Search results for "Proband"

showing 10 items of 99 documents

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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Semiquantitative multiplex PCR: a useful tool for large rearrangement screening and characterization

2006

Methods presently employed for detection of large rearrangements have several drawbacks, such as the amount of sample and time required, technical difficulty, or the probability of false-negative carriers. Using the low-density-lipoprotein receptor (LDLR) gene, whose mutations are responsible for familial hypercholesterolemia (FH), we have developed a procedure to detect large rearrangements in this gene based on semiquantitative PCR, with important improvements as compared to previous methods. Our method covers the complete LDLR gene and introduces an internal control in the reaction. The procedure discriminates the four different large rearrangements (two deletions and two insertions) tha…

Chromosome AberrationsGeneticsProbandMutationLdlr geneExonsBiologymedicine.disease_causePolymerase Chain ReactionHyperlipoproteinemia Type IIExonReceptors LDLLDL receptorMultiplex polymerase chain reactionGeneticsmedicineHumansGenetic TestingGeneGene DeletionGenetics (clinical)Apolipoproteins BSouthern blotHuman Mutation
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Rare variants in the genetic background modulate the expressivity of neurodevelopmental disorders

2018

AbstractPurposeTo assess the contribution of rare variants in the genetic background towards variability of neurodevelopmental phenotypes in individuals with rare copy-number variants (CNVs) and gene-disruptive mutations.MethodsWe analyzed quantitative clinical information, exome-sequencing, and microarray data from 757 probands and 233 parents and siblings who carry disease-associated mutations.ResultsThe number of rare secondary mutations in functionally intolerant genes (second-hits) correlated with the expressivity of neurodevelopmental phenotypes in probands with 16p12.1 deletion (n=23, p=0.004) and in probands with autism carrying gene-disruptive mutations (n=184, p=0.03) compared to …

GeneticsProband0303 health sciencesCandidate geneMutationGenetic heterogeneityDiseaseBiologymedicine.diseasemedicine.disease_cause03 medical and health sciences0302 clinical medicinemedicineAutismExpressivity (genetics)Family history030217 neurology & neurosurgery030304 developmental biology
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Identification of Novel Wsf1 Mutations in a Sicilian Child with Wolfram Syndrome

2014

Wolfram Syndrome (WS) is a rare hereditary disease with autosomal recessive inheritance with incomplete penetrance. It is characterized by diabetes mellitus associated with progressive optic atrophy. The diagnosis is essentially clinical and mutation analysis is used to confirm the diagnosis. In the present study we describe the clinical and molecular features of a diabetic child carrying two novel WFS1 mutations. The Sicilian proband and his non-affected family were studied. Ophthalmologic examination included: visual acuity determination and funduscopy, optical coherent tomography, retinal fluorangiography, perimetry and electroretinogram. Molecular methods: automatic sequencing of PCR am…

GeneticsProbandMutationWolfram syndromebusiness.industryWolfram syndromeDiabetesWFS1medicine.disease_causemedicine.diseasePenetranceSettore MED/13 - EndocrinologiaAtrophyDIDMOADDiabetes mellitusMutation testingMedicineAllelebusinessJournal of Genetic Syndromes & Gene Therapy
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Genetics of the Charcot-Marie-Tooth disease in the Spanish Gypsy population: the hereditary motor and sensory neuropathy-Russe in depth

2012

Four private mutations responsible for three forms demyelinating of Charcot-Marie-Tooth (CMT) or hereditary motor and sensory neuropathy (HMSN) have been associated with the Gypsy population: the NDRG1 p.R148X in CMT type 4D (CMT4D/HMSN-Lom); p.C737_P738delinsX and p.R1109X mutations in the SH3TC2 gene (CMT4C); and a G>C change in a novel alternative untranslated exon in the HK1 gene causative of CMT4G (CMT4G/HMSN-Russe). Here we address the findings of a genetic study of 29 Gypsy Spanish families with autosomal recessive demyelinating CMT. The most frequent form is CMT4C (57.14%), followed by HMSN-Russe (25%) and HMSN-Lom (17.86%). The relevant frequency of HMSN-Russe has allowed us to inv…

GeneticsProbandcongenital hereditary and neonatal diseases and abnormalitiesWeaknesseducation.field_of_studyHaplotypePopulationBiologymedicine.diseaseTooth diseaseDistal sensory lossGeneticsmedicinemedicine.symptomeducationHereditary motor and sensory neuropathyFounder mutationGenetics (clinical)Clinical Genetics
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Mitochondrial DNA variations in patients with Type 2 (non-insulin dependent) diabetes mellitus and a Welsh control population

1999

The LDL-receptor gene point mutation FH-Genoa/Palermo is the most frequent mutation responsible for Familial Hypercholesterolemia in Sicily. The mutation does not introduce or abolish any useful restriction site. We establish a GeneComb-based strategy to identify this mutation in a population of Sicilian unrelated clinically diagnosed FH probands. The method was very sensitive and specific; 12 out of 90 (13.3%) unrelated FH probands were found to carry the FH-Genoa/Palermo mutation. According to these results, the FH-Genoa/Palermo is the more frequent LDL-receptor gene mutation among the Sicilian FH patients. Moreover FH-Genoa/Palermo is the mutation cluster to date more represented in Sout…

GeneticsProbandcongenital hereditary and neonatal diseases and abnormalitieseducation.field_of_studyPoint mutationPopulationnutritional and metabolic diseasesFamilial hypercholesterolemiaGene mutationBiologymedicine.diseaseRestriction siteLDL receptorMutation (genetic algorithm)Geneticsmedicineskin and connective tissue diseaseseducationGenetics (clinical)Human Mutation
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The landscape of epilepsy-related GATOR1 variants

2019

Purpose:\ud \ud To define the phenotypic and mutational spectrum of epilepsies related to DEPDC5, NPRL2 and NPRL3 genes encoding the GATOR1 complex, a negative regulator of the mTORC1 pathway.\ud \ud Methods:\ud \ud We analyzed clinical and genetic data of 73 novel probands (familial and sporadic) with epilepsy-related variants in GATOR1-encoding genes and proposed new guidelines for clinical interpretation of GATOR1 variants.\ud \ud Results:\ud \ud The GATOR1 seizure phenotype consisted mostly in focal seizures (e.g., hypermotor or frontal lobe seizures in 50%), with a mean age at onset of 4.4 years, often sleep-related and drug-resistant (54%), and associated with focal cortical dysplasia…

Male0301 basic medicineProbandDEPDC5SUDEP030105 genetics & heredityBioinformaticsLoss of Function Mutation/geneticsEpilepsyINDEL MutationLoss of Function MutationmTORC1 pathwayGenetics(clinical)ChildGenetics (clinical)Multiprotein Complexes/geneticsBrugada SyndromeDNA Copy Number VariationBrugada syndromeINDEL Mutation/geneticsGTPase-Activating ProteinsNPRL3SeizureDEPDC5PhenotypePedigree3. Good healthBrugada Syndrome/geneticsChild PreschoolFemaleHumanSignal TransductionDNA Copy Number VariationsAdolescentSeizures/complicationsMechanistic Target of Rapamycin Complex 1/geneticsDNA Copy Number Variations/geneticsMechanistic Target of Rapamycin Complex 1Tumor Suppressor Proteins/geneticsArticleFocal cortical dysplasia03 medical and health sciencesSeizuresGTPase-Activating Proteins/geneticsmedicineHumansGenetic Predisposition to DiseaseDEPDC5; Focal cortical dysplasia; Genetic focal epilepsy; mTORC1 pathway; SUDEPGenetic focal epilepsyEpilepsy/complicationsRepressor Proteins/geneticsEpilepsybusiness.industryGTPase-Activating ProteinTumor Suppressor ProteinsInfant NewbornCorrectionInfantRepressor ProteinCortical dysplasiamedicine.diseaseddc:616.8Repressor Proteins030104 developmental biologyFrontal lobe seizures[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMultiprotein ComplexesMultiprotein ComplexeSignal Transduction/geneticsHuman medicinebusiness
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A new family with an SLC9A6 mutation expanding the phenotypic spectrum of Christianson syndrome

2016

Using targeted next generation sequencing, we have identified a splicing mutation (c.526-9_526-5del) in the SLC9A6 gene in a 9-year-old boy with mild intellectual disability (ID), microcephaly, and social interaction disabilities. This intronic microdeletion leads to the skipping of exon 3 and to an in-frame deletion of 26 amino acids in the TM4 domain. It segregates with cognitive impairment or learning difficulties in other members of the family. Mutations in SLC9A6 have been reported in X-linked Christianson syndrome associating severe to profound intellectual deficiency and an Angelman-like phenotype with microcephaly, absent speech, ataxia with progressive cerebellar atrophy, ophthalmo…

