Development and Psychometric Properties of the Emotional Intelligence Admission Essay Scale

The purpose was to describe the development and psychometric properties of the Emotional Intelligence Admission Essay scale. The authors developed an admission essay question and rating scale designed to provide information about applicants’ emotional intelligence (EI). Content validity, convergent validity, interrater reliability, and internal consistency were established. The scale was also examined to determine if it could discriminate between students with and without professional behavior problems in the academic and fieldwork settings. Content validity was found to be high by a panel of three experts in EI (content validity index = 1.0). Convergent validity with the Assessing Emotions Scale was moderate (r = .46, p \u3c .02). Interrater reliability between two trained faculty raters was high (ICC = .91, p \u3c .000). Internal consistency of the scale was high with a Cronbach’s alpha of .95. This version of the scale was not able to discriminate between students with and without professional behavior problems. The moderate to strong psychometric properties suggest that the EI Admission Essay Scale has the ability to provide information about applicants’ EI. The wording of the essay question must be modified to better instruct applicants to address interpersonal conflict

Variants in PRKAR1B cause a neurodevelopmental disorder with autism spectrum disorder, apraxia, and insensitivity to pain

Purpose We characterize the clinical and molecular phenotypes of six unrelated individuals with intellectual disability and autism spectrum disorder who carry heterozygous missense variants of the PRKAR1B gene, which encodes the R1 beta subunit of the cyclic AMP-dependent protein kinase A (PKA). Methods Variants of PRKAR1B were identified by single- or trio-exome analysis. We contacted the families and physicians of the six individuals to collect phenotypic information, performed in vitro analyses of the identified PRKAR1B-variants, and investigated PRKAR1B expression during embryonic development. Results Recent studies of large patient cohorts with neurodevelopmental disorders found significant enrichment of de novo missense variants in PRKAR1B. In our cohort, de novo origin of the PRKAR1B variants could be confirmed in five of six individuals, and four carried the same heterozygous de novo variant c.1003C>T (p.Arg335Trp; NM_001164760). Global developmental delay, autism spectrum disorder, and apraxia/dyspraxia have been reported in all six, and reduced pain sensitivity was found in three individuals carrying the c.1003C>T variant. PRKAR1B expression in the brain was demonstrated during human embryonal development. Additionally, in vitro analyses revealed altered basal PKA activity in cells transfected with variant-harboring PRKAR1B expression constructs. Conclusion Our study provides strong evidence for a PRKAR1B-related neurodevelopmental disorder