The Developmental Trajectory of Empathy and Its Association with Early Symptoms of Psychopathology in Children with and without Hearing Loss

Empathy enables people to share, understand, and show concern for others’ emotions. However, this capacity may be more difficult to acquire for children with hearing loss, due to limited social access, and the effect of hearing on empathic maturation has been unexplored. This four-wave longitudinal study investigated the development of empathy in children with and without hearing loss, and how this development is associated with early symptoms of psychopathology. Seventy-one children with hearing loss and cochlear implants (CI), and 272 typically-hearing (TH) children, participated (aged 1–5 years at Time 1). Parents rated their children’s empathic skills (affective empathy, attention to others’ emotions, prosocial actions, and emotion acknowledgment) and psychopathological symptoms (internalizing and externalizing behaviors). Children with CI and TH children were rated similarly on most of the empathic skills. Yet, fewer prosocial actions were reported in children with CI than in TH children. In both groups, affective empathy decreased with age, while prosocial actions and emotion acknowledgment increased with age and stabilized when children entered primary schools. Attention to emotions increased with age in children with CI, yet remained stable in TH children. Moreover, higher levels of affective empathy, lower levels of emotion acknowledgment, and a larger increase in attention to emotions over time were associated with more psychopathological symptoms in both groups. These findings highlight the importance of social access from which children with CI can learn to process others’ emotions more adaptively. Notably, interventions for psychopathology that tackle empathic responses may be beneficial for both groups, alike

Interplay between SIN3A and STAT3 Mediates Chromatin Conformational Changes and GFAP Expression during Cellular Differentiation

BACKGROUND: Neurons and astrocytes are generated from common neural precursors, yet neurogenesis precedes astrocyte formation during embryogenesis. The mechanisms of neural development underlying suppression and de-suppression of differentiation-related genes for cell fate specifications are not well understood. METHODOLOGY/PRINCIPAL FINDINGS: By using an in vitro system in which NTera-2 cells were induced to differentiate into an astrocyte-like lineage, we revealed a novel role for Sin3A in maintaining the suppression of GFAP in NTera-2 cells. Sin3A coupled with MeCP2 bound to the GFAP promoter and their occupancies were correlated with repression of GFAP transcription. The repression by Sin3A and MeCP2 may be an essential mechanism underlying the inhibition of cell differentiation. Upon commitment toward an astrocyte-like lineage, Sin3A- MeCP2 departed from the promoter and activated STAT3 simultaneously bound to the promoter and exon 1 of GFAP; meanwhile, olig2 was exported from nuclei to the cytoplasm. This suggested that a three-dimensional or higher-order structure was provoked by STAT3 binding between the promoter and proximal coding regions. STAT3 then recruited CBP/p300 to exon 1 and targeted the promoter for histone H3K9 and H3K14 acetylation. The CBP/p300-mediated histone modification further facilitates chromatin remodeling, thereby enhancing H3K4 trimethylation and recruitment of RNA polymerase II to activate GFAP gene transcription. CONCLUSIONS/SIGNIFICANCE: These results provide evidence that exchange of repressor and activator complexes and epigenetic modifications are critical strategies for cellular differentiation and lineage-specific gene expression