Search results for "Lipidoses"

showing 10 items of 11 documents

A lipidomic cell-based assay for studying drug-induced phospholipidosis and steatosis

2017

Phospholipidosis and steatosis are two toxic effects, which course with overaccumulation of different classes of lipids in the liver. MS-based lipidomics has become a powerful tool for the comprehensive determination of lipids. LC-MS lipid profiling of HepG2 cells is proposed as an in vitro assay to study and anticipate phospholipidosis and steatosis. Cells with and without pre-incubation with a mixture of free fatty acids (FFA) (i.e., oleic and palmitic) were exposed to a set of well-known steatogenic and phospholipidogenic compounds. The use of FFA pre-loading accelerated the accumulation of phospholipids thus leading to a better discrimination of phospholipidosis, and magnified the lipid…

0301 basic medicineDrugmedia_common.quotation_subjectClinical BiochemistryLipidosesModels BiologicalBiochemistryMass SpectrometryAnalytical Chemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineLipidomicsmedicineHumansPhosphatidylserinesLeast-Squares AnalysisPhospholipidsmedia_commonPhospholipidosisChemistryComputational BiologyHep G2 Cellsmedicine.diseaseIn vitroFatty LiverOleic acid030104 developmental biologyBiochemistry030220 oncology & carcinogenesislipids (amino acids peptides and proteins)Chemical and Drug Induced Liver InjurySteatosisIntracellularChromatography LiquidELECTROPHORESIS
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Mucolipidosis I: increased sialic acid content and deficiency of an alpha-N-acetylneuraminidase in cultured fibroblasts.

1977

Abstract Extracts of fibroblasts derived from a patient with mucolipidosis I exhibited a fivefold increase in sialic acid content as compared to those of normal cells. About 80% of this sialic acid was linked to other molecules. Using neuraminlactose as a substrate, mucolipidosis I fibroblasts were found to be severely deficient in an “acid” α-N-acetylneuraminidase. Since other lysosomal hydrolase activities were normal, we hypothesize that the basic metabolic lesion in mucolipidosis I lies in a defective degradation of sialic acid-containing compounds due to the genetic deficiency of a neuraminidase.

BiophysicsNeuraminidaseBiochemistryLesionchemistry.chemical_compoundMucolipidosesMucolipidosis IHydrolasemedicineHumansSialidosisMolecular BiologyCells CulturedSkinbiologyMucolipidosesSubstrate (chemistry)Cell BiologyFibroblastsmedicine.diseaseSialic acidBiochemistrychemistrybiology.proteinSialic Acidsmedicine.symptomNeuraminidaseBiochemical and biophysical research communications
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Neuraminidase deficiency presenting as non-immune hydrops fetalis

1984

A newborn infant with oedema, ascites and hepatosplenomegaly is described. In ascites fluid foamy macrophages were found, in a liver biopsy cytoplasmic inclusions and membrane-bound vacuoles were seen. Furthermore the child excreted excessive amounts of sialic acid-rich oligosaccharides in the urine, and therefore a neurovisceral degenerative disorder was assumed. The diagnosis of sialidosis was confirmed by enzymatic assay in cultured fibroblasts, in which a complete deficiency of the lysosomal enzyme neuraminidase could be demonstrated. After recurrent septicaemias the child became dystrophic and died at the age of 6 months. Our case is compared with sialidosis observed by other authors, …

Cytoplasmic inclusionHepatosplenomegalyNeuraminidaseOligosaccharidesMucolipidosesalpha-MannosidaseHydrops fetalisMannosidasesAscitesLeukocytesmedicineLysosomal storage diseaseEdemaHumansSialidosisalpha-L-Fucosidasemedicine.diagnostic_testbiologybusiness.industryInfant NewbornFibroblastsbeta-Galactosidasemedicine.diseasebeta-N-AcetylhexosaminidasesHexosaminidasesLiverLiver biopsyPediatrics Perinatology and Child HealthImmunologybiology.proteinFemalemedicine.symptomLysosomesbusinessNeuraminidaseEuropean Journal of Pediatrics
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Presenting signs and patient co-variables in Gaucher disease: outcome of the Gaucher Earlier Diagnosis Consensus (GED-C) Delphi initiative.

