4,242 research outputs found
Brisures du romaneque: 'La Malédiction de la Madone', ou d'une pratique ironique du docufiction.
No full textLa Malédiction de la Madone, pubblicato nel 2022, è il primo romanzo in cui Philippe Vilain, scrittore tra i maggiori rappresentanti dell’autofinzione, ab- bandona la narrazione in prima persona per un “docufiction” in terza persona basato sulla vita della camorrista Pupetta Maresca. questo cambio di rotta, an- cor più sorprendente per un autore come Vilain che aveva sempre vilipeso que- sto genere letterario, è occasione di mettere in questione le sue concezioni del romanzo e della letteratura. Ne vien fuori una narrazione tesa tra l’aspirazione a far corpo unico con la sua precedente produzione letteraria e le condizioni im- poste dalla “docufinzionalizzazione” della storia. La Malédiction de la Madone diventa così un vero e proprio laboratorio letterario dove la sperimentazione più fine e pensosa svela inattese punte d’ironia.La Malédiction de la Madone, published in 2022, is the first novel in which Philippe Vilain, a writer among the greatest representatives of autofiction, abandons the first-person narration for a third-person “docufiction” based on the life of the camorrist Pupetta Maresca. This change of course, even more surprising for an author like Vilain who had always vilified this literary genre, is an opportunity to question his conceptions of the novel and of literature. The result is a narrative tended between the aspiration to merge with his previous literary pro- duction and the conditions imposed by “docufictionalization” of the history. The Malédiction de la Madone thus becomes a real literary laboratory where the finest and most thoughtful experimentation reveals unexpected hints of irony
The discovery of male Caligus brevicaudatus Scott, 1901 (Copepoda: Caligidae) parasitic on tub gurnard, Chelidonichthys lucerna (Linnaeus) from the eastern Mediterranean
No full text© Institute of Parasitology, Biology Centre CAS. Folia Parasitologica is an open access journal since 2015, this article is published under the terms of a Creative Commons License (http://creativecommons.org/licenses/by/4.0/). The file attached is the published version of the article.NHM Repositor
Concerto en re mineur pour deux pianos et orchestre FP 61 / Francis Poulenc, comp. ; Francis Poulenc, Jacques Février, p ; Orchestre de la Société des Concerts du Conservatoire ; Georges Prêtre, dir.. Concerto champêtre pour clavecin et orchestre FP 49 / Francis Poulenc, comp. ; Aimée Van de Wiele, clav. ; Orchestre de la Société des Concerts du Conservatoire ; Georges Prêtre, dir.
No full textTitre uniforme : Poulenc, Francis (1899-1963). Compositeur. [Concertos. Pianos (2), orchestre. FP 61. Ré mineur]Titre uniforme : Poulenc, Francis (1899-1963). Compositeur. [Concert champêtre. FP 49]Comprend : Concerto en re mineur pour deux pianos et orchestre FP 61 / Francis Poulenc, comp. ; Francis Poulenc, Jacques Février, p ; Orchestre de la Société des Concerts du Conservatoire ; Georges Prêtre, dir. ; Concerto champêtre pour clavecin et orchestre FP 49 / Francis Poulenc, comp. ; Francis Poulenc, Jacques Février, p ; Orchestre de la Société des Concerts du Conservatoire ; Georges Prêtre, dir.BnF-Partenariats, Collection sonore - BelieveContient une table des matière
Remnants and Revenants: politics and violence in the work of Agamben and Derrida
No full textThis is the peer reviewed version of the following article: Frazer, Elizabeth, and Kimberly Hutchings. "Remnants and revenants: politics and violence in the work of Agamben and Derrida." The British Journal of Politics & International Relations 13.2 (2011): 127-144, which has been published in final form at http://dx.doi.org/10.1111/j.1467-856X.2010.00428.x. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.Jacques Derrida and Giorgio Agamben both consider the question of whether there can be politics without violence, offering contrasting responses. In the case of Agamben, the remnant (that which remains) is disruptive and destabilising of present institutions; in the case of Derrida the revenant, the spectre, promises a future that is open. This reading of the two theories suggests that Derrida's response to the question of politics and violence is more persuasive than Agamben's. But the abstraction of his argument, like the tensions and contradictions in Agamben's, means that we are not hereby furnished with the resources to think politically about violence
Modulation allostérique du récepteur FP dans le cancer colorectal
No full textLes prostaglandines modulent d’importants rôles physiologiques. Elles sont aussi impliquées dans le développement d’une variété de conditions pathologiques telles l’inflammation, la douleur et le cancer. La prostaglandine PGF2α et son récepteur (récepteur FP) se trouvent impliqué dans la modulation de nombreuses pathologies tels lors de l’accouchement préterme et le cancer colorectal. Récemment, nous avons fait partie d’un groupe de recherche ayant développé des modulateurs allostériques du récepteur FP.
