Editorial: Addressing community priorities in autism research

Autism is a form of neurodiversity, currently characterized by differences compared to the neurotypical population across multiple domains including sensory processing (Proff et al., 2021), social communication style (Crompton et al., 2021), attentional processing (Murray et al., 2005), and movement and motor processing (Miller et al., 2021). Historically, autism (and thus autistic people) has been studied through a medical lens (Chapman and Carel, 2022), owing primarily to the characterization of autism as a disorder of childhood development. These conceptualizations led to dehumanizing narratives about autistic people (Botha) and have impacted on who we consider to be knowledgeable about what it is like to be autistic (Kourti). In recent years, there has been a shift toward recognition of autism as a form of neurodivergence; a naturally occurring variation in the human population that may lead to a differential profile of strengths and challenges in comparison to the non-autistic population (Den Houting, 2019). This shift has been primarily driven by the autistic self-advocacy and neurodiversity movements (Kapp et al., 2013; Walker, 2021), which have campaigned for better understanding of autistic people

Impact and process evaluation of Forward Thinking Birmingham, the 0-25 Mental Health Service : Final Report

This report provides the findings of a year-long evaluation of Forward Thinking Birmingham (FTB) which started just after the service went live in October 2015. Undertaken by a team from the University of Warwick and the GIFT Partnership, the purpose of the evaluation was to understand how the changes to mental health service provision for children and young people aged 0-25 and their parents and carers outlined in the new FTB model impact on key stakeholders across a range of service settings and types. The aim was to generate learning about the new model as to whether it worked/was achieving its specified objectives, what was perhaps less successful and needed amendment or further development. The evaluation would also provide an opportunity to think about the future development of the service in order to ensure a robust and sustainable model of provision

A20 and ABIN1 Suppression of a Keratinocyte Inflammatory Program with a Shared Single-Cell Expression Signature in Diverse Human Rashes.

Genetic variation in the NF-κB inhibitors, ABIN1 and A20, increase risk for psoriasis. While critical for hematopoietic immune cell function, these genes are believed to additionally inhibit psoriasis by dampening inflammatory signaling in keratinocytes. We dissected ABIN1 and A20's regulatory role in human keratinocyte inflammation using an RNA sequencing-based comparative genomic approach. Here we show subsets of the IL-17 and tumor necrosis factor-α signaling pathways are robustly restricted by A20 overexpression. In contrast, ABIN1 overexpression inhibits these genes more modestly for IL-17, and weakly for tumor necrosis factor-α. Our genome-scale analysis also indicates that inflammatory program suppression appears to be the major transcriptional influence of A20/ABIN1 overexpression, without obvious influence on keratinocyte viability genes. Our findings thus enable dissection of the differing anti-inflammatory mechanisms of two distinct psoriasis modifiers, which may be directly exploited for therapeutic purposes. Importantly, we report that IL-17-induced targets of A20 show similar aberrant epidermal layer-specific transcriptional upregulation in keratinocytes from diseases as diverse as psoriasis, atopic dermatitis, and erythrokeratodermia variabilis, suggesting a contributory role for epidermal inflammation in a broad spectrum of rashes