Bursting out of our bubble: using creative techniques to communicate within the systematic review process and beyond

This is the final version. Available on open access from BMC via the DOI in this recordBACKGROUND: Increasing pressure to publicise research findings and generate impact, alongside an expectation from funding bodies to go beyond publication within academic journals, has generated interest in alternative methods of science communication. Our aim is to describe our experience of using a variety of creative communication tools, reflect on their use in different situations, enhance learning and generate discussion within the systematic review community. METHODS: Over the last 5 years, we have explored several creative communication tools within the systematic review process and beyond to extend dissemination beyond traditional academic mechanisms. Central to our approach is the co-production of a communication plan with potential evidence users which facilitates (i) the identification of key messages for different audiences, (ii) discussion of appropriate tools to communicate key messages and (iii) exploration of avenues to share them. We aim to involve evidence users in the production of a variety of outputs for each research project cognisant of the many ways in which individuals engage with information. RESULTS: Our experience has allowed us to develop an understanding of the benefits and challenges of a wide range of creative communication tools. For example, board games can be a fun way of learning, may flatten power hierarchies between researchers and research users and enable sharing of large amounts of complex information in a thought provoking way, but they are time and resource intensive both to produce and to engage with. Conversely, social media shareable content can be quick and easy to produce and to engage with but limited in the depth and complexity of shareable information. DISCUSSION: It is widely recognised that most stakeholders do not have time to invest in reading large, complex documents; creative communication tools can be a used to improve accessibility of key messages. Furthermore, our experience has highlighted a range of additional benefits of embedding these techniques within our project processes e.g. opening up two-way conversations with end-users of research to discuss the implications of findings.National Institute for Health Research (NIHR

Impaired oligodendroglial turnover is associated with myelin pathology in focal cortical dysplasia and tuberous sclerosis complex

Conventional antiepileptic drugs suppress the excessive firing of neurons during seizures. In drug-resistant patients, treatment failure indicates an alternative important epileptogenic trigger. Two epilepsy-associated pathologies show myelin deficiencies in seizure-related brain regions: Focal Cortical Dysplasia IIB (FCD) and cortical tubers in Tuberous Sclerosis Complex (TSC). Studies uncovering white matter-pathology mechanisms are therefore urgently needed to gain more insight into epileptogenesis, the propensity to maintain seizures, and their associated comorbidities such as cognitive defects. We analyzed epilepsy surgery specimens of FCD IIB (n = 22), TSC (n = 8), and other malformations of cortical development MCD (n = 12), and compared them to autopsy and biopsy cases (n = 15). The entire lesional pathology was assessed using digital immunohistochemistry, immunofluorescence and western blotting for oligodendroglial lineage, myelin and mTOR markers, and findings were correlated to clinical parameters. White matter pathology with depleted myelin and oligodendroglia were found in 50% of FCD IIB and 62% of TSC cases. Other MCDs had either a normal content or even showed reactive oligodendrolial hyperplasia. Furthermore, myelin deficiency was associated with increased mTOR expression and the lower amount of oligodendroglia was linked with their precursor cells (PDGFRa). The relative duration of epilepsy (normalized to age) also correlated positively to mTOR activation and negatively to myelination. Decreased content of oligodendroglia and missing precursor cells indicated insufficient oligodendroglial development, probably mediated by mTOR, which may ultimately lead to severe myelin loss. In terms of disease management, an early and targeted treatment could restore normal myelin development and, therefore, alter seizure threshold and improve cognitive outcom