Search results for "Phenotype"

showing 10 items of 1875 documents

Mutation analyses in 17 patients with deficiency in acid β-galactosidase: three novel point mutations and high correlation of mutation W273L with Mor…

2001

An inherited deficiency in beta-galactosidase can result in GM1 gangliosidosis, with several phenotypes of generalized or chronic psychomotor deterioration, as well as in Morquio disease type B, a characteristic mucopolysaccharidosis free of neurological symptoms. We performed mutation analyses in 17 juvenile and adult patients from various European regions with a deficiency in beta-galactosidase and skeletal abnormalities. Fifteen of these had the Morquio B phenotype and have remained neurologically healthy until now while the two others exhibited psychomotor retardation of juvenile onset. A two-base substitution (851-852TG--CT; W273L) was present in 14 of the 15 Morquio B cases. Even if o…

AdultMaleAdolescentMucopolysaccharidosisDNA Mutational AnalysisRestriction MappingMutation MissenseBiologyGeneticsmedicineHumansPoint MutationMissense mutationRNA MessengerChildGenetics (clinical)DNA PrimersGeneticsPsychomotor retardationReverse Transcriptase Polymerase Chain ReactionPoint mutationMucopolysaccharidosis IVHeterozygote advantageMiddle Agedbeta-Galactosidasemedicine.diseasePhenotypePedigreePhenotypeGLB1Child PreschoolMutation (genetic algorithm)Femalemedicine.symptomHuman Genetics
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Hereditary angioedema in a single family with specific mutations in both plasminogen and SERPING1 genes

2019

BACKGROUND Hereditary angioedema (HAE) is a group of genetic diseases characterized by recurrent, painful and potentially lethal tissue swelling. The most common form results from mutations in the SERPING1 gene, leading to reduced function of complement 1 inhibitor (C1-INH). Rarer forms with normal C1-INH may arise from mutations in the coagulation factor F12 gene, but mostly the genetic background is unknown. Recently, a novel HAE mutation in the plasminogen (PLG) gene was shown. PATIENTS AND METHODS We analyzed the various clinical manifestations of HAE in 14 related patients using clinical data, biochemical analysis for C1-INH and C4 as well as gene sequencing. RESULTS Patients' symptoms…

AdultMaleAdolescentMutation MissenseDermatologymedicine.disease_causeYoung Adult030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicineTonguemedicineHumansFamilyChildGeneSingle familyMutationGastrointestinal tractbusiness.industryAngioedemas HereditaryPlasminogenMiddle Agedmedicine.diseasePhenotype3. Good healthPhenotypemedicine.anatomical_structureCoagulationChild PreschoolMutationHereditary angioedemaImmunologyFemalebusinessComplement C1 Inhibitor ProteinJDDG: Journal der Deutschen Dermatologischen Gesellschaft
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Hydroxylation of collagen type I: evidence that both lysyl and prolyl residues are overhydroxylated in osteogenesis imperfecta

1995

The composition of the collagens secreted into the media of fibroblast cultures of 39 patients with osteogenesis imperfecta (OI) was the same in controls and OI cultures. An abnormal migration pattern of collagens upon SDS-PAGE was evident in one third of the cultures investigated. Lysyl and prolyl hydroxylation of HPLC-purified alpha 1(I) chains was elevated in about 60% of cultures. The degree of hydroxylation was highest in the lethal forms. The extent of lysyl and prolyl hydroxylation showed a strong correlation (r = 0.74, P < 0.001). While high levels of hydroxylation are frequently observed in OI patients, a direct correlation between lysyl or prolyl hydroxylation and fracture rate or…

AdultMaleAdolescentProlineClinical BiochemistryAlpha (ethology)Fibroblast culturesHydroxylationHydroxylysineBiochemistryHydroxylationFractures Bonechemistry.chemical_compoundHydroxyprolinePregnancymedicineHumansChildCells CulturedCollagen typeGrowth retardationLysineInfantGeneral MedicineFibroblastsMiddle AgedOsteogenesis Imperfectamedicine.diseaseMolecular biologyBody HeightHydroxyprolineHydroxylysinePhenotypechemistryBiochemistryOsteogenesis imperfectaChild PreschoolFemaleCollagenEuropean Journal of Clinical Investigation
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Single-Nucleotide Polymorphism Array-Based Characterization of Ring Chromosome 18

