Education Department

This study employed an A-B singled subject design to explore the extent to which a peer-mediated intervention supported a first-grade student with autism's usage both in purpose and frequency of a speech-generating device (SGD) during mathematics activities. The intervention involved teaching a peer without a disability to encourage the student with autism to use the SGD during partnered mathematics activities. Our analysis involved visual and descriptive examination of trends and patterns over time, and comparison of means between and within phases. We found during the course of this study that (1) the student with autism's level of overall communication, which included the relevancy of these communicative behaviors, increased; (2) the student with autism's level of spontaneous communication acts increased; and (3) the peer became more independent with supporting the student with autism's communication. Implications for future research and practice are provided.

Determining the layers of gene regulation within the innate immune response is critical to our understanding of the cellular responses to infection and dysregulation in disease. We identified a conserved mechanism of gene regulation in human and mouse via changes in alternative first exon (AFE) usage following inflammation, resulting in changes to the isoforms produced. Of these AFE events, we identified 95 unannotated transcription start sites in mice using a de novo transcriptome generated by long-read native RNA-sequencing, one of which is in the cytosolic receptor for dsDNA and known inflammatory inducible gene, Aim2. We show that this unannotated AFE isoform of Aim2 is the predominant isoform expressed during inflammation and contains an iron-responsive element in its 5'UTR enabling mRNA translation to be regulated by iron levels. This work highlights the importance of examining alternative isoform changes and translational regulation in the innate immune response and uncovers novel regulatory mechanisms of Aim2.