Search results for "Muscular Dystrophies"

showing 10 items of 24 documents

Targeted Re-Sequencing Emulsion PCR Panel for Myopathies: Results in 94 Cases.

2016

BACKGROUND Molecular diagnostics in the genetic myopathies often requires testing of the largest and most complex transcript units in the human genome (DMD, TTN, NEB). Iteratively targeting single genes for sequencing has traditionally entailed high costs and long turnaround times. Exome sequencing has begun to supplant single targeted genes, but there are concerns regarding coverage and needed depth of the very large and complex genes that frequently cause myopathies. OBJECTIVE To evaluate efficiency of next-generation sequencing technologies to provide molecular diagnostics for patients with previously undiagnosed myopathies. METHODS We tested a targeted re-sequencing approach, using a 45…

0301 basic medicineBiologyPolymerase Chain ReactionMuscular Dystrophies03 medical and health sciencesExon0302 clinical medicineMuscular DiseasesHumansGenetic TestingGeneExomeExome sequencingGeneticsMassive parallel sequencingHigh-Throughput Nucleotide SequencingSequence Analysis DNAMolecular diagnostics030104 developmental biologyNeurologyMolecular Diagnostic TechniquesRe sequencingMutationHuman genomeNeurology (clinical)030217 neurology & neurosurgery
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Congenital muscular dystrophy: from muscle to brain.

2016

Congenital muscular dystrophies (CMDs) are a wide group of muscular disorders that manifest with very early onset of muscular weakness, sometime associated to severe brain involvement. The histologic pattern of muscle anomalies is typical of dystrophic lesions but quite variable depending on the different stages and on the severity of the disorder. Recent classification of CMDs have been reported most of which based on the combination of clinical, biochemical, molecular and genetic findings, but genotype/phenotype correlation are in constant progression due to more diffuse utilization of the molecular analysis. In this article, the Authors report on CMDs belonging to the group of dystroglyc…

0301 basic medicinePediatricsmedicine.medical_specialtyMuscle-eye-brain diseaseMuscular dystrophiesDiseaseReviewSeverity of Illness IndexNODiagnosis Differential03 medical and health sciencesMuscular dystrophie0302 clinical medicineBrain involvement; Congenital muscle diseases; Fukuyama congenital muscular dystrophy; Muscle-eye-brain disease; Muscular dystrophies; Walker-Warburg syndrome;Fukuyama congenital muscular dystrophySeverity of illnessmedicineHumansFukuyama congenital muscular dystrophyBrain involvement; Congenital muscle diseaseWalker–Warburg syndromeCongenital muscle diseasesWalker-Warburg syndromebusiness.industryInfant NewbornBrainmedicine.diseaseVery early onsetMolecular analysis030104 developmental biologyClinical diagnosisCongenital muscle diseaseCongenital muscular dystrophyPhysical therapybusinessBrain involvement030217 neurology & neurosurgery
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A Roma founder BIN1 mutation causes a novel phenotype of centronuclear myopathy with rigid spine

2018

ObjectiveTo describe a large series of BIN1 patients, in which a novel founder mutation in the Roma population of southern Spain has been identified.MethodsPatients diagnosed with centronuclear myopathy (CNM) at 5 major reference centers for neuromuscular disease in Spain (n = 53) were screened for BIN1 mutations. Clinical, histologic, radiologic, and genetic features were analyzed.ResultsEighteen patients from 13 families carried the p.Arg234Cys variant; 16 of them were homozygous for it and 2 had compound heterozygous p.Arg234Cys/p.Arg145Cys mutations. Both BIN1 variants have only been identified in Roma, causing 100% of CNM in this ethnic group in our cohort. The haplotype analysis confi…

Adult0301 basic medicinemedicine.medical_specialtyRomaNeuromuscular diseaseAdolescentPopulationMallory BodiesCompound heterozygosityArticleMuscular DystrophiesCohort StudiesYoung Adult03 medical and health sciences0302 clinical medicineInternal medicinemedicineHumansProspective StudiesCentronuclear myopathyChildeducationProspective cohort studyAdaptor Proteins Signal TransducingRetrospective Studieseducation.field_of_studybusiness.industryTumor Suppressor ProteinsHaplotypeNuclear ProteinsRetrospective cohort studyMiddle Agedmedicine.diseaseFounder EffectPhenotype030104 developmental biologyScoliosisSpainMutation[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Neurology (clinical)business030217 neurology & neurosurgeryMyopathies Structural CongenitalFounder effect
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Oculopharyngeal muscular dystrophy in a northern German family linked to chromosome 14q, and presenting carnitine deficiency

