L'éveil de l'âme française devant l'appel aux armes.

At head of title: Abbés G. Ardant., J. Desgranges, Ch. Thellier de Poncheville.

Documents allemands relatifs à l'origine de la guerre : collection complète des documents officiels rassemblés avec quelques compléments /

t. 1. De l'attentat de Sarajevo à la réception de la réponse serbe avec quelques documents des semaines qui ont prédédé. -- t. 2. De la réception de la réponse serbe à la nouvelle de la mobilisation générale russe. -- t. 3. De la nouvelle de la mobilisation générle russe à la déclaration de guerre à la France. -- t. 4. De la déclaration de guerre à la France à la declaration de guerre de l'Autriche-Hongrie à la Russie (avec annexes)

The best short stories of 1915 : and the yearbook of the American short story /

The water-hole / Maxwell Struthers Burt -- The wake / Donn Byrne -- Chautonville / Will Levington Comfort -- La Derniere mobilisation / W. A. Dwiggins -- The citizen / James Francis Dwyer -- Whose dog? / Frances Gregg -- Life / Ben Hecht -- T. B. / Fannie Hurst -- Mr. Eberdeen's house / Arthur Johnson -- Vengeance is mine / Virgil Jordan -- The weaver who clad the summer / Harris Merton Lyon.

International Labour Movement Responses to Globalization /

This book examines international labour movement opposition to globalisation. It chronicles and critically scrutinizes the emergence of distinctively new forms of labour movement organisation and mobilisation that constitute creative initiatives on the part of labour, which present capitalism with fresh challenges.

The role of glucocorticoids in the induction of zinc-α2-glycoprotein expression in adipose tissue in cancer cachexia

Loss of adipose tissue in cancer cachexia in mice bearing the MAC16 tumour arises from an increased lipid mobilisation through increased expression of zinc-α2-glycoprotein (ZAG) in white (WAT) and brown (BAT) adipose tissue. Glucocorticoids have been suggested to increase ZAG expression, and this study examines their role in cachexia and the mechanisms involved. In mice bearing the MAC16 tumour, serum cortisol concentrations increased in parallel with weight loss, and the glucocorticoid receptor antagonist RU38486 (25 mg kg-1) attenuated both the loss of body weight and ZAG expression in WAT. Dexamethasone (66 μg kg-1) administration to normal mice produced a six-fold increase in ZAG expression in both WAT and BAT, which was also attenuated by RU38486. In vitro studies using 3T3-L1 adipocytes showed dexamethasone (1.68 μM) to stimulate lipolysis and increase ZAG expression, and both were attenuated by RU38486 (10 μM), anti-ZAG antibody (1 μ gml-1), and the β3-adrenoreceptor (β3-AR) antagonist SR59230A (10 μM). Zinc-α2-glycoprotein also increased its own expression and this was attenuated by SR59230A, suggesting that it was mediated through the β3-AR. This suggests that glucocorticoids stimulate lipolysis through an increase in ZAG expression, and that they are responsible for the increase in ZAG expression seen in adipose tissue of cachectic mice. © 2005 Cancer Research UK.

Queer enough? Contested terrains of identity deployment in the context of gay and lesbian public activism in Poland

