Reappraising contemporary theories of subcortical participation in language: Proposing an interhemispheric regulatory function for the subthalamic nucleus (STN) in the mediation of high-level linguistic processes

Apropos the basal ganglia, the dominant striatum and globus pallidus internus (GPi) have been hypothesised to represent integral components of subcortical language circuitry. Working subcortical language theories, however, have failed thus far to consider a role for the STN in the mediation of linguistic processes, a structure recently defined as the driving force of basal ganglia output. The aim of this research was to investigate the impact of surgically induced functional inhibition of the STN upon linguistic abilities, within the context of established models of basal ganglia participation in language. Two males with surgically induced 'lesions' of the dominant and non-dominant dorsolateral STN, aimed at relieving Parkinsonian motor symptoms, served as experimental subjects. General and high-level language profiles were compiled for each subject up to 1 month prior to and 3 months following neurosurgery, within the drug-on state (i.e., when optimally medicated). Comparable post-operative alterations in linguistic performance were observed subsequent to surgically induced functional inhibition of the left and right STN. More specifically, higher proportions of reliable decline as opposed to improvement in post-operative performance were demonstrated by both subjects on complex language tasks, hypothesised to entail the interplay of cognitive-linguistic processes. The outcomes of the current research challenge unilateralised models of functional basal ganglia organisation with the proposal of a potential interhemispheric regulatory function for the STN in the mediation of high-level linguistic processes.

Exits, entrances and entrepreneurship : an exploration of economic theories of entrepreneurship through new independent entry and infant exit

The thesis began as a study of new firm formation. Preliminary research suggested that infant death rate was considered to be a closely related problem and the search was for a theory of new firm formation which would explain both. The thesis finds theories of exit and entry inadequate in this respect and focusses instead on theories of entrepreneurship, particularly those which concentrate on entrepreneurship as an agent of change. The role of information is found to be fundamental to economic change and an understanding of information generation and dissemination and the nature and direction of information flows is postulated to lead coterminously to an understanding of entrepreneurhsip and economic change. The economics of information is applied to theories of entrepreneurhsip and some testable hypotheses are derived. The testing relies on etablishing and measuring the information bases of the founders of new firms and then testing for certain hypothesised differences between the information bases of survivors and non-survivors. No theory of entrepreneurship is likely to be straightforwardly testable and many postulates have to be established to bring the theory to a testable stage. A questionnaire is used to gather information from a sample of firms taken from a new micro-data set established as part of the work of the thesis. Discriminant Analysis establishes the variables which best distinguish between survivors and non-survivors. The variables which emerge as important discriminators are consistent with the theory which the analysis is testing. While there are alternative interpretations of the important variables, collective consistency with the theory under test is established. The thesis concludes with an examination of the implications of the theory for policy towards stimulating new firm formation.

A critical evaluation of theories of nationalism

This thesis considers the main theoretical positions within the contemporary sociology of nationalism. These can be grouped into two basic types, primordialist theories which assert that nationalism is an inevitable aspect of all human societies, and modernist theories which assert that nationalism and the nation-state first developed within western Europe in recent centuries. With respect to primordialist approaches to nationalism, it is argued that the main common explanation offered is human biological propensity. Consideration is concentrated on the most recent and plausible of such theories, sociobiology. Sociobiological accounts root nationalism and racism in genetic programming which favours close kin, or rather to the redirection of this programming in complex societies, where the social group is not a kin group. It is argued that the stated assumptions of the sociobiologists do not entail the conclusions they draw as to the roots of nationalism, and that in order to arrive at such conclusions further and implausible assumptions have to be made. With respect to modernists, the first group of writers who are considered are those, represented by Carlton Hayes, Hans Kohn and Elie Kedourie, whose main thesis is that the nation-state and nationalism are recent phenomena. Next, the two major attempts to relate nationalism and the nation-state to imperatives specific either to capitalist societies (in the `orthodox' marxist theory elaborated about the turn of the twentieth century) or to the processes of modernisation and industrialisation (the `Weberian' account of Ernest Gellner) are discussed. It is argued that modernist accounts can only be sustained by starting from a definition of nationalism and the nation-state which conflates such phenomena with others which are specific to the modern world. The marxist and Gellner accounts form the necessary starting point for any explanation as to why the nation-state is apparently the sole viable form of polity in the modern world, but their assumption that no pre-modern society was national leaves them without an adequate account of the earliest origins of the nation-state and of nationalism. Finally, a case study from the history of England argues both the achievement of a national state form and the elucidation of crucial components of a nationalist ideology were attained at a period not consistent with any of the versions of the modernist thesis.

Assessing the efficacy of structural merger remedies:choosing between theories of harm?

