Relevant bibliographies by topics / Dystrophie musculaire de Becker

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Academic literature on the topic 'Dystrophie musculaire de Becker'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Dystrophie musculaire de Becker"

1

Opoko, A. P., A. Labied, S. El Moussaoui, and G. Belmejdoub. "Dystrophie musculaire de Becker et acromégalie : association fortuite." Annales d'Endocrinologie 75, no. 5-6 (October 2014): 424. http://dx.doi.org/10.1016/j.ando.2014.07.514.

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Dahimène, Fayçal, Julien Durigneux, Aleksandra Nadaj, Sandra Mercier, Yann Péréon, and Armelle Magot. "Cas clinique 3 : dystrophie musculaire de Becker et atteinte cognitive." Revue Neurologique 174 (April 2018): S179. http://dx.doi.org/10.1016/j.neurol.2018.02.052.

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Magot, A., S. Mercier, and Y. Péréon. "Particularités de la dystrophie musculaire de Becker et des femmes conductrices." Archives de Pédiatrie 22, no. 12 (December 2015): 12S31–12S36. http://dx.doi.org/10.1016/s0929-693x(16)30006-9.

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4

Lescaut, W., C. Butori, M. H. Soriani, and C. Desnuelles. "À propos de quatre cas féminins de dystrophie musculaire de Duchenne et Becker." La Revue de Médecine Interne 25, no. 6 (June 2004): 464–67. http://dx.doi.org/10.1016/j.revmed.2004.03.001.

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Allart, M. E., M. N. Olivier, V. Wieczorek, H. Hovart, A. Thevenon, and V. Tiffreau. "Évaluation de l’oxygénation musculaire à l’effort chez des patients porteurs de dystrophie musculaire de Becker par la spectroscopie du proche infrarouge (NIRS)." Annals of Physical and Rehabilitation Medicine 54 (October 2011): e152. http://dx.doi.org/10.1016/j.rehab.2011.07.523.

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Tselikas, L., E. Rodrigues, M. Jammal, K. Tiev, C. Chayet, L. Josselin-Mahr, M. Gain, C. Toledano, J. Cabane, and A. Kettaneh. "Dystrophie musculaire de Becker à révélation tardive. À propos d’un nouveau patient et de 12 observations de la littérature." La Revue de Médecine Interne 32, no. 3 (March 2011): 181–86. http://dx.doi.org/10.1016/j.revmed.2010.10.353.

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7

Srivastava, Niraj Kumar, Somnath Mukherjee, and Vijay Nath Mishra. "Metabolic Disturbance in Patients with Muscular Dystrophy and Reflection of Altered Enzyme Activity in Dystrophic Muscle: One Critical View." Journal of Biomedical Research & Environmental Sciences 1, no. 8 (December 2020): 393–403. http://dx.doi.org/10.37871/jbres1171.

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Muscular dystrophies are inherited myogenic diseases and considered by progressive muscle wasting and weakness with variable distribution and severity. The essential characteristics of muscular dystrophies are selective involvement, significant wasting and weakness of muscles. The most common and frequent types of muscular dystrophies are Duchenne Muscular Dystrophy (DMD), Becker Muscular Dystrophy (BMD), Facioscapulohumeral Dystrophy (FSHD) and Limb Girdle Muscular Dystrophy (LGMD). Metabolic disturbance is observed in muscular dystrophy patients (DMD, BMD, FSHD and LGMD-2B). Alteration in the level of metabolites (BCAA, Glu/ Gln, Ace, alanine, glucose, histidine, propionate, tyrosine and fumarate) in dystrophic muscle reflects the alteration in the activity of enzymes. Collectively, these observations propose that there is alteration in the rate of glycolysis, TCA cycle, fatty acid oxidation, gluconeogenesis pathway and protein metabolism (catabolism & anabolism) in the muscular dystrophy patients. Metabolic disturbance, further provide the explanation about the pathophysiology of muscular dystrophy.
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8

Teramoto, Naomi, Hidetoshi Sugihara, Keitaro Yamanouchi, Katsuyuki Nakamura, Koichi Kimura, Tomoko Okano, Takanori Shiga, et al. "Pathological evaluation of rats carrying in-frame mutations in the dystrophin gene: a new model of Becker muscular dystrophy." Disease Models & Mechanisms 13, no. 9 (August 28, 2020): dmm044701. http://dx.doi.org/10.1242/dmm.044701.