2012

Objective To study genotype–phenotype correlation of ring chromosome 18 [r(18)] in 9 patients with 46,XN karyotype. Study design In 9 patients with a de novo 46,XN,r(18) karyotype (7 females, 2 males), we performed high-resolution single-nucleotide polymorphism array analysis (Illumina Human Omni1-QuadV1 array in 6 patients, Affymetrix 6.0 array in 3 patients), investigation of parental origin, and genotype–phenotype correlation. Results No breakpoint was recurrent. Single metaphases with loss of the ring, double rings, or secondarily rearranged rings were found in some cases, but true mosaicism was present in none of these cases. In 3 patients, additional duplications in 18p (of 1.4 Mb, 2 …

AdultMaleAdolescentRing chromosomeSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideCROMOSSOMOS HUMANOS (ANORMALIDADES;COMPLICAÇÕES)Young AdultMeiosisPolymorphism (computer science)SNPBody SizeHumansRing ChromosomesChildGenetic Association StudiesOligonucleotide Array Sequence AnalysisGeneticsBreakpointInfant NewbornInfantKaryotypeMiddle AgedPhenotypeChild PreschoolKaryotypingPediatrics Perinatology and Child HealthFemaleChromosome DeletionChromosomes Human Pair 18HeadMaternal AgeMicrosatellite Repeats
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Studies on serum groups in the Kumaon region, India

1970

A total of 469 individuals belonging to 4 endogamous groups (Brahamins, Rajputs, Doms and Tharus) from the Kumaon region (North India) were tested for Hp, Gc, Gm and Inv systems.

AdultMaleAdolescentStatistics as TopicIndian populationIndiaEuropean populationMiddle AgedBiologyNorth indiaWhite PeopleHuman geneticsPhenotypeAsian PeopleSocial ClassGenetic distanceEndogamyBlood Group AntigensGeneticsHumansMarriageMetabolic diseaseSocioeconomicsAllelesGenetics (clinical)Humangenetik
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Expanding the clinical phenotype of patients with a ZDHHC9 mutation.

2013

In 2007, 250 families with X-linked intellectual disability (XLID) were screened for mutations in genes on the X-chromosome, and in 4 of these families, mutations in the ZDHHC9 gene were identified. The ID was either isolated or associated with a marfanoid habitus. ZDHHC9 encodes a palmitoyl transferase that catalyzes the posttranslational modification of NRAS and HRAS. Since this first description, no additional patient with a ZDHHC9 mutation has been reported in the literature. Here, we describe a large family in which we identified a novel pathogenic ZDHHC9 nonsense mutation (p.Arg298*) by parallel sequencing of all X-chromosome exons. The mutation cosegregated with the clinical phenotyp…

AdultMaleAdolescentX-linked intellectual disabilityGenetic counselingNonsense mutationNeuropsychological TestsBioinformaticsYoung AdultFatal OutcomeGenes X-LinkedIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumansHRASChildGenetics (clinical)GeneticsMassive parallel sequencingAcrocyanosisbusiness.industryBrainFaciesmedicine.diseaseMagnetic Resonance ImagingPedigreePhenotypeMutation (genetic algorithm)MutationbusinessAcyltransferasesAmerican journal of medical genetics. Part A
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Incomplete penetrance and phenotypic variability of 6q16 deletions including SIM1.

2015

International audience; 6q16 deletions have been described in patients with a Prader-Willi-like (PWS-like) phenotype. Recent studies have shown that certain rare single-minded 1 (SIM1) loss-of-function variants were associated with a high intra-familial risk for obesity with or without features of PWS-like syndrome. Although SIM1 seems to have a key role in the phenotype of patients carrying 6q16 deletions, some data support a contribution of other genes, such as GRIK2, to explain associated behavioural problems. We describe 15 new patients in whom de novo 6q16 deletions were characterised by comparative genomic hybridisation or single-nucleotide polymorphism (SNP) array analysis, including…

AdultMaleAdolescent[SDV]Life Sciences [q-bio]PenetranceBioinformaticsPolymorphism Single NucleotideArticlePregnancyGRIK2Basic Helix-Loop-Helix Transcription FactorsGeneticsHumansSNPObesityChildGeneGenetic Association StudiesGenetics (clinical)GeneticsComparative Genomic Hybridizationbiology[ SDV ] Life Sciences [q-bio]InfantPenetrancePhenotypeRepressor ProteinsChild PreschoolAborted FetusSIM1biology.proteinChromosomes Human Pair 6FemaleHaploinsufficiencyPrader-Willi SyndromeComparative genomic hybridization
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Pure Progressive Amnesia and the APPV717G Mutation

