Strength in Numbers: The Impact of Trade Union Mergers on Trade Union Power

This study investigates the consequences of the growth in mergers amongst trade unions. It is conventional wisdom that unions which engage in mergers, pooling their resources and releasing economies of scale, become more powerful and serve their members’ more efficiently. The notion that unions truly achieve a strength in numbers, through pursuing a strategy for growth based around mergers and amalgamations, will be examined in relation to union structure and collective bargaining with a view to determining the impact of mergers on trade union power. Given that the merger activity of trade unions has not been neglected by academics, particularly during the 1980s, it is perhaps surprising that, hitherto, studies have preferred to investigate the reasons for mergers rather than the consequences. It is to be hoped therefore that This study can add something new to the studies of union merger and reinvigorate, the debate. The interest in, and prevalence of, merger activity amongst trade unions has shown no sign of abating during the 1990s. The research conducted for this study involved three distinct methods. An extensive survey of practitioners in employee relations from employers and trade unions in the public and private sector was conducted, in conjunction with follow-up interviews in which respondents were asked to elaborate on (and to justify) their responses. The research was supplemented by two case studies involving different mergers in different sectors which aimed to control for any subjectivity residing in the findings of the initial research by allowing for the views of an independent observer to be taken into account. Moreover, case studies allowed the dynamics of the merger process to be taken into account by delivering a mechanism by which the development of the merger over time could be studied in a way that a static survey response could not. The study concluded that on a number of counts the growth in mergers had had some impact on trade union power, both in relation to bargaining and organisation. It also concluded that the consequences of the merger stemmed from two distinct facets of the merger. There is a direct impact through the growth or stability of union members or resources and a secondary impact, whereby the merger unfroze the union’s reluctance to rationalise through an organisational and structural review. In generating a focus for organisational change within the union, there was some evidence that the merger acted as a catalyst for an efficiency reviews which stemmed beyond the immediate and direct confines of the merger. Not unsurprisingly, the study indicated that an accurate assessment of union power and power relations is very difficult. Given the number of potential determinants of union power, it is extremely difficult to isolate the effects of a single determinant. More work needs to be conducted in generating a workable model for union power that, whilst allowing for a range of interrelated determinants, can be applied in practice. It is to be hoped that in some way this study, in addition to refocusing the debate on union mergers per se, can also contribute to an investigation of the determinants of union power and how they can be measured. The thesis is set out in five parts beginning with the academic literature relating to the study. Given that the investigation is primarily a study of trade union mergers the literature relating to merger theory is outlined. Where there are conclusions that have an impact on the thesis, particularly for example in the classification of mergers, this is reviewed in some detail. The notion of power is important in the study and consideration of the literature relating to power theory forms the next section of the thesis. Where authors have directed their studies towards a robust definition of the concept of power this is discussed in relation to trade unions and the bargaining environment. Where research on collective bargaining has been conducted to identify the major components and determinants of union power these are examined and applied. In both cases, literature going back to the 1960s from both the UK and abroad, has been included. A brief overview of trade union mergers during the period covered by the study is included in the next section. This will describe the mergers which occurred in the late 1980s to the mid-1990s, as well as placing them in the economic and political environment of the period, indicating where necessary, developments which had a notable impact on merger activity. In the next section. The results of the research are necessarily covered in some detail in the third section and they are preceded with a brief summary. The range of issues, under examination and the variety of different sectors and organisations which submitted information demanded that adequate space was allocated to investigating the different responses from within and between unions and employers operating in different sectors and industries. Lastly, in the final section of the thesis, the findings of the research are collated and evaluated. The degree to which trade union power has been affected by mergers, either directly or through legitimising a review programme, are considered in relation to a range of mergers and different industries. The question of whether the dramatic increase in trade a range of mergers over the last decade or so has benefited union members, either in terms of the services they enjoy or through the enhanced performance of their unions in collective bargaining, is considered

