Search results for " Heterogeneity"

showing 10 items of 358 documents

Search for a gene responsible for Floating-Harbor syndrome on chromosome 12q15q21.1.

2012

International audience; Floating-Harbor syndrome (FHS) is characterized by characteristic facial dysmorphism, short stature with delayed bone age, and expressive language delay. To date, the gene(s) responsible for FHS is (are) unknown and the diagnosis is only made on the basis of the clinical phenotype. The majority of cases appeared to be sporadic but rare cases following autosomal dominant inheritance have been reported. We identified a 4.7 Mb de novo 12q15-q21.1 microdeletion in a patient with FHS and intellectual deficiency. Pangenomic 244K array-CGH performed in a series of 12 patients with FHS failed to identify overlapping deletions. We hypothesized that FHS is caused by haploinsuf…

AdultHeart Septal Defects VentricularMaleCandidate geneFloating Harbor syndrome[SDV.GEN] Life Sciences [q-bio]/GeneticsHaploinsufficiencyBiologyBioinformaticsShort statureCraniofacial Abnormalities03 medical and health sciences12q15q21.1 microdeletion[SDV.BDD] Life Sciences [q-bio]/Development BiologyGeneticsmedicineHumansAbnormalities MultipleGenetic Predisposition to Disease[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyChild[SDV.BDD]Life Sciences [q-bio]/Development BiologyGenetics (clinical)Growth Disorders030304 developmental biologySequence DeletionPhenocopyGenetics0303 health sciencesComparative Genomic Hybridization[SDV.GEN]Life Sciences [q-bio]/GeneticsChromosomes Human Pair 12Genetic heterogeneity030305 genetics & heredityChromosomeHigh-Throughput Nucleotide Sequencinghigh-throughput sequencingmedicine.disease3. Good healthPhenotypeFloating–Harbor syndromeChild PreschoolMutation (genetic algorithm)Femalemedicine.symptomHaploinsufficiency[ SDV.GEN ] Life Sciences [q-bio]/Genetics
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Not All Floating-Harbor Syndrome Cases are Due to Mutations in Exon 34 of SRCAP

2013

International audience; Floating-Harbor syndrome (FHS) is a rare disorder characterized by short stature, delayed bone age, speech delay, and dysmorphic facial features. We report here the molecular analysis of nine cases, fulfilling the diagnostic criteria for FHS. Using exome sequencing, we identified SRCAP as the disease gene in two cases and subsequently found SRCAP truncating mutations in 6/9 cases. All mutations occurred de novo and were located in exon 34, in accordance with the recent report of Hood et al. However, the absence of SRCAP mutations in 3/9 cases supported genetic heterogeneity of FH syndrome. Importantly, no major clinical differences were observed supporting clinical h…

AdultHeart Septal Defects VentricularMaleDNA Mutational AnalysisBiologyShort statureCraniofacial Abnormalitiesgenetic heterogeneity03 medical and health sciencesExonGeneticsmedicineHumansAbnormalities MultipleGenetic Predisposition to DiseaseChildFloating-Harbor syndromeGenetics (clinical)Exome sequencingGrowth Disorders030304 developmental biologyDisease geneGeneticsAdenosine Triphosphatases0303 health sciences[SDV.GEN]Life Sciences [q-bio]/GeneticsGenetic heterogeneity030305 genetics & heredityBone ageExonsmedicine.diseaseSRCAP3. Good healthFloating–Harbor syndromeSpeech delayMutationFemalemedicine.symptom[ SDV.GEN ] Life Sciences [q-bio]/Genetics
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Heterogeneity of obesity-asthma association disentangled by latent class analysis, the SAPALDIA cohort

2017

Although evidence for the heterogeneity of asthma accumulated, consensus for definitions of asthma phenotypes is still lacking. Obesity may have heterogeneous effects on various asthma phenotypes. We aimed to distinguish asthma phenotypes by latent class analysis and to investigate their associations with different obesity parameters in adults using a population-based Swiss cohort (SAPALDIA). We applied latent class analysis to 959 self-reported asthmatics using information on disease activity, atopy, and age of onset. Associations with obesity were examined by multinomial logistic regression, after adjustments for age, sex, smoking status, educational level, and study centre. Body mass ind…

AdultHypersensitivity ImmediateMalePulmonary and Respiratory MedicineWaistAdolescentEpidemiologyPopulationBody Mass IndexCohort Studies03 medical and health sciencesYoung Adult0302 clinical medicineWaist–hip ratioimmune system diseasesRisk FactorsMedicineBody Fat DistributionHumans030212 general & internal medicineObesityeducationAsthmaWaist-to-height ratioeducation.field_of_studyAsthma heterogeneitybusiness.industrySmokingMiddle Agedmedicine.diseaseObesityLatent class modelAsthmarespiratory tract diseasesPhenotype030228 respiratory systemSpirometryBody fatImmunologyFemaleSelf ReportWaist CircumferencebusinessSettore SECS-S/01 - StatisticaBody mass indexSwitzerlandDemographyRespiratory Medicine
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Mutations in theMORC2gene cause axonal Charcot–Marie–Tooth disease

2015

Charcot-Marie-Tooth disease (CMT) is a complex disorder with wide genetic heterogeneity. Here we present a new axonal Charcot-Marie-Tooth disease form, associated with the gene microrchidia family CW-type zinc finger 2 (MORC2). Whole-exome sequencing in a family with autosomal dominant segregation identified the novel MORC2 p.R190W change in four patients. Further mutational screening in our axonal Charcot-Marie-Tooth disease clinical series detected two additional sporadic cases, one patient who also carried the same MORC2 p.R190W mutation and another patient that harboured a MORC2 p.S25L mutation. Genetic and in silico studies strongly supported the pathogenicity of these sequence variant…

AdultMale0301 basic medicinePathologymedicine.medical_specialtyGene ExpressionSchwann cellSural nerveBiologyFasciculationMiceYoung Adult03 medical and health sciences0302 clinical medicineAtrophySural NerveCharcot-Marie-Tooth DiseasemedicineAnimalsHumansAxonAgedGenetic heterogeneityInfantSensory lossMiddle Agedmedicine.diseaseSciatic NerveAxonsPedigreePhenotype030104 developmental biologymedicine.anatomical_structureMutationFemaleNeurology (clinical)Myokymiamedicine.symptomNeuroscience030217 neurology & neurosurgeryTranscription FactorsBrain
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Novel findings in patients with primary hyperoxaluria type III and implications for advanced molecular testing strategies

2012

Identification of mutations in the HOGA1 gene as the cause of autosomal recessive primary hyperoxaluria (PH) type III has revitalized research in the field of PH and related stone disease. In contrast to the well-characterized entities of PH type I and type II, the pathophysiology and prevalence of type III is largely unknown. In this study, we analyzed a large cohort of subjects previously tested negative for type I/II by complete HOGA1 sequencing. Seven distinct mutations, among them four novel, were found in 15 patients. In patients of non-consanguineous European descent the previously reported c.700+5G>T splice-site mutation was predominant and represents a potential founder mutation, w…

AdultMaleAdolescentIn silicoCell Culture TechniquesMedizinGene ExpressionContext (language use)Biologymedicine.disease_causeArticlePrimary hyperoxaluriaKidney CalculiGeneticsmedicineHumansGenetic TestingGeneGenetics (clinical)Genetic testingGeneticsMutationmedicine.diagnostic_testGenetic heterogeneityOxo-Acid-LyasesMiddle Agedmedicine.diseasePhenotypePedigreeHyperoxaluria PrimaryMutationFemale
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Two novel mutations at exon 8 of the Sequestosome 1 (SQSTM1) gene in an Italian series of patients affected by Paget's disease of bone (PDB).

2003

PDB is genetically heterogeneous. Mutations of the sequestosome1 gene have been reported in sporadic and familial forms of Paget's in patients of French Canadian and British descent. Mutational analyses in different ethnic groups are needed to accurately investigate hereditary diseases. We describe two novel mutations of sequestosome1 in 62 Italian sporadic patients, confirming the role of the encoded protein in this disorder. Introduction: Paget's disease of bone (PDB) is a relatively common disease of bone metabolism reported to affect up to 3% of whites over 55 years of age. The disorder is genetically heterogeneous, and at present, there is scientific evidence that at least eight differ…

AdultMaleEndocrinology Diabetes and MetabolismPopulationExonSequestosome 1GenotypeSequestosome-1 ProteinmedicineHumansOrthopedics and Sports MedicineeducationAdaptor Proteins Signal TransducingAgedDNA PrimersGeneticsAged 80 and overeducation.field_of_studyBase SequenceGenetic heterogeneitybusiness.industryProteinsExonsMiddle Agedmedicine.diseaseOsteitis DeformansPenetrancePaget's disease of boneHereditary DiseasesMutationFemalebusinessJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
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Further evidence of genetic heterogeneity in familial essential tremor.

