bluuebunny/crossref_metadata_2025_split huggingface dataset:
La grande enfance
Authors: Dupeyron Jean-François 
Published: December 2013

Il s’agit dans ce texte de faire le point sur les représentations de l’enfance en Occident, en pointant les insuffisances et les difficultés de la représentation contemporaine de l’enfant comme un sujet. Celle-ci alimente pourtant aujourd’hui une véritable « rumeur savante » sur la découverte de l’enfance par la modernité et constitue le noyau dur d’un paradigme. La critique de ce paradigme s’accompagne de quelques propositions pour repenser la subjectivité enfantine à partir de la phénoménologie de la vie enfantine et avec le soutien des travaux de Michel Henry et de Georges Canguilhem. Du coup la forme scolaire française est renvoyée à une emprise orthopédique ancienne que l’actuelle « pédagogie des compétences » ne fait que prolonger : de ce fait, les difficultés de subjectivation de l’enfant sont vues comme les conséquences d’une activité empêchée. In fine, le modèle nietzschéen d’une Grande Enfance propose un autre horizon philosophique pour l’accueil pédagogique de cette forme de vie emplie de puissance d’agir qu’est la petite enfance.
Représentations sociales des nanosciences et nanotechnologies chez des lycéens
Authors: Grivopoulos Konstantinos 
Published: December 2013

L’éducation au développement durable ne doit pas évincer les Nanosciences et Nanotechnologies, un secteur en plein essor, prometteur et, à la fois, sujet à controverse pour les défis socio-économiques et écologiques. Cet article porte sur les représentations sociales des nanosciences et nanotechnologies chez les lycéens de terminales générales. Le sens attribué à cet objet pluridisciplinaire et hors programmes, très peu étudié jusqu’à ce jour, s’érige en système d’accueil du savoir, pouvant faire obstacle ou, au contraire, servir d’appui à l’apprentissage, lors de la transposition didactique (cf. projets d’« éducation à… »). La recherche s’appuie sur la théorie structurale des représentations, ainsi que sur la didactique des Questions scientifiques socialement vives. Suivant l’analyse prototypique et catégorielle pour le traitement des données du questionnaire, notre hypothèse générale s’avère en partie vérifiée dans le cadre des limites de cette recherche.
Role for σ38 in Prolonged Survival of Escherichia coli in Drosophila melanogaster
Authors: Shiratsuchi Akiko , Shimamoto Naoto , Nitta Mao , Tuan Tran Quoc , Firdausi Afwa , Gawasawa Mitsuko , Yamamoto Kaneyoshi , Ishihama Akira , Nakanishi Yoshinobu 
Published: December 2013

Abstract
Bacteria adapt themselves to host environments by altering the pattern of gene expression. The promoter-recognizing subunit σ of bacterial RNA polymerase plays a major role in the selection of genes to be transcribed. Among seven σ factors of Escherichia coli, σ38 is responsible for the transcription of genes in the stationary phase and under stressful conditions. We found a transient increase of σ38 when E. coli was injected into the hemocoel of Drosophila melanogaster. The loss of σ38 made E. coli rapidly eliminated in flies, and flies infected with σ38-lacking E. coli stayed alive longer than those infected with the parental strain. This was also observed in fly lines defective in humoral immune responses, but not in flies in which phagocytosis was impaired. The lack of σ38 did not influence the susceptibility of E. coli to phagocytosis, but made them vulnerable to killing after engulfment. The changes caused by the loss of σ38 were recovered by the forced expression of σ38-encoding rpoS as well as σ38-regulated katE and katG coding for enzymes that detoxify reactive oxygen species. These results collectively suggested that σ38 contributes to the prolonged survival of E. coli in Drosophila by inducing the production of enzymes that protect bacteria from killing in phagocytes. Considering the similarity in the mechanism of innate immunity against invading bacteria between fruit flies and humans, the products of these genes could be new targets for the development of more effective antibacterial remedies.
ADAM17-Mediated Shedding of FcγRIIIA on Human NK Cells: Identification of the Cleavage Site and Relationship with Activation
Authors: Lajoie Laurie , Congy-Jolivet Nicolas , Bolzec Armelle , Gouilleux-Gruart Valérie , Sicard Elodie , Sung Hsueh Cheng , Peiretti Frank , Moreau Thierry , Vié Henri , Clémenceau Béatrice , Thibault Gilles 
Published: December 2013

