Pamela Cox, Heather Shore (Eds.), Becoming Delinquent: British and European Youth, 1650-1950

Produit à la suite d’un congrès international tenu à Cambridge en 1999, ce livre rassemble différentes études ouest-européennes portant sur le thème la délinquance juvénile selon une perspective qui met l’accent sur l’histoire et la longue durée. Alors que l’expansion de la criminologie a permis la prolifération de travaux relatifs à la criminalité et à la protection de l’enfance, Pamela Cox et Heather Shore estiment que les études publiées jusqu’à présent ont quelque peu négligé l’aspect his..

Les mesures destinées à redresser l'enfance délinquante au Québec : le cas de l'Institut Saint-Antoine pour garçons (1873-1910)

Cet article porte sur la première expérience québécoise en matière d'institutionnalisation spécialisée pour les garçons délinquants. Le portrait des traitements en vigueur dans la principale institution d'enfermement destinée à cette clientèle au Québec, l'Institut Saint-Antoine, illustre bien l'évolution des mesures destinées à redresser l'enfance délinquante jusqu'à l'adoption des lois de 1908 et 1910 permettant la création d'un tribunal pour mineurs à Montréal. Nous pouvons de cette façon évaluer comment l'expérience québécoise s'inscrit dans le courant de l'époque en matière de traitement de l'enfance délinquante.Measures intended to raise delinquent childhood in Quebec: the case of Saint Antoine institute for boys ( 1873-1910)       This article deals with the first experience in institutionalization for delinquent boys in Quebec. The portrait of treatment methods used in the principle institution intended for this clientele in Quebec, Saint Antoine institute, allows us to illustrate the evolution of measures designed to address the problems of delinquent children until the adoption of the 1908 and 1910 laws that allowed for the creation of a juvenile court in Montreal. We shall, in this way, be able to estimate to what extent Quebec’s experience reflects trends elsewhere in the treatment of juvenile delinquents

Pamela Cox, Heather Shore (Eds.), Becoming Delinquent: British and European Youth, 1650-1950

Produit à la suite d’un congrès international tenu à Cambridge en 1999, ce livre rassemble différentes études ouest-européennes portant sur le thème la délinquance juvénile selon une perspective qui met l’accent sur l’histoire et la longue durée. Alors que l’expansion de la criminologie a permis la prolifération de travaux relatifs à la criminalité et à la protection de l’enfance, Pamela Cox et Heather Shore estiment que les études publiées jusqu’à présent ont quelque peu négligé l’aspect his..

Jean-Claude Vimont (dir.), Jeunes, déviances et identités (XVIIIe-XXe siècles)

Produit par le Groupe de Recherche en Histoire de l’Université de Rouen, cet ouvrage rassemble les textes des communications présentées dans le cadre d’une journée d’études portant sur les relations entre la construction identitaire et la construction de catégories sociales chez les jeunes déviants. Les coordonnateurs de cette journée (Jean-Pierre Jessenne, Anne-Marie Sohn et Jean-Claude Vimont) ont également commandé des articles à d’éminents chercheurs de l’histoire pénale ainsi qu’à de jeu..

Critical Role of TLR9 in Acute Graft-versus-Host Disease

Abstract Graft-vs-host disease (GVHD) is a major complication after allogeneic bone marrow transplantation. Different studies have demonstrated that intestinal bacterial breakdown products and loss of gastrointestinal tract integrity, both induced by conditioning regiments, are critical in the pathogenesis of acute GVHD. Using C57BL/6 knockout mice, we evaluated the role of TLR4 and TLR9, which recognize bacterial LPS and DNA, respectively, in the GVHD associated with allogeneic bone marrow transplantation. When myeloablative-irradiated TLR9 knockout (TLR9−/−) mice were used as graft recipients, survival and clinical score of acute GVHD were improved as compared with the wild-type recipient mice (18/30 vs 1/31 mice still alive at day 70 in a total of four experiments); while no differences were observed using recipient TLR4 knockout (TLR4−/−) mice. The reduced mortality and morbidity in TLR9−/− mice related with reduced stimulatory activity of TLR9−/− spleen APCs after conditioning and reduced proliferation of allogeneic donor T cells. Experiments using TLR9+/+ into TLR9−/− and TLR9−/− into TLR9+/+ chimeric mice as recipients indicated a critical role for nonhematopoietic TLR9+/+ cells interacting with bacterial breakdown products released in myeloablated mice. Altogether these data reveal a novel important role of TLR9 in GVHD, a finding that might provide tools to reduce this complication of allogeneic transplantation

Une politique de l'enfance délinquante et en danger : la mise en place des écoles de réforme et d'industrie au Québec (1840-1873)

