Search results for "Myopathies"

showing 10 items of 85 documents

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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Circulating miR-323-3p is a biomarker for cardiomyopathy and an indicator of phenotypic variability in Friedreich’s ataxia patients

2017

AbstractMicroRNAs (miRNAs) are noncoding RNAs that contribute to gene expression modulation by regulating important cellular pathways. In this study, we used small RNA sequencing to identify a series of circulating miRNAs in blood samples taken from Friedreich’s ataxia patients. We were thus able to develop a miRNA biomarker signature to differentiate Friedreich’s ataxia (FRDA) patients from healthy people. Most research on FDRA has focused on understanding the role of frataxin in the mitochondria, and a whole molecular view of pathological pathways underlying FRDA therefore remains to be elucidated. We found seven differentially expressed miRNAs, and we propose that these miRNAs represent …

AdultMale0301 basic medicineSmall RNAAtaxiaSciencePopulationCardiomyopathyBioinformaticsArticleYoung Adult03 medical and health sciencesmicroRNAmedicineHumanseducationCells CulturedAgedCell ProliferationGeneticseducation.field_of_studyMultidisciplinarybiologyQRHigh-Throughput Nucleotide SequencingMiddle AgedPrognosismedicine.diseasePhenotypeMicroRNAs030104 developmental biologyBiological Variation PopulationFriedreich AtaxiaCase-Control StudiesFrataxinbiology.proteinBiomarker (medicine)MedicineFemalemedicine.symptomCardiomyopathiesBiomarkersFollow-Up StudiesScientific Reports
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Anatomical features and clinical correlations in Caucasian patients with definite arrhythmogenic right ventricular dysplasia/cardiomyopathy.

2014

AIM: Arrhythmogenic right ventrticular dysplasia/cardiomyopathy (ARVD/C) is an inherited cardiomyopathy characterized by fibrofatty replacement and a high risk of ventricular arrhythmias (VA) and sudden cardiac death (SCD). The aim of the present investigation is to examine the pathological profile and the clinical correlations in a group of ARVD/C patients. METHODS: We conducted a multicenter study evaluating 47 patients (31 men; mean age 37±14 years) with definite ARVD/C. Diagnosis was established according to the actual clinicomorphologic criteria at autopsy or clinically. We divided the study population in 2 different groups. First group included 28 alive patients and the second 19 pati…

AdultMaleAdolescentEuropean Continental Ancestry GroupLeftAge FactorsAdolescent; Adult; Age Factors; Aged; Arrhythmogenic Right Ventricular Dysplasia; Death Sudden Cardiac; European Continental Ancestry Group; Humans; Male; Middle Aged; Retrospective Studies; Ventricular Dysfunction Left; Young AdultMiddle AgedSettore MED/11 - Malattie Dell'Apparato CardiovascolareSuddenWhite PeopleDeathVentricular Dysfunction LeftYoung AdultDeath Sudden CardiacVentricular DysfunctionHumansCardiomyopathies - Death sudden - Young adult - ExerciseCardiacArrhythmogenic Right Ventricular DysplasiaAgedRetrospective StudiesMinerva cardioangiologica
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Manifestation and ultrastructural typing of amyloid deposits in the heart

1983

Using light and electron microscopy, 65 cases of amyloid deposits in the heart were examined. Five different groups were distinguished: I. isolated atrial amyloidosis, II. senile cardiac amyloidosis, III. cardiac amyloid accompanying chronic infections and tumors, IV. cardiac amyloid accompanying plasma cell dyscrasia, V. idiopathic cardiac amyloidosis. Seen structurally, no principal differences in the precise localization of the amyloid deposits were found in any of the groups investigated. Amyloid is always deposited in the vicinity of cells with myocytic cell differentiation (i.e. the heart muscle cells, non-striated muscle cells of the vessels), whereby the relevant basement membranes …

AdultMaleAmyloidPathologymedicine.medical_specialtyHistologyAdolescentAmyloidHeart diseasePlasma cell dyscrasiaAutopsyBasement MembranePathology and Forensic Medicinemental disordersmedicineHumansIsolated atrial amyloidosisHeart AtriaMolecular BiologyAgedbusiness.industryMyocardiumAmyloidosisCell DifferentiationAmyloidosisCell BiologyGeneral MedicineMiddle Agedmedicine.diseaseCoronary VesselsMicroscopy ElectronCardiac amyloidosisHeart failurecardiovascular systemFemaleAnatomyCardiomyopathiesbusinessVirchows Archiv A Pathological Anatomy and Histopathology
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Vulnerability of the right ventricle to cathodal, anodal, and bipolar stimulation at double diastolic threshold strength