AbstractFcγRIIIA/CD16A, the low-affinity receptor for the IgG Fc portion expressed on human CD56dim NK cells and involved in Ab-dependent cell cytotoxicity, is shed upon NK cell activation. We found that recombinant a disintegrin and metalloprotease (ADAM) 17 cleaved the ectodomain of FcγRIIIA/CD16A and a peptide for which the sequence encompasses aa 191–201 of the FcγRIIIA/CD16A stalk region but not ADAM10. MALDI-TOF analysis revealed that the peptide was cleaved between Ala195 and Val196 (i.e., 1 aa upstream of the expected position). This location of the cleavage site was confirmed by the finding that ADAM17 failed to cleave a peptide in which Ala and Val were reversed. ADAM17 was found to be expressed on NK cells, and stimulation with PMA or N-ethyl-maleimide resulted in the shedding of FcγRIIIA/CD16A and CD62L, a specific substrate of ADAM17. Selective inhibition of ADAM17 prevented the shedding of both molecules. Moreover, the shedding of FcγRIIIA/CD16A was strongly correlated with degranulation when a wide range of CD56dim NK cell activating receptors were stimulated, whereas both ADAM17-dependent shedding and internalization were involved in FcγRIIIA/CD16A downmodulation when the latter was engaged. Finally, the shedding of FcγRIIIA/CD16A was restricted to activated cells, suggesting that ADAM17 acts mainly, if not exclusively, in cis. Taken together, our results demonstrated for the first time, to our knowledge, at the molecular level that ADAM17 cleaves the stalk region of FcγRIIIA/CD16A and identified its cleavage site. The shedding of FcγRIIIA/CD16A was at least partially ADAM17 dependent, and it may be considered as a marker of FcγRIIIA/CD16A-independent NK cell activation highly correlated with degranulation.
Arsenic Trioxide and Other Arsenical Compounds Inhibit the NLRP1, NLRP3, and NAIP5/NLRC4 Inflammasomes
Authors: Maier Nolan K. , Crown Devorah , Liu Jie , Leppla Stephen H. , Moayeri Mahtab 
Published: December 2013

Abstract
Inflammasomes are large cytoplasmic multiprotein complexes that activate caspase-1 in response to diverse intracellular danger signals. Inflammasome components termed nucleotide-binding oligomerization domain–like receptor (NLR) proteins act as sensors for pathogen-associated molecular patterns, stress, or danger stimuli. We discovered that arsenicals, including arsenic trioxide and sodium arsenite, inhibited activation of the NLRP1, NLRP3, and NAIP5/NLRC4 inflammasomes by their respective activating signals, anthrax lethal toxin, nigericin, and flagellin. These compounds prevented the autoproteolytic activation of caspase-1 and the processing and secretion of IL-1β from macrophages. Inhibition was independent of protein synthesis induction, proteasome-mediated protein breakdown, or kinase signaling pathways. Arsenic trioxide and sodium arsenite did not directly modify or inhibit the activity of preactivated recombinant caspase-1. Rather, they induced a cellular state inhibitory to both the autoproteolytic and substrate cleavage activities of caspase-1, which was reversed by the reactive oxygen species scavenger N-acetylcysteine but not by reducing agents or NO pathway inhibitors. Arsenicals provided protection against NLRP1-dependent anthrax lethal toxin–mediated cell death and prevented NLRP3-dependent neutrophil recruitment in a monosodium urate crystal inflammatory murine peritonitis model. These findings suggest a novel role in inhibition of the innate immune response for arsenical compounds that have been used as therapeutics for a few hundred years.
Aged Mice Are Unable To Mount an Effective Myeloid Response to Sepsis
Authors: Nacionales Dina C. , Gentile Lori F. , Vanzant Erin , Lopez M. Cecilia , Cuenca Angela , Cuenca Alex G. , Ungaro Ricardo , Li Yi , Baslanti Tezcan Ozrazgat , Bihorac Azra , Moore Frederick A. , Baker Henry V. , Leeuwenburgh Christiaan , Moldawer Lyle L. , Efron Philip A. 
Published: December 2013