À partir du milieu du XIXe siècle, diverses sociétés occidentales mettent en place, à des rythmes et à des degrés divers, une politique de l'enfance délinquante et en danger. Chacune de ces sociétés organise ses politiques de l'enfance selon un contexte qui lui est propre, et selon les besoins de ses élites qui veulent assurer la reconstruction de l'ordre existant à promouvoir ou à construire. Le Québec constitue en ce sens un exemple intéressant. L'analyse de la mise en place de ses premières institutions de traitement de l'enfance délinquante et en danger nous permet de voir comment et à quel rythme, dans un contexte socio-politique donné, les différents enjeux d'une politique de l'enfance se cristallisent et aboutissent à une structuration particulière.In the mid-nineteenth century, various Western societies, each at its own place and intensity, began putting in place policies for the surveillance and care of delinquent and endangered children. Each society organized these policies in accordance with its own context and the needs of its élites, who were desirous of ensuring the continuity of the existing order, or of promoting or constructing a new one. Quebec is an interesting example. An analysis of its early institutions for dealing with delinquent and endangered children reveals the way and the speed at which in a given socio-political context, the various issues at stake in a child-welfare policy crystallize and result in a particular structuring

The 67-kDa laminin receptor originated from a ribosomal protein that acquired a dual function during evolution.

The 67-kDa laminin receptor (67LR) is a nonintegrin cell surface receptor that mediates high-affinity interactions between cells and laminin. Overexpression of this protein in tumor cells has been related to tumor invasion and metastasis. Thus far, only a full-length gene encoding a 37-kDa precursor protein (37LRP) has been isolated. The finding that the cDNA for the 37LRP is virtually identical to a cDNA encoding the ribosomal protein p40 has suggested that 37LRP is actually a component of the translational machinery, with no laminin-binding activity. On the other hand, a peptide of 20 amino acids deduced from the sequence of 37LR/p40 was shown to exhibit high laminin-binding activity. The evolutionary relationship between 23 sequences of 37LRP/p40 proteins was analyzed. This phylogenetic analysis indicated that all of the protein sequences derive from orthologous genes and that the 37LRP is indeed a ribosomal protein that acquired the novel function of laminin receptor during evolution. The evolutionary analysis of the sequence identified as the laminin-binding site in the human protein suggested that the acquisition of the laminin-binding capability is linked to the palindromic sequence LMWWML, which appeared during evolution concomitantly with laminin

vanA in Enterococcus faecium, Enterococcus faecalis, and Enterococcus casseliflavus detected in French cattle.

The goal of this study was to assess the presence of enterococci species presenting van-mediated glycopeptide resistance in French cattle. Fecal samples were collected from healthy and sick animals, and enterococci were screened for vancomycin resistance. Vancomycin resistance was principally encountered in Enterococcus gallinarum and Enterococcus casseliflavus strains. However, glycopeptide resistance was detected in three different species of enterococci (E. faecalis, E. faecium, and E. casseliflavus). Molecular characterization of the genetic support proved that they all presented the prototypic VanA element. Interestingly, the E. casseliflavus strain displayed a remarkable VanB phenotype/vanA-vanC genotype. Transferability, associated resistances, and factors of vanA cotransfer were sought. This study proved that acquired vanA genes can still be detected in food-producing animals more than a decade after the avoparcin ban. Indeed, calves, which are recurrently exposed to antibiotics in France, may allow the re-emergence of glycopeptide resistance through coselection factors, and this might potentially be concerning for human health

Relationship between p53 and p27 expression following HER2 signaling

HER2, frequently associated with low p27 expression in breast tumors, when activated has been found to upmodulate p53 in tumor cells. The aim of this work was to investigate the role of p53 in the connection between HER2 and p27. Fifty-two breast tumor specimens, characterized for p53 mutations, were analyzed immunohistochemically (IHC) for HER2, p53 and p27 expression. p27, inversely associated with HER2, was found in 29% of tumors with IHC-negative mutated p53 versus 93% of tumors with accumulation of p53 protein and 59% with wild-type p53 (p=0.001), indicating a direct association between p53 and p27 expression. HER2-overexpressing cell lines carrying wild-type or null p53 protein, and treated with heregulin beta1 (HRG), were analyzed for expression and subcellular localization of p53 and p27. In HER2-overexpressing cells stimulated with HRG, p27 protein expression increased in parallel with p53 with no corresponding increase in p27 transcript. No p27 increase was observed in p53-null cells. Transfection with wild-type p53 restored p27 upmodulation in HRG-stimulated cells, indicating a crucial role of p53 in determining p27 upmodulation following HER2 activation. Together, our data demonstrate the crucial role of p53 in determining p27 upmodulation following HER2 activation. This could have implications in the response to Transtuzumab therapy