1997

We report the evaluation of oculopharyngeal muscular dystrophy (OPMD) in a large northern German family, which can be traced back six generations and is unrelated to French-Canadian families. The symptoms in this family start at about 50 years of age and include dysphagia, bilateral ptosis, and in some cases a slowly progressive atrophy and weakness of other extraocular, facial or limb girdle muscles. The muscle biopsies showed the pathognomonic ultrastructural finding of characteristic intranuclear filaments. Linkage analysis confirmed that this family is also linked to chromosome 14q markers. Haplotype analysis revealed that a unique haplotype segregates with the disease which is differen…

AdultMaleProbandPathologymedicine.medical_specialtyWeaknessGenetic LinkageBiopsyBiologyMuscular DystrophiesOculopharyngeal muscular dystrophySural NervePathognomonicGenetic linkageCarnitineGermanymedicineHumansCarnitineGenetics (clinical)AgedChromosomes Human Pair 14Family HealthGeneticsElectromyographyHaplotypeMiddle Agedmedicine.diseaseDysphagiaMitochondriaPedigreeMicroscopy ElectronPhenotypeNeurologyOculomotor MusclesPediatrics Perinatology and Child HealthPharyngeal MusclesFemaleNeurology (clinical)medicine.symptommedicine.drugNeuromuscular Disorders
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Evoked potential study in facio-scapulo-humeral muscular dystrophy.

1997

Nerve conduction velocities (NCVs), somatosensory (SEPs) and auditory evoked potentials (BAEPs) were recorded in 9 patients with facio-scapulo-humeral dystrophy (FSHD) and in 20 age-matched controls. In FSHD patients a significant increase of the nerve distal sensory latencies and of the absolute SEP latencies revealed a subclinical involvement of the afferent sensory pathways, as well as the abnormal slowing of the later components of the BAEPs, pointed to a central auditory dysfunction. Moreover all patients underwent brain MRI that showed the presence of white matter hyperintense lesions in 4 of them (44%). No correlations were found between individual or total number of SEP and BAEP abn…

AdultMalemedicine.medical_specialtyShoulderNeural ConductionSensory systemSomatosensory systemSeverity of Illness IndexNerve conduction velocityMuscular DystrophiesWhite matterInternal medicineEvoked Potentials SomatosensorymedicineEvoked Potentials Auditory Brain StemHumansMuscular dystrophyAuditory Diseases CentralSubclinical infectionChi-Square DistributionDystrophyBrainGenetic VariationGeneral MedicineMiddle Agedmedicine.diseaseMagnetic Resonance ImagingMedian Nervemedicine.anatomical_structureNeurologySomatosensory evoked potentialCase-Control StudiesFaceCardiologyArmFemaleNeurology (clinical)Tibial NervePsychologyNeuroscienceActa neurologica Scandinavica
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MMP-10 Is Required for Efficient Muscle Regeneration in Mouse Models of Injury and Muscular Dystrophy

2013

Abstract Matrix metalloproteinases (MMPs), a family of endopeptidases that are involved in the degradation of extracellular matrix components, have been implicated in skeletal muscle regeneration. Among the MMPs, MMP-2 and MMP-9 are upregulated in Duchenne muscular dystrophy (DMD), a fatal X-linked muscle disorder. However, inhibition or overexpression of specific MMPs in a mouse model of DMD (mdx) has yielded mixed results regarding disease progression, depending on the MMP studied. Here, we have examined the role of MMP-10 in muscle regeneration during injury and muscular dystrophy. We found that skeletal muscle increases MMP-10 protein expression in response to damage (notexin) or diseas…

Duchenne muscular dystrophyMatrix metalloproteinaseBiologyMuscle disorderMuscular DystrophiesExtracellular matrixMiceMatrix Metalloproteinase 10medicineAnimalsHumansRegenerationMuscular dystrophyMuscle SkeletalRegeneration (biology)Skeletal muscleCell BiologyAnatomymedicine.diseaseCell biologyDisease Models Animalmedicine.anatomical_structureMatrix Metalloproteinase 9Mice Inbred mdxMatrix Metalloproteinase 2Molecular MedicineITGA7Developmental BiologyStem Cells
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Absence of dysferlin alters myogenin expression and delays human muscle differentiation 'in vitro'

2006

Mutations in dysferlin cause a type of muscular dystrophy known as dysferlinopathy. Dysferlin may be involved in muscle repair and differentiation. We compared normal human skeletal muscle cultures expressing dysferlin with muscle cultures from dysferlinopathy patients. We quantified the fusion index of myoblasts as a measure of muscle development and conducted optic and electronic microscopy, immunofluorescence, Western blot, flow cytometry, and real-time PCR at different developmental stages. Short interference RNA was used to corroborate the results obtained in dysferlin-deficient cultures. A luciferase reporter assay was performed to study myogenin activity in dysferlin-deficient cultur…