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ABSTRACTDystrophin, encoded by the DMD gene on the X chromosome, stabilizes the sarcolemma by linking the actin cytoskeleton with the dystrophin-glycoprotein complex (DGC). In-frame mutations in DMD cause a milder form of X-linked muscular dystrophy, called Becker muscular dystrophy (BMD), characterized by the reduced expression of truncated dystrophin. So far, no animal model with in-frame mutations in Dmd has been established. As a result, the effect of in-frame mutations on the dystrophin expression profile and disease progression of BMD remains unclear. In this study, we established a novel rat model carrying in-frame Dmd gene mutations (IF rats) and evaluated the pathology. We found that IF rats exhibited reduced expression of truncated dystrophin in a proteasome-independent manner. This abnormal dystrophin expression caused dystrophic changes in muscle tissues but did not lead to functional deficiency. We also found that the expression of additional dystrophin named dpX, which forms the DGC in the sarcolemma, was associated with the appearance of truncated dystrophin. In conclusion, the outcomes of this study contribute to the further understanding of BMD pathology and help elucidate the efficiency of dystrophin recovery treatments in Duchenne muscular dystrophy, a more severe form of X-linked muscular dystrophy.
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9

Sarkozy, Anna, Mariacristina Scoto, Francesco Muntoni, and Joana Domingos. "Dystrophinopathies and Limb-Girdle Muscular Dystrophies." Neuropediatrics 48, no. 04 (April 20, 2017): 262–72. http://dx.doi.org/10.1055/s-0037-1601860.

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AbstractMuscular dystrophies are a heterogeneous group of inherited diseases. The natural history of these disorders along with their management have changed mainly due to a better understanding of their pathophysiology, the evolution of standards of care, and new treatment options. Dystrophinopathies include both Duchenne's and Becker's muscular dystrophies, but in reality they are a spectrum of muscle diseases caused by mutations in the gene that encodes the protein dystrophin. Duchenne's muscular dystrophy is the most common form of inherited muscle disease of childhood. The current standards of care considerably prolong independent ambulation and survival. Several therapeutic options either aiming at substituting/correcting the primary protein defect or limiting the progression of the dystrophic process are currently being explored in clinical trials.Limb-girdle muscular dystrophies (LGMDs) are rare and heterogeneous conditions, characterized by weakness and wasting of the pelvic and shoulder girdle muscles. Originally classified into dominant and recessive, > 30 genetic forms of LGMDs are currently recognized. Further understanding of the pathogenic mechanisms of LGMD will help identifying novel therapeutic approaches that can be tested in clinical trials.
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10

Bellayou, Hanane, Khalil Hamzi, Mohamed Abdou Rafai, Mehdi Karkouri, Ilham Slassi, Houssine Azeddoug, and Sellama Nadifi. "Duchenne and Becker Muscular Dystrophy: Contribution of a Molecular and Immunohistochemical Analysis in Diagnosis in Morocco." Journal of Biomedicine and Biotechnology 2009 (2009): 1–5. http://dx.doi.org/10.1155/2009/325210.

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Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are X-linked recessive disorders caused by mutations of the DMD gene located at Xp21. In DMD patients, dystrophin is virtually absent; whereas BMD patients have 10% to 40% of the normal amount. Deletions in the dystrophin gene represent 65% of mutations in DMD/BMD patients. To explain the contribution of immunohistochemical and genetic analysis in the diagnosis of these dystrophies, we present 10 cases of DMD/BMD with particular features. We have analyzed the patients with immunohistochemical staining and PCR multiplex to screen for exons deletions. Determination of the quantity and distribution of dystrophin by immunohistochemical staining can confirm the presence of dystrophinopathy and allows differentiation between DMD and BMD, but dystrophin staining is not always conclusive in BMD. Therefore, only identification involved mutation by genetic analysis can establish a correct diagnosis.
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Dissertations / Theses on the topic "Dystrophie musculaire de Becker"

1

Gaïda, Philippe. "Dystrophie musculaire de Becker : étude d'une série de 31 patients." Bordeaux 2, 1996. http://www.theses.fr/1996BOR23051.