Dans une première étude, l’action du PGF2α sur le déclenchement des contractions myométriales a été évaluée, car peu d’information est connue sur la signalisation de cette prostaglandine lors de l’accouchement. Ainsi, nous avons utilisé un peptidomimétique de la deuxième boucle extracellulaire, dénommée PDC113.824. Nos résultats ont démontré que le PDC113.824 permettait de retarder la mise bas chez des souris gestantes, mais agissait de manière différente sur les multiples voies de signalisation de la PGF2α. Ainsi, le PDC113.824 inhibait la voie RhoA-ROCK, dépendante de l’activation de la protéine Gα12 par le. Les protéines RhoA-ROCK sont des acteurs clés dans le remodelage du cytosquelette d’actine et des contractions myométriales lors de l’accouchement. De plus, le PDC113.824 en présence de PGF2α agit comme un modulateur positif sur la voie dépendante de l’activation de la protéine Gαq. Le PDC113.824 serait donc un modulateur allostérique non compétitif possédant des actions à la fois de modulateurs positifs et négatifs sur la signalisation du récepteur FP
Dans une seconde étude, des analogues du PDC113.824 ont été conçus et analysés dans un second modèle pathologique, le cancer colorectal. Ce cancer possède de hauts niveaux de récepteur FP. Nous avons donc étudié le rôle du récepteur FP dans le développement et la progression du cancer colorectal et l’effet de modulateurs allostériques. Il est généralement accepté que dans le cancer colorectal, la prostaglandine PGE2 permet la croissance et l’invasion tumorale, ainsi que l’angiogenèse. Toutefois, peu d’informations sont connues sur le rôle du PGF2α dans le cancer colorectal. C’est dans ce contexte que nous avons décidé d’examiner la contribution de ce récepteur dans la progression du cancer colorectal et cherché à déterminer si la modulation des fonctions du récepteur FP a un impact sur la croissance de tumeurs colorectales. Nos recherches ont révélé que l’activation du récepteur FP permet la migration et la prolifération de plusieurs lignées cellulaires humaines et murines d’adénocarcinomes colorectaux. Dans ce contexte, nos expériences ont démontré que la migration des cellules cancéreuses était dépendante de l’activation de la voie Rho. Nos résultats démontrent qu’en effet, l’activation de RhoA, une petite GTPase clé de la voie Gα12, est inhibée de façon sélective par nos composés. De plus, nos molécules allostériques sont également efficaces pour inhiber la voie de signalisation de la ß-caténine, une protéine impliquée dans la genèse du cancer colorectal. In vivo, le traitement de souris avec un des ces modulateurs a permis une inhibition effective de la croissance tumorale. Dans l’ensemble, nos résultats suggèrent donc que les modulateurs allostériques des récepteurs FP pourraient constituer une nouvelle classe de médicaments utilisés pour le traitement du cancer colorectal.Prostaglandins play many important physiological roles. They are also involved in the development of a variety of pathological conditions such as inflammation, pain and preterm labor. The prostaglandin PGF2α and the FP receptor are implicated in the modulation of many pathological diseases, for example in preterm labor and in colorectal cancer. Our group has recently developed FP receptor allosteric modulators and focused on the role of this receptor and its ligand PGF2α in different models.
In a first study, the action of PGF2α on myometrial contraction was evaluated because there is little information about the pathway signalling regulating these contractions. We used a peptidomimectic whose structure is based on the second extracellular loop of the FP receptor and who is an inhibitor of parturition in mice, the PDC113.824. Our results have demonstrated that PDC113.824 is able to delay parturition in mice, affecting multiple pathways activated by the FP receptor and PGF2α. PDC113.824 inhibited the PGF2α mediated activation of the Gα12 dependent activation of the RhoA-ROCK signalling pathway. RhoA and ROCK proteins are keys actors in the remodelling of actin cytosqueleton and in myometrial contractions. Furthermore, PDC113.824 with the presence of PGF2α acted positively by increasing the activation of the Gαq pathway. Our finding suggests that PDC113.824 is an allosteric modulator with dual actions, acting in a positive and negative way on the FP receptor signalling.
