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Journal articles on the topic 'Duchenne'

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Published: 4 June 2021
Last updated: 15 June 2025

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1

Senatorova, A., and I. Khodun. "ERB-DUCHENNE PALSY (CASE REPORT)." Inter Collegas 5, no. 2 (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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2

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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3

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 (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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4

Ibrahim Sory, P., T. Sidi, L. Guida, et al. "Dystrophie Musculaire de Duchenne: Aspects cliniques, biologiques et évolutifs à propos de cinq cas dans le service de Rhumatologie au CHU du Point G." Rhumatologie Africaine Francophone 6, no. 2 (2024): 18–23. http://dx.doi.org/10.62455/raf.v6i2.53.

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Résumé 
 La dystrophie musculaire de Duchenne (DMD) due à la non expression de la dystrophine est liée au chromosome X. Décrite au 19e siècle, est la plus courante dystrophie musculaire de l’enfant [1, 2]. L’incidence est estimée à 30 cas pour 100 000 naissances [1, 2].
 But- étudier les caractères cliniques, biologiques et évolutifs de la dystrophie musculaire de Duchenne.
 Patients et Méthodes :
 Il s’est agi d’une étude rétrospective portant sur 5 dossiers de DMD, colligés en 7 ans.
 Résultats
 Nous rapportons cinq dossiers de garçons colligés entre 2005 et 2012,
 2012, d’âge moyen de 7 ans avec des extrêmes de 1 et 12 ans. L’hypertrophie des mollets et la présence d’un signe de Gowers chez 4/5 patients. Le caractère familial était présent chez 2 garçons âgés de 5 et 10 ans à l’inclusion dont un mariage consanguin. L’examen anatomopathologique musculaire a conclu à des lésions dystrophiques. L’immunohistochimie n’a pas trouvé d’expression de la dystrophine. La corticothérapie précocement instituée à 0,5 mg/kg/jour associée à la rééducation kinésithérapie a maintenu l’autonomie des patients.
 Conclusion
 La corticothérapie retarderait les complications cardio-pulmonaires. Associée à la rééducation kinésithérapie et aux conseils pratiques elle a diminué les chutes.
 Mots clés : Dystrophie – Musculaire – Duchenne, Rhumatologie Bamako
 
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 Introduction Duchenne’s muscular dystrophy (DMD) caused by no dystrophin expression is linked to X chromosome. Described in the 19th century, it is the most common muscular dystrophy of the child [1, 2]. The incidence is estimated at 30 cases per 100 000 births [1, 2]. Goal - Study clinical, biological and evolutive aspects of the Duchenne's Muscular Dystrophy.
 Patients and Methods:
 It was a retrospective study about 5 cases of DMD, collected in 7 years [2005-2012].
 Results During our study from the period of 2005 to 2012, we had 5 cases of boys with an average age of 7 years and the extreme age from 1 year to 12 years. The calf’s hypertrophy and the presence of a Gowers’s sign in 4/5 patients. Family caracteristic was present in two boys aged 5 and 10 years with a consanguineous marriage. Muscular Histological examination concluded dystrophic lesions. The immunohistiochemistry found no expression of dystrophin. Corticosteroids early established at 0.5 mg / kg / day combined with physiotherapy rehabilitation maintained the autonomy of patients. .
 Conclusion Corticosteroids would slow douwn cardiopulmonary complications. Associated with the physiotherapy rehabilitation and practical advice, it has decreased falls.
 Keywords: Duchenne’s muscular dystrophy, Rheumatology, Bamako
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5

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 (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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6

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 (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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7

Soim, Aida, Bailey Wallace, Nedra Whitehead, et al. "Health Profile of Preterm Males With Duchenne Muscular Dystrophy." Journal of Child Neurology 36, no. 12 (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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8

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 (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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9

Meißner, Thomas. "Duchenne-Muskeldystrophie." MMW - Fortschritte der Medizin 157, no. 13 (2015): 81. http://dx.doi.org/10.1007/s15006-015-3369-7.

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10

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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11

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 (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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12

Mwiinga, Fair Banji, Roster Chihwaka Malimba, Mutinta Mirriam Nzima, et al. "Early detection and rehabilitation in Erb-Duchenne paralysis before age 1 year: A Case Report From Lusaka Zambia." Medical Journal of Zambia 50, no. 2 (2023): 192–96. http://dx.doi.org/10.55320/mjz.50.2.353.

