The Industrial Context of Occupational Mobility: Change in Structure

The neglect of a consideration of history has been a feature of mobility research. ‘History’ affects the results of analyses of social mobility by altering the occupational/industrial structure and by encouraging exchange mobility. Changes in industrial structure are rooted more directly in historical causes and can be seen as more fundamental than changes in occupational structure. Following a substantial review of the secondary literature on changes in industrial and occupational structure in Northern Ireland, loglinear analyses of intra- and intergenerational mobility tables for sociologically-derived cohort generations that incorporate occupational and industrial categories are presented. Structural and inheritance effects for industry are as significant as those for occupation. Given the well-established finding of ‘constant social fludity’ in mobility tables once structural effects are controlled, the inclusion of categorization by industry is necessary in order to reach an accurate understanding of occupational mobility and the role of historical change in mobility.

Northern Ireland:The Development Context

This article provides a contextual framework for the new agenda for development, represented in the economic strategy known as Strategy 2010, and the regional spatial plan known as Shaping Our Future. These are considered in the following two articles. This article begins by setting a perspective on the political economy of Northern Ireland and follows with an outline of the spatial planning process. In conclusion, it raises the key challenges facing attempts to renew the region.

Cox-2 Promotes Chromogranin A Expression and Bioactivity: Evidence for a PGE2-Dependent Mechanism and the Involvement of a Proximal cAMP-Responsive Element.

Abstract The prostanoid biosynthetic enzyme cyclooxygenase-2 (Cox-2) is upregulated in several neuroendocrine tumors. The aim of the current study was to employ a neuroendocrine cell (PC12) model of Cox-2 over-expression to identify gene products that might be implicated in the oncogenic and/or inflammatory actions of this enzyme in the setting of neuroendocrine neoplasia. Expression array and real-time PCR analysis demonstrated that levels of the neuroendocrine marker chromogranin A (CGA) were 2-fold and 3.2-fold higher, respectively, in Cox-2 over-expressing cells (PCXII) vs their control (PCMT) counterparts. Immunocytochemical and immunoblotting analyses confirmed that both intracellular and secreted levels of CGA were elevated in response to Cox-2 induction. Moreover, exogenous addition of prostaglandin E2 (1u�­M), mimicked this effect in PCMT cells, while treatment of PCXII cells with the Cox-2 selective inhibitor NS-398 (100 nM) reduced CGA expression levels, thereby confirming the biospecificity of this finding. Levels of neurone specific enolase (NSE) were similar in the two cell lines, suggesting that the effect of Cox-2 on CGA expression was specific and not due to a global enhancement of neuroendocrine marker expression/differentiation. Cox-2-dependent CGA upregulation was associated with significantly increased chromaffin granule number and intracellular and secreted levels of dopamine. CGA promoter-driven reporter gene expression studies provided evidence that prostaglandin E2-dependent upregulation required a proximal cAMP-responsive element (CRE; -71 - -64 bp). This study is the first to demonstrate that Cox-2 upregulates both CGA expression and bioactivity in a neuroendocrine cell line and has major implications for the role of this polypeptide in the pathogenesis of neuroendocrine cancers in which Cox-2 is upregulated.