Gay and lesbian prides and marches are of crucial relevance to the way in which non-heterosexual lives are imagined internationally despite regional and national differences. Quite often, these events are connected not only with increased activist mobilisation, but also with great controversy, which is the case of Poland, where gay and lesbian marches have been attacked by right-wing protesters and cancelled by right-wing city authorities on a number of occasions. Overall, the scholars analysing these events have largely focused on the macro-context of the marches, paying less attention to the movement actors behind these events. The contribution of this thesis lies not only in filling a gap when it comes to research on sexual minorities in Eastern Europe/Poland, but also in its focus on micro-level movement processes and engagement with theories of collective identity and citizenship. Furthermore, this thesis challenges the inscription of Eastern European/Polish movements into the narrative of victimhood and delayed development when compared to LGBT movements in the Global North. This thesis is grounded in qualitative research including participant observation of public activist events as well as forty semi-structured interviews with the key organisers of gay and lesbian marches in Warsaw, Poznan and Krakow between 2001 and 2007, and five of these interviews were further accompanied by photo-elicitation (self-directed photography) methods. Starting from the processes whereby from 2001 onwards, marches, pride parades and demonstrations became the most visible and contested activity of the Polish lesbian and gay movement, this thesis examines how the activists redefined the meanings of citizenship in the post-transformation context, by incorporating the theme of sexual minorities' rights. Using Bernstein's (1997, 2002, 2005, 2008) concept of identity deployment, I show how and when movement actors use identity tactically, depending on their goals. Specifically, in the context of movement-media interactions, I examine the ways in which the activists use marches to challenge the negative representations of sexual minorities in Poland. I also broaden Bernstein's framework to include the discussion of emotion work as relevant to public LGBT activism in Poland. Later, I discuss how the emotions of protests allowed the activists to inscribe their efforts into the "revolutionary" narrative of the Polish Solidarity movement and by extension, the frame of citizenship. Finally, this thesis engages with the dilemmas of identity deployment strategies, and seeks to problematise the dichotomy between identity-based gay and lesbian assimilationist strategies and the anti-identity queer politics.

Informal boundary-spanning links and networks in successful technological innovation

The sources of ideas embodied within successful technological innovation has been a subject of interest in many studies since the 1950s. This research suggests that sources external to the innovating organisation account for between one and two-thirds of the inputs important to the innovation process. In addition, studies have long highlighted the important role played by the personal boundary-spanning relationships of engineers and scientists as a channel for the transference of such inputs. However, research concerning the role and nature of personal boundary-spanning links in the innovation process have either been primarily structurally orientated, seeking to map out the informal networks of scientists and engineers, or more typically, anecdotal. The objective of this research was to reveal and build upon our knowledge of the role, nature and importance of informal exchange activity in the innovation process. In order to achieve this, an empirical study was undertaken to determine the informal sources, channels and mechanisms employed in the development of thirty five award-winning innovations. Through the adoption of the network perspective, the multiple sources and pluralistic patterns of collaboration and communication in the innovation process were systematically explored. This approach provided a framework that allowed for the detailed study of both the individual dyadic links and morphology of the innovation action-sets in which these dyads were embedded. The research found, for example, that the mobilisation of boundary-spanning links and networks was an important or critical factor in nineteen (54%) of the development projects. Of these, informal boundary-spanning exchange activity was considered to be important or critical in eight (23%).

The mode of action of a lipid mobilising factor in cancer cachexia

Cachexia is characterised by a progressive weight loss due to depletion of both skeletal muscle and adipose tissue. The loss of adipose tissue is due to the production of a tumour-derived lipid mobilising factor (LMF), which has been shown to directly induce lipolysis in isolated epididymal murine white adipocytes. The administration of LMF to a non-tumour bearing mice produced a rapid weight loss, with a specific reduction in carcass lipid with also some redistribution of lipid with the accumulation of lipid in the liver. There was also up-regulation of uncoupling protein-1 and -2 mRNA and protein expression in brown adipose tissue, suggesting that an adaptive process occurs due to increased energy mobilisation. There was also up-regulation of UCP-2 in the livers of LMF treated mice, suggesting a protective mechanism to the build up of lipid in the livers, which would produce free radical by-products. LMF was also shown to stimulate cyclic AMP production in CHO-K1 cells transfected with human -3 adrenergic receptors and inhibited by the -β3 antagonist SR59230A. LMF binding was also inhibited by SR59230A in isolated receptors. This suggests that LMF mediates its effects through a β3 adrenergic receptor. There were also changes in glucose and fatty acid uptake in LMF treated mice, which suggests metabolic changes are occurring. The study suggests that a tumour derived lipolytic factor acts through the 3 adrenoceptor producing effects on lipid mobilisation, energy expenditure and glucose metabolism.