1984

The repetitive ventricular response (RVR) to three stimulation techniques (bipolar, cathodal and anodal) was investigated in 35 patients. 26 patients suffered from coronary heart disease and 9 patients from dilative cardiomyopathy. The stimulation study was performed at a ventricular driving rate of 120/min with one and two premature ventricular extrastimuli. We used rectangular impulses of 1.8 ms duration at duable diastolic threshold strength. RVR was scored as follows: 0: no RVR, 1: one nonstimulated RVR, 2: two nonstimulated RVR, 3: three nonstimulated RVR, 4: four to ten nonstimulated RVR, 5: more than ten nonstimulated RVR lasting less than 2 minutes, 6: sustained ventricular tachycar…

AdultMaleCardiac Catheterizationmedicine.medical_specialtyPhysiologyHeart VentriclesDiastoleCoronary DiseaseStimulationDilative cardiomyopathyElectrocardiographyPhysiology (medical)Internal medicinemedicineHumansAgedStimulation techniquebusiness.industryEffective refractory periodMiddle Agedmedicine.diseaseElectric StimulationBipolar stimulationmedicine.anatomical_structureVentricleAnesthesiaVentricular fibrillationCardiologyFemaleCardiomyopathiesCardiology and Cardiovascular MedicinebusinessBasic Research in Cardiology
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ICD implantation in noncompaction of the left ventricular myocardium: a case report

2009

Isolated noncompaction of the ventricular myocardium (INVM) is an uncommon cardiomyopathy characterized by the persistence of fetal myocardium with prominent trabecular meshwork and deep intertrabecular recesses, often associated with systolic dysfunction and ventricular dilatation. A 23-year-old man from Burkina Faso was referred to our operative unit with a diagnosis of INVM, made with echocardiogram and magnetic resonance imaging and nonsustained ventricular tachycardia. The literature reports the incidence of malignant ventricular arrhythmias in as many as 47% of the patients and sudden cardiac death in almost 50% of them and this supported our decision to perform implantable cardiovert…

AdultMaleICD noncompactionTreatment Outcomeleft ventricle noncompactionICDVentricular Dysfunction RightTachycardia VentricularHumansCardiomyopathiesSettore MED/11 - Malattie Dell'Apparato CardiovascolareDefibrillators Implantable
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A series of West European patients with severe cardiac and skeletal myopathy associated with a de novo R406W mutation in desmin.

2003

Desminopathy is a familial or sporadic cardiac and skeletal muscular dystrophy associated with mutations in desmin. We have previously characterized a de novo desmin R406W mutation in a patient of European origin with early onset muscle weakness in the lower extremities and atrioventricular conduction block requiring a permanent pacemaker. The disease relentlessly progressed resulting in severe incapacity within 5 years after onset. We have now identified three other patients with early onset rapidly progressive cardiac and skeletal myopathy caused by this same desmin R406W mutation. The mutation was present in each studied patient, but not in their parents or other unaffected family member…

AdultMaleModels Molecularmedicine.medical_specialtyPathologyNeurologyHeart diseaseAdolescentAmino Acid MotifsCardiomyopathymacromolecular substancesDiseaseBiologyProtein Structure SecondaryDesmin03 medical and health sciences0302 clinical medicineMuscular DiseasesmedicineHumansMuscular dystrophyMyopathyMuscle SkeletalConserved Sequence030304 developmental biology0303 health sciencesMuscle WeaknessBase SequenceMyocardiumMuscle weaknessAnatomymedicine.diseasePedigreeEuropeHeart BlockNeurologyAmino Acid SubstitutionMutationDisease ProgressionDesminFemaleNeurology (clinical)medicine.symptomCardiomyopathies030217 neurology & neurosurgeryJournal of neurology
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Reducing Body Myopathy with Cytoplasmic Bodies and Rigid Spine Syndrome: A Mixed Congenital Myopathy

