Relevant bibliographies by topics / Duchenne

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Duchenne'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "Duchenne"

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Senatorova, A., and I. Khodun. "ERB-DUCHENNE PALSY (CASE REPORT)." Inter Collegas 5, no. 2 (July 26, 2018): 80–83. http://dx.doi.org/10.35339/ic.5.2.80-83.

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ERB–DUCHENNE PALSY (case study)Senatorova A.V., Khodun I.I.The frequency of damage to the brachial plexus is 0.5-2 per 1000 live births. Most of them (about 90 % cases) are Erb-Duchesnne palsy. Birth trauma of the brachial plexus occurs mainly in in full-term newborns. Correct diagnosis of Erb-Duchesnne palsy allows to avoid long-term complications as late treatment leads to disability. The article presents a clinical observation of Erb-Duchesnne palsy in a newborn patient, who was diagnosed on the first day of life. Conservative therapy was an effective strategy of baby’s recovery.Key words: Erb-Duchenne palsy, birth injury, brachial plexus, newborn. ПАРАЛІЧ ДЮШЕНА-ЕРБА (клінічний випадок)Сенаторова А.В., Ходун І.І.Частота пошкодження плечового сплетення становить 0,5-2 на 1000 живонароджених; серед них 90% випадків - це параліч Дюшена-Ерба. Причиною його можуть бути травми плечового сплетення у доношених новонароджених під час пологів. Своєчасна діагностика паралічу Дюшена-Ерба дозволяє уникнути відстрочених ускладнень. Несвоєчасне розпочате лікування призводить до інвалідизації. У статті наведено клінічне спостереження паралічу Дюшена - Ерба у новонародженого діагностували в першу добу. Своєчасна розпочата консервативна терапія призвела до одужання дитини.Ключові слова: параліч Ерб-Дюшенна, родова травма, плечове сплетіння, новонароджений. ПАРАЛИЧ ДЮШЕНА-ЭРБА (клинический случай)Сенаторова А.В., Ходун И.И.Частота повреждения плечевого сплетения составляет 0,5-2 на 1000 живорожденных; среди них 90% случаев – это паралич Дюшена-Эрба. Причиной его могут быть травмы плечевого сплетения у доношенных новорожденных во время родов. Своевременная диагностика паралича Дюшена-Эрба позволяет избежать отсроченных осложнений. Несвоевременно начатое лечение приводит к инвалидизации. В статье приведено клиническое наблюдение паралича Дюшена - Эрба у новорожденного, диагностированного в первые сутки. Своевременно начатая консервативная терапия способствовала выздоровлению ребенка.Ключевые слова: паралич Эрб-Дюшенна, родовая травма, плечевое сплетение, новорожденный.
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Goldblatt, David. "A Gentleman of Bologna Duchenne, Duchesne, etc." Seminars in Neurology 8, no. 01 (1988): 115–16. http://dx.doi.org/10.1055/s-2008-1041363.

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Parent, André. "Duchenne De Boulogne: A Pioneer in Neurology and Medical Photography." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 32, no. 3 (August 2005): 369–77. http://dx.doi.org/10.1017/s0317167100004315.

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ABSTRACT:Guillaume-Benjamin-Amand Duchenne was born 200 years ago in Boulogne-sur-Mer (Pas-de-Calais, France). He studied medicine in Paris and became a physician in 1831. He practiced general medicine in his native town for about 11 years and then returned to Paris to initiate pioneering studies on electrical stimulation of muscles. Duchenne used electricity not only as a therapeutic agent, as it was commonly the case earlier in the 19th century, but chiefly as a physiological investigation tool to study the anatomy of the living body. Without formal appointment he visited hospital wards across Paris searching for rare cases of neuromuscular disorders. He built a portable electrical device that he used to functionally map all bodily muscles and to study their coordinating action in health and disease. He gave accurate descriptions of many neuromuscular disorders, including pseudohypertrophic muscular dystrophy to which his name is still attached (Duchenne muscular dystrophy). He also invented a needle system (Duchenne's histological harpoon) for percutaneous sampling of muscular tissue without anesthesia, a forerunner of today's biopsy. Duchenne summarized his work in two major treatises entitled De l'électrisation localisée (1855) and Physiologie des mouvements (1867). Duchenne's iconographic work stands at the crossroads of three major discoveries of the 19th century: electricity, physiology and photography. This is best exemplified by his investigation of the mechanisms of human physiognomy in which he used localized faradic stimulation to reproduce various forms of human facial expression. The album that complements his book on this issue is considered a true incunabulum of photography. Duchenne de Boulogne, a shy but hard-working, acute and ingenious observer, became one of most original clinicians of the 19th century. He died in Paris in 1875.
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Lwi, Sandy J., James J. Casey, Alice Verstaen, Dyan E. Connelly, Jennifer Merrilees, and Robert W. Levenson. "Genuine Smiles by Patients During Marital Interactions are Associated with Better Caregiver Mental Health." Journals of Gerontology: Series B 74, no. 6 (January 27, 2018): 975–87. http://dx.doi.org/10.1093/geronb/gbx157.

