Search results for "Dystrophy"

showing 10 items of 268 documents

TEMPORAL STRUCTURE OF THE MUSCULAR DYSTROPHY X-LINKED MOUSE BEHAVIOUR TESTED IN OPEN FIELD

2017

In comparison with wilde type mice, animal models of Duchenne Muscolar Dystrophy (mdx mice) show a different behavioral organization with a more articulated structure of the temporal patterns. Present study sheds light, for the first time, on specific temporal features of behavior in an animal model of DMD.

Duchenne Muscolar Dystrophy mdx mice behavioral organization temporal patternsSettore BIO/09 - Fisiologia
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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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Evidence of oxidative stress in very long chain fatty acid--treated oligodendrocytes and potentialization of ROS production using RNA interference-di…

2011

X-linked adrenoleukodystrophy (X-ALD) and pseudo neonatal adrenoleukodystrophy (P-NALD) are neurodegenerative demyelinating diseases resulting from the functional loss of the peroxisomal ATP-binding cassette transporter D (ABCD1) and from single peroxisomal enzyme deficiency (Acyl-CoA oxidase1: ACOX1), respectively. As these proteins are involved in the catabolism of very long chain fatty acids (VLCFA: C24:0, C26:0), X-ALD and P-NALD patients are characterized by the accumulation of VLCFA in plasma and tissues. Since peroxisomes are involved in the metabolism of reactive oxygen species (ROS) and nitrogen species (RNS), we examined the impact of VLCFA on the oxidative status of 158N murine o…

congenital hereditary and neonatal diseases and abnormalitiesendocrine systemendocrine system diseasesVery long chain fatty acidBlotting Westernmedicine.disease_causeReal-Time Polymerase Chain ReactionTransfectionATP Binding Cassette Transporter Subfamily D Member 1Gas Chromatography-Mass SpectrometrySuperoxide dismutaseLipid peroxidationchemistry.chemical_compoundMicemedicinePeroxisomesAnimalsAdrenoleukodystrophyCells Culturedchemistry.chemical_classificationReactive oxygen speciesbiologyReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceFatty Acidsnutritional and metabolic diseasesPeroxisomemedicine.diseaseFlow CytometryOligodendrogliaOxidative StressBiochemistrychemistryGene Knockdown Techniquesbiology.proteinACOX1AdrenoleukodystrophyATP-Binding Cassette TransportersRNA InterferenceAcyl-CoA OxidaseReactive Oxygen SpeciesOxidation-ReductionOxidative stressNeuroscience
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Psychological aspects in children affected by duchenne de boulogne muscular dystrophy.

2012

Impairment of intelligence in Duchenne muscular dystrophy (DMD) patients was described by Duchenne de Boulogne himself in 1868. Further studies report intelligence disorders with mayor impairment of memory. The aim of the present study was to assess the presence of affective and personality disorders in a group of children affected by DMD. Twenty six male DMD patients, mean age eleven and four months years old, were assessed for their affective and personality disorder. Only eight subjects had a total IQ below average with major difficulties in verbal and visual-spatial memory, comprehension, arithmetic and vocabulary. All the subjects presented some disorders: tendency to marginalization a…

Duchenne muscular dystrophymedicine.medical_specialtylcsh:RC435-571media_common.quotation_subjectDuchenne muscular dystrophylcsh:MedicineDiseaseArticlelcsh:PsychiatrymedicineDuchenne muscular dystrophy psychopathological assessment affective development psychology disorderPersonalityMuscular dystrophyPsychiatrymedia_commonaffective developmentlcsh:Rmedicine.diseasePersonality disordersSettore MED/39 - Neuropsichiatria InfantileComprehensionPsychiatry and Mental healthpsychology disorderAnxietyPsychological aspectsmedicine.symptomPsychologypsychopathological assessmentMental illness
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Fibrate induction of the adrenoleukodystrophy-related gene (ABCD2)

2001

X-linked adrenoleukodystrophy (X-ALD) is a neurodegenerative disease due to a defect in the ABCD1 (ALD) gene. ABCD1, and the two close homologues ABCD2 (ALDR) and ABCD3 (PMP70), are genes encoding ATP-binding cassette half-transporters of the peroxisomal membrane. As overexpression of the ABCD2 or ABCD3 gene can reverse the biochemical phenotype of X-ALD (reduced beta-oxidation of very-long-chain fatty acids), pharmacological induction of these partially redundant genes may represent a therapeutic approach to X-ALD. We previously reported that the ABCD2 and ABCD3 genes could be strongly induced by fibrates, which are hypolipidaemic drugs and peroxisome-proliferators in rodents. We provide e…

MaleTranscription GeneticMolecular Sequence DataResponse elementReceptors Cytoplasmic and NuclearATP-binding cassette transporterATP Binding Cassette Transporter Subfamily DBiochemistryMiceFenofibrateABCD3Sequence Homology Nucleic AcidABCD2medicineAnimalsHumansRats WistarAdrenoleukodystrophyPromoter Regions GeneticGeneHypolipidemic AgentsMice KnockoutBase SequencebiologyDNATransfectionPeroxisomemedicine.diseaseMolecular biologyRatsGene Expression Regulationbiology.proteinATP-Binding Cassette TransportersAdrenoleukodystrophyTranscription FactorsEuropean Journal of Biochemistry
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Further delineation of eye manifestations in homozygous 15q13.3 microdeletions including TRPM1: a differential diagnosis of ceroid lipofuscinosis.