2001

At the age of five years a male child started to develop a progressive rigid spine, torsion scoliosis, and flexion contractures of his elbows, knees, hips, and ankles owing to severe proximal and distal muscle weakness. He had three muscle biopsies from three different muscles at ages 7, 11, and 14 years, respectively. Myopathologically, these muscle tissues contained numerous inclusions which, at the ultrastructural level, turned out to be reducing bodies and cytoplasmic bodies, often in close spatial proximity. Similar histological inclusions, although not further identified by histochemistry and electron microscopy, were seen in his maternal grandmother's biopsied muscle tissue who had d…

AdultMaleMuscle tissuePathologymedicine.medical_specialtyWeaknessScoliosisSpinal Muscular Atrophies of ChildhoodSarcomereMyositis Inclusion BodymedicineHumansGenetic Predisposition to DiseaseMuscle SkeletalMyopathyMyositisAgedInclusion Bodiesbusiness.industrySyndromeGeneral MedicineAnatomymedicine.diseasePenetrancePedigreemedicine.anatomical_structureChild PreschoolPediatrics Perinatology and Child HealthDisease ProgressionLordosisFemaleDesminNeurology (clinical)medicine.symptombusinessMyopathies Structural CongenitalNeuropediatrics
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Genotype-phenotype correlations in nemaline myopathy caused by mutations in the genes for nebulin and skeletal muscle alpha-actin.

2003

We present comparisons of the clinical pictures in a series of 60 patients with nemaline myopathy in whom mutations had been identified in the genes for nebulin or skeletal muscle alpha-actin. In the patients with nebulin mutations, the typical form of nemaline myopathy predominated, while severe, mild or intermediate forms were less frequent. Autosomal recessive inheritance had been verified or appeared likely in all nebulin cases. In the patients with actin mutations, the severe form of nemaline myopathy was the most common, but some had the mild or typical form, and a few showed other associated features such as intranuclear rods or actin accumulation. Most cases were sporadic, but in ad…

AdultMalePathologymedicine.medical_specialtyAdolescentGenotypeNonsense mutationDNA Mutational AnalysisMuscle ProteinsBiologymedicine.disease_causeMyopathies Nemaline03 medical and health sciencesNebulin0302 clinical medicineNemaline myopathyGenotypemedicineHumansChildMuscle SkeletalGenetics (clinical)Actin030304 developmental biologyGenetics0303 health sciencesMutationInfantmedicine.diseaseCongenital myopathyPhenotypeActinsPhenotypeNeurologyChild PreschoolPediatrics Perinatology and Child HealthMutationbiology.proteinFemaleNeurology (clinical)030217 neurology & neurosurgeryNeuromuscular disorders : NMD
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The planimetric Grothoff's criteria by cardiac magnetic resonance can improve the specificity of left ventricular non-compaction diagnosis in thalass…

2020

We differentiated the left ventricle non-compaction (LVNC) from hypertrabeculated myocardium due to a negative remodeling in thalassemia intermedia (TI) patients applying linear and planimetric criteria and comparing the cardiovascular magnetic resonance (CMR) findings. CMR images were analyzed in 181 TI patients enrolled in the Myocardial Iron Overload in Thalassemia Network and 27 patients with proved LVNC diagnosis. The CMR diagnostic criteria applied in TI patients were: a modified linear CMR Petersen’s criterion based on a more restrictive ratio of diastolic NC/C > 2.5 at segmental level and the combination of planimetric Grothoff’s criteria (percentage of trabeculated LV myocardial…

AdultMaleThalassemia intermedia · Magnetic resonance imaging · Isolated non-compaction of the ventricular myocardium · ventricular remodelingmedicine.medical_specialtyDatabases FactualThalassemiaIronDiastoleMagnetic Resonance Imaging CineVentricular Function LeftDiagnosis DifferentialYoung AdultPredictive Value of TestsInternal medicinemedicineHumansRadiology Nuclear Medicine and imagingVentricular remodelingCardiac imagingObserver VariationIsolated Noncompaction of the Ventricular Myocardiummedicine.diagnostic_testVentricular Remodelingbusiness.industryMyocardiumbeta-ThalassemiaReproducibility of ResultsMagnetic resonance imagingMiddle Agedmedicine.diseaseFibrosismedicine.anatomical_structureVentricleCase-Control StudiesCardiologyFemaleThalassemia intermediaCardiology and Cardiovascular MedicinebusinessCardiac magnetic resonanceCardiomyopathiesBiomarkers
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