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Abstract Objective Providing care for a spouse with dementia is associated with an increased risk for poor mental health. To determine whether this vulnerability in caregivers is related to the expression of positive emotion, we examined 57 patients with Alzheimer’s disease and behavioral variant frontotemporal dementia and their spouses as they discussed a marital conflict. Method Facial behavior during the discussion was objectively coded to identify Duchenne (i.e., genuine) smiles and non-Duchenne (i.e., polite) smiles. Caregiver mental health was measured using the Medical Outcomes Survey. Results Greater expression of Duchenne smiles by patients was associated with better caregiver mental health, even when accounting for covariates (i.e., diagnosis, patient cognitive functioning, and caregiver marital satisfaction). Greater expression of non-Duchenne smiles by patients was associated with worse caregiver health, but only when covariates were entered in the model. Expression of Duchenne and non-Duchenne smiles by caregivers was not associated with caregiver mental health. Discussion Patients’ expression of Duchenne and non-Duchenne smiles may reveal important aspects of the emotional quality of the patient–caregiver relationship that influence caregiver burden and mental health.
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Meißner, Thomas. "Duchenne-Muskeldystrophie." MMW - Fortschritte der Medizin 157, no. 13 (July 2015): 81. http://dx.doi.org/10.1007/s15006-015-3369-7.

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Sekelj Fureš, J., and V. Đuranović. "Female Duchenne." European Journal of Paediatric Neurology 21 (June 2017): e229. http://dx.doi.org/10.1016/j.ejpn.2017.04.1244.

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Thibault, Pascal, Manon Levesque, Pierre Gosselin, and Ursula Hess. "The Duchenne Marker is Not a Universal Signal of Smile Authenticity – But it Can Be Learned!" Social Psychology 43, no. 4 (January 2012): 215–21. http://dx.doi.org/10.1027/1864-9335/a000122.

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The Duchenne marker has been proposed as a universal marker of smile authenticity. However, Elfenbein, Beaupré, Levesque, and Hess (2007 ) found that, whereas Canadians typically show the Duchenne marker when posing happiness, Gabonese do not. We therefore investigated whether the Duchenne marker is perceived as a marker of smile authenticity by Gabonese and by Mainland Chinese living in Quebec, Canada. The results show that Gabonese do not use the Duchenne marker to assess smile authenticity at all. Mainland Chinese immigrants to Quebec showed sensitivity to the Duchenne marker only when judging smiles by French-Canadian encoders, suggesting learning of the use of this cultural dialect through cultural exposure. In sum, the use of Duchenne marker is not universal, but rather limited to certain cultures.
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Soim, Aida, Bailey Wallace, Nedra Whitehead, Michael G. Smith, Joshua R. Mann, Shiny Thomas, and Emma Ciafaloni. "Health Profile of Preterm Males With Duchenne Muscular Dystrophy." Journal of Child Neurology 36, no. 12 (October 2021): 1095–102. http://dx.doi.org/10.1177/08830738211047019.