2019

Background: Gaucher disease (GD) presents with a range of signs and symptoms. Physicians can fail to recognise the early stages of GD owing to a lack of disease awareness, which can lead to significant diagnostic delays and sometimes irreversible but avoidable morbidities. Aim: The Gaucher Earlier Diagnosis Consensus (GED-C) initiative aimed to identify signs and co-variables considered most indicative of early type 1 and type 3 GD, to help non-specialists identify ‘at-risk’ patients who may benefit from diagnostic testing. Methods: An anonymous, three-round Delphi consensus process was deployed among a global panel of 22 specialists in GD (median experience 17.5 years, collectively managin…

Delphi TechniqueDisease outcomethrombocytopeniaMedicina Clínica030204 cardiovascular system & hematology0302 clinical medicine//purl.org/becyt/ford/3.2 [https]Lysosomal storage disease030212 general & internal medicinecomputer.programming_languageGaucher Malaltia de:Ciencias de la información::análisis de sistemas::técnica Delfos [CIENCIA DE LA INFORMACIÓN]lysosomal storage diseaseINBORN ERROR:Information Science::Systems Analysis::Delphi Technique [INFORMATION SCIENCE]Original Article//purl.org/becyt/ford/3 [https]Corrigendum:Diagnosis::Early Diagnosis [ANALYTICAL DIAGNOSTIC AND THERAPEUTIC TECHNIQUES AND EQUIPMENT]medicine.medical_specialtyCIENCIAS MÉDICAS Y DE LA SALUDSPLENOMEGALYConsensusPrognosiLYSOSOMAL STORAGE DISEASEMETABOLISMinborn error03 medical and health sciencesPhysiciansInternal MedicinemedicineHumansHematologíaALGORITHM:enfermedades del sistema nervioso::enfermedades del sistema nervioso central::enfermedades cerebrales::enfermedades cerebrales metabólicas::enfermedades cerebrales metabólicas congénitas::enfermedades por almacenamiento lisosómico del sistema nervioso::esfingolipidosis::enfermedad de Gaucher [ENFERMEDADES]splenomegalyalgorithmGaucher Diseasebusiness.industryTHROMBOCYTOPENIA:Nervous System Diseases::Central Nervous System Diseases::Brain Diseases::Brain Diseases Metabolic::Brain Diseases Metabolic Inborn::Lysosomal Storage Diseases Nervous System::Sphingolipidoses::Gaucher Disease [DISEASES]Original Articlesmedicine.disease:diagnóstico::diagnóstico precoz [TÉCNICAS Y EQUIPOS ANALÍTICOS DIAGNÓSTICOS Y TERAPÉUTICOS]Early DiagnosisFamily medicinebusinessmetabolismcomputerDelphiInternal medicine journal
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Mucolipidosis I — A sialidosis

1977

Mucolipidosis I is characterized by Hurler-like features and skeletal dysplasia with a cherry-red macular spot and signs of neurodegeneration involving neuronal cells and myelin. Excessive amounts of sialic acid-containing compounds were found in cultured fibroblasts, leukocytes, and urine of a patient with a clinical phenotype of mucolipidosis I. In cultured fibroblasts, profoundly diminished activity of an alpha-N-acetylneuraminidase (sialidase) was found. Mucolipidosis I thus appears to be a distinct disorder of complex carbohydrate catabolism caused by the genetic deficiency of a neuraminidase.

Malemedicine.medical_specialtyHydrolasesNeuraminidaseSialidaseMyelinMucolipidosesInternal medicinemedicineHumansSialidosisChildCells CulturedGenetics (clinical)SkinbiologyMucolipidosisCatabolismNeurodegenerationmedicine.diseasePhenotypeEndocrinologymedicine.anatomical_structureDysplasiaChild PreschoolImmunologySialic Acidsbiology.proteinLysosomesNeuraminidaseFollow-Up StudiesAmerican Journal of Medical Genetics
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Splice donor site mutation in the lysosomal neuraminidase gene causing exon skipping and complete loss of enzyme activity in a sialidosis patient.

2001

Sialidosis is a lysosomal storage disease caused by the deficiency of K K-N-acetylneuraminidase (NEU1; sialidase), the key enzyme for the intralysosomal catabolism of sialylated glycoconjugates. We have identified a homozygous transversion in the last intron (IVSE +1 Gs C) in neu1 of a sialidosis patient. Sequencing of the truncated cDNA revealed an alternatively spliced neu1 transcript which lacks the complete sequence of exon 5. Skipping of exon 5 leads to a frameshift and results in a premature termination codon. This is the first description of an intronic point mutation causing a complete deficiency of the lysosomal neuraminidase activity. fl 2001 Federation of Euro- pean Biochemical S…

Molecular Sequence DataBiophysicsNeuraminidaseBiochemistryFrameshift mutationNEU1ExonLysosomal neuraminidaseStructural BiologyMucolipidosesGeneticsLysosomal storage diseasemedicineHumansSialidosisAmino Acid SequenceMolecular BiologyGeneticsSialidosisSplice site mutationbiologySequence Homology Amino AcidReverse Transcriptase Polymerase Chain ReactionDonor splice siteCell BiologyExonsFibroblastsmedicine.diseaseMolecular biologyExon skippingMutationbiology.proteinRNA Splice SitesLysosomesNeuraminidaseExon skippingGene DeletionFEBS letters
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Oligosaccharide and Ganglioside Neuraminidase Activities of Mucolipidosis I (Sialidosis) and Mucolipidosis II (I-Cell Disease) Fibroblasts

