Search results for "DELE"

showing 10 items of 631 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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Chromosome 15q BP3 to BP5 deletion is a likely locus for speech delay and language impairment: Report on a four‐member family and an unrelated boy

2020

Abstract Background Deletions in chromosome 15q13 have been reported both in healthy people and individuals with a wide range of behavioral and neuropsychiatric disturbances. Six main breakpoint (BP) subregions (BP1‐BP6) are mapped to the 15q13 region and three further embedded BP regions (BP3‐BP5). The deletion at BP4‐BP5 is the rearrangement most frequently observed compared to other known deletions in BP3‐BP5 and BP3‐BP4 regions. Deletions of each of these three regions have previously been implicated in a variable range of clinical phenotypes, including minor dysmorphism, developmental delay/intellectual disability, epilepsy, autism spectrum disorders, behavioral disturbances, and speec…

AdultMale0301 basic medicinespeech delayAdolescentlcsh:QH426-470BP3-BP5 deletionspeech delay.Chromosome DisordersLocus (genetics)030105 genetics & heredity03 medical and health sciencesEpilepsySettore MED/38 - Pediatria Generale E SpecialisticaSeizuresIntellectual DisabilityIntellectual disabilitychromosome 15 q13GeneticsmedicineHumansLanguage Development DisordersChildMolecular BiologyGenetics (clinical)GeneticsChromosomes Human Pair 15business.industryBreakpointlanguage impairmentOriginal Articlesmedicine.diseasePhenotypePedigreeBP3‐BP5 deletiondevelopmental delayLanguage developmentlcsh:GeneticsPhenotype030104 developmental biologyBP3-BP5 deletion; chromosome 15 q13; developmental delay; language impairment; speech delaySpeech delayAutismFemaleOriginal ArticleChromosome Deletionmedicine.symptombusinessMolecular Genetics & Genomic Medicine
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Does angiotensin-converting enzyme gene polymorphism affect blood pressure? Findings after 6 years of follow-up in healthy subjects.

2003

Background: There has been an increase in research into the association between angiotensin-converting enzyme (ACE) gene deletion polymorphism and cardiovascular disease, with conflicting results. The present prospective long-term study was conducted to evaluate whether the DD genotype could also be associated with a higher prevalence of hypertension in healthy subjects, over 6 years of follow-up. Methods: Population: 684 healthy volunteers (aged, 25–55 years): normotensive and free of cardiovascular diseases, with acceptable echocardiographic window. All subjects had to have a normal electrocardiogram (ECG) and echocardiogram (ECHO) at entry. Study protocol: All subjects underwent a comple…

AdultMaleACE-I/D gene polymorphismmedicine.medical_specialtyTime FactorsGenotypePopulationBlood PressurePeptidyl-Dipeptidase AReference ValuesInternal medicineMedicineHumansProspective StudiesFamily historyeducationeducation.field_of_studyPolymorphism Geneticbiologybusiness.industryIncidence (epidemiology)IncidenceAngiotensin-converting enzymeVenous bloodMiddle Agedmedicine.diseaseMutagenesis InsertionalEndocrinologyBlood pressureHeart failureHypertensionbiology.proteinFemaleGene polymorphismCardiology and Cardiovascular MedicinebusinessHealthy subjectGene DeletionFollow-Up StudiesEuropean journal of heart failure
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Two systems of maintenance in verbal working memory: evidence from the word length effect.

2013

The extended time-based resource-sharing (TBRS) model suggested a working memory architecture in which an executive loop and a phonological loop could both support the maintenance of verbal information. The consequence of such a framework is that phonological effects known to impact the maintenance of verbal information, like the word length effect (WLE), should depend on the use of the phonological loop, but should disappear under the maintenance by the executive loop. In two previous studies, introducing concurrent articulation in complex span tasks barely affected WLE, contradicting the prediction from the TBRS model. The present study re-evaluated the WLE in a complex span task while co…

