60 research outputs found
Victoria K, Delphine Seyrig et moi ou La petite chaise jaune : un matrimoine en conversion d’archives
No full textLe texte lauréat du Prix RFI Théâtre (2019) Victoria K, Delphine Seyrig et moi ou La petite chaise jaune (2021) de Valérie Cachard s’inscrit dans la mouvance de la « littérature hors du livre » (Rosenthal et Ruffel, 2010 : 4), où l’auteur·trice légitime la réception de son texte à travers une performance narrative. Après avoir interrogé la nature et le bien-fondé des archives intimes de Victoria K, lettres extraites de son journal intime abandonné dans sa maison, l’article s’intéresse aux allers-retours entre la fiction et le réel fictionnel qui systématisent une mémoire solidaire de la guerre civile en apparence fragmentaire. La performance du texte à Beyrouth par la dramaturge et son acolyte artistique Hadi Deaibes tend à éroder les dimensions sociopolitiques de l’archivage au profit d’une hybridation des identités scéniques. Cette contribution, coécrite par Noha Nemer et son amie de longue date Valérie Cachard, propose une réflexion sur l’expropriation discursive, esthétique et scénique d’une littérature intimiste.The award-winning text of the RFI Theater Prize (2019), Victoria K, Delphine Seyrig et moi ou La petite chaise jaune (2021) by Valérie Cachard, falls within the trend of “literature beyond the book” (“littérature hors du livre”; Rosenthal and Ruffel, 2010: 4), where the author legitimizes the reception of their text through a narrative performance. After questioning the nature and validity of the intimate archives of Victoria K – letters taken from her diary left behind in her house – the article focuses on the back-and-forth between fiction and fictional reality, which creates a cohesive memory of the seemingly fragmented civil war. The text’s performance in Beirut by the playwright and her artistic collaborator Hadi Deaibes tends to erode the sociopolitical dimensions of archiving in favor of a hybridization of stage identities. This contribution, co-written by Noha Nemer and her long-time friend Valérie Cachard, offers a reflection on the discursive, aesthetic, and scenic expropriation of intimate literature
Tbx5 et l’adaptation du cœur à la vie sur terre
No full text[No abstract available]Anderson RH, 2003, HEART, V89, P949, DOI 10.1136-heart.89.8.949; Basson CT, 1997, NAT GENET, V15, P30, DOI 10.1038-ng0197-30; Bruneau BG, 2001, CELL, V106, P709, DOI 10.1016-S0092-8674(01)00493-7; Contreras-Ramos A, 2008, ANAT HISTOL EMBRYOL, V37, P344, DOI 10.1111-j.1439-0264.2008.00852.x; delaCruz MV, 1997, ANAT REC, V247, P512, DOI 10.1002-(SICI)1097-0185(199704)247:4512::AID-AR103.0.CO;2-S; Koshiba-Takeuchi K, 2009, NATURE, V461, P95, DOI 10.1038-nature08324; Nemer M, 2008, CARDIOVASC PATHOL, V17, P48, DOI 10.1016-j.carpath.2007.06.005; Wyneken Jeanette, 2009, Veterinary Clinics of North America Exotic Animal Practice, V12, P51, DOI 10.1016-j.cvex.2008.08.0010
T-box factors: Insights into the evolutionary emergence of the complex heart
No full textThe heart as a functional organ first appeared in bilaterians as a single peristaltic pump and evolved through arthropods, fish, amphibians, and finally mammals into a four-chambered engine controlling blood-flow within the body. The acquisition of cardiac complexity in the evolving heart was a product of gene duplication events and the co-option of novel signaling pathways to an ancestral cardiac-specific gene network. T-box factors belong to an evolutionary conserved family of transcriptional regulators with diverse roles in development. Their regulatory functions are integral in the initiation and potentiation of heart development, and mutations in these genes are associated with congenital heart defects. 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Panniculitis ossificans traumatica of the neck region: Report of a rare case in an unusual location
