Search results for "Inborn"

showing 10 items of 62 documents

Left ventricular hypertrophy or storage disease? the incremental value of speckle tracking strain bull's-eye

2017

Left ventricular hypertrophy (LVH) develops in response to a variety of physical, genetic, and biochemical stimuli and represents the early stage of ventricular remodeling. In patients with LVH, subclinical left ventricular (LV) dysfunction despite normal ejection fraction (EF) may be present before the onset of symptoms, which portends a dismal prognosis. Strain measurement with two-dimensional speckle tracking echocardiography (STE) represents a highly reproducible and accurate alternative to LVEF determination. The present review focuses on current available evidence that supports the incremental value of STE in the diagnostic and prognostic workup of LVH. When assessing the components o…

Radiology Nuclear Medicine and ImagingSpeckle tracking echocardiographyDisease030204 cardiovascular system & hematologyLeft ventricular hypertrophytwo-dimensional strain0302 clinical medicineCardiomegaly Exercise-Induced030212 general & internal medicineanabolic steroidSubclinical infectionamyloidosiEvidence-Based MedicineEjection fractionHypertrophic cardiomyopathyleft ventricular hypertrophyEchocardiographyCardiologyElasticity Imaging TechniquesHypertrophy Left VentricularRadiologyCardiomyopathiesCardiology and Cardiovascular MedicineHumanendocrine systemmedicine.medical_specialtyarterial hypertensionReproducibility of ResultSensitivity and SpecificityDiagnosis Differential03 medical and health sciencesElasticity Imaging TechniqueInternal medicinemedicineathlete's heartHumanscardiovascular diseasesVentricular remodelingspeckle tracking echocardiographyCardiomyopathiebusiness.industryReproducibility of ResultsStroke Volumeaortic stenosiImage Enhancementmedicine.diseasehypertrophic cardiomyopathyDifferential diagnosisMetabolism Inborn ErrorbusinessMetabolism Inborn Errors
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eNOS Activation by HDL Is Impaired in Genetic CETP Deficiency.

2014

Mutations in the CETP gene resulting in defective CETP activity have been shown to cause remarkable elevations of plasma HDL-C levels, with the accumulation in plasma of large, buoyant HDL particles enriched in apolipoprotein E. Genetic CETP deficiency thus represents a unique tool to evaluate how structural alterations of HDL impact on HDL atheroprotective functions. Aim of the present study was to assess the ability of HDL obtained from CETP-deficient subjects to protect endothelial cells from the development of endothelial dysfunction. HDL isolated from one homozygous and seven heterozygous carriers of CETP null mutations were evaluated for their ability to down-regulate cytokine-induced…

Settore MED/09 - Medicina InternaCHOLESTEROL EFFLUXApolipoprotein BEpidemiologylcsh:MedicineANTIINFLAMMATORY PROPERTIESmedicine.disease_causeBiochemistryVascular Medicinechemistry.chemical_compoundHigh-density lipoproteinEnosMedicine and Health SciencesEndothelial dysfunctionlcsh:ScienceMutationMultidisciplinarybiologyHomozygoteCETP; eNOS; HDL;NeurochemistryLipidsGenetic EpidemiologyeNOSlipids (amino acids peptides and proteins)AnatomyNeurochemicalsLipoproteins HDLResearch Articlemedicine.medical_specialtyDrug Research and DevelopmentHDLNitric Oxide Synthase Type IIILipoproteinsENDOTHELIAL FUNCTIONINHIBITIONCardiologyDown-RegulationVascular Cell Adhesion Molecule-1Nitric OxideCELL-ADHESION MOLECULE-1Lipid Metabolism Inborn ErrorsESTER TRANSFER PROTEINInternal medicineCETPCholesterylester transfer proteinHuman Umbilical Vein Endothelial CellsmedicineHumansNITRIC-OXIDE SYNTHASEInflammationClinical GeneticsPharmacologyCholesterollcsh:RTorcetrapibEndothelial CellsBiology and Life SciencesProteinsnutritional and metabolic diseasesLipid MetabolismAtherosclerosismedicine.diseasebiology.organism_classificationCholesterol Ester Transfer Proteinscarbohydrates (lipids)MetabolismEndocrinologychemistryOther Clinical MedicineMutationImmunologyCardiovascular Anatomybiology.proteinlcsh:QTORCETRAPIBClinical MedicineHIGH-DENSITY-LIPOPROTEINSCAVENGER RECEPTOR BI
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SiRNA-mediated selective inhibition of mutant keratin mRNAs responsible for the skin disorder pachyonychia congenita.

