Search results for "DYSTROPHY"

showing 10 items of 268 documents

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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Spontaneous mechanical activity and evoked responses in isolated gastric preparations from normal and dystrophic (mdx) mice

2002

This study examined whether alterations of the spontaneous and evoked mechanical activity are present in the stomach of the mdx mouse, the animal model for Duchenne muscular dystrophy. The gastric mechanical activity from whole-organ of normal and mdx mice was recorded in vitro as changes of intraluminal pressure. All gastric preparations developed spontaneous tone and phasic contractions, although the tone of the mdx preparations was significantly greater. Atropine reduced the tone of the two preparations by the same degree. Nomega-nitro-l-arginine methyl ester (l-NAME) significantly increased the tone and spontaneous contractions only in the stomach from normal animals, but did not affect…

MaleNitroprussideDuchenne muscular dystrophymedicine.medical_specialtymdx mouseContraction (grammar)PhysiologyDuchenne muscular dystrophyTetrodotoxinCholinergic AgonistsSettore BIO/09 - FisiologiaContractilityMicechemistry.chemical_compoundOrgan Culture TechniquesInternal medicinemedicineAnimalsNitric Oxide Donorsmdx mouseAnesthetics LocalEnzyme InhibitorsNeuroscience (all)Endocrine and Autonomic SystemsChemistryStomachStomachGastroenterologyMuscle SmoothNitric oxideAnatomyMuscular Dystrophy AnimalGastric smooth musclemedicine.diseaseElectric StimulationMuscular Dystrophy DuchenneGastric mechanical activityAtropineNG-Nitroarginine Methyl Estermedicine.anatomical_structureEndocrinologyMice Inbred mdxTetrodotoxinCholinergicCarbacholMuscle Contractionmedicine.drug
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Dehydroepiandrosterone up-regulates the Adrenoleukodystrophy-related gene (ABCD2) independently of PPAR alpha in rodents

2007

International audience; X-linked adrenoleukodystrophy (X-ALD) is a neurodegenerative disease caused by mutations in the ABCD1 gene, which encodes a peroxisomal ABC transporter, ALDP, supposed to participate in the transport of very long chain fatty acids (VLCFA). The adrenoleukodystrophyrelated protein (ALDRP), which is encoded by the ABCD2 gene, is the closest homolog of ALDP and is considered as a potential therapeutic target since functional redundancy has been demonstrated between the two proteins. Pharmacological induction of Abcd2 by fibrates through the activation of PPARa has been demonstrated in rodent liver. DHEA, the most abundant steroid in human, is described as a PPARa activat…

MalePEROXISOMEProhormonePeroxisome proliferator-activated receptorATP-binding cassette transporterBiochemistryMice0302 clinical medicineABC TRANSPORTERSPPAR-ALPHAAdrenal GlandsTestisDHEACells Culturedchemistry.chemical_classification0303 health sciencesSex CharacteristicsbiologyBrainGeneral MedicineOrgan SizePeroxisome3. Good healthUp-RegulationLiverAdrenoleukodystrophyFemalemedicine.drugAndrostenediolmedicine.medical_specialtyADRENOLEUKODYSTROPHYATP Binding Cassette Transporter Subfamily D03 medical and health sciencesABCD3Internal medicinemedicineABCD2AnimalsPPAR alpha[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRats Wistar030304 developmental biologyActivator (genetics)Body Weightnutritional and metabolic diseasesMembrane ProteinsDehydroepiandrosteronemedicine.diseaseRatsMice Inbred C57BLEndocrinologychemistrybiology.proteinHepatocytesATP-Binding Cassette TransportersAcyl-CoA Oxidase030217 neurology & neurosurgery
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Axonal pathology of the skin in infantile neuroaxonal dystrophy.

1987

Ultrastructural studies on the skin of two patients affected by infantile neuroaxonal dystrophy (INAD) were performed to evaluate its diagnostic value and to discuss the etiology of INAD. While the majority of terminal axons around intradermal glands were dystophic consisting of tubulomembranous and tubulovesicular profiles sometimes accompanied by synaptic vesicles, there were only few dystophic axons inside intradermal nerve bundles. These observations suggest that the primary lesion of INAD is located in terminal and presynaptic axons. Therefore, terminal axons have to be investigated when a diagnostic skin biopsy is performed in INAD.

MalePathologymedicine.medical_specialtyAxonal pathologySynaptic vesiclePathology and Forensic MedicineInfantile neuroaxonal dystrophyCellular and Molecular NeurosciencemedicineHumansAxonNeuroaxonal dystrophySkinmedicine.diagnostic_testbusiness.industryLeukodystrophyInfantAnatomyPrimary lesionmedicine.diseaseAxonsSweat Glandsmedicine.anatomical_structurenervous systemChild PreschoolSkin biopsyFemaleNeurology (clinical)Nervous System DiseasesbusinessActa neuropathologica
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Ultrastructural Pathology of Eccrine Sweat Gland Epithelial Cells in Globoid Cell Leukodystrophy

1993

Three of four children were recognized by deficient β-galactocerebrosidase activities as having globoid cell leukodystrophy inclusions in sweat gland epithelial cells, similar in ultrastructure to those seen in Schwann cells. This observation in globoid cell leukodystrophy emphasizes the need to include sweat gland epithelial cells in examinations of skin in globoid cell leukodystrophy, as well as in any neurometabolic disorder. ( J Child Neurol 1993;8:171-174).