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In this retrospective cohort study, we characterize the health profile of preterm males with Duchenne muscular dystrophy. Major clinical milestones (ambulation cessation, assisted ventilation use, and onset of left ventricular dysfunction) and corticosteroids use in males with Duchenne muscular dystrophy identified through a population-based surveillance system were analyzed using Kaplan-Meier survival curves and Cox proportional hazards modeling. The adjusted risk of receiving any respiratory intervention among preterm males with Duchenne muscular dystrophy was 87% higher than among the corresponding full-term males with Duchenne muscular dystrophy. The adjusted risks for ambulation cessation and left ventricular dysfunction were modestly elevated among preterm compared to full-term males, but the 95% confidence intervals contained the null. No difference in the start of corticosteroid use between preterm and full-term Duchenne muscular dystrophy males was observed. Overall, the disease course seems to be similar between preterm and full-term males with Duchenne muscular dystrophy; however, pulmonary function seems to be affected earlier among preterm males with Duchenne muscular dystrophy.
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Denetclaw, W. F., G. Bi, D. V. Pham, and R. A. Steinhardt. "Heterokaryon myotubes with normal mouse and Duchenne nuclei exhibit sarcolemmal dystrophin staining and efficient intracellular free calcium control." Molecular Biology of the Cell 4, no. 9 (September 1993): 963–72. http://dx.doi.org/10.1091/mbc.4.9.963.

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Duchenne and mdx muscle tissues lack dystrophin where it normally interacts with glycoproteins in the sarcolemma. Intracellular free calcium ([Ca2+]i) is elevated in Duchenne and mdx myotubes and is correlated with abnormally active calcium-specific leak channels in dystrophic myotubes. We fused Duchenne human and normal mouse myoblasts and identified heterokaryon myotubes by Hoechst 33342 staining to measure the degree to which dystrophin introduced by normal nuclei could incorporate throughout the myotube at the sarcolemma and restore normal calcium homeostasis. Dystrophin expression in myotubes was determined by immunofluorescence and confocal laser scanning microscopy. Dystrophin was expressed at the sarcolemma in normal mouse and heterokaryon myotubes, but not in Duchenne myotubes. In heterokaryons, extensive dystrophin localization occurred at the sarcolemma even where only Duchenne nuclei were present, indicating that dystrophin does not exhibit nuclear domains. Heterokaryon, normal mouse and Duchenne myotube [Ca2+]i was measured using fura-2 and fluorescence ratio imaging. Heterokaryon and normal mouse myotubes were found to maintain similar levels of [Ca2+]i. In contrast, Duchenne myotubes had significantly higher [Ca2+]i (p < 0.001). Furthermore, the ability of heterokaryons to maintain normal [Ca2+]i did not depend on greater numbers of normal nuclei than Duchenne being present in the myotube. These results support the view that dystrophin expression in heterokaryons allows for efficient control of [Ca2+]i.
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Heutinck, Lotte, Nadine van Kampen, Merel Jansen, and Imelda J. M. de Groot. "Physical Activity in Boys With Duchenne Muscular Dystrophy Is Lower and Less Demanding Compared to Healthy Boys." Journal of Child Neurology 32, no. 5 (January 23, 2017): 450–57. http://dx.doi.org/10.1177/0883073816685506.

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This study describes the amount of physical activity and perception of physical activity in boys with Duchenne muscular dystrophy (DMD) compared to healthy boys. A questionnaire described 6 domains of physical activity. Four Duchenne muscular dystrophy subgroups were made: early and late ambulatory, nonambulatory with relative good, or limited arm function. Eighty-four boys with Duchenne muscular dystrophy (15.0 ± 6.4 years) and 198 healthy boys (14.0 ± 4.3 years) participated. Daily activities were more passive for boys with Duchenne muscular dystrophy. Physical activity was less and low demanding compared to healthy boys. It decreased with disease severity ( P < .05), whereas screen time increased ( P < .05). Benefits of physical activity in boys with Duchenne muscular dystrophy were having fun and making friends. Barriers were lack of sport facilities and insufficient health. This study helps to quantify poor engagement in physical activity by boys with Duchenne muscular dystrophy, and demonstrates factors that contribute to it. Suggestions to stimulate physical activity are made.
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Dissertations / Theses on the topic "Duchenne"

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Busch, H. F. M. "Het begon bij Duchenne." [S.l.] : Rotterdam : [de auteur] ; Erasmus University [Host], 1994. http://hdl.handle.net/1765/7462.

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Rabinowitz, Adam Howard. "Antisense therapies for Duchenne muscular dystrophy." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444590.

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Smith, T. J. "Molecular analysis of Duchenne muscular dystrophy." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233559.

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Hodgson, Shirley V. "Genetic studies in Duchenne muscular dystrophy." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235878.

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Wakefield, Philip M. "Gene therapy for duchenne muscular dystrophy." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365743.

