bluuebunny/crossref_metadata_2025_split huggingface dataset:
La défense sociale en Belgique, entre soin et sécurité.
Authors: Cartuyvels Yves , Champetier Brice , Wyvekens Anne 
Published: March 2011

En application de la loi de défense sociale en Belgique, l’auteur d’un fait qualifié infraction considéré comme irresponsable fait l’objet d’une mesure d’internement, soit dans une annexe psychiatrique rattachée à une prison, soit dans un établissement de défense sociale prévu à cet effet, soit encore dans un hôpital psychiatrique. La mesure d’internement est décrite comme une mesure de sécurité et de soin. Dans les faits, tant en annexe psychiatrique de prison qu’en établissement de défense sociale, la place faite au soin reste problématique : le manque de moyens est chronique et le recours à la médication systématique dans des lieux d’internement souvent surpeuplés. La scission entre les fonctions de soin et d’expertise, intervenue dans certains lieux d’internement, constitue à cet égard un enjeu important.
Surveiller et punir à l'âge actuariel
Authors: Harcourt Bernard E. 
Published: March 2011

Les méthodes actuarielles pénètrent aujourd’hui la sphère pénale des États-Unis. À la seule exception du profilage racial des Africains-Américains et des Hispaniques, la majeure partie de la population considère que l’adoption des méthodes actuarielles est efficace, rationnelle et rentable. Bernard Harcourt met en question ce consensus naissant en prônant, dans la sphère pénale, l’échantillonnage aléatoire : la randomisation dans le maintien de l’ordre. C’est la seule façon d’obtenir une sphère carcérale qui reflète impartialement et ressemble réellement à la distribution des personnes commettant des délits. Donc, dans le droit pénal et son application, c’est sur la prédiction que les interrogations devraient porter. Dans le premier article, B. Harcourt trace une généalogie des méthodes actuarielles aux États-Unis. Dans le second article, B. Harcourt démontre mathématiquement les effets contre-productifs du profilage et des méthodes actuarielles.
Règle d'or et logique d'équivalence
Authors: Michel Johann 
Published: March 2011

Résumé	Issue originellement du testament judéo-chrétien, la Règle d'or (« Ne pas faire à autrui ce que l'on ne voudrait pas que l'on nous fasse ») s'est sécularisée dans la culture morale occidentale au point de tenir lieu fréquemment de maxime de nos interactions quotidiennes. L'objectif de cet article consiste à se demander si cette règle peut fonder des principes de morale et de justice. Si l'on se place dans le cadre déontologique d'une philosophie procédurale, la règle d'or est considérée comme un stade inférieure de normativité dans la mesure où il s'agit d'une maxime tirée d'une éthique narrative particulière impropre à s'élever au rang de principes. Si l'on suit au contraire l'herméneutique critique que propose Paul Ricœur, la Règle d'or s'élève au rang de maxime suprême de la normativité présupposée par toute entreprise de fondation procédurale des principes de morale et de justice. La thèse défendue par Johann Michel cherche à montrer que c'est moins la Règle d'or que la logique d'équivalence qui est à même de jouer cette fonction principielle, la première n'étant qu'une expression particulière de la prétention à l'universalité de la seconde.
Du poids relatif des morts
Authors: Detienne Marcel , Esquerre Arnaud 
Published: March 2011

Résumé Dans cet entretien, Marcel Detienne explique tout d'abord comment, pour les Grecs de l'Antiquité qui partent fonder des colonies, les morts sont « légers » : ils ne sont pas attachés aux vivants ni à un endroit particulier. Le rapport aux morts mis en place par les historiens en France depuis le 19e siècle jusqu'à Braudel est très différent : il lie ensemble les morts et les vivants dans une communauté nationale, « enracinée » dans un territoire. Pour mieux comprendre la place des morts en France et en Europe aujourd'hui, Marcel Detienne propose, enfin, de travailler en procédant à des comparaisons.
The Food Preference Paradigm: A Review of Autumn–Winter Food Use by North American Dabbling Ducks (1900–2009)
Authors: Callicutt James T. , Hagy Heath M. , Schummer Michael L. 
Published: March 2011