This paper shows that many structural remedies in a sample of European merger cases result in market structures which would probably not be cleared by the Competition Authority (CA) if they were the result of merger (rather than remedy).This is explained by the fact that the CA’s objective through remedy is to restore premerger competition, but markets are often highly concentrated even before merger. If so, the CA must often choose between clearing an ‘uncompetitive’merger, or applying an unsatisfactory remedy. Here, the CA appears reluctant to intervene against coordinated effects, if doing so enhances a leader’s dominance.

Assessing the efficacy of structural merger remedies:choosing between theories of harm?

Previous empirical assessments of the effectiveness of structural merger remedies have focused mainly on the subsequent viability of the divested assets. Here, we take a different approach by examining how competitive are the market structures which result from the divestments. We employ a tightly specified sample of markets in which the European Commission (EC) has imposed structural merger remedies. It has two key features: (i) it includes all mergers in which the EC appears to have seriously considered, simultaneously, the possibility of collective dominance, as well as single dominance; (ii) in a previous paper, for the same sample, we estimated a model which proved very successful in predicting the Commission’s merger decisions, in terms of the market shares of the leading firms. The former allows us to explore the choices between alternative theories of harm, and the latter provides a yardstick for evaluating whether markets are competitive or not – at least in the eyes of the Commission. Running the hypothetical post-remedy market shares through the model, we can predict whether the EC would have judged the markets concerned to be competitive, had they been the result of a merger rather than a remedy. We find that a significant proportion were not competitive in this sense. One explanation is that the EC has simply been inconsistent – using different criteria for assessing remedies from those for assessing the mergers in the first place. However, a more sympathetic – and in our opinion, more likely – explanation is that the Commission is severely constrained by the pre-merger market structures in many markets. We show that, typically, divestment remedies return the market to the same structure as existed before the proposed merger. Indeed, one can argue that any competition authority should never do more than this. Crucially, however, we find that this pre-merger structure is often itself not competitive. We also observe an analogous picture in a number of markets where the Commission chose not to intervene: while the post-merger structure was not competitive, nor was the pre-merger structure. In those cases, however, the Commission preferred the former to the latter. In effect, in both scenarios, the EC was faced with a no-win decision. This immediately raises a follow-up question: why did the EC intervene for some, but not for others – given that in all these cases, some sort of anticompetitive structure would prevail? We show that, in this sample at least, the answer is often tied to the prospective rank of the merged firm post-merger. In particular, in those markets where the merged firm would not be the largest post-merger, we find a reluctance to intervene even where the resulting market structure is likely to be conducive to collective dominance. We explain this by a willingness to tolerate an outcome which may be conducive to tacit collusion if the alternative is the possibility of an enhanced position of single dominance by the market leader. Finally, because the sample is confined to cases brought under the ‘old’ EC Merger Regulation, we go on to consider how, if at all, these conclusions require qualification following the 2004 revisions, which, amongst other things, made interventions for non-coordinated behaviour possible without requiring that the merged firm be a dominant market leader. Our main conclusions here are that the Commission appears to have been less inclined to intervene in general, but particularly for Collective Dominance (or ‘coordinated effects’ as it is now known in Europe as well as the US.) Moreover, perhaps contrary to expectation, where the merged firm is #2, the Commission has to date rarely made a unilateral effects decision and never made a coordinated effects decision.

Unravelling the theories of pre-eclampsia:Are the protective pathways the new paradigm?

Pre-eclampsia is a vascular disorder of pregnancy where anti-angiogenic factors, systemic inflammation and oxidative stress predominate, but none can claim to cause pre-eclampsia. This review provides an alternative to the 'two-stage model' of pre-eclampsia in which abnormal spiral arteries modification leads to placental hypoxia, oxidative stress and aberrant maternal systemic inflammation. Very high maternal soluble fms-like tyrosine kinase-1 (sFlt-1 also known as sVEGFR) and very low placenta growth factor (PlGF) are unique to pre-eclampsia; however, abnormal spiral arteries and excessive inflammation are also prevalent in other placental disorders. Metaphorically speaking, pregnancy can be viewed as a car with an accelerator and brakes, where inflammation, oxidative stress and an imbalance in the angiogenic milieu act as the 'accelerator'. The 'braking system' includes the protective pathways of haem oxygenase 1 (also referred as Hmox1 or HO-1) and cystathionine-γ-lyase (also known as CSE or Cth), which generate carbon monoxide (CO) and hydrogen sulphide (H2S) respectively. The failure in these pathways (brakes) results in the pregnancy going out of control and the system crashing. Put simply, pre-eclampsia is an accelerator-brake defect disorder. CO and H2S hold great promise because of their unique ability to suppress the anti-angiogenic factors sFlt-1 and soluble endoglin as well as to promote PlGF and endothelial NOS activity. The key to finding a cure lies in the identification of cheap, safe and effective drugs that induce the braking system to keep the pregnancy vehicle on track past the finishing line.