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Koppaka, Sisir. "Imaging biomarkers for Duchenne muscular dystrophy." Thesis, Massachusetts Institute of Technology, 2015. http://hdl.handle.net/1721.1/106959.

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Thesis: S.M., Massachusetts Institute of Technology, School of Engineering, Center for Computational Engineering, Computation for Design and Optimization Program, 2015.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 75-78).
Duchenne muscular dystrophy (DMD) is the most common muscular dystrophy of childhood and affects 1 in 3600 male births. The disease is caused by mutations in the dystrophin gene leading to progressive muscle weakness which ultimately results in death due to respiratory and cardiac failure. Accurate, practical, and painless tests to diagnose DMD and measure disease progression are needed in order to test the effectiveness of new therapies. Current clinical outcome measures such as the sixminute walk test and North Star Ambulatory Assessment (NSAA) can be subjective and limited by the patient's degree of effort and cannot be accurately performed in the very young or severely affected older patients. We propose the use of image-based biomarkers with suitable machine learning algorithms instead. We find that force-controlled (precise acquisition at a certain force) and force-correlated (acquisition over a force sweep) ultrasound helps to reduce variability in the imaging process. We show that there is a high degree of inter-operator and intra-operator reliability with this integrated hardware-software setup. We also discuss how other imaging biomarkers, segmentation algorithms to target specific subregions, and better machine learning techniques may provide a boost to the performance reported. Optimizing the ultrasound image acquisition process by maximizing the peak discriminatory power of the images vis-à-vis force applied at the contact force is also discussed. The techniques presented here have the potential for providing a reliable and non-invasive method to discriminate, and eventually track the progression of DMD in patients.
by Sisir Koppaka.
S.M.
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Tay, Shaun Li Jian. "Duchenne Muscular Dystrophy—Insight and Treatment." Thesis, The University of Arizona, 2015. http://hdl.handle.net/10150/595055.

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Duchenne Muscular Dystrophy (DMD) is a genetic disorder characterized by progressive degeneration of muscle fibers and dystrophic changes on muscle biopsy¹. DMD accounts for approximately 50% of all dystrophinopathies, with around 21,000 male babies born with the disease each year², ³, ⁴, ⁵. It is also the most lethal X-linked recessive disorder as phenotypic traits are not immediately present at birth¹¹, ³. Patients usually do not live past their 20's without medical intervention to treat associated respiratory and cardiac dysfunctions¹¹, ³. For these reasons DMD remains one of the greatest threats, amongst a range of pediatric pathologies, to the normalcy of child development and parental care. Although treatment options have shown to mitigate the progression of DMD, most are controversial and costly - the estimated annual treatment cost of DMD per patient is $50,953⁵⁸. In light of this, disease awareness and public health education are critical components for acquiring funds needed for research towards a cure¹². My hope is that through this integrated overview of DMD, the medical layman will better understand the depths of this lethal disease, and how it can be detrimental to both the affected child and his caretaker.
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Matecki, Stefan. "Fonction respiratoire et myopathie de Duchenne." Montpellier 1, 1997. http://www.theses.fr/1997MON11135.

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vianello, sara. "Molecular modifiers in Duchenne muscular dystrophy." Doctoral thesis, Università degli studi di Padova, 2018. http://hdl.handle.net/11577/3426720.