No full textPanniculitis ossificans is a rare, self-limiting form of heterotopic ossification that might involve the subcutis as a reaction to trauma. To the best of the author′s knowledge, there is no published report in the English literature describing such a case in the neck region. Herein is a report of a 47-year-old male who presented with a well-circumscribed firm mass in the supraclavicular area, a location that led to clinical suspicion of lymphoma. Definite pathological diagnosis was made after excision and no further interventions were needed. Awareness of this pseudomalignant condition is crucial for the clinician, radiologist and pathologist to avoid a diagnosis of malignancy
Differential duplication of an intronic region in the NFATC1 gene in patients with congenital heart disease
No full textMost forms of congenital heart disease (CHD) result from aberrations in cardiac morphogenesis including errors in septation, valve formation, and proper patterning of the great vessels. Transcription factors are key proteins that dictate mRNA synthesis rate and subsequent protein production in most eukaryotes. NFATC1 belongs to the Rel family of transcription factors. In mice, it is expressed in the embryonic heart and is restricted to the endocardium where it plays a major role in valve formation. To establish a role for NFATC1 in CHD, we started screening for mutations in the exons encoding the DNA-binding domain of NFATC1 in patients enrolled in our study on CHD in Lebanon. DNA was extracted from patients with pulmonary stenosis (PS), tricuspid atresia (TA) and ventricular septal defect (VSD). PCR amplification and DNA sequencing were done on the patients and their parents and (or) siblings. PCR amplification of the exon 7 region showed that 2 bands are obtained in 57percent of patients with CHD (32-56) and in 45percent of their healthy parents and (or) siblings. Sequencing of the 2 bands revealed that both are amplicons of the exon 7 region, and that the additional band harbors an additional 44 nucleotides segment in the intronic region. The homozygous form of this allele was only present in patients with VSD (2-21). A screen of a pool of 81 healthy, unrelated individuals showed no presence for the homozygous form of this allele, suggesting that NFATC1 is a potential VSD-susceptibility gene. © 2006 NRC.Basson CT, 1997, NAT GENET, V15, P30, DOI 10.1038-ng0197-30; Bitar F F, 2001, J Med Liban, V49, P304; Bruneau BG, 2001, CELL, V106, P709, DOI 10.1016-S0092-8674(01)00493-7; Chang CP, 2004, CELL, V118, P649, DOI 10.1016-j.cell.2004.08.010; Crispino JD, 2001, GENE DEV, V15, P839, DOI 10.1101-gad.875201; de la Pompa JL, 1998, NATURE, V392, P182; DLOTT B, 1990, J BIOL CHEM, V265, P17921; Donovan J, 2002, CURR BIOL, V12, P1605, DOI 10.1016-S0960-9822(02)01149-1; Eldadah ZA, 2001, HUM MOL GENET, V10, P163, DOI 10.1093-hmg-10.2.163; Garg V, 2003, NATURE, V424, P443, DOI 10.1038-nature01827; Goldmuntz E, 2001, CLIN PERINATOL, V28, P1, DOI 10.1016-S0095-5108(05)70067-1; GRAETZEL M, 1999, CATECH, V3, P4; Gruber PJ, 2004, CIRC RES, V94, P273, DOI 10.1161-01.RES.0000116144.43797.3B; Johnson EN, 2003, J BIOL CHEM, V278, P1686, DOI 10.1074-jbc.M210250200; Kumar P, 2000, EDN, V45, P127; Lange AW, 2004, DEV BIOL, V266, P346, DOI 10.1016-j.ydbio.2003.10.036; Lin CR, 1999, NATURE, V401, P279; Mani A, 2002, P NATL ACAD SCI USA, V99, P15054, DOI 10.1073-pnas.192582999; Molkentin JD, 1998, CELL, V93, P215, DOI 10.1016-S0092-8674(00)81573-1; Molkentin JD, 1997, GENE DEV, V11, P1061, DOI 10.1101-gad.11.8.1061; Musaro A, 1999, NATURE, V400, P581; Nabulsi MM, 2003, AM J MED GENET A, V116A, P342, DOI 10.1002-ajmg.a.10020; Nemer G, 2002, DEVELOPMENT, V129, P4045; Nemer G, 2001, ANN MED, V33, P604, DOI 10.3109-07853890109002106; Nemer Georges, 2006, Hum Mutat, V27, P293, DOI 10.1002-humu.9410; Pizzuti A, 2003, HUM MUTAT, V22, P372, DOI 10.1002-humu.10261; Ranger AM, 1998, NATURE, V392, P186; Robbins J, 2004, J MOL CELL CARDIOL, V36, P643, DOI 10.1016-j.yjmcc.2004.02.012; Schott JJ, 1998, SCIENCE, V281, P108, DOI 10.1126-science.281.5373.108; Serfling E, 2000, BBA-MOL CELL RES, V1498, P1, DOI 10.1016-S0167-4889(00)00082-3; Srivastava D, 1999, CURR OPIN CARDIOL, V14, P263, DOI 10.1097-00001573-199905000-00011; Srivastava D, 2000, NATURE, V407, P221, DOI 10.1038-35025190; Svensson EC, 2000, NAT GENET, V25, P353; Yagi H, 2003, LANCET, V362, P1366, DOI 10.1016-S0140-6736(03)14632-613141