2006

RNA interference offers a novel approach for treating genetic disorders including the rare monogenic skin disorder pachyonychia congenita (PC). PC is caused by mutations in keratin 6a (K6a), K6b, K16, and K17 genes, including small deletions and single nucleotide changes. Transfection experiments of a fusion gene consisting of K6a and a yellow fluorescent reporter (YFP) resulted in normal keratin filament formation in transfected cells as assayed by fluorescence microscopy. Similar constructs containing a single nucleotide change (N171K) or a three-nucleotide deletion (N171del) showed keratin aggregate formation. Mutant-specific small inhibitory RNAs (siRNAs) effectively targeted these site…

Small interfering RNABiologymedicine.disease_causeTransfectionGeneral Biochemistry Genetics and Molecular BiologyFusion geneHistory and Philosophy of ScienceCell Line TumorKeratinmedicinePachyonychia congenitaHumansRNA MessengerRNA Small Interferingchemistry.chemical_classificationMutationKeratin Filamentintegumentary systemGeneral NeuroscienceGenetic Diseases InbornKeratin-6RNAKeratin 6Amedicine.diseaseMolecular biologychemistryPachyonychia CongenitaMutationMutagenesis Site-DirectedKeratinsDimerizationAnnals of the New York Academy of Sciences
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Investigation on a MMACHC mutant from cblC disease: The c.394C>T variant

2022

The cblC disease is an inborn disorder of the vitamin B12 (cobalamin, Cbl) metabolism characterized by methylmalonic aciduria and homocystinuria. The clinical consequences of this disease are devastating and, even when early treated with current therapies, the affected children manifest symptoms involving vision, growth, and learning. The illness is caused by mutations in the gene codifying for MMACHC, a 282aa protein that transports and transforms the different Cbl forms. Here we present data on the structural properties of the truncated protein p.R132X resulting from the c.394C > T mutation that, along with c.271dupA and c.331C > T, is among the most common mutations in cblC. Althou…

Vitamin B12 (cobalamin)Structure-function relationshipBiophysicsBiochemistryAnalytical ChemistryVitamin B 12MutationMMACHC proteinHumansMethylmalonic aciduria and homocystinuria cblC typeHomocystinuriaCarrier ProteinsChildOxidoreductasesAmino Acid Metabolism Inborn ErrorsMolecular BiologyBiochimica et Biophysica Acta (BBA) - Proteins and Proteomics
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B and T lymphocytes are affected in lysosomal disorders--an immunoelectron microscopic study.

1991

Circulating lymphocytes of four patients with mucopolysaccharidoses II and IIIA, four patients with juvenile neuronal ceroid-lipofuscinosis, one patient each with glycogenosis type II, infantile neuronal ceroid-lipofuscinosis, and Gaucher disease were classified by immunoelectron microscopy as B or T lymphocytes. Disease-specific lysosomal inclusions as well as non-specific lysosomal organelles, especially Gall bodies were identified in B and T lymphocytes. These non-quantitative studies indicate that both B and T lymphocytes participate in the lysosomal storage process.

congenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtyHistologyImmunoelectron microscopyMucopolysaccharidosisT-LymphocytesCentral nervous systemVacuoleBiologyPathology and Forensic MedicinePhysiology (medical)OrganellemedicineLysosomal storage diseaseHumansMicroscopy ImmunoelectronB-Lymphocytesnutritional and metabolic diseasesT lymphocytemedicine.diseasemedicine.anatomical_structureNeurologyNeuronal ceroid lipofuscinosisNeurology (clinical)Metabolism Inborn ErrorsNeuropathology and applied neurobiology
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Molecular Approaches Fighting Nonsense

2021

Nonsense mutations are the result of single nucleotide substitutions in the DNA that change a sense codon (coding for an amino acid) to a nonsense or premature termination codon (PTC) within the coding region of the mRNA [...]

endocrine system diseasesQH301-705.5media_common.quotation_subjectNonsenseNonsense mutationBiologyCatalysisInorganic ChemistrySense Codonchemistry.chemical_compoundHumansCoding regionNucleotideBiology (General)Physical and Theoretical ChemistryQD1-999Molecular BiologySpectroscopymedia_commonchemistry.chemical_classificationGeneticsMessenger RNAOrganic ChemistryGenetic Diseases InbornSettore CHIM/06 - Chimica OrganicaGeneral MedicineNonsense Mediated mRNA DecayComputer Science ApplicationsAmino acidChemistryn/aEditorialchemistryCodon NonsenseGenetic DiseasesProtein BiosynthesisMutationsense organsDNAInternational Journal of Molecular Sciences
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A case of combined Farber and Sandhoff disease