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Erb-Duchenne paralysis is a neurological condition characterized by paralysis of the arm which occurs due to injury of the upper trunk of C5-C6 of the brachial plexus and can lead to disturbances in movement and sensation. Erb-Duchenne paralysis commonly presents with a “Waiter’s Tip” deformity characterized by elbow extension, medial rotation of the arm, forearm pronation, and wrist flexion. Management of Erb-Duchenne paralysis may involve strengthening exercises, range of motion exercises, manual therapy, and neuromuscular electrical stimulation. However, in most cases, the diagnosis of Erb-Duchenne paralysis is not detected early enough for rehabilitation outcomes to be maximized. We herein report a case of a 6-months old child who had Erb-Duchenne paralysis in the left upper limb. The aim of this case report is to highlight the importance of early detection and rehabilitation of Erb-Duchenne paralysis. Furthermore, the report also discusses the physiotherapy techniques that can be used to optimize outcomes.
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13

Robert, D., TN Willig, P. Leger, and J. Paulus. "Long-term nasal ventilation in neuromuscular disorders: report of a consensus conference." European Respiratory Journal 6, no. 4 (1993): 599–606. http://dx.doi.org/10.1183/09031936.93.06040599.

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Following the colloquium entitled "Nasal Ventilation and Neuromuscular Disease", which took place in Lyon, France, October 24, 1991, a group of authorities on neuromuscular disorders met to establish a consensus concerning the application of this technique, in the clinical setting, for patients with Duchenne's muscular dystrophy, non-Duchenne myopathies and the spinal muscular atrophies. This report summarizes recommendations issuing from this conference. The conclusions drawn from this work should not be applied to patients with other diagnoses.
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Khatri, Ravi Shankar, Mridul Ranajan, and Shalini . "A COMPARATIVE AYURVEDIC REVIEW OF ETIOPATHOGENESIS OF DUCHENNE MUSCULAR DYSTROPHY (INHERITED DISORDER)." International Journal of Research in Ayurveda and Pharmacy 12, no. 1 (2021): 124–25. http://dx.doi.org/10.7897/2277-4343.120127.

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Duchenne muscular dystrophy (DMD) is an inherited disorder with severe progressive muscle weakness. In Ayurveda, Adibala Pravritta Vyadhi are also known as inherited diseases that caused by Matruja beeja dushti (Shonita) and Pitruja beeja dushti (Shukra). Duchenne muscular dystrophy (DMD) has been classified under Adibala Pravritta Vyadhi as per Ayurveda. The main objective of this article is to describe the various aspect of etiopathogenesis of Duchenne muscular dystrophy (DMD) as per Ayurvedic literature. This article will be helpful to making the Nidana (Diagnosis) as per Ayurveda and also help in the Chikitsa (Treatment) of Duchenne muscular dystrophy.
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15

Sanadhya, Anuradha, Ritvika Jyani, Suresh Goyal, Neha Asora, and Mukesh Kumar Gurjar. "Duchenne muscular dystrophy in a female with x-autosome translocation." International Journal of Contemporary Pediatrics 8, no. 4 (2021): 770. http://dx.doi.org/10.18203/2349-3291.ijcp20211094.

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Duchenne’s muscular dystrophy is the most common hereditary neuromuscular disease, which affects all races. Its classical characteristic clinical features being progressive muscular weakness, intellectual impairment and hypertrophy of the calves with proliferation of connective tissue and progressive fibrosis in muscles. As the disease is inherited as an X-linked recessive trait, thus females not manifesting the disease and acting as carriers only, as second X chromosome prevents the manifestation of disease. We report a case of classical Duchenne muscular dystrophy in 10 year old female with no intellectual deficit and no family history of similar type of muscular dystrophy.
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16

Melis Gönülal, Melis Gönülal, and Didem Didar Balcı Didem Didar Balcı. "ADALİMUMAB: USAGE İN A CASE WİTH PSORİASİS AND DUCHENNE MUSCULAR DYSTROPHY." INTERNATIONAL JOURNAL OF INNOVATIVE MEDICINE & HEALTHCARE 01, no. 01 (2022): 04–07. http://dx.doi.org/10.55858/ijimh01012022-04.

