Politically motivated former prisoner groups: community activism and conflict transformation

Aims and objectives: This study represents the first sustained quantitative and qualitative attempt to involve both Republicans and Loyalists in an investigation of the impact of imprisonment and the role of politically motivated former prisoners in the process of conflict transformation in Northern Ireland. The overall aim of the project is to examine the ways in which groups of former prisoners are involved in peace-building and conflict transformation work and to evaluate the constraints and impediments placed upon their activities by the effects of the imprisonment process, politically motivated release and residual criminalisation. In pursuing the evaluation of the role of politically motivated former prisoners working within and without their own communities, the research has six specific objectives: To trace the evolution and development of former prisoner groups; To evaluate the impacts of imprisonment and release on the personal lives of former prisoners; To assess the constraints imposed on former prisoners as agents of change by the residual criminalisation arising from their status; To determine the potential of the former prisoner community in challenging intra-community tensions and evaluate their potential and actual contribution to conflict transformation at the inter-community level; To compare and contrast the effectiveness of Loyalist and Republican former prisoners as agents of change within their own communities; To explore the notion of former prisoners as agents of social and communal transformation within broader political processes through grounding the knowledge and practical experience of the former prisoner community within the broader conceptual context of conflict transformation.

Redox remodelling in diaphragm muscle adaptation to chronic sustained hypoxia

Chronic sustained hypoxia (CH) induces functional weakness, atrophy, and mitochondrial remodelling in the diaphragm muscle. Animal models of CH present with changes similar to patients with respiratory-related disease, thus, elucidating the molecular mechanisms driving these adaptations is clinically important. We hypothesize that ROS are pivotal in diaphragm muscle adaptation to CH. C57BL6/J mice were exposed to CH (FiO2=0.1) for one, three, and six weeks. Sternohyoid (upper airway dilator), extensor digitorum longus (EDL), and soleus were studied as reference muscles as well as the diaphragm. The diaphragm was profiled using a redox proteomics approach followed by mass spectrometry. Following this, redox-modified metabolic enzyme activities and atrophy signalling were assessed using spectrophotometric assays and ELISA. Diaphragm isotonic performance was assessed after six weeks of CH ± chronic antioxidant supplementation. Protein carbonyl and free thiol content in the diaphragm were increased and decreased respectively after six weeks of CH – indicative of protein oxidation. These changes were temporally modulated and muscle specific. Extensive remodelling of metabolic proteins occurred and the stress reached the cross-bridge. Metabolic enzyme activities in the diaphragm were, for the most part, decreased by CH and differential muscle responses were observed. Redox sensitive chymotrypsin-like proteasome activity of the diaphragm was increased and atrophy signalling was observed through decreased phospho-FOXO3a and phospho-mTOR. Phospho-p38 MAPK content was increased and this was attenuated by antioxidant treatment. Hypoxia decreased power generating capacity of the diaphragm and this was restored by N-acetyl-cysteine (NAC) but not by tempol. Redox remodelling is pivotal for diaphragm adaptation to chronic sustained hypoxia. Muscle changes are dependent on duration of the hypoxia stimulus, activity profile of the muscle, and molecular composition of the muscle. The working respiratory muscles and slow oxidative fibres are particularly susceptible. NAC (antioxidant) may be useful as an adjunct therapy in respiratory-related diseases characterised by hypoxic stress.