Trade union policy and new technology: the Civil and Public Services Association

The introduction of a micro-electronic based technology to the workplace has had a far reaching and widespread effect on the numbers and content of jobs. The importance of the implications of new technology were recognised by the trade unions, leading to a plethora of advice and literature in the late 70s and early 80s, notably the TUC 'Technology and Employment ' report. However, studies into the union response have consistently found an overall lack of influence by unions in the introduction of technology. Whilst the advent of new technology has coincided with an industrial relations climate of unprecedented hostility to union activity in the post-war period, there are structural weaknesses in unions in coming to terms with the process of technological change. In particular was the identification of a lack of suitable technological expertise. Addressing itself to this perceived weakness of the union response, this thesis is the outcome of a collaborative project between a national union and an academic institution. The thesis is based on detailed case studies concerning technology bargaining in the Civil Service and the response of the Civil and Public Services Associations (CPSA), the union that represents lower grade white collar civil servants. It is demonstrated that the application of expertise to union negotiators is insufficient on its own to extend union influence and that for unions to effectively come to terms with technology and influence its development requires a re-assessment across all spheres of union activity. It is suggested that this has repercussions for not only the internal organisation and quality of union policy formation and the extent, form and nature of collective bargaining with employer representatives, but also in the relationship with consumer and interest groups outside the traditional collective bargaining forum. Three policy options are developed in the thesis with the 'adversarial' and 'co~operative' options representing the more traditional reactive and passive forms of involvement. These are contrasted with an 'independent participative' form of involvement which was a 'pro-active' policy option and utilised the expertise of the Author in the CPSA's response to technological change.

Monocyte subpopulation counts and TNF alpha associations with clinical outcome post ST elevation myocardial infarction

Background Monocytes are implicated in the initiation and progression of the atherosclerotic plaque contributing to its instability and rupture. Although peripheral monocytosis has been related to poor clinical outcome post ST elevation myocardial infarction (STEMI), only scarce information is available of mechanisms of this association. Tumour necrosis factor alpha (TNFα) is a key cytokine in the acute phase inflammatory response, and it is predominantly produced by inflammatory macrophages. Little is known about TNFα association with circulating monocyte subpopulations post STEMI. Method A total of 142 STEMI patients (mean age 62±13 years; 72% male) treated with percutaneous revascularization were recruited with blood samples obtained within first 24 hours from the onset and on day 10-14. Peripheral blood monocyte subpopulations were enumerated and characterized using flow cytometry after staining for CD14, CD16 and CCR2 and were defined as: CD14++CD16-CCR2+ (Mon1), CD14++CD16+CCR+ (Mon2) and CD14+CD16++CCR2- (Mon3) cells. Plasma levels of TNFα were measured by enzyme-linked immunosorbent assay (ELISA, Peprotec system, UK). Major adverse cardiac events (MACE), defined as recurrent STEMI, new diagnosis of heart failure and death were recorded at follow up, mean of 164±134 days. Results TNFα levels were significantly higher 24 hours post STEMI, compared to day 14 (paired t-test, p <0.001) with day 1 levels weakly correlated with total monocyte count as well as Mon1 (Spearman’s correlation, r=0.19, p=0.02 and r=0.22, p=0.01, respectively). There was no correlation between TNFα and Mon2 or Mon3 subpopulations. TNFα levels were significantly higher in patients with a recorded MACE (n=28, Mann-Whitney test, p<0.001) (figure 1).⇓