In a second study, analogues of PDC113.824 were made and analysed in a second pathological model, colorectal cancer development and progression. Colorectal cancer seems to posses high levels of FP receptor but it is generally accepted that PGE2 promotes tumor growth, invasion and angiogenesis. However, little is known about the effect of PGF2α in colorectal cancer and only one report has suggested that this prostaglandin can stimulate motility and invasion. Its in this context, whether modulation of FP receptor function can impact colorectal tumors growth remains to be defined. Using our allosteric modulator, we investigated the contribution of FP receptor in the malignant progression of colorectal cancer. Our findings indicate that activation of FP receptors promote migration and proliferation of different human and murine colorectal cell lines. In this context, we demonstrated that this migration was dependent upon the activation of the Rho signalling pathway. Our results indicate that the activation of RhoA, a key small GTPase of the Gα12/13 pathway, is selectively inhibited by our compounds. We also showed that our allosteric modulator could act negatively on the β-catenin pathway, which is a protein with multiple effects on the progression of colorectal cancer. In vivo, treatment of mice with one this allosteric modulator is effective in inhibiting colorectal tumor growth in a xenograph mouse model. Together these findings suggest that PGF2α and the receptor FP, may play a considerable role in the development and progression of colorectal cancer
Characterization of signalling cross-talk between the EP2 and FP receptors in endometrial epithelial cells
No full textUterine fibroids are benign tumors that arise from the smooth-muscle uterine cells (myometrium) and are the most common uterine disorder occurring in as many as 30% of women over 35 years of age. Despite their frequent occurrence, the etiology of uterine fibroids is not well elucidated. Several studies have shown that numerous tumors can be regulated by cyclooxygenase (COX) enzyme products but their role in uterine fibroids is not well established. The initial aim of the study was to determine the expression level of COX enzymes and prostaglandin receptors in fibroids and autologous myometrium samples from women with fibroids. Real-Time reverse-transcriptase polymerase chain reaction (RT-PCR) revealed that the expression of COX enzymes, EP1, EP2 and EP4 prostanoid receptors and prolactin were not significantly altered while the EP3 subtype receptor was significantly down-regulated in fibroids compared to adjacent myometrium samples. The EP3 receptor has a protective role in tumor development suggesting the role for down-regulation of the receptor in uterine fibroids pathology. In addition, the expression of COX enzymes, prostaglandin receptors and prostaglandin-mediated genes were assessed in endometrium samples from women with and without uterine fibroids in different stages of the menstrual cycle. COX-2 and interleukin-8 (IL-8) mRNA expressions were significantly higher in both proliferative stage and early-mid secretory, EP2 receptor and IL-11 were elevated in the proliferative stage, vascular endothelial growth factor (VEGF) was highly expressed in the early-mid secretory phase while FP receptor was up-regulated in all stages of the menstrual cycle in endometrium samples from women with fibroids. These data suggest that up-regulation of COX-2 and prostaglandin receptors (EP2 and FP) in endometrium can induce expression of angiogenic and mitogenic factors such as VEGF, IL-8 and IL-11 which might act in a paracrine manner on neighboring myometrial/fibroid tissue to promote angiogenesis and facilitate tumor growth. XVII Furthermore, since EP2 and FP receptors were up-regulated in the proliferative phase of endometrium from uterine fibroid patients and the receptors are co-expressed in endometrial adenocarcinoma (Ishikawa) cells, this study investigated a possible cross-talk that influences intracellular signalling by using Ishikawa cells stably expressing the EP2 and FP receptors (FPEP2 cells) as a model cell line. Real-Time RT-PCR, Western blot analysis and immunofluorescence microscopy confirmed stable expression of the EP2 and FP receptors in FPEP2 cells localized to the perinuclear and plasma membrane. Using FPEP2 cells, the integrated effect of Butaprost (EP2 receptor ligand) and PGF (FP receptor ligand) co-administration on inositol phosphate (IP3) and adenosine 3-,5-cyclic monophosphate (cAMP) release was assessed to study a possible heterologous-interaction or cross-talk between the EP2 and FP receptors. The study showed that in FPEP2 cells, PGF alone does not alter cAMP production, but in combination with Butaprost augments EP2 receptor-mediated cAMP release. PGF-mediated potentiation of cAMP release was abolished by antagonism of the FP receptor, inhibition of phospholipase C (PLC) and IP3-receptor whereas inhibition of protein kinase C (PKC) had no effect suggesting the cross-talk is mediated by FP receptor activation of IP3 release. Moreover, inhibition of calcium effectors using calmodulin antagonist (W7) or Ca2+/calmodulin-dependent kinase II (CaMK-II) inhibitor (KN-93) abolished PGF potentiation of Butaprost-mediated cAMP release. Using short interfering RNA (siRNA) molecules targeted against the adenylyl cyclase 3 (AC3) isoform, the study showed the isoform to be