AdultMaleAdolescentCognitive NeuroscienceMnemonicsShort-term memorylcsh:MedicineSocial and Behavioral SciencesVerbal learningTask (project management)Young AdultMemoryHuman PerformancePsychologyHumansWorking Memorylcsh:ScienceBiologyBehaviorMultidisciplinaryRecallVerbal BehaviorWorking memorylcsh:RCognitive PsychologyExperimental PsychologyLinguisticsPhonologyVerbal LearningMental HealthMemory Short-TermMental RecallMedicineFemalelcsh:QBaddeley's model of working memoryAttention (Behavior)PsychologyArticulation (phonetics)Research ArticleNeuroscienceCognitive psychologyPLoS ONE
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Characterization of 14 novel deletions underlying Rubinstein–Taybi syndrome: an update of the CREBBP deletion repertoire

2015

Rubinstein–Taybi syndrome (RSTS) is a rare, clinically heterogeneous disorder characterized by cognitive impairment and several multiple congenital anomalies. The syndrome is caused by almost private point mutations in the CREBBP (~55 % of cases) and EP300 (~8 %) genes. The CREBBP mutational spectrum is variegated and characterized by point mutations (30–50 %) and deletions (~10 %). The latter are diverse in size and genomic position and remove either the whole CREBBP gene and its flanking regions or only an intragenic portion. Here, we report 14 novel CREBBP deletions ranging from single exons to the whole gene and flanking regions which were identified by applying complementary cytomolecu…

AdultMaleAdolescentContiguous gene syndromeCohort StudiesExonGeneticmedicineGeneticsHumansPoint MutationCREB-binding proteinEP300ChildPreschoolGenetics (clinical)Sequence DeletionGeneticsRubinstein-Taybi Syndromebiologymedicine.diagnostic_testRubinstein–Taybi syndromeBase SequencePoint mutationMedicine (all)Infant NewbornInfantMiddle Agedmedicine.diseaseNewbornCREB-Binding ProteinHuman geneticsAdolescent; Adult; CREB-Binding Protein; Child; Child Preschool; Cohort Studies; Female; Humans; Infant; Infant Newborn; Male; Middle Aged; Rubinstein-Taybi Syndrome; Base Sequence; Point Mutation; Sequence Deletion; Genetics (clinical); Genetics; Medicine (all)Child Preschoolbiology.proteinFemaleCohort StudieAdolescent; Adult; CREB-Binding Protein; Child; Child Preschool; Cohort Studies; Female; Humans; Infant; Infant Newborn; Male; Middle Aged; Rubinstein-Taybi Syndrome; Base Sequence; Point Mutation; Sequence Deletion; Medicine (all); Genetics; Genetics (clinical)Fluorescence in situ hybridizationHuman
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Molecular analysis of Gaucher disease: distribution of eight mutations and the complete gene deletion in 27 patients from Germany

1997

Gaucher disease is the most common lysosomal storage disease with a high prevalence in the Ashkenazi Jewish population but it is also present in other populations. The presence of eight mutations (1226G, 1448C, IVS2+1. 84GG, 1504T, 1604T, 1342C and 1297T) and the complete deletion of the beta-glucocerebrosidase gene was investigated in 25 unrelated non-Jewish patients with Gaucher's disease in Germany. In the Jewish population, three of these mutations account for more than 90% of all mutated alleles. In addition, relatives of two patients were included in our study. Restriction fragment length polymorphism analysis and sequencing of PCR products obtained from DNA of peripheral blood leukoc…

AdultMaleAdolescentGenotypePopulationBiologymedicine.disease_causeCompound heterozygosityFrameshift mutationGermanyGenotypeGeneticsmedicineHumansAlleleChildeducationGeneAllelesGenetics (clinical)GeneticsMutationeducation.field_of_studyGaucher DiseaseMiddle AgedPhenotypeChild PreschoolMutationFemaleRestriction fragment length polymorphismGene DeletionPolymorphism Restriction Fragment LengthHuman Genetics
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Translocations Disrupting PHF21A in the Potocki-Shaffer-Syndrome Region Are Associated with Intellectual Disability and Craniofacial Anomalies

2012

Contains fulltext : 110038.pdf (Publisher’s version ) (Closed access) Potocki-Shaffer syndrome (PSS) is a contiguous gene disorder due to the interstitial deletion of band p11.2 of chromosome 11 and is characterized by multiple exostoses, parietal foramina, intellectual disability (ID), and craniofacial anomalies (CFAs). Despite the identification of individual genes responsible for multiple exostoses and parietal foramina in PSS, the identity of the gene(s) associated with the ID and CFA phenotypes has remained elusive. Through characterization of independent subjects with balanced translocations and supportive comparative deletion mapping of PSS subjects, we have uncovered evidence that t…

AdultMaleAdolescentGenotypePotocki–Shaffer syndromeChromosome DisordersHaploinsufficiencyBiologyHistone DeacetylasesSodium ChannelsTranslocation GeneticArticleChromatin remodelingCraniofacial Abnormalities03 medical and health sciencesSCN3A0302 clinical medicineIntellectual DisabilityNAV1.3 Voltage-Gated Sodium ChannelmedicineTranscriptional regulationGeneticsAnimalsHumansDeletion mappingGenetics(clinical)CraniofacialZebrafishGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesChromosomes Human Pair 11Infant Newbornmedicine.diseaseGenetics and epigenetic pathways of disease DCN MP - Plasticity and memory [NCMLS 6]Child PreschoolHomeoboxFemaleChromosome DeletionHaploinsufficiencyExostoses Multiple Hereditary030217 neurology & neurosurgeryThe American Journal of Human Genetics
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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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C4, BF, C3 Allele Distribution and Complement Activity in Healthy Aged People and Centenarians

1999

The aim of this study was to examine the complement system and the distribution of some human leukocyte antigen (HLA) class III alleles (C4, BF) in healthy aged people (77 centenarians and 89 elderly subjects). We have also studied the alleles of C3, a complement component genetically unrelated to HLA, the immunochemical levels of C4 and C3 and serum functional hemolytic activity for classical (CH50) and alternative (AP50) complement pathway. The levels of C3 and C4 and the CH50 and AP50 were found to be within the normal range. The frequencies of C3, BF, and C4A alleles were similar in the cohorts that have been studied. For C4B null allele (C4BQ0) a trend toward an increase in the older c…

AdultMaleAgingComplement Pathway AlternativeHuman leukocyte antigenBiologyComplement Hemolytic Activity AssayHemolysisComplement factor BCohort StudiesHLA AntigensHumansComplement Pathway ClassicalAlleleComplement ActivationAllelesAgedAged 80 and overPolymorphism GeneticC4AComplement C4Complement C3DNAMiddle AgedNull alleleComplement systemImmunologyCohortFemaleGeriatrics and GerontologyGene DeletionComplement Factor BThe Journals of Gerontology Series A: Biological Sciences and Medical Sciences
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PAI-1 plasma levels in a general population without clinical evidence of atherosclerosis: relation to environmental and genetic determinants.

1998

Abstract —Plasminogen activator inhibitor-1 (PAI-1) plasma levels have been consistently related to a polymorphism (4G/5G) of the PAI-1 gene. The renin-angiotensin pathway plays a role in the regulation of PAI-1 plasma levels. An insertion ( I )/deletion ( D ) polymorphism of the angiotensin-converting enzyme (ACE) gene has been related to plasma and cellular ACE levels. In 1032 employees (446 men and 586 women; 22 to 66 years old) of a hospital in southern Italy, we investigated the association between PAI-1 4G/5G and the ACE I/D gene variants and plasma PAI-1 antigen levels. None of the individuals enrolled had clinical evidence of atherosclerosis. In univariate analysis, PAI-1 levels we…

AdultMaleAgingmedicine.medical_specialtyAlcohol DrinkingGenotypePopulationPeptidyl-Dipeptidase ABody Mass Indexchemistry.chemical_compoundInsulin resistanceGene FrequencyInternal medicinePlasminogen Activator Inhibitor 1Blood plasmaGenotypemedicineHumanseducationAllele frequencyTriglyceridesAgedSex Characteristicseducation.field_of_studyPolymorphism GeneticbiologySmokingAngiotensin-converting enzymeMiddle Agedmedicine.diseaseCholesterolEndocrinologychemistryPlasminogen activator inhibitor-1Hypertensionbiology.proteinFemaleCardiology and Cardiovascular MedicineBody mass indexGene Deletion
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