Abstract
The elderly have increased morbidity and mortality following sepsis; however, the cause(s) remains unclear. We hypothesized that these poor outcomes are due in part to defects in innate immunity, rather than to an exaggerated early inflammatory response. Young (6–12 wk) or aged (20–24 mo) mice underwent polymicrobial sepsis, and subsequently, the aged mice had increased mortality and defective peritoneal bacterial clearance compared with young mice. No differences were found in the magnitude of the plasma cytokine responses. Although septic aged mice displayed equivalent or increased numbers of circulating, splenic, and bone marrow myeloid cells, some of these cells exhibited decreased phagocytosis, reactive oxygen species production, and chemotaxis. Blood leukocyte gene expression was less altered in aged versus young mice 1 d after sepsis. Aged mice had a relative inability to upregulate gene expression of pathways related to neutrophil-mediated protective immunity, chemokine/chemokine receptor binding, and responses to exogenous molecules. Expression of most MHC genes remained more downregulated in aged mice at day 3. Despite their increased myeloid response to sepsis, the increased susceptibility of aged mice to sepsis appears not to be due to an exaggerated inflammatory response, but rather, a failure to mount an effective innate immune response.
Cutting Edge: DNAX Accessory Molecule 1–Deficient CD8+ T Cells Display Immunological Synapse Defects That Impair Antitumor Immunity
Authors: Ramsbottom Kelly M. , Hawkins Edwin D. , Shimoni Raz , McGrath Mairi , Chan Christopher J. , Russell Sarah M. , Smyth Mark J. , Oliaro Jane 
Published: December 2013

Abstract
DNAX accessory molecule 1 (DNAM-1) is expressed on all CD8+ T cells and promotes their activation and effector function. DNAM-1 interacts with LFA-1, a critical molecule for immunological synapse formation between T cells and APCs, and for cytotoxic killing of target cells. Mice that lack DNAM-1 display abnormal T cell responses and antitumor activity; however, the mechanism involved is unclear. In this article, we show that DNAM-1 deficiency results in reduced proliferation of CD8+ T cells after Ag presentation and impaired cytotoxic activity. We also demonstrate that DNAM-1–deficient T cells show reduced conjugations with tumor cells and decreased recruitment of both LFA-1 and lipid rafts to the immunological synapse, which correlates with reduced tumor cell killing in vitro. This synapse defect may explain why DNAM-1–deficient mice cannot clear tumors in vivo, and highlights the importance of DNAM-1 and the immunological synapse in T cell–mediated antitumor immunity.
Cytosolic Group IVA and Calcium-Independent Group VIA Phospholipase A2s Act on Distinct Phospholipid Pools in Zymosan-Stimulated Mouse Peritoneal Macrophages
Authors: Gil-de-Gómez Luis , Astudillo Alma M. , Guijas Carlos , Magrioti Victoria , Kokotos George , Balboa María A. , Balsinde Jesús 
Published: December 2013

