Search results for "Generalized muscle weakness"

showing 2 items of 2 documents

HACD1, a regulator of membrane composition and fluidity, promotes myoblast fusion and skeletal muscle growth

2015

International audience; The reduced diameter of skeletal myofibres is a hallmark of several congenital myopathies, yet the underlying cellular and molecular mechanisms remain elusive. In this study, we investigate the role of HACD1/PTPLA, which is involved in the elongation of the very long chain fatty acids, in muscle fibre formation. In humans and dogs, HACD1 deficiency leads to a congenital myopathy with fibre size disproportion associated with a generalized muscle weakness. Through analysis of HACD1-deficient Labradors, Hacd1-knockout mice, and Hacd1-deficient myoblasts, we provide evidence that HACD1 promotes myoblast fusion during muscle development and regeneration. We further demons…

Male[SPI.GPROC] Engineering Sciences [physics]/Chemical and Process EngineeringCellular differentiationGeneralized muscle weaknessBiologyMuscle Developmentcentronuclear myopathyCell LineMyoblasts03 medical and health scienceschemistry.chemical_compoundMyoblast fusionMice0302 clinical medicineDogsVLCFA[SDV.IDA]Life Sciences [q-bio]/Food engineeringGeneticsmedicineMyocyteAnimalsHumans[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process EngineeringMUFACentronuclear myopathyMuscle SkeletalMolecular Biology030304 developmental biologyMice Knockout0303 health sciencesPTPLACell MembraneSkeletal muscleCell DifferentiationCell BiologyGeneral MedicineArticles[SDV.IDA] Life Sciences [q-bio]/Food engineeringmedicine.diseaseCongenital myopathyLysophosphatidylcholinemedicine.anatomical_structureLPCchemistryBiochemistryFemaleProtein Tyrosine Phosphatasescentronuclear myopathy;lpc;mufa;ptpla;vlcfa030217 neurology & neurosurgery
researchProduct

Clinical and Genetic Aspects of Juvenile Onset Pompe Disease

2021

AbstractLittle is known about clinical symptomatology and genetics of juvenile onset Pompe disease (JOPD). The aims of this study were to analyze how these children are diagnosed, what clinical problems they have, and how phenotype is related to genotype. To accomplish this, we analyzed retrospectively data of 34 patients diagnosed after their first and before completion of their 18th birthday. Median age at diagnosis was 3.9 (range 1.1–17) years. Eight patients (23.5%) developed initial symptoms in the first year, 12 (35%) between 1 and 7 years, and 6 (18%) thereafter. Eight (23.5%) had no clinical symptoms at the time of diagnosis. Indications for diagnostics were a positive family histor…

Pediatricsmedicine.medical_specialtyGeneralized muscle weaknessDisease03 medical and health sciences0302 clinical medicineGenotypeHumansMedicineFamily historyRetrospective Studies030304 developmental biology0303 health sciencesGlycogen Storage Disease Type IIbusiness.industryHypertrophic cardiomyopathyMuscle weaknessalpha-GlucosidasesGeneral Medicinemedicine.disease3. Good healthPhenotypeJuvenile onsetMutationPediatrics Perinatology and Child HealthFailure to thriveNeurology (clinical)medicine.symptombusiness030217 neurology & neurosurgeryNeuropediatrics
researchProduct