Mediators of monocyte activity in inflammation

C-reactive protein (CRP) is the prototypic acute phase serum protein in humans. CRP is currently one of the best markers of inflammatory disease and disease activity. One of the keys cells involved in inflammation within chronic inflammatory diseases is the monocyte. Monocytes are able to modulate inflammation through cytokine expression, cytosolic peroxide formation, adhesion molecule expression and subsequent adhesion/migration to sites of inflammation. CRP has been previously shown to bind directly to monocytes through Fc receptors. However this observation is not conclusive and requires further investigation. The effects of incubation of CRP with human primary and monocytic cell lines were examined using monocytic cytokine expression, adhesion molecule expression and adhesion to endothelial cells and intracellular peroxide formation, as end points. Monocytic intracellular signalling events were investigated after interaction of CRP with specific CRP receptors on monocytes. These initial signalling events were examined for their role in modulating monocytic adhesion molecule and cytokine expression. Monocyte recruitment and retention in the vasculature is also influenced by oxidative stress. Therefore the effect of 6 weeks of antioxidant intervention in vivo was examined on monocytic adhesion molecule expression, adhesion to endothelial cells ex vivo and on serum CRP concentrations, pre- and post- supplementation with the antioxidants vitamin C and vitaInin E. In summary, CRP is able to bind FcγRIIa. CRP binding FcγR initiates an intracellular signalling cascade that phosphorylates the non-receptor tyrosine kinase, Syk, associated with intracellular tyrosine activating motifs on the cytoplasmic tail of Fcγ receptors. CRP incubations increased phosphatidyl inositol turnover and Syk phosphorylation ultimately lead to Ca2+ mobilisation in monocytes. CRP mediated Syk phosphorylation in monocytes leads to an increase in CD 11b and IL-6 expression. CRP engagement with monocytes also leads to an increase in peroxide production, which can be inhibited in vitro using the antioxidants α-tocopherol and ascorbic acid. CRP mediated CD 11b expression is not redox regulated by CRP mediated changes in cytosolic peroxides. The FcyRIla polymorphism at codon 131 effects the phenotypic driven changes described in monocytes by CRP, where R/R allotypes have a greater increase in CD11b, in response to CRP, which may be involved in promoting the monocytic inflammatory response. CRP leads to an increase in the expression of pro-inflammatory cytokines, which alters the immune phenotype of circulating monocytes. Vitamin C supplementation reduced monocytic adhesion to endothelial cells, but had no effect on serum levels of CRP. Where long-term antioxidant intervention may provide benefit from the risk of developing vascular inflammatory disease, by reducing monocytic adhesion to the vasculature. In conclusion CRP appears to be much more than just a marker of ongoing inflammation or associated inflammatory disease and disease activity. This data suggests that at pathophysiological concentrations, CRP may be able to directly modulate inflammation through interacting with monocytes and thereby alter the inflammatory response associated with vascular inflammatory diseases.

Second messenger pathways in the action of cachectic factors

Cachexia in cancer is characterised by progressive depletion of both adipose tissue stores and skeletal muscle mass. Two catabolic factors produced by cachexia-inducing tumours have the potential for inducing these changes in body composition: (i) proteolysis-inducing factor (PIF) which acts on skeletal muscle to induce both protein degradation and inhibit protein synthesis, (ii) lipid-mobilising factor (LMF), which has been shown to directly induce lipolysis in isolated epididymal murine white adipocytes. Administration of lipid-mobilising factor (LMF) to mice produced a specific reduction in carcass lipid with a tendency to increase non-fat carcass mass. Treatment of murine myoblasts, myotubes and tumour cells with tumour-produced LMF, caused concentration dependent stimulation of protein synthesis, within a 24hr period. It produced an increase in intracellular cyclic AMP levels, which was linearly related to the increase in protein synthesis. The observed effect was attenuated by pretreating cells with the adenylate cyclase inhibitor, MDL12330A and was additive with stimulation produced by forskolin. Both propranolol and a specific 3 adrenergic antagonist SR59230A, significantly reduced the stimulation of protein synthesis induced by LMF. LMF also affected protein degradation in vitro, as demonstrated by a reduction in proteasome activity, a key component of the ubiquitin-dependent proteolytic pathway. These effects were opposite to those produced by PIF which caused both a decrease in the rate of protein synthesis and an elevation on protein breakdown when incubated in vitro.Incubation of LMF with a fat cell line produced alterations in the levels of guanine-nucleotide binding proteins (G proteins). This was also evident in adipocyte plasma membranes isolated from mice bearing the tumour model of cachexia, MAC16 adenocarcinoma and from patients with cancer cachexia. Progression through the cachectic state induced an upregulation of stimulatory G proteins paralleled with a downregulation of inhibitory G proteins. These changes would contribute to the increased lipid mobilisation seen in cancer cachexia.

