bluuebunny/crossref_metadata_2025_split huggingface dataset:
La tarification du téléphone : une réforme de grande ampleur
Authors: Le Foll Jean 
Published: March 2011

La tarification du téléphone : une réforme de grande ampleur,
par Jean Le Foll.

Depuis 1981, plusieurs décisions ont modifié sensiblement les tarifs du téléphone : prélèvements au profit du budget général, de la poste et des industries électroniques, modulation horaire, tarification à la durée des communications locales... Ces décisions s'inscrivent-elles dans le cadre d'une réforme d'ensemble tendant à rapprocher les coûts et les prix de ces services ? L'article a pour objet d'apporter quelques éléments de réponse à cette question et de décrire les paramètres principaux sur lesquels pourraient porter les changements futurs.

Il rappelle tout d'abord quelques exemples de distorsions tarifaires dans plusieurs pays développés ainsi que les résultats d'une étude récente de la Direction générale des télécommunications qui évalue l'importance des transferts de revenus induits par la tarification téléphonique. Après avoir indiqué le cadre général propre à la France, où cette activité est gérée en tant que monopole public par une administration d'Etat, on s'interroge sur le contexte international de déréglementation dont le démembrement d'Att aux Etats-Unis est le précurseur.

L'évolution globale des recettes et, plus précisément, le niveau général des tarifs conduisent à deux catégories d'observations : d'une part, l'intérêt économique et social indéniable de cette activité commande d'éviter le rationnement par les prix, d'autre part, l'instauration récente de divers prélèvements invite à étudier de façon plus approfondie l'assu- jetissement des télécommunications au régime fiscal de droit commun des entreprises.

Les principaux développements de l'article sont consacrés à la structure des tarifs et aux différents paramètres qui devraient guider son évolution. D'abord, ceux qui caractérisent les divers usages ou catégories de services rendus, l'équipement téléphonique (raccordement, transfert et abonnement) et surtout quatre d'entre eux déterminant l'essentiel des coûts et des recettes : le moment, le lieu, la distance et la durée de la communication. La modulation horaire devra encore être accentuée. Cependant réduire l'importance de la distance pour le trafic interurbain et particulièrement accroître celle de la durée pour les liaisons locales sont certainement les réformes qui, déjà commencées, auront les conséquences les plus profondes d'abord sur les transferts entre usagers, puis sur le comportement des divers agents économiques concernés. L'article indique enfin l'ampleur des changements tarifaires envisageables dans le cadre d'un rapprochement significatif des prix et des coûts : division par deux ou trois des tarifs de longue distance et forte hausse des prix des communications locales.
Mise en œuvre des budgets économiques au Niger
Authors: Mathis Jean , de Monchy Guy , Rocca Marc 
Published: March 2011

Developing economic budgets in Niger,
by Jean Mathis, Guy de Monchy et Marc Rocca.

Under a United Nations Development Programm (Undp) project to develop short-term economic analysis and forecasting in the Niger Republic, several teams of experts have visited this country since the end of 1983.

The aim of this article is to show through a tentative experiment earned out in Niger the stages which can be reached in developing this type of forecasting depending on the economic information available and the existing administrative structures. The stages described here do not take into account the most recent missions and therefore do not reflect the latest situation with regard to the Undp's work to develop its short- term forecasting policy in the Niger Republic.

After an introductory section explaining the approach used, three other sections show the transition process from analysis of how the economy functions to various stages of formalization thereof.

First of all, therefore, the physical characteristics of the economy of Niger and its major macroeconomic circuits are described. The authors then explain the model-building stage and what can be learned in this way when statistical information is lacking. The last section presents a short-term forecasting model derived from an analogous pedagogical model developed for a macroeconomic forecast seminar organized by the Un at Niamey in July 1984.

The conclusion touches on possible ways of improving on the work presented and certain conditions to be fulfilled if it is to be integrated into the economic policy development process.
Du côtoiement à l'engagement : la portée politique de la civilité
Authors: Gayet-Viaud Carole 
Published: March 2011

