Childbirth-related post-traumatic stress disorder symptoms and mother-infant neurophysiological and behavioral co-regulation during dyadic interaction: study protocol

BackgroundMother's childbirth-related posttraumatic stress disorder (PTSD) symptoms have a negative impact on mother and infant's behaviors during dyadic interactions which may increase mother-infant neurophysiological and behavioral co-regulation difficulties, leading to dysregulated mother-infant interactions. This study was specifically designed to analyze: (1) the sociodemographic and obstetric factors associated with mother's childbirth-related PTSD symptoms; (2) mother-infant neurophysiological functioning and behavioral co-regulation during dyadic interaction; (3) the impact of mother's childbirth-related PTSD symptoms on neurophysiological and behavioral mother-infant co-regulation during dyadic interaction; (4) the moderator role of previous trauma on the impact of mother's childbirth-related PTSD symptoms on neurophysiological and behavioral mother-infant co-regulation during dyadic interaction; and (5) the moderator role of comorbid symptoms of anxiety and depression on the impact of mother's childbirth-related PTSD symptoms on neurophysiological and behavioral mother-infant co-regulation during dyadic interaction.MethodsAt least 250 mothers will be contacted in order to account for refusals and dropouts and guarantee at least 100 participating mother-infant dyads with all the assessment waves completed. The study has a longitudinal design with three assessment waves: (1) 1-3 days postpartum, (2) 8 weeks postpartum, and (3) 22 weeks postpartum. Between 1 and 3 days postpartum, mothers will report on-site on their sociodemographic and obstetric characteristics. At 8 weeks postpartum, mothers will complete online self-reported measures of birth trauma, previous trauma, childbirth-related PTSD, anxiety, and depressive symptoms. At 22 weeks postpartum, mothers will complete online self-reported measures of childbirth-related PTSD, anxiety, and depressive symptoms. Mothers and infants will then be home-visited to observe and record their neurophysiological, neuroimaging and behavioral data during dyadic interactions using the Still-face Paradigm. Activation patterns in the prefrontal cortices of mother and infant will be recorded simultaneously using hyperscanning acquisition devices. Unadjusted and adjusted multilevel linear regression models will be performed to analyze objectives 1 to 3. Moderation models will be performed to analyze objectives 4 and 5.DiscussionData from this study will inform psychological interventions targeting mother-infant interaction, co-regulation, and infant development. Moreover, these results can contribute to designing effective screenings to identify mothers at risk of perinatal mental health problems and those who may need specialized perinatal mental health care

Dissociable Effects of Psychopathic Traits on Executive Functioning: Insights From the Triarchic Model

The relationship between executive functioning and psychopathy lacks consistent findings. The heterogeneity of the psychopathic personality structure may contribute to the mixed data that emerged from clinical-categorical approaches. Considering the link between antisocial behavior and executive dysfunction from the perspective of the Triarchic Model of Psychopathy, it is suggested that executive impairments in psychopathy are specifically explained by meanness and disinhibition traits, reflecting externalizing vulnerability. In turn, boldness is conceptualized as an adaptive trait. The current study assessed updating (N-back), inhibition (Stroop), and shifting (Trail Making Test) in a forensic (n = 56) and non-forensic sample (n = 48) that completed the Triarchic Psychopathy Measure. A positive association between boldness and inhibition was found, while meanness accounted for the lack of inhibitory control. In addition, disinhibition explained updating dysfunction. These findings provide empirical evidence for dissociable effects of psychopathic traits on executive functioning, in light of the Triarchic Model of Psychopathy

Effects of age on the identification of emotions in facial expressions: a meta-analysis

© 2018 Gonçalves et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited.Background: Emotion identification is a fundamental component of social cognition. Although it is well established that a general cognitive decline occurs with advancing age, the effects of age on emotion identification is still unclear. A meta-analysis by Ruffman and colleagues (2008) explored this issue, but much research has been published since then, reporting inconsistent findings. Methods: To examine age differences in the identification of facial expressions of emotion, we conducted a meta-analysis of 24 empirical studies (N = 1,033 older adults, N = 1,135 younger adults) published after 2008. Additionally, a meta-regression analysis was conducted to identify potential moderators. Results: Results show that older adults less accurately identify facial expressions of anger, sadness, fear, surprise, and happiness compared to younger adults, strengthening the results obtained by Ruffman et al. (2008). However, meta-regression analyses indicate that effect sizes are moderated by sample characteristics and stimulus features. Importantly, the estimated effect size for the identification of fear and disgust increased for larger differences in the number of years of formal education between the two groups. Discussion: We discuss several factors that might explain the age-related differences in emotion identification and suggest how brain changes may account for the observed pattern. Furthermore, moderator effects are interpreted and discussed.This research was supported by a grant from the Fundação BIAL. Carina Fernandes was supported by a doctoral grant from the Fundação para a Ciência e Tecnologia (Carina Fernandes - SFRH/BD/112101/2015).info:eu-repo/semantics/publishedVersio

Sensor Placement via Optimal Experiment Design in EMI Sensing of Metallic Objects

