Search results for "Mitochondrial myopathy"

showing 8 items of 8 documents

Mutations of mitochondrial DNA and human death.

1990

In the skeletal muscle of patients with mitochondrial myopathies (Kearns-Sayre syndrome and chronic progressive external ophthalmoplegia) and in the heart and skeletal muscle of healthy persons cells lacking cytochrome c oxidase are found. The respiratory-defective cells have the following features in common: onset of the defect at juvenile or adult age; progressive character of the defect with increasing age; and focal pattern of respiratory-deficient cells (fibers). A statistic mutation of mtDNA in affected cells is suggested to cause the defect of mitochondrial function. It is postulated that the continuous accumulation of respiratory-deficient cells, mainly in the human heart with incre…

Mitochondrial DNAmedicine.medical_specialtyCytochrome-c Oxidase DeficiencyMitochondrionBiologyHuman mitochondrial geneticsDNA MitochondrialMitochondria HeartKearns–Sayre syndromeElectron Transport Complex IVMitochondrial myopathyMuscular DiseasesReference ValuesInternal medicinemedicineAnimalsHumansEcology Evolution Behavior and SystematicsGeneticsMammalsHomoplasmySkeletal muscleGeneral Medicinemedicine.diseaseMitochondria MuscleDeathEndocrinologymedicine.anatomical_structureMutationChronic progressive external ophthalmoplegiaDie Naturwissenschaften
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Mitochondria-related encephalomyopathies.

1989

Owing to advances in morphological and biochemical techniques, the mitochondria-related myopathies and encephalomyopathies have emerged as a still rapidly growing group of primary and secondary metabolic disorders, which may extend from infancy to late adulthood. Impairment of the biochemically diversified mitochondria is reflected in an enormous number of deficiencies, often affecting several mitochondrial enzymes in the same patient; morphologically abnormal mitochondria are common and are thus not specific to individual mitochondrial enzyme deficiencies. Skeletal muscle biopsies have provided a wealth of data through histological and histochemical studies and from isolated mitochondria. …

Isolated mitochondriaPathologymedicine.medical_specialtyBrain DiseasesHistologyAbnormal mitochondriaEncephalopathySkeletal muscleMitochondrionBiologymedicine.diseasePathology and Forensic MedicineMitochondriaDegenerative diseasemedicine.anatomical_structureNeurologyMitochondrial myopathyMetabolic DiseasesMuscular DiseasesPhysiology (medical)medicineHumansNeurology (clinical)Mitochondrial EncephalomyopathiesNeuropathology and applied neurobiology
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Myo-, neuro-, gastrointestinal encephalopathy (MNGIE syndrome) due to partial deficiency of cytochrome-c-oxidase

1987

A 42-year-old woman had a 10-year history of external ophthalmoplegia, malabsorption resulting in chronic malnutrition, muscle atrophy and polyneuropathy. Computer tomography revealed hypodensity of her cerebral white matter. A metabolic disturbance consisted of lactic acidosis after moderate glucose loads with increased excretion of hydroxybutyric and fumaric acids. Post-mortem studies revealed gastrointestinal scleroderma as the morphological manifestation of her malabsorption syndrome, ocular and skeletal myopathy with ragged red fibers, peripheral neuropathy, vascular abnormalities of meningeal and peripheral nerve vessels. Biochemical examination of the liver and muscle tissues reveale…

AdultPathologymedicine.medical_specialtyMalabsorptionGastrointestinal DiseasesEncephalopathyRespiratory chainCytochrome-c Oxidase DeficiencyEyePathology and Forensic Medicine03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineMuscular DiseasesMitochondrial myopathymedicineHumansMuscular dystrophy030304 developmental biology2. Zero hungerBrain Diseases0303 health sciencesbusiness.industryPeripheral Nervous System DiseasesSyndromemedicine.diseaseMitochondria MusclePeripheral neuropathyLactic acidosisFemaleNeurology (clinical)businessPolyneuropathy030217 neurology & neurosurgeryActa Neuropathologica
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Differential expression of PGC-1α and metabolic sensors suggest age-dependent induction of mitochondrial biogenesis in Friedreich ataxia fibroblasts.

2011

11 pages, 6 figures. PMID:21687738[PubMed] PMCID: PMC3110204

MaleAgingMitochondrial DiseasesMitochondrial MyopathyUbiquinoneCardiomyopathylcsh:MedicineMitochondrionAMP-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesAntioxidantsAdenosine TriphosphateAMP-activated protein kinaseTrinucleotide RepeatsFibrosisMolecular Cell BiologyChildlcsh:ScienceHeat-Shock ProteinsRegulation of gene expressionMultidisciplinaryMovement DisordersbiologyNeuromuscular DiseasesMiddle AgedCatalasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCell biologyMitochondriaDNA-Binding ProteinsNeurologyDisease ProgressionMedicineFemalemedicine.symptomSignal TransductionResearch ArticleAdultcongenital hereditary and neonatal diseases and abnormalitiesAtaxiaAdolescentMitochondrial ProteinsmedicineGeneticsHumansBiologyAllelesGlutathione PeroxidaseSuperoxide Dismutaselcsh:RHuman GeneticsFibroblastsmedicine.diseaseMolecular biologyOxidative StressMitochondrial biogenesisGene Expression RegulationFriedreich Ataxiabiology.proteinFrataxinlcsh:QEnergy MetabolismReactive Oxygen SpeciesTranscription FactorsPLoS ONE
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Maternally inherited diabetes and deafness (MIDD): unusual occult exocrine pancreatic manifestation in an affected German family

