The Fantastic Genre in the Novel "The Maze" of Maurice Sandoz

This article examines the structure of Maurice Sandoz’s novel Le Labyrinthe (The Maze) in order to determine to what extent that novel belongs to the fantastic genre. Drawing on classical theories of the fantastic, the present article demonstrates that Sandoz’s Labyrinthe raises terminological issues, since it contains elements that canonical theories consider as fantastiques but also merveilleux (Todorov, Caillois). A detailed analysis of the Sandozian forewords’ characteristics makes it possible to show that the author plays with the notions of limit and hesitation. The latter are crucial in the seminal theories on the fantastique and are at the core of the Sandozian strategy that consists in the blurring of the boundaries between author, narrator, narrative, and “reality”. This study constitutes a first step towards a more detailed analysis of Sandoz’s fantastique and its goal is to underlines the necessity of a perspective shift in the comprehension thereof.Cet article examine la structure du roman Le Labyrinthe de Maurice Sandoz dans le but de déterminer dans quelle mesure le roman appartient au genre fantastique. En se basant sur les théories classiques du fantastique, l’article démontre que Le Labyrinthe de Sandoz soulève des problèmes terminologiques étant donné qu’il contient des éléments considérés par les théories canoniques comme fantastiques mais aussi merveilleux (Todorov, Caillois). Une analyse détaillée des caractéristiques des avant-propos sandoziens permet de montrer que l’auteur joue sur la notion de limite et d’hésitation. Ces dernières sont cruciales dans les théories majeures du fantastique et sont au coeur de la stratégie de Sandoz, qui consiste à brouiller les frontières entre l’auteur, le narrateur, le récit et la « réalité ». Cette étude constitue une première étape vers une analyse plus détaillée du fantastique de Sandoz et son but est de souligner la nécessité d’un changement de perspective dans l’appréhension de ce dernier

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Construction of 12 EST libraries and characterization of a 12,226 EST dataset for chicory (Cichorium intybus) root, leaves and nodules in the context of carbohydrate metabolism investigation

<p>Abstract</p> <p>Background</p> <p>The industrial chicory, <it>Cichorium intybus</it>, is a member of the <it>Asteraceae </it>family that accumulates fructan of the inulin type in its root. Inulin is a low calories sweetener, a texture agent and a health promoting ingredient due to its prebiotic properties. Average inulin chain length is a critical parameter that is genotype and temperature dependent. In the context of the study of carbohydrate metabolism and to get insight into the transcriptome of chicory root and to visualize temporal changes of gene expression during the growing season, we obtained and characterized 10 cDNA libraries from chicory roots regularly sampled in field during a growing season. A leaf and a nodule libraries were also obtained for comparison.</p> <p>Results</p> <p>Approximately 1,000 Expressed Sequence Tags (EST) were obtained from each of twelve cDNA libraries resulting in a 12,226 EST dataset. Clustering of these ESTs returned 1,922 contigs and 4,869 singlets for a total of 6,791 putative unigenes. All ESTs were compared to public sequence databases and functionally classified. Data were specifically searched for sequences related to carbohydrate metabolism. Season wide evolution of functional classes was evaluated by comparing libraries at the level of functional categories and unigenes distribution.</p> <p>Conclusion</p> <p>This chicory EST dataset provides a season wide outlook of the genes expressed in the root and to a minor extent in leaves and nodules. The dataset contains more than 200 sequences related to carbohydrate metabolism and 3,500 new ESTs when compared to other recently released chicory EST datasets, probably because of the season wide coverage of the root samples. We believe that these sequences will contribute to accelerate research and breeding of the industrial chicory as well as of closely related species.</p

Phase Ib/II Study of the Efficacy and Safety of Binimetinib (MEK162) Plus Panitumumab for Mutant or Wild-Type RAS Metastatic Colorectal Cancer

RAS mutation; Binimetinib; Colorectal cancerMutació RAS; Binimetinib; Càncer colorectalMutación RAS; Binimetinib; Cáncer colorrectalIntroduction Activating RAS gene mutations occur in approximately 55% of patients with metastatic colorectal cancer (mCRC) and are associated with poorer clinical outcomes due to epidermal growth factor receptor (EGFR) blockade resistance. Combined EGFR and mitogen-activated protein kinase (MEK) inhibition may extend response to EGFR inhibition and overcome acquired resistance. This phase Ib/II dose escalation trial evaluated the safety and activity of dual inhibition with binimetinib (MEK1/2 inhibitor) and panitumumab (EGFR inhibitor [EGFRi]) in patients with RAS mutant or BRAF wild type (WT)/RAS WT mCRC. Methods Phase Ib dose escalation started with binimetinib 45 mg twice daily plus panitumumab 6 mg/kg administered every 2 weeks. In the phase II study, patients with measurable mCRC were enrolled into 4 groups based on previous anti-EGFR monoclonal antibody therapy and RAS mutational status. Results No patients in the phase Ib portion (n = 10) had a response; 70% of patients had stable disease. In the phase II portion (n = 43), overall response rate (ORR, confirmed) was 2.3% with one partial response in the RAS WT group, DCR was 30.2%, and median progression-free survival was 1.8 months (95%CI, 1.6-3.3). All patients experienced ≥1 adverse event, with the most common being diarrhea (71.7%), vomiting (52.8%), nausea (50.9%), fatigue (49.1%), dermatitis acneiform (43.4%), and rash (41.5%). Most patients required treatment interruption or dose reduction due to difficulties tolerating treatment. Conclusions The combination of binimetinib and panitumumab had substantial toxicity and limited clinical activity for patients with mutant or WT RAS mCRC, independent of EGFRi treatment history (Trial registration: NCT01927341).This study was sponsored by Array Biopharma in collaboration with Novartis. Array Biopharma was acquired by Pfizer in July 2019. Medical writing and editorial assistance were provided by Namiko Abe of Caudex and were funded by Pfizer. Research was supported by the National Institutes of Health Cancer Center Core Grant P30 CA 008748