Search results for "MYOPATHY"

showing 10 items of 352 documents

D-2-hydroxyglutarate produced by mutant IDH2 causes cardiomyopathy and neurodegeneration in mice.

2014

Mutations in isocitrate dehydrogenase 1 and 2 (IDH1/2) have been discovered in several cancer types and cause the neurometabolic syndrome D2-hydroxyglutaric aciduria (D2HGA). The mutant enzymes exhibit neomorphic activity resulting in production of D2-hydroxyglutaric acid (D-2HG). To study the pathophysiological consequences of the accumulation of D-2HG, we generated transgenic mice with conditionally activated IDH2R140Q and IDH2R172K alleles. Global induction of mutant IDH2 expression in adults resulted in dilated cardiomyopathy, white matter abnormalities throughout the central nervous system (CNS), and muscular dystrophy. Embryonic activation of mutant IDH2 resulted in more pronounced ph…

Genetically modified mouseTransgeneMutantCardiomyopathyMice NudeBiologyIDH2Cell LineGlutarateschemistry.chemical_compoundMiceGeneticsmedicineAnimalsHumansMuscular dystrophyMice Inbred BALB CGlycogenGene Expression ProfilingGene Expression Regulation DevelopmentalHeartNeurodegenerative Diseasesmedicine.diseaseMolecular biologyIsocitrate DehydrogenaseIsocitrate dehydrogenasechemistryMutationCardiomyopathiesDevelopmental BiologyResearch PaperGenesdevelopment
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Desmin-related myopathy with mallory body-like inclusions is caused by mutations of the selenoprotein N gene

2004

Desmin-related myopathies (DRMs) are a heterogeneous group of muscle disorders, morphologically defined by intrasarcoplasmic aggregates of desmin. Mutations in the desmin and the alpha-B crystallin genes account for approximately one third of the DRM cases. The genetic basis of the other forms remain unknown, including the early-onset, recessive form with Mallory body-like inclusions (MB-DRMs), first described in five related German patients. Recently, we identified the selenoprotein N gene (SEPN1) as responsible for SEPN-related myopathy (SEPN-RM), a unique early-onset myopathy formerly divided in two different nosological categories: rigid spine muscular dystrophy and the severe form of c…

Genetics0303 health scienceseducation.field_of_studyPathologymedicine.medical_specialtySelenoprotein NLocus (genetics)Muscle disorderBiologymedicine.disease03 medical and health sciences0302 clinical medicineNeurologyCrystallinmedicineDesminNeurology (clinical)Muscular dystrophymedicine.symptomeducationMyopathyGene030217 neurology & neurosurgery030304 developmental biologyAnnals of Neurology
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Genome wide association analysis in dilated cardiomyopathy reveals two new key players in systolic heart failure on chromosome 3p25.1 and 22q11.23

2020

SummaryWe present the results of the largest genome wide association study (GWAS) performed so far in dilated cardiomyopathy (DCM), a leading cause of systolic heart failure and cardiovascular death, with 2,719 cases and 4,440 controls in the discovery population. We identified and replicated two new DCM-associated loci, one on chromosome 3p25.1 (lead SNP rs62232870, p = 8.7 × 10−11 and 7.7 × 10−4 in the discovery and replication step, respectively) and the second on chromosome 22q11.23 (lead SNP rs7284877, p = 3.3 × 10−8 and 1.4 × 10−3 in the discovery and replication step, respectively) while confirming two previously identified DCM loci on chromosome 10 and 1, BAG3 and HSPB7. The genetic…

Genetics0303 health scienceseducation.field_of_studyPopulationGenome-wide association studyDilated cardiomyopathyLocus (genetics)030204 cardiovascular system & hematologyBiologymedicine.diseaseGenomeGenetic architecture03 medical and health sciences0302 clinical medicinemedicineSNPeducationGene030304 developmental biology
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Desmin‐related Myopathies

