Search results for "4-alpha-Glucosidase"

showing 4 items of 4 documents

Skeletal alterations, developmental delay and new mutations in juvenile-onset Pompe disease.

2018

Abstract Pompe disease is an autosomal recessive disorder caused by a deficiency of acid α-glucosidase. In addition to the severe infantile form with cardiac involvement, late-onset variants can affect older children, adolescents (aged >1 year old) or adults. Patients with juvenile (a subgroup of late-onset type) Pompe disease typically do not have cardiac alterations e.g. hypertrophic cardiomyopathy, and the diagnosis is often difficult because it can clinically resemble myriad other neuromuscular disorders. A high level of clinical suspicion is necessary for a timely and accurate diagnosis. We describe 3 interesting cases of patients with juvenile-onset Pompe disease who presented some un…

0301 basic medicineMalePediatricsmedicine.medical_specialtyAdolescentDevelopmental DisabilitiesDisease03 medical and health sciences0302 clinical medicinemedicineJuvenileHumansMuscle SkeletalGenetics (clinical)business.industryGlycogen Storage Disease Type IIGenetic variantsalpha-Glucosidases030104 developmental biologyJuvenile onsetNeurologyPediatrics Perinatology and Child HealthMutationNeurology (clinical)Glucan 14-alpha-Glucosidasebusiness030217 neurology & neurosurgeryNeuromuscular disorders : NMD
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Safety, tolerability, pharmacokinetics, pharmacodynamics, and exploratory efficacy of the novel enzyme replacement therapy avalglucosidase alfa (neoG…

2019

This multicenter/multinational, open-label, ascending-dose study (NCT01898364) evaluated safety, tolerability, pharmacokinetics, pharmacodynamics, and exploratory efficacy of repeat-dose avalglucosidase alfa (neoGAA), a second-generation, recombinant acid α-glucosidase replacement therapy, in late-onset Pompe disease (LOPD). Patients ≥18 years, alglucosidase alfa naïve (Naïve) or previously receiving alglucosidase alfa for ≥9 months (Switch), with baseline FVC ≥50% predicted and independently ambulatory, received every-other-week avalglucosidase alfa 5, 10, or 20 mg/kg over 24 weeks. 9/10 Naïve and 12/14 Switch patients completed the study. Avalglucosidase alfa was well-tolerated; no deaths…

Avalglucosidase alfa (neoGAA)0301 basic medicineMaleGLUCOSE TETRASACCHARIDELysosomal acid alpha-glucosidase (GAA) deficiencyCHILDRENPulmonary function testingMOTOR FUNCTION0302 clinical medicineMedicineGenetics (clinical)Late-onset Pompe disease (LOPD)Glycogen Storage Disease Type IIAlglucosidase alfaMOUSE MODELEnzyme replacement therapyMiddle AgedTreatment OutcomeNeurologyTolerabilityEnzyme replacement therapySKELETAL-MUSCLEFemaleLife Sciences & BiomedicineMUSCLE TRAINING RMTGlycogen6-MINUTE WALKmedicine.drugAdultmedicine.medical_specialtyClinical NeurologyGLYCOGEN03 medical and health sciencesFEV1/FVC ratioPharmacokineticsInternal medicineHumansEnzyme Replacement TherapyAdverse effectAlglucosidase alfaScience & Technologybusiness.industryNeurosciencesalpha-GlucosidasesADULTSGlycogen storage disease type IISEVERITY030104 developmental biologyPharmacodynamicsPediatrics Perinatology and Child HealthNeurosciences & NeurologyNeurology (clinical)Glucan 14-alpha-Glucosidasebusiness030217 neurology & neurosurgeryNeuromuscular Disorders
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A Microassay for Measuring Glycogen in 96-Well-Cultured Cells

1996

Abstract This study describes a rapid, sensitive, and automated spectrophotometric enzymatic microassay that measures the intracellular glycogen of primary cultured hepatocytes and other cultured cells in 96-well plates and can be adapted for other samples that are transferred to these plates. The procedure involves in situ disruption of cells, followed by hydrolysis of glycogen into glucosyl units by fungal glucoamylase (exo-1,4-α- D -glucosidase, EC 3.2.1.3), and glucose determination with the glucose oxidase colorimetric method. The color intensity can be measured in conventional ELISA readers, and the data can be fed to an on-line computer for rapid processing. The advantages of this me…

MaleTime FactorsBiophysicsSensitivity and SpecificityBiochemistryRats Sprague-DawleyHydrolysischemistry.chemical_compoundCarbohydrate ConformationAnimalsGlucose oxidaseMolecular BiologyCells CulturedSample handlingchemistry.chemical_classificationChromatographybiologyGlycogenHydrolysisMicrochemistryfungiColor intensityRapid processingReproducibility of Resultsfood and beveragesDNACell BiologyLiver GlycogenRatsGlucoseEnzymeLiverBiochemistrychemistrybiology.proteinColorimetryGlucan 14-alpha-GlucosidaseIntracellularAnalytical Biochemistry
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Methods for a prompt and reliable laboratory diagnosis of Pompe disease : report from an international consensus meeting

2008

Pompe disease is an autosomal recessive disorder of glycogen metabolism caused by a deficiency of the lysosomal enzyme acid alpha-glucosidase (GAA). It presents at any age, with variable rates of progression ranging from a rapidly progressive course, often fatal by one-year of age, to a more slowly, but nevertheless relentlessly progressive course, resulting in significant morbidity and premature mortality. In infants, early initiation of enzyme replacement therapy is needed to gain the maximum therapeutic benefit, underscoring the need for early diagnosis. Several new methods for measuring GAA activity have been developed. The Pompe Disease Diagnostic Working Group met to review data gener…

Pediatricsmedicine.medical_specialtyEndocrinology Diabetes and MetabolismDiseaseBiochemistryEarly initiationchemistry.chemical_compoundEndocrinologyInternal medicineGlycogen storage disease type IIGeneticsmedicineHumansMolecular BiologyAcarboseMuscle biopsyGlycogenmedicine.diagnostic_testClinical Laboratory TechniquesGlycogen Storage Disease Type IIbusiness.industryInfantEnzyme replacement therapymedicine.diseasePompe disease; laboratory diagnosisEndocrinologychemistryAcid alpha-glucosidaseGlucan 14-alpha-Glucosidasebusinessmedicine.drug
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