Search results for "Pedigree"

showing 10 items of 313 documents

A novel L1CAM mutation in a fetus detected by prenatal diagnosis

2010

X-linked hydrocephalus is due to mutations in the L1 neuronal cell adhesion molecule (L1CAM) gene. L1 protein plays a key role in neurite outgrowth, axonal guidance, and pathfinding during the development of the nervous system. We report on a familial case diagnosed by prenatal ultrasonographic examination, with cerebellar hypoplasia, agenesis of the corpus callosum, and the bilateral overlapping of the second and third fingers of the hand. Sequencing of the L1CAM gene showed a novel missense mutation in exon 14: transition of a guanine to cytosine at position 1777 (c.1777G > C), which led to an amino acid change of alanine to proline at position 593 (Ala593Pro) in the sixth immunoglobulin …

Adultmedicine.medical_specialtyPathologyL1Neural Cell Adhesion Molecule L1Prenatal diagnosismedicine.disease_causeL1CAM L1-desease prenatal diagnosis hydrocephalus HSAS CRASH syndromeExonSettore MED/38 - Pediatria Generale E SpecialisticaPregnancyPrenatal DiagnosisInternal medicinemedicineHumansPoint MutationMissense mutationAgenesis of the corpus callosumUltrasonographyMutationbusiness.industrymedicine.diseasePedigreeFetal DiseasesEndocrinologyKaryotypingPediatrics Perinatology and Child HealthFemaleNeural cell adhesion moleculeCerebellar hypoplasia (non-human)businessHydrocephalus
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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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Missense mutations in the fas gene resulting in autoimmune lymphoproliferative syndrome: A molecular and immunological analysis

1997

AbstractProgrammed cell death (or apoptosis) is a physiological process essential to the normal development and homeostatic maintenance of the immune system. The Fas/Apo-1 receptor plays a crucial role in the regulation of apoptosis, as demonstrated by lymphoproliferation in MRL-lpr/lpr mice and by the recently described autoimmune lymphoproliferative syndrome (ALPS) in humans, both of which are due to mutations in the Fas gene. We describe a novel family with ALPS in which three affected siblings carry two distinct missense mutations on both the Fas gene alleles and show lack of Fas-induced apoptosis. The children share common clinical features including splenomegaly and lymphadenopathy, b…

Antigens Differentiation T-LymphocyteMaleAdolescentT-LymphocytesCD3ImmunologyLymphoproliferative disordersBiologyLymphocyte ActivationAutoimmune DiseaseBiochemistryFas ligandImmunophenotypingImmune systemPedigree; Antigens Differentiation T-Lymphocyte; Solubility; Apoptosis; Autoimmune Diseases; Humans; Antigens CD95; Child; Lymphocytes; Child Preschool; Lymphocyte Activation; Syndrome; Lymphoproliferative Disorders; Adolescent; Mutation; Immunophenotyping; Male; Biological Markers; T-LymphocytesmedicineChildAutoimmune diseaseApoptosiSyndromeCell BiologyHematologymedicine.diseaseFas receptorPedigreeAntigens CD95SolubilityApoptosisChild PreschoolLymphoproliferative DisorderAutoimmune lymphoproliferative syndromeMutationBiological MarkerImmunologybiology.proteinLymphocyteHuman
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APOE epsilon variation in multiple sclerosis susceptibility and disease severity: some answers

2006

Background: Previous studies have examined the role of APOE variation in multiple sclerosis (MS), but have lacked the statistical power to detect modest genetic influences on risk and disease severity. The meta- and pooled analyses presented here utilize the largest collection, to date, of MS cases, controls, and families genotyped for the APOE epsilon polymorphism. Methods: Studies of MS and APOE were identified by searches of PubMed, Biosis, Web of Science, Cochrane Review, and Embase. When possible, authors were contacted for individual genotype data. Meta-analyses of MS case-control data and family-based analyses were performed to assess the association of APOE epsilon genotype with dis…

Apolipoprotein EOncologyRiskmedicine.medical_specialtyPathologyMultiple SclerosisGenotypeApolipoprotein E2Apolipoprotein E4Polymorphism Single NucleotideSeverity of Illness IndexLinkage DisequilibriumPrimary progressiveCentral nervous system disease03 medical and health sciences0302 clinical medicineApolipoproteins EDisease severityPolymorphism (computer science)Internal medicineGenotypemedicineHumansGenetic Predisposition to Disease10. No inequalityAlleles030304 developmental biology0303 health sciencesExpanded Disability Status ScalePolymorphism GeneticScience & Technologybusiness.industryMultiple sclerosismedicine.disease3. Good healthPedigreePhenotypeCase-Control StudiesSettore MED/26 - NeurologiaNeurology (clinical)businessMultiple Sclerosis APOE disease severity meta-analysis030217 neurology & neurosurgery
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Two Italian kindreds carrying the Arg136--Ser mutation of the Apo E gene: development of premature and severe atherosclerosis in the presence of epsi…

