Search results for " myopathy"

showing 10 items of 69 documents

Novel slow-skeletal myosin (MYH7) mutation in the original myosin storage myopathy kindred

2006

Abstract Myosin storage myopathy (OMIM 608358), a congenital myopathy characterised by subsarcolemmal, hyaline-like accumulations of myosin in Type I muscle fibres, was first described by Cancilla and Colleagues in 1971 [Neurology 1971;21:579–585] in two siblings as ‘familial myopathy with probable lysis of myofibrils in type I muscle fibres'. Two mutations in the slow skeletal myosin heavy chain gene ( MYH7 ) have recently been associated with the disease in other families. We have identified a novel heterozygous Leu1793Pro mutation in MYH7 in DNA from paraffin sections of one of the original siblings. This historical molecular analysis confirms the original cases had myosin storage myopat…

MaleHeterozygotemacromolecular substancesMyosinsBiologymedicine.disease_causeMuscular DiseasesMyofibrilsMyosinmedicineHumansMyopathyGeneGenetics (clinical)GeneticsMutationMyosin Heavy ChainsMyosin storage myopathyDNAExonsmedicine.diseaseMolecular biologyCongenital myopathyMuscle Fibers Slow-TwitchNeurologyChild PreschoolMutationPediatrics Perinatology and Child HealthFemaleMYH7Neurology (clinical)medicine.symptomMyofibrilCardiac MyosinsNeuromuscular Disorders
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Actin-related myopathy without any missense mutation in the ACTA1 gene.

2004

Actinopathies are defined by missense mutations in the ACTA1 gene coding for sarcomeric actin, of which some 70 families have, so far, been identified. Often, but not always, muscle fibers carry large patches of actin filaments. Many such patients also have nemaline myopathy, qualifying actinopathies as a subgroup of nemaline myopathies. This article concerns a then newborn, now 21/2-year-old boy, the first and single child of nonconsanguineous parents, who was born floppy, requiring immediate postnatal assisted ventilation. A quadriceps muscle biopsy revealed large patches of thin myofilaments reacting at light and electron microscopic levels with antibodies against actin but only a few s…

MaleMyofilamentBiopsyDNA Mutational AnalysisMutation MissenseGene mutationBiologymedicine.disease_cause03 medical and health sciences0302 clinical medicineNemaline myopathyMuscular Diseases030225 pediatricsmedicineMissense mutationHumansPoint MutationMyopathyMuscle SkeletalActinMutationInfantmedicine.diseaseMolecular biologyCongenital myopathyActinsPediatrics Perinatology and Child HealthNeurology (clinical)medicine.symptom030217 neurology & neurosurgeryJournal of child neurology
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A new familial congenital myopathy in children with desmin and dystrophin reacting plaques.

1995

In 5 children with a progressive congenital myopathy representing 3 different families, unusual histological, immunohistochemical and ultrastructural changes in skeletal muscle have been found. Histologically, this myopathy was characterized by the presence of fine hyaline plaques devoid of oxidative as well as ATPase enzyme activities. At the ultrastructural level plaques were composed of helical filaments and amorphous dense material. Helical filament storage corresponded to strong desmin as well as ubiquitin immunoreactivity. In addition they were also dystrophin positive. The exclusive appearance of desmin, ubiquitin and dystrophin positive plaques in muscle specimens from 5 children em…

MalePathologymedicine.medical_specialtyAdolescentImmunocytochemistryBiologyDesminDystrophinMyofibrilsBiopsymedicineHumansMyopathyChildUbiquitinsHyalinemedicine.diagnostic_testMusclesSkeletal muscleNeuromuscular Diseasesmedicine.diseaseCongenital myopathyImmunohistochemistryMicroscopy Electronmedicine.anatomical_structureNeurologyChild Preschoolbiology.proteinDesminFemaleNeurology (clinical)medicine.symptomDystrophinJournal of the neurological sciences
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Myofibrillar disorganization characterizes myopathy of camptocormia in Parkinson’s disease

2011

Camptocormia is a highly disabling syndrome that occurs in various diseases but is particularly associated with Parkinson’s disease (PD). Although first described nearly 200 years ago, the morphological changes associated with camptocormia are still under debate and the pathophysiology is unknown. We analyzed paraspinal muscle biopsies of 14 PD patients with camptocormia and compared the findings to sex-matched postmortem controls of comparable age to exclude biopsy site-specific changes. Camptocormia in PD showed a consistent lesion pattern composed of myopathic changes with type-1 fiber hypertrophy, loss of type-2 fibers, loss of oxidative enzyme activity, and acid phosphatase reactivity …

