Discurs del rector de la Universitat de Girona, Dr.Joan Batlle, en l'acte d'investidura com doctors honoris causa de Robert Brian Tate, Joan Bertran Rusca i Jaume Gil Aluja

Discurs d'investidura de doctors honoris causa per la Universitat de Girona, del rector Joan Batlle

Marques de biblioteca: Robert Brian Tate

Explicació del motius que Robert Brian Tate podia tenir per a triar l’humanista quatrecentista Joan Margarit i Pau com a figura del seu ex-libris

Adaptación para niños de la prueba de amplitud lectora de Daneman y Carpenter (PAL-N).

Resumen basado en el de la publicación: Incluye apéndices

Dancing in translation: Irina Brook’s mise en scène of 'Danser à Lughnasa', Jean-Marie Besset’s translation of Brian Friel’s 'Dancing at Lughnasa'

This essay contributes to debates about theatre and cross-cultural encounter through an analysis of Irina Brook’s 1999 Swiss / French co-production of Irish playwright Brian Friel’s Dancing at Lughnasa, in a French translation by Jean-Marie Besset. While the translation and Brook’s mise en scène clearly identified the source text and culture as Irish, they avoided cultural stereotypes, and rendered the play accessible to francophone audiences without entirely assimilating it to a specific Swiss or French cultural context. Drawing on discourses of theatre translation, and concepts of cosmopolitanism and conviviality, the essay focuses on the potential of such textual and theatrical translation to acknowledge specific cultural traces but also to estrange the familiar perceptions and boundaries of both the source and target cultures, offering modes of interconnection across diverse cultural affiliations.

Carpenter Syndrome: Extended RAB23 Mutation Spectrum and Analysis of Nonsense-mediated mRNA Decay

Carpenter syndrome, a rare autosomal recessive disorder characterized by a combination of craniosynostosis, polysyndactyly, obesity, and other congenital malformations, is caused by mutations in RAB23, encoding a member of the Rab-family of small GTPases. In 15 out of 16 families previously reported, the disease was caused by homozygosity for truncating mutations, and currently only a single missense mutation has been identified in a compound heterozygote. Here, we describe a further 8 independent families comprising 10 affected individuals with Carpenter syndrome, who were positive for mutations in RAB23. We report the first homozygous missense mutation and in-frame deletion, highlighting key residues for RAB23 function, as well as the first splice-site mutation. Multi-suture craniosynostosis and polysyndactyly have been present in all patients described to date, and abnormal external genitalia have been universal in boys. High birth weight was not evident in the current group of patients, but further evidence for laterality defects is reported. No genotype-phenotype correlations are apparent. We provide experimental evidence that transcripts encoding truncating mutations are subject to nonsense-mediated decay, and that this plays an important role in the pathogenesis of many RAB23 mutations. These observations refine the phenotypic spectrum of Carpenter syndrome and offer new insights into molecular pathogenesis. (C) 2011 Wiley-Liss, Inc.