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There are different biological treatments for psoriasis and one of these treatments is adalimumab. Here we want to present a case with psoriasis and Duchenne muscular dystrophy treated with adalimumab. A 23-year-old male patient with psoriasis and Duchenne muscular dystrophy applied to our dermatology clinic. At the sixth week control of the patient we achieved PASI 90 response. Duchenne muscular dystrophy is a rare disease and its coexistence with psoriasis is a very rare status. No similar case report was found in the literature. We wanted to present both this rare status and psoriasis progression under adalimumab treatment. Keywords: psoriasis, adalimumab, Duchenne muscular dystrophy
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Ihmsen, Harald, Joachim Schmidt, Helmut Schwilden, Hubert J. Schmitt, and Tino Muenster. "Influence of Disease Progression on the Neuromuscular Blocking Effect of Mivacurium in Children and Adolescents with Duchenne Muscular Dystrophy." Anesthesiology 110, no. 5 (2009): 1016–19. http://dx.doi.org/10.1097/aln.0b013e31819daf31.

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Background Studies with nondepolarizing neuromuscular blocking agents showed a delayed onset and prolonged recovery in patients with Duchenne muscular dystrophy. The objective of this study was to investigate if these alterations depend on disease progression. Methods The authors studied 11 children (6-9 yr) with moderate Duchenne muscular dystrophy, 11 adolescents (12-16 yr) with advanced Duchenne muscular dystrophy, and 2 age-matched control groups of 8 patients each (5-9 and 10-17 yr). Anesthesia was performed with propofol and remifentanil. Patients received a single intravenous dose of 0.2 mg/kg mivacurium. Neuromuscular transmission was monitored by acceleromyography. The time course of neuromuscular blockade was characterized by the onset time and the times to different levels of recovery. Results Onset and duration of neuromuscular blockade were significantly prolonged in adolescent Duchenne muscular dystrophy patients (onset time, 4.0 min; recovery index, 12.3 min; median), as compared with Duchenne muscular dystrophy children (onset time, 2.3 min; recovery index, 6.8 min), and also as compared with young controls (onset time, 2.0 min; recovery index, 4.4 min) and adolescent controls (onset time, 2.5 min; recovery index, 4.8 min). Within the Duchenne muscular dystrophy patients, onset time and recovery index increased significantly with age. In the control group, age had no effect. Conclusions The neuromuscular blocking effects of mivacurium showed a significant age dependency in Duchenne muscular dystrophy patients, which was most probably caused by the progression of the disease.
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Sarvutiene, Julija, Arunas Ramanavicius, Simonas Ramanavicius, and Urte Prentice. "Advances in Duchenne Muscular Dystrophy: Diagnostic Techniques and Dystrophin Domain Insights." International Journal of Molecular Sciences 26, no. 8 (2025): 3579. https://doi.org/10.3390/ijms26083579.

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Abnormalities in X chromosomes, either numerical or structural, cause X-linked disorders, such as Duchenne muscular dystrophy (DMD). Recent molecular and cytogenetic techniques can help identify DMD gene mutations. The accurate diagnosis of Duchenne is crucial, directly impacting patient treatment management, genetics, and the establishment of effective prevention strategies. This review provides an overview of X chromosomal disorders affecting Duchenne and discusses how mutations in Dystrophin domains can impact detection accuracy. Firstly, the efficiency and use of cytogenetic and molecular techniques for the genetic diagnosis of Duchenne disease have, thus, become increasingly important. Secondly, artificial intelligence (AI) will be instrumental in developing future therapies by enabling the aggregation and synthesis of extensive and heterogeneous datasets, thereby elucidating underlying molecular mechanisms. However, despite advances in diagnostic technology, understanding the role of Dystrophin in Duchenne disease remains a challenge. Therefore, this review aims to synthesize this complex information to significantly advance the understanding of DMD and how it could affect patient care.
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Werneck, Lineu Cesar, and Eduardo Bonilla. "Distrofina na diferenciação das distrofias de duchenne e becker estudo imuno-histoquímico comparado com o estádio clínico, enzimas séricas e biópsia muscular." Arquivos de Neuro-Psiquiatria 48, no. 4 (1990): 454–64. http://dx.doi.org/10.1590/s0004-282x1990000400009.

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Foram estudados 55 casos de distrofia muscular progressiva (34 Duchenne, 12 Duchenne com distrofina residual e 9 Becker), comparando idade, época de início e tempo de sintomas, graduação na escala de Vignos e Archibald, níveis de enzimas séricas e presença de distrofina nas biópsias musculares por imunofluorescência. A intensidade dos sintomas, gravidade do quadro clínico, proliferação de tecido ccnjuntivo endomisial e infiltração por tecido adiposo estão inversamente relacionadas à quantidade de distrofina presente nas biópsias e, diretamente, à presença de fibras hipertróficas e fibras angulares escuras atróficas. Nos comentários são abordados alguns aspectos sobre a diferenciação da distrofia muscular de Duchenne e Becker, a distrofina residual nos casos de Duchenne e a importância do teste para o diagnóstico adequado.
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20

Sheldon, Kennon M., Mike Corcoran, and Melanie Sheldon. "Duchenne Smiles as Honest Signals of Chronic Positive Mood." Perspectives on Psychological Science 16, no. 3 (2021): 654–66. http://dx.doi.org/10.1177/1745691620959831.