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Duchenne muscular dystrophy (DMD) is an X-linked progressive neuromuscular disease affecting 1:3500 –1/5000 boys at birth. It is caused by the absence of dystrophin, a subsarcolemmal protein that confers membrane stability linking cytoskeletal actin to the extracellular matrix. Dystrophin is part of a multi-protein complex called dystrophin associated protein complex (DAPC), which contains, among the other components, β-dystroglycan and nitric oxide synthase (NOS). The consequences of the absence of dystrophin are: deregulation of calcium homeostasis, tissue necrosis, and progressive accumulation of fat and fibrosis and loss of contractile muscle fibers. The ensuing muscle weakness leads to progressive and severe disability, with loss of independent ambulation around the early teens, and cardiac and respiratory failure leading to patient’s death, usually around the age of 20-30 years.Despite all patients having a complete lack of dystrophin in muscle fibers, a relevant inter-patient variability in disease severity is observed (e.g. loss of ambulation may range from 8 to beyond 15 years of age). Emerging evidence points to genetic modifiers, i.e. polymorphisms in genes different form the disease gene, as one of the causes of this variability, but little is yet known about the underlying molecular mechanisms.My PhD work can be divided into 4 aims: Aim 1: To characterize the molecular mechanism underlying the modifier effect of the rs28357094 T>G SNP in the SPP1gene, encoding osteopontin (OPN) the first identified genetic modifier of DMD. I treated dystrophic and healthy cell line with two different concentrations of deflazacort (DFZ), one of the glucocorticoids mainly used to treat DMD patients, in order to analyze osteopontin expression in relation to genetic background at rs24357094. The results obtained revealed: (I) a developmental regulated expression pattern of OPN; (II) no difference of osteopontin expression are observed related to rs28357094 genotype; (III) an increase in OPN expression only in TG DFZ-treated myotubes, suggesting a possible interaction between glucocorticoid responsive elements (GRs) in the promoter of the SPP1gene and the glucocorticoid.Aim 2: To investigate the possible roles of SPP1splicing isoforms in DMDmuscle biopsies and cells. Three SPP1isoforms, named a, b and c, were analyzed. SPP1mRNA studies revealed that all three isoforms are overexpressed in DMD muscle compared to controls, but not in myogenic cell cultures. Moreover, SPP1isoforms expression was directly correlated withage in DMD patients’ muscle biopsies. Finally, muscle biopsies carrying the rs24357094 TT genotype showed an increased expression of all three SPP1isoforms compared to TG genotype. Aim 3: To validate the known DMD geneticmodifiers in novel cohorts of DMD patients utilizing different outcome measures. First, we asked if SPP1genotype and LTBP4haplotype (the second identified modifier of DMD) can modulate the cardiac involvement in DMD. LTBP4haplotye and the SPP1rs28357094 were genotyped in 168 DMD patients. LTBP4haplotype is composed of 4 polymorphisms in perfect linkage disequilibrium (LD). The genotype at rs10880 resulted, as expected, to be associated to a delay at age of loss of ambulation (LoA) and, as novel finding, also to a delay in cardiomyopathy onset. The SPP1minor G allele at rs28357094 resulted also associated to a later cardiomyopathy onset.Finally, I participate to the identification of the third genetic modifier in DMD: CD40. CD40was identified through a GWAS approach in a large cohort of DMD patients.The CD40rs1883832 C>T polymorphism is located within the Kozak sequence of the gene and it causes a decrease of transcriptional activity of the promoter resulting in an increase of the CD40 secreted isoform. In order to validate CD40 as a genetic modifier in DMD in an independent cohort from the discovery cohort, rs1883832 was genotyped in 96 DMD patients.DMD patients carrying the minor T allele lost ambulation earlier compared to patients carrying the C allele. Moreover, in order to study the functional role of CD40 in DMD, RT-PCR and immunoblot were performed in a subset of patients’ muscle biopsies stratified according to rs1883832 genotype. Our results reveal that the minor T allele is associated to an increase of the transcript and a decrease of the protein compared to C genotype.Taken together these data contribute to clarify some aspects of the molecular mechanisms underlying the downstream consequences of genetic modifiers in DMD. Further studies are needed to fully translate the knowledge acquired in thefield of genetic modifiers in DMD to the clinic, e.g. to implement patient genotyping for genetic counseling, prognosis, planning of treatments, and stratification in clinical trials
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MARCHI, Michele. "DESIGN FOR DUCHENNE. Linee guida per il progetto di costruzione o ristrutturazione di abitazioni per famiglie Duchenne." Doctoral thesis, Università degli studi di Ferrara, 2015. http://hdl.handle.net/11392/2389086.

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Books on the topic "Duchenne"

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Duchenne muscular dystrophy. Oxford: Oxford University Press, 1987.

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Duchenne muscular dystrophy. 3rd ed. Oxford: Oxford University Press, 2003.

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Bernardini, Camilla, ed. Duchenne Muscular Dystrophy. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7374-3.

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Duchenne muscular dystrophy. 2nd ed. Oxford: Oxford University Press, 1993.

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i15, Institut Garches Entretiens. Myopathies de Duchenne-Becker. Paris: Frison-Roche, 2002.

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Marcil-Denault, Éveline. Le sourire de Duchenne. Montréal (Québec): Stanké, 2013.