MalePathologymedicine.medical_specialtyParkinson's diseaseMyopathyClinical Neurology610BiologySpinal CurvaturesMuscle hypertrophyPathology and Forensic MedicineLesionMuscular Atrophy Spinal03 medical and health sciencesCamptocormiaMyofibrillar disorganizationCellular and Molecular Neuroscience0302 clinical medicineMyofibrilsBiopsymedicineHumansProspective StudiesMyopathyMuscle SkeletalParkinson’s disease; Camptocormia; Myopathy; Myofibrillar disorganization; ProprioceptionMyositis030304 developmental biologyAgedAged 80 and over0303 health sciencesOriginal Papermedicine.diagnostic_testParkinson DiseaseMiddle Agedmedicine.diseaseProprioceptionPathophysiologyCamptocormiaParkinson’s diseaseFemaleNeurology (clinical)medicine.symptomMedicine & Public Health; Neurosciences; Pathology030217 neurology & neurosurgeryActa Neuropathologica
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169th ENMC International Workshop Rare Structural Congenital Myopathies 6–8 November 2009, Naarden, The Netherlands

2011

This international ENMC workshop assembled 18 clinicians and scientists from Europe, the United States of America, South America, Japan and Australia to discuss “Rare Structural Congenital Myopathies (CM)”. This workshop can be considered a follow-up to an earlier one [1], then and now excluding classical CM on which separate workshops have repeatedly been held at ENMC and respective consortia exist such as on nemaline myopathies, centronuclear myopathies, core myopathies, as well as protein aggregate myopathies. CM can be classified according to CM-specific morphological features, certain epidemiological aspects or on molecular grounds. This workshop addressed those rare CM which, to date,…

MalePediatricsmedicine.medical_specialtybusiness.industryeducationZebra bodiesInfantArticleTubular aggregates myopathyNeurologyChild PreschoolPediatrics Perinatology and Child HealthHumansMedicineFemaleNeurology (clinical)medicine.symptomChildbusinessMyopathyGenetics (clinical)Myopathies Structural CongenitalNetherlandsNeuromuscular Disorders
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Intranuclear nemaline rod myopathy

2006

The clinical, pathologic, and genetic findings of a boy with intranuclear nemaline rod myopathy are described. Serial muscle biopsies revealed myocyte nuclei containing inclusions that were immunoreactive for α-actinin and increased with age. Genetic analysis revealed a Val163Leu ACTA1 mutation previously associated with nemaline rod myopathy. Although initially delayed, he has reached all milestones and remains stable. These findings suggest intranuclear rods may increase with time and do not necessarily imply a poor prognosis. Muscle Nerve, 2006

MalePoor prognosisPathologymedicine.medical_specialtyPhysiologyBiopsyIntranuclear Inclusion BodiesMyopathies Nemalinemedicine.disease_causeCellular and Molecular NeuroscienceNemaline myopathyPhysiology (medical)BiopsymedicineHumansMyocyteIntranuclear Nemaline Rod MyopathyChildMuscle SkeletalMyopathyActinCell NucleusMutationmedicine.diagnostic_testbusiness.industrymedicine.diseaseNeurology (clinical)medicine.symptombusinessMuscle & Nerve
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Pilot study of safety and efficacy of polyprenols in combination with coenzyme Q10 in patients with statin-induced myopathy

2016

Background and objective: Statin-induced myopathy (SIM) has been partially attributed to deficiency of dolichol and coenzyme Q10 (CoQ10). We aimed to test the safety and efficacy of plant polyprenols in combination with CoQ10 for alleviation of SIM. Materials and methods: In an open-label, one-center prospective pilot study patients with SIM received conifer-tree needle polyprenols (4 mg/day) and CoQ10 (100 mg/day) for 8 weeks. Symptoms and safety were evaluated according to symptom severity score (0–10), creatine kinase (CK) levels, exercise test, dynamometry, complete blood count, clinical biochemistry and electrocardiography. Results: Of the 14 patients, 11 completed the study per protoc…

MaleUbiquinoneMyopathyPilot Projects030204 cardiovascular system & hematologyGastroenterologyElectrocardiography0302 clinical medicine030212 general & internal medicineProspective StudiesProspective cohort studyPain MeasurementAged 80 and overMedicine(all)lcsh:R5-920Muscle Weaknessbiologymedicine.diagnostic_testComplete blood countMiddle AgedTreatment OutcomeDrug Therapy CombinationFemalemedicine.symptomlcsh:Medicine (General)Glomerular Filtration Ratemedicine.medical_specialtyStatinmedicine.drug_classRenal functionAsymptomaticPolyprenols03 medical and health sciencesDouble-Blind MethodInternal medicinemedicineHumansMyopathyAgedbusiness.industryTerpenesStatinsMyalgiamedicine.diseaseTracheophytaAutomotive EngineeringPhysical therapybiology.proteinExercise TestCoenzyme Q10Creatine kinaseHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessStatins; Myopathy; Polyprenols; Coenzyme Q10; UbiquinoneBiomarkersKidney diseaseMedicina
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HACD1, a regulator of membrane composition and fluidity, promotes myoblast fusion and skeletal muscle growth