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Chronic positive mood (CPM) has been shown to confer a wide variety of social, functional, and health benefits. Some researchers have argued that humans evolved to feel CPM, which explains why most people report better than neutral mood (the “positivity offset bias”) and why particularly happy people have particularly good outcomes. Here, we argue that the Duchenne smile evolved as an honest signal of high levels of CPM, alerting others to the psychological fitness of the smiler. Duchenne smiles are honest because they express felt positive emotion, making it difficult for unhappy people to produce them. Duchenne smiles enable happy people to signal and cooperate with one another, boosting their advantages. In our literature review, we found (a) that not all Duchenne smiles are “honest,” although producing them in the absence of positive emotion is difficult and often detectable, and (b) that the ability to produce and recognize Duchenne smiles may vary somewhat by a person’s cultural origin. In the final section of the article, we consider behavioral influences on CPM, reviewing research showing that engaging in eudaimonic activity reliably produces CPM, as posited by the eudaimonic-activity model. This research suggests that frequent Duchenne smiling may ultimately signal eudaimonic personality as well as CPM.
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21

Lupu-Merca, Violeta, and Sebastian Vaida. "Benefits of the Duchenne Smile and Positive Emotions. A Systematic Review." Educatia 21, no. 27 (May 14, 2024): 93–102. http://dx.doi.org/10.24193/ed21.2024.27.09.

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The Duchenne smile is the genuine smile characterized by the activation of the muscles around the eyes and mouth. It has been associated, in the specialized literature, with the experience of positive emotions. Through the present work, using a qualitative approach, we aimed to identify and systematize the studies carried out in the period 2010-2023 that investigated the relationship between the Duchenne smile and positive emotions. Following the application of specific keywords, 611 studies were identified, from which, after applying the inclusion-exclusion criteria, 8 studies were included in the review. A conclusion could not be drawn regarding the idea that the Duchenne smile is indisputably an indicator of positive emotions, but the data provide us with important information such as the following: the Duchenne smile is associated with experiencing positive emotions (happiness, joy, hope, contentment) and manifests itself in the context of affiliation and cooperation. It has an important role in triggering extended cognitive states (attentional ones) and can be performed voluntarily (in the presence/absence of a positive emotion), having the same health benefits as spontaneous smiling. In addition, the Duchenne smile increases the acceptance rate of feedback given by teachers in class. The relationship between the Duchenne smile and positive emotions is context dependent.
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22

Khmyzov, Sergij, Anastasiia Hrytsenko, Genadii Kykosh та Anton Hrytsenko. "BIRTH INJURY, DUCHENNE-ERBʼS OBSTETRIC PALSY. DIAGNOSIS AND TREATMENT (LITERATURE REVIEW)". ORTHOPAEDICS TRAUMATOLOGY and PROSTHETICS, № 3 (18 жовтня 2023): 69–78. http://dx.doi.org/10.15674/0030-59872023369-78.

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Obstetric practice dates back thousands of years, providing assistance to women in labor is often complicated by the rapid course of labor, pelvic presentation of the fetus, shoulder dystocia with a possible clavicle fracture. Damage to CV–CVI roots, classic Duchenne–Erb palsy, accounts for 46 % of the total number of obstetric palsies. Objective. To analyze the scientific and medical literature in order to identify historical scientific and practical information about the study of childbirth injuries, and, in particular, Duchenne–Erb's obstetric palsy. Methods. To study and analyze sources of scientific and medical information, publications from Google search engines, electronic databases PubMed, Google Scholar, archival medical journals. Results. The first data on obstetric paralysis were provided by Duchesne in 1872, highlighting thorough reports on upper extremity muscle damage. Subsequently, in 1874, Erb performed electrical stimulation of the affected muscles, finding out the zone of neurological damage. The history of the development and formation of this scientific issue is quite ambiguous, because it borders on two medical fields: neurosurgery and orthopedics. According to literary sources, it is obvious that the pathohistology and pathophysiology of the direct injury zone (roots CV–CVI), delayed changes in the function of the upper limb, and the latest diagnostic technologies simplify the understanding of the presentation. The existing methods of operative interventions allow physicians to improve the child's life. However, the question remains open regarding the use of certain operative interventions in relation to the child's age and further rehabilitation. Conclusions. Despite a significant stratum of scientific and practical research on Duchenne–Erb's obstetric palsy, there are still a number of questions regarding the diagnosis and treatment of children with this abnormality. The search for improving the functional state of the upper limb in children should continue.
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23