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S, Chamberlain Jeffrey, and Rando Thomas A, eds. Duchenne muscular dystrophy: Advances in therapeutics. New York: Taylor & Francis, 2005.

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Kate, Stone, ed. Occupational therapy and Duchenne muscular dystrophy. Chichester, West Sussex, England: John Wiley & Sons, 2007.

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Voices of hope: Coping with muscular dystrophy in Mauritius. Port-Louis: Best Graphics Ltd., 2008.

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Bergman, Thomas. Precious time: Children living with muscular dystrophy. Milwaukee: Gareth Stevens Pub., 1996.

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Book chapters on the topic "Duchenne"

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de Die-Smulders, C. E. M., C. G. Faber, Y. Pinto, and C. T. R. M. Schrander-Stumpel. "Duchenne-Spierdystrofie." In Klinische genetica, 217–27. Houten: Bohn Stafleu van Loghum, 2003. http://dx.doi.org/10.1007/978-90-313-9437-1_21.

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Johannesmeyer, David, and Reed Estes. "Duchenne Muscular Dystrophy." In Orthopedic Surgery Clerkship, 581–82. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52567-9_122.

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Gilbert, Patricia. "Duchenne muscular dystrophy." In The A-Z Reference Book of Syndromes and Inherited Disorders, 94–98. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-6918-7_24.

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Angelini, Corrado. "Duchenne Muscular Dystrophy." In Genetic Neuromuscular Disorders, 3–7. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56454-8_1.

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Verschuren, Olaf. "Ziekte van Duchenne." In Fysiotherapeutische casuïstiek, 733–40. Houten: Bohn Stafleu van Loghum, 2006. http://dx.doi.org/10.1007/978-90-313-8645-1_121.

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Dickson, George, and Susan C. Brown. "Duchenne muscular dystrophy." In Molecular and Cell Biology of Human Gene Therapeutics, 261–80. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0547-7_14.

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Markert, Chad D., Martin K. Childers, and Robert W. Grange. "Duchenne Muscular Dystrophy." In Encyclopedia of Exercise Medicine in Health and Disease, 262–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_250.

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Angelini, Corrado. "Duchenne Muscular Dystrophy." In Genetic Neuromuscular Disorders, 3–7. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-07500-6_1.

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Cantor, Richard M., Charles V. Pollack, and Victoria G. Riese. "Duchenne Muscular Dystrophy." In Differential Diagnosis of Cardiopulmonary Disease, 379–89. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-63895-9_25.

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Dillane, Derek. "Duchenne Muscular Dystrophy." In Preoperative Assessment, 205–10. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-58842-7_31.

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Conference papers on the topic "Duchenne"

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Vandeventer, Jason, and Eric Patterson. "Differentiating Duchenne from non-Duchenne smiles using active appearance models." In 2012 IEEE Fifth International Conference On Biometrics: Theory, Applications And Systems (BTAS). IEEE, 2012. http://dx.doi.org/10.1109/btas.2012.6374595.

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Rossoni, Tainara Emanuele, Ranieri Alvin Stroher Junior, and Bruna Hoeller. "Duchenne Muscular Dystrophy - Case Report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.129.

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Context: Duchenne Muscular Dystrophy (DMD) is an inherited recessive disease linked to the X chromosome, it is a progressive neuromuscular disease most prevalent in the world, affecting 1/3600 male births. It is associated with mutations that lead to loss of dystrophin protein expression, loss of severe muscle, respiratory and cardiac failure. At birth, the signs are generally nonspecific. At 3 years of age there is the appearance of specific changes, starting with muscle weakness, which occurs in an ascending, symmetrical and bilateral manner, becoming evident at around 5 years of age, with difficulty walking, jumping and running, in addition to frequent falls. The disease progresses with cardiorespiratory failure, leading to death between 18 and 25 years. Case Report: Male, 3 years old, with frequent falls, difficulty climbing stairs and rising from the floor, even with support, medical guidance for expectant conduct. At 5 years, clinical worsening, investigation of the condition, changes alteration in the creatinophosphokinase test (8918 U / L), suggesting a hypothesis of Muscular Dystrophy. Karyotype performed, with revelation of genetic changes compatible with DMD. Family heredogram, showing a brother without traits for DMD and a mother with an allele for the disease. The patient evolved with progressive loss of motor functions, reaching inability to move around at 9 years of age and the appearance of cardiac changes - left ventricular systolic dysfunction and extrasystoles. Currently, the patient presents marked movement restriction and undergoes palliative treatment. Conclusions: A DMD relies only on palliative therapy, the recognition of the initial clinical manifestations is essential for its investigation, diagnosis and early treatment, enabling improvement in quality and life expectancy.
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Fiorentino, Giuseppe, Anna Annunziata, Maria Antonietta Mazza, Rosa Cauteruccio, Gianfranco Scotto di Frega, and Anna Michela Gaeta. "Mouthpiece ventilation in Duchenne muscular dystrophy." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2166.

