The Economic and Electoral Consequences of Austerity Policies in Britain

The aim of this paper is to examine the relationship between electoral support and the economy over the period 2004 to 2014, paying particular attention to the impact of the economic strategy pursued by the Coalition government in Britain since the general election in May 2010. This involves modelling the relationship between voting intentions, perceptions of economic performance, and a variety of other variables using survey data collected each month from 2004. The evidence shows that when Labour was in office, support for the party was strongly influenced by the state of the economy, as was support for the opposition parties. However, since the Coalition came to power, the relationship between the economy and political support has changed, with neither the Conservatives nor the Liberal Democrats gaining from a fairly rapid growth in economic optimism which has taken place since early 2013. The paper explains this change in terms of a growing perception among the public that none of the major parties can effectively manage Britain?s economic problems. It is also the case that optimism about the national economy has not significantly percolated down to the level of the individual voter. So individuals may be more optimistic about the future of the national economy but they are still being badly affected by the recession

Like Father, Like Son: Justin Trudeau and Valence Voting in Canada's 2015 Federal Election

This is the author accepted manuscript. The final version is available from Cambridge University Press via the DOI in this record.Canada’s 2015 federal election was an exiting, as well as a nostalgia provoking, contest. After nine years in office, Prime Minister Stephen Harper and the governing Conservatives were defeated by the resurgent Liberals led by Justin Trudeau. Trudeau is the son of Pierre Trudeau, perhaps Canada’s best known prime minister. Analyses of national survey data demonstrate that party leader images—a major component of the “valence politics” model of electoral choice—were important in both cases. Unlike his father, Justin Trudeau was castigated as a “lightweight” and “just not ready.” However, articulating plausible policies to jump-start Canada’s sluggish economy and espousing “sunny ways,” the younger Trudeau was warmly received by many voters. In contrast, Harper’s image of managerial competence was tarnished by bad economic news, and his attempt to refocus the campaign on emotionally charged cultural issues failed. The result was a Liberal majority government and a prime minister named Trudeau

Patients, caregivers and health‐care professionals’ experience with an interdisciplinary intervention for people with multimorbidity in primary care: a qualitative study

Background : Multimorbidity challenges the health‐care system and requires innovative approaches. In 2015, a 4‐month patient‐centred interdisciplinary pragmatic intervention was implemented in primary care with the aim of supporting self‐management for patients with multimorbidity. Objective : To explore the perceptions and experiences of health‐care professionals, patients and their caregivers with a 4‐month patient‐centred interdisciplinary pragmatic intervention in primary care. Design : A descriptive, qualitative study using semi‐structured interviews was conducted. Setting and participants : A purposive sample of 30 participants was recruited from seven family medicine groups including patients, caregivers and health‐care professionals (HCPs). Interviews were analysed using Thorne's interpretive description approach. Results : Findings were grouped into the benefits and challenges of participating in the intervention. The programme allowed patients to adopt realistic and adapted objectives; to customize interventions to the patient's reality; and to help patients gain confidence, improve their knowledge, skills and motivation to manage their condition. Interprofessional collaboration eased the exchange of information via team meetings and electronic medical records. Challenges were related to collaboration, communication, coordination of work and integration of newly relocated HCPs mainly due to part‐time assignments and staff turnover. HCPs part‐time schedules limited their availability and hindered patients’ follow‐up. Discussion and conclusion : This intervention was useful and rewarding from the HCPs, patients and caregivers’ perspective. However, to ensure the success of this complex interdisciplinary intervention, implementers and managers should anticipate organizational barriers such as availability and time management of relocated HCPs

The intestinal expulsion of the roundworm Ascaris suum is associated with eosinophils, intra-epithelial T cells and decreased intestinal transit time

Ascaris lumbricoides remains the most common endoparasite in humans, yet there is still very little information available about the immunological principles of protection, especially those directed against larval stages. Due to the natural host-parasite relationship, pigs infected with A. suum make an excellent model to study the mechanisms of protection against this nematode. In pigs, a self-cure reaction eliminates most larvae from the small intestine between 14 and 21 days post infection. In this study, we investigated the mucosal immune response leading to the expulsion of A. suum and the contribution of the hepato-tracheal migration. Self-cure was independent of previous passage through the liver or lungs, as infection with lung stage larvae did not impair self-cure. When animals were infected with 14-day-old intestinal larvae, the larvae were being driven distally in the small intestine around 7 days post infection but by 18 days post infection they re-inhabited the proximal part of the small intestine, indicating that more developed larvae can counter the expulsion mechanism. Self-cure was consistently associated with eosinophilia and intra-epithelial T cells in the jejunum. Furthermore, we identified increased gut movement as a possible mechanism of self-cure as the small intestinal transit time was markedly decreased at the time of expulsion of the worms. Taken together, these results shed new light on the mechanisms of self-cure that occur during A. suum infections