MaleDysferlinopathyMuscle ProteinsIn Vitro TechniquesBiochemistryMuscular DystrophiesDysferlinmedicineMyocyteHumansMuscular dystrophyMuscle SkeletalMolecular BiologyDysferlinMyogeninCells CulturedbiologyMyogenesisMusclesSkeletal muscleMembrane ProteinsCell DifferentiationCell Biologymedicine.diseaseMolecular biologyCD56 Antigenmedicine.anatomical_structureGene Expression RegulationCase-Control Studiesbiology.proteinFemaleMyogeninMyofibrilSignal Transduction
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Inhibition of autophagy rescues muscle atrophy in a LGMDD2 Drosophila model

2021

Limb-girdle muscular dystrophy D2 (LGMDD2) is an ultrarare autosomal dominant myopathy caused by mutation of the normal stop codon of the TNPO3 nuclear importin. The mutant protein carries a 15 amino acid C-terminal extension associated with pathogenicity. Here we report the first animal model of the disease by expressing the human mutant TNPO3 gene in Drosophila musculature or motor neurons and concomitantly silencing the endogenous expression of the fly protein ortholog. A similar genotype expressing wildtype TNPO3 served as a control. Phenotypes characterization revealed that mutant TNPO3 expression targeted at muscles or motor neurons caused LGMDD2-like phenotypes such as muscle degener…

MaleMutantBiochemistryAnimals Genetically ModifiedMutant proteinAutophagyGeneticsmedicineAnimalsHumansGene silencingMuscular dystrophyMyopathyMolecular BiologyMotor NeuronsbiologyMusclesAutophagyChloroquinebeta Karyopherinsmedicine.diseasebiology.organism_classificationMuscle atrophyCell biologySurvival RateDisease Models AnimalMuscular AtrophyDrosophila melanogasterPhenotypeMuscular Dystrophies Limb-GirdleInsect HormonesFemalemedicine.symptomDrosophila melanogasterLocomotionBiotechnologyThe FASEB Journal
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Macrophagic myofasciitis plus (distinct types of muscular dystrophy).

2009

Macrophagic myofasciitis (MMF) is a well-known lesion following vaccination with aluminium-containing vaccines. It has abundantly been reported in adults and several times in children, often in single patients or in rather small cohorts. Only few of these published reports on children have shown distinct myopathology of another neuromuscular disease except for MMF. Indications for biopsy often were nondescript clinical features in children, such as hypotonia or delay in motor development but, apparently, never that of suspected MMF. Thus, in previous reports as well as in our two patients, encountering MMF in the biopsied tissue specimens was coincidental. Our two unrelated patients with MM…

MalePathologymedicine.medical_specialtyNeuromuscular diseaseBiopsyMuscle Fibers SkeletalMuscular DystrophiesLesionMicroscopy Electron TransmissionBiopsymedicineHumansMuscular dystrophyMuscle SkeletalMuscle biopsymedicine.diagnostic_testbusiness.industryMacrophagesMacrophagic myofasciitisInfantGeneral Medicinemedicine.diseaseDermatologyHypotoniaPediatrics Perinatology and Child HealthFemaleNeurology (clinical)medicine.symptombusinessNeuropediatrics
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Deflazacort vs. prednisone in Duchenne muscular dystrophy: trends of an ongoing study

1995

Several studies have demonstrated the slowing effect of corticosteroids on the decline of muscle strength in Duchenne muscular dystrophy (DMD). Deflazacort (DFC) is supposed to have fewer side effects than prednisone (PRED). An ongoing double blind multicenter study is comparing the effects and side effects of deflazacort (0.9 mg/kg/day) and prednisone (0.75 mg/kg/day) in DMD. This interim report includes data for 67 boys between age 5 years and loss of ambulation. Besides the common clinical and laboratory data for chronic corticoid treatment, motor performance has been tested. Interim results, 3-15 months after starting the medication, show some scattering but no grouping of data for all …

Malemedicine.medical_specialtyDuchenne muscular dystrophyAnti-Inflammatory AgentsMuscular DystrophiesDouble-Blind MethodDevelopmental NeurosciencePregnenedionesPrednisoneInternal medicinemedicineHumansChildCreatine KinaseDose-Response Relationship Drugbiologybusiness.industryBody WeightGeneral MedicineAlkaline Phosphatasemedicine.diseaseClinical trialDeflazacortDose–response relationshipEndocrinologyNeurologyMulticenter studyChild PreschoolAnesthesiaPediatrics Perinatology and Child HealthOsteocalcinbiology.proteinPrednisoneNeurology (clinical)medicine.symptombusinessWeight gainMuscle Contractionmedicine.drugBrain and Development
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