2006

Outstanding progress in elucidating the pathology of muscular disorders at light and electron microscopic levels has allowed the identification of proteins involved in pathological alterations. This, in turn, has led to discoveries of multiple genes and mutations associated with previously poorly understood conditions. An unexpected result is that phenotypically similar and pathogenetically related neuromuscular disorders are associated with mutations in one or the other of several interacting proteins. Keywords: desmin-related myopathy; distal myopathy; cardiomyopathy; desmin and alpha-B crystallin gene mutations; functional analysis; molecular pathogenesis; genotype–phenotype correlations

GeneticsCrystallinMolecular pathogenesismedicineCardiomyopathyDesminGene mutationmedicine.symptomBiologyMyopathymedicine.diseaseGenePathologicaleLS
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Intermediate Filament Diseases: Desminopathy

2008

Desminopathy is one of the most common intermediate filament human disorders associated with mutations in closely interacting proteins, desmin and alphaB-crystallin. The inheritance pattern in familial desminopathy is characterized as autosomal dominant or autosomal recessive, but many cases have no family history. At least some and likely most sporadic desminopathy cases are associated with de novo DES mutations. The age of disease onset and rate of progression may vary depending on the type of inheritance and location of the causative mutation. Typically, the illness presents with lower and later upper limb muscle weakness slowly spreading to involve truncal, neck-flexor, facial and bulba…

GeneticsPathologymedicine.medical_specialtyPoint mutationMutantCardiomyopathyIntermediate Filamentsalpha-Crystallin B ChainGene mutationBiologymedicine.diseaseSudden deathPolymorphism Single NucleotideArticleUpper limb muscle weaknessDesminMuscular DiseasesmedicineDisease ProgressionAnimalsHumansDesminIntermediate filament
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THE NONCOMPACTION OF THE LEFT VENTRICULAR MYOCARDIUM: OUR PEDIATRIC EXPERIENCE

2007

OBJECTIVES: The noncompaction of the left ventricular myocardium is a rare congenital heart disease, characterized by an excessive prominence of trabecular meshwork, spaced out by deep intertrabecular recesses, consequent to the arrest of the normal myocardium embryogenesis. Although there are numerous descriptions, the physiopathological effects of the structural alterations, just like the clinical spectrum and the evolution of the disease, are not totally clarified. In the present study, we have evaluated the natural history of the disease, the familial incidence and the alterations of the systolic and diastolic function. METHODS: We collected a series of 21 young patients who were affect…

Heart Defects CongenitalMalemedicine.medical_specialtygenetic structuresHeart diseaseCardiomyopathyInternal medicineHumansMedicinecardiovascular diseasesNoncompactionChildVentricular dysfunctionUltrasonographybusiness.industryHeart Septal DefectsMyocardiumGeneral Medicinemedicine.diseaseeye diseasesmedicine.anatomical_structureChild Preschoolcardiovascular systemCardiologyLeft ventricular myocardiumFemalesense organsTrabecular meshworkTissue DopplerUltrasonographyCardiology and Cardiovascular Medicinebusiness
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Liver transplantation and combined liver-heart transplantation in patients with familial amyloid polyneuropathy: A single-center experience

2010

Liver transplantation (LT) is the only curative option for patients with familial amyloid polyneuropathy (FAP) at present. Twenty patients with FAP underwent LT between May 1998 and June 2007. Transthyretin mutations included predominantly the Val30Met mutation but also 10 other mutations. Seven patients received a pacemaker prior to LT, and because of impairment of mechanical cardiac function, 4 combined heart-liver transplants were performed, 1 simultaneously and 3 sequentially. The first patient, who underwent simultaneous transplantation, died. Seven patients died after LT, with 5 dying within the first year after transplantation. The causes of death were cardiac complications (4 patien…

Heart transplantationTransplantationmedicine.medical_specialtyHepatologybiologybusiness.industrymedicine.medical_treatmentRestrictive cardiomyopathyLiver transplantationmedicine.diseaseSingle CenterGastroenterologySurgeryTransplantationTransthyretinInternal medicineHeart failuremedicinebiology.proteinSurgerybusinessPolyneuropathyLiver Transplantation
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SYMPTOMATIC ACUTE MYOCARDIAL INFARCTION IN A PATIENT BEARER OF HEART TRANSPLANTATION FOLLOWING ISCHEMIC HEART DISEASE