1979

Fibroblasts cultured from the skin of patients with the genetic diseases mucolipidosis I and mucolipidosis II were found deficient in a neuraminidase specific for both an α23 and and α2 6 type of neuraminosyl linkage of sialyl oligosaccharides. Obligate heterozygotes (parents) showed an intermediate activity in mucolipidosis I, but a normal one in mucolipidosis II. The neuraminidase activity of mucolipidosis I fibroblasts towards gangliosides, measured at pH 4.5 in the presence of Triton X-100, was within the range of normal controls with gangliosides Gm3 and GD3, but somewhat diminished with a bovine brain ganglioside preparation. In mucolipidosis II, neuraminidase activity was markedly de…

NeuraminidaseOligosaccharidesBiochemistryCell LinePolyethylene GlycolsSubstrate SpecificityMucolipidosesGangliosidesmedicineHumansGanglioside GD3SialidosisCells CulturedSkinchemistry.chemical_classificationGangliosidebiologyMucolipidosisGenetic Carrier ScreeningHeterozygote advantageFibroblastsOligosaccharidemedicine.diseaseKineticschemistryBiochemistrybiology.proteinlipids (amino acids peptides and proteins)I-cell diseaseNeuraminidaseEuropean Journal of Biochemistry
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Cytotoxic effects of oxysterols associated with human diseases: Induction of cell death (apoptosis and/or oncosis), oxidative and inflammatory activi…

2009

Oxysterols resulting from spontaneous or enzymatic oxidation of cholesterol are present in numerous foodstuffs and have been identified at increased levels in the plasma and the vascular walls of patients with cardiovascular diseases, especially in atherosclerotic lesions. Consequently, their role in lipid disorders is widely suspected, but they may also contribute to the development of important degenerative diseases such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, osteoporosis, age-related macular degeneration, and cataract. Since these pathologies can be associated with the presence of apoptotic cells, oxidative and inflammatory processes, and lipid disorders, the ab…

Programmed cell deathClinical BiochemistryInflammationApoptosisOxidative phosphorylationPharmacologyBiologyLipidosesBiochemistrychemistry.chemical_compoundMacular DegenerationNeoplasmspolycyclic compoundsmedicineCytotoxic T cellHumansMolecular BiologyKetocholesterolsPhospholipidsPhospholipidosisInflammationCholesterolGeneral MedicineAtherosclerosisHydroxycholesterolsOxidative StresschemistryApoptosisImmunologyMolecular Medicinelipids (amino acids peptides and proteins)Signal transductionmedicine.symptomMolecular aspects of medicine
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Side effects of oxysterols: cytotoxicity, oxidation, inflammation, and phospholipidosis.

2008

Oxysterols are 27-carbon atom molecules resulting from autoxidation or enzymatic oxidation of cholesterol. They are present in numerous foodstuffs and have been demonstrated to be present at increased levels in the plasma of patients with cardiovascular diseases and in atherosclerotic lesions. Thus, their role in lipid disorders is widely suspected, and they might also be involved in important degenerative diseases such as Alzheimer's disease, osteoporosis, and age-related macular degeneration. Since atherosclerosis is associated with the presence of apoptotic cells and with oxidative and inflammatory processes, the ability of some oxysterols, especially 7-ketocholesterol and 7β-hydrox…

Programmed cell deathPhysiologyImmunologyBiophysicsInflammationApoptosisOxidative phosphorylationPharmacologyLipidosesBiochemistryPhospholipidosischemistry.chemical_compoundmedicinepolycyclic compoundsAnimalsHumansGeneral Pharmacology Toxicology and PharmaceuticsCytotoxicitylcsh:QH301-705.5PhospholipidsPhospholipidosisInflammationlcsh:R5-920ChemistryCholesterolGeneral NeuroscienceCell BiologyGeneral MedicineOxysterolsAtherosclerosisHydroxycholesterolsBiochemistrylcsh:Biology (General)Apoptosislipids (amino acids peptides and proteins)medicine.symptomSignal transductionlcsh:Medicine (General)Oxidation-ReductionBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
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Lysosomal and Peroxisomal Disorders. Recent Advances: Introduction

2006

SymposiumBiochemistryGeneral NeuroscienceSphingolipidosesPeroxisomal disordermedicineGlycogen storage diseaseNeurology (clinical)Biologymedicine.diseasePathology and Forensic Medicine
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