2000

The mitochondrial (mt) 3243 DNA mutation is an underlying cause of maternally inherited diabetes and deafness (MIDD) syndrome and the syndrome of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). We report an affected German MIDD pedigree with maternal lineage over three generations. The index patient, her mother, her maternal aunt and her maternal grandmother all suffered from diabetes and premature hearing loss and were positive on testing for the mt 3243 DNA mutation. The 27-year-old index patient had a history of grand mal seizures. As sequela of abdominal ultrasound and confirmed by magnetic resonance cholangio-pancreaticography, she was diagnose…

AdultPathologymedicine.medical_specialtyPancreatic diseaseEndocrinology Diabetes and MetabolismEncephalopathyDeafnessMELAS syndromeDNA MitochondrialDiabetes ComplicationsEndocrinologyMitochondrial myopathyGermanyDiabetes MellitusInternal MedicineHumansMedicinePancreatic ductCommon bile ductbusiness.industryPancreatic DuctsCalcinosisPancreatic DiseasesSyndromeGeneral MedicineMiddle Agedmedicine.diseasePedigreemedicine.anatomical_structurePancreatitisLactic acidosisMutationPancreatitisFemalebusinessDilatation PathologicExperimental and Clinical Endocrinology & Diabetes
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Further delineation of a rare recessive encephalomyopathy linked to mutations in GFER thanks to data sharing of whole exome sequencing data

2017

Background Alterations in GFER gene have been associated with progressive mitochondrial myopathy, congenital cataracts, hearing loss, developmental delay, lactic acidosis and respiratory chain deficiency in 3 siblings born to consanguineous Moroccan parents by homozygosity mapping and candidate gene approach (OMIM#613076). Next generation sequencing recently confirmed this association by the finding of compound heterozygous variants in 19-year-old girl with a strikingly similar phenotype, but this ultra-rare entity remains however unknown from most of the scientific community. Materials and methods Whole exome sequencing was performed as part of a "diagnostic odyssey" for suspected mitochon…

AdultMale0301 basic medicineHeterozygoteCandidate geneAdolescentdata sharingMitochondrial diseaseCompound heterozygosityBioinformaticsYoung Adult03 medical and health sciencesMitochondrial myopathyMitochondrial EncephalomyopathiesExome SequencingGeneticsHumansMedicineGenetic Predisposition to DiseaseOxidoreductases Acting on Sulfur Group Donorswhole-exome sequencingChildExomeCytochrome ReductasesGenetics (clinical)Exome sequencing[SDV.GEN]Life Sciences [q-bio]/Geneticsbusiness.industryGFERDisease gene identificationmedicine.diseasePedigree3. Good health030104 developmental biologymitochondrial conditionMutationCongenital cataractsFemale[ SDV.GEN ] Life Sciences [q-bio]/GeneticsbusinessClinical Genetics
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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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Mitochondrial myopathy--a result of clofibrate/etofibrate treatment? Case report.

1985

A 66-year-old man had developed a myopathy while undergoing several periods of etofibrate and clofibrate therapy over the past 5 years. Discontinuation of etofibrate treatment failed to reverse his muscle illness which, however, did not progress. A muscle biopsy revealed a chronic myopathy marked by abundant, abnormally structured muscle mitochondria. His mitochondrial myopathy may represent a forme fruste of the Kearns-Sayre syndrome or other types of mitochondrial myopathy, clinically made evident by the etofibrate/clofibrate therapy, or a permanent, adverse side effect of clofibrate treatment. If the latter assumption proves to be correct, it will indicate that clofibrate therapy may ind…

Malemedicine.medical_specialtySide effectKearns-Sayre SyndromePathology and Forensic Medicine03 medical and health sciencesCellular and Molecular NeuroscienceClofibric Acid0302 clinical medicineMitochondrial myopathyMuscular DiseasesInternal medicinemedicineHumansClofibrateMyopathy030304 developmental biologyAgedHypolipidemic Agents0303 health sciencesMuscle biopsyClofibratemedicine.diagnostic_testbusiness.industryMusclesForme frustemedicine.disease3. Good healthDiscontinuationMitochondria MuscleMicroscopy ElectronEndocrinologyEtofibrateNeurology (clinical)medicine.symptombusiness030217 neurology & neurosurgerymedicine.drugActa neuropathologica
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