Le Musée de l'histoire de l'immigration à Paris: une collection et un musée en devenir

Globalization and the emergence of political issues in the European Union have propelled the topic of immigration into the center of the current political climate. In this contemporary context, museums that are focused on immigration are gaining more importance due to the impetus for preserving and providing visibility for the heritage of immigrants. In Paris during October 2007 the Cité nationale de l'Histoire de l'Immigration (CNHI) opened its doors but in 2013 it changed its name to Musée de l'histoire de l'immigration (MHI). The museum presents a historical and cultural approach to immigration as well as displaying contemporary works of art that deal with the theme of immigration. In this paper we will analyze how this museum is an attempt to integrate the History of immigration as a national heritage.Com a globalização e o surgimento da Comunidade Europeia, a questão das migrações se apresenta no centro das preocupações políticas mundiais contemporâneas. E nesse contexto histórico de países de imigração ou de emigração organizam-se os museus de estudos das migrações que pertencem à categoria dos museus de história e de sociedade. Em outubro de 2007, é criada, em Paris, a Cité nationale de l'Histoire de l'Immigration (CNHI) que desde 2013 passou a se chamar Musée de l'histoire de l'immigration (MHI): um museu que apresenta ao público uma abordagem histórica e cultural da imigração assim como obras de arte contemporânea que tratam do tema. Neste artigo, bucaremos compreender como este museu constitui uma tentativa de reconhecimento do patrimônio da imigração como um patrimônio nacional.Avec la mondialisation et l'émergence de nouvelles politiques d'immigration dans la Communauté Européenne, la question des migrations est centrale dans le monde politique d'aujourd'hui. C'est dans ce contexte historique de pays d'immigration ou d'émigration que se met en place et s'organise l'étude des musées d'immigration qui appartiennent à la catégorie des musées d'histoire et de société. En France, la Cité nationale de l'Histoire de l'Immigration, qui a ouvert ses portes en octobre 2007, depuis 2013 Musée de l'histoire de l'immigration (MHI), se distingue, dans ce contexte mondial, par l'originalité de son projet et les discussions qu'il suscite dans divers domaines (aussi bien dans le milieu académique que dans les réseaux d'associations qui s'occupent des immigrés en France). Le musée présente au public une approche historique et culturelle de l'immigration ainsi que des œuvres d'art contemporain sur ce sujet. Dans cet article, on s'interrogera sur comment ce musée constitue une tentative de reconnaître le patrimoine de l'immigration comme un patrimoine national

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Mutations in PIK3CA are infrequent in neuroblastoma

BACKGROUND: Neuroblastoma is a frequently lethal pediatric cancer in which MYCN genomic amplification is highly correlated with aggressive disease. Deregulated MYC genes require co-operative lesions to foster tumourigenesis and both direct and indirect evidence support activated Ras signaling for this purpose in many cancers. Yet Ras genes and Braf, while often activated in cancer cells, are infrequent targets for activation in neuroblastoma. Recently, the Ras effector PIK3CA was shown to be activated in diverse human cancers. We therefore assessed PIK3CA for mutation in human neuroblastomas, as well as in neuroblastomas arising in transgenic mice with MYCN overexpressed in neural-crest tissues. In this murine model we additionally surveyed for Ras family and Braf mutations as these have not been previously reported. METHODS: Sixty-nine human neuroblastomas (42 primary tumors and 27 cell lines) were sequenced for PIK3CA activating mutations within the C2, helical and kinase domain "hot spots" where 80% of mutations cluster. Constitutional DNA was sequenced in cases with confirmed alterations to assess for germline or somatic acquisition. Additionally, Ras family members (Hras1, Kras2 and Nras) and the downstream effectors Pik3ca and Braf, were sequenced from twenty-five neuroblastomas arising in neuroblastoma-prone transgenic mice. RESULTS: We identified mutations in the PIK3CA gene in 2 of 69 human neuroblastomas (2.9%). Neither mutation (R524M and E982D) has been studied to date for effects on lipid kinase activity. Though both occurred in tumors with MYCN amplification the overall rate of PIK3CA mutations in MYCN amplified and single-copy tumors did not differ appreciably (2 of 31 versus 0 of 38, respectively). Further, no activating mutations were identified in a survey of Ras signal transduction genes (including Hras1, Kras2, Nras, Pik3ca, or Braf genes) in twenty-five neuroblastic tumors arising in the MYCN-initiated transgenic mouse model. CONCLUSION: These data suggest that activating mutations in the Ras/Raf-MAPK/PI3K signaling cascades occur infrequently in neuroblastoma. Further, despite compelling evidence for MYC and RAS cooperation in vitro and in vivo to promote tumourigenesis, activation of RAS signal transduction does not constitute a preferred secondary pathway in neuroblastomas with MYCN deregulation in either human tumors or murine models

RESCUE OF HIPPO CO-ACTIVATOR YAP1 TRIGGERS DNA DAMAGE-INDUCED APOPTOSIS IN HEMATOLOGICAL CANCERS

Oncogene–induced DNA damage elicits genomic instability in epithelial cancer cells, but apoptosis is blocked through inactivation of the tumor suppressor p53. In hematological cancers, the relevance of ongoing DNA damage and mechanisms by which apoptosis is suppressed are largely unknown. We found pervasive DNA damage in hematologic malignancies including multiple myeloma, lymphoma and leukemia, which leads to activation of a p53–independent, pro-apoptotic network centered on nuclear relocalization of ABL1 kinase. Although nuclear ABL1 triggers cell death through its interaction with the Hippo pathway co–activator YAP1 in normal cells, we show that low YAP1 levels prevent nuclear ABL1–induced apoptosis in these hematologic malignancies. YAP1 is under the control of a serine–threonine kinase, STK4. Importantly, genetic inactivation of STK4 restores YAP1 levels, triggering cell death in vitro and in vivo. Our data therefore identify a novel synthetic–lethal strategy to selectively target cancer cells presenting with endogenous DNA damage and low YAP1 levels

Lecture by Michael Kimmelman, given at Florida International University, January 8, 1993

Michael Kimmelman discusses collecting modernist art in America in the 20th century. Introduction by Dahlia Morgan

Restauration d'un trésor de l'art islamique au Maroc

Kimmelman Michael, Benjelloun Mohamed Othmane. Restauration d'un trésor de l'art islamique au Maroc. In: Horizons Maghrébins - Le droit à la mémoire, N°39, 1999. Place Jema' el Fna : Patrimoine Oral de l'Humanité. Héritage commun en Méditerranée. pp. 21-23