Abstract
Studies describing food use (i.e., diet) of nonbreeding dabbling ducks Anas spp. are essential to understanding physiological needs of and recommending habitat management for these birds. We conducted a review of published autumn and winter food-use studies of dabbling ducks in North America to characterize the current state of knowledge and identify remaining research needs. We initiated our review to determine whether valuations of duck foods and the term “preference” commonly used by researchers and in waterfowl management guides (i.e., the food preference paradigm) were supported by available peer-reviewed literature. We analyzed peer-reviewed literature (1900–2009) on autumn–winter food use of dabbling ducks (n  =  59 studies). Most studies (68%) used methods known to contain substantial bias including data from gizzards and hunter-collected ducks. Only 5% of published articles reliably determined food selection by concurrently measuring food use and availability, and no study determined food use at a scale appropriate for winter home ranges of dabbling ducks. In some habitats commonly managed for waterfowl (e.g., agricultural lands), few if any collections of ducks are available to obtain data on food use. The limited geographic and habitat scope of unbiased food use and selection studies for dabbling ducks during autumn and winter suggests that the food-preference paradigm found in waterfowl management literature is not supported by empirical evidence and that managers must continue to use best judgment in managing foraging habitats for waterfowl. Researchers and conservation planners should aim to reduce uncertainty regarding the value of waterfowl foods by conducting contemporary food-selection studies using unbiased collection and processing methodologies. Further, we suggest future researchers conduct concurrent behavioral observations, habitat use, and food selection studies within winter home ranges of dabbling ducks to aid managers in meeting the nutritional requirements of dabbling ducks during autumn and winter in North America.
Exposure to IL-15 and IL-21 Enables Autoreactive CD8 T Cells To Respond to Weak Antigens and Cause Disease in a Mouse Model of Autoimmune Diabetes
Authors: Ramanathan Sheela , Dubois Stephanie , Chen Xi-Lin , Leblanc Chantal , Ohashi Pamela S. , Ilangumaran Subburaj 
Published: March 2011

Abstract
Autoreactive CD8+ T lymphocytes play a key role in the pathogenesis of several autoimmune diseases. It is not yet well understood how autoreactive CD8+ T cells, which express TCRs with low reactivity toward self-Ags, gain the ability to respond to autoantigens to cause disease. Previously, we have shown that prior stimulation of CD8+ T cells with synergistic combinations of cytokines produced by the innate immune response, such as IL-21 and IL-15, induces Ag-independent proliferation. Such “cytokine-primed” CD8 T cells displayed increased responsiveness to limiting quantities of the cognate Ag. In this paper, we report that prior stimulation with IL-15 and IL-21 also enables CD8+ T cells to respond to weakly agonistic TCR ligands, resulting in proliferation, cytokine secretion, and cytolytic activity. Using a transgenic mouse model of autoimmune diabetes, we show that cytokine-primed autoreactive CD8+ T cells induce disease following stimulation by weak TCR ligands, but their diabetogenic potential is dependent on continuous availability of IL-15 in vivo. These findings suggest that inflammatory cytokines could facilitate the triggering of autoreactive CD8+ T cells by weak autoantigens, and this mechanism may have important implications for autoimmune diseases associated with microbial infections and chronic inflammation.
Lipopolysaccharide Signaling without a Nucleus: Kinase Cascades Stimulate Platelet Shedding of Proinflammatory IL-1β–Rich Microparticles
Authors: Brown G. Thomas , McIntyre Thomas M. 
Published: March 2011

Abstract
Platelets contain unspliced heteronuclear IL-1β RNA, which is rapidly spliced and translated upon activation. LPS is a superior agonist for this atypical platelet response, but how LPS induces proinflammatory cytokine production in anucleate cells lacking NF-κB is unknown. Platelets express functional TLR4, and stimulation by LPS induced rapid splicing, translation, and secretion of mature IL-1β after caspase-1 processing. LPS stimulated microparticle shedding, and secreted IL-1β was exclusively present in these particles. Microparticles from LPS-stimulated platelets induced VCAM-1 production by cultured human endothelial cells, and blockade of endothelial IL-1β receptor with IL-1 receptor antagonist completely suppressed endothelial activation. Splicing was posttranscriptional as the SR kinase inhibitor TG003 blocked IL-1β RNA production by platelets, but not by monocytes, and was dependent on exogenous CD14—a property of platelets. We used a combination of small-molecule inhibitors, cell-penetrating chimeric peptide inhibitors, and gene-targeted animals to show splicing required MyD88 and TIRAP, and IRAK1/4, Akt, and JNK phosphorylation and activation. Traf6 couples MyD88 to the Akt pathway and, remarkably, a Traf6 interacting peptide–antennapedia chimera was more effective than LPS in stimulating IL-1β splicing. The Traf6 chimera did not, however, stimulate microparticle shedding, nor was IL-1β released. We conclude LPS-induced kinase cascades are sufficient to alter cellular responses, that three signals emanate from platelet TLR4, and that Akt and JNK activation are sufficient to initiate posttranscriptional splicing while another event couples microparticle shedding to TLR4 activation. Platelets contribute to the inflammatory response to LPS through production of microparticles that promote endothelial cell activation.
Enhanced Sensitivity to IL-2 Signaling Regulates the Clinical Responsiveness of IL-12–Primed CD8+ T Cells in a Melanoma Model
Authors: Lisiero Dominique N. , Soto Horacio , Liau Linda M. , Prins Robert M. 
Published: March 2011