Co-opetition models for governing professional football

In recent years, models for co-creating value in a business-to-business context have often been examined with the aim of studying the strategies implemented by and among organisations for competitive and co-operative purposes. The traditional concepts of competition and co-operation between businesses have now evolved, both in terms of the sector in which the businesses operate and in terms of the type of goods they produce. Many researchers have, in recent times, investigated the determinants that can influence the way in which the model of co-opetition can be applied to the football world. Research interest lies in the particular features of what makes a good football. In this paper, the aim is to conduct an analysis of the rules governing the “football system”, while also looking at the determinants of the demand function within football entertainment. This entails applying to football match management the co-opetition model, a recognised model that combines competition and co-operation with the view of creating and distributing value. It can, therefore, be said that, for a spectator, watching sport is an experience of high suspense, and this suspense, in turn, depends upon the degree of uncertainty in the outcome. It follows that the rules ensuring that both these elements can be satisfied are a fertile ground for co-operation between clubs, as it is in the interest of all stakeholders to offer increasingly more attractive football, in comparison with other competing products. Our end purpose is to understand how co-opetition can be achieved within professional football

Primary and malignant cholangiocytes undergo CD40 mediated Fas dependent Apoptosis, but are insensitive to direct activation with exogenous fas ligand

Introduction Cholangiocarcinoma is a rare malignancy of the biliary tract, the incidence of which is rising, but the pathogenesis of which remains uncertain. No common genetic defects have been described but it is accepted that chronic inflammation is an important contributing factor. We have shown that primary human cholangiocyte and hepatocyte survival is tightly regulated via co-operative interactions between two tumour necrosis family (TNF) receptor family members; CD40 and Fas (CD95). Functional deficiency of CD154, the ligand for CD40, leads to a failure of clearance of biliary tract infections and a predisposition to cholangiocarcinoma implying a direct link between TNF receptor-mediated apoptosis and the development of cholangiocarcinoma. Aims To determine whether malignant cholangiocytes display defects in CD40 mediated apoptosis. By comparing CD40 and Fas-mediated apoptosis and intracellular signalling in primary human cholangiocytes and three cholangiocyte cell lines. Results Primary cholangiocytes and cholangiocyte cell lines were relatively insensitive to direct Fas-mediated killing with exogenous FasL when compared with Jurkat cells, which readily underwent Fas-mediated apoptosis, but were extremely sensitive to CD154 stimulation. The sensitivity of cells to CD40 activation was similar in magnitude in both primary and malignant cells and was STAT-3 and AP-1 dependent in both. Conclusions 1) Both primary and malignant cholangiocytes are relatively resistant to Fas–mediated killing but show exquisite sensitivity to CD154, suggesting that the CD40 pathway is intact and fully functional in both primary and malignant cholangiocytes 2) The relative insensitivity of cholangiocytes to Fas activation demonstrates the importance of CD40 augmentation of Fas dependent death in these cells. Agonistic therapies which target CD40 and associated intracellular signalling pathways may be effective in promoting apoptosis of malignant cholangiocytes

Limited Urban Growth: London's Street Network Dynamics since the 18th Century

We investigate the growth dynamics of Greater London defined by the administrative boundary of the Greater London Authority, based on the evolution of its street network during the last two centuries. This is done by employing a unique dataset, consisting of the planar graph representation of nine time slices of Greater London's road network spanning 224 years, from 1786 to 2010. Within this time-frame, we address the concept of the metropolitan area or city in physical terms, in that urban evolution reveals observable transitions in the distribution of relevant geometrical properties. Given that London has a hard boundary enforced by its long-standing green belt, we show that its street network dynamics can be described as a fractal space-filling phenomena up to a capacitated limit, whence its growth can be predicted with a striking level of accuracy. This observation is confirmed by the analytical calculation of key topological properties of the planar graph, such as the topological growth of the network and its average connectivity. This study thus represents an example of a strong violation of Gibrat's law. In particular, we are able to show analytically how London evolves from a more loop-like structure, typical of planned cities, toward a more tree-like structure, typical of self-organized cities. These observations are relevant to the discourse on sustainable urban planning with respect to the control of urban sprawl in many large cities, which have developed under the conditions of spatial constraints imposed by green belts and hard urban boundaries.Comment: PlosOne, in publicatio