Is Music Piracy Normal? Behavioral Effects of Social and Technological Barriers

Music piracy, once a novel issue covered in technology magazines, has become an issue of considerable importance and is discussed regularly in mainstream media. Despite the strategies and alternatives aimed at reducing piracy behaviour, the phenomenon remains a major issue for the industry. This paper continues from previous work by testing a further section of the previously proposed model using Structural Equation Modelling (SEM). The Economic and Complexity factors were found to be relevant, but, surprisingly, age was unexpectedly found not to be significant. Users from lower income brackets were more likely to engage in music piracy, and the relative complexity of the legal process of music downloading was found to be a barrier to legally downloading music, thus operating to turn users toward music piracy. Our work and other studies suggest that some degree of music piracy is actually beneficial to the industry, and further research should confirm this notion and determine whether an optimum level exists

A Model of Music Piracy

Music piracy has evolved from a minor concern in technology magazines to a major issue discussed almost daily in the media. The industry claims potentially billions of dollars are at stake and we seek to determine why extensive anti-piracy strategies don't appear successful. We propose a Model of Music Piracy and, using a survey, test and validate a section of the model using SEM. The majority of propositions were upheld, but contrary to expectations, age was not significant. All users are well aware of the law, prominent cases, and penalties incurred, however these deterrents do not change behaviour or attitudes to piracy. They feel online anonymity affords some protection, and there is safety in numbers (music companies cannot catch everyone). Our work and other studies suggest a certain level of music piracy is efficacious, and further research should confirm this notion and determine whether an optimum level exists

Complex structural rearrangements are present in high-grade dysplastic Barrett\u27s oesophagus samples

Background: Oesophageal adenocarcinoma (EAC) incidence is increasing and has a poor survival rate. Barrett’s oesophagus (BE) is a precursor condition that is associated with EAC and often occurs in conjunction with chronic gastro-oesophageal reflux, however many individuals diagnosed with BE never progress to cancer. An understanding of the genomic features of BE and EAC may help with the early identification of at-risk individuals. Methods: In this study, we assessed the genomic features of 16 BE samples using whole-genome sequencing. These included non-dysplastic samples collected at two time-points from two BE patients who had not progressed to EAC over several years. Seven other non-dysplastic samples and five dysplastic BE samples with high-grade dysplasia were also examined. We compared the genome profiles of these 16 BE samples with 22 EAC samples. Results: We observed that samples from the two non-progressor individuals had low numbers of somatic single nucleotide variants, indels and structural variation events compared to dysplastic and the remaining non-dysplastic BE. EAC had the highest level of somatic genomic variations. Mutational signature 17, which is common in EAC, was also present in non-dysplastic and dysplastic BE, but was not present in the non-progressors. Many dysplastic samples had mutations in genes previously reported in EAC, whereas only mutations in CDKN2A or in the fragile site genes appeared common in non-dysplastic samples. Rearrangement signatures were used to identify a signature associated with localised complex events such as chromothripsis and breakage fusion-bridge that are characteristic of EACs. Two dysplastic BE samples had a high contribution of this signature and contained evidence of localised rearrangements. Two other dysplastic samples also had regions of localised structural rearrangements. There was no evidence for complex events in non-dysplastic samples. Conclusions: The presence of complex localised rearrangements in dysplastic samples indicates a need for further investigations into the role such events play in the progression from BE to EAC

Phylogenetic relationships and molecular evolution in uropeltid snakes (Serpentes: Uropeltidae): allozymes and albumin immunology

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73950/1/j.1095-8312.1990.tb00541.x.pd

Complex structural rearrangements are present in high-grade dysplastic Barrett’s oesophagus samples

This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.Abstract Background Oesophageal adenocarcinoma (EAC) incidence is increasing and has a poor survival rate. Barrett’s oesophagus (BE) is a precursor condition that is associated with EAC and often occurs in conjunction with chronic gastro-oesophageal reflux, however many individuals diagnosed with BE never progress to cancer. An understanding of the genomic features of BE and EAC may help with the early identification of at-risk individuals. Methods In this study, we assessed the genomic features of 16 BE samples using whole-genome sequencing. These included non-dysplastic samples collected at two time-points from two BE patients who had not progressed to EAC over several years. Seven other non-dysplastic samples and five dysplastic BE samples with high-grade dysplasia were also examined. We compared the genome profiles of these 16 BE samples with 22 EAC samples. Results We observed that samples from the two non-progressor individuals had low numbers of somatic single nucleotide variants, indels and structural variation events compared to dysplastic and the remaining non-dysplastic BE. EAC had the highest level of somatic genomic variations. Mutational signature 17, which is common in EAC, was also present in non-dysplastic and dysplastic BE, but was not present in the non-progressors. Many dysplastic samples had mutations in genes previously reported in EAC, whereas only mutations in CDKN2A or in the fragile site genes appeared common in non-dysplastic samples. Rearrangement signatures were used to identify a signature associated with localised complex events such as chromothripsis and breakage fusion-bridge that are characteristic of EACs. Two dysplastic BE samples had a high contribution of this signature and contained evidence of localised rearrangements. Two other dysplastic samples also had regions of localised structural rearrangements. There was no evidence for complex events in non-dysplastic samples. Conclusions The presence of complex localised rearrangements in dysplastic samples indicates a need for further investigations into the role such events play in the progression from BE to EAC

Grb2 controls phosphorylation of FGFR2 by inhibiting receptor kinase and Shp2 phosphatase activity

Constitutive receptor tyrosine kinase phosphorylation requires regulation of kinase and phosphatase activity to prevent aberrant signal transduction. A dynamic mechanism is described here in which the adaptor protein, growth factor receptor–bound protein 2 (Grb2), controls fibroblast growth factor receptor 2 (FGFR2) signaling by regulating receptor kinase and SH2 domain–containing protein tyrosine phosphatase 2 (Shp2) phosphatase activity in the absence of extracellular stimulation. FGFR2 cycles between its kinase-active, partially phosphorylated, nonsignaling state and its Shp2-dephosphorylated state. Concurrently, Shp2 cycles between its FGFR2-phosphorylated and dephosphorylated forms. Both reciprocal activities of FGFR2 and Shp2 were inhibited by binding of Grb2 to the receptor. Phosphorylation of Grb2 by FGFR2 abrogated its binding to the receptor, resulting in up-regulation of both FGFR2’s kinase and Shp2’s phosphatase activity. Dephosphorylation of Grb2 by Shp2 rescued the FGFR2–Grb2 complex. This cycling of enzymatic activity results in a homeostatic, signaling-incompetent state. Growth factor binding perturbs this background cycling, promoting increased FGFR2 phosphorylation and kinase activity, Grb2 dissociation, and downstream signaling. Grb2 therefore exerts constitutive control over the mutually dependent activities of FGFR2 and Shp2

Loss-of-function fibroblast growth factor receptor-2 mutations in melanoma

We report that 10% of melanoma tumors and cell lines harbor mutations in the fibroblast growth factor receptor 2 (FGFR2) gene. These novel mutations include three truncating mutations and 20 missense mutations occurring at evolutionary conserved residues in FGFR2 as well as among all four FGFRs. The mutation spectrum is characteristic of those induced by UV radiation. Mapping of these mutations onto the known crystal structures of FGFR2 followed by in vitro and in vivo studies show that these mutations result in receptor loss of function through several distinct mechanisms, including loss of ligand binding affinity, impaired receptor dimerization, destabilization of the extracellular domains, and reduced kinase activity. To our knowledge, this is the first demonstration of loss-of-function mutations in a class IV receptor tyrosine kinase in cancer. Taken into account with our recent discovery of activating FGFR2 mutations in endometrial cancer, we suggest that FGFR2 may join the list of genes that play context-dependent opposing roles in cancer