2008

In 2005 Syeda et al. reported that the major factor limiting the long term of cardiac transplantation is the development of accelerated arteriosclerosis that occurs in the coronary arteries of the cardiac allograft. Transplant arteriosclerosis is characterized by diffuse, uniform, concentric narrowing of the artery by a fibrous proliferation of sub-intima cells. This atherosclerosis was estimate to occur in approximately 50% of patients by 5 years after transplantation. Unfortunately, as a consequence of cardiac denervation, symptoms are often atypical or completely absent. When these are present, the symptoms are those typical of effort angina. Very uncommon is the acute coronary syndrome.…

Heart transplantationmedicine.medical_specialtyAcute coronary syndromeIschemic cardiomyopathybusiness.industrymedicine.medical_treatmentArteriosclerosismedicine.diseaseSettore MED/11 - Malattie Dell'Apparato CardiovascolareSurgeryCoronary artery diseaseTransplantationCoronary arteriessurgical procedures operativemedicine.anatomical_structureInternal medicineAtherosclerosis Heart transplantation Coronary artery diseasemedicineCardiologyMyocardial infarctionCardiology and Cardiovascular Medicinebusiness
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Macrophagic myofasciitis in a 3-month-old child

2015

Macrophagic myofasciitis (MMF) is a rare inflammatory myopathy which occurs after injection of aluminium-containing vaccines against hepatitis B virus (HBV), hepatitis A virus, and tetanus toxoid. Most of the cases reported are from France and are adult patients. We report a rare case of MMF in a 3-month-old male child of Indian origin. He was immunized for HBV at birth after which he developed generalized hypotonia, and central nervous system and peripheral nervous system manifestations at 1 month of age. Muscle biopsy showed typical features of MMF and aluminium could be detected in the muscle biopsy macrophages by ultrastructural examination and LAMMA technique. Our case is the youngest …

Hepatitis B virusPathologymedicine.medical_specialtyMuscle biopsymedicine.diagnostic_testTetanusbusiness.industryGeneralized hypotoniaMacrophagic myofasciitisToxoidmedicine.diseasemedicine.disease_causeInflammatory myopathymedicine.anatomical_structurePeripheral nervous systemPediatrics Perinatology and Child HealthmedicineNeurology (clinical)businessJournal of Pediatric Neurology
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Identification of a novel compound heterozygote SCO2 mutation in cytochrome c oxidase deficient fatal infantile cardioencephalomyopathy

2006

UNLABELLED Fatal infantile cardioencephalomyopathy (OMIM No. 604377) is a disorder of the mitochondrial respiratory chain and is characterised by neonatal progressive muscular hypotonia and cardiomyopathy because of severe Cytochrome c oxidase deficiency. Here we report a novel mutation in the Cytochrome c oxidase assembly gene SCO2 in an infant with fatal infantile cardioencephalomyopathy despite normal initial metabolic screening. CONCLUSION In newborns with unexplained muscular hypotonia and cardiomyopathy genetic testing of mitochondrial respiratory chain disorders might be helpful to establish a final diagnosis and guide treatment decisions.

Heterozygotemedicine.medical_specialtyPathologyCardiomyopathyCytochrome-c Oxidase DeficiencyCompound heterozygositymedicine.disease_causeMitochondrial ProteinsFatal OutcomeMitochondrial EncephalomyopathiesInternal medicinemedicineHumansCytochrome c oxidaseGeneGenetic testingMutationMuscular hypotoniamedicine.diagnostic_testbiologybusiness.industryInfantGeneral Medicinemedicine.diseaseEndocrinologyMitochondrial respiratory chainMutationPediatrics Perinatology and Child Healthbiology.proteinFemaleCardiomyopathiesCarrier ProteinsbusinessMolecular ChaperonesActa Paediatrica
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