Search results for "Heterozygote"

showing 10 items of 240 documents

CC chemokine receptor 5 polymorphism in Italian patients with Beḩet's disease

2012

OBJECTIVE: To evaluate the potential role of CC chemokine receptor 5 (CCR5)Δ32 polymorphism in the susceptibility to and clinical expression of Behcet's disease (BD) in a cohort of Italian patients. METHODS: One hundred and ninety-six consecutive Italian patients satisfying the ISG criteria for BD were followed up for 8 years, and 180 healthy age- and sex-matched blood donors were molecularly genotyped for the CCR5Δ32 polymorphism. A standard microlymphocytotoxicity technique was used to serotype HLA-B51. The patients were subgrouped on the basis of the presence or absence of clinical manifestations. RESULTS: The distribution of the CCR5Δ32 genotype differed between BD patients and controls…

AdultMalemedicine.medical_specialtyHeterozygoteReceptors CCR5Behcet's disease CCR5 polymorphismBehcet's diseaseGastroenterologyRheumatologyGeneticGene FrequencyInternal medicineGenotypeReceptorsMedicineHumansPharmacology (medical)Genetic Predisposition to DiseaseAllelePolymorphismAllele frequencyPolymorphism Geneticbusiness.industryBehcet SyndromeHomozygoteCase-control studyOdds ratiomedicine.diseaseBeḩet's disease; CC chemokine receptor 5 Δ32 olymorphism; Chemokines; Disease manifestations; Adult; Behcet Syndrome; Case-Control Studies; Female; Gene Frequency; Genetic Predisposition to Disease; HLA-B Antigens; Heterozygote; Homozygote; Humans; Italy; Male; Polymorphism Genetic; Receptors CCR5; Rheumatology; Pharmacology (medical)Adult; Behcet Syndrome; Case-Control Studies; Female; Gene Frequency; Genetic Predisposition to Disease; HLA-B Antigens; Heterozygote; Homozygote; Humans; Italy; Male; Polymorphism Genetic; Receptors CCR5ItalyHLA-B AntigensCase-Control StudiesImmunologyCohortFemalebusinessCC chemokine receptorsCCR5
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Familial HDL deficiency due to ABCA1 gene mutations with or without other genetic lipoprotein disorders

2004

Mutations in ABCA1 have been shown to be the cause of Tangier disease (TD) and some forms of familial hypoalphalipoproteinemia (HA), two genetic disorders characterized by low plasma HDL levels. Here we report six subjects with low HDL, carrying seven ABCA1 mutations, six of which are previously unreported. Two mutations (R557X and H160FsX173) were predicted to generate short truncated proteins; two mutations (E284K and Y482C) were located in the first extracellular loop and two (R1901S and Q2196H) in the C-terminal cytoplasmic domain of ABCA1. Two subjects found to be compound heterozygotes for ABCA1 mutations did not have overt clinical manifestations of TD. Three subjects, all with prema…

AdultMalemedicine.medical_specialtyHeterozygoteSettore MED/09 - Medicina InternaApolipoprotein BAdolescentPremature coronary artery diseaseTangier diseaseCoronary DiseaseBiologyGene mutationmedicine.disease_causeCompound heterozygosityTangier diseaseInternal medicineGenotypeABCA1 genemedicineHumansChildHypoalphalipoproteinemiaSelection BiasAgedApolipoproteins BGeneticsMutationFamilial defective Apo B (FDB)Apolipoprotein A-ICholesterol HDLnutritional and metabolic diseasesMiddle Agedmedicine.diseaseLipoprotein lipaseTangier disease; Familial HDL deficiency; ABCA1 gene; Familial defective Apo B (FDB); Lipoprotein lipase; Premature coronary artery diseaseEndocrinologyChild PreschoolMutationbiology.proteinlipids (amino acids peptides and proteins)Allelic heterogeneityATP-Binding Cassette TransportersFemaleCardiology and Cardiovascular MedicineFamilial HDL deficiencyATP Binding Cassette Transporter 1
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Improved identification of heterozygotes for phenylketonuria using blood neopterin and biopterin