Timonen, Anne, Michele Lloyd-Puryear, David M. Hougaard, et al. "Duchenne Muscular Dystrophy Newborn Screening: Evaluation of a New GSP® Neonatal Creatine Kinase-MM Kit in a US and Danish Population." International Journal of Neonatal Screening 5, no. 3 (2019): 27. http://dx.doi.org/10.3390/ijns5030027.

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Duchenne muscular dystrophy (DMD/Duchenne) is a progressive X-linked disease and is the most common pediatric-onset form of muscular dystrophy, affecting approximately 1:5000 live male births. DNA testing for mutations in the dystrophin gene confirms the diagnosis of this disorder. This study involves assessment of screening newborns for DMD using an immunoassay for muscle-type (MM) creatine kinase (CK) isoform—the GSP Neonatal CK-MM kit. Comparisons were made with CK activity determination by fluorescence measurement. In addition, the study evaluated the effect of gestational age, age of infant at time of sampling and how stable the CK-MM was over time. This assay discriminates well between normal, unaffected and Duchenne affected populations and is suitable for Duchenne newborn screening.
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24

Jufan, Akhmad Yun, Djayanti Sari, and Karlina Mahardieni. "DUCHENNE MUSCULER DYSTROPHY." Jurnal Komplikasi Anestesi 3, no. 2 (2023): 47–53. http://dx.doi.org/10.22146/jka.v3i2.7242.

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Duchenne muscular dystrophy merupakan suatu kelainan otot yang sering ditemui. Penyakit ini terpaut pada kromosom X yang disebabkan oleh mutasi gen dystrophin. Gejalanya berupa kelemahan otot proksimal yang berat, bersifat degenerasi progresif dan infi ltrasi lemak ke otot. Efek duchenne muscular dystrophy terhadap otot respirasi dan berhubungan dengan kardio-miopati yang dapat mengarah ke kematian.Dilaporkan anak laki-laki usia 12 tahun dengan diagnosa duchenne muscular dystrophy dd/ Baker’s muscular dystrophy dilakukan prosedur biopsi. Pasien dinilai sebagai status fi sik ASA 2 yang dilakukan general anesthesia dengan teknik TIVA. Setelah persiapan preoperasi, pasien diberikan ko induksi dengan midazolam 1,5mg, induksi dengan ketamine 20mg. Pemeliharaan anestesi dengan O2 melalui nasal kanul. Hemodinamik durante operasi stabil dengan jalan nafas terjaga dengan kepala ekstensi. Operasiberlangsung selama 20menit. Perdarahan minimal dan urine output 25cc. Kondisi pasien setelah operasi stabil dan kembali ke bangsal.
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25

Dubey, Abhishek, Gaurav Dubey, Sambodhan Dhawane, and Rishikesh Sharma. "Duchenne Muscular Disease." American Journal of PharmTech Research 8, no. 5 (2018): 33–54. http://dx.doi.org/10.46624/ajptr.2018.v8.i5.003.

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26

Biggar, W. D. "Duchenne Muscular Dystrophy." Pediatrics in Review 27, no. 3 (2006): 83–88. http://dx.doi.org/10.1542/pir.27-3-83.

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27

Juříková, Lenka, Zdeňka Bálintová, and Jana Haberlová. "Duchenne muscular dystrophy." Neurologie pro praxi 20, no. 3 (2019): 180–82. http://dx.doi.org/10.36290/neu.2019.111.

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28

Kornberg, AndrewJ, and EppieM Yiu. "Duchenne muscular dystrophy." Neurology India 56, no. 3 (2008): 236. http://dx.doi.org/10.4103/0028-3886.43441.

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29

Sussman, Michael. "Duchenne Muscular Dystrophy." Journal of the American Academy of Orthopaedic Surgeons 10, no. 2 (2002): 138–51. http://dx.doi.org/10.5435/00124635-200203000-00009.

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30

Torreggiani, William C., Iain D. Lyburn, Alison C. Harris, and V. A. Rowley. "Duchenne-Landouzy Dystrophy." American Journal of Roentgenology 174, no. 5 (2000): 1467–68. http://dx.doi.org/10.2214/ajr.174.5.1741467a.

