Academic literature on the topic 'Achille Duchêne'
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Journal articles on the topic "Achille Duchêne"
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Hyde, Sylvia A., Ida Fløytrup, Sara Glent, Anna-Karin Kroksmark, Betty Salling, Birgit F. Steffensen, Ulla Werlauff, and Mogens Erlandsen. "A randomized comparative study of two methods for controlling Tendo Achilles contracture in Duchenne muscular dystrophy." Neuromuscular Disorders 10, no. 4-5 (June 2000): 257–63. http://dx.doi.org/10.1016/s0960-8966(99)00135-2.
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Śliwińska, Martyna, Anna Rakuś-Kwiatosz, and Katarzyna Wojciechowska. "Duchenne muscular dystrophy diagnosed in infancy – a case report." Pediatria i Medycyna Rodzinna 18, no. 3 (December 30, 2022): 285–89. http://dx.doi.org/10.15557/pimr.2022.0044.
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Duchenne muscular dystrophy is the most common inherited neuromuscular disorder. The onset of myopathic symptoms is observed at an average age of 2.5 years. However, the definitive diagnosis is not reached until between 3 and 5 years of age, indicating a delay in relation to the onset of first symptoms. The diagnosis is confirmed with genetic testing. This paper presents a case of a 6.5-month-old boy with reduced motor activity already in the foetal period, hypertransaminasaemia, constipation and reduced muscle tone. Extensive differential diagnosis of these abnormalities, including genetic testing, confirmed Duchenne muscular dystrophy. Detection of this disease at an early, poorly symptomatic stage offers a chance to achieve better treatment outcomes and improve the patient’s quality of life. Modern gene therapies implemented before irreversible changes are induced by the disease may in the future give the patient a chance to be completely cured. In the presented case, the symptoms of myopathy were present already in foetal life, and the diagnosis was reached at a younger age than the typical age reported in most of the available literature data.
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Ohtsuka, Yoshikazu, Keiko Udaka, Yuichiro Yamashiro, Hideo Yagita, and Ko Okumura. "Dystrophin Acts as a Transplantation Rejection Antigen in Dystrophin-Deficient Mice: Implication for Gene Therapy." Journal of Immunology 160, no. 9 (May 1, 1998): 4635–40. http://dx.doi.org/10.4049/jimmunol.160.9.4635.
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Abstract Duchenne muscular dystrophy is a lethal and common X-linked recessive disease caused by a defect in dystrophin. Normal myoblast transplantation and dystrophin gene transfer have been expected to correct the deficiency in the muscles, but their clinical application has been hampered by the limited preservation of dystrophin-positive myofibers. In this study we investigated the mechanism for immunologic rejection of normal C57BL/10 (B10) myoblasts transplanted into dystrophin-deficient mdx mice, an animal model of Duchenne muscular dystrophy. We found that mdx mice develop CTL specific for dystrophin itself, which were CD8 dominant and restricted by H-2Kb. We identified several antigenic peptides derived from dystrophin that bind to H-2Kb and are recognized by the mdx anti-B10 CTL. Immunologic tolerance against dystrophin was successfully induced by i.v. injection of these peptides before B10 myoblast transplantation, which resulted in sustained preservation of dystrophin-expressing myofibers in mdx mice. These results demonstrate that dystrophin is antigenic in dystrophin-deficient mice and that immunologic regimen would be necessary to achieve the persistent expression of introduced dystrophin in the muscles of dystrophin-deficient individuals.
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Ho, Peggy P., Lauren J. Lahey, Foteini Mourkioti, Peggy E. Kraft, Antonio Filareto, Moritz Brandt, Klas E. G. Magnusson, et al. "Engineered DNA plasmid reduces immunity to dystrophin while improving muscle force in a model of gene therapy of Duchenne dystrophy." Proceedings of the National Academy of Sciences 115, no. 39 (September 4, 2018): E9182—E9191. http://dx.doi.org/10.1073/pnas.1808648115.