1993

A novel approach that combines information provided by the metabolism of pteridines and that of phenylalanine has been applied to the detection of heterozygotes for phenylketonuria. Phenylalanine, tyrosine, biopterin and neopterin have been measured in serum from normal controls and heterozygotes for classical phenylketonuria, before and after a phenylalanine oral load. Significant differences in neopterin and biopterin mean values in fasting serum and in the mean increase of biopterin induced by the phenylalanine load were found between groups. Inclusion of pteridine data in the discriminant analysis significantly improved the resolution of the classical phenylalanine loading test for the …

AdultMalemedicine.medical_specialtyPhenylalanineBiopterinPhenylalanineNeopterinchemistry.chemical_compoundPhenylketonuriasInternal medicineClassical phenylketonuriaGeneticsmedicineHumansTyrosineGenetics (clinical)ChemistryGenetic Carrier ScreeningNeopterinHeterozygote advantageTetrahydrobiopterinBiopterinEndocrinologyTyrosineFemalemedicine.drugPteridineJournal of Inherited Metabolic Disease
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Lack of association of the -463 G/A myeloperoxidase promoter polymorphism with Behcet's disease in Italian patients.

2007

Objective. To investigate potential associations between the � 463G/A myeloperoxidase (MPO) promoter polymorphism and susceptibility to, and clinical expression of, Behcet's disease (BD). Methods. One hundred and seventy-five Italian patients who satisfied the International Study Group criteria for BD and 235 healthy age- and sex-matched blood donors were genotyped for the �463G/A promoter polymorphism of the MPO gene by molecular methods. The patients were subgrouped according to the presence or absence of clinical manifestations. Results. The distribution of allele and genotype frequencies of the MPO �463A/G polymorphism did not differ significantly between the BD patients and the healthy…

AdultMalemedicine.medical_specialtySystemic diseaseAdult; Behcet Syndrome; Female; Gene Frequency; Genetic Predisposition to Disease; Genotype; Heterozygote; Histocompatibility Testing; Humans; Male; Peroxidase; Promoter Regions Genetic; Polymorphism GeneticHeterozygoteGenotypeBehcet's diseaseBehçet's disease; Disease manifestation; Myeloperoxidase; Myeloperoxidase gene polymorphism; Adult; Behcet Syndrome; Female; Gene Frequency; Genetic Predisposition to Disease; Genotype; Heterozygote; Histocompatibility Testing; Humans; Male; Peroxidase; Promoter Regions Genetic; Polymorphism Genetic; Rheumatology; Pharmacology (medical)Promoter RegionsRheumatologyGeneticGene FrequencyInternal medicineGenotypemedicineHumansPharmacology (medical)Genetic Predisposition to DiseaseAllelePolymorphismPromoter Regions GeneticPeroxidasePolymorphism Geneticbiologybusiness.industryBehcet SyndromeHistocompatibility TestingOdds ratiomedicine.diseaseRheumatologyGenotype frequencyMyeloperoxidaseImmunologybiology.proteinFemalebusinessRheumatology (Oxford, England)
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Electrophysiological findings of neuronal ceroid lipofuscinosis in heterozygotes.

1988

Nineteen obligate heterozygotes, 8 individuals at risk of being heterozygote, and 10 patients afflicted with four different forms of neuronal ceroid lipofuscinosis were examined electrophysiologically. The group of obligate heterozygotes was compared to age-matched control groups. Statistically significant differences were found between scotopic b-wave amplitudes, P-ERG amplitudes, and EOG light peaks of the obligate carriers of the juvenile type and the control subjects. The photopic L-ERGs and the latencies of the VEPs were mostly within the normal range. The findings represent the first evidence of functional ophthalmological changes in obligate carriers of neuronal ceroid lipofuscinosis…

AdultPathologymedicine.medical_specialtyHeterozygotegenetic structuresAdolescentPhysiologyBiologyCellular and Molecular NeuroscienceNeuronal Ceroid-LipofuscinosesRisk FactorsmedicineElectroretinographyHumansScotopic visionChildmedicine.diagnostic_testObligateHeterozygote advantageElectrooculographymedicine.diseaseSensory SystemsOphthalmologyElectrophysiologyElectrooculographyChild PreschoolEvoked Potentials VisualNeuronal ceroid lipofuscinosissense organsElectroretinographyPhotopic visionGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie
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Enzyme replacement therapy in heterozygous females with Fabry disease: results of a phase IIIB study.

