Search results for "ceramide"

showing 10 items of 94 documents

Enzyme replacement therapy with agalsidase alfa in children with Fabry disease.

2006

Aim: To assess the effects of enzyme replacement therapy (ERT) in children with Fabry disease. Methods: Safety and efficacy of ERT with agalsidase alfa, 0.2 mg/kg infused over 40 minutes every 2 weeks for 23 weeks, were studied in a multicentre open-label trial in nine boys and four girls. Median age at the start of the study was 11.0 years (range 3.5–18 years). Results: Fifty-four adverse events were reported in 11 patients. No serious adverse events related to ERT were reported. Twelve of the 54 adverse events were considered possibly or probably related to ERT. Infusion reactions (8 mild, 3 moderate) occurred in four boys, in seven infusions. One boy developed IgG antibodies, although he…

MalePediatricsmedicine.medical_specialtyAdolescentGlobotriaosylceramideSweatingchemistry.chemical_compoundQuality of lifemedicineHumansBrief Pain InventoryAdverse effectChildPain Measurementbusiness.industryTrihexosylceramidesGeneral MedicineEnzyme replacement therapymedicine.diseaseFabry diseaseRecombinant ProteinsSurgeryClinical trialIsoenzymesTreatment OutcomeEl NiñochemistryChild Preschoolalpha-GalactosidasePediatrics Perinatology and Child HealthFabry DiseaseFemalebusinessActa paediatrica (Oslo, Norway : 1992)
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Clinical and neuroradiological findings in classic infantile and late-onset globoid-cell leukodystrophy (Krabbe disease)

1996

In the present study the clinical course and imaging of early and late-onset forms of Krabbe disease are analyzed. We report on 11 patients with a biochemical diagnosis of galactosyl ceramide β-galactoside deficiency. Two presented as the classic infantile form and died within the second year of life. In 9 children the first clinical signs, such as gait difficulties and visual failure, started after age 2 years. All these patients developed slow regression of motor and mental capacities, and most of them died within their first decade. In patients of both groups computed tomography (CT) and magnetic resonance imaging (MRI) were performed. In the late-onset form, hypodensities of the central…

MalePediatricsmedicine.medical_specialtyGalactosylceramidesDiseaseWhite matterCentral nervous system diseasemedicineHumansAge of OnsetGenetics (clinical)Pyramidal tractsmedicine.diagnostic_testbusiness.industryBrainInfantMagnetic resonance imagingmedicine.diseaseMagnetic Resonance ImagingLeukodystrophy Globoid Cellmedicine.anatomical_structureEl NiñoSpinal CordChild PreschoolKrabbe diseaseFemaleAge of onsetbusinessTomography X-Ray Computed
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Nitric Oxide Mediates Natural Polyphenol-induced Bcl-2 Down-regulation and Activation of Cell Death in Metastatic B16 Melanoma

2007

Intravenous administration to mice of trans-pterostilbene (t-PTER; 3,5-dimethoxy-4'-hydroxystilbene) and quercetin (QUER; 3,3',4',5,6-pentahydroxyflavone), two structurally related and naturally occurring small polyphenols, inhibits metastatic growth of highly malignant B16 melanoma F10 (B16M-F10) cells. t-PTER and QUER inhibit bcl-2 expression in metastatic cells, which sensitizes them to vascular endothelium-induced cytotoxicity. However, the molecular mechanism(s) linking polyphenol signaling and bcl-2 expression are unknown. NO is a potential bioregulator of apoptosis with controversial effects on Bcl-2 regulation. Polyphenols may affect NO generation. Short-term exposure (60 min/day) t…

MaleProgrammed cell deathCeramideEndotheliumDown-RegulationBiologyNitric OxideBiochemistryMicechemistry.chemical_compoundPhenolsCell Line TumorCell AdhesionmedicineAnimalsRNA MessengerNeoplasm MetastasisCytotoxicityMelanomaMolecular BiologyNitritesFlavonoidsNitratesCell DeathReverse Transcriptase Polymerase Chain ReactionPolyphenolsHydrogen PeroxideCell BiologyGenes bcl-2Cell biologyMice Inbred C57BLEndothelial stem cellmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2Mitochondrial permeability transition porechemistryCell cultureApoptosisMitochondrial MembranesCancer researchEndothelium VascularJournal of Biological Chemistry
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The expression of the Goodpasture antigen-binding protein (ceramide transporter) in adult rat brain

