Humility, Self-Awareness, and Religious Ambivalence: Another Look at Beckett's ‘Humanistic Quietism’

This is the accepted manuscript. The final version is available from Edinburgh University Press at http://www.euppublishing.com/doi/abs/10.3366/jobs.2014.0104. This article provides a commentary on the opaque and often contradictory arguments of ‘Humanistic Quietism’, Samuel Beckett's 1934 review of Thomas MacGreevy's Poems. Using Beckett's complicated relationship to both his own Protestant upbringing and the Catholicism of MacGreevy as a starting point, the article proposes new ways of understanding Beckett's ambivalent comments about MacGreevy's interiority, prayer-like poetry, humility, and quietism. It draws on Beckett's comments on Rilke, André Gide, and Arnold Geulincx, as well as his familiarity with Dante, to unpack the review's dense allusions and make sense of Beckett's aesthetic allegiances. </jats:p

L' Escalade de 1602 : ballade historique

par H. Fréd. Amie

L' Escalade de 1602 : ballade historique

par H. Fréd. Amie

Fragments d'un journal intime. Tome 2 / Henri-Frédéric Amiel ; introduction de Bernard Bouvier

[Journal intime (français). Extrait]Appartient à l’ensemble documentaire : RfnEns0Appartient à l’ensemble documentaire : RfnEuro1Appartient à l’ensemble documentaire : RfnLang1Avec mode text

Philine : pages du Journal intime /

Schoentjes, Pierr

In-Frame Mutations in Exon 1 of SKI Cause Dominant Shprintzen-Goldberg Syndrome

International audienceShprintzen-Goldberg syndrome (SGS) is characterized by severe marfanoid habitus, intellectual disability, camptodactyly, typical facial dysmorphism, and craniosynostosis. Using family-based exome sequencing, we identified a dominantly inherited heterozygous in-frame deletion in exon 1 of SKI. Direct sequencing of SKI further identified one overlapping heterozygous in-frame deletion and ten heterozygous missense mutations affecting recurrent residues in 18 of the 19 individuals screened for SGS; these individuals included one family affected by somatic mosaicism. All mutations were located in a restricted area of exon 1, within the R-SMAD binding domain of SKI. No mutation was found in a cohort of 11 individuals with other marfanoid-craniosynostosis phenotypes. The interaction between SKI and Smad2/3 and Smad 4 regulates TGF-β signaling, and the pattern of anomalies in Ski-deficient mice corresponds to the clinical manifestations of SGS. These findings define SGS as a member of the family of diseases associated with the TGF-β-signaling pathway