2003

Summary: Fabry disease is an X-linked glycosphingolipid storage disorder caused by a deficiency of α-galactosidase A. Affected patients experience debilitating neuropathic pain and have premature mortality due to renal failure, cardiovascular disease or cerebrovascular complications. The disease may be X-linked dominant, since most females heterozygous for Fabry disease are affected clinically. We evaluated the safety, efficacy and pharmacokinetics of agalsidase alfa (Replagal) administered intravenously to female patients with Fabry disease in an open-label, single-centre study. Fifteen severely affected patients received agalsidase alfa at 0.2 mg/kg every other week for up to 55 weeks. Ag…

Adultmedicine.medical_specialtyHeterozygoteAdolescentArthritisRenal functionKidneyGastroenterologyAntibodiesArthritis RheumatoidElectrocardiographyPharmacokineticsInternal medicineGeneticsmedicineHumansGenetics (clinical)Vascular diseasebusiness.industryTrihexosylceramidesEnzyme replacement therapymedicine.diseaseFabry diseaseRecombinant ProteinsSurgeryClinical trialIsoenzymesEchocardiographyalpha-GalactosidaseNeuropathic painMutationFabry DiseaseFemalebusinessJournal of inherited metabolic disease
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Spectrum of mutations and phenotypic expression in patients with autosomal dominant hypercholesterolemia identified in Italy.

2013

Abstract Objective To determine the spectrum of gene mutations and the genotype–phenotype correlations in patients with Autosomal Dominant Hypercholesterolemia (ADH) identified in Italy. Methods The resequencing of LDLR , PCSK9 genes and a selected region of APOB gene were conducted in 1018 index subjects clinically heterozygous ADH and in 52 patients clinically homozygous ADH. The analysis was also extended to 1008 family members of mutation positive subjects. Results Mutations were detected in 832 individuals: 97.4% with LDLR mutations, 2.2% with APOB mutations and 0.36% with PCSK9 mutations. Among the patients with homozygous ADH, 51 were carriers of LDLR mutations and one was an LDLR / …

Adultmedicine.medical_specialtyHeterozygoteSettore MED/09 - Medicina InternaApolipoprotein BCoronary DiseaseBiologyGene mutationmedicine.disease_causeHyperlipoproteinemia Type IITendonschemistry.chemical_compoundReference ValuesInternal medicinemedicineXanthomatosisHumansGeneAllelesGenetic Association StudiesAgedGeneticsMutationCholesterolPCSK9Cholesterol HDLSerine EndopeptidasesSmokingAlcohol Dehydrogenasenutritional and metabolic diseasesCholesterol LDLMiddle AgedEndocrinologyPhenotypechemistryItalyLDL receptorMutationbiology.proteinAutosomal dominanthypercholesterolemia LDL receptor Apolipoprotein B PCSK9 Mutationslipids (amino acids peptides and proteins)Allelic heterogeneityFemaleProprotein ConvertasesProprotein Convertase 9Cardiology and Cardiovascular MedicineAtherosclerosis
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Cardiac manifestations of Anderson-Fabry disease in heterozygous females.

2002

AbstractObjectivesWe sought to define the prevalence of cardiac involvement in female patients with Anderson–Fabry disease (AFD).BackgroundAnderson–Fabry disease is a rare inborn X-linked lysosomal storage disorder. Globotriaosylceramide (Gb3), the major substrate of the deficient α-galactosidase A enzyme, accumulates progressively in vulnerable cells, including the cardiovascular system. It has been believed that heterozygous females have less cardiac involvement than hemizygous males with AFD.MethodsWe performed two-dimensional echocardiographic examinations of female patients heterozygous for AFD.ResultsSince 1997, a total of 55 female patients (mean age, 39.6 years; range, 6.1 to 70.8 y…