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In gene therapy for Duchenne muscular dystrophy there are two potential immunological obstacles. An individual with Duchenne muscular dystrophy has a genetic mutation in dystrophin, and therefore the wild-type protein is “foreign,” and thus potentially immunogenic. The adeno-associated virus serotype-6 (AAV6) vector for delivery of dystrophin is a viral-derived vector with its own inherent immunogenicity. We have developed a technology where an engineered plasmid DNA is delivered to reduce autoimmunity. We have taken this approach into humans, tolerizing to myelin proteins in multiple sclerosis and to proinsulin in type 1 diabetes. Here, we extend this technology to a model of gene therapy to reduce the immunogenicity of the AAV vector and of the wild-type protein product that is missing in the genetic disease. Following gene therapy with systemic administration of recombinant AAV6-microdystrophin to mdx/mTRG2 mice, we demonstrated the development of antibodies targeting dystrophin and AAV6 capsid in control mice. Treatment with the engineered DNA construct encoding microdystrophin markedly reduced antibody responses to dystrophin and to AAV6. Muscle force in the treated mice was also improved compared with control mice. These data highlight the potential benefits of administration of an engineered DNA plasmid encoding the delivered protein to overcome critical barriers in gene therapy to achieve optimal functional gene expression.
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Naidoo, Michael, and Karen Anthony. "Dystrophin Dp71 and the Neuropathophysiology of Duchenne Muscular Dystrophy." Molecular Neurobiology 57, no. 3 (December 13, 2019): 1748–67. http://dx.doi.org/10.1007/s12035-019-01845-w.
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AbstractDuchenne muscular dystrophy (DMD) is caused by frameshift mutations in the DMD gene that prevent the body-wide translation of its protein product, dystrophin. Besides a severe muscle phenotype, cognitive impairment and neuropsychiatric symptoms are prevalent. Dystrophin protein 71 (Dp71) is the major DMD gene product expressed in the brain and mutations affecting its expression are associated with the DMD neuropsychiatric syndrome. As with dystrophin in muscle, Dp71 localises to dystrophin-associated protein complexes in the brain. However, unlike in skeletal muscle; in the brain, Dp71 is alternatively spliced to produce many isoforms with differential subcellular localisations and diverse cellular functions. These include neuronal differentiation, adhesion, cell division and excitatory synapse organisation as well as nuclear functions such as nuclear scaffolding and DNA repair. In this review, we first describe brain involvement in DMD and the abnormalities observed in the DMD brain. We then review the gene expression, RNA processing and functions of Dp71. We review genotype-phenotype correlations and discuss emerging cellular/tissue evidence for the involvement of Dp71 in the neuropathophysiology of DMD. The literature suggests changes observed in the DMD brain are neurodevelopmental in origin and that their risk and severity is associated with a cumulative loss of distal DMD gene products such as Dp71. The high risk of neuropsychiatric syndromes in Duchenne patients warrants early intervention to achieve the best possible quality of life. Unravelling the function and pathophysiological significance of dystrophin in the brain has become a high research priority to inform the development of brain-targeting treatments for Duchenne.
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Starosta, Alicja, and Patryk Konieczny. "Therapeutic aspects of cell signaling and communication in Duchenne muscular dystrophy." Cellular and Molecular Life Sciences 78, no. 11 (April 7, 2021): 4867–91. http://dx.doi.org/10.1007/s00018-021-03821-x.
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AbstractDuchenne muscular dystrophy (DMD) is a devastating chromosome X-linked disease that manifests predominantly in progressive skeletal muscle wasting and dysfunctions in the heart and diaphragm. Approximately 1/5000 boys and 1/50,000,000 girls suffer from DMD, and to date, the disease is incurable and leads to premature death. This phenotypic severity is due to mutations in the DMD gene, which result in the absence of functional dystrophin protein. Initially, dystrophin was thought to be a force transducer; however, it is now considered an essential component of the dystrophin-associated protein complex (DAPC), viewed as a multicomponent mechanical scaffold and a signal transduction hub. Modulating signal pathway activation or gene expression through epigenetic modifications has emerged at the forefront of therapeutic approaches as either an adjunct or stand-alone strategy. In this review, we propose a broader perspective by considering DMD to be a disease that affects myofibers and muscle stem (satellite) cells, as well as a disorder in which abrogated communication between different cell types occurs. We believe that by taking this systemic view, we can achieve safe and holistic treatments that can restore correct signal transmission and gene expression in diseased DMD tissues.
