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Melodic expectancies among children and adults were examined. In Experiment 1, adults, 11-year-olds, and 8-year-olds rated how well individual test tones continued fragments of melodies. In Experiment 2, 11-, 8-, and 5-year-olds sang continuations to 2-tone stimuli. Response patterns were analyzed using 2 models of melodic expectancy. Despite having fewer predictor variables, the 2-factor model (E. G. Schellenberg, 1997) equaled or surpassed the implication-realization model (E. Narmour, 1990) in predictive accuracy. Listeners of all ages expected the next tone in a melody to be proximate in pitch to the tone heard most recently. Older listeners also expected reversals of pitch direction, specifically for tones that changed direction after a disruption of proximity and for tones that formed symmetric patterns.

This paper provides a synopsis of findings from the first two phases of a larger campus-based participatory action research study, which examines the factors that contribute to health within a university setting. Theoretical underpinnings of this study were rooted in concepts of socio-ecological thinking and healthy settings and in the Ottawa Charter and the Okanagan Charter on Health Promoting Universities. In Phase 1 (February 2016), a multidisciplinary team of student and faculty researchers used a campus survey to identify perceived facilitators and barriers to health within the university context. Participants (n = 181) included students, faculty, staff and administration. Findings from Phase 1 were used to create a second survey that itemised possible priority areas for action. In Phase 2 (April 2017), this health priorities survey was sent via the university-wide email listserv to the campus community for input. There was consensus among respondents on which areas should be prioritized for action. Areas identified include health enhancing food-environments (e.g., access to healthy food), health enhancing social environments (e.g., coping and stress management), and teaching and learning environments that support healthy living and well-being (e.g., work-life balance). The findings from Phases 1 and 2 of this study will guide student-engaged and community-driven interventions in subsequent phases of this research. [ABSTRACT FROM AUTHOR]

Background: Moral injury (MI) is consistently associated with adverse mental health outcomes, including the development of posttraumatic stress disorder (PTSD) and suicidality. Methods: We investigated neural activation patterns associated with MI event recall using functional magnetic resonance imaging in participants with military and public safety‐related PTSD, relative to civilian MI‐exposed controls. Results: MI recall in the PTSD as compared to control group was associated with increased neural activation among salience network nodes involved in viscerosensory processing and hyperarousal (right posterior insula, dorsal anterior cingulate cortex; dACC), regions involved in defensive responding (left postcentral gyrus), and areas responsible for top‐down cognitive control of emotions (left dorsolateral prefrontal cortex; dlPFC). Within the PTSD group, measures of state and trait shame correlated negatively with activity among default mode network regions associated with self‐related processing and moral cognition (dorsomedial prefrontal cortex; dmPFC) and salience network regions associated with viscerosensory processing (left posterior insula), respectively. Conclusions: These findings suggest that MI event processing is altered in military and public safety‐related PTSD, relative to MI‐exposed controls. Here, it appears probable that as individuals with PTSD recall their MI event, they experience a surge of blame‐related processing of bodily sensations within salience network regions, including the right posterior insula and the dACC, which in turn, prompt regulatory strategies at the level of the left dlPFC aimed at increasing cognitive control and inhibiting emotional affect. These results are consistent with previous findings showing enhanced sensory processing and altered top‐down control in PTSD samples during autobiographical memory recall. [ABSTRACT FROM AUTHOR]

Background Dysfunction of histone methyltransferases and chromatin modifiers has been implicated in complex neurodevelopmental syndromes and cancers. SETD1B encodes a lysine-specific methyltransferase that assists in transcriptional activation of genes by depositing H3K4 methyl marks. Previous reports of patients with rare variants in SETD1B describe a distinctive phenotype that includes seizures, global developmental delay and intellectual disability. Methods Two of the patients described herein were identified via genome-wide and exome-wide testing, with microarray and research-based exome, through the CAUSES (Clinical Assessment of the Utility of Sequencing and Evaluation as a Service) Research Clinic at the University of British Columbia. The third Vancouver patient had clinical trio exome sequencing through Blueprint Genetics. The fourth patient underwent singleton exome sequencing in Nantes, with subsequent recruitment to this cohort through GeneMatcher. Results Here we present clinical reports of four patients with rare coding variants in SETD1B that demonstrate a shared phenotype, including intellectual disability, language delay, conserved musculoskeletal findings and seizures that may be treatment-refractory. We include supporting evidence from next-generation sequencing among a cohort of paediatric patients with epilepsy. Conclusion Rare coding variants in SETD1B can cause a diagnosable syndrome and could contribute as a risk factor for epilepsy, autism and other neurodevelopmental phenotypes. In the long term, some patients may also be at increased risk for cancers and other complex diseases. Thus, longitudinal studies are required to further elucidate the precise role of SETD1B in neurodevelopmental disorders and other systemic disease. [ABSTRACT FROM AUTHOR]