MalePathologymedicine.medical_specialtyBiopsyCellEccrine GlandsBiologyEpitheliumInclusion bodiesUltrastructural Pathology03 medical and health sciences0302 clinical medicine030225 pediatricsSweat glandmedicineHumansEccrine sweat glandChildSkinInclusion Bodiesintegumentary systemLeukodystrophyInfantLipid Metabolismmedicine.diseaseEpitheliumLeukodystrophy Globoid CellMicroscopy Electronmedicine.anatomical_structureChild PreschoolVacuolesPediatrics Perinatology and Child HealthUltrastructureFemaleNeurology (clinical)030217 neurology & neurosurgeryJournal of Child Neurology
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Infantile neuroaxonal dystrophy: Diagnosis by skin biopsy

1991

A child who shows progressive motor and mental deterioration after the first year of life, who has pyramidal signs, marked muscle hypotonia, but no seizures, suggests to have infantile neuroaxonal dystrophy (INAD). Beyond the age of two years, the EEG also entails characteristic findings. Diagnosis may be obtained by an ultrastructural examination of biopsied skin. The respective clinical and morphological findings are recorded and illustrated from four patients in this report.

MalePathologymedicine.medical_specialtyMuscle HypotoniaBiopsySural nerveInfantile neuroaxonal dystrophyDegenerative diseaseDevelopmental NeuroscienceBiopsyHumansMedicineSkinmedicine.diagnostic_testMental deteriorationbusiness.industryLeukodystrophyInfantPeripheral Nervous System DiseasesNeuromuscular DiseasesGeneral Medicinemedicine.diseaseChild PreschoolPediatrics Perinatology and Child HealthSkin biopsyFemaleNeurology (clinical)businessBrain and Development
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Macrophagic myofasciitis plus (distinct types of muscular dystrophy).

2009

Macrophagic myofasciitis (MMF) is a well-known lesion following vaccination with aluminium-containing vaccines. It has abundantly been reported in adults and several times in children, often in single patients or in rather small cohorts. Only few of these published reports on children have shown distinct myopathology of another neuromuscular disease except for MMF. Indications for biopsy often were nondescript clinical features in children, such as hypotonia or delay in motor development but, apparently, never that of suspected MMF. Thus, in previous reports as well as in our two patients, encountering MMF in the biopsied tissue specimens was coincidental. Our two unrelated patients with MM…

MalePathologymedicine.medical_specialtyNeuromuscular diseaseBiopsyMuscle Fibers SkeletalMuscular DystrophiesLesionMicroscopy Electron TransmissionBiopsymedicineHumansMuscular dystrophyMuscle SkeletalMuscle biopsymedicine.diagnostic_testbusiness.industryMacrophagesMacrophagic myofasciitisInfantGeneral Medicinemedicine.diseaseDermatologyHypotoniaPediatrics Perinatology and Child HealthFemaleNeurology (clinical)medicine.symptombusinessNeuropediatrics
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Amyloidosis and Ocular Involvement: an Overview.

2019

Purpose: To describe the ophthalmic manifestations of amyloidosis and the corresponding therapeutic measures.Methods: The 178 patients included in the study had different types of amyloidosis, diagnosed at a single internal medicine institution (Bari, Italy). To provide a comprehensive review of the types of amyloidosis that can be associated with ocular involvement, the images and clinical descriptions of patients with amyloidosis structurally related to gelsolin, keratoepithelin and lactoferrin were obtained in collaborations with the ophthalmology departments of hospitals in Mainz (Germany) and Helsinki (Finland).Results: Overall, ocular morbidity was detected in 41 of the 178 patients w…

MalePathologymedicine.medical_specialtygenetic structuresEye Diseasesmedicine.medical_treatmentCorneal dystrophyDiagnostic Techniques OphthalmologicalEye03 medical and health sciences0302 clinical medicineAA amyloidosismedicineAL amyloidosisHumansCorneal transplantationCorneal epitheliumRetrospective Studiesbiologybusiness.industryAmyloidosisGeneral MedicineAmyloidosisMiddle Agedmedicine.diseaseeye diseases3. Good healthOphthalmologyTransthyretinmedicine.anatomical_structure030221 ophthalmology & optometrybiology.proteinLattice corneal dystrophyFemalesense organsbusiness030217 neurology & neurosurgeryFollow-Up StudiesSeminars in ophthalmology
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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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Recurrent Granular Dystrophy of the Cornea

2006

Purpose: To describe a case of severe corneal granular dystrophy with clinicopathologic and molecular genetic findings. Methods: The DNAs of a 53-year-old male patient suffering from corneal granular dystrophy and nonaffected family members was analyzed by molecular genetic methods. Clinical features, and histopathologic and immunohistochemical findings from the penetrating keratoplasty specimen, are described. Results: Histopathologic and molecular genetic findings confirmed the diagnosis. A new genetic polymorphism is described. Histopathologic evidence supports the assumption of the epithelial origin of the described dystrophy. Conclusions: A severe course of corneal granular dystrophy c…

MalePathologymedicine.medical_specialtymedicine.medical_treatmentDNA Mutational AnalysisBiologyPolymerase Chain ReactionPhototherapeutic keratectomyRecurrenceTransforming Growth Factor betaCorneamedicineHumansMutational statusMolecular BiologyCorneal Dystrophies HereditaryExtracellular Matrix ProteinsPolymorphism GeneticUnusual caseDystrophyExonsMiddle AgedOphthalmologymedicine.anatomical_structureMutationImmunohistochemistrySevere courseNovel mutationKeratoplasty PenetratingCornea
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