Search results for "Hypotonia"

showing 9 items of 49 documents

Branching enzyme deficiency/glycogenosis storage disease type IV presenting as a severe congenital hypotonia: muscle biopsy and autopsy findings, bio…

2010

The fatal infantile neuromuscular presentation of branching enzyme deficiency (glycogen storage disease type IV) due to mutations in the gene encoding the glycogen branching enzyme, is a rare but probably underdiagnosed cause of congenital hypotonia. We report an infant girl with severe generalized hypotonia, born at 33 weeks gestation who required ventilatory assistance since birth. She had bilateral ptosis, mild knee and foot contractures and echocardiographic evidence of cardiomyopathy. A muscle biopsy at 1 month of age showed typical polyglucosan storage. The autopsy at 3.5 months of age showed frontal cortex polymicrogyria and polyglucosan bodies in neurons of basal ganglia, thalamus, …

Pathologymedicine.medical_specialtyMuscle HypotoniaCardiomyopathyAutopsyGlycogen Storage Disease Type IVFatal Outcome14-alpha-Glucan Branching EnzymemedicineGlycogen branching enzymePolymicrogyriaHumansGlycogen storage disease type IVMuscle SkeletalGenetics (clinical)Muscle biopsymedicine.diagnostic_testbiologyInfant NewbornBrainInfantmedicine.diseaseNeurologyPediatrics Perinatology and Child Healthbiology.proteinMuscle HypotoniaFemaleNeurology (clinical)Differential diagnosisInfant PrematureNeuromuscular disorders : NMD
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Muscle degeneration in neuramindase 1 deficient mice results from infiltration of the muscle fibers by expanded connective tissue

2010

AbstractNeuraminidase 1 (NEU1) regulates the catabolism of sialoglycoconjugates in lysosomes. Congenital NEU1 deficiency in children is the basis of sialidosis, a severe neurosomatic disorder in which patients experience a broad spectrum of clinical manifestations varying in the age of onset and severity. Osteoskeletal deformities and muscle hypotonia have been described in patients with sialidosis. Here we present the first comprehensive analysis of the skeletal muscle pathology associated with loss of Neu1 function in mice. In this animal model, skeletal muscles showed an expansion of the epimysial and perimysial spaces, associated with proliferation of fibroblast-like cells and abnormal …

Pathologymedicine.medical_specialtyMuscle HypotoniaMuscle Fibers SkeletalNeuraminidaseConnective tissueApoptosisNEU1BiologyArticleMiceNecrosisNEU1SarcolemmaCell MovementSettore BIO/10 - BiochimicamedicineAnimalsSialidosisMuscular dystrophyMyopathyMolecular BiologySialidosiMetalloproteinaseCell ProliferationMice KnockoutMuscle biopsySialidosisECMmedicine.diagnostic_testSkeletal muscleFibroblastsMuscular Dystrophy Animalmedicine.diseaseLysosomeExtracellular MatrixMuscular Atrophymedicine.anatomical_structureConnective TissueImmunologyMolecular MedicineMuscle biopsymedicine.symptom
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2q13 microdeletion syndrome: Report on a newborn with additional features expanding the phenotype

2021

In this paper we describe an additional newborn patient with craniofacial dysmorphisms, congenital heart disease, hypotonia and a 2q13 deletion of 1.7 Mb, whose clinical and genomic findings are consistent with the diagnosis of 2q13 microdeletion syndrome.

Pediatricsmedicine.medical_specialtyMedicine (General)Heart diseaseCNVgenotype-phenotype correlationR5-920newborngenotype‐phenotype correlationsfollow-upmedicineCraniofacialGenotype-Phenotype Correlationschromosome 2newborn.GeneticsCNVsfollow‐upbusiness.industryRGeneral MedicineMicrodeletion syndromemedicine.diseasePhenotypeHypotoniaMedicinemedicine.symptombusinessClinical Case Reports
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PURA- Related Developmental and Epileptic Encephalopathy: Phenotypic and Genotypic Spectrum

2021

Background and ObjectivesPurine-rich element-binding protein A (PURA) gene encodes Pur-α, a conserved protein essential for normal postnatal brain development. Recently, a PURA syndrome characterized by intellectual disability, hypotonia, epilepsy, and dysmorphic features was suggested. The aim of this study was to define and expand the phenotypic spectrum of PURA syndrome by collecting data, including EEG, from a large cohort of affected patients.MethodsData on unpublished and published cases were collected through the PURA Syndrome Foundation and the literature. Data on clinical, genetic, neuroimaging, and neurophysiologic features were obtained.ResultsA cohort of 142 patients was include…

Pediatricsmedicine.medical_specialtySocio-culturale[SDV.GEN] Life Sciences [q-bio]/GeneticsElectroencephalographyEpilepsyDevelopmental and Epileptic EncephalopathyIntellectual disabilitymedicineGenetics (clinical)feeding difficulties[SDV.GEN]Life Sciences [q-bio]/Geneticsmedicine.diagnostic_testbusiness.industryfungimedicine.diseaseHypotoniaEpileptic spasmsNeonatal hypotonianeonatal hypotoniaEpilepsy syndromesCohortepilepsyNeurology (clinical)medicine.symptombusiness
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An organelle-specific protein landscape identifies novel diseases and molecular mechanisms.