This work, under the optimal experimental design framework, investigates the sensor placement problem that aims to guide electromagnetic induction (EMI) sensing of multiple objects. We use the linearized model covariance matrix as a measure of estimation error to present a sequential experimental design (SED) technique. The technique recursively minimizes data misfit to update model parameters and maximizes an information gain function for a future survey relative to previous surveys. The fundamental process of the SED seeks to increase weighted sensitivities to targets when placing sensors. The synthetic and field experiments demonstrate that SED can be used to guide the sensing process for an effective interrogation. It also can serve as a theoretic basis to improve empirical survey operation. We further study the sensitivity of the SED to the number of objects within the sensing range. The tests suggest that an appropriately overrepresented model about expected anomalies might be a feasible choice

Frequent 4EBP1 Amplification Induces Synthetic Dependence on FGFR Signaling in Cancer

Simple Summary Our work establishes that amplification of 4EBP1, as a part of Chr. 8p11, creates a synthetic dependency on FGFR1 signaling in cancer. 4EBP1 is phosphorylated by FGFR1 and PI3K signaling, and accordingly cancer with 4EBP1-FGFR1 amplification is more sensitive to FGFR1 and PI3K inhibition due to inhibition of 4EBP1 phosphorylation. Moreover, we characterize the translational targets of 4EBP1 and identify that 4EBP1 specifically regulates the translation of genes involved in insulin signaling, glucose metabolism, and the inositol pathway that plays a role in cancer progression. The eIF4E translation initiation factor has oncogenic properties and concordantly, the inhibitory eIF4E-binding protein (4EBP1) is considered a tumor suppressor. The exact molecular effects of 4EBP1 activation in cancer are still unknown. Surprisingly, 4EBP1 is a target of genomic copy number gains (Chr. 8p11) in breast and lung cancer. We noticed that 4EBP1 gains are genetically linked to gains in neighboring genes, including WHSC1L1 and FGFR1. Our results show that FGFR1 gains act to attenuate the function of 4EBP1 via PI3K-mediated phosphorylation at Thr37/46, Ser65, and Thr70 sites. This implies that not 4EBP1 but instead FGFR1 is the genetic target of Chr. 8p11 gains in breast and lung cancer. Accordingly, these tumors show increased sensitivity to FGFR1 and PI3K inhibition, and this is a therapeutic vulnerability through restoring the tumor-suppressive function of 4EBP1. Ribosome profiling reveals genes involved in insulin signaling, glucose metabolism, and the inositol pathway to be the relevant translational targets of 4EBP1. These mRNAs are among the top 200 translation targets and are highly enriched for structure and sequence motifs in their 5 ' UTR, which depends on the 4EBP1-EIF4E activity. In summary, we identified the translational targets of 4EBP1-EIF4E that facilitate the tumor suppressor function of 4EBP1 in cancer

The post-transcriptional trans-acting regulator, TbZFP3, co-ordinates transmission-stage enriched mRNAs in Trypanosoma brucei

Post-transcriptional gene regulation is essential to eukaryotic development. This is particularly emphasized in trypanosome parasites where genes are co-transcribed in polycistronic arrays but not necessarily co-regulated. The small CCCH protein, TbZFP3, has been identified as a trans-acting post-transcriptional regulator of Procyclin surface antigen expression in Trypanosoma brucei. To investigate the wider role of TbZFP3 in parasite transmission, a global analysis of associating transcripts was carried out. Examination of a subset of the selected transcripts revealed their increased abundance through mRNA stabilization upon TbZFP3 ectopic overexpression, dependent upon the integrity of the CCCH zinc finger domain. Reporter assays demonstrated that this regulation was mediated through 3′-UTR sequences for two target transcripts. Global developmental expression profiling of the cohort of TbZFP3-selected transcripts revealed their significant enrichment in transmissible stumpy forms of the parasite. This analysis of the specific mRNAs selected by the TbZFP3mRNP provides evidence for a developmental regulon with the potential to co-ordinate genes important in parasite transmission

The Cell Cycle Regulated Transcriptome of Trypanosoma brucei

Progression of the eukaryotic cell cycle requires the regulation of hundreds of genes to ensure that they are expressed at the required times. Integral to cell cycle progression in yeast and animal cells are temporally controlled, progressive waves of transcription mediated by cell cycle-regulated transcription factors. However, in the kinetoplastids, a group of early-branching eukaryotes including many important pathogens, transcriptional regulation is almost completely absent, raising questions about the extent of cell-cycle regulation in these organisms and the mechanisms whereby regulation is achieved. Here, we analyse gene expression over the Trypanosoma brucei cell cycle, measuring changes in mRNA abundance on a transcriptome-wide scale. We developed a “double-cut” elutriation procedure to select unperturbed, highly synchronous cell populations from log-phase cultures, and compared this to synchronization by starvation. Transcriptome profiling over the cell cycle revealed the regulation of at least 430 genes. While only a minority were homologous to known cell cycle regulated transcripts in yeast or human, their functions correlated with the cellular processes occurring at the time of peak expression. We searched for potential target sites of RNA-binding proteins in these transcripts, which might earmark them for selective degradation or stabilization. Over-represented sequence motifs were found in several co-regulated transcript groups and were conserved in other kinetoplastids. Furthermore, we found evidence for cell-cycle regulation of a flagellar protein regulon with a highly conserved sequence motif, bearing similarity to consensus PUF-protein binding motifs. RNA sequence motifs that are functional in cell-cycle regulation were more widespread than previously expected and conserved within kinetoplastids. These findings highlight the central importance of post-transcriptional regulation in the proliferation of parasitic kinetoplastids