Abstract
Phospholipase A2s generate lipid mediators that constitute an important component of the integrated response of macrophages to stimuli of the innate immune response. Because these cells contain multiple phospholipase A2 forms, the challenge is to elucidate the roles that each of these forms plays in regulating normal cellular processes and in disease pathogenesis. A major issue is to precisely determine the phospholipid substrates that these enzymes use for generating lipid mediators. There is compelling evidence that group IVA cytosolic phospholipase A2 (cPLA2α) targets arachidonic acid–containing phospholipids but the role of the other cytosolic enzyme present in macrophages, the Ca2+-independent group VIA phospholipase A2 (iPLA2β) has not been clearly defined. We applied mass spectrometry–based lipid profiling to study the substrate specificities of these two enzymes during inflammatory activation of macrophages with zymosan. Using selective inhibitors, we find that, contrary to cPLA2α, iPLA2β spares arachidonate-containing phospholipids and hydrolyzes only those that do not contain arachidonate. Analyses of the lysophospholipids generated during activation reveal that one of the major species produced, palmitoyl-glycerophosphocholine, is generated by iPLA2β, with minimal or no involvement of cPLA2α. The other major species produced, stearoyl-glycerophosphocholine, is generated primarily by cPLA2α. Collectively, these findings suggest that cPLA2α and iPLA2β act on different phospholipids during zymosan stimulation of macrophages and that iPLA2β shows a hitherto unrecognized preference for choline phospholipids containing palmitic acid at the sn-1 position that could be exploited for the design of selective inhibitors of this enzyme with therapeutic potential.
Lack of Galactosylation Enhances the Pathogenic Activity of IgG1 but Not IgG2a Anti-Erythrocyte Autoantibodies
Authors: Ito Kiyoaki , Furukawa Jun-ichi , Yamada Kazunori , Tran Ngoc Lan , Shinohara Yasuro , Izui Shozo 
Published: December 2013

Abstract
IgG bears asparagine-linked oligosaccharide side chains in the Fc region. Variations in their extent of galactosylation and sialylation could modulate IgG Fc-dependent effector functions, and hence Ab activity. However, it has not yet been clarified whether the pathogenic potential of IgG autoantibodies is consistently enhanced by the absence of galactose residues per se or the lack of terminal sialylation, which is dependent on galactosylation. Moreover, it remains to be defined whether the increased pathogenicity of agalactosylated IgG is related to activation of the complement pathway by mannose-binding lectin, as suggested by in vitro studies. Using a murine model of autoimmune hemolytic anemia, we defined the contribution of galactosylation or sialylation to the pathogenic activity of IgG1 and IgG2a anti-erythrocyte class-switch variants of 34-3C monoclonal autoantibody. We generated their degalactosylated or highly sialylated glycovariants and compared their pathogenic effects with those of highly galactosylated or desialylated counterparts. Our results demonstrated that lack of galactosylation, but not sialylation, enhanced the pathogenic activity of 34-3C IgG1, but not IgG2a autoantibodies. Moreover, analysis of in vivo complement activation and of the pathogenic activity in mice deficient in C3 or IgG FcRs excluded the implication of mannose-binding lectin-mediated complement activation in the enhanced pathogenic effect of agalactosylated IgG1 anti-erythrocyte autoantibodies.
Thymic Medullary Epithelium and Thymocyte Self-Tolerance Require Cooperation between CD28–CD80/86 and CD40–CD40L Costimulatory Pathways
Authors: Williams Joy A. , Zhang Jingjing , Jeon Hyein , Nitta Takeshi , Ohigashi Izumi , Klug David , Kruhlak Michael J. , Choudhury Baishakhi , Sharrow Susan O. , Granger Larry , Adams Anthony , Eckhaus Michael A. , Jenkinson S. Rhiannon , Richie Ellen R. , Gress Ronald E. , Takahama Yousuke , Hodes Richard J. 
Published: December 2013

