problem‐Focused Disengagement. Conclusions: The findings suggest that lower TEI is associated with the likelihood for maladaptive coping in response to EMS. The preference for certain coping styles associated with a particular domain of EMS may be explained by an individual's perceived metacognitive ability to regulate their stress and emotions. When individuals’ needs for love, safety, and acceptance from others are not met, there might be poorer perceived self‐efficacies in Emotionality and the tendency to cope through emotional avoidance. Individuals with difficulties establishing internal limits are more likely to respond with problem avoidance, possibly due to deficient distress tolerance. Longitudinal studies with a clinical population are warranted to replicate these findings

A systems-level framework for drug discovery identifies Csf1R as an anti-epileptic drug target

The identification of drug targets is highly challenging, particularly for diseases of the brain. To address this problem, we developed and experimentally validated a general computational framework for drug target discovery that combines gene regulatory information with causal reasoning (“Causal Reasoning Analytical Framework for Target discovery”—CRAFT). Using a systems genetics approach and starting from gene expression data from the target tissue, CRAFT provides a predictive framework for identifying cell membrane receptors with a direction-specified influence over disease-related gene expression profiles. As proof of concept, we applied CRAFT to epilepsy and predicted the tyrosine kinase receptor Csf1R as a potential therapeutic target. The predicted effect of Csf1R blockade in attenuating epilepsy seizures was validated in three pre-clinical models of epilepsy. These results highlight CRAFT as a systems-level framework for target discovery and suggest Csf1R blockade as a novel therapeutic strategy in epilepsy. CRAFT is applicable to disease settings other than epilepsy

AKT Signaling Mediates IGF-I Survival Actions on Otic Neural Progenitors

Background: Otic neurons and sensory cells derive from common progenitors whose transition into mature cells requires the coordination of cell survival, proliferation and differentiation programmes. Neurotrophic support and survival of post-mitotic otic neurons have been intensively studied, but the bases underlying the regulation of programmed cell death in immature proliferative otic neuroblasts remains poorly understood. The protein kinase AKT acts as a node, playing a critical role in controlling cell survival and cell cycle progression. AKT is activated by trophic factors, including insulin-like growth factor I (IGF-I), through the generation of the lipidic second messenger phosphatidylinositol 3-phosphate by phosphatidylinositol 3-kinase (PI3K). Here we have investigated the role of IGF-dependent activation of the PI3K-AKT pathway in maintenance of otic neuroblasts. Methodology/Principal Findings: By using a combination of organotypic cultures of chicken (Gallus gallus) otic vesicles and acoustic-vestibular ganglia, Western blotting, immunohistochemistry and in situ hybridization, we show that IGF-I-activation of AKT protects neural progenitors from programmed cell death. IGF-I maintains otic neuroblasts in an undifferentiated and proliferative state, which is characterised by the upregulation of the forkhead box M1 (FoxM1) transcription factor. By contrast, our results indicate that post-mitotic p27Kip-positive neurons become IGF-I independent as they extend their neuronal processes. Neurons gradually reduce their expression of the Igf1r, while they increase that of the neurotrophin receptor, TrkC. Conclusions/Significance: Proliferative otic neuroblasts are dependent on the activation of the PI3K-AKT pathway by IGF-I for survival during the otic neuronal progenitor phase of early inner ear development

Study protocol: evaluation of an online, father-inclusive, universal parenting intervention to reduce child externalising behaviours and improve parenting practices

Abstract Background Parenting interventions that focus on enhancing the quality and consistency of parenting are effective for preventing and reducing externalising problems in children. There has been a recent shift towards online delivery of parenting interventions in order to increase their reach and impact on the population prevalence of child externalising problems. Parenting interventions have low rates of father participation yet research suggests that father involvement may be critical to the success of the intervention. Despite this, no online parenting interventions have been specifically developed to meet the needs and preferences of fathers, as well as mothers. This paper describes the protocol of a study examining the effectiveness of an online, father-inclusive parenting intervention called ‘ParentWorks’, which will be delivered as a universal intervention to Australian families. Methods/design A single group clinical trial will be conducted to examine the effectiveness of ParentWorks for reducing child externalising problems and improving parenting, as well as to explore the impact of father engagement (in two-parent families) on child outcomes. Australian parents/caregivers with a child aged 2–16 years will be recruited. Participants will provide informed consent, complete pre-intervention measures and will then complete the intervention, which consists of five compulsory video modules and three optional modules. The primary outcomes for this study are changes in child externalising behaviour, positive and dysfunctional parenting practices and parental conflict, and the secondary outcome is changes in parental mental health. Demographic information, satisfaction with the intervention, and measures of parental engagement will also be collected. Questionnaire data will be collected at pre-intervention, post-intervention and three-month follow-up, as well as throughout the program. Discussion This paper describes the study protocol of a single group clinical trial of a national, online, father-inclusive parenting intervention. The results from this study could be used to inform public policy about providing support to parents of children with behaviour problems, and enhancing the engagement of fathers in parenting interventions. Trial registration ACTRN12616001223426 , registered 05/09/201