2014

The 15q13.3 heterozygous microdeletion is a fairly common microdeletion syndrome with marked clinical variability and incomplete penetrance. The average size of the deletion, which comprises six genes including CHRNA7, is 1.5 Mb. CHRNA7 has been identified as the gene responsible for the neurological phenotype in this microdeletion syndrome. Only seven patients with a homozygous microdeletion that includes at least CHRNA7, and is inherited from both parents have been described in the literature. The aim of this study was to further describe the distinctive eye manifestations from the analysis in the three French patients diagnosed with the classical 1.5 Mb homozygous microdeletion. Patients…

MalePathologymedicine.medical_specialtygenetic structuresalpha7 Nicotinic Acetylcholine ReceptorEncephalopathyTRPM Cation ChannelsChromosome DisordersBiologyBlindnessEyePupilNeuronal Ceroid-LipofuscinosesNight BlindnessSeizuresIntellectual DisabilityRetinal DystrophiesGeneticsmedicineElectroretinographyMyopiaHumansEye AbnormalitiesChildGenetics (clinical)TRPM1Genetic Association StudiesCongenital stationary night blindnessGeneticsChromosomes Human Pair 15DystrophyEye Diseases HereditaryGenetic Diseases X-LinkedOptic NerveMicrodeletion syndromemedicine.diseasePenetranceChild PreschoolFemalesense organsDifferential diagnosisChromosome DeletionAmerican journal of medical genetics. Part A
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Muscle NAD+ depletion and Serpina3n as molecular determinants of murine cancer cachexia—the effects of blocking myostatin and activins

2020

Objective Cancer cachexia and muscle loss are associated with increased morbidity and mortality. In preclinical animal models, blocking activin receptor (ACVR) ligands has improved survival and prevented muscle wasting in cancer cachexia without an effect on tumour growth. However, the underlying mechanisms are poorly understood. This study aimed to identify cancer cachexia and soluble ACVR (sACVR) administration-evoked changes in muscle proteome. Methods Healthy and C26 tumour-bearing (TB) mice were treated with recombinant sACVR. The sACVR or PBS control were administered either prior to the tumour formation or by continued administration before and after tumour formation. Muscles were an…

MaleEXPRESSIONActivin receptor; APR; C26; Cancer cachexia; Nrk2; OXPHOSlcsh:Internal medicineCachexiaREVERSALActivin ReceptorsMETABOLISMactivin receptorOxidative PhosphorylationCell Line TumorAnimalsMuscle Skeletallcsh:RC31-1245aineenvaihduntaSerpinslihassolut318 Medical biotechnologyNrk2Cancer cachexiaMyostatinNADOXPHOSMUSCULAR-DYSTROPHYActivinsMitochondriaActivin receptorDisease Models AnimalMuscular AtrophyMICESIRTUINSOriginal ArticlesyöpätauditproteiinitC26lihassurkastumasairaudetAPRAcute-Phase Proteinscancer cachexia
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Phenotypic spectrum and genomics of undiagnosed arthrogryposis multiplex congenital

2022

BackgroundArthrogryposis multiplex congenita (AMC) is characterised by congenital joint contractures in two or more body areas. AMC exhibits wide phenotypic and genetic heterogeneity. Our goals were to improve the genetic diagnosis rates of AMC, to evaluate the added value of whole exome sequencing (WES) compared with targeted exome sequencing (TES) and to identify new genes in 315 unrelated undiagnosed AMC families.MethodsSeveral genomic approaches were used including genetic mapping of disease loci in multiplex or consanguineous families, TES then WES. Sanger sequencing was performed to identify or validate variants.ResultsWe achieved disease gene identification in 52.7% of AMC index pati…

musculoskeletal diseasesArtrogriposi múltiple congènitaSettore BIO/18 - GENETICAhuman geneticsneuromuscular diseasesGenomicsBiologyCONTRACTURESCLASSIFICATIONdiseasessymbols.namesakeDiagnòsticGene mappingarthrogryposis multiplex congenitaExome SequencingOF-FUNCTION MUTATIONSGeneticsMedicine and Health SciencesgenomicsHumansGenetics (clinical)Exome sequencingArthrogryposisSanger sequencingGeneticsArthrogryposis multiplex congenitaGenetic heterogeneitySPINAL MUSCULAR-ATROPHYProteinsnervous system malformationsDYSTROPHYDisease gene identificationGENEHuman geneticsPedigreeETIOLOGYPhenotypesymbolsneuromuscularGenèticaTranscription Factors
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Mitochondrial Toxicity in HAART: An Overview of In Vitro Evidence

2011

The combined antiretroviral therapeutic approach currently employed for the treatment of HIV infection, known as Higly Active Antiretroviral Therapy (HAART), has dramatically reduced AIDS-related morbidity and mortality. However, the adverse reactions associated with the long term use of this therapy have now become a major issue and researchers have focused on understanding the cellular mechanisms underlying these drug-induced detrimental effects which englobe a large list of different events including rash and hypersensibility reactions, hepatotoxicity, metabolic disturbances including lipodystrophy, and other metabolic syndrome-like disturbances such as hyperlactatemia, hyperlipedimia, i…

PharmacologyMitochondrial DNAAnti-HIV AgentsMitochondrionBiologyPharmacologymedicine.diseaseDNA MitochondrialReverse transcriptaseMitochondriaMitochondrial toxicityInsulin resistancePharmacotherapyAntiretroviral Therapy Highly ActiveDrug DiscoverymedicineHumansDrug Therapy CombinationHyperlactatemiaLipodystrophyCurrent Pharmaceutical Design
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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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