Search results for "MUTATION"

showing 10 items of 2830 documents

Role of the pyrin M694V (A2080G) allele in acute myocardial infarction and longevity: a study in the Sicilian population

2006

Abstract A proinflammatory genotype seems to contribute significantly to the risk of developing coronary heart disease (CHD). Conversely, the susceptibility alleles to inflammatory disease should be infrequent in the genetic background favoring longevity. In fact, in a modern environment, attainment of longevity is facilitated by an anti-inflammatory status. To evaluate whether inflammatory alleles of pyrin, the gene responsible for familial Mediterranean fever (FMF) may play an opposite role in CHD and in longevity, we examined three FMF-associated mutations, M694V (A2080G), M694I (G2082A), and V726A (T2177C), encoded by the FMF gene (MEFV) in 121 patients affected by acute myocardial infa…

AdultMaleHeterozygotemedia_common.quotation_subjectImmunologyPopulationDNA Mutational AnalysisLongevityMyocardial InfarctionMEFVFamilial Mediterranean feverEnvironmentPyrin domainProinflammatory cytokineAMIGene FrequencyRisk FactorsGenotypeImmunology and AllergyMedicineHumansProtein IsoformsGenetic Predisposition to DiseaseGenetic TestingAlleleeducationSicilyAllelesmedia_commonAged 80 and overeducation.field_of_studybusiness.industryLongevityAge FactorsCell BiologyMiddle AgedPyrinmedicine.diseaseMEFVCytoskeletal ProteinsinflammationImmunologyAcute DiseaseMutationFemalebusiness
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Evaluation of clinical diagnosis criteria of familial ligand defective apoB 100 and lipoprotein phenotype comparison between LDL receptor gene mutati…

2007

Familial hypercholesterolemia (FH) and familial defective apoB 100 (FDB) are characterized by increased plasma low-density lipoprotein cholesterol (LDLc) levels and risk of coronary heart disease (CHD). FDB is clinically indistinguishable from FH. The aims of this study were to evaluate clinical diagnosis criteria for FDB and to compare the lipoprotein phenotype between carriers of LDL receptor (LDLR) gene mutations that affect the ligand-binding domain and subjects with the R3500Q mutation in apoB gene. We studied 213 subjects (113 probands) with FH and 19 heterozygous FDB subjects. Genetic diagnosis was determined by following a protocol based on Southern blot and polymerase chain reactio…

AdultMaleHeterozygotemedicine.medical_specialtyGenotypeApolipoprotein BPopulationMutation MissenseCoronary DiseaseFamilial hypercholesterolemiaGene mutationBiologyWhite PeopleHyperlipoproteinemia Type IIchemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineHumansMissense mutationeducationPolymorphism Single-Stranded Conformationaleducation.field_of_studyBinding SitesCholesterolGenetic Carrier ScreeningBiochemistry (medical)Public Health Environmental and Occupational HealthCholesterol LDLGeneral MedicineMiddle Agedmedicine.diseaseFounder EffectProtein Structure TertiaryEuropePhenotypeEndocrinologyReceptors LDLchemistryApolipoprotein B-100LDL receptorbiology.proteinFemalelipids (amino acids peptides and proteins)LipoproteinTranslational Research
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Thrombosis in inherited factor VII deficiency

2003

Thrombosis in congenital factor (F) VII deficiency was investigated through extensive phenotypic and molecular-genetic studies. Patients with a history of thrombosis among 514 entries in the FVII Deficiency Study Group database were evaluated. Thrombotic events were arterial in one case, disseminated intravascular coagulation in another and venous in seven. Gene mutations were characterized in eight patients: three were homozygous, three compound heterozygous and two heterozygous. FXa and IIa generation assays were consistent with the genetic lesions. One patient was heterozygous for the FV Leiden and one for the FIIG20210A mutation. In seven patients, surgical interventions and/or replacem…

AdultMaleHeterozygotemedicine.medical_specialtyPathologyTime FactorsAdolescentFactor VII DeficiencyGene mutationCompound heterozygosityThrombophiliaGastroenterologyInternal medicinemedicineHumansThrombophiliaAgedVenous ThrombosisDisseminated intravascular coagulationbiologybusiness.industryHomozygoteFactor VFactor VThrombosisHematologyCongenital FVII deficiency; Replacement therapy; Surgery; Thrombophilia; Thrombosis;Disseminated Intravascular CoagulationMiddle Agedmedicine.diseaseThrombosisZygosityVenous thrombosisPhenotypeDatabases as TopicFactor XaMutationbiology.proteinFemaleProthrombinbusinessJournal of Thrombosis and Haemostasis
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Genetic Variation at the ApoA-IV Gene Locus and Response to Diet in Familial Hypercholesterolemia