A comparative study of the effects of hypoxia upon isolated arterial muscle from the rat

Contractile response of rat aorta, mesenteric artery and femoral artery to noradrenaline and potassium chloride were studied under standard and hypoxic conditions and the effect of hypoxia was dependent upon both the vessel and the stimulant. Hypoxia had less effect upon contractions to potassium chloride than those to noradrenaline. The effects of hypoxia on potassium chloride induced responses in different vessels were relatively similar although responses to noradrenaline were vessel dependent. Noradrenaline induced contractions of the femoral artery were most affected by hypoxia whilst those of the mesenteric artery were least affected. Hypoxia changed the well maintained response of the femoral artery to noradrenaline to a transient form; this effect of hypoxia was not evident in the aorta or the mesenteric artery. The aorta and mesenteric artery contracted in calcium free EGTA PSS suggesting that these vessels displayed a release component. Hypoxia reduced the magnitude of this component. The effects of verapamil on noradrenaline and potassium chloride induced responses were investigated and were found to be different to those of hypoxia. Verapamil exerted a greater effect on contractions to potassium chloride than on those to noradrenaline. The effects of hypoxia on 45calcium flux were also vessel dependent. In the mesenteric and femoral arteries hypoxia increased basal 45calcium accumulation. However, the magnitude of noradrenaline stimulated 45calcium accumulation was reduced in the femoral artery and aorta but was unchanged in the mesenteric artery. The effects of hypoxia on 45calcium accumulation were similar to verapamil only in the aorta. The results provide evidence that the effects of hypoxia may arise from alterations in calcium mobilisation processes and that differences between vessels in these processes accounts for the heterogeneity between vessels in their response to hypoxia.

Mechanisms of tumour-induced cachexia

The effect of cancer cachexia on host metabolism has been studied in mice transplanted with either the MAC16 adenocarcinoma which induces profound loss of host body weight and depletion of lipid stores or, the MAC13 adenocarcinoma which is of the same histological type, but which grows without an effect on host body weight. Oxidation of D-[U-14C]glucose was elevated in both tumour-bearing states irrespective of cachexia, when compared with non tumour-bearing controls. Both the MAC16 and MAC13 tumours in vivo utilised glucose at the expense of the brain, where its use was partially replaced by 3-hydroxybutyrate, a ketone body. Oxidation of both [U-14C]palmitic acid and [1-14C]triolein was significantly increased in MAC16 tumour-bearing animals and decreased in MAC13 tumour-bearing animals when compared with non tumour-bearing controls, suggesting that in cachectic tumour-bearing animals, mobilisation of body lipids is accompanied by an increased utilisation by the host. Weight loss in MAC16 tumour-bearing animals is associated with the production of a lipolytic factor. Injection of this partially purified lipolytic factor induced weight loss in recipient animals which could be maintained over time in tumour-bearing animals. This suggests that the tumour acts as a sink for the free fatty acids liberated as a result of the mobilisatation of adipose stores. Lipids are important as an energy source in cachectic animals because of their high calorific value and because glucose is being diverted away from host tissues to support tumour growth. Their importance is further demonstrated by the evidence of a MAC16 tumour-associated lipolytic factor. This lipolytic factor is the key to understanding the alterations in host metabolism that occur in tumour-induced cachexia, and may provide future alternatives for the reversal of cachexia and the treatment of cancer itself.