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Cavache, Alina, Diana Zaharia, Raluca Ioana Teleanu, Diana Anamaria Epure, Dana Vasile, Magdalena Sandu, Ioana Adriana Ghiorghiu, and Doina Anca Plesca. "P315 Electrocardiographic changes in duchenne muscular dystrophy." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.403.

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Grinio, L. "A new hypothesis of duchenne muscular dystrophy." In Scientific achievements of the third millennium. SPC "LJournal", 2021. http://dx.doi.org/10.18411/scienceconf-03-2021-41.

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Reichert, S., M. Schmuck, C. Kalbe, B. Kessler, LM Fonteyne, N. Klymiuk, E. Wolf, et al. "Exon-Skipping im Schweinemodell der Duchenne Muskeldystrophie." In 24. Kongress des Medizinisch-Wissenschaftlichen Beirates der Deutschen Gesellschaft für Muskelkranke (DGM) e.V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1685090.

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Dell'Acqua, Guido, and Filippo Castiglione. "A Mathematical Model of Duchenne Muscular Dystrophy." In Selected Contributions from the 9th SIMAI Conference. WORLD SCIENTIFIC, 2009. http://dx.doi.org/10.1142/9789814280303_0028.

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Molloy, Helen, Victoria Beesley, Dipansu Ghosh, and Mark Elliot. "NIV in Duchenne Muscular Dystrophy : A qualitative study." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa1890.

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Gushue, C. A., and R. Shell. "Effectiveness of Airway Clearance in Duchenne Muscular Dystrophy." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3679.

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Koppaka, Sisir, Matthew W. Gilbertson, Jim S. Wu, Seward B. Rutkove, and Brian W. Anthony. "Assessing duchenne muscular dystrophy with force-controlled ultrasound." In 2014 IEEE 11th International Symposium on Biomedical Imaging (ISBI 2014). IEEE, 2014. http://dx.doi.org/10.1109/isbi.2014.6867965.

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Reports on the topic "Duchenne"

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Cnaan, Avital. CINRG: Infrastructure for Clinical Trials in Duchenne Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada567633.

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Cnaan, Avital. CINRG: Infrastructure for Clinical Trials in Duchenne Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada599521.

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Martin, Paul T. Translational Studies of GALGT2 Gene Therapy for Duchenne Muscular Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613577.

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Martin, Paul T. Translational Studies of GALGT2 Gene Therapy for Duchenne Muscular Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada598203.

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Byrne, Barry J. Advanced Gene Therapy for Treatment of Cardiomyopathy and Respiratory Insufficiency in Duchenne Muscular Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada613171.

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Constenius, Kurt N. U-Pb Zircon Geochronology Results from the Provo and Duchesne 30' x 60' Quadrangles, Utah. Utah Geological Survey, July 2020. http://dx.doi.org/10.34191/ofr-719.

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Waanders, Gerald L. Palynology Evaluation Results from the Provo, Duchesne, and Rush Valley 30' x 60' Quadrangles, Utah. Utah Geological Survey, July 2020. http://dx.doi.org/10.34191/ofr-720.

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Bluebell field drill-hole database, Duchesne and Uintah Counties, Utah. Utah Geological Survey, 1995. http://dx.doi.org/10.34191/c-90.

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Geologic map of the Mount Powell quadrangle, Duchesne and Summit Counties, Utah. Utah Geological Survey, 2016. http://dx.doi.org/10.34191/mp-16-5dm.

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Geologic map of the Kings Peak 7.5 minute quadrangle, Duchesne and Summit Counties, Utah. Utah Geological Survey, 2015. http://dx.doi.org/10.34191/mp-15-3.

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