1998

Abstract —Plasma lipid response to dietary fat and cholesterol is, in part, genetically controlled. The apolipoprotein A-IV (apoA-IV protein; APOA4, gene) has been shown to influence the response to dietary changes in normolipidemic individuals. The response to diet in subjects with familial hypercholesterolemia (FH) is also variable, and no studies are available on the influence of APOA4 mutations on dietary response in these subjects. We studied the effect of 2 common apoA-IV genetic variants (Gln 360 →His and Thr 347 →Ser) on the lipid response to the National Cholesterol Education Program type I (NCEP-I) diet in 67 FH heterozygotes (43 women and 24 men). Subjects were studied at baseli…

AdultMaleHeterozygotemedicine.medical_specialtyVery low-density lipoproteinGenotypeApolipoprotein BHypercholesterolemiaFamilial hypercholesterolemiaStatistics Nonparametricchemistry.chemical_compoundHigh-density lipoproteinInternal medicinemedicineHumansAlleleNational Cholesterol Education ProgramAllelesApolipoproteins AGeneticsAnalysis of VariancebiologyCholesterolGenetic VariationMiddle Agedmedicine.diseaseDietary FatsLipidsEndocrinologychemistryLow-density lipoproteinMutationbiology.proteinFemalelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineArteriosclerosis, Thrombosis, and Vascular Biology
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Evaluation of the autoimmune regulator (AIRE) gene mutations in a cohort of Italian patients with autoimmune-polyendocrinopathy-candidiasis-ectoderma…

2009

Summary Objective   Autoimmune-polyendocrinopathy-candidiasis-ectodermal-dystrophy (APECED) is a rare syndrome characterized by chronic candidiasis, chronic hypoparathyroidism and Addison's disease. APECED has been associated with mutations in autoimmune regulator (AIRE) gene. Our aim is to perform a genetic analysis of the AIRE gene in Italian APECED patients and in their relatives. Design  AIRE mutations were determined by DNA sequencing in all subjects. Patients were tested for clinical autoimmune or non-autoimmune diseases, or for organ and non-organ specific autoantibodies. Patients   A total of 24 Italian patients with APECED (15 from the Venetian region, 2 from Southern-Tyrol, 4 from…

AdultMaleHeterozygotemedicine.medical_specialtyanimal structuresAdolescentHypoparathyroidismEndocrinology Diabetes and MetabolismGene mutationmedicine.disease_causeCompound heterozygositySettore MED/13 - EndocrinologiaCohort StudiesLoss of heterozygosityYoung AdultEndocrinologyAddison DiseaseInternal medicinemedicineHumansChildPolyendocrinopathies AutoimmuneAgedGeneticsMutationGenetic heterogeneitybusiness.industryHomozygoteCandidiasisAutoantibodyAutoimmune polyendocrinopathyMiddle AgedAutoimmune regulatorEndocrinologyItalyCase-Control StudiesMutationAPS1 AIRE APECEDFemalebusinessTranscription Factors
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Mutation screening for the prothrombin variant G20210A by melting point analysis with the Light Cycler system: atypical results, detection of the var…

2005

In the differential diagnosis of thrombophilic disorders genotyping of prothrombin and factor V are nowadays performed as a routine analysis. In the following we describe the unusual results of the mutation screening using melting point analysis for two patients and the consecutive detection of the mutation C20209T by sequencing the corresponding gene fragments. The molecular result is discussed with special respect to the medical history, ethnic background and clinical findings of both patients.

AdultMaleHot TemperatureDNA Mutational AnalysisClinical BiochemistryBiologyNucleic Acid DenaturationThrombophiliaPolymerase Chain Reactionlaw.inventionlawmedicineHumansPoint MutationThrombophiliaMedical historyGenotypingPolymerase chain reactionGeneticsPoint mutationBiochemistry (medical)Factor VSequence Analysis DNAHematologyGeneral Medicinemedicine.diseaseMutation (genetic algorithm)biology.proteinFemaleProthrombinDifferential diagnosisClinical and Laboratory Haematology
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Molecular basis of a new type of C1q-deficiency associated with a non-functional low molecular weight (LMW) C1q: parallels and differences to other k…

1998

Analysis of an abnormal C1q molecule of individuals of a Moroccan family by ultracentrifugation in sucrose gradients revealed a low molecular weight C1q (LMW-C1q). We investigated the molecular basis of this defect by sequencing all six exons of the three C1q genes. One point mutation in the codon for Gly at position 15 (GGT) of the B chain was found resulting in an amino acid substitution to Asp (GAT). The exchange not only leads to an interruption of the collagen-like motif Gly-X-Y, but also introduces one negatively charged residue per B chain which results in two additional charges per structural subunit (A-B, C-C, A-B). The mutation which has been identified by DNA-sequencing in the C1…