responsible for the cross-talk between the FP and EP2 receptors. In order to determine the integrative effects of the EP2 and FP receptors co-activation on gene expression, a whole genome array profiling in FPEP2 cells in response to Butaprost and/or PGF was performed. The gene array revealed 228 genes that are regulated by co-activation of the EP2 and FP receptors that are involved in cell morphology, proliferation and differentiation. XVIII In addition, co-activation of EP2 and FP receptors with their respective ligands enhanced or repressed a set of EP2 receptor-regulated genes. One of the genes identified, SAT1 (Spermidine/ N1-acetyltransferase), was regulated by the EP2 and FP receptors cross-talk via the calcium sensitive AC3 isoform. SAT1, with known role in regulation of tumorigenesis was also up-regulated in the proliferative stage of endometrium samples from women with uterine fibroids suggesting the EP2 and FP receptor cross-talk characterized in vitro can also happen in vivo. In conclusion, this study reports that COX-2, EP2 and FP receptors, VEGF, IL-8, IL-11 and SAT1 are up-regulated in endometrium from women with uterine fibroids. These genes play a major role in development of fibroids by facilitating angiogenesis and cell growth and by inhibiting apoptosis via autocrine/paracrine mechanisms. In addition, this study demonstrates that co-activation of the EP2 and FP receptors results in enhanced release of cAMP via the FP receptor-G +-q-Ca2+-calmodulin pathway by activating the calcium-sensitive AC3 isoform and modulates a molecular switch which alters the trans-activation of a subset single-receptor induced genes that have important functions in the pathogenesis of reproductive pathologies
FP-INJECTIVE SEMIRINGS, SEMIGROUP RINGS AND LEAVITT PATH ALGEBRAS
No full textIn this paper we give characterisations of FP-injective semirings (previously termed “exact” semirings in work of the first author). We provide a basic connection between FP-injective semirings and P-injective semirings, and establish that FP-injectivity of semirings is a Morita invariant property. We show that the analogue of the Faith-Menal conjecture (relating FP-injectivity and self-injectivity for rings satisfying certain chain conditions) does not hold for semirings. We prove that the semigroup ring of a locally finite inverse monoid over an FP-injective ring is FP-injective and give a criterion for the Leavitt path algebra of a finite graph to be FP-injective
Alive-FP: Automated Verification of Floating Point Based Peephole Optimizations in LLVM
No full textPeephole optimizations optimize and canonicalize code to enable other optimizations but are error-prone. Our prior research on Alive, a domain-specific language for specifying LLVM’s peephole optimizations, automatically verifies the correctness of integer-based peephole optimizations and generates C++ code for use within LLVM. This paper proposes Alive-FP, an automated verification and code generation framework for floating point based peephole optimizations in LLVM. Alive-FP handles bit precise floating point optimizations and a class of fast-math optimizations involving signed zeros, not-a-number, and infinities. This paper provides multiple encodings for various floating point operations to account for the various kinds of undefined behavior and under-specification in the LLVM’s language reference manual. We have translated all optimizations that belong to this category into Alive-FP. In this process, we have discovered seven wrong optimizations in LLVM.Technical report DCS-TR-72
Impédance d'entrée d'antennes planaires à BIE ou à cavité FP
No full text4 pagesNational audienceRarement abordée dans la littérature, l'étude théorique de l'impédance d'entrée d'une antenne à Bande Interdite Electromagnétique (BIE) ou à cavité Fabry Pérot (FP) est un réel challenge du point de vue mathématique et électromagnétique. Dans ce travail, nous présenterons une méthode originale pour évaluer l'impédance d'entrée d'une source (primaire) cylindrique ou sphérique placée au sein d'une cavité FP ou d'une structure à BIE. La méthode est basée sur la généralisation aux ondes cylindriques (ou sphériques) du développement en onde plane du champ interne de la cavité. Les formules analytiques simples et rigoureuses obtenues permettent d'une part, de mieux comprendre les phénomènes physiques associés aux antennes à BIE ou à cavité FP et d'autre part, de faciliter la conception de ces antennes
Impédance d'entrée d'antennes planaires à BIE ou à cavité FP
No full text4 pagesNational audienceRarement abordée dans la littérature, l'étude théorique de l'impédance d'entrée d'une antenne à Bande Interdite Electromagnétique (BIE) ou à cavité Fabry Pérot (FP) est un réel challenge du point de vue mathématique et électromagnétique. Dans ce travail, nous présenterons une méthode originale pour évaluer l'impédance d'entrée d'une source (primaire) cylindrique ou sphérique placée au sein d'une cavité FP ou d'une structure à BIE. La méthode est basée sur la généralisation aux ondes cylindriques (ou sphériques) du développement en onde plane du champ interne de la cavité. Les formules analytiques simples et rigoureuses obtenues permettent d'une part, de mieux comprendre les phénomènes physiques associés aux antennes à BIE ou à cavité FP et d'autre part, de faciliter la conception de ces antennes
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