Abstract
The optimal expansion, trafficking, and function of adoptively transferred CD8+ T cells are parameters that currently limit the effectiveness of antitumor immunity to established tumors. In this study, we addressed the mechanisms by which priming of self tumor-associated Ag-specific CD8+ T cells influenced antitumor functionality in the presence of the inflammatory cytokine IL-12. In vitro priming of mouse tumor-specific CD8+ T cells in the presence of IL-12 induced a diverse and rapid antitumor effector activity while still promoting the generation of memory cells. Importantly, IL-12–primed effector T cells dramatically reduced the growth of well-established s.c. tumors and significantly increased survival to highly immune resistant, established intracranial tumors. Control of tumor growth by CD8+ T cells was dependent on IL-12–mediated upregulation of the high-affinity IL-2R (CD25) and a subsequent increase in the sensitivity to IL-2 stimulation. Finally, IL-12–primed human PBMCs generated tumor-specific T cells both phenotypically and functionally similar to IL-12–primed mouse tumor-specific T cells. These results highlight the ability of IL-12 to obviate the strict requirement for administering high levels of IL-2 during adoptive cell transfer-mediated antitumor responses. Furthermore, acquisition of a potent effector phenotype independent of cytokine support suggests that IL-12 could be added to adoptive cell transfer clinical strategies in cancer patients.
IFN-α Production by Plasmacytoid Dendritic Cells Stimulated with RNA-Containing Immune Complexes Is Promoted by NK Cells via MIP-1β and LFA-1
Authors: Hagberg Niklas , Berggren Olof , Leonard Dag , Weber Gert , Bryceson Yenan T. , Alm Gunnar V. , Eloranta Maija-Leena , Rönnblom Lars 
Published: March 2011

Abstract
Several systemic autoimmune diseases display a prominent IFN signature. This is caused by a continuous IFN-α production by plasmacytoid dendritic cells (pDCs), which are activated by immune complexes (ICs) containing nucleic acid. The IFN-α production by pDCs stimulated with RNA-containing IC (RNA-IC) consisting of anti-RNP autoantibodies and U1 small nuclear ribonucleoprotein particles was recently shown to be inhibited by monocytes, but enhanced by NK cells. The inhibitory effect of monocytes was mediated by TNF-α, PGE2, and reactive oxygen species, but the mechanisms for the NK cell-mediated increase in IFN-α production remained unclear. In this study, we investigated the mechanisms whereby NK cells increase the RNA-IC–induced IFN-α production by pDCs. Furthermore, NK cells from patients with systemic lupus erythematosus (SLE) were evaluated for their capacity to promote IFN-α production. We found that CD56dim NK cells could increase IFN-α production &gt;1000-fold after RNA-IC activation, whereas CD56bright NK cells required costimulation by IL-12 and IL-18 to promote IFN-α production. NK cells produced MIP-1α, MIP-1β, RANTES, IFN-γ, and TNF-α via RNA-IC–mediated FcγRIIIA activation. The IFN-α production in pDCs was promoted by NK cells via MIP-1β secretion and LFA-mediated cell–cell contact. Moreover, NK cells from SLE patients displayed a reduced capacity to promote the RNA-IC–induced IFN-α production, which could be restored by exogenous IL-12 and IL-18. Thus, different molecular mechanisms can mediate the NK cell-dependent increase in IFN-α production by RNA-IC–stimulated pDCs, and our study suggests that the possibility to therapeutically target the NK–pDC axis in IFN-α–driven autoimmune diseases such as SLE should be investigated.
Attenuated Bordetella pertussis Vaccine Candidate BPZE1 Promotes Human Dendritic Cell CCL21-Induced Migration and Drives a Th1/Th17 Response
Authors: Fedele Giorgio , Bianco Manuela , Debrie Anne-Sophie , Locht Camille , Ausiello Clara Maria 
Published: March 2011