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31

Millichap, J. Gordon. "Duchenne Muscular Dystrophy." Pediatric Neurology Briefs 3, no. 5 (1989): 40. http://dx.doi.org/10.15844/pedneurbriefs-3-5-11.

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32

Biggar, W. Douglas. "Duchenne Muscular Dystrophy." Pediatrics In Review 27, no. 3 (2006): 83–88. http://dx.doi.org/10.1542/pir.27.3.83.

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33

Bushby, K. "Duchenne Muscular Dystrophy." Journal of Medical Genetics 31, no. 6 (1994): 506. http://dx.doi.org/10.1136/jmg.31.6.506.

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34

Bundey, S. "Duchenne Muscular Dystrophy." Journal of Medical Genetics 25, no. 2 (1988): 140. http://dx.doi.org/10.1136/jmg.25.2.140.

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35

Bundey, S. "Duchenne Muscular Dystrophy." Journal of Medical Genetics 26, no. 6 (1989): 416. http://dx.doi.org/10.1136/jmg.26.6.416.

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36

Heckmatt, J. Z. "Duchenne Muscular Dystrophy." Archives of Disease in Childhood 64, no. 5 (1989): 767. http://dx.doi.org/10.1136/adc.64.5.767.

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37

McDonald, Craig M., Richard T. Abresch, Gregory T. Carter, et al. "Duchenne Muscular Dystrophy." American Journal of Physical Medicine & Rehabilitation 74, Supplement 1 (1995): S70—S92. http://dx.doi.org/10.1097/00002060-199509001-00003.

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38

Gomez-Merino, Elia, and John R. Bach. "Duchenne Muscular Dystrophy." American Journal of Physical Medicine & Rehabilitation 81, no. 6 (2002): 411–15. http://dx.doi.org/10.1097/00002060-200206000-00003.

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39

Harper, P. "Duchenne Muscular Dystrophy." Journal of Neurology, Neurosurgery & Psychiatry 50, no. 9 (1987): 1249. http://dx.doi.org/10.1136/jnnp.50.9.1249.

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40

Marles, Hugh C. "Duchenne de Boulogne." History of Photography 16, no. 4 (1992): 395–96. http://dx.doi.org/10.1080/03087298.1992.10442576.

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41

Scott, Oona M. "Duchenne Muscular Dystrophy." Physiotherapy 76, no. 3 (1990): 138. http://dx.doi.org/10.1016/s0031-9406(10)62140-2.

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42

Villanova, Marcello, Beatrice Brancalion, and Anokhi D. Mehta. "Duchenne Muscular Dystrophy." American Journal of Physical Medicine & Rehabilitation 93, no. 7 (2014): 595–99. http://dx.doi.org/10.1097/phm.0000000000000074.

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43

Shieh, Perry B. "Duchenne muscular dystrophy." Current Opinion in Neurology 28, no. 5 (2015): 542–46. http://dx.doi.org/10.1097/wco.0000000000000243.

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44

Roper, Helen P. "Duchenne muscular dystrophy." Neuromuscular Disorders 14, no. 5 (2004): 346–47. http://dx.doi.org/10.1016/j.nmd.2004.02.001.

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45

Davies, Kay E. "Duchenne muscular dystrophy." Trends in Genetics 3 (January 1987): 231–32. http://dx.doi.org/10.1016/0168-9525(87)90244-7.

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46

Topaloglu, Haluk. "Duchenne Muscular Dystrophy." European Journal of Paediatric Neurology 8, no. 5 (2004): 269. http://dx.doi.org/10.1016/j.ejpn.2004.05.004.

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47

Bolhuis, P. A. "Duchenne muscular dystrophy." Journal of the Neurological Sciences 80, no. 1 (1987): 118–19. http://dx.doi.org/10.1016/0022-510x(87)90230-9.

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48

Bolhuis, P. A. "Duchenne muscular dystrophy." Journal of the Neurological Sciences 90, no. 3 (1989): 348. http://dx.doi.org/10.1016/0022-510x(89)90125-1.

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49

Samson, Kurt. "DUCHENNE MUSCULAR DYSTROPHY." Neurology Today 3, no. 9 (2003): 1. http://dx.doi.org/10.1097/00132985-200309000-00001.

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50

Casademont, Jordi. "Duchenne Muscular Dystrophy." Clinical Neurophysiology 115, no. 10 (2004): 2426. http://dx.doi.org/10.1016/j.clinph.2004.05.006.

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