2003

Abstract Background and Aims: Type III hyperlipoproteinemia, or dysbetalipoproteinemia, is commonly associated with apolipoprotein E2 homozygosity (Cy Background and Aims: 12, Cy Background and Aims: 58). Apo E2-Christchurch (Arg136→Ser), a rare mutation of the Apo E gene, located in the receptor-binding domain of the protein, has been found to be associated in the vast majority of cases of dysbetalipoproteinemia. Methods and Results: This is the first report of two Italian kindreds carrying the Arg136→Ser mutation. One family is a four-generation kindred from Genoa (Liguria, Italy) with a high rate of mortality due to coronary artery disease: the proband was a 51-year-old woman with previo…

Apolipoprotein EProbandMaleSettore MED/09 - Medicina InternaGenotypeApolipoprotein E2ArteriosclerosisEndocrinology Diabetes and MetabolismMedicine (miscellaneous)Sequence HomologyBiologyArteriosclerosiPolymerase Chain ReactionCoronary artery diseaseApolipoproteins EGenotypeHyperlipoproteinemia Type IIImedicineHaplotypeHumansAlleleGenotypingAllelesGeneticsAlleleNutrition and DieteticsBase SequenceHaplotypeLipidMiddle Agedmedicine.diseaseLipidsPedigreeSettore MED/03 - Genetica MedicaHaplotypesMutationFemaleCardiology and Cardiovascular MedicineApolipoprotein E2HumanNutrition, metabolism, and cardiovascular diseases : NMCD
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Distal Arthrogryposis type 5 in an Italian family due to an autosomal dominant gain-of-function mutation of the PIEZO2 gene

2022

Abstract Background Arthrogryposis multiplex congenita (AMC) is a group of clinically and etiologically heterogeneous conditions, characterized by prenatal onset contractures affecting two or more joints. Its incidence is about 1 in 3000 live births. AMC may be distinguished into amyoplasia, distal and syndromic arthrogryposis. Distal arthrogryposis (DA) predominantly affects hands and feet. It is currently divided into more than ten subtypes (DA1, DA2A/B, DA3–10), based on clinical manifestations, gene mutations and inheritance pattern. Among them, only a few patients with DA5 have been reported. It is associated to a gain-of-function pathogenic variant of the PIEZO2 gene, encoding for an …

ArthrogryposisContractureOphthalmoplegiaArthrogryposis multiplex congenita Case report DA5 Gain-of-function mutation NGS Ophthalmoplegia PIEZO2 gene Gain of Function Mutation Humans Infant Newborn Inheritance Patterns Ion Channels Mutation Pedigree Retinal Diseases Arthrogryposis Contracture OphthalmoplegiaRetinal DiseasesGain of Function MutationMutationInfant NewbornInheritance PatternsHumansGeneral MedicineIon ChannelsPedigreeItalian Journal of Pediatrics
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Sensory neuropathy with bone destruction due to a mutation in the membrane-shaping atlastin GTPase 3.

2014

Many neurodegenerative disorders present with sensory loss. In the group of hereditary sensory and autonomic neuropathies loss of nociception is one of the disease hallmarks. To determine underlying factors of sensory neurodegeneration we performed whole-exome sequencing in affected individuals with the disorder. In a family with sensory neuropathy with loss of pain perception and destruction of the pedal skeleton we report a missense mutation in a highly conserved amino acid residue of atlastin GTPase 3 (ATL3), an endoplasmic reticulum-shaping GTPase. The same mutation (p.Tyr192Cys) was identified in a second family with similar clinical outcome by screening a large cohort of 115 patients …

AtlastinAdultMaleIntracellular SpaceMutation MissenseSensory systemBiologymedicine.disease_causeEndoplasmic ReticulumGTP PhosphohydrolasesCohort StudiesFractures BoneYoung AdultmedicineMissense mutationHumansExomenociceptionAxonAge of OnsetHereditary Sensory and Autonomic NeuropathiesGenes DominantaxonGeneticsMutationEndoplasmic reticulumNeurodegenerationneurodegenerationmedicine.diseasePenetrancePedigreeHSANsensory neuronsmedicine.anatomical_structurePhenotypeCoughHaplotypesMutationGastroesophageal RefluxFemaleNeurology (clinical)Human medicineBone DiseasesNeuroscienceBrain : a journal of neurology
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An inherited deficiency of the third component of complement, C3, in guinea pigs