2016

Cellular organelles provide opportunities to relate biological mechanisms to disease. Here we use affinity proteomics, genetics and cell biology to interrogate cilia: poorly understood organelles, where defects cause genetic diseases. Two hundred and seventeen tagged human ciliary proteins create a final landscape of 1,319 proteins, 4,905 interactions and 52 complexes. Reverse tagging, repetition of purifications and statistical analyses, produce a high-resolution network that reveals organelle-specific interactions and complexes not apparent in larger studies, and links vesicle transport, the cytoskeleton, signalling and ubiquitination to ciliary signalling and proteostasis. We observe sub…

Proteomics0301 basic medicineSystems AnalysisDNA Mutational Analysislnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]General Physics and AstronomyDatasets as Topicmethods [Chromatography Affinity]ProteomicsSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Chromatography AffinityMass SpectrometryProtein Interaction Mappingtherapy [Ciliopathies]genetics [Ciliopathies]methods [Molecular Targeted Therapy]Molecular Targeted TherapyProtein Interaction MapsMultidisciplinaryCiliumChemistry (all)Qabnormalities [Spine]pathology [Ciliopathies]genetics [Muscle Hypotonia]therapy [Muscle Hypotonia]Metabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]metabolism [Proteins]isolation & purification [Proteins]physiology [Biological Transport]3. Good healthCell biologyVesicular transport proteinpathology [Dwarfism]metabolism [Cilia]Muscle Hypotoniaddc:500pathology [Muscle Hypotonia]pathology [Spine]genetics [Dwarfism]Rare cancers Radboud Institute for Health Sciences [Radboudumc 9]ScienceDwarfismExocystBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyPhysics and Astronomy (all)03 medical and health sciencesIntraflagellar transportCiliogenesisOrganelleHumansCiliaBiochemistry Genetics and Molecular Biology (all)ProteinsBiological TransportGeneral Chemistrytherapy [Dwarfism]Fibroblastsgenetics [Proteins]CiliopathiesSpinemethods [Protein Interaction Mapping]Renal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]030104 developmental biologyProteostasisHEK293 Cellsmethods [Proteomics]
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BCL11A intellectual developmental disorder: defining the clinical spectrum and genotype-phenotype correlations

2021

AbstractPurposeHeterozygous variants in BCL11A underlie an intellectual developmental disorder with persistence of fetal hemoglobin (BCL11A-IDD, a.k.a. Dias-Logan syndrome). We sought to delineate the genotypic and phenotypic spectrum of BCL11A-IDD.MethodsWe performed an in-depth analysis of 42 patients with BCL11A-IDD ascertained through a collaborative network of clinical and research colleagues. We also reviewed 33 additional affected individuals previously reported in the literature or available through public repositories with clinical information.ResultsMolecular and clinical data analysis of 75 patients with BCL11A-IDD identified 60 unique variants (30 frameshift, 7 missense, 6 splic…

business.industryPostnatal microcephalyMicrodeletion syndromemedicine.diseaseBioinformaticsHypotoniaDevelopmental disorderAutism spectrum disorderIntellectual disabilityFetal hemoglobinmedicineMissense mutationmedicine.symptombusiness
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Arteriovenous fistula of the vertebral artery in a female infant with hypotonia and cephalocorporal disproportion

2010

Background:  Congenital arteriovenous fistulas are exceptional in childhood and imply a therapeutic challenge. Case report: A 9-month-old female infant was studied for cephalocorporal disproportion, hypotonia, progressive muscular atrophy and hyperreflexia. Computed tomography of the brain and electroencephalography were normal. Electromyographic patterns suggested proximal myopathic involvement. A continuous murmur with systolic reinforcement was audible in the neck. Angioresonance detected intracranial aneurysmal dilatations behind the bulbo-medullary junction and cerebral panangiography evidenced a direct vertebrovertebral fistula with extra- and intra-cranial varices and extreme medulla…

medicine.medical_specialtybusiness.industryVertebral arteryFistulamedicine.medical_treatmentArteriovenous fistulaArteriovenous malformationGeneral MedicineHyperreflexiamedicine.diseaseHypotoniaSurgerymedicine.arteryPediatrics Perinatology and Child HealthmedicineRadiologyEmbolizationmedicine.symptombusinessVaricesActa Paediatrica
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The campomelic syndrome: review, report of 17 cases, and follow-up on the currently 17-year-old boy first reported by Maroteaux et al in 1971.

1983

We report 17 cases of the campomelic syndrome (CS) and a follow-up of one of the original patients of Maroteaux et al who is now 17 years old. Our review is based on 97 patients, including our own. An infant with the CS presents at birth with spectacularly short and bowed femora and tibiae. The initial chest radiograph confirms the diagnosis by demonstrating extremely small bladeless scapulae and hypoplastic pedicles of many thoracic vertebrae. Ossification of the sternal segments, pubis, talus, and knee epiphyses is also retarded. Usually the hips are dislocated and talipes equinovarus deformities are present. There is a small chondrocranium and a disproportionately large neurocranium. The…

musculoskeletal diseasesMaleAdolescentH-Y AntigenRespiratory SystemBone and BonesmedicineHumansAbnormalities MultipleGenitaliaHydronephrosisGenetics (clinical)Respiratory Distress Syndrome NewbornRespiratory distressmedicine.diagnostic_testOssificationbusiness.industryInfant NewbornAnatomySyndromemusculoskeletal systemmedicine.diseaseRenal hypoplasiaHypotoniaCampomelic dysplasiamedicine.anatomical_structureCartilageThoracic vertebraeFemalemedicine.symptomChest radiographbusinessAmerican journal of medical genetics
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The Skull in Achondroplasia

1988

The growth disorder in achondroplasia results from abnormalities of endochondral bone formation. Cranial abnormalities originate from the occipital bone, the only region where enchondral bone is formed.

musculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesMuscular hypotoniaThanatophoric dysplasiabusiness.industryOccipital boneAnatomymedicine.diseaseEndochondral bone formationSkullmedicine.anatomical_structuremedicineAchondroplasiabusinessJugular foramen
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