Identification of new GATA4-small molecule inhibitors by structure-based virtual screening
No full textMembers of the GATA family of transcription factors are zinc finger proteins that were shown to play evolutionary conserved roles in cell differentiation and proliferation in different organisms. We hypothesized that by finding new molecules that inhibit their function to be crucial in future therapeutical interventions for various diseases. By virtual high throughput screening using a version of glide (Schrodinger®) program with both crystal and NMR structure of GATA C-terminal zinc finger, we identified new small molecular weight chemicals with lead-like properties. We used in vitro cell-based assays to show that these molecules selectively and efficiently inhibit GATA4 activity by inhibiting its interaction with the DNA. In addition we showed that these molecules can block the activation of downstream target genes by GATA4. Moreover these compounds can moderately enhanced a mouse model of myoblast differentiation into myotubes. This might be partially due to decreased GATA4-DNA interaction as shown by gel retardation assays. Further investigation is needed to reach selectivity and efficacy. Our study however do show that in silico screening combined with in vitro studies are efficient tools to unravel new molecules that interact with zinc finger proteins such as GATA4. © 2011 Elsevier Ltd. All rights reserved.Abba MC, 2006, BREAST CANCER RES, V8, DOI 10.1186-bcr1617; Agnihotri S, 2009, ONCOGENE, V28, P3033, DOI 10.1038-onc.2009.159; Aries A, 2004, P NATL ACAD SCI USA, V101, P6975, DOI 10.1073-pnas.0401833101; Bates DL, 2008, J MOL BIOL, V381, P1292, DOI 10.1016-j.jmb.2008.06.072; Boidot R, 2010, ONCOGENE, V29, P2577, DOI 10.1038-onc.2009.525; Burch JBE, 2005, SEMIN CELL DEV BIOL, V16, P71, DOI 10.1016-j.semcdb.2004.10.002; Cai KQ, 2009, PLOS ONE, V4, DOI 10.1371-journal.pone.0006454; Capo-Chichi CD, 2009, MOL CELL BIOL, V29, P4766, DOI 10.1128-MCB.00087-09; Charron F, 2001, GENE DEV, V15, P2702, DOI 10.1101-gad.915701; Charron F, 1999, SEMIN CELL DEV BIOL, V10, P85, DOI 10.1006-scdb.1998.0281; Fu BJ, 2007, CANCER BIOL THER, V6, P1546; Georges R, 2008, MOL CELL BIOL, V28, P4052, DOI 10.1128-MCB.02100-07; Guo MZ, 2006, INT J CANCER, V119, P2078, DOI 10.1002-ijc.22092; Irwin JJ, 2005, J CHEM INF MODEL, V45, P177, DOI 10.1021-ci049714+; Kentsis A, 2004, P NATL ACAD SCI USA, V101, P18105, DOI 10.1073-pnas.0406927102; Kim BH, 2010, BRIT J HAEMATOL, V148, P132, DOI 10.1111-j.1365-2141.2009.07925.x; Kodo K, 2009, P NATL ACAD SCI USA, V106, P13933, DOI 10.1073-pnas.0904744106; Kyronlahti A, 2008, ENDOCRINOLOGY, V149, P5635, DOI 10.1210-en.2008-0148; Lowry JA, 2000, J MOL EVOL, V50, P103; Mott BH, 2004, BIOCHEM BIOPH RES CO, V316, P910, DOI 10.1016-j.bbrc.2004.02.142; Nemer Georges, 2006, Hum Mutat, V27, P293, DOI 10.1002-humu.9410; OMICHINSKI JG, 1993, SCIENCE, V261, P438, DOI 10.1126-science.8332909; Piccagli L, 2009, CHEMMEDCHEM, V4, P2024, DOI 10.1002-cmdc.200900362; Riazi AM, 2005, J BIOL CHEM, V280, P10716, DOI 10.1074-jbc.M500028200; Rojas A, 2008, MOL CELL BIOL, V28, P5420, DOI 10.1128-MCB.00717-08; Siddiquee K, 2007, P NATL ACAD SCI USA, V104, P7391, DOI 10.1073-pnas.0609757104; Trainor CD, 2000, J BIOL CHEM, V275, P28157; Van E.H., 2000, NATURE, V406, P419; Vonderfecht TR, 2008, BIOCHEM BIOPH RES CO, V369, P1052, DOI 10.1016-j.bbrc.2008.02.136; Zhang SJ, 2009, LEUKEMIA RES, V33, P1141, DOI 10.1016-j.leukres.2009.02.0250
Le romanesque chanté dans l’œuvre bipolaire d’Yves Simon : du transfert générique comme ré(é)criture
No full textYves Simon occupe une place inédite dans la littérature et dans la chanson française. Depuis trois décennies, l’auteur fréquente deux mondes qui ne se connaissent que de loin et dont il constitue l’une des rares passerelles. Cette place inédite amène Simon à l’assumer suivant une esthétique de la réception qui lui est propre : « J’ai vu dans des salons du livre des gens qui ne savaient pas que je suis chanteur et d’autres qui découvraient là que j’écris. L’idéal est que les choses se joignent..
La chanson dans l’œuvre écrite de Mathias Malzieu : métamorphose de la fiction ou fiction de la métamorphose ?
No full textDepuis une dizaine d’années, Mathias Malzieu, le chanteur et musicien du groupe rock Dyonisus, a entamé une carrière d’écrivain originale. S’inspirant à la fois du roman victorien et du conte picaresque, il réussit à évoquer d’un récit à l’autre un univers qui tient son enchantement d’une triple imbrication du fantastique dans le merveilleux, du merveilleux dans le quotidien et du quotidien dans le surnaturel. Outre son recueil de nouvelles 38 mini westerns (2003), ses trois romans Maintenant qu’il fait tout le temps nuit sur toi (2005), La Mécanique du cœur (2007) et Métamorphose en bord de ciel (2011) ont en commun de mettre en scène des personnages mélomanes qui subissent des rites de passage cruciaux, des métamorphoses allégoriques. La chanson accompagne souvent ces rites, occupant des places stratégiques dans le récit qui en dynamisent le schéma narratif et parcellisent l’histoire en trois genres (autobiographie, conte, roman).La portée narratologique de la chanson est d’autant plus significative qu’elle immunise “ces romans pour grands enfants” à la Roald Dahl contre toute restriction générique. En effet, chacune de ces trois parutions romanesques est suivie d’un album musical correspondant dont deux – Monsters in love (2005) et Bird’nRoll (2012) – mettent en voix les avatars infantilisés du personnage victorien Jack l’Éventreur à partir duquel se construit la trame de ces métamorphoses initiatiques.En partant de cette fonction de la chanson comme transfert en tant qu’instance métamorphosant les personnages des romans, et neutralisant le registre pathétique par le merveilleux, je montrerai à travers le conte musical La Mécanique du cœur (2007) inspiré du roman du même titre, que cette fonction de transfert est la source des métamorphoses génériques et de leurs appareils énonciatifs
Familial Hypercholesterolemia: The Lipids or the Genes?
No full textAbstract Familial Hypercholesterolemia (FH) is a common cause of premature cardiovascular disease and is often undiagnosed in young people. Although the disease is diagnosed clinically by high LDL cholesterol levels and family history, to date there are no single internationally accepted criteria for the diagnosis of FH. Several genes have been shown to be involved in FH; yet determining the implications of the different mutations on the phenotype remains a hard task. The polygenetic nature of FH is being enhanced by the discovery of new genes that serve as modifiers. Nevertheless, the picture is still unclear and many unknown genes contributing to the phenotype are most likely involved. Because of this evolving polygenetic nature, the diagnosis of FH by genetic testing is hampered by its cost and effectiveness. In this review, we reconsider the clinical versus genetic nomenclature of FH in the literature. After we describe each of the genetic causes of FH, we summarize the known correlation with phenotypic measures so far for each genetic defect. We then discuss studies from different populations on the genetic and clinical diagnoses of FH to draw helpful conclusions on cost-effectiveness and suggestions for diagnosis.</p
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