Adultmedicine.medical_specialtyPediatricsHeterozygoteendocrine system diseasesHeart diseaseAdolescentSystoleHeart Valve DiseasesDiseaseVentricular Dysfunction LeftFemale patientotorhinolaryngologic diseasesmedicinePrevalenceHumanscardiovascular diseasesProspective StudiesSystoleProspective cohort studyChildneoplasmsAgedVascular diseasebusiness.industryAge FactorsMiddle Agedmedicine.diseaseFabry diseasehumanitiesSurgeryPedigreeAnderson-Fabry DiseaseEchocardiographyFabry Diseaselipids (amino acids peptides and proteins)FemaleHypertrophy Left VentricularCardiology and Cardiovascular MedicinebusinessJournal of the American College of Cardiology
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Influence of microsomal triglyceride transfer protein promoter polymorphism -493 GT on fasting plasma triglyceride values and interaction with treatm…

2005

Familial hypercholesterolaemia (FH) is an autosomal dominant disease characterized by elevated levels of low-density lipoprotein-cholesterol (LDL-C). Phenotypic expression is highly variable, being influenced by diet, age, gender, body mass index, apolipoprotein E genotype and type of LDL-receptor gene mutation. Microsomal triglyceride (TG) transfer protein (MTP) is a protein involved in lipid metabolism. Polymorphism MTP -493 GT has been shown to modulate lipid levels in several populations. To analyse the effect of this polymorphism in the lipid phenotype expression of FH and treatment response, we studied a sample of 222 Spanish FH patients, of whom 147 were studied before and after trea…

Apolipoprotein EMaleAtorvastatinPolymerase Chain ReactionMicrosomal triglyceride transfer proteinBody Mass Indexchemistry.chemical_compoundAtorvastatinGeneral Pharmacology Toxicology and PharmaceuticsPromoter Regions GeneticGenetics (clinical)Polymorphism Single-Stranded ConformationalGeneticsbiologyAutosomal dominant traitFastingLipoproteins LDLCholesterolPhenotypeMolecular Medicinelipids (amino acids peptides and proteins)Femalemedicine.drugmedicine.medical_specialtyHeterozygoteGenotypeLipoproteinsHyperlipoproteinemia Type IIApolipoproteins ESex FactorsInternal medicineGeneticsmedicineHumansPyrrolesMolecular BiologyAllelesTriglyceridesPolymorphism GeneticTriglycerideCholesterolGenetic VariationCholesterol LDLDNALipid MetabolismEndocrinologychemistryHeptanoic AcidsPharmacogeneticsMutationbiology.proteinHydroxymethylglutaryl-CoA Reductase InhibitorsCarrier ProteinsBody mass indexPharmacogeneticsPharmacogenetics and genomics
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In silico and in vitro comparative analysis to select, validate and test SNPs for human identification.

2007

Abstract Background The recent advances in human genetics have recently provided new insights into phenotypic variation and genome variability. Current forensic DNA techniques involve the search for genetic similarities and differences between biological samples. Consequently the selection of ideal genomic biomarkers for human identification is crucial in order to ensure the highest stability and reproducibility of results. Results In the present study, we selected and validated 24 SNPs which are useful in human identification in 1,040 unrelated samples originating from three different populations (Italian, Benin Gulf and Mongolian). A Rigorous in silico selection of these markers provided …

Asialcsh:QH426-470lcsh:BiotechnologyIn silicoPolymorphism Single Nucleotide; Heterozygote Detection; Gene Frequency; Humans; Africa; Europe; Computational Biology; Sequence Analysis DNA; Forensic Anthropology; Asia; Chromosome MappingSingle-nucleotide polymorphismBiologyHeterozygote DetectionGenomePolymorphism Single NucleotideGene Frequencylcsh:TP248.13-248.65GeneticsHumansPolymorphismAllele frequencySelection (genetic algorithm)GeneticsGenetic Carrier ScreeningChromosome MappingComputational BiologySingle NucleotideDNASequence Analysis DNAHuman geneticsEuropelcsh:GeneticsSettore MED/03 - Genetica MedicaAfricaSNPs HUMAN IDENTIFICATION comparative analysisForensic AnthropologyHuman genomeDNA microarraySequence AnalysisBiotechnologyResearch ArticleBMC genomics
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