2007

Familial essential tremor (FET) is a common hereditary movement disorder with phenotypic variability and genetic heterogeneity. To date, linkage analyses revealed three loci associated to essential tremor (ET) (ETM1 on 3q13, ETM2 on 2p22-25, and a locus on 6p23). We performed a genetic analysis of these candidate chromosomal regions in a fifth-generation Italian kindred with autosomal-dominant ET. Of the 22 clinically evaluated family members, nine were affected by ET. The genetic study indicates that the ET in this family is not associated to any of the known ET loci. These findings support evidence of further genetic heterogeneity for such disease. (C) 2007 Elsevier Ltd. All rights reserv…

AdultMaleGenetic LinkageLocus (genetics)DiseaseBiologyGenetic analysisGenetic HeterogeneityGenetic linkagemedicineHumansAge of OnsetAgedGeneticsEssential tremorGenetic heterogeneityMiddle Agedmedicine.diseasePhenotypePedigreeNeurologySettore MED/03 - Genetica MedicaDisease ProgressionEssential tremorFemaleSettore MED/26 - NeurologiaNeurology (clinical)Geriatrics and GerontologyAge of onsetLinkage analysiNeurological disease
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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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HETEROGENEITY OF METATROPIC DYSPLASIA

1983

Metatropic dysplasia is a neonatally manifest entity that is characterized clinically by a rapidly progressing kyphoscoliosis leading to severe shortening of the originally long trunk ("metatropism"). Major radiographic features include flattening and defective ossification of the vertebral bodies, a narrow thorax and a marked hypoplasia of the basilar portions of the ilia with crescent-shaped iliac crests. There is some evidence of genetic heterogeneity. From five personal observations and from a review of the literature we conclude that metatropic dysplasia comprises at least three genetic entities: (1) a nonlethal type with autosomal recessive transmission; (2) a nonlethal dominant type …

AdultMalePathologymedicine.medical_specialtyDwarfismDwarfismShort staturemedicineHumansKyphosisChildKyphoscoliosisBone Diseases DevelopmentalGenetic heterogeneityOssificationbusiness.industryAnatomymedicine.diseaseOsteochondrodysplasiaTrunkHypoplasiaScoliosisPediatrics Perinatology and Child HealthFemalemedicine.symptombusiness
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Distinct neuropsychological profiles correspond to distribution of cortical thinning in inherited prion disease caused by insertional mutation

2012

Background The human prion diseases are a group of universally fatal neurodegenerative disorders associated with the auto-catalytic misfolding of the normal cell surface prion protein (PrP). Mutations causative of inherited human prion disease (IPD) include an insertion of six additional octapeptide repeats (6-OPRI) and a missense mutation (P102L) with large families segregating for each mutation residing in southern England. Here we report for the first time the neuropsychological and clinical assessments in these two groups. Method The cognitive profiles addressing all major domains were obtained for 26 patients (18 6-OPRI, 8 P102L) and the cortical thickness determined using 1.5T MRI in …

AdultMalePathologymedicine.medical_specialtyPrionsprion diseaseNeuroimagingDiseaseNeuropsychological Testsmedicine.disease_causePrion DiseasesExecutive FunctionYoung AdultHumansMedicineDementiaMissense mutationStrokeMemory DisordersMutationSettore M-PSI/02 - Psicobiologia E Psicologia Fisiologicabusiness.industryGenetic heterogeneityNeuropsychologyBrainMiddle Agedmedicine.diseaseMagnetic Resonance ImagingUnited KingdomMutagenesis InsertionalPsychiatry and Mental healthFemaleSurgeryNeurology (clinical)Cognition DisordersbusinessExecutive dysfunctionJournal of Neurology, Neurosurgery and Psychiatry
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