Abstract
A critical process during thymic development of the T cell repertoire is the induction of self-tolerance. Tolerance in developing T cells is highly dependent on medullary thymic epithelial cells (mTEC), and mTEC development in turn requires signals from mature single-positive thymocytes, a bidirectional relationship termed thymus crosstalk. We show that CD28–CD80/86 and CD40–CD40L costimulatory interactions, which mediate negative selection and self-tolerance, upregulate expression of LTα, LTβ, and receptor activator for NF-κB in the thymus and are necessary for medullary development. Combined absence of CD28–CD80/86 and CD40–CD40L results in profound deficiency in mTEC development comparable to that observed in the absence of single-positive thymocytes. This requirement for costimulatory signaling is maintained even in a TCR transgenic model of high-affinity TCR–ligand interactions. CD4 thymocytes maturing in the altered thymic epithelial environment of CD40/CD80/86 knockout mice are highly autoreactive in vitro and are lethal in congenic adoptive transfer in vivo, demonstrating a critical role for these costimulatory pathways in self-tolerance as well as thymic epithelial development. These findings demonstrate that cooperativity between CD28–CD80/86 and CD40–CD40L pathways is required for normal medullary epithelium and for maintenance of self-tolerance in thymocyte development.
T Cell Ig and Mucin Domain–Containing Protein 3 Is Recruited to the Immune Synapse, Disrupts Stable Synapse Formation, and Associates with Receptor Phosphatases
Authors: Clayton Kiera L. , Haaland Matthew S. , Douglas-Vail Matthew B. , Mujib Shariq , Chew Glen M. , Ndhlovu Lishomwa C. , Ostrowski Mario A. 
Published: December 2013

Abstract
CD8+ CTLs are adept at killing virally infected cells and cancer cells and releasing cytokines (e.g., IFN-γ) to aid this response. However, during cancer and chronic viral infections, such as with HIV, this CTL response is progressively impaired due to a process called T cell exhaustion. Previous work has shown that the glycoprotein T cell Ig and mucin domain–containing protein 3 (Tim-3) plays a functional role in establishing T cell exhaustion. Tim-3 is highly upregulated on virus and tumor Ag-specific CD8+ T cells, and antagonizing Tim-3 helps restore function of CD8+ T cells. However, very little is known of how Tim-3 signals in CTLs. In this study, we assessed the role of Tim-3 at the immunological synapse as well as its interaction with proximal TCR signaling molecules in primary human CD8+ T cells. Tim-3 was found within CD8+ T cell lipid rafts at the immunological synapse. Blocking Tim-3 resulted in a significantly greater number of stable synapses being formed between Tim-3hiCD8+ T cells and target cells, suggesting that Tim-3 plays a functional role in synapse formation. Further, we confirmed that Tim-3 interacts with Lck, but not the phospho-active form of Lck. Finally, Tim-3 colocalizes with receptor phosphatases CD45 and CD148, an interaction that is enhanced in the presence of the Tim-3 ligand, galectin-9. Thus, Tim-3 interacts with multiple signaling molecules at the immunological synapse, and characterizing these interactions could aid in the development of therapeutics to restore Tim-3–mediated immune dysfunction.
Simulating global and local surface temperature changes due to Holocene anthropogenic land cover change
Authors: He Feng , Vavrus Steve J. , Kutzbach John E. , Ruddiman William F. , Kaplan Jed O. , Krumhardt Kristen M. 
Published: December 2013

AbstractSurface albedo changes from anthropogenic land cover change (ALCC) represent the second largest negative radiative forcing behind aerosol during the industrial era. Using a new reconstruction of ALCC during the Holocene era by Kaplan et al. (2011), we quantify the local and global temperature response induced by Holocene ALCC in the Community Climate System Model, version 4. We find that Holocene ALCC causes a global cooling of 0.17°C due to the biogeophysical effects of land‐atmosphere exchange of momentum, moisture, and radiative and heat fluxes. On the global scale, the biogeochemical effects of Holocene ALCC from carbon emissions dominate the biogeophysical effects by causing 0.9°C global warming. The net effects of Holocene ALCC amount to a global warming of 0.73°C during the preindustrial era, which is comparable to the ~0.8°C warming during industrial times. On local to regional scales, such as parts of Europe, North America, and Asia, the biogeophysical effects of Holocene ALCC are significant and comparable to the biogeochemical effect.
A sampling method for improving the representation of spatially varying precipitation and soil moisture using the Simple Biosphere Model
Authors: Medina Isaac D. , Denning A. Scott , Baker Ian T. , Ramirez Jorge A. , Randall David A. 
Published: December 2013