AdultMaleImmunodiffusionAdolescentSequence analysisProtein subunitchemical and pharmacologic phenomenaBiologyComplement Hemolytic Activity AssayPolymerase Chain Reactionlaw.inventionExonlawHumansLupus Erythematosus SystemicPoint MutationChildGenePolymerase chain reactionPharmacologychemistry.chemical_classificationPoint mutationComplement C1qDNAExonsMolecular biologyAmino acidMolecular WeightMoroccoBiochemistrychemistryFemaleUltracentrifugeCollagenSequence AnalysisImmunopharmacology
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KIAA0556 is a novel ciliary basal body component mutated in Joubert syndrome

2015

Background Joubert syndrome (JBTS) and related disorders are defined by cerebellar malformation (molar tooth sign), together with neurological symptoms of variable expressivity. The ciliary basis of Joubert syndrome related disorders frequently extends the phenotype to tissues such as the eye, kidney, skeleton and craniofacial structures. Results Using autozygome and exome analyses, we identified a null mutation in KIAA0556 in a multiplex consanguineous family with hallmark features of mild Joubert syndrome. Patient-derived fibroblasts displayed reduced ciliogenesis potential and abnormally elongated cilia. Investigation of disease pathophysiology revealed that Kiaa0556-/- null mice possess…

AdultMaleK04F10.2KIAA0556MicrotubuleMicrotubulesRetinaMiceJoubert syndromeCerebellumAnimalsHumansAbnormalities MultipleExomeCiliaEye AbnormalitiesSensory disorders Radboud Institute for Molecular Life Sciences [Radboudumc 12]Caenorhabditis elegansChildCells CulturedAdenosine TriphosphatasesADP-Ribosylation FactorsResearchBrainMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]Kidney Diseases CysticBasal BodiesPedigreeMice Inbred C57BLRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]Basal bodyChild PreschoolMutationFemaleKataninMicrotubule-Associated ProteinsProtein BindingGenome Biology
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Impact of HBV genotypes A and D genetic variability on infection evolution

2015

HBV is characterized by a high genetic variability, which is the basis of its classification into eight genotypes (A-H). HBV infection is associated with different outcomes, from self-limiting acute hepatitis to active chronic hepatitis, asymptomatic carriage, and occult infection. The aim of this study was to analyze the genetic variability of HBV genotypes A and D isolates from 79 cases of self-limiting acute hepatitis and chronic hepatitis, in order to identify HBV variants associated with resolution or chronicity of acute HBV infection. The entire preS-S sequence and a fragment of 346 bp of the preC-C region, containing Enhancer II and Basal Core Promoter sequences, were analyzed. A phy…

AdultMaleMicrobiology (medical)Hepatitis B virusSettore MED/07 - Microbiologia E Microbiologia ClinicaGenotypeAcute hepatitis BBiologymedicine.disease_causeMicrobiologyLiver diseaseViral ProteinspreC/C mutationGeneticImmune-escape mutationGenetic variationGenotypeGeneticsmedicineHumansViral ProteinGenetic variabilityMolecular BiologyEcology Evolution Behavior and SystematicsPhylogenyAgedHepatitis B virusPolymorphism GeneticpreS/S mutationGenetic VariationHepatitis B viruHepatitis BMiddle Agedmedicine.diseaseHepatitis BVirologyBiological EvolutionEcology Evolution Behavior and SystematicInfectious DiseasesAmino Acid SubstitutionViral evolutionImmunologyMutationFemaleViral hepatitisHuman
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Ten new cases further delineate the syndromic intellectual disability phenotype caused by mutations in DYRK1A.

2015

The dual-specificity tyrosine-phosphorylation-regulated kinase 1A (DYRK1A) gene, located on chromosome 21q22.13 within the Down syndrome critical region, has been implicated in syndromic intellectual disability associated with Down syndrome and autism. DYRK1A has a critical role in brain growth and development primarily by regulating cell proliferation, neurogenesis, neuronal plasticity and survival. Several patients have been reported with chromosome 21 aberrations such as partial monosomy, involving multiple genes including DYRK1A. In addition, seven other individuals have been described with chromosomal rearrangements, intragenic deletions or truncating mutations that disrupt specificall…

AdultMaleMicrocephalyMonosomyDown syndromeAdolescentChromosomes Human Pair 21BiologyProtein Serine-Threonine KinasesArticleIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumansAutistic DisorderChildGenetics (clinical)Chromosomal DeletionGeneticsProtein-Tyrosine Kinasesmedicine.diseasePhenotypeChild PreschoolSpeech delayMutationMicrocephalyAutismFemalemedicine.symptomChromosome DeletionDown SyndromeChromosome 21European journal of human genetics : EJHG
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