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The research enquiry for this thesis, from an insider/outsider position, is a deeply held reflection of personal values, convictions and professional experiences stemming from the researcher's life's work in school leadership both in the United States and abroad. The intent of this study is to engage with the sacred discourse of evangelical Christian school leaders and the discourse of the sacred and secular scholarly literature. This is a qualitative study of a constructivist/interpretivist approach where sem1- structured interviews, with 12 senior school leaders, four in each of three Anglophone countries, inform the data. A more in-depth case study of one school is utilised as a comprehensive illustration of thematic elements revealed through multiple data sources. The preliminary literature for this research was based on the readings of various contemporary theories of leadership and literature around servant-leadership from which the initial research question was framed. As the data analysis advanced, a new framework emerged around attributes of leadership and community building through leadership, making it imperative to accommodate a new set of transformational/relational/ethical literature, taking the story on a completely different journey with a new research question and sub-questions; therefore, leaving behind the initial research question. Two descriptors of leadership became the primary framework for the thesis: the 'sacred' and the 'secular' discourses relating to school leadership. Standing in the doorway, as it were, the researcher took on a role of interpreting and translating one discourse to the other rather than acting solely as observer and interpreter of the data. The findings, the utilisation of two discourses, and the interpretive stance make a positive and original contribution to knowledge and are significant in two ways. First, the participants, speaking through the sacred discourse, express an extension to or linkage with the secular literature, revealing much more overlap between the two discourses than was expected. Second, the secular literature does not capture the sacred discourse; there is an appurtenance - an add-on - a more spiritual dimension, to consider.

Proteinase activated receptor-2 (PAR-2) is a novel G-protein coupled receptor, that is activated by means of proteolytic cleavage (Macfarlane et al, 2001) and has both pro and anti-inflammatory actions depending upon the system examined. PAR-2 have been linked to the stress-activated protein kinases (SAPKs), JNK and p38 MAP kinase and NFK13 signalling (Kanke et al, 2001; Sabri et al, 2000), pathways known to be involved in proinflammatory responses in several cell types. TNFa has been demonstrated to up-regulate PAR-2 expression in a variety of cell types (Nystedt et al, 1996; Ritchie et al, 2007). Since both TNFa and PAR-2 are implicated in inflammation, we examined the possibility of altered PAR-2 trafficking under inflammatory conditions and possible crosstalk between PAR-2 and TNFa at the level of intracellular signalling. Previous studies have characterised P AR-2 trafficking in transfected cell lines, however the effects of inflammatory stimuli on the kinetics of PAR-2 trafficking has not been investigated. The study sought to re-characterise PAR-2 trafficking in the presence of inflammatory stimuli. NCTC2544 cells transfected with YFP epitope tagged PAR-2, demonstrated clear PAR-2 expression and trafficking of the receptor was successfully characterised, however no significant differences in the kinetics of P AR-2 trafficking under inflammatory conditions compared to control was observed. The latter part of the study examined PAR-2 and TNFa mediated activation of the MAPK and NFK13 pathways. In a keratinocyte cell line stably expressing PAR-2 (CloneG), trypsin, SLIGKV-OH, and TNFa, caused a time and concentration-dependent increase in p38 MAPK and JNK phosphorylation however, preliminary results failed to show evidence of synergy between the receptors. Surprisingly however, pre-activation of P AR-2 substantially reduced the ability of TNFa to activate JNK. The inhibitory effect of P AR-2 was mimicked by the protein kinase C activator PMA, partially reversed by the PKC inhibitor GF109203X, and completely reversed by the novel Gaqlll inhibitor YM-254890, consistent with a role for both Ca2+ -dependent and independent PKC isoforms and for P AR-2 coupling to Gaq/11 to mediate this agonist driven inhibitory response. These results indicate a potential mechanistic explanation for both the anti and pro-inflammatory actions of P AR- 2, and highlight a possible novel therapeutic avenue for the development ofPAR-2 agonists as anti-inflammatory drugs.