Danh Vo : de l’objet à l’histoire, du nom à l’objet, de l’histoire au nom, de la sculpture au nom.

Le titre de l’exposition consacrée à Danh Vo au Musée d’art moderne, à première vue énigmatique, Go Mo Ni Ma Da, s’avère être un « Good Morning, Madam » revisité sur le mode monosyllabique propre à la langue vietnamienne, sans les diacritiques qui en modulent les sons et le sens. Le ton hybride est donné, le visiteur abandonné à la croisée d’histoires, celles des Etats-Unis, du Viêt Nam et de la France, dans un espace au dépouillement parfaitement maîtrisé. Danh Vo s’éclipse là : derrière les..

L’abstraction au cœur de l’Exposition. Ilya Bolotowsky, Study for the Hall of Medical Sciences Mural at the 1939 World's Fair in New York (1938/39)

Ilya Bolotowsky (1907-1981), Study for the Hall of Medical Sciences Mural at the 1939 World’s Fair in New York, 1938/39 Huile sur toile, 76,2 x 121,9 cm. Wilson L. Mead Fund, 1977.1. The Art Institute of Chicago Photo credit: The Art Institute of Chicago / Art Resource, NY. * Study for the Hall of Medical Sciences Mural at the 1939 World’s Fair in New York (1938/39) est à la fois projection d’une œuvre à venir et survivance d’une peinture murale dont l’existence n’est connue que par le biais..

Danh Vo : de l’objet à l’histoire, du nom à l’objet, de l’histoire au nom, de la sculpture au nom.

Le titre de l’exposition consacrée à Danh Vo au Musée d’art moderne, à première vue énigmatique, Go Mo Ni Ma Da, s’avère être un « Good Morning, Madam » revisité sur le mode monosyllabique propre à la langue vietnamienne, sans les diacritiques qui en modulent les sons et le sens. Le ton hybride est donné, le visiteur abandonné à la croisée d’histoires, celles des Etats-Unis, du Viêt Nam et de la France, dans un espace au dépouillement parfaitement maîtrisé. Danh Vo s’éclipse là : derrière les..

Sculpteurs d’une cause perdue : statues et causes d’une perte ?

Dans les débats que suscitent les statues dédiées aux Confédérés, l’attention accordée aux artistes est souvent inexistante. Ils ont pourtant participé à cette entreprise de commémoration aujourd’hui contestée, puisque ce sont eux qui ont donné forme à des généraux et des soldats que les défenseurs de la cause perdue avaient décidé d’honorer et de placer dans des lieux publics. Afin d’éclairer certains aspects du processus mis en œuvre pour ériger de tels monuments dans le Sud de la fin du XIXe et du début du XXe siècle, et de saisir ce qu’implique leur présence dans le monde actuel, cet article s’intéresse à quelques-uns de ces artistes, Antonin Mercié, Alexander Doyle, Frederick W. Ruckstull, Alexander Phimister Proctor, et aux procédures qui ont conduit à les choisir.In the conversations that Confederate statues have provoked, little attention, if any, has been paid to the authors of those statues. These artists willingly participated in the commemorative movement that is so highly contested today; they also gave shape to the generals and soldiers that the Lost Cause advocates honored and sited in public places. In order to grasp the process that led to the monumentalizing of the late-nineteenth- and early-twentieth-century South and thus in part help us to understand the ramifications of the very existence of those works in today’s world, this article looks at a number of these artists—Antonin Mercié, Alexander Doyle, Frederick W. Ruckstull, Alexander Phimister Proctor—as well as the procedures which led to their selection

DUX4c Is Up-Regulated in FSHD. It Induces the MYF5 Protein and Human Myoblast Proliferation

Facioscapulohumeral muscular dystrophy (FSHD) is a dominant disease linked to contractions of the D4Z4 repeat array in 4q35. We have previously identified a double homeobox gene (DUX4) within each D4Z4 unit that encodes a transcription factor expressed in FSHD but not control myoblasts. DUX4 and its target genes contribute to the global dysregulation of gene expression observed in FSHD. We have now characterized the homologous DUX4c gene mapped 42 kb centromeric of the D4Z4 repeat array. It encodes a 47-kDa protein with a double homeodomain identical to DUX4 but divergent in the carboxyl-terminal region. DUX4c was detected in primary myoblast extracts by Western blot with a specific antiserum, and was induced upon differentiation. The protein was increased about 2-fold in FSHD versus control myotubes but reached 2-10-fold induction in FSHD muscle biopsies. We have shown by Western blot and by a DNA-binding assay that DUX4c over-expression induced the MYF5 myogenic regulator and its DNA-binding activity. DUX4c might stabilize the MYF5 protein as we detected their interaction by co-immunoprecipitation. In keeping with the known role of Myf5 in myoblast accumulation during mouse muscle regeneration DUX4c over-expression activated proliferation of human primary myoblasts and inhibited their differentiation. Altogether, these results suggested that DUX4c could be involved in muscle regeneration and that changes in its expression could contribute to the FSHD pathology

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead