Search results for " deletion"

showing 10 items of 361 documents

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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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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C4A deficiency and nonresponse to hepatitis B vaccination

2002

Hepatitis B vaccination failure has been linked to the presence of certain human leukocyte antigen class II alleles. However, the functional background of these associations has remained unclear. Complement component C 4 is encoded within the major histocompatibility complex and is essential for classical pathway activation.Healthy individuals (n=4269) were vaccinated in a prospective trial with Engerix B. Nonresponse was classified as anti-HBs10 U/l after the last vaccination. Seventy-three nonresponders (NR) (1.7%) were identified. For comparison 53 responders (R) (anti-HBs10 IU/l) were drawn randomly from the same cohort. C4 allotyping was carried out by high-voltage agarose gel electrop…

AdultMaleBiologyMajor histocompatibility complexClassical complement pathwaySeroepidemiologic StudiesHumansHepatitis B VaccinesProspective StudiesTreatment FailureHepatitis B AntibodiesSouthern blotGel electrophoresisB-LymphocytesHepatologyHaplotypeComplement C4aHLA-DR AntigensMiddle AgedHepatitis BVirologyComplement systemLogistic ModelsHaplotypesAgarose gel electrophoresisImmunologybiology.proteinFemaleVaccine failureGene DeletionHLA-DRB1 ChainsJournal of Hepatology
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Rapid and reliable genotyping procedure for detection of alleles with mutations, deletion, or/and duplication of the CYP2D6 gene

2009

Abstract Background Polymorphisms of cytochrome P450 2D6 (CYP2D6) have a significant effect on the pharmacokinetics of most tricyclic antidepressants. More than 150 alleles lead to four distinct phenotypes of drug metabolism. The phenotypes are described as ultrarapid, extensive, intermediate, and poor metabolizers. Therapeutic plasma levels of CYP2D6 substrates may be difficult to achieve. Here we describe a rapid and reliable procedure for CYP2D6*4, *3, *6, and *9 genotyping. Design and methods Serum concentrations of venlafaxine and its pharmacologically active metabolite, O-desmethylvenlafaxine, were measured in patients treated with the antidepressant venlafaxine, a substrate of CYP2D6…

AdultMaleCYP2D6GenotypeDNA Mutational AnalysisMolecular Sequence DataClinical BiochemistrySingle-nucleotide polymorphismBiologyPolymerase Chain ReactionSensitivity and Specificitydigestive systemGene DuplicationGene duplicationGenotypeHumansAlleleskin and connective tissue diseasesGeneGenotypingAllelesSequence DeletionGeneticsPolymorphism GeneticBase SequenceDepressionVenlafaxine HydrochlorideReproducibility of ResultsSequence Analysis DNAGeneral MedicineMiddle AgedCyclohexanolsMolecular biologyReal-time polymerase chain reactionCytochrome P-450 CYP2D6MutationAntidepressive Agents Second-GenerationFemaleClinical Biochemistry
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Predictive chromosomal clusters of synchronous and metachronous brain metastases in clear cell renal cell carcinoma

2014

Synchronous (early) and metachronous (late) brain metastasis (BM) events of sporadic clear cell renal cell carcinoma (ccRCC) (n = 148) were retrospectively analyzed using comparative genomic hybridization (CGH). Using oncogenetic tree models and cluster analyses, chromosomal imbalances related to recurrence-free survival until BM (RFS-BM) were analyzed. Losses at 9p and 9q appeared to be hallmarks of metachronous BM events, whereas an absence of detectable chromosomal changes at 3p was often associated with synchronous BM events. Correspondingly, k-means clustering showed that cluster 1 cases generally exhibited low copy number chromosomal changes that did not involve 3p. Cluster 2 cases ha…

AdultMaleCancer ResearchDNA Copy Number VariationsMedizinChromosome 9BiologySporadic Clear Cell Renal Cell Carcinoma03 medical and health sciences0302 clinical medicineGeneticsmedicineHumansCarcinoma Renal CellMolecular BiologyAgedRetrospective StudiesSequence Deletion030304 developmental biologyAged 80 and overChromosome AberrationsGeneticsComparative Genomic Hybridization0303 health sciencesBase SequenceBrain NeoplasmsChromosomeDNA NeoplasmMiddle Agedmedicine.diseaseKidney NeoplasmsClear cell renal cell carcinomaTumor progression030220 oncology & carcinogenesisCancer researchFemaleNeoplasm Recurrence LocalLow copy numberComparative genomic hybridizationBrain metastasisCancer Genetics
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