Co-designing Possible Flooding Solutions : Participatory Mapping Methods to Identify Flood Management Options from a UK Borders Case Study

This paper reports on the findings developed by a funded project within the UK Rural Economy and Land Use Programme: ‘Managing borderlands: adaptive decision making amongst specialists and non-specialists’. The project focuses specifically on the development of a nested-scale participatory GIS (PGIS) method to identify spatially local perceptions and experiential knowledge of the risk and vulnerability of two catchments in the Scottish–English Borders. The method attempts to move beyond mapping risk towards the co-design of possible solutions. This will highlight the potential for improved inclusion of local perspectives on risk afforded by using PGIS mapping approaches in the UK context. The potential of the approach to generate co-designed community preferences leading to more resilient solutions (particularly in terms of social and economic consequences) to environmental change will also be discussed

Lymph node removal enhances corneal graft survival in mice at high risk of rejection

Peer reviewedPublisher PD

The roles of calcium signaling and ERK1/2 phosphorylation in a Pax6(+/- )mouse model of epithelial wound-healing delay

BACKGROUND: Congenital aniridia caused by heterozygousity at the PAX6 locus is associated with ocular surface disease including keratopathy. It is not clear whether the keratopathy is a direct result of reduced PAX6 gene dosage in the cornea itself, or due to recurrent corneal trauma secondary to defects such as dry eye caused by loss of PAX6 in other tissues. We investigated the hypothesis that reducing Pax6 gene dosage leads to corneal wound-healing defects. and assayed the immediate molecular responses to wounding in wild-type and mutant corneal epithelial cells. RESULTS: Pax6(+/- )mouse corneal epithelia exhibited a 2-hour delay in their response to wounding, but subsequently the cells migrated normally to repair the wound. Both Pax6(+/+ )and Pax6(+/- )epithelia activated immediate wound-induced waves of intracellular calcium signaling. However, the intensity and speed of propagation of the calcium wave, mediated by release from intracellular stores, was reduced in Pax6(+/- )cells. Initiation and propagation of the calcium wave could be largely decoupled, and both phases of the calcium wave responses were required for wound healing. Wounded cells phosphorylated the extracellular signal-related kinases 1/2 (phospho-ERK1/2). ERK1/2 activation was shown to be required for rapid initiation of wound healing, but had only a minor effect on the rate of cell migration in a healing epithelial sheet. Addition of exogenous epidermal growth factor (EGF) to wounded Pax6(+/- )cells restored the calcium wave, increased ERK1/2 activation and restored the immediate healing response to wild-type levels. CONCLUSION: The study links Pax6 deficiency to a previously overlooked wound-healing delay. It demonstrates that defective calcium signaling in Pax6(+/- )cells underlies this delay, and shows that it can be pharmacologically corrected. ERK1/2 phosphorylation is required for the rapid initiation of wound healing. A model is presented whereby minor abrasions, which are quickly healed in normal corneas, transiently persist in aniridic patients, compromising the corneal stroma

In-vivo evidence that high mobility group box 1 exerts deleterious effects in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model and Parkinson's disease which can be attenuated by glycyrrhizin

Acknowledgements Samples were obtained from the Neuro Biobank of the University of Tuebingen, Germany (http://www.hih-tuebingen.de/nd/biobank/for-researchers/). This biobank is supported by the Hertie Institute and the DZNE. We are grateful to the staff of the Medical Research Facility for their help with the animal care. We thank Dr. Kinnari Sathe for her help with the experiments. We thank Claire A. Walker for assisting with western blot analysis. This study was supported by: Tenovus Scotland, Parkinson's Disease Foundation, Royal Society 2006/R1, NHS Endowment 14-42, and Wellcome Trust WT080782MF.Peer reviewedPublisher PD