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Educational psychologists seek to keep abreast of significant theoretical and practical developments within the field of inclusive education. This paper outlines and discusses Universal Design for Learning as a theory of inclusion, highly applicable for use by educational psychologists. The Universal Design for Learning (UDL) framework is introduced by exploring the contextual history of its development and explaining the three pillars of the framework; the ‘affective networks’, the ‘recognition networks’, and the ‘strategic networks’. Application of the UDL framework is demonstrated with classroom-based examples, drawing on existing research. A critical stance is taken towards understanding the current drawbacks of UDL, and direct links to educational psychology practice are made and critically reviewed considering these.

Purpose Children with medical complexity (MC) must rely on others to notice and address pain. Parents are aware of child pain behaviors and can serve as reliable proxy reporters. Thus, there is a critical need to understand parent perspectives to improve pain practices. Design Individual interviews were used as a data collection method in this qualitative study. Methods Participants were recruited via mail and social media postings. Interviews were audio-recorded and transcribed verbatim. Transcribed documents were imported to NVIVO for qualitative analysis. Conventional and directed approaches to qualitative content analysis were used. Results From the data analysis, major themes included: pain experiences, confidence in caregivers, parents are partners, proactive communication, and a spontaneous theme, “they can hear us.” Emotional pain and challenges identifying the source pain were identified as sub-themes of pain experiences. Conclusions Parents in this study shared methods helpful to identifying pain in their children, as well as suggestions for discussing pain with caregivers. Priorities for future research include identifying methods for sharing pain information that are thorough, but do not burden parents or providers. Researchers should also determine how parents and caregivers can partner to identify and address pain in children with MC. Going forward, conversations about pain should be a key part of any admission assessment or first encounter. As pain episodes among children with MC can be complex and may not always be re-created in front of a provider, nurses may advise parents to take photos or videos to share with caregivers.

[Image: see text] Despite intense attention from biomedical and chemical researchers, there are few approved treatments for amyotrophic lateral sclerosis (ALS), with only riluzole (Rilutek) and edaravone (Radicava) currently available to patients. Moreover, the mechanistic basis of the activity of these drugs is currently not well-defined, limiting the ability to design new medicines for ALS. This Letter describes the synthesis of triazole-containing riluzole analogues, and their testing in a novel neuroprotective assay. Seven compounds were identified as having neuroprotective activity, with two compounds having similar activity to riluzole.

The Forkhead transcription factor, FoxO3a induces genomic death responses in neurones following translocation from the cytosol to the nucleus. Nuclear translocation of FoxO3a is triggered by trophic factor withdrawal, oxidative stress and the stimulation of extrasynaptic NMDA receptors. Receptor activation of phosphatidylinositol 3-kinase (PI3K) - Akt signalling pathways retains FoxO3a in the cytoplasm thereby inhibiting the transcriptional activation of death promoting genes. We hypothesised that phenolic antioxidants such as tert-Butylhydroquinone (tBHQ), which is known to stimulate PI3K-Akt signalling, would inhibit FoxO3a translocation and activity. Treatment of cultured cortical neurones with NMDA increased the nuclear localisation of FoxO3a, reduced the phosphorylation of FoxO3a, increased caspase activity and upregulated Fas ligand expression. In contrast the phenolic antioxidant tBHQ caused retention of FoxO3a in the cytosol coincident with enhanced PI3K- dependent phosphorylation of FoxO3a. tBHQ-induced nuclear exclusion of FoxO3a was associated with reduced FoxO-mediated transcriptional activity. Exposure of neurones to tBHQ inhibited NMDA-induced nuclear translocation of FoxO3a prevented NMDA-induced upregulation of FoxO-mediated transcriptional activity, blocked caspase activation and protected neurones from NMDA-induced excitotoxic death. Collectively, these data suggest that phenolic antioxidants such as tBHQ oppose stress-induced activation of FoxO3a and therefore have potential neuroprotective utility in neurodegeneration. © 2012 The Authors Journal of Neurochemistry © 2012 International Society for Neurochemistry.