Male0301 basic medicineProbandMicrocephalyDNA Mutational Analysisx-chromosome inactivationSLC9A6Gene mutationexchangerEpilepsyOcular Motility Disorders0302 clinical medicineangelman-syndromeX Chromosome InactivationIntellectual disabilitymicrocephalyChild10. No inequalityGenetics (clinical)Sequence DeletionGeneticsBrainGenetic Diseases X-LinkedtoolMagnetic Resonance ImagingPedigree3. Good healthPhenotypeFemaleCerebellar atrophyChristianson syndromemedicine.symptomAdultHeterozygoteSodium-Hydrogen ExchangersAtaxiaAdolescentlearning disabilities linked mental-retardation03 medical and health sciencescerebellar atrophyIntellectual Disability[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyAngelman syndromeGeneticsmedicineHumansFamilygeneGenetic Association Studiesbusiness.industryFaciesmedicine.disease030104 developmental biologysplicing signalsMutationepilepsyAtaxiaRNA Splice Sitesbusiness030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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First report of X-linked hypohidrotic ectodermal dysplasia with a hemizygous c.1142G > C in the EDA gene: variant of uncertain significance or new pa…

2021

AbstractBackgroundHypohidrotic Ectodermal Dysplasia (HED) is a genetic disorder which affects structures of ectodermal origin. X-linked hypohidrotic ectodermal dysplasia (XLHED) is the most common form of disease. XLHED is characterized by hypotrichosis, hypohydrosis and hypodontia. The cardinal features of classic HED become obvious during childhood.Identification of a hemizygous EDA pathogenic variant in an affected male confirms the diagnosis.Case presentationWe report on a male newborn with the main clinical characteristics of the X-linked HED including hypotrichosis, hypodontia and hypohidrosis. Gene panel sequencing identified a new hemizygous missense variant of uncertain significanc…

Male0301 basic medicineProbandMutation MissenseVariants of uncertain significance (VUS)Case ReportX-linked.030105 genetics & heredityPediatricsRJ1-57003 medical and health sciencesEDA geneHumansMedicineMissense mutationHypohidrotic ectodermal dysplasiaX chromosomeHemizygoteGeneticsX-linkedChromosomes Human XEctodermal Dysplasia 1 Anhidroticbusiness.industryInfant NewbornGenetic disorderGeneral MedicineEctodysplasinsmedicine.diseaseHypoidrotic ectodermal dysplasiaHypodontia030104 developmental biologyHypotrichosisEctodysplasin AbusinessItalian Journal of Pediatrics
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Expanding the β-III Spectrin-Associated Phenotypes toward Non-Progressive Congenital Ataxias with Neurodegeneration

2021

(1) Background: A non-progressive congenital ataxia (NPCA) phenotype caused by b-III spectrin (SPTBN2) mutations has emerged, mimicking spinocerebellar ataxia, autosomal recessive type 14 (SCAR14). The pattern of inheritance, however, resembles that of autosomal dominant classical spinocerebellar ataxia type 5 (SCA5). (2) Methods: In-depth phenotyping of two boys studied by a customized gene panel. Candidate variants were sought by structural modeling and protein expression. An extensive review of the literature was conducted in order to better characterize the SPTBN2-associated NPCA. (3) Results: Patients exhibited an NPCA with hypotonia, developmental delay, cerebellar syndrome, and cogni…

Male0301 basic medicineProbandPathologyProtein ConformationSequence Homology<i>SPTBN2 </i>geneb-III spectrin030105 genetics & heredityFluid-attenuated inversion recoveryCohort Studieslcsh:ChemistryNon-progressive congenital ataxia0302 clinical medicineβ-III spectrinSpectrin:enfermedades del sistema nervioso::enfermedades neurodegenerativas [ENFERMEDADES]Age of OnsetChildlcsh:QH301-705.5Spectroscopy:Otros calificadores::Otros calificadores::/genética [Otros calificadores]NeurodegenerationneurodegenerationNeurodegenerative Diseasesnon-progressive congenital ataxiaSyndromeGeneral MedicinePhenotypeHypotoniaComputer Science ApplicationsPhenotype:Nervous System Diseases::Neurodegenerative Diseases [DISEASES]Spinocerebellar ataxiamedicine.symptomSPTBN2 genemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesCerebellar AtaxiaNeuroimagingBiologyCatalysisArticleInorganic Chemistry03 medical and health sciences:Nervous System Diseases::Central Nervous System Diseases::Brain Diseases::Cerebellar Diseases::Cerebellar Ataxia [DISEASES]:Other subheadings::Other subheadings::/genetics [Other subheadings]medicineHumansAmino Acid SequencePhysical and Theoretical ChemistryNeurodegenerationMolecular BiologyGenetic Association StudiesOrganic ChemistrySpectrinmedicine.diseaseHyperintensitySistema nerviós - Degeneració - Aspectes genèticslcsh:Biology (General)lcsh:QD1-999:enfermedades del sistema nervioso::enfermedades del sistema nervioso central::enfermedades cerebrales::enfermedades cerebelosas::ataxia cerebelosa [ENFERMEDADES]Mutation030217 neurology & neurosurgeryInternational Journal of Molecular Sciences
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