A collaborative project funded by the Iraqi Research Fellowship Programme of the Council for Assisting Refugee Academics was set up to transfer laboratory and clinical skills in between three clinical research teams in the UK, Jordan and Iraq. The project was set up to study the genetics of the potentially debilitating condition, Behçet's Disease (BD). Blood samples were collected from: 38 BD patients, 28 patients with oral ulcers not related to BD and 32 healthy controls. All samples were analysed using Micro SSP HLA Class I B locus kit (B locus, generic). Logistic regression analysis revealed that samples positive for HLA-B51 were 7.4 times more likely to have BD than the healthy control subjects. The results of this study make a valuable addition to the scientific literature. Additional valuable outcomes include the intellectual exchange and transfer of skills in between the collaborating teams, which led to the establishment of an international research collaboration.
abstract:Objectives: Behçet's disease (BD) is an immune-mediated small vessel systemic vasculitis. Human β-defensins are antimicrobial peptides associated with many inflammatory diseases and are encoded by the β-defensin family of multiple-copy genes. However, their role in BD necessitates further investigation. The aim of the present study was to investigate the possible association of BD in its various clinical forms with defensin β-4 (DEFB4) genomic copy numbers. Methods: This case-control study was conducted from January to September 2011 and included 50 control subjects and 27 unrelated Iraqi BD patients registered at Baghdad Teaching Hospital, Bagdad, Iraq. Copy numbers of the DEFB4 gene were determined using the comparative cycle threshold method by duplex real-time polymerase chain reaction technology at the Department of Dermatology of Jena University Hospital, Jena, Germany. Results: DEFB4 genomic copy numbers were significantly higher in the BD group compared to the control group (P = 0.010). However, no statistically significant association was found between copy numbers and clinical variables within the BD group. Conclusion: The DEFB4 copy number polymorphism may be associated with BD; however, it is not associated with different clinical manifestations of the disease.
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