Résumé De nombreuses critiques ont été formulées quant à la portée politique du rapprochement aujourd’hui croissant entre questions politiques et questions urbaines, civilité et citoyenneté. Ces critiques ont souligné les effets en trompe-l’œil imputables à « l’orientation localiste et urbaniciste de l’action publique? 1 », ainsi que les risques d’un confinement de l’engagement militant dans le local. Sans prétendre trancher ici ces débats, on propose de suspendre toute présomption concernant « ce que veut dire » le fait de parler d’engagement de proximité, de citadinité, ou de civilité, pour considérer ce que peuvent faire certaines de ces façons de parler? 2 et d’agir, dans des contextes particuliers, ici celui d’une activité associative. L’analyse portera sur un discours de la proximité, mis en œuvre dans le cadre d’une démarche de communication, entreprise en 2009 par l’association Les Morts de la Rue , engagée dans le soutien aux personnes à la rue, et dont la principale activité consiste à offrir des funérailles aux personnes décédées à la rue. Cette démarche offre une occasion intéressante d’aborder l’articulation possible de gestes civils élémentaires et de l’engagement citoyen.
Impasse du capitalisme, chemins de l'utopie
Authors: Bourdeau Vincent , Flory Julienne , Haeringer Nicolas 
Published: March 2011

Résumé Mouvements a rencontré Isabelle Frémeaux? 1 et John Jordan? 2 auteurs du Livre – film Les Sentiers de L’utopie . Cette œuvre propose une exploration de quelques formes de vie post-capitalistes en Europe. Quelles sont ces utopies ? Comment vivre en résistance à la société capitaliste actuelle, en proposant des alternatives ? Quelles sont les luttes et les revendications de ces communautés ? Comment fonctionnent-elles ? C’est ce que nous vous proposons de découvrir, à travers cet entretien avec les auteurs.
« Pour une résistance culturelle permanente »
Authors: Lemoine Stéphanie , Ouardi Samira 
Published: March 2011

Résumé Depuis 1987, Le Critical Art Ensemble (CAE) s’attache à inventer « une culture de l’opposition et de la résistance ». Ses travaux protéiformes, faits de publications théoriques, d’interventions, d’installations, de performances et de production d’images, sont notamment destinés à doter les citoyens d’outils de réflexion et d’action critique. Quand d’autres initiatives du même type se sont penchées sur la vie quotidienne ou l’économie, les membres du CAE ont choisi la technologie pour « théâtre des opérations »? 1 . Ils sont ainsi les théoriciens de la « désobéissance civile électronique », concept repris en pratique par des mouvements comme la guérilla zapatiste. Plus généralement, ils ont produit une critique radicale des usages des nouveaux médias et du web. Depuis le début des années 2000 le groupe se consacre au développement d’une nouvelle forme de hacking : la biologie contestataire. L’objectif des projets nés dans cette perspective est « la réappropriation des matériaux et processus scientifiques qui ne profitent aujourd’hui qu’aux grands groupes et à l’armée ». Parfois dispositifs participatifs de prise de conscience des enjeux des biotechnologies, d’autres fois expériences scientifiques d’intervention sur les OGM pour les désactiver, ces travaux ont valu à Steve Kurtz, co-fondateur du collectif, d’être inculpé de « bio-terrorisme » en 2004. Si toutes les charges retenues contre lui ont finalement été abandonnées en 2008, ce procès est venu démontrer une fois encore que, sans conteste, la science est l’un des lieux du pouvoir contemporain. Nous avons rencontré Steve Kurtz à Paris, il est revenu pour nous sur l’histoire et les pratiques du CAE.
Suppressor of Cytokine Signaling 1 Regulates Embryonic Myelopoiesis Independently of Its Effects on T Cell Development
Authors: O’Sullivan Lynda A. , Noor Suzita M. , Trengove Monique C. , Lewis Rowena S. , Liongue Clifford , Sprigg Naomi S. , Nicholson Sandra E. , Ward Alister C. 
Published: March 2011

Abstract
Suppressor of cytokine signaling 1 (SOCS1) has been shown to play important roles in the immune system. It acts as a key negative regulator of signaling via receptors for IFNs and other cytokines controlling T cell development, as well as Toll receptor signaling in macrophages and other immune cells. To gain further insight into SOCS1, we have identified and characterized the zebrafish socs1 gene, which exhibited sequence and functional conservation with its mammalian counterparts. Initially maternally derived, the socs1 gene showed early zygotic expression in mesodermal structures, including the posterior intermediate cell mass, a site of primitive hematopoiesis. At later time points, expression was seen in a broad anterior domain, liver, notochord, and intersegmental vesicles. Morpholino-mediated knockdown of socs1 resulted in perturbation of specific hematopoietic populations prior to the commencement of lymphopoiesis, ruling out T cell involvement. However, socs1 knockdown also lead to a reduction in the size of the developing thymus later in embryogenesis. Zebrafish SOCS1 was shown to be able to interact with both zebrafish Jak2a and Stat5.1 in vitro and in vivo. These studies demonstrate a conserved role for SOCS1 in T cell development and suggest a novel T cell-independent function in embryonic myelopoiesis mediated, at least in part, via its effects on receptors using the Jak2–Stat5 pathway.
Anthrax Lethal Factor Activates K+ Channels To Induce IL-1β Secretion in Macrophages
Authors: Thomas Johnson , Epshtein Yulia , Chopra Arun , Ordog Balazs , Ghassemi Mahmood , Christman John W. , Nattel Stanley , Cook James L. , Levitan Irena 
Published: March 2011