1986

Hereditary deficiency of the third component of complement, C3, is found very seldom in the human. C3 deficiency is associated with severe bacterial infections revealing the central role of C3 in complement activation via the classical or alternative pathway. We describe a new hereditary C3 deficiency in strain 2 guinea pigs. Serum from these animals had a markedly reduced lytic activity in a standard assay for complement-dependent, antibody-mediated cytotoxicity. In functional assays of individual components, the hemolytic activity of the components C4, C2, C5 and of factors B, D and H was in the normal range. The functional C3 titer, and similarly C3 antigenic activity in the serum of the…

Blood Bactericidal ActivityGuinea PigsImmunologyMacrophage-1 Antigenchemical and pharmacologic phenomenaBiologyHemolysisMajor Histocompatibility ComplexGuinea pigInbred strainAntigenIn vivoAnimalsImmunology and AllergyComplement ActivationRecombination GeneticComplement C3Molecular biologyIn vitroPedigreeReceptors ComplementComplement systemImmunologyAlternative complement pathwaybiology.proteinC3a receptorEuropean Journal of Immunology
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Insulin resistance in patients with familial combined hyperlipidemia and coronary artery disease.

1997

The minimum model modified by the administration of insulin provides an objective and relatively easily measured index of peripheral sensitivity to insulin which was significantly lower (p <0.02) in familial combined hyperlipidemia (FCH) with ischemic heart disease (IHD) than in FCH without IHD and in control subjects (1.2 +/- 0.6, 1.9 +/- 1.0, 2.9 +/- 1.2 x 10(-4) mU/L/ min, respectively). In patients with FCH, insulin resistance explains, at least in part, their metabolic alterations (hypertension, abnormal glucose tolerance, hyperinsulinemia) and elevated IHD.

Blood GlucoseMalemedicine.medical_specialtymedicine.medical_treatmentLipoproteinsHyperlipidemia Familial CombinedCoronary DiseaseDiseaseCoronary artery diseaseInsulin resistanceRisk FactorsInternal medicineHyperinsulinemiaMedicineHumansInsulinIn patientcardiovascular diseasesbusiness.industryInsulinGlucose Tolerance TestMiddle Agedmedicine.diseasePeripheralPedigreeEndocrinologyPhenotypeCardiologyInsulin ResistanceCardiology and Cardiovascular MedicinebusinessLipoproteinThe American journal of cardiology
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The analysis of 51 genes in DSM-IV combined type attention deficit hyperactivity disorder: association signals in DRD4, DAT1 and 16 other genes.

2006

Contains fulltext : 35205.pdf (Publisher’s version ) (Closed access) Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder, starting in early childhood and persisting into adulthood in the majority of cases. Family and twin studies have demonstrated the importance of genetic factors and candidate gene association studies have identified several loci that exert small but significant effects on ADHD. To provide further clarification of reported associations and identify novel associated genes, we examined 1,038 single-nucleotide polymorphisms (SNPs) spanning 51 candidate genes involved in the regulation of neurotransmitter pathways, particularly dopamine, nor…

Candidate geneGenetics and epigenetic pathways of disease [NCMLS 6]MedizinReceptors NicotinicTryptophan HydroxylaseNeuroinformatics [DCN 3]0302 clinical medicinePerception and Action [DCN 1]Determinants in Health and Disease [EBP 1]ChildOncogene ProteinsGenetics0303 health sciencesbiologyDNA POOLING ANALYSISPedigree3. Good healthserotoninPsychiatry and Mental healthConduct disorderChild Preschool/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingMonoamine oxidase AdopaminePsychologyFunctional Neurogenomics [DCN 2]Genetic MarkersAdolescentSynaptosomal-Associated Protein 25Single-nucleotide polymorphismassociation studyPolymorphism Single NucleotideMental health [NCEBP 9]Genetic determinismGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular NeuroscienceMONOAMINE-OXIDASE-ACognitive neurosciences [UMCN 3.2]SDG 3 - Good Health and Well-beingmental disordersmedicineHumansAttention deficit hyperactivity disorderADHDGenetic Predisposition to Disease5-HT1B RECEPTOR GENEddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersMonoamine OxidaseMolecular Biology030304 developmental biologyGenetic associationDopamine Plasma Membrane Transport ProteinsSEROTONIN TRANSPORTER GENEDOPAMINE-BETA-HYDROXYLASESiblingsReceptors Dopamine D4candidate genemedicine.diseaseTwin studyPREFERENTIAL TRANSMISSIONHaplotypesCATECHOL-O-METHYLTRANSFERASEAttention Deficit Disorder with HyperactivityCONDUCT DISORDERbiology.proteinnoradrenalineDEFICIT/HYPERACTIVITY DISORDERNO EVIDENCE030217 neurology & neurosurgerylinkage disequilibriumMolecular Psychiatry
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