Abstract
New vaccines against pertussis are needed to evoke full protection and long-lasting immunological memory starting from the first administration in neonates—the major target of the life-threatening pertussis infection. A novel live attenuated Bordetella pertussis vaccine strain, BPZE1, has been developed by eliminating or detoxifying three important B. pertussis virulence factors: pertussis toxin, dermonecrotic toxin, and tracheal cytotoxin. We used a human preclinical ex vivo model based on monocyte-derived dendritic cells (MDDCs) to evaluate BPZE1 immunogenicity. We studied the effects of BPZE1 on MDDC functions, focusing on the impact of Bordetella-primed dendritic cells in the regulation of Th and suppressor T cells (Ts). BPZE1 is able to activate human MDDCs and to promote the production of a broad spectrum of proinflammatory and regulatory cytokines. Moreover, conversely to its parental wild-type counterpart BPSM, BPZE1-primed MDDCs very efficiently migrate in vitro in response to the lymphatic chemokine CCL21, due to the inactivation of pertussis toxin enzymatic activity. BPZE1-primed MDDCs drove a mixed Th1/Th17 polarization and also induced functional Ts. Experiments performed in a Transwell system showed that cell contact rather than the production of soluble factors was required for suppression activity. Overall, our findings support the potential of BPZE1 as a novel live attenuated pertussis vaccine, as BPZE1-challenged dendritic cells might migrate from the site of infection to the lymph nodes, prime Th cells, mount an adaptive immune response, and orchestrate Th1/Th17 and Ts responses.
The Role of ChemR23 in the Induction and Resolution of Cigarette Smoke-Induced Inflammation
Authors: Demoor Tine , Bracke Ken R. , Dupont Lisa L. , Plantinga Maud , Bondue Benjamin , Roy Marie-Odile , Lannoy Vincent , Lambrecht Bart N. , Brusselle Guy G. , Joos Guy F. 
Published: March 2011

AbstractChronic obstructive pulmonary disease is mainly triggered by cigarette smoke (CS) and progresses even after smoking cessation. CS induces an exaggerated influx of inflammatory cells to the bronchoalveolar space and lung parenchyma, likely resulting from a complex interplay between chemoattractants and their respective receptors. In a murine CS model of chronic obstructive pulmonary disease, we studied the importance of chemokine-like receptor ChemR23 for the induction and resolution of inflammation in CS-exposed lungs. Subacute and chronic CS exposure increased protein levels of the ChemR23 ligand and chemoattractant, chemerin, in bronchoalveolar lavage (BAL) fluid of wild-type (WT) mice. Moreover, the proinflammatory chemokines CXCL1, CCL2, and CCL20 were increased in the airways of CS-exposed WT mice, accompanied by a massive accumulation of inflammatory neutrophils and monocytes, CD11bhiCD103− and CD11bloCD103+ dendritic cells (DCs), and CD4+ and CD8+ T cells. The lung parenchyma of WT mice was infiltrated with inflammatory neutrophils, CD11bhiCD103− DCs, and activated CD4+ T cells after CS exposure. CS-induced inflammation was severely attenuated in BAL fluid and lungs of ChemR23 knockout mice with regard to the induction of inflammatory chemokines and the recruitment of inflammatory cells. Neutrophils and CD8+ T cells persisted in the airways of WT mice, as did the airway-derived conventional DCs in the mediastinal lymph nodes, for at least 14 d after smoking cessation. In the BAL fluid of CS-exposed ChemR23 knockout mice, there was a remarkable delayed accumulation of T cells 14 d after the final exposure. Our data support a role for ChemR23 in directing innate and adaptive immune cells to CS-exposed lungs.
Measurement of CO3-610, a Potential Liver Biomarker Derived from Matrix Metalloproteinase-9 Degradation of Collagen Type III, in a Rat Model of Reversible Carbon-Tetrachloride-Induced Fibrosis
Authors: Vassiliadis Efstathios , Vang Larsen Dorthe , Clausen Rikke Elgaard , Veidal Sanne Skovgård , Barascuk Natasha , Larsen Lise , Simonsen Henrik , Silvestre Toni Segovia , Hansen Christina , Overgaard Trine , Leeming Diana Julie , Karsdal Morten A 
Published: March 2011