2009

The Goodpasture antigen-binding protein (GPBP) plays a critical role in brain development. Knockdown of GPBP leads to loss of myelinated tracts in the central nervous system and to extensive apoptosis in the brain during early embryogenesis. GPBP was initially identified as a protein associated with the autoantigen in Goodpasture autoimmune syndrome, where it was shown to be a kinase that regulates type IV collagen organization. GPBP isoforms bind and transport ceramide from the endoplasmic reticulum to the Golgi apparatus and are therefore also known as ceramide transporters (CERT). Ceramide dysregulation is involved in autoimmunity and neurodegenerative disorders. In order to analyze the …

MaleTelencephalonmedicine.medical_specialtyCeramideBlotting WesternCentral nervous systemGolgi ApparatusProtein Serine-Threonine KinasesBiologyHippocampal formationCeramidesEndoplasmic ReticulumCellular and Molecular NeuroscienceType IV collagenchemistry.chemical_compoundInternal medicinemedicineAnimalsDiencephalonRats WistarNeuroinflammationBrain MappingNeurodegenerationBrainmedicine.diseaseImmunohistochemistryRatsmedicine.anatomical_structureEndocrinologychemistryCerebral cortexNeuronJournal of Chemical Neuroanatomy
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Treatment of Fabry Disease management with migalastat-outcome from a prospective 24 months observational multicenter study (FAMOUS).

2020

Abstract Aims Fabry disease (FD) is an X-linked lysosomal storage disorder caused by a deficiency of the lysosomal enzyme α-galactosidase A (GLA/AGAL), resulting in the lysosomal accumulation of globotriaosylceramide (Gb3). Patients with amenable GLA mutations can be treated with migalastat, an oral pharmacological chaperone increasing endogenous AGAL activity. In this prospective observational multicentre study, safety as well as cardiovascular, renal, and patient-reported outcomes and disease biomarkers were assessed after 12 and 24 months of migalastat treatment under ‘real-world’ conditions. Methods and results A total of 54 patients (26 females) (33 of these [61.1%] pre-treated with en…

Malemedicine.medical_specialty1-DeoxynojirimycinGlobotriaosylceramideRenal functionDiseaseGastroenterology03 medical and health scienceschemistry.chemical_compoundInternal medicineMigalastatmedicineHumansPharmacology (medical)Prospective Studies030304 developmental biology0303 health sciencesbusiness.industry030305 genetics & heredityDisease ManagementEnzyme replacement therapymedicine.diseaseFabry diseaseMulticenter studychemistryFabry DiseaseObservational studyFemaleCardiology and Cardiovascular MedicinebusinessEuropean heart journal. Cardiovascular pharmacotherapy
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Clinical manifestations of Fabry disease in children: data from the Fabry Outcome Survey.

2006

Background Fabry disease is a rare X-linked disorder caused by deficient activity of the enzyme alpha-galactosidase A. This produces progressive lysosomal accumulation of globotriaosylceramide throughout the body, leading to organ failure and premature death. Aim Here, we present the clinical manifestations of Fabry disease in children enrolled in FOS--the Fabry Outcome Survey--a European database of the natural history of Fabry disease and the effects of enzyme replacement therapy with agalsidase alfa (Replagal). Methods Currently, there are 545 patients in FOS, from 11 European countries. We analysed the baseline demographic and clinical characteristics of 82 of these patients (40 boys, 4…

Malemedicine.medical_specialtyAbdominal painPediatricsHeterozygoteAdolescentDNA Mutational AnalysisGlobotriaosylceramidechemistry.chemical_compoundOutcome Assessment Health CaremedicineHumansAge of OnsetChildStrokebusiness.industryVascular diseaseGeneral MedicineEnzyme replacement therapymedicine.diseaseFabry diseaseRecombinant ProteinsSurgeryAngiokeratomaIsoenzymeschemistryChild Preschoolalpha-GalactosidasePediatrics Perinatology and Child HealthFabry DiseaseFemaleAge of onsetmedicine.symptombusinessActa paediatrica (Oslo, Norway : 1992)
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Fabry disease: enzyme replacement therapy

2003

Fabry disease is a multisystem disorder associated with wide variability in clinical expression. Fabry disease is an X-linked lysosomal storage disorder caused by a deficiency of alpha-galactosidase A. The enzyme defect leads to the systemic accumulation of glycosphingolipids with alpha-galactosyl moieties consisting predominantly of globotriaosylceramide, galabiosylceramide and two additional glycosphingolipids. Four hemizygotes patients with a family history of Fabry disease and deficiency of the enzyme alpha-galactosidase A were selected. Each patient received purified alpha-galactosidase by intravenous infusion (0.2 mg/kg). The infusion was administered every 2 weeks, for 40 min, for a …

Malemedicine.medical_specialtyGlobotriaosylceramideRenal functionVasomotionCorneal dystrophyDermatologyRisk AssessmentGastroenterologyDrug Administration ScheduleSampling Studieschemistry.chemical_compoundInternal medicineHumansMedicineFamily historyInfusions IntravenousDose-Response Relationship Drugbusiness.industryBiopsy NeedleOutcome measuresEnzyme replacement therapymedicine.diseaseImmunohistochemistryFabry diseaseTreatment OutcomeInfectious DiseasesEndocrinologychemistryalpha-GalactosidaseFabry DiseaseFemalebusinessFollow-Up StudiesJournal of the European Academy of Dermatology and Venereology
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Fabry disease defined: baseline clinical manifestations of 366 patients in the Fabry Outcome Survey.

2004

Background  Fabry disease is a rare X-linked disorder caused by deficient activity of the lysosomal enzyme α-galactosidase A. Progressive accumulation of the substrate globotriaosylceramide in cells throughout the body leads to major organ failure and premature death. In response to the recent introduction of enzyme replacement therapy, the Fabry Outcome Survey (FOS) was established to pool data from European clinics on the natural history of this little-known disease and to monitor the long-term efficacy and safety of treatment. This paper presents the first analysis of the FOS database and provides essential baseline data against which the effects of enzyme replacement can be measured. De…

Malemedicine.medical_specialtyPediatricsGenotypeClinical BiochemistryGlobotriaosylceramideDiseaseBiochemistryCohort StudiesDiagnosis Differentialchemistry.chemical_compoundmedicineHumansCornea verticillataVascular diseasebusiness.industryAge FactorsGeneral MedicineEnzyme replacement therapymedicine.diseaseFabry diseaseSurgeryEuropeIsoenzymesTreatment Outcomechemistryalpha-GalactosidaseCohortFabry DiseaseFemaleDifferential diagnosismedicine.symptombusinessEuropean journal of clinical investigation
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The Shwartzman reaction repealed

2007

The article, “ -Galactosylceramide induces protection against lipopolysaccharide-induced shock” (doi:10.1189/jlb.0506298), was selected as a Pivotal Advance because the results suggest that -galactosylceramide ( GalCer), a glycolipid isolated from marine sponges, can protect against the complete morbidity and mortality characterisitic of endotoxin shock by inducing NKT cells to produce TH2 cytokines.

Marine sponges1 o (alpha galactopyranosyl) 2 hexacosanoylamino 134 octadecanetriol alpha galactosylceramide lipopolysaccharideImmunologyCell BiologyTh2 cytokinesBiologyNatural killer T cellMicrobiologyEndotoxin shockGlycolipidShock (circulatory)medicineImmunology and Allergylipids (amino acids peptides and proteins)medicine.symptom
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Frequency of Fabry disease in patients with small-fibre neuropathy of unknown aetiology: a pilot study

2010

Background:  Early occurrence of small-fibre neuropathy (SFN) is a common feature of Fabry disease (FD) – an X-linked storage disorder caused by reduced activity of the α-galactosidase A (α-GAL). Although SFN may result from different disorders, the cause is often unclear. Therefore, we investigated the frequency of FD in patients with SFN of unknown aetiology. Methods:  Patients with idiopathic SFN, established by sensory quantitative testing and/or skin biopsy, were examined for mutations in the α-GAL gene. Where mutations in the α-GAL gene were identified, levels of globotriaosylceramide (Gb3) were measured in urine and blood and the α-GAL activity was evaluated. When new mutations were …

Mutationmedicine.medical_specialtyPathologyAlpha-galactosidasemedicine.diagnostic_testbiologybusiness.industryHaplotypeGlobotriaosylceramideEnzyme replacement therapymedicine.diseasemedicine.disease_causeFabry diseaseGastroenterologyPathogenesischemistry.chemical_compoundNeurologychemistryInternal medicineSkin biopsymedicinebiology.proteinNeurology (clinical)businessEuropean Journal of Neurology
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