2015

International audience; The reduced diameter of skeletal myofibres is a hallmark of several congenital myopathies, yet the underlying cellular and molecular mechanisms remain elusive. In this study, we investigate the role of HACD1/PTPLA, which is involved in the elongation of the very long chain fatty acids, in muscle fibre formation. In humans and dogs, HACD1 deficiency leads to a congenital myopathy with fibre size disproportion associated with a generalized muscle weakness. Through analysis of HACD1-deficient Labradors, Hacd1-knockout mice, and Hacd1-deficient myoblasts, we provide evidence that HACD1 promotes myoblast fusion during muscle development and regeneration. We further demons…

Male[SPI.GPROC] Engineering Sciences [physics]/Chemical and Process EngineeringCellular differentiationGeneralized muscle weaknessBiologyMuscle Developmentcentronuclear myopathyCell LineMyoblasts03 medical and health scienceschemistry.chemical_compoundMyoblast fusionMice0302 clinical medicineDogsVLCFA[SDV.IDA]Life Sciences [q-bio]/Food engineeringGeneticsmedicineMyocyteAnimalsHumans[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process EngineeringMUFACentronuclear myopathyMuscle SkeletalMolecular Biology030304 developmental biologyMice Knockout0303 health sciencesPTPLACell MembraneSkeletal muscleCell DifferentiationCell BiologyGeneral MedicineArticles[SDV.IDA] Life Sciences [q-bio]/Food engineeringmedicine.diseaseCongenital myopathyLysophosphatidylcholinemedicine.anatomical_structureLPCchemistryBiochemistryFemaleProtein Tyrosine Phosphatasescentronuclear myopathy;lpc;mufa;ptpla;vlcfa030217 neurology & neurosurgery
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Prophylactic Implantable Cardioverter Defibrillator Placement in a Sporadic Desmin Related Myopathy and Cardiomyopathy

2004

Desminopathy is a neuromuscular disorder associated with the accumulation of the protein desmin. This article reports a case of a man with a mutation in the desmin gene suffering from cardiomyopathy and skeletal myopathy. This patient underwent implantable cardioverter defibrillator (ICD) implantation for prognostic considerations and subsequently developed a sustained ventricular tachycardia (SVT). While nonsustained VTs (NSVT) have previously been reported, this is the first time that a SVT could be seen in a patient with this disease.

Malemedicine.medical_specialtyAdolescentmedicine.medical_treatmentCardiomyopathyDiseaseDesminInternal medicineHumansMedicineDESMIN-RELATED MYOPATHYbusiness.industryImplantable Cardioverter-Defibrillator PlacementGeneral MedicineImplantable cardioverter-defibrillatormedicine.diseaseSkeletal myopathyDefibrillators ImplantableSustained ventricular tachycardiaMutationTachycardia VentricularCardiologyDesminCardiomyopathiesCardiology and Cardiovascular MedicinebusinessMyopathies Structural CongenitalPacing and Clinical Electrophysiology
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Mitochondrial myopathy with lactic acidosis and deficient activity of muscle succinate cytochrome-c-oxidoreductase

1984

A male infant had severe muscular hypotonia from birth. Recurrent vomiting with dehydration and severe metabolic acidosis complicated the course. Elevated lactate (up to 12.3 mmol/l; n less than 2), pyruvate (0.4 mmol/l; n less than 0.05) and alanine levels were found in serum with an abnormal lactate/pyruvate ratio (greater than 30; n less than 15). In urine the concentrations of lactate, pyruvate, alanine and of several intermediates of the citric acid cycle were increased. In muscle, numerous disseminated "ragged red fibres" were found by light microscopy; muscle fibres were found to contain subsarcolemmal aggregates of mitochondria, lipid droplets and glycogen by electromicroscopical me…

Malemedicine.medical_specialtySevere muscular hypotoniaRespiratory chainMitochondria Livermacromolecular substancesMitochondrionBiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineMuscular DiseasesMitochondrial myopathy030225 pediatricsInternal medicinemedicineHumansGlycogenMusclesInfantMetabolic acidosismedicine.diseaseMitochondriaMitochondria Muscle3. Good healthCitric acid cycleEndocrinologyBiochemistrychemistryLactic acidosisPediatrics Perinatology and Child HealthLactatesSuccinate Cytochrome c OxidoreductaseAcidosisOxidoreductases030217 neurology & neurosurgeryEuropean Journal of Pediatrics
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