Abstract
Anthrax lethal toxin (LeTx) is a virulence factor of Bacilillus anthracis that is a bivalent toxin, containing lethal factor (LF) and protective Ag proteins, which causes cytotoxicity and altered macrophage function. LeTx exposure results in early K+ efflux from macrophages associated with caspase-1 activation and increased IL-1β release. The mechanism of this toxin-induced K+ efflux is unknown. The goals of the current study were to determine whether LeTx-induced K+ efflux from macrophages is mediated by toxin effects on specific K+ channels and whether altered K+-channel activity is involved in LeTx-induced IL-1β release. Exposure of macrophages to LeTx induced a significant increase in the activities of two types of K+ channels that have been identified in mouse macrophages: Ba2+-sensitive inwardly rectifying K+ (Kir) channels and 4-aminopyridine–sensitive outwardly rectifying voltage-gated K+ (Kv) channels. LeTx enhancement of both Kir and Kv required the proteolytic activity of LF, because exposure of macrophages to a mutant LF-protein (LFE687C) combined with protective Ag protein had no effect on the currents. Furthermore, blocking Kir and Kv channels significantly decreased LeTx-induced release of IL-1β. In addition, retroviral transduction of macrophages with wild-type Kir enhanced LeTx-induced release of IL-1β, whereas transduction of dominant-negative Kir blocked LeTx-induced release of IL-1β. Activation of caspase-1 was not required for LeTx-induced activation of either of the K+ channels. These data indicate that a major mechanism through which LeTx stimulates macrophages to release IL-1β involves an LF-protease effect that enhances Kir and Kv channel function during toxin stimulation.
The Adaptor Protein TRADD Is Essential for TNF-Like Ligand 1A/Death Receptor 3 Signaling
Authors: Pobezinskaya Yelena L. , Choksi Swati , Morgan Michael J. , Cao Xiumei , Liu Zheng-gang 
Published: March 2011

Abstract
TNFR-associated death domain protein (TRADD) is a key effector protein of TNFR1 signaling. However, the role of TRADD in other death receptor (DR) signaling pathways, including DR3, has not been completely characterized. Previous studies using overexpression systems suggested that TRADD is recruited to the DR3 complex in response to the DR3 ligand, TNF-like ligand 1A (TL1A), indicating a possible role in DR3 signaling. Using T cells from TRADD knockout mice, we demonstrate in this study that the response of both CD4+ and CD8+ T cells to TL1A is dependent upon the presence of TRADD. TRADD knockout T cells therefore lack the appropriate proliferative response to TL1A. Moreover, in the absence of TRADD, both the stimulation of MAPK signaling and activation of NF-κB in response to TL1A are dramatically reduced. Unsurprisingly, TRADD is required for recruitment of receptor interacting protein 1 and TNFR-associated factor 2 to the DR3 signaling complex and for the ubiquitination of receptor interacting protein 1. Thus, our findings definitively establish an essential role of TRADD in DR3 signaling.
Temporal Regulation of Intracellular Organelle Homeostasis in T Lymphocytes by Autophagy
Authors: Jia Wei , He You-Wen 
Published: March 2011

Abstract
The highly conserved self-degradation pathway known as autophagy plays important roles in regulating T lymphocyte homeostasis. Recently, we found that T lymphocytes lacking the autophagy-related gene Atg5 or Atg7 have defective survival and contain expanded mitochondria and endoplasmic reticulum (ER); however, whether these defects are caused by impaired autophagy or by defects in their autophagy-independent signaling capacity of Atg5 or Atg7 in T lymphocytes remains unknown. Furthermore, the function of the microtubule-associated protein L chain 3 (LC3) conjugation system in T lymphocytes remains unclear. To address these questions, we generated conditional knockout mice with specific deletion of Atg3, a ubiquitin enzyme E2-like molecule involved in the LC3 conjugation system, in T lymphocytes. Atg3-deficient T lymphocytes displayed a phenotype similar to those of Atg7- and Atg5-deficient T cells. The survival of Atg3-deficient naive CD4+ and CD8+ T cells was defective. Furthermore, the mitochondria and ER were expanded in Atg3-deficient T cells. Interestingly, mitochondrial and ER content did not change instantly upon inducible deletion of Atg3 in mature T lymphocytes in vitro. Instead, it began to expand 10 d after inducible deletion of Atg3 in mature T lymphocytes, and mitochondrial content continued to increase on day 18. Cell death began to increase 24 d after inducible deletion of Atg3. These data show that the LC3 conjugation system is essential for autophagy in T lymphocytes. Our data suggest that autophagy promotes T lymphocyte survival by regulating organelle homeostasis and that the decreased survival of autophagy-deficient T cells is due to the temporal accumulation of these autophagy-related defects.
Clonal Analysis Reveals Uniformity in the Molecular Profile and Lineage Potential of CCR9+ and CCR9− Thymus-Settling Progenitors
Authors: Desanti Guillaume E. , Jenkinson William E. , Parnell Sonia M. , Boudil Amine , Gautreau-Rolland Laetitia , Eksteen Bertus , Ezine Sophie , Lane Peter J. L. , Jenkinson Eric J. , Anderson Graham 
Published: March 2011

Abstract
The entry of T cell progenitors to the thymus marks the beginning of a multistage developmental process that culminates in the generation of self–MHC-restricted CD4+ and CD8+ T cells. Although multiple factors including the chemokine receptors CCR7 and CCR9 are now defined as important mediators of progenitor recruitment and colonization in both the fetal and adult thymi, the heterogeneity of thymus-colonizing cells that contribute to development of the T cell pool is complex and poorly understood. In this study, in conjunction with lineage potential assays, we perform phenotypic and genetic analyses on thymus-settling progenitors (TSP) isolated from the embryonic mouse thymus anlagen and surrounding perithymic mesenchyme, including simultaneous gene expression analysis of 14 hemopoietic regulators using single-cell multiplex RT-PCR. We show that, despite the known importance of CCL25-CCR9 mediated thymic recruitment of T cell progenitors, embryonic PIR+c-Kit+ TSP can be subdivided into CCR9+ and CCR9− subsets that differ in their requirements for a functional thymic microenvironment for thymus homing. Despite these differences, lineage potential studies of purified CCR9+ and CCR9− TSP reveal a common bias toward T cell-committed progenitors, and clonal gene expression analysis reveals a genetic consensus that is evident between and within single CCR9+ and CCR9− TSP. Collectively, our data suggest that although the earliest T cell progenitors may display heterogeneity with regard to their requirements for thymus colonization, they represent a developmentally homogeneous progenitor pool that ensures the efficient generation of the first cohorts of T cells during thymus development.
Differentiation of Inflammatory Dendritic Cells Is Mediated by NF-κB1–Dependent GM-CSF Production in CD4 T Cells
Authors: Campbell Ian K. , van Nieuwenhuijze Annemarie , Segura Elodie , O’Donnell Kristy , Coghill Elise , Hommel Mirja , Gerondakis Steve , Villadangos José A. , Wicks Ian P. 
Published: March 2011

Abstract
Rel/NF-κB transcription factors regulate inflammatory and immune responses. Despite possible subunit redundancy, NF-κB1–deficient (Nfkb1−/−) mice were profoundly protected from sterile CD4 T cell-dependent acute inflammatory arthritis and peritonitis. We evaluated CD4 T cell function in Nfkb1−/− mice and found increased apoptosis and selectively reduced GM-CSF production. Apoptosis was blocked by expression of a Bcl-2 transgene without restoring a disease response. In contrast with wild-type cells, transfer of Nfkb1−/− or GM-CSF–deficient CD4 T cells into RAG-1–deficient (Rag1−/−) mice failed to support arthritis induction. Injection of GM-CSF into Nfkb1−/− mice fully restored the disease response, suggesting that T cells are an important source of GM-CSF during acute inflammation. In Ag-induced peritonitis, NF-κB1–dependent GM-CSF production in CD4 T cells was required for disease and for generation of inflammatory monocyte-derived dendritic cells (MoDC), but not conventional dendritic cells. MoDC were identified in inflamed synovium and draining lymph nodes during arthritis. These MoDC produced high levels of MCP-1, a potent chemoattractant for monocytes. This study revealed two important findings: NF-κB1 serves a critical role in the production of GM-CSF by activated CD4 T cells during inflammatory responses, and GM-CSF derived from these cells drives the generation of MoDC during inflammatory disease.
Sphingosine 1-Phosphate–Induced Motility and Endocytosis of Dendritic Cells Is Regulated by SWAP-70 through RhoA
Authors: Ocaña-Morgner Carlos , Reichardt Peter , Chopin Michaël , Braungart Sarah , Wahren Christine , Gunzer Matthias , Jessberger Rolf 
Published: March 2011

Abstract
The phospholipid mediator sphingosine 1-phosphate (S1P) enhances motility and endocytosis of mature dendritic cells (DCs). We show that in vitro migration of Swap-70−/− bone marrow-derived DCs (BMDCs) in response to S1P and S1P-induced upregulation of endocytosis are significantly reduced. S1P-stimulated movement of Swap-70−/− BMDCs, specifically retraction of their trailing edge, in a collagen three-dimensional environment is impaired. These in vitro observations correlate with delayed entry into lymphatic vessels and migration to lymph nodes of skin DCs in Swap-70−/− mice. Expression of S1P receptors (S1P1–3) by wild-type and Swap-70−/− BMDCs is similar, but Swap-70−/− BMDCs fail to activate RhoA and to localize Rac1 and RhoA into areas of actin polymerization after S1P stimulus. The Rho-activating G protein Gαi interacts with SWAP-70, which also supports the localization of Gα13 to membrane rafts in BMDCs. LPS-matured Swap-70−/− BMDCs contain significantly more active RhoA than wild-type DCs. Preinhibition of Rho activation restored migration to S1P, S1P-induced upregulation of endocytosis in mature Swap-70−/− BMDCs, and localization of Gα13 to membrane rafts. These data demonstrate SWAP-70 as a novel regulator of S1P signaling necessary for DC motility and endocytosis.
Leptin Enhances Survival and Induces Migration, Degranulation, and Cytokine Synthesis of Human Basophils
Authors: Suzukawa Maho , Nagase Hiroyuki , Ogahara Ikuko , Han Kaiyu , Tashimo Hiroyuki , Shibui Akiko , Koketsu Rikiya , Nakae Susumu , Yamaguchi Masao , Ohta Ken 
Published: March 2011

Abstract
Basophils are the rarest leukocytes in human blood, but they are now recognized as one of the most important immunomodulatory as well as effector cells in allergic inflammation. Leptin, a member of the IL-6 cytokine family, has metabolic effects as an adipokine, and it is also known to participate in the pathogenesis of inflammatory reactions. Because there is an epidemiologic relationship between obesity and allergy, we examined whether basophil functions are modified by leptin. We found that human basophils express leptin receptor (LepR) at both the mRNA and surface protein levels, which were upregulated by IL-33. Leptin exerted strong effects on multiple basophil functions. It induced a strong migratory response in human basophils, similar in potency to that of basophil-active chemokines. Also, leptin enhanced survival of human basophils, although its potency was less than that of IL-3. Additionally, CD63, a basophil activation marker expressed on the cell surface, was upregulated by leptin, an effect that was neutralized by blocking of LepR. Assessments of basophil degranulation and cytokine synthesis found that leptin showed a strong priming effect on human basophil degranulation in response to FcεRI aggregation and induced Th2, but not Th1, cytokine production by the cells. In summary, the present findings indicate that leptin may be a key molecule mediating the effects of adipocytes on inflammatory cells such as basophils by binding to LepR and activating the cellular functions, presumably exacerbating allergic inflammation.
Classification of Inductive Limits of Outer Actions of ℝ on Approximate Circle Algebras
Authors: Dean Andrew J. 
Published: March 2011

AbstractIn this paper we present a classification, up to equivariant isomorphism, of C*-dynamical systems (A, ℝ, α) arising as inductive limits of directed systems ﹛(An, ℝ, αn), φnm﹜, where each An is a finite direct sum of matrix algebras over the continuous functions on the unit circle, and the αns are outer actions generated by rotation of the spectrum.
On the Distribution of Irreducible Trinomials
Authors: Shparlinski Igor E. 
Published: March 2011

AbstractWe obtain new results about the number of trinomials tn + at + b with integer coefficients in a box (a, b) ∈ [C,C + A] × [D,D + B] that are irreducible modulo a prime p. As a by-product we show that for any p there are irreducible polynomials of height at most p1/2+o(1), improving on the previous estimate of p2/3+o(1) obtained by the author in 1989.