1989

We describe a patient with the biochemically established combination of Farber and Sandhoff disease. A 6-month-old girl of consanguineous Turkish parents presented with hoarseness, stridor, scattered skin nodules, painful swelling of hand joints and ankles, and cherry-red macular spots. Until the age of 2 years her motor and physical condition deteriorated distinctly, however her mental state remained unchanged. A biopsied skin nodule disclosed lysosomal inclusions within storage cells that were typical of Farber disease (curved tubular structures). However, other inclusions (e.g. zebra bodies) were also found. Biochemical findings included ceramide accumulation in skin nodules and cultured…

medicine.medical_specialtyCeramidePathologyBiopsySandhoff diseaseCeramidesLipid Metabolism Inborn Errorschemistry.chemical_compoundInternal medicinemedicineHumansHexosaminidaseSkinSphingolipidsFarber diseasebusiness.industryInfantSandhoff DiseaseCeramidasemedicine.diseaseSkin NoduleEndocrinologyCeramidase activitychemistryPediatrics Perinatology and Child HealthFemalebusinessSphingomyelinEuropean Journal of Pediatrics
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The policy of public health genomics in Italy.

2013

Abstract Italy has a monitoring system for genetic testing, consisting in a periodic census of clinical and laboratory activities performed in the country. The experience is limited, however, concerning the translation of genomic testing for complex diseases into clinical practice. For the first time the Italian Ministry of Health has introduced a policy strategic plan on genomics and predictive medicine within the 2010–2012 National Prevention Plan. This achievement was supported by the Italian Network for Public Health Genomics (GENISAP) and will likely contribute to the integration of public health genomics into health care in the country. Our experience might be of interest not only in …

medicine.medical_specialtyEconomic growthpublic health genomicsSettore MED/03 - GENETICA MEDICASettore MED/42 - Igiene Generale E ApplicataPredictive medicinepredictive medicineEnvironmental healthHealth caremedicineNational PolicyHumansGenetic Testingpolicy genomicsHealth policyGenetic testingStrategic planningnational policyPublic health genomicsmedicine.diagnostic_testbusiness.industryPublic healthHealth PolicyGenetic Diseases InbornGenomicspublic health genomics public health policyHealth PlanningInbornItalyGenetic DiseasesPublic HealthbusinessDelivery of Health Carepolicypublic health genomics; predictive medicine; national policyHealth policy (Amsterdam, Netherlands)
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Lysine triggers apoptosis through a NADPH oxidase-dependent mechanism in human renal tubular cells

2012

Progressive chronic kidney disease (CKD) is common in lysinuric protein intolerance (LPI), a primary inherited aminoaciduria characterized by massive Lysine excretion in urine. However, by which mechanisms Lysine may cause kidney damage to tubule cells is still not understood. This study determined whether Lysine overloading of human proximal tubular cells (HK-2) in culture enhances apoptotic cell loss and its associated mechanisms. Overloading HK-2 with Lysine levels reproducing those observed in urine of patients affected by LPI (10 mM) increased apoptosis (+30%; p < 0.01 vs.C), as well as Bax and Apaf-1 expressions (+30-50% p < 0.05), while downregulated Bcl-2 (-40% p < 0.05). Apoptosis …

medicine.medical_specialtyLysineGene ExpressionApoptosisNADPH Oxidasecomplex mixturesAntioxidantsCell LineExcretionKidney Tubules ProximalInternal medicineGeneticsmedicineHumansRenal Insufficiency ChronicAmino Acid Metabolism Inborn ErrorsProtein SubunitGenetics (clinical)Membrane Potential MitochondrialKidneyNADPH oxidasebiologyLysineAmino Acid Metabolism Inborn ErrorNADPH OxidasesApoptosimedicine.diseaseCaspase InhibitorsLysinuric protein intoleranceIn vitroProtein SubunitsEndocrinologymedicine.anatomical_structureCell cultureApoptosisbiology.proteinCaspase InhibitorDisease ProgressionAntioxidantReactive Oxygen SpeciesReactive Oxygen SpecieHuman
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Tyrosinaemia type Ia without excess of urinary succinylacetone.

1993

medicine.medical_specialtyPediatricsHeptanoates; Amino Acid Metabolism Inborn Errors; Humans; Tyrosine; Female; Child Preschoolbusiness.industryUrinary systemAmino Acid Metabolism Inborn Errormedicine.diseaseHuman geneticsHeptanoatesTyrosinemiaEndocrinologySuccinylacetoneInternal medicineChild PreschoolGeneticsMedicineHumansTyrosineFemaleHeptanoatebusinessAmino Acid Metabolism Inborn ErrorsGenetics (clinical)HumanJournal of inherited metabolic disease
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