"Can I Play Too?" A Qualitative Study of Outdoor Play and Participation Among Autistic Preschoolers.

IMPORTANCE: Outdoor play in homes, schools, and communities provides children with unique opportunities to explore their worlds, develop fundamental life skills, and experience belonging. However, few studies have explored outdoor free play among autistic preschoolers in natural settings from a neurodivergent-informed perspective. OBJECTIVE: To explore the play preferences, opportunities, and challenges in outdoor play for autistic preschoolers. DESIGN: In this qualitative study, the authors used a multimethod approach to data collection using visual, verbal, and projective techniques and thematic analysis to identify and describe outdoor play occupation as expressed by autistic preschoolers. SETTING: Home, community, and preschool environments in a city in Ireland. PARTICIPANTS: Seven autistic children and their parents, from seven diverse preschool settings in Ireland. RESULTS: Two overarching themes were identified: (1) outdoor play preferences and meaning and (2) the physical and social environments of outdoor play. The findings suggest that autistic preschoolers demonstrate distinctive play styles and preferences when playing freely outdoors, with physical and social barriers to outdoor play existing in community and educational contexts. CONCLUSIONS AND RELEVANCE: The findings suggest that autistic preschoolers' outdoor play styles and preferences require support from adult advocates. Although the importance of relationships and social play cannot be overlooked, infrastructural accommodations for parents and schools are required if we are to create supportive and inclusive outdoor play environments and opportunities for freedom of expression for autistic children. Plain-Language Summary: This study explored the distinctive outdoor play preferences, opportunities, and challenges for autistic preschoolers. The findings show that autistic preschoolers face physical and social barriers to outdoor play and that they need parents, schools, and communities to create supportive and inclusive play environments and opportunities for freedom of expression.

Beyond housekeeping: autophagy regulates PKA signaling at synapses.

Autophagy modulates synaptic function and plasticity, but the molecular basis for this process is largely unknown. A recent tour de force study by Overhoff and colleagues identifies a novel role for autophagy in regulating PKA signaling at synapses to modulate the organization of the postsynaptic proteome and neuronal excitability.

A circuit logic for sexually shared and dimorphic aggressive behaviors in Drosophila.

Aggression involves both sexually monomorphic and dimorphic actions. How the brain implements these two types of actions is poorly understood. We have identified three cell types that regulate aggression in Drosophila: one type is sexually shared, and the other two are sex specific. Shared common aggression-promoting (CAP) neurons mediate aggressive approach in both sexes, whereas functionally downstream dimorphic but homologous cell types, called male-specific aggression-promoting (MAP) neurons in males and fpC1 in females, control dimorphic attack. These symmetric circuits underlie the divergence of male and female aggressive behaviors, from their monomorphic appetitive/motivational to their dimorphic consummatory phases. The strength of the monomorphic → dimorphic functional connection is increased by social isolation in both sexes, suggesting that it may be a locus for isolation-dependent enhancement of aggression. Together, these findings reveal a circuit logic for the neural control of behaviors that include both sexually monomorphic and dimorphic actions, which may generalize to other organisms.

The p53 Pathway in Glioblastoma.

The tumor suppressor and transcription factor p53 plays critical roles in tumor prevention by orchestrating a wide variety of cellular responses, including damaged cell apoptosis, maintenance of genomic stability, inhibition of angiogenesis, and regulation of cell metabolism and tumor microenvironment. TP53 is one of the most commonly deregulated genes in cancer. The p53-ARF-MDM2 pathway is deregulated in 84% of glioblastoma (GBM) patients and 94% of GBM cell lines. Deregulated p53 pathway components have been implicated in GBM cell invasion, migration, proliferation, evasion of apoptosis, and cancer cell stemness. These pathway components are also regulated by various microRNAs and long non-coding RNAs. TP53 mutations in GBM are mostly point mutations that lead to a high expression of a gain of function (GOF) oncogenic variants of the p53 protein. These relatively understudied GOF p53 mutants promote GBM malignancy, possibly by acting as transcription factors on a set of genes other than those regulated by wild type p53. Their expression correlates with worse prognosis, highlighting their potential importance as markers and targets for GBM therapy. Understanding mutant p53 functions led to the development of novel approaches to restore p53 activity or promote mutant p53 degradation for future GBM therapies.