AbstractRepresenting spatially varying precipitation for current grid length scales used in General Circulation Models (GCMs) is a continuing challenge. Furthermore, to fully capture the hydrologic effects of nonuniform precipitation, a representation of soil moisture heterogeneity and distribution of spatially varying precipitation must exist within the same framework. For this study, the explicit and sampling methods of Sellers et al. (2007) are tested off‐line using the Simple Biosphere Model (SiB3) in an arid, semiarid, and wet site, and are numerically compared to the bulk method, which is currently used in GCMs. To carry out the numerical experiments, an arbitrary grid area was defined by (1) a single instance of SiB3 (bulk method), (2) 100 instances of SiB3 (explicit method), and (3) less than 100 instances of SiB3 (sampling method). Precipitation was randomly distributed over fractions of the grid area for the explicit and sampling methods, while the standard SiB3 exponential distribution relating precipitation intensity to the grid area wet fraction was used in the bulk method. Comparing the sampling and bulk method to the explicit method indicates that 10 instances of SiB3 in the sampling method better captures the spatial variability in soil moisture and grid area flux calculations produced by the explicit method, and deals realistically with spatially varying precipitation at little additional computational cost to the bulk method.
Welche anorganischen Strukturen sind am komplexesten?
Authors: Krivovichev Sergey V. 
Published: December 2013

AbstractDie Entdeckung, dass Röntgenstrahlen an Kristallen gebeugt werden, markierte den Beginn einer neuen wissenschaftlichen Ära, die eine Vielzahl von erstaunlichen Entdeckungen über die Strukturen und Funktionen von Materie auf atomarer und molekularer Skala hervorgebracht hat. Über die letzten hundert Jahre wurden ungefähr 150 000 anorganische Kristallstrukturen aufgeklärt und bildlich dargestellt. Das Aufkommen neuer Technologien wie Flächendetektoren und Synchrotronstrahlung führte zur Strukturlösung von kristallinen Verbindungen nie dagewesener Komplexität. Allerdings fehlt bis heute eine klare quantitative Definition der strukturellen Komplexität von Kristallen. In diesem Kurzaufsatz nutzen wir die mathematische Informationstheorie, um den Komplexitätsgrad anorganischer Strukturen in Form ihres Informationsgehaltes zu charakterisieren.
Rheology and morphology of polyester/thermoplastic flour blends
Authors: Démé Florian , Peuvrel‐Disdier Edith , Vergnes Bruno 
Published: December 2013

ABSTRACTTwo maize flours (standard and waxy grades) were plasticized in an internal mixer with a constant amount of water and two glycerol contents. The resulting thermoplastic flours (TPFs) were characterized in dynamic oscillatory shear and creep/recovery rheometry. They displayed two different behaviors: the viscoelastic behavior of a high‐molecular‐weight polymer for the first one and a gel‐like behavior for the second one. The TPFs were then mixed with a copolyester [poly(butylene adipate–terephtalate)]. All of the blends contained the same volume fractions and were prepared with the same mixing conditions. The morphology and rheological behavior of each blend were characterized. Different morphologies, ranging from cocontinuous to nodular, were observed. In fixed mixing conditions, the blend morphology was shown to be governed by the rheological behavior of the starchy phase and the plasticizer content. The gel‐like behavior of the second TPF seemed to prevent droplet coalescence; this led to a very fine dispersion. The rheological behavior of each blend appeared to be linked to both the morphology and the rheological behavior of the two phases. © 2013 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2014, 131, 40222.