Background and AimThe current study utilized a carbon tetrachloride (CCl4)-induced liver fibrosis model to measure levels of the MMP9-mediated collagen type III degradation fragment CO3-610 (site of cleavage: KNGETGPQGP), during disease progression and regression, and to investigate a potential prognostic role of the biomarker.Materials and Methods72 female Sprague-Dawley rats aged 6 months old were injected with CCl4twice a week over different periods of time to induce varying degrees of liver fibrosis. After 4, 6 and 8 weeks of treatment, administration of CCl4was stopped. The 6- and 8-week treatment groups were left to regress for a further 6 or 12 weeks at which point they were sacrificed and livers removed and sectioned. Liver fibrosis was quantified using Visiopharm software to analyse Sirius red-stained sections. Serum levels of CO3-610 were measured in all animals using an ELISA assay as described by Barascuk et al.1ResultsQuantitative histology revealed total collagen deposition in the liver increased as fibrosis progressed. In animals treated with CCl4for 4 weeks, collagen comprised on average 4.94% of the total tissue in liver sections, while after 6 weeks the mean was 8.25%, and after 8 weeks, 9.11%. During the regression phase, the total collagen deposition gradually decreased to a mean of 6.9% and 5.09% for animals regressing 6 and 12 weeks respectively after 6 weeks treatment, and 6.27% for animals regressed 12 weeks after 8 weeks treatment. CO3-610 values increased progressively in rats treated for 4 weeks (by a mean of 55.0 ng/ml), 6 weeks (mean 61.1 ng/ml) and 8 weeks (mean 70.2 ng/ml). During the regression phase, CO3-610 values rapidly decreased by a mean of 28.9 ng/ml at 6 weeks and 21.6 ng/ml at 12 weeks in animals previously treated for 6 weeks, and by a mean of 19.52 ng/ml in animals treated for 8 weeks and regressed for 12 weeks. CO3-610 levels were statistically significantly correlated with total collagen during disease progression ( r = 0.5701, P < 0.0001). No statistically significant correlation was observed during regression ( r = 0.2081, P = 0.1138).ConclusionLevels of the MMP-9 generated fragment of collagen type III, CO3-610, correlated with the degree of liver fibrosis in rats during the progression phase, but were not correlated with total collagen levels during regression. CO3-610 seems to be produced only under the CCL4stimulus, and signifies CO3-610 as a potential marker of progression rather than regression. The corresponding steep elevations in levels of CO3-610 total collagen and collagen type III during liver fibrosis progression underline a potential prognostic capacity of the biomarker.
Retinal Nerve Fiber Layer Measurement and Diagnostic Capability of Spectral-Domain versus Time-Domain Optical Coherence Tomography
Authors: Kaushik Sushmita , Pandav Surinder Singh , Ichhpujani Parul , Gupta Amod , Gupta Pramod 
Published: March 2011

Purpose To compare retinal nerve fiber layer (RNFL) thickness and diagnostic capability of spectral-domain (Cirrus™) versus time-domain (Stratus®) optical coherence tomography (OCT). Methods A total of 123 eyes of 123 subjects including 68 normal, 32 glaucoma suspect, and 23 patients with glaucoma were prospectively recruited for the study. All subjects were scanned by Stratus® and Cirrus™ OCT in the same session. Average and quadrant peripapillary RNFL measurements by both machines were correlated using Spearman correlation coefficient, and agreement between testing methods was analyzed by Bland-Altman plots. The area under receiver operating characteristic curves (AUC) for glaucoma diagnosis was calculated. Results Average RNFL thickness were significantly thinner on the Cirrus™ compared to the Stratus® OCT in normal subjects and glaucoma suspects (p<0.001), but thicker on the Cirrus™ OCT in glaucoma patients, though the difference was not statistically significant (p=0.53). There was good correlation between the measurements in all 3 groups. In normal controls, the average, superior, nasal, inferior, and temporal correlations were r=0.668, 0.601, 0.508, 0.620, and 0.660, p<0.001, respectively. In glaucomatous eyes, the corresponding values were r=0.560, p=0.005; r=0.423, p=0.04; r=0.117, p=0.596; r=0.742, p<0.001; r=0.669, p<0.001, respectively. The 95% limits of agreement of average RNFL thickness were −30.2 to 13.8 μm. Area under receiver operating characteristic curves for diagnosing glaucoma were comparable (superior RNFL thickness by Cirrus™ 0.925; average RNFL thickness by Stratus® 0.987). Highest correlated AUCs were for inferior and temporal quadrants. Conclusions Retinal nerve fiber layer measurements on the Cirrus™ and Stratus® OCT correlate well but do not have clinically acceptable agreement between their measurements. The instruments may not be used interchangeably.