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Marchenko, L. A. "Productivity of garden strawberry and breeding possibilities to improve it." Siberian Herald of Agricultural Science 51, no. 3 (July 29, 2021): 65–74. http://dx.doi.org/10.26898/0370-8799-2021-3-7.
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The information on the productivity trait of garden strawberry Fragaria × ananassa (Duchesne ex Weston) Duchesne ex Rozier has been summarized on the basis of literary sources. The productivity trait has a complex polygenic character. Independent inheritance of individual productivity components allows modeling their optimal combination in a new variety. The creation of highly productive varieties of strawberries is based on intraspecific hybridization. The established positive correlation between the size of berries and the yield indicates the possibility of increasing the productivity of varieties by using large-fruited forms in breeding. At present, in various zones of horticulture, researchers distinguish large-fruited varieties of domestic breeding: ‘Atlas', ‘Bereginya', ‘Vityaz', ‘Grenada', ‘Zabelinskaya', ‘Kemiya', ‘Nashe Podmoscovie', ‘Nelly', ‘Pervoklassnitsa', ‘Rusich', ‘Solnechnaya Polyanka', ‘Solovushka', ‘Festivalnaya Romashka', ‘Fruktovaya', ‘Tsaritsa', ‘Yaponka', and foreign breeding: ‘Alba', ‘Asia', ‘Elsanta', ‘Finesse', ‘Florense', ‘Vivaldi', ‘Galia', ‘Jive', ‘Joly', ‘M. Champion', ‘Merced', ‘Murano', ‘Onda', ‘Roxana', ‘Rumba', ‘Tarda Vicoda', ‘Vima Kimberly', ‘Vima Tarda', ‘Vima Rina', ‘Vima Xima'. It was noted that when using the inbreeding method, it is possible to achieve a heterotic effect on the basis of the productivity trait. The method of genetic modifications of plants is of great importance for breeding of complex quantitative traits of productivity, including yield. Expansion of the genetic base of garden strawberry by means of octoploid and polyploid forms of wild species will ensure an increase in the productivity of new varieties due to the inclusion of traits of adaptability to biotic and abiotic factors in the genotype. The use of modern research methods (screening of the metabolomic and biochemical profile, DNA certification, molecular labeling) increases the objectivity of research and the efficiency of the breeding process.
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Makkar, Raj R., Dean J. Kereiakes, Frank Aguirre, Glenn Kowalchuk, Tarun Chakravarty, Konstantinos Malliaras, Gary S. Francis, et al. "Intracoronary ALLogeneic heart STem cells to Achieve myocardial Regeneration (ALLSTAR): a randomized, placebo-controlled, double-blinded trial." European Heart Journal 41, no. 36 (August 4, 2020): 3451–58. http://dx.doi.org/10.1093/eurheartj/ehaa541.
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Abstract Aims Cardiosphere-derived cells (CDCs) are cardiac progenitor cells that exhibit disease-modifying bioactivity in various models of cardiomyopathy and in previous clinical studies of acute myocardial infarction (MI), dilated cardiomyopathy, and Duchenne muscular dystrophy. The aim of the study was to assess the safety and efficacy of intracoronary administration of allogeneic CDCs in the multicentre, randomized, double-blinded, placebo-controlled, intracoronary ALLogeneic heart STem cells to Achieve myocardial Regeneration (ALLSTAR) trial. Methods and results We enrolled patients 4 weeks to 12 months after MI, with left ventricular ejection fraction (LVEF) ≤45% and LV scar size ≥15% of LV mass by magnetic resonance imaging (MRI). A pre-specified interim analysis was performed when 6-month MRI data were available. The trial was subsequently stopped due to the low probability of detecting a significant treatment effect of CDCs based on the primary endpoint. Patients were randomly allocated in a 2:1 ratio to receive CDCs or placebo in the infarct-related artery by stop-flow technique. The primary safety endpoint was the occurrence, during 1-month post-intracoronary infusion, of acute myocarditis attributable to allogeneic CDCs, ventricular tachycardia- or ventricular fibrillation-related death, sudden unexpected death, or a major adverse cardiac event (death or hospitalization for heart failure or non-fatal MI or need for left ventricular assist device or heart transplant). The primary efficacy endpoint was the relative percentage change in infarct size at 12 months post-infusion as assessed by contrast-enhanced cardiac MRI. We randomly allocated 142 eligible patients of whom 134 were treated (90 to the CDC group and 44 to the placebo group). The mean baseline LVEF was 40% and the mean scar size was 22% of LV mass. No primary safety endpoint events occurred. There was no difference in the percentage change from baseline in scar size (P = 0.51) between CDCs and placebo groups at 6 months. Compared with placebo, there were significant reductions in LV end-diastolic volume (P = 0.02), LV end-systolic volume (P = 0.02), and N-terminal pro b-type natriuretic peptide (NT-proBNP) (P = 0.02) at 6 months in CDC-treated patients. Conclusion Intracoronary infusion of allogeneic CDCs in patients with post-MI LV dysfunction was safe but did not reduce scar size relative to placebo at 6 months. Nevertheless, the reductions in LV volumes and NT-proBNP reveal disease-modifying bioactivity of CDCs. Trial registration Clinicaltrials.gov identifier: NCT01458405.