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Robert, Bernard. "La myopathie de becker : donnees classiques et actuelles ; a propos de 60 observations." Lyon 1, 1988. http://www.theses.fr/1988LYO1M473.

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LANG, CATHERINE. "Aspects moleculaires des myopathies de duchenne et de becker." Strasbourg 1, 1994. http://www.theses.fr/1994STR15058.

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Guilbaud, Marine. "Identification d'ARNs non-codants impliqués dans les dystrophinopathies." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS042/document.

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Les dystrophies musculaires de Duchenne (DMD) et de Becker (BMD) sont dues à des mutations dans le gène DMD codant la Dystrophine. De nombreux aspects des mécanismes pathophysiologiques de ces maladies ne sont pas encore expliqués. Nous nous sommes intéressés à l'étude d'ARN non-codants pouvant participer à ces processus. Une première étude a été centrée sur l’identification de micro-ARNs (miARNs) impliqués dans la régulation de l’oxyde nitrique synthase neuronale (nNOS) une protéine partenaire de la Dystrophine et associée à des caractéristiques de ces pathologies telles que la fatigabilité musculaire. 617 miARNs ont été criblés par Taqman Low Density Array dans des muscles de sujets sains et de patients BMDdel45-55. 4 miARNs candidats ont été sélectionnés de cette étude pour leur surexpression chez les patients BMDdel45-55 et leur capacité théorique à cibler nNOS. Des expériences de modulation de l’expression de ces miARNs dans des myoblastes humains sains ou dystrophiques nous ont permis d’identifier que le miR-708-5p et le miR-34-5p pouvaient cibler nNOS et moduler son expression.Un deuxième axe a été mené sur l’étude des longs ARNs non-codants (lncARNs). Les introns 44 et 55, qui bornent les exons 45 à 55 délétés chez les patients BMDdel45-55, sont de grandes régions contenant des lncARNs décrits comme régulant la Dystrophine. Les points de cassure introniques des mutations de ces patients n’étant pas décrites, nous avons supposé l’existence de profils de lncARNs différents. L’analyse de l’ADN de ces patients montre en effet des profils de lncARNs différents, révélant ainsi l’importance d’une étude plus précise des zones de délétion des patients BMDdel45-55
Duchenne (DMD) and Becker (BMD) muscular dystrophies are due to mutations in DMD gene, encoding Dystrophin. Many aspects of pathophysiological mechanisms of these diseases are not yet well understood. We were interested in the study of non-coding RNAs that could be involved in these pathological processes. A first study focused on micro-RNAs (miRNAs) that could modulate expression of the neuronal nitric oxide synthase (nNOS), a partner of Dystrophin which is linked to pathological features as muscular fatigability. 617 miRNAs were screened by Taqman Low Density Array in muscle biopsies of healthy subjects or BMDdel45-55 patients. 4 candidate miRNAs were selected from this study since they were overexpressed in BMDdel45-55 patients and for their theoretical ability to target nNOS. Experiments modulating the expression of these miRNAs in healthy or dystrophic human myoblasts enabled us to identify that miR-708-5p and miR-34-5p could target nNOS and modulate its expression.A second axis was conducted on long non-coding RNA (lncRNA). Introns 44 and 55, which bound exons 45-55 deleted in BMDdel45-55 patients, are large regions containing lncRNAs described as regulating Dystrophin. Since intronic breakpoints of DMD mutations of these pateints were not described, we have assumed the existence of different profiles of lncRNAs. DNA analysis of these patients actually showed different lncRNAs profiles, thus revealing the significance of a more precise analysis of deletion areas in DMD gene of BMDdel45-55 patients
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Humbertclaude, Véronique. "Variabilité phénotypique et corrélations génotype – phénotype des dystrophinopathies : contribution des banques de données." Thesis, Montpellier 1, 2011. http://www.theses.fr/2011MON1T028/document.

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L'objectif de ce travail est de développer la partie clinique de la banque de données du gène DMD, afin d'étudier l'histoire naturelle des dystrophinopathies et les corrélations génotype–phénotype, et de faciliter la sélection des patients pour les futurs essais thérapeutiques. La méthodologie créée pour le gène DMD peut être généralisée et utilisée pour d'autres banques de données dédiées à des maladies génétiques. La collecte de 70 000 données cliniques chez 600 patients avec un suivi longitudinal moyen de 12 ans permet de décrire l'histoire naturelle des dystrophies musculaires de Duchenne et de Becker et des formes symptomatiques chez les femmes. Nous avons pu préciser l'hétérogénéité phénotypique sur le plan moteur, orthopédique et respiratoire (forme sévère et forme intermédiaire de la dystrophie musculaire de Duchenne), sur le plan cardiaque (absence de corrélation entre les atteintes motrice et cardiaque, variabilité de l'atteinte cardiaque), et sur le plan cérébral (atteinte intellectuelle chez les patients avec dystrophie musculaire de Becker, troubles psychologiques des dystrophinopathies). L'utilisation de cet outil par les cliniciens et les généticiens devrait faciliter le travail de recherche clinique et la réalisation des futurs essais cliniques. Ceci nécessite maintenant de développer l'accessibilité de la banque de données et d'envisager sa pérennisation
The objective of this work is to develop the clinical part of the French dystrophinopathy data-base, in order to study the natural history and the genotype-phenotype correlations, and to facilitate the selection of the patients for the future therapeutic trials. The methodology developed for the DMD gene can be generalized and used for the other databases dedicated to genetic diseases. The collection of 70 000 clinical data for 600 patients with an average lon-gitudinal follow-up of 12 years allows to clarify the natural history of the muscular dystrophies of Duchenne and Becker and in symptomatic females. We were able to specify the pheno-typic heterogeneity of the motor, orthopaedic and respiratory involvements (severe form and intermediary form of the Duchenne muscular dystrophy), of the cardiac disorder (absence of correlation between motor and cardiac involvements, variability of the cardiomyopathy), and of the brain function (mental deficiency in the patients with Becker muscular dystrophy, psychological disorders in dystrophinopathies). The use of this tool by the clinicians and the ge-neticists should facilitate their clinical research work and the realization of the future clinical trials. This requires now to develop the accessibility of the database and to ensure its continued existence
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Couillandre, Annabelle. "Incidence de la posture initiale sur la programmation de la marche : contrôle du centre des masses lors de l'initiation de la marche sur l'avant-pied." Paris 11, 2002. http://www.theses.fr/2002PA112296.

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Par rapport à un objectif vitesse, la progression du corps au cours de l'initiation de la marche (IM) résulte du contrôle des forces gravitaires par les forces musculaires et du choix des paramètres locomoteurs. Dans ce travail, nous utilisons le modèle d'analyse de l'IM pour comprendre l'incidence de la posture initiale sur la programmation de la marche: d'une part, chez le sujet sain à qui on impose une posture, talons décollés du sol et d'autre part, chez le sujet avec la Dystrophie Musculaire de Becker (BMD), qui présente fréquemment naturellement cette posture. Celle-ci a pour conséquence de réduire la base posturale, restreindre l'amplitude de recul du centre des pressions des pieds (CP) au cours des Ajustements Posturaux Anticipateurs (APA). En associant les techniques dynamique, électromyographique (EMG) et dynamométrique, nous mettons en évidence, dans chacune des phases de l'IM, des modifications mais aussi des invariances des paramètres biomécaniques et EMG. Le contrôle des forces gravitaires par les forces musculaires chez le sujet sain adoptant la posture, talons décollés du sol diffère de celui mis en évidence chez le sujet présentant la BMD. Cette différence de contrôle est à l'origine de la perturbation de la séquence motrice normalement observée. Chez le sujet adoptant la posture, talons décollés du sol comme chez le patient, des synergies musculaires autres que celles normalement observées assistent la mise en place de cette séquence motrice, dans le but de conserver des APA adéquats pour la progression. Ceux-ci préparent la configuration posturale pour le mouvement à venir, assistent la performance motrice et présentent des caractéristiques dépendant des paramètres de la posture et du mouvement. De plus, l'ajustement entre vitesse du centre de gravité et du CP traduit des adaptations du schéma corporel dynamique. La stratégie de modulation de la vitesse du CP permet de discerner un comportement locomoteur spécifique des contraintes posturales
According to a velocity objective, body progression during gait initiation results from a control of the gravity forces by the muscular forces and a choice of the locomotor parameters. In this study, we use a gait initiation analysis model in order to understand the incidence of the initial posture on gait programming: on one hand, on the healthy subject to whom a heel-off posture is imposed and on the other hand, on the subject with Becker Muscular Dystrophy (BMD), who naturally frequently displays this posture. This latter consequently reduces the postural basis, limits the centre of foot pressure (CP) backward shift during the Anticipatory Postural Adjustments (APA). Using dynamic, electromyographical (EMG) and dynamometric techniques, we show, in each of the gait initiation phases, some modifications but also some invariances of the biomechanical and EMG parameters. The control of the gravity forces by the muscular forces in the healthy subject, adopting the heel-off posture differs from the one displayed by the subject with BMD. This difference of control is at the origin of the perturbation on the motor sequence normally observed. In the healthy subject adopting the heel-off posture as well as in the patient, muscular synergies other than the ones normally observed assist the occurence of this motor sequence in order to preserve appropriate APA for progression. These prepare the postural configuration for the forthcoming movement, assist the motor performance and present characteristics in relation with the parameters of the posture and movement. Moreover, the adjustement between centre of gravity and CP velocities may represent adaptations of the dynamic body scheme. The strategy of CP velocity modulation allows to distinguish a locomotor behaviour specific to the postural constraints
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7

Vincent, Lacaze Nathalie. "Expression du gène de la dystrophine et perspectives thérapeutiques des dystrophines musculaires de Duchenne et de Becker." Paris 5, 1996. http://www.theses.fr/1996PA05CD12.

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Le gène de la dystrophine dont l'atteinte est responsable de la dystrophie musculaire de Duchenne (DMD) code pour un transcrit musculaire de 14 kilobases et pour une famille de transcrits issus de promoteurs et/ou d'épissages alternatifs. Il existe une hétérogénéité des manifestations cliniques associées à la présence de mutations dans le gène de la dystrophine qui incitent à rechercher un ou plusieurs autres gènes non encore caractérisés tout entiers contenus dans une des introns de ce gène, ou intriqués avec lui. Nous avons caractérisé différents transcrits initiés à partir d'un promoteur alternatif localisé dans l'intron 62. Le criblage de banques d' ADNc de foie et de lymphocytes humains ne nous a pas permis de mettre en évidence de nouveaux transcrits alternatifs. Afin d'élargir la recherche à des transcrits totalement distincts de ceux déjà connus, nous avons entrepris d'utiliser la sélection d' ADNc par hybridation sur des chromosomes artificiels de levures (YAC). Nous avons utilisé des fragments de PCR-Alu obtenus à partir d'un YAC couvrant la région génomique correspondant aux exons 1 à 25 de la dystrophine pour sélectionner dans une banque de cœur d'éventuels ADNc issus du locus DMD. Nous avons isolé un clone de 270 bases, dont nous avons localisé l'origine dans l'intron 2 du gène. La deuxième partie de ce travail a été consacrée à une collaboration avec le laboratoire de Michel Perricaudet (Villejuif), portant sur le transfert d'un minigène de dystrophine médié par un vecteur adénoviral dans le muscle de souris mdx. Nous avons démontré l'efficacité de cette approche chez des souris nouveau-nées, en obtenant une expression dans 5 à 60% des fibres musculaires et une correction à long terme (6 mois) des anomalies histologiques observées chez ces mutants dépourvus de dystrophine. Nous avons testé l'effet de la dose injectée, et de l'âge des animaux au moment de l'injection. Ceci a permis de mettre en évidence, en même temps que d'autres équipes, l'existence d'une réaction immunologique chez les animaux lorsqu'ils ne sont pas injectés dans les premiers jours de vie, ainsi qu'une baisse nette du nombre de fibres infectées à partir de l'âge de 25 jours.
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Kaspar, Rita Wen. "Genotype-Phenotype Association Analysis of Dilated Cardiomyopathy in Becker Muscular Dystrophy." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1243469474.

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Frishman, Natalia, Kristin Caspers Conway, Jennifer Andrews, Jacob Oleson, Katherine Mathews, Emma Ciafaloni, Joyce Oleszek, et al. "Perceived quality of life among caregivers of children with a childhood-onset dystrophinopathy: a double ABCX model of caregiver stressors and perceived resources." BIOMED CENTRAL LTD, 2017. http://hdl.handle.net/10150/623121.

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Background: Duchenne and Becker muscular dystrophies, collectively referred to as dystrophinopathies, are recessive X-linked disorders characterized by progressive muscle weakness and ultimately cardiac and respiratory failure. Immediate family members are often primary caregivers of individuals with a dystrophinopathy. Methods: We explored the impact of this role by inviting primary caregivers (n = 209) of males diagnosed with childhood-onset dystrophinopathy who were identified by the Muscular Dystrophy Surveillance, Tracking, and Research Network (MD STARnet) to complete a mailed questionnaire measuring perceived social support and stress, spirituality, and family quality of life (FQoL). Bivariate and multivariate analyses examined associations between study variables using the Double ABCX model as an analytic framework. Results: Higher stressor pile-up was associated with lower perceived social support (r = -0.29, p <.001), availability of supportive family (r = -0.30, p <.001) or non-family (r = -0.19, p <.01) relationships, and higher perceived stress (r = 0.33, p <.001); but not with spirituality (r = -0.14, p > 0.05). FQoL was positively associated with all support measures (correlations ranged from: 0.25 to 0.58, p-values 0.01-0.001) and negatively associated with perceived stress and control (r = -0.49, p <.001). The association between stressor pile-up and FQoL was completely mediated through global perceived social support, supportive family relationships, and perceived stress and control; supportive non-family relationships did not remain statistically significant after controlling for other mediators. Conclusions: Findings suggest caregiver adaptation to a dystrophinopathy diagnosis can be optimized by increased perceived control, supporting family resources, and creation of a healthy family identity. Our findings will help identify areas for family intervention and guide clinicians in identifying resources that minimize stress and maximize family adaptation.
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Tandon, Animesh. "Dystrophin genotype-cardiac phenotype correlations in Duchenne and Becker muscular dystrophy using cardiac magnetic resonance imaging." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1396453528.

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Books on the topic "Dystrophie musculaire de Becker"

1

Herrmann, Falko H. X-linked muscular dystrophies (Duchenne and Becker): A bibliography. Jena: Universitaẗsbibliothek, 1985.

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Herrmann, Falko H. X-linked muscular dystrophies (Duchenne and Becker): A bibliography. Jena: Universita tsbibliothek, 1985.

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Herrmann, Falko H. X-linked muscular dystrophies (Duchenne and Becker): A bibliography. Jena: Universitätsbibliothek, 1985.

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US GOVERNMENT. An Act to Amend the Public Health Service Act to Provide for Research with Respect to Various Forms of Muscular Dystrophy, Including Duchenne, Becker, Limb Girdle, Congenital, Facioscapulohumeral, Myotonic, Oculopharyngeal, Distal, and Emery-Dreifuss Muscular Dystrophies. [Washington, D.C: U.S. G.P.O., 2001.

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Emery, Alan E. H. Muscular dystrophy, the facts. 2nd ed. Oxford: Oxford University Press, 2000.

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Jean-Guy, Bégin, ed. Einstein, chien-guide? Saint-Alphonse-de-Granby, Québec: Éditions de la Paix, 2006.

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Kaplan, Tamara, and Tracey Milligan. Myopathy (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190650261.003.0017.

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The video in this chapter discusses myopathy, including its symptoms (pain, stiffness, cramps, exertional fatigue, myoglobinuria, shortness of breath, rash), muscular dystrophy and dystrophinopathies (Becker with reduced dystrophin and Duchenne with no dystrophin), polymyositis, dermatomyositis, and inclusion body myositis.
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1932-, Kakulas Byron A., Mastaglia Frank L, and Neuromuscular Foundation of Western Australia., eds. Pathogenesis and therapy of Duchenne and Becker muscular dystrophy. New York: Raven Press, 1990.

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Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. An 18-Year-Old Male with Slowly Progressive Weakness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0028.

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Slow progression of proximal weakness in an adult may suggest Becker muscular dystrophy, but limb-girdle muscular dystrophy needs to be considered. This chapter discusses a diagnostic approach that includes the utility of ever-evolving genetic tests. Electromyography is helpful in cases of suspected muscular dystrophy without a family history, if creatine kinase levels are low, or in evaluation of possible female carriers for BMD who are symptomatic. Management considerations are also outlined. A muscular dystrophy clinic with a multidisciplinary approach is helpful for coordination of care. A consult from a clinical geneticist is often very helpful.
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Terence, Partridge, ed. Molecular and cell biology of muscular dystrophy. London: Chapman & Hall, 1993.