Polyunsaturated fatty acids in tumour-induced cachexia

A transplantable murine colon adenocarcinoma (MAC16) was utilised as a model of human cancer cachexia. This tumour has been found to produce extensive weight loss, characterised by depletion of host body protein and lipid stores at a small tumour burden. This weight loss has been found to be associated with production by the tumour of a lipolytic factor, activity of which was inhibited in vitro by the polyunsaturated fatty acid (PUFA) eicosapentaenoic acid (EPA). EPA has also been shown to possess anti-tumour and anti-cachectic activity in vivo, leading to the hypothesis that fatty acids mobilised by the lipolytic factor supply a growth requirement of the MAC16 tumour. In this study mobilisation and sequestration of fatty acids by the tumour was found to be non-specific, although a relationship between weight loss and arachidonic acid (AA) concentration was found in both tumour-bearing mice, and human cancer patients. The anti-tumour effect of EPA, which was found to be associated with an increase in cell loss, but not its anti-cachectic activity, was reversed by the administration of the PUFAs oleic acid (OA) and linoleic acid (LA). LA was also found to be capable of stimulating tumour growth. Inhibition of either the cyclooxygenase or lipoxygenase pathways was found to result in reduction of tumour growth, leading to the implication of one of the metabolites of LA or AA in tumour growth and cachexia. The ethyl ester of EPA was found to be inactive against the growth and cachexia of the MAC16 tumour, due to its retarded uptake compared with the free acid. The anti-proliferative agent 5-fluorouracil was found to cause tumour growth inhibition, and when given in combination with EPA, reduced the phase of tumour regrowth observed after 4 to 5 days of treatment with EPA.

Negotiating proximity:expert testimony and collective memory in the trials of environmental activists in France and the United Kingdom

This article analyzes the role of expert witness testimony in the trials of social movement actors, discussing the trial of the "Kingsnorth Six" in Britain and the trials of activists currently mobilising against airport construction at Notre Dame des Landes in western France. Though the study of expert testimony has so far overwhelmingly concentrated on fact-finding and admissibility, the cases here reveal the importance of expert testimony not simply in terms of legal argument, but in "moral" or political terms, as it reflects and constitutes movement cognitive praxis. In the so-called climate change defence presented by the Kingsnorth Six, I argue that expert testimony attained a "negotiation of proximity," connecting different types of contributory expertise to link the scales and registers of climate science with those of everyday understanding and meaning. Expert testimony in the trials of activists in France, however, whilst ostensibly able to develop similar bridging narratives, has instead been used to construct resistance to the airport siting as already proximate, material, and embedded. To explain this, I argue that attention to the symbolic, as well as instrumental, functions of expert testimony reveals the crucial role that collective memory plays in the construction of both knowledge and grievance in these cases. Collective memory is both a constraint on and catalyst for mobilisation, defining the boundaries of the sayable. Testimony in trials both reflects and reproduces these elements and is a vital explanatory tool for understanding the narrativisation and communication of movement identities and objectives. © 2013 The Author. Law & Policy © 2013 The University of Denver/Colorado Seminary.

Representing religion in the European Union:does God matter?

Religious actors are becoming part of the EU bureaucratic system, and their mobilisation in Brussels and Strasbourg in the last decade has increased dramatically. This book explores the mechanism and impact of religious representation by examining relations between religious practitioners and politicians in the European Union from the Second World War until today. This book seeks to answer the following questions: How do (trans)national religious groups enter into contact with European institutions? What are the rationale and the mechanisms of religious representation in the European Union? How are religious values transposed into political strategies? What impact has relations between religious practitioners, EU officials and politicians on the construction of the European Union? Examining religious representation at the state, transnational and institutional levels, this volume demonstrates that ‘faith’ is becoming an increasingly important element of the decision-making process. It includes chapters written by both academics and religious practitioners in dialogue with European institutions and will be of great interest to students and scholars of European politics, history, sociology of religion, law and international relations.