This paper aims to provide an overview of current research in cognitive behavioural interventions which address verbal impairment in children with autism. The studies are evaluated based on methodological quality and the validity of the data collected. Studies examining behavioural interventions for children with autism were selected from a number of databases, namely Ovid, PsychINFO, and Embase. Multiple filtration rounds were conducted to ensure that papers met the inclusion criteria, followed the DSM IV autism definition, and met the methodological quality standards. A CONSORT style observational longitudinal checklist was used to evaluate the methodological quality of the studies. Criteria pertaining to study designs were more commonly addressed than those focusing on internal validity. Analysis of literature subsequent to the year 2000 demonstrated an emergence of behavioural therapies focused on remediating verbal impairment in children diagnosed with autism. Common limitations amongst all reviewed papers were discussed in terms of impact on validity and reliability. Finally, the discussion consolidated the future directives noted in all papers to discuss trajectories for further research. The chosen literature often neglected to include essential quantitative information that affected their validity. Inclusion of control groups and appropriate sample sizes should be investigated, and future directions of this research should include the use of a diverse sample that is representative of different ethnic backgrounds and socioeconomic statuses.

Background: Pemphigus vulgaris (PV) is an IgG-mediated autoimmune disease characterised by epithelial cell–cell detachment (acantholysis) resulting in mucocutaneous blistering. The exact pathogenesis of blister formation is unknown and this has hampered the development of non-steroidal, mechanism-based treatments for this autoimmune disease. This systematic review aims to investigate the role of caspases in the pathogenesis of PV to inform the choice of more targeted therapeutic agents. Methods: A systematic search of MEDLINE/PubMed and Scopus databases was conducted to identify eligible studies. Multiple phases of inclusion and exclusion of the primary articles were conducted in pairs, and studies were recorded and analysed according to the latest version of the preferred reporting items for systematic reviews and meta-analyses (PRISMA). Risk of bias assessment was conducted for extracted in vivo animal intervention studies using SYRCLE’s risk of bias tool. Results: Eight articles from a total of 2338 in vitro, in vivo, and human studies met the inclusion criteria, with a high degree of inter-rater reliability. By and large, the results show that caspase activation was pathogenic in experimental PV because pan-caspase inhibitors could block or reduce PV acantholysis and blistering in vitro and in vivo, respectively. The pathogenic pathways identified involved caspase-1 and caspase-3. One study failed to show any improvement in the PV model with a caspase inhibitor. The majority of animal studies had high or unclear risk of bias. Conclusion: There are consistent data pointing towards a pathogenic role of caspase activation in PV acantholysis. However, high-quality evidence to confirm that caspase inhibition can prevent PV-induced blistering in vivo is limited. Therefore, further research is required to test the preclinical efficacy of caspase inhibitors in PV.