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Nesmith, Alexander P., Matthew A. Wagner, Francesco S. Pasqualini, Blakely B. O’Connor, Mark J. Pincus, Paul R. August, and Kevin Kit Parker. "A human in vitro model of Duchenne muscular dystrophy muscle formation and contractility." Journal of Cell Biology 215, no. 1 (October 3, 2016): 47–56. http://dx.doi.org/10.1083/jcb.201603111.
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Tongue weakness, like all weakness in Duchenne muscular dystrophy (DMD), occurs as a result of contraction-induced muscle damage and deficient muscular repair. Although membrane fragility is known to potentiate injury in DMD, whether muscle stem cells are implicated in deficient muscular repair remains unclear. We hypothesized that DMD myoblasts are less sensitive to cues in the extracellular matrix designed to potentiate structure–function relationships of healthy muscle. To test this hypothesis, we drew inspiration from the tongue and engineered contractile human muscle tissues on thin films. On this platform, DMD myoblasts formed fewer and smaller myotubes and exhibited impaired polarization of the cell nucleus and contractile cytoskeleton when compared with healthy cells. These structural aberrations were reflected in their functional behavior, as engineered tongues from DMD myoblasts failed to achieve the same contractile strength as healthy tongue structures. These data suggest that dystrophic muscle may fail to organize with respect to extracellular cues necessary to potentiate adaptive growth and remodeling.
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Guiraud, Simon, Benjamin Edwards, Arran Babbs, Sarah E. Squire, Adam Berg, Lee Moir, Matthew J. Wood, and Kay E. Davies. "The potential of utrophin and dystrophin combination therapies for Duchenne muscular dystrophy." Human Molecular Genetics 28, no. 13 (March 5, 2019): 2189–200. http://dx.doi.org/10.1093/hmg/ddz049.
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Abstract Duchenne muscular dystrophy (DMD) is a lethal neuromuscular disorder caused by loss of dystrophin. Several therapeutic modalities are currently in clinical trials but none will achieve maximum functional rescue and full disease correction. Therefore, we explored the potential of combining the benefits of dystrophin with increases of utrophin, an autosomal paralogue of dystrophin. Utrophin and dystrophin can be co-expressed and co-localized at the same muscle membrane. Wild-type (wt) levels of dystrophin are not significantly affected by a moderate increase of utrophin whereas higher levels of utrophin reduce wt dystrophin, suggesting a finite number of actin binding sites at the sarcolemma. Thus, utrophin upregulation strategies may be applied to the more mildly affected Becker patients with lower dystrophin levels. Whereas increased dystrophin in wt animals does not offer functional improvement, overexpression of utrophin in wt mice results in a significant supra-functional benefit over wt. These findings highlight an additive benefit of the combined therapy and potential new unique roles of utrophin. Finally, we show a 30% restoration of wt dystrophin levels, using exon-skipping, together with increased utrophin levels restores dystrophic muscle function to wt levels offering greater therapeutic benefit than either single approach alone. Thus, this combination therapy results in additive functional benefit and paves the way for potential future combinations of dystrophin- and utrophin-based strategies.
