Search results for "Proband"

showing 10 items of 99 documents

Exclusion of PAX9 and MSX1 mutation in six families affected by tooth agenesis. A genetic study and literature review

2013

Objectives: In the present study, it is described the phenotypical analysis and the mutational screening, for genes PAX9 and MSX1, of six families affected by severe forms of tooth agenesis associated with other dental anomalies and systemic entities. Study Design: Six families affected by severe tooth agenesis associated with other dental anomalies and systemic entities were included. Oral exploration, radiological examination, medical antecedents consideration and mutational screening for PAX9 and MSX1 were carried out. Results: No mutations were discovered despite the fact that numerous teeth were missing. An important phenotypical variability was observed within the probands, not being …

ProbandMaleNonsense mutationOdontologíaGene mutationmedicine.disease_causeGene dosageAnodontiaGenetic transformationstomatognathic systemDental abnormalitiesmedicineMalalties hereditàriesMissense mutationHumansGeneral DentistryGenetic Association StudiesAnodontiaGeneticsMSX1 Transcription FactorMutationOral Medicine and Pathologybusiness.industryResearchmedicine.disease:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludFenotipstomatognathic diseasesPhenotypeOtorhinolaryngologyGenesUNESCO::CIENCIAS MÉDICASMutationSurgeryFemalePAX9 Transcription FactorbusinessMalformacions dentalsTransformació genèticaPAX9GensGenetic diseases
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Malformations in newborn: results based on 30,940 infants and fetuses from the Mainz congenital birth defect monitoring system (1990-1998).

2002

Prevalence rates of birth defects in the Federal Republic of Germany are informative to assess the general background risk of having a child with a birth defect. They provide basic figures to determine temporal and regional prevalence trends, to evaluate and initiate preventive measures and to initiate research projects. To avoid observer, definition and collection bias, active monitoring systems are required. Data collected in the active monitoring system of the Mainz Birth Defects Registry are presented. From 1990-1998, 30,940 live-births, stillbirths and abortions underwent standardized physical and sonographic examinations. Anamnestic data were collected from prenatal care records, mate…

ProbandMalePediatricsmedicine.medical_specialtyPolyhydramniosPrevalenceOligohydramniosPrenatal careCongenital AbnormalitiesCohort StudiesRisk FactorsGermanyPrevalenceMedicineHumansRegistriesPregnancybusiness.industryInfant NewbornObstetrics and GynecologyGestational ageGeneral Medicinemedicine.diseaseFemalebusinessCohort studyArchives of gynecology and obstetrics
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Inheritance and variable expression in Rubinstein-Taybi syndrome.

2010

Familial Rubinstein-Taybi syndrome (RTS) is very rare. Here we report on the 6th and 7th case of inherited RTS. Family 1 presents with incomplete or mild RTS over three generations; a 13-year-old girl (proband 1) with mild but typical facial features and learning disabilities, her very mildly affected mother (proband 2), and the maternal grandmother (proband 3). Family 2 includes three females with classical RTS (probands 4-6) and their father (proband 7) with broad thumbs and halluces. Proband 5 also had a brain tumor (ganglioglioma) at the age of 3 years. In probands 1-3, direct sequencing identified a novel CREBBP missense mutation, c.2728A > G (predicting p.Thr910Ala), that was absent i…

ProbandMaleRiskAdolescentDNA Mutational AnalysisMutation MissenseBiologyVariable ExpressionGenetic HeterogeneityGeneticsmedicineMissense mutationHumansPoint MutationFamilyAlleleGenetics (clinical)GeneticsRubinstein-Taybi SyndromeRubinstein–Taybi syndromeGenetic heterogeneityMosaicismPoint mutationmedicine.diseaseCREB-Binding ProteinPedigreePhenotypeChild PreschoolMutation (genetic algorithm)FemaleAmerican journal of medical genetics. Part A
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Excess of de novo variants in genes involved in chromatin remodelling in patients with marfanoid habitus and intellectual disability.

2020

PurposeMarfanoid habitus (MH) combined with intellectual disability (ID) (MHID) is a clinically and genetically heterogeneous presentation. The combination of array CGH and targeted sequencing of genes responsible for Marfan or Lujan–Fryns syndrome explain no more than 20% of subjects.MethodsTo further decipher the genetic basis of MHID, we performed exome sequencing on a combination of trio-based (33 subjects) or single probands (31 subjects), of which 61 were sporadic.ResultsWe identified eight genes with de novo variants (DNVs) in at least two unrelated individuals (ARID1B, ATP1A1, DLG4, EHMT1, NFIX, NSD1, NUP205 and ZEB2). Using simulation models, we showed that five genes (DLG4, NFIX, …

ProbandMale[SDV]Life Sciences [q-bio]intellectual deficiencyMESH: NFI Transcription Factorschromatin remodelingMarfan SyndromeCraniofacial AbnormalitiesMESH: ChildIntellectual disabilityMESH: Craniofacial AbnormalitiesMESH: Mental Retardation X-LinkedExomeChildde novo variantsGenetics (clinical)Exome sequencingGeneticsMESH: ExomeMESH: Middle AgedbiologyMESH: Genetic Predisposition to DiseaseMiddle AgedNFIXMESH: Young AdultFemaleAdultMESH: MutationAdolescentChromatin remodelingMESH: Intellectual DisabilityMESH: Marfan SyndromeEHMT1Young AdultMESH: Whole Exome SequencingIntellectual DisabilityExome SequencingGeneticsmedicineHumansGenetic Predisposition to Diseasemarfanoid habitusGeneMESH: Neurodevelopmental DisordersMESH: AdolescentMESH: HumansGenetic heterogeneityMESH: Chromatin Assembly and DisassemblyMESH: Histone-Lysine N-MethyltransferaseMESH: AdultHistone-Lysine N-Methyltransferasemedicine.diseaseChromatin Assembly and DisassemblyMESH: MaleNFI Transcription FactorsNeurodevelopmental DisordersMutationbiology.proteinMental Retardation X-LinkedMESH: FemaleJournal of medical genetics
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Lack of phenotypic additive effect of familial defective apolipoprotein B3531 in familial hypercholesterolaemia.

2020

Familial defective apolipoprotein (apo) B (FDB) and familial hypercholesterolaemia (FH) are the two common genetic conditions that cause hypercholesterolaemia. R3531C mutation of the APOB gene is a rare cause of FDB. Individuals with both FDB and FH are rare. A 51-year-old man with hypercholesterolaemia (11.4 mmol/L) and his family were studied. Low-density lipoprotein (LDL) receptor (LDLR) and APOB genes were analysed by direct sequencing. LDL of four subjects were studied in a fibroblast LDL receptor-binding displacement assay. We found a mutation of the LDLR gene (p.Y398X) in the proband and in four other family members: the p.R3531C APOB gene mutation was also found in the proband, his …

ProbandMalemedicine.medical_specialtyApolipoprotein B030204 cardiovascular system & hematologyCompound heterozygosityHyperlipoproteinemia Type II03 medical and health scienceschemistry.chemical_compoundFDB35310302 clinical medicineInternal medicineInternal MedicinemedicineHumans030212 general & internal medicineApolipoproteins Bdouble heterozygotebiologybusiness.industryCholesterolLDL receptornutritional and metabolic diseasesHeterozygote advantageMiddle AgedEndocrinologychemistryItalyReceptors LDLLDL receptorMutation (genetic algorithm)Mutationfamilial hypercholesterolaemiabiology.proteinlipids (amino acids peptides and proteins)businessLipoproteinInternal medicine journalReferences
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The impact of the endogenous subtype on the familial aggregation of unipolar depression.

1991

The endogenous/non-endogenous distinction of unipolar major depression is widely accepted, as is the family study approach to the validation of diagnostic distinctions. Rates of affective disorders were examined in 689 first-degree relatives of 184 patients with unipolar major depression and were compared with 312 first-degree relatives of 80 healthy controls. Only unipolar depression and alcoholism were more common in families of depressed probands compared with families of healthy controls. As a variety of diagnostic definitions of endogenous depression have been proposed, probands and relatives were diagnosed in a polydiagnostic manner. None of the five diagnostic definitions of endogeno…

ProbandMalemedicine.medical_specialtyEndogenybehavioral disciplines and activitiesDelusionsArousalDiagnosis DifferentialChild of Impaired ParentsRisk Factorsmental disordersmedicineHumansPharmacology (medical)PsychiatryBiological PsychiatryDepression (differential diagnoses)Depressive DisorderGeneral NeuroscienceMental DisordersFamily aggregationGeneral MedicineFamilial riskMiddle AgedCircadian RhythmPsychiatry and Mental healthNeuropsychology and Physiological PsychologyPhenotypeEndogenous depressionFemalePsychologyArousalClinical psychologyEuropean archives of psychiatry and clinical neuroscience
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A genotype-phenotype correlation in Sicilian patients with GJB2 biallelic mutations

2015

The aim of this work was to study the genotype distribution of Sicilian patients with biallelic GJB2 mutations; to correlate genotype classes and/or specific mutations of GJB2 gene (35delG-non-35delG) with audiologic profiles. A total of 10 different mutations and 11 different genotypes were evidenced in 73 SNHL subjects; 35delG (90.36 % of cases) and IVS1+1 (13.69 %) were the most common mutations found in the cohort with a significant difference in the distribution between North and South Sicily. Audiological evaluation revealed a severe (16/73) to profound (47/73) hearing loss (HL) in 86.13 % of cases without significant difference between the degree of HL and the province of origin of t…

ProbandMalemedicine.medical_specialtyGenotypeHearing lossHearing Loss SensorineuralGJB2 mutations Sensorineural hearing loss Genetic hearing loss · Cx26BiologyDeafnessCompound heterozygositymedicine.disease_causeGastroenterologySeverity of Illness IndexConnexinsCorrelationYoung AdultAudiometryInternal medicineGenotypemedicineHumansChildHearing LossSicilyGenetic Association StudiesGeneticsMutationGeneral Medicinemedicine.diseaseSettore MED/32 - AudiologiaConnexin 26Settore MED/31 - OtorinolaringoiatriaOtorhinolaryngologyChild PreschoolCohortMutationSensorineural hearing lossFemalemedicine.symptom
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Newborn screening for 3-methylcrotonyl-CoA carboxylase deficiency: population heterogeneity of MCCA and MCCB mutations and impact on risk assessment.

2006

New technology enables expansion of newborn screening (NBS) of inborn errors aimed to prevent adverse outcome. In conditions with a large share of asymptomatic phenotypes, the potential harm created by NBS must carefully be weighed against benefit. Policies vary throughout the United States, Australia, and Europe due to limited data on outcome and treatability of candidate screening conditions. We elaborated the rationale for decision making in 3-methylcrotonyl-coenzyme A (CoA) carboxylase deficiency (MCCD), which afflicts leucine catabolism, with reported outcomes ranging from asymptomatic to death. In Bavaria, we screened 677,852 neonates for 25 conditions, including MCCD, based on elevat…

ProbandMalemedicine.medical_specialtyGenotypePenetranceBiologyAsymptomaticRisk AssessmentCohort StudiesGenetic HeterogeneityNeonatal ScreeningInternal medicineGermanyGeneticsmedicineHumansExpressivity (genetics)Genetics (clinical)AllelesGeneticsNewborn screeningGenetic heterogeneityInfant Newborn3-Methylcrotonyl-CoA carboxylase deficiencymedicine.diseasePenetranceCarbon-Carbon LigasesInborn error of metabolismMutationFemalemedicine.symptomDeficiency DiseasesHuman mutation
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A homozygous mutation in the TUB gene associated with retinal dystrophy and obesity.

2013

Inherited retinal dystrophies are a major cause of childhood blindness. Here, we describe the identification of a homozygous frameshift mutation (c.1194_1195delAG, p.Arg398Serfs*9) in TUB in a child from a consanguineous UK Caucasian family investigated using autozygosity mapping and whole-exome sequencing. The proband presented with obesity, night blindness, decreased visual acuity, and electrophysiological features of a rod cone dystrophy. The mutation was also found in two of the proband's siblings with retinal dystrophy and resulted in mislocalization of the truncated protein. In contrast to known forms of retinal dystrophy, including those caused by mutations in the tubby-like protein …

ProbandMaleobesity030209 endocrinology & metabolismGenes RecessiveConsanguinityBiologymedicine.disease_causeWhite PeopleFrameshift mutation03 medical and health sciencesConsanguinity0302 clinical medicineRetinitis pigmentosaGeneticsRod-cone dystrophymedicineHomeostasisHumansretinal dystrophyTUBChildEye ProteinsFrameshift MutationGenetics (clinical)030304 developmental biologyAdaptor Proteins Signal TransducingGenetics0303 health sciencesMutationHomozygoteChildhood blindnessciliatubbyChromosome MappingProteinsmedicine.diseaseUnited Kingdom3. Good healthPedigreeBrief ReportsFemaleRetinal DystrophiesRetinitis Pigmentosa
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Contribution of molecular analyses in diagnosing Marfan syndrome and type I fibrillinopathies: an international study of 1009 probands.

2008

International audience; BACKGROUND: The diagnosis of Marfan syndrome (MFS) is usually initially based on clinical criteria according to the number of major and minor systems affected following international nosology. The number of FBN1 mutation carriers, at risk of aortic complications who would not be properly diagnosed based only on clinical grounds, is of growing importance owing to the increased availability of molecular screening. The aim of the study was to identify patients who should be considered for FBN1 mutation screening. METHODS: Our international series included 1009 probands with a known FBN1 mutation. Patients were classified as either fulfilling or not fulfilling "clinical"…

ProbandNosologyMarfan syndromeMalePediatricsSystemic diseaseMESH : International CooperationFibrillin-1International CooperationMESH : Aged[SDV.GEN] Life Sciences [q-bio]/GeneticsMarfan SyndromeMESH : ChildMESH: ChildEpidemiologyMESH : FemaleEctopia lentisChildGenetics (clinical)AortaAortic dissectionMESH: Aged0303 health sciences030305 genetics & heredityMicrofilament ProteinsMESH: AortaMESH : AdultConnective tissue disease3. Good healthFemaleMESH : Mutationmusculoskeletal diseasesAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesMESH: MutationMESH : Microfilament ProteinsAdolescentMESH : MaleFibrillinsMESH: Marfan Syndrome03 medical and health sciencesMESH: Microfilament ProteinsMESH : AdolescentGeneticsmedicineHumans030304 developmental biologyAgedMESH: Adolescent[SDV.GEN]Life Sciences [q-bio]/GeneticsMESH : Marfan SyndromeMESH: Humansbusiness.industryMESH : HumansMESH : AortaMESH: Adultmedicine.diseaseMESH: MaleMESH: International CooperationMutation[ SDV.GEN ] Life Sciences [q-bio]/GeneticsbusinessMESH: FemaleJournal of medical genetics
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