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Book chapters on the topic "Dystrophie musculaire de Becker"

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Leung, Alexander K. C., Marcus Schmitt, Christie P. Thomas, Cord Sunderkötter, Meinhard Schiller, Thomas Schwarz, Mark Berneburg, et al. "Becker Muscular Dystrophy." In Encyclopedia of Molecular Mechanisms of Disease, 212. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8372.

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Angelini, Corrado. "Becker Muscular Dystrophy." In Genetic Neuromuscular Disorders, 13–16. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56454-8_3.

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Angelini, Corrado. "Becker Muscular Dystrophy." In Genetic Neuromuscular Disorders, 13–17. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-07500-6_3.

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Mah, Jean K. "Duchenne and Becker Muscular Dystrophies: Underlying Genetic and Molecular Mechanisms." In Muscular Dystrophy, 21–35. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17362-7_4.

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Khadilkar, Satish V., Rakhil S. Yadav, and Bhagyadhan A. Patel. "Duchenne and Becker Muscular Dystrophies." In Neuromuscular Disorders, 85–98. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-5361-0_9.

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Oette, Mark, Marvin J. Stone, Hendrik P. N. Scholl, Peter Charbel Issa, Monika Fleckenstein, Steffen Schmitz-Valckenberg, Frank G. Holz, et al. "Muscular Dystrophy, Duchenne and Becker." In Encyclopedia of Molecular Mechanisms of Disease, 1384–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_517.

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Hoffman, Eric P. "Genotype/phenotype correlations in Duchenne/Becker dystrophy." In Molecular and Cell Biology of Muscular Dystrophy, 12–36. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1528-5_2.

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Srivastava, Niraj Kumar, Ramakant Yadav, and Deepak Sharma. "Aging: Influence on Duchenne Muscular Dystrophy (DMD) and Becker Muscular Dystrophy (BMD)." In Models, Molecules and Mechanisms in Biogerontology, 149–76. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-3585-3_8.

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Davies, K. E., H. R. Dorkins, S. McGlade, S. P. Ball, S. J. Kenwrick, T. Smith, S. Forrest, et al. "DNA Analysis of Duchenne and Becker Muscular Dystrophies." In Topics in the Neurosciences, 123–30. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2321-1_11.

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Monaco, Anthony P. "Molecular human genetics and the Duchenne/Becker muscular dystrophy gene." In Molecular and Cell Biology of Muscular Dystrophy, 1–11. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1528-5_1.

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Conference papers on the topic "Dystrophie musculaire de Becker"

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Marin, Marija. "Immunogold localization of dystrophin in the erythrocytes of patients with Duchenne-Becker muscular dystrophy." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.373.

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de Feraudy, Yvan, Rabah Yaou, Karim Wahbi, France Leturcq, and Helge Amthor. "Residual Very Low Dystrophin Levels Mitigate Dystrophinopathy towards Becker’s Muscular Dystrophy." In Abstracts of the 47th Annual Meeting of the SENP (Société Européenne De Neurologie Pédiatrique). Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1685441.

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"Mutations in Duchenne and Becker Muscular Dystrophy Patients." In AEBMS-2017, ICCET-2017, BBMPS-17, UPACEE-17, LHESS-17, TBFIS-2017, IC4E-2017, AMLIS-2017 & BEFM-2017. Higher Education and Innovation Group (HEAIG), 2018. http://dx.doi.org/10.15242/heaig.c1217230.

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Sheehan, Daniel W., Daniel A. Mandel, Shree Pandya, Christina P. Westfield, Deborah J. Fox, Sarah K. Nabukera, Katherine Mathews, Christopher Cunniff, Carolyn M. Constantin, and David Birnkrant. "Pulmonologist Involvement In Duchenne And Becker Muscular Dystrophies: Data From The MD STARnet Caregiver Interview, 2007-2008." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5049.

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You might also be interested in the extended bibliographies on the topic 'Dystrophie musculaire de Becker' for particular source types:
Journal articles Dissertations / Theses Books
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