Dissertations / Theses on the topic "Achille Duchêne"
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LEGE', ALICE SILVIA. "LES CAHEN D'ANVERS EN FRANCE ET EN ITALIE. DEMEURES ET CHOIX CULTURELS D'UNE LIGNÉE D'ENTREPRENEURS (I CAHEN D'ANVERS IN FRANCIA E IN ITALIA. DIMORE E SCELTE CULTURALI DI UNA DINASTIA DI IMPRENDITORI)." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/726976.
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Founding member of a banking network related to the actual BNP Paribas Group, Meyer Joseph Cahen (1804-1881), adopted the “d’Anvers” when he settled in Paris in 1849. Born in Bonn, of an Ashkenazi family, he made his fortune in the Belgian city to which he associated his name, and he continued his career in France. Owner of Nainville’s castle (Essonne) and of the Petit Hôtel de Villars (Paris), he became a naturalized French citizen in 1865. The next year, he obtained the title of Count, bestowed upon him by the King of Italy Victor-Emmanuel II, thanks to the economic support he offered to the Italian Unification. Nineteen years later, King Humbert I surpassed his predecessor and raised Meyer Joseph’s eldest son, Édouard (1832-1894), to the status of Marquis of Torre Alfina. If his siblings – Emma (1833-1901), Louis (1837-1922), Raphaël (1841-1900) and Albert (1846-1903) – enrooted their pathways in the French capital, the eldest lived between Florence, Naples and Rome: he was one of the great investors involved in the urban renovation of the Italian capital, after the fall of the papacy. In France, as well as in Italy, art, and especially architecture, served to legitimize the recent nobility of a family that wished to express the fullness of its civil rights. As targets of the anti-Semitic press, the Cahen d’Anvers family experienced the consequences of the Dreyfus Affair and the horrors of the racial laws. Before the latter, they adopted what could be defined as a “top-down model of integration”. This thesis focuses on its mechanisms and development. After tracing the patriarch’s origins, it analyses the family’s matrimonial policies and it continues with an exploration of Cahen d’Anvers’ “choices” in the vast field of culture. In their salons, the readers will meet Guy de Maupassant, Paul Bourget, Marcel Proust and Gabriele D’Annunzio, as well as Auguste Renoir and Léon Bonnat. Twelve mansions offered a perfect stage for these intellectual gatherings. As a public manifestation of the family’s economic and social power, the historicist eclecticism of these properties aimed to represent the owners as a new phalanx of the old nobility. While Forge-Philippe’s manor (Wallonia), Gérardmer’s chalet (Vosges) and Villa della Selva (Umbria) expressed a certain openness to the twentieth century novelties, the three residences rented by the family (Hôtel du Plessis-Bellière, Paris; Palazzo Núñez-Torlonia, Rome; Château de la Jonchère, Yvelines) and the two properties of Meyer Joseph, as well as Rue de Bassano’s mansion (Paris) or the castles of Champs (Seine-et-Marne), Bergeries (Essonne) and Torre Alfina (Latium) dressed up their nineteenth century spaces with Ancien Régime motifs. Thanks to their historical knowledge and taste, the architects Destailleur, Giuseppe Partini and Eugène Ricard, as well as the landscapers Henri and Achille Duchêne, were able to bend the Middle Age, the Renaissance and the 18th century’s “grammars” to their patrons’ taste and ambitions.
Books on the topic "Achille Duchêne"
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Dwyer, Michael Middleton. Carolands: Ernest Sanson, Achille Duchêne, Willis Polk. San Mateo, Calif: San Mateo County Historical Association, 2006.
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Claire, Frange, ed. Le style Duchêne: Henri & Achille Duchêne, architectes paysagistes, 1841-1947. Neuilly: Editions du Labyrinthe, 1998.
Find full textBook chapters on the topic "Achille Duchêne"
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"Henri and Achille Duchêne and the Reinvention of Le Nôtre." In The Architecture of Western Gardens: A Design History from the Renaissance to the Present Day. MIT Press, 1991. http://dx.doi.org/10.37862/aaeportal.00122.066.
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