Search results for "candidate"

showing 10 items of 304 documents

Lack of association between angiotensin converting enzyme polymorphism and sporadic Alzheimer's disease

2002

Epidemiological and pathogenetic evidences suggest a strong association between vascular risk factors and sporadic Alzheimer's disease (sAD). In agreement with the vascular hypothesis of AD, the role of various candidate genes for atherosclerosis has been investigated, leading to conflicting results. In order to clarify the significance of angiotensin-converting enzyme (ACE) gene insertion (I)/deletion (D) polymorphism in a group of patients with sAD, we conducted a case-control study including 149 cases and 149 age and sex matched controls. All subjects were genotyped for ACE and Apolipoprotein E (APOE). There were no significant differences in ACE genotype or allele frequencies between ca…

MaleApolipoprotein ECandidate genemedicine.medical_specialtySettore MED/09 - Medicina InternaGenotypeDiseasePeptidyl-Dipeptidase ABiologyApolipoproteins EGene FrequencyAlzheimer DiseaseRisk FactorsInternal medicineGenetic predispositionmedicineHumansPolymorphismAllele frequencyAgedAged 80 and overPolymorphism GeneticNeuroscience (all)General NeuroscienceCase-control studyCase-control studyAngiotensin-converting enzymeMiddle AgedAlzheimer's diseasemedicine.diseaseEndocrinologyCase-Control Studiesbiology.proteinFemaleSettore MED/26 - NeurologiaApolipoprotein EAlzheimer's diseaseAngiotensin-converting enzymeNeuroscience Letters
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Association of estrogen receptor α gene with Alzheimer's disease: A case-control study

2006

Abstract Recent experimental data have offered the biological background to study the estrogen receptor (ER) alpha gene as a candidate gene for AD. Genetic association studies proposed ERalpha PvuII and XbaI gene polymorphisms as susceptibility factors for AD, although subsequent studies did not replicate this finding. To verify this association in a Caucasian Italian sample, we conducted a case-control study in a dataset of 172 clinic-based probable AD cases and 172 age- and sex-matched controls. Possible interaction between ERalpha polymorphisms and sex, age at onset of AD or apolipoprotein E (APOE) was examined. The xx-genotype of the XbaI polymorphism was associated with the risk of dev…

MaleApolipoprotein EOncologymedicine.medical_specialtyCandidate geneGenotypeEstrogen receptorNeuropsychological TestsBioinformaticsRisk AssessmentApolipoproteins ESex FactorsGene FrequencyAlzheimer DiseasePolymorphism (computer science)Internal medicineOdds RatiomedicineHumansRisk factorAllelesAgedGenetic associationAged 80 and overPolymorphism Geneticbusiness.industryGeneral NeuroscienceAge FactorsEstrogen Receptor alphaCase-control studyDNAGeneral MedicineMiddle AgedPsychiatry and Mental healthClinical PsychologyItalyCase-Control StudiesSettore MED/26 - NeurologiaFemaleGeriatrics and GerontologypolymorphismsbusinessEstrogen receptor alphaAPOEestrogen receptor
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Large-scale gene-centric analysis identifies novel variants for coronary artery disease.

2011

Coronary artery disease (CAD) has a significant genetic contribution that is incompletely characterized. To complement genome-wide association (GWA) studies, we conducted a large and systematic candidate gene study of CAD susceptibility, including analysis of many uncommon and functional variants. We examined 49,094 genetic variants in ∼2,100 genes of cardiovascular relevance, using a customised gene array in 15,596 CAD cases and 34,992 controls (11,202 cases and 30,733 controls of European descent; 4,394 cases and 4,259 controls of South Asian origin). We attempted to replicate putative novel associations in an additional 17,121 CAD cases and 40,473 controls. Potential mechanisms through w…

MaleCancer ResearchCandidate geneEpidemiologyGenome-wide association studyCoronary Artery Disease030204 cardiovascular system & hematologyCardiovascular0302 clinical medicineGENETICS & HEREDITYGenetics (clinical)Genetics0303 health sciencesCardiovascular diseases [NCEBP 14]Middle Aged3. Good healthCYP17A1Genetic EpidemiologyGenome-wide association; Myocardial-infarction; Susceptibility loci; Risk; Atherosclerosis; Metanalysis; LipoproteinMedicineFemaleLife Sciences & BiomedicineResearch ArticleAsian Continental Ancestry GroupAdultRiskSUSCEPTIBILITY LOCIlcsh:QH426-470European Continental Ancestry GroupBiologyPolymorphism Single Nucleotidecoronary artery disease; geneticsWhite People03 medical and health sciencesSDG 3 - Good Health and Well-beingAsian PeopleGenetic variationGeneticsHumansGenetic Predisposition to DiseaseGENOME-WIDE ASSOCIATIONAlleleMolecular BiologyGeneBiologyMETAANALYSISEcology Evolution Behