bluuebunny/crossref_metadata_2025_split huggingface dataset:
Une approche par l'art dans la formation en animation socioculturelle
Authors: della Croce Claudia 
Published: September 2014

Cet article propose une réflexion philosophique et pratique sur la notion de « médiation culturelle ». Partant d’une conception issue de la philosophie pragmatiste et s’inspirant d’auteurs tels que Spinoza et Deleuze, l’auteur montre que la sphère de la création est issue d’une continuité de l’expérience humaine qui dépasse et transcende celle de l’individu pris isolément. La médiation culturelle permet d’assurer cette dimension expérientielle fondamentale avec tous les publics, laissant au médiateur une place distincte de celle de l’artiste.
Politique de l'art : une politique du réel ?
Authors: Chassagne Annie 
Published: September 2014

Ce texte relate l’histoire du festival de cinéma documentaire grand public « Traces de vies », né en 1991, à partir d’un centre de formation au travail social. Quelles sont les conditions d’émergence de la création artistique dans les secteurs du soin, du social et des institutions ? La richesse des signifiants qui circulent dans un lieu à la réflexion exigeante, la volonté de ce lieu de soutenir les initiatives atypiques et peu raisonnables peuvent permettre des croisements inédits. C’est l’occasion d’ébaucher une réflexion sur la notion de réel dans le champ cinématographique et pour l’art en général aujourd’hui.
Des voleurs d'enfants ? Une recherche sur les représentations de l'assistante sociale dans les médias
Authors: Allegri Elena 
Published: September 2014

Cet article présente une recherche analytique à partir de vingt films et vingt et un romans, complétée par des entretiens semi-directifs, sur le thème de l’image des assistants de service social dans les médias. Cinq catégories de personnages ont été identifiées : les héros, les personnages positifs et négatifs, les ambivalents et les personnages neutres. Une majorité des caractères étudiés sont des femmes. Peu correspondent à l’image du héros et, contrairement aux attentes, peu véhiculent une image négative. À partir de la construction d’une typologie, l’auteure montre toute l’importance pour les travailleurs sociaux de prendre conscience des stéréotypes dont ils sont l’objet et de développer des stratégies pour influencer les médias.
L'accompagnement global par le gestionnaire de cas pour un changement dans la situation de la personne âgée
Authors: Hugues Leïla 
Published: September 2014

Il s’agit ici de rendre compte d’une recherche, à partir d’un petit échantillon, sur le rôle du gestionnaire de cas dans l’accompagnement d’une personne âgée aux prises avec un changement de situation. La caractéristique de cet accompagnement est de devoir à la fois s’adapter à la personne et aux circonstances qui nécessitent cette intervention. « La définition du besoin n’est donc plus à la charge du seul usager, l’élaboration de solutions à la charge du seul professionnel. [...] Chacun apprend au contact de l’autre, dans le cours d’une résolution d’un problème mal défini et à construire. » L’échantillon était constitué de onze personnes, huit gestionnaires de cas et trois aidants naturels. Cette recherche met en valeur la qualité d’un accompagnement de proximité, au plus près de la personne en situation de grande vulnérabilité, pour que les ressources possibles et disponibles soient au service d’un mieux-être quotidien.
Le Mouvement d’occupation d’espaces publics : Occupy Dame Street et Occupy Galway
Authors: Royall Frederic , Desbos Clément 
Published: September 2014

Cet article revient sur des épisodes contestataires
inédits en République d’Irlande : des occupations d’espaces publics
entre 2001 et 2012 qui se veulent, à l’origine, une critique des
conséquences du néolibéralisme rampant sur le pays. Malgré une
occupation de plusieurs mois, ces protestataires ont eu beaucoup de
mal à susciter un engouement chez le grand public et à dépasser le
cadre extrêmement réduit des campements eux-mêmes. Cet article revient
sur le sens et la valeur de ces occupations et les analyse à l’aune
d’une certaine spécificité irlandaise.
A Multiple Sclerosis–Associated Variant of CBLB Links Genetic Risk with Type I IFN Function
Authors: Stürner Klarissa Hanja , Borgmeyer Uwe , Schulze Christian , Pless Ole , Martin Roland 
Published: September 2014

AbstractMultiple sclerosis (MS) is an autoimmune disease of the CNS, and autoreactive CD4+ T cells are considered important for its pathogenesis. The etiology of MS involves a complex genetic trait and environmental triggers that include viral infections, particularly the EBV. Among the risk alleles that have repeatedly been identified by genome-wide association studies, three are located near the Casitas B-lineage lymphoma proto-oncogene b gene (CBLB). The CBLB protein (CBL-B) is a key regulator of peripheral immune tolerance by limiting T cell activation and expansion and hence T cell–mediated autoimmunity through its ubiquitin E3-ligase activity. In this study, we show that CBL-B expression is reduced in CD4+ T cells from relapsing-remitting MS (RR-MS) patients during relapse. The MS risk-related single nucleotide polymorphism of CBLB rs12487066 is associated with diminished CBL-B expression levels and alters the effects of type I IFNs on human CD4+ T cell proliferation. Mechanistically, the CBLB rs12487066 risk allele mediates increased binding of the transcription factor C/EBPβ and reduced CBL-B expression in human CD4+ T cells. Our data suggest a role of the CBLB rs12487066 variant in the interactions of a genetic risk factor and IFN function during viral infections in MS.
Bullous Pemphigoid Autoantibodies Directly Induce Blister Formation without Complement Activation
Authors: Ujiie Hideyuki , Sasaoka Tetsumasa , Izumi Kentaro , Nishie Wataru , Shinkuma Satoru , Natsuga Ken , Nakamura Hideki , Shibaki Akihiko , Shimizu Hiroshi 
Published: September 2014

Abstract
Complement activation and subsequent recruitment of inflammatory cells at the dermal/epidermal junction are thought to be essential for blister formation in bullous pemphigoid (BP), an autoimmune blistering disease induced by autoantibodies against type XVII collagen (COL17); however, this theory does not fully explain the pathological features of BP. Recently, the involvement of complement-independent pathways has been proposed. To directly address the question of the necessity of the complement activation in blister formation, we generated C3-deficient COL17-humanized mice. First, we show that passive transfer of autoantibodies from BP patients induced blister formation in neonatal C3-deficient COL17-humanized mice without complement activation. By using newly generated human and murine mAbs against the pathogenic noncollagenous 16A domain of COL17 with high (human IgG1, murine IgG2), low (murine IgG1), or no (human IgG4) complement activation abilities, we demonstrate that the deposition of Abs, and not complements, is relevant to the induction of blister formation in neonatal and adult mice. Notably, passive transfer of BP autoantibodies reduced the amount of COL17 in lesional mice skin, as observed in cultured normal human keratinocytes treated with the same Abs. Moreover, the COL17 depletion was associated with a ubiquitin/proteasome pathway. In conclusion, the COL17 depletion induced by BP autoantibodies, and not complement activation, is essential for the blister formation under our experimental system.
IL-17A Influences Essential Functions of the Monocyte/Macrophage Lineage and Is Involved in Advanced Murine and Human Atherosclerosis
Authors: Erbel Christian , Akhavanpoor Mohammadreza , Okuyucu Deniz , Wangler Susanne , Dietz Alex , Zhao Li , Stellos Konstantinos , Little Kristina M. , Lasitschka Felix , Doesch Andreas , Hakimi Maani , Dengler Thomas J. , Giese Thomas , Blessing Erwin , Katus Hugo A. , Gleissner Christian A. 
Published: September 2014

Abstract
Atherosclerosis is a chronic inflammatory disease. Lesion progression is primarily mediated by cells of the monocyte/macrophage lineage. IL-17A is a proinflammatory cytokine, which modulates immune cell trafficking and is involved inflammation in (auto)immune and infectious diseases. But the role of IL-17A still remains controversial. In the current study, we investigated effects of IL-17A on advanced murine and human atherosclerosis, the common disease phenotype in clinical care. The 26-wk-old apolipoprotein E–deficient mice were fed a standard chow diet and treated either with IL-17A mAb (n = 15) or irrelevant Ig (n = 10) for 16 wk. Furthermore, essential mechanisms of IL-17A in atherogenesis were studied in vitro. Inhibition of IL-17A markedly prevented atherosclerotic lesion progression (p = 0.001) by reducing inflammatory burden and cellular infiltration (p = 0.01) and improved lesion stability (p = 0.01). In vitro experiments showed that IL-17A plays a role in chemoattractance, monocyte adhesion, and sensitization of APCs toward pathogen-derived TLR4 ligands. Also, IL-17A induced a unique transcriptome pattern in monocyte-derived macrophages distinct from known macrophage types. Stimulation of human carotid plaque tissue ex vivo with IL-17A induced a proinflammatory milieu and upregulation of molecules expressed by the IL-17A–induced macrophage subtype. In this study, we show that functional blockade of IL-17A prevents atherosclerotic lesion progression and induces plaque stabilization in advanced lesions in apolipoprotein E–deficient mice. The underlying mechanisms involve reduced inflammation and distinct effects of IL-17A on monocyte/macrophage lineage. In addition, translational experiments underline the relevance for the human system.
NF-κB–Inducing Kinase in Thymic Stroma Establishes Central Tolerance by Orchestrating Cross-Talk with Not Only Thymocytes but Also Dendritic Cells
Authors: Mouri Yasuhiro , Nishijima Hitoshi , Kawano Hiroshi , Hirota Fumiko , Sakaguchi Nobuo , Morimoto Junko , Matsumoto Mitsuru 
Published: September 2014

Abstract
Essential roles of NF-κB–inducing kinase (NIK) for the development of medullary thymic epithelial cells (mTECs) and regulatory T cells have been highlighted by studies using a strain of mouse bearing a natural mutation of the NIK gene (aly mice). However, the exact mechanisms underlying the defect in thymic cross-talk leading to the breakdown of self-tolerance in aly mice remain elusive. In this study, we demonstrated that production of regulatory T cells and the final maturation process of positively selected conventional αβ T cells are impaired in aly mice, partly because of a lack of mature mTECs. Of note, numbers of thymic dendritic cells and their expression of costimulatory molecules were also affected in aly mice in a thymic stroma–dependent manner. The results suggest a pivotal role of NIK in the thymic stroma in establishing self-tolerance by orchestrating cross-talk between mTECs and dendritic cells as well as thymocytes. In addition, we showed that negative selection was impaired in aly mice as a result of the stromal defect, which accounts for the development of organ-specific autoimmunity through a lack of normal NIK.
Dynamic Changes in Macrophage Activation and Proliferation during the Development and Resolution of Intestinal Inflammation
Authors: Little Matthew C. , Hurst Rebecca J. M. , Else Kathryn J. 
Published: September 2014

Abstract
Macrophages (Mφs) accumulate at sites of inflammation, and, because they can assume several functionally distinct states of activation, they can either drive or restrain inflammatory responses. Once believed to depend on the recruitment of blood monocytes, it is now clear that the accumulation of Mφs in some tissues can result from the proliferation of resident Mφs in situ. However, little is known about the proliferation and activation state of Mφ subsets in the gut during the development and resolution of intestinal inflammation. We show that inflammatory Mφs accumulate in the large intestine of mice during the local inflammatory response to infection with the gastrointestinal nematode parasite Trichuris muris. Classically activated Mφs predominate initially (as the inflammation develops) and then, following worm expulsion (as the inflammation resolves), both the resident and inflammatory populations of Mφs become alternatively activated. A small but significant increase in the proliferation of inflammatory Mφs is seen but only during the resolution phase of the inflammatory response following both worm expulsion and the peak in Mφ accumulation. In contrast to recent studies in the pleural and peritoneal cavities, the proliferation of resident and alternatively activated Mφs does not increase during the inflammatory response. Furthermore, in CCR2−/− mice, monocyte recruitment to the gut is impeded, and the accumulation of alternatively activated Mφs is greatly reduced. In conclusion, the recruitment of blood monocytes is the principle mechanism of Mφ accumulation in the large intestine. This study provides a novel insight into the phenotype and behavior of intestinal Mφ during infection-driven inflammation.
Recognition of Lysophosphatidylcholine by Type II NKT Cells and Protection from an Inflammatory Liver Disease
Authors: Maricic Igor , Girardi Enrico , Zajonc Dirk M. , Kumar Vipin 
Published: September 2014

Abstract
Lipids presented by the MHC class I–like molecule, CD1d, are recognized by NK T (NKT) cells, which can be broadly categorized into two subsets. The well-characterized type I NKT cells express a semi-invariant TCR and can recognize both α- and β-linked glycolipids, whereas type II NKT cells are less well studied, express a relatively diverse TCR repertoire, and recognize β-linked lipids. Recent structural studies have shown a distinct mode of recognition of a self-glycolipid sulfatide bound to CD1d by a type II NKT TCR. To further characterize Ag recognition by these cells, we have used the structural data and screened other small molecules able to bind to CD1d and activate type II NKT cells. Using plate-bound CD1d and APC-based Ag presentation assay, we found that phospholipids such as lysophosphatidylcholine (LPC) can stimulate the sulfatide-reactive type II NKT hybridoma Hy19.3 in a CD1d-dependent manner. Using plasmon resonance studies, we found that this type II NKT TCR binds with CD1d-bound LPC with micromolar affinities similar to that for sulfatide. Furthermore, LPC-mediated activation of type II NKT cells leads to anergy induction in type I NKT cells and affords protection from Con A–induced hepatitis. These data indicate that, in addition to self-glycolipids, self-lysophospholipids are also recognized by type II NKT cells. Because lysophospholipids are involved during inflammation, our findings have implications for not only understanding activation of type II NKT cells in physiological settings, but also for the development of immune intervention in inflammatory diseases.
Intrinsic Self-DNA Triggers Inflammatory Disease Dependent on STING
Authors: Ahn Jeonghyun , Ruiz Phillip , Barber Glen N. 
Published: September 2014

Abstract
Inflammatory diseases such as Aicardi–Goutières syndrome and severe systemic lupus erythematosus are generally lethal disorders that have been traced to defects in the exonuclease TREX1 (DNase III). Mice lacking TREX1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the stimulator of IFN genes (STING) pathway. In this study, we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into TREX1−/− mice. TREX1−/− macrophages did not exhibit significant augmented ability to produce proinflammatory cytokines compared with normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies.
Vizantin Inhibits Endotoxin-Mediated Immune Responses via the TLR 4/MD-2 Complex
Authors: Oda Masataka , Yamamoto Hirofumi , Shibutani Masahiro , Nakano Mayo , Yabiku Kenta , Tarui Takafumi , Kameyama Naoya , Shirakawa Daiki , Obayashi Sumiyo , Watanabe Naoyuki , Nakase Hiroshi , Suenaga Midori , Matsunaga Yoichi , Nagahama Masahiro , Takahashi Hironobu , Imagawa Hiroshi , Kurosawa Mie , Terao Yutaka , Nishizawa Mugio , Sakurai Jun 
Published: September 2014

Abstract
Vizantin has immunostimulating properties and anticancer activity. In this study, we investigated the molecular mechanism of immune activation by vizantin. THP-1 cells treated with small interfering RNA for TLR-4 abolished vizantin-induced macrophage activation processes such as chemokine release. In addition, compared with wild-type mice, the release of MIP-1β induced by vizantin in vivo was significantly decreased in TLR-4 knockout mice, but not in TLR-2 knockout mice. Vizantin induced the release of IL-8 when HEK293T cells were transiently cotransfected with TLR-4 and MD-2, but not when they were transfected with TLR-4 or MD-2 alone or with TLR-2 or TLR-2/MD-2. A dipyrromethene boron difluoride–conjugated vizantin colocalized with TLR-4/MD-2, but not with TLR-4 or MD-2 alone. A pull-down assay with vizantin-coated magnetic beads showed that vizantin bound to TLR-4/MD-2 in extracts from HEK293T cells expressing both TLR-4 and MD-2. Furthermore, vizantin blocked the LPS-induced release of TNF-α and IL-1β and inhibited death in mice. We also performed in silico docking simulation analysis of vizantin and MD-2 based on the structure of MD-2 complexed with the LPS antagonist E5564; the results suggested that vizantin could bind to the active pocket of MD-2. Our observations show that vizantin specifically binds to the TLR-4/MD-2 complex and that the vizantin receptor is identical to the LPS receptor. We conclude that vizantin could be an effective adjuvant and a therapeutic agent in the treatment of infectious diseases and the endotoxin shock caused by LPS.
Cutting Edge: Discrete Functions of mTOR Signaling in Invariant NKT Cell Development and NKT17 Fate Decision
Authors: Wei Jun , Yang Kai , Chi Hongbo 
Published: September 2014

Abstract
Invariant NKT (iNKT) cells recently were classified into NKT1, NKT2, and NKT17 lineages with distinct transcription factor and cytokine profiles, but the mechanisms underlying such fate decisions remain elusive. In this article, we report crucial roles for mechanistic target of rapamycin (mTOR) signaling, especially mTORC2, in iNKT cell development and fate determination of NKT17 cells. Loss of Rictor, an obligatory component of mTORC2, decreased thymic and peripheral iNKT cells, which was associated with defective survival. Strikingly, Rictor deficiency selectively abolished the NKT17 lineage, as indicated by a marked reduction in RORγt and IL-17 expression. Moreover, deletion of phosphatase and tensin homolog (Pten) upregulated mTORC2 activity and enhanced NKT17 generation, but concomitant loss of Rictor reversed the NKT17 dysregulation. In contrast, mTORC1 regulators Raptor and Rheb are dispensable for NKT17 differentiation, despite their importance in iNKT cell thymic development. Our findings establish pivotal and unique roles for mTORC2 signaling, which is reciprocally regulated by Rictor and Pten, in NKT17 lineage determination.
Contrasting vulnerability of drained tropical and high‐latitude peatlands to fluvial loss of stored carbon
Authors: Evans Chris D. , Page Susan E. , Jones Tim , Moore Sam , Gauci Vincent , Laiho Raija , Hruška Jakub , Allott Tim E. H. , Billett Michael F. , Tipping Ed , Freeman Chris , Garnett Mark H. 
Published: September 2014

AbstractCarbon sequestration and storage in peatlands rely on consistently high water tables. Anthropogenic pressures including drainage, burning, land conversion for agriculture, timber, and biofuel production, cause loss of pressures including drainage, burning, land conversion for agriculture, timber, and biofuel production, cause loss of peat‐forming vegetation and exposure of previously anaerobic peat to aerobic decomposition. This can shift peatlands from net CO2 sinks to large CO2 sources, releasing carbon held for millennia. Peatlands also export significant quantities of carbon via fluvial pathways, mainly as dissolved organic carbon (DOC). We analyzed radiocarbon (14C) levels of DOC in drainage water from multiple peatlands in Europe and Southeast Asia, to infer differences in the age of carbon lost from intact and drained systems. In most cases, drainage led to increased release of older carbon from the peat profile but with marked differences related to peat type. Very low DOC‐14C levels in runoff from drained tropical peatlands indicate loss of very old (centuries to millennia) stored peat carbon. High‐latitude peatlands appear more resilient to drainage; 14C measurements from UK blanket bogs suggest that exported DOC remains young (<50 years) despite drainage. Boreal and temperate fens and raised bogs in Finland and the Czech Republic showed intermediate sensitivity. We attribute observed differences to physical and climatic differences between peatlands, in particular, hydraulic conductivity and temperature, as well as the extent of disturbance associated with drainage, notably land use changes in the tropics. Data from the UK Peak District, an area where air pollution and intensive land management have triggered Sphagnum loss and peat erosion, suggest that additional anthropogenic pressures may trigger fluvial loss of much older (>500 year) carbon in high‐latitude systems. Rewetting at least partially offsets drainage effects on DOC age.
Scree Test
Authors: B. D'agostino Ralph , Russell Heidy K. 
Published: September 2014

Abstract
The scree test is a test for determining the number of factors to retain in a factor analysis or principal components analysis. The scree test involves plotting the eigenvalues in descending order of their magnitude against their factor numbers and determining where they level off. The break between the steep slope and a leveling off indicates the number of meaningful factors, different from random error. The technique is illustrated and compared with alternative techniques for determining the number of factors to retain.
Dendrogram
Authors: CaliŃski Tadeusz 
Published: September 2014

Abstract
The term “dendrogram” is used in numerical taxonomy for any graphical drawing or diagram giving a treelike description of a taxonomic system. More generally, a dendrogram is a two‐dimensional diagram representing a tree of relationships, whatever their nature.
The representation of a taxonomic system by a dendrogram is particularly suitable in connection with a cluster analysis applied to investigate the structure of the corresponding operational taxonomic units, such as individual patients or case histories initially used to construct disease classifications. This becomes apparent when it is desirable to interpret the results of the analysis in terms of a natural nonoverlapping taxonomic hierarchy. The usual basis for a cluster analysis is a resemblance matrix, its rows and columns referring to the operational taxonomic units, and its entries being the estimates of the resemblances between the corresponding units.
Examples of dendrograms and methods of their presentation are described in many textbooks on numerical taxonomy and cluster analysis.
Among the various clustering methods, the single linkage cluster analysis is particularly relevant to a dendrogram representation.
Spearman Rank Correlation: Overview
Authors: Zar Jerrold H. 
Published: September 2014

AbstractIn a nonparametric (distribution‐free) approach to the correlation between two sets of measurements made on the same individuals, each set may be ranked in order of magnitude. The standard (Pearson) product‐moment correlation coefficient is calculated on the two sets of ranks. Simple formulae are available, and adjustments are made for tied ranks. Test and estimation procedures are described. The relationship with the Kendall rank correlation coefficient is discussed.