Involvement of Noradrenergic Neurotransmission in the Stress- but not Cocaine-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in Mice: Role for β-2 Adrenergic Receptors

The responsiveness of central noradrenergic systems to stressors and cocaine poses norepinephrine as a potential common mechanism through which drug re-exposure and stressful stimuli promote relapse. This study investigated the role of noradrenergic systems in the reinstatement of extinguished cocaine-induced conditioned place preference by cocaine and stress in male C57BL/6 mice. Cocaine- (15 mg/kg, i.p.) induced conditioned place preference was extinguished by repeated exposure to the apparatus in the absence of drug and reestablished by a cocaine challenge (15 mg/kg), exposure to a stressor (6-min forced swim (FS); 20–25°C water), or administration of the α-2 adrenergic receptor (AR) antagonists yohimbine (2 mg/kg, i.p.) or BRL44408 (5, 10 mg/kg, i.p.). To investigate the role of ARs, mice were administered the nonselective β-AR antagonist, propranolol (5, 10 mg/kg, i.p.), the α-1 AR antagonist, prazosin (1, 2 mg/kg, i.p.), or the α-2 AR agonist, clonidine (0.03, 0.3 mg/kg, i.p.) before reinstatement testing. Clonidine, prazosin, and propranolol failed to block cocaine-induced reinstatement. The low (0.03 mg/kg) but not high (0.3 mg/kg) clonidine dose fully blocked FS-induced reinstatement but not reinstatement by yohimbine. Propranolol, but not prazosin, blocked reinstatement by both yohimbine and FS, suggesting the involvement of β-ARs. The β-2 AR antagonist ICI-118551 (1 mg/kg, i.p.), but not the β-1 AR antagonist betaxolol (10 mg/kg, i.p.), also blocked FS-induced reinstatement. These findings suggest that stress-induced reinstatement requires noradrenergic signaling through β-2 ARs and that cocaine-induced reinstatement does not require AR activation, even though stimulation of central noradrenergic neurotransmission is sufficient to reinstate

Probing host pathogen cross-talk by transcriptional profiling of both Mycobacterium tuberculosis and infected human dendritic cells and macrophages

This study provides the proof of principle that probing the host and the microbe transcriptomes simultaneously is a valuable means to accessing unique information on host pathogen interactions. Our results also underline the extraordinary plasticity of host cell and pathogen responses to infection, and provide a solid framework to further understand the complex mechanisms involved in immunity to M. tuberculosis and in mycobacterial adaptation to different intracellular environments

Cellular Radiosensitivity: How much better do we understand it?

Purpose: Ionizing radiation exposure gives rise to a variety of lesions in DNA that result in genetic instability and potentially tumorigenesis or cell death. Radiation extends its effects on DNA by direct interaction or by radiolysis of H2O that generates free radicals or aqueous electrons capable of interacting with and causing indirect damage to DNA. While the various lesions arising in DNA after radiation exposure can contribute to the mutagenising effects of this agent, the potentially most damaging lesion is the DNA double strand break (DSB) that contributes to genome instability and/or cell death. Thus in many cases failure to recognise and/or repair this lesion determines the radiosensitivity status of the cell. DNA repair mechanisms including homologous recombination (HR) and non-homologous end-joining (NHEJ) have evolved to protect cells against DNA DSB. Mutations in proteins that constitute these repair pathways are characterised by radiosensitivity and genome instability. Defects in a number of these proteins also give rise to genetic disorders that feature not only genetic instability but also immunodeficiency, cancer predisposition, neurodegeneration and other pathologies. Conclusions: In the past fifty years our understanding of the cellular response to radiation damage has advanced enormously with insight being gained from a wide range of approaches extending from more basic early studies to the sophisticated approaches used today. In this review we discuss our current understanding of the impact of radiation on the cell and the organism gained from the array of past and present studies and attempt to provide an explanation for what it is that determines the response to radiation