2009

We report an isolated, slowly progressive, pure amnestic phenotype in a 59-year-old member of a family affected by autosomal dominant familial Alzheimer disease. Early-onset Alzheimer disease in this family was associated with a V717G mutation in the amyloid precursor protein gene (APP). Subjective impairment of episodic memory began in our subject at the age of 44 years and subsequent, longitudinal neuropsychologic assessment confirmed progressive, severe, global impairment of memory functions over a period of 14 years with preservation of other cognitive domains. The mean annual hippocampal atrophy rate, determined by volumetric magnetic resonance imaging was intermediate between values p…

AdultMaleAgingPathologymedicine.medical_specialtyGlycineAmnesiaHippocampusAmyloid beta-Protein PrecursorAtrophyAlzheimer DiseasemedicineHumansDementiaMemory disorderEpisodic memoryAgedSettore M-PSI/02 - Psicobiologia E Psicologia FisiologicaCognitive disorderValineMiddle Agedmedicine.diseaseAPPV717G mutation.PedigreePsychiatry and Mental healthClinical PsychologyPhenotypeMutationDisease ProgressionPure progressive amnesiaFemaleAmnesiaAtrophyGeriatrics and Gerontologymedicine.symptomAlzheimer's diseasePsychologyGerontologyFrontotemporal dementia
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Two Italian kindreds with familial amyotrophic lateral sclerosis due to FUS mutation

2009

Recently, fused in sarcoma/translated in liposarcoma (FUS/TLS) gene, located on chromosome 16p11.2, has been identified as a disease gene in familial amyotrophic lateral sclerosis (FALS). We have analyzed FUS/TLS in a cohort of 52 index cases from seven Italian regions with non-SOD1 and non-TARDBP FALS. We identified a heterozygous c.G1542C missense mutation in a family of northern Italian origin, and a heterozygous c.C1574T missense mutation in a family of Sicilian origin. Both variants are located in exon 15 encoding the RNA-recognition motif, and result in a substitution of an arginine with a serine in position 514 (p.R514S) and substitution of a proline with a leucine at position 525 (p…

AdultMaleAgingamyotrophic lateral sclerosisAdolescentDNA Mutational AnalysisMutation MissenseBiologyArticleCohort StudiesExonYoung AdultDegenerative diseasemedicineMissense mutationHumansFamilygeneticsAmyotrophic lateral sclerosisAge of OnsetGeneamyotrophic lateral sclerosis; geneticsAgedGeneticsGeneral NeuroscienceMiddle Agedmedicine.diseasePhenotypePedigreePhenotypeSLA - FUS mutation - geneticsItalyMutationDisease ProgressionRNA-Binding Protein FUSFemaleSettore MED/26 - NeurologiaNeurology (clinical)Geriatrics and GerontologyAge of onsetMissenseAmyotrophic lateral sclerosis; Family pedigrees; FUS gene; Genetics;Developmental BiologyRNA-Binding Protein FUS
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Sex-specific phenotypical and functional differences in peripheral human Vγ9/Vδ2 T cells

2006

Abstract Vγ9/Vδ2 T cells constitute a minor proportion of human peripheral blood T cells that can expand rapidly upon infection with microbial pathogens. Vγ9/Vδ2 T cell numbers change characteristically with age, rising from birth to puberty and gradually decreasing again beyond 30 years of age. In adults, female blood donors have significantly higher levels than males, implying that circulating Vγ9/Vδ2 T cells in women remain elevated for a longer period in life and drop less strikingly than in men. This loss in men is accompanied by a substantial depletion of CD27−CD45RA− and CD27−CD45RA+ effector T cells and a parallel increase in CD27+CD45RA− central memory T cells while in women, the d…

AdultMaleAgingmedicine.medical_specialtyAdolescentT-LymphocytesT cellImmunologyIsopentenyl pyrophosphateStimulationBiologygamma delta T cells Phenotype effector functionsInterferon-gammachemistry.chemical_compoundHemiterpenesOrganophosphorus CompoundsSex FactorsT-Lymphocyte SubsetsInternal medicinemedicineHumansImmunology and AllergySecretionLongitudinal StudiesChildAgedSex CharacteristicsEffectorCell DifferentiationReceptors Antigen T-Cell gamma-deltaCell BiologyMiddle AgedPhenotypeIn vitroPeripheralPhenotypemedicine.anatomical_structureEndocrinologychemistryChild PreschoolFemaleJournal of Leukocyte Biology
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