To investigate the effects of freeze-drying on the structural and biochemical properties of amniotic membrane (AM) and defining parameters for its use as a battlefield dressing for ocular surface injuries.
AM has been used to treat burns to the front of the eye since the late 1930s, and more recently has become firmly established as a biomaterial for treating OS burns and acute injuries, as a graft and as a protective overlay to relieve pain and prevent chronic inflammatory sequelae such as neovascularisation and scarring (Dua H et al, 2004). AM is typically cryopreserved at -80°C before use, and is therefore unsuitable for use in a battlefield environment. Freeze-dried AM preparations have recently become available as an alternative and are used in various countries in civilian ophthalmic surgery and by the United States Army. However the specific indications for military use have not been conclusively demonstrated. Although desiccation produces a brittle and thin membrane, following reconstitution the effects on AM physical properties are reported to be minimal. Freeze-drying simplifies membrane storage and stabilises degradation, which has clear potential benefits for battle field application.
My early research career began by studying for a PhD with the Tumour Immunology group, in the Division of Breast Surgery, University of Nottingham. The backbone of my thesis was the preliminary development of a novel autoantibody screening assay to over-expressed antigen markers in breast and ovarian cancer. This was to aid in earlier diagnosis of these diseases prior to symptomatic presentation in women <50 years old, who are not routinely screened by mammography. And to be used in conjunction with current screening strategies for earlier diagnosis and to improve patients prognosis and overall survival. Further validation of these assays in these diseases are presently being carried out. However this group have recently published data on the clinical validation of an autoantibody panel as a diagnostic tool and the potential to monitor pateints that are at high risk of lung cancer (Boyle P, Chapman CJ et al, 2010). My first postdoctoral research position paid particular emphasis on the vascular endothelium, endothelial cell biology, and associated signalling pathways. Primarily my investigations looked at the role of angiotensin II and PDGF-BB on migration and proliferation of coronary artery smooth muscle cells, with particular emphasis on pro-oxidant and antioxidant enzyme activities, proliferative and migratory responses, the signal transduction pathways involved in atherogen-mediated oxidative stress regulation and the effects of angiotensin receptor blockers, antioxidants, free radical scavengers or stains on the aforementioned activities (Allen CL, Bayraktutan U et al, 2008). This was continued by studying the contribution of hyperglycaemia-mediated generation of oxidative stress and its contribution towards cerebral microvascular endothelial dysfunction, BBB integrity, and to explore the signal transduction pathways involved by employing specific inhibitors of PKC, p38MAPK and PI3 kinase and whether antioxidants and glucose normalisation reverse these phenomena (Allen CL, Bayraktutan U et al, 2009). Penultimately my latter research has focused on the role of small GTP-binding protein RhoA and its effector protein Rho kinase in BBB disintegration under ischaemic conditions (Allen CL, Bayraktutan U et al). This was achieved by looking at protein expression levels, BBB permeability, MLC phosphorylation and actin cytoskeletal organisation in HBMEC, and HBMEC over-expressing constitutively active His RhoA or anti-RhoA Ig in the presence or absence of a specific inhibitor of Rho kinase, under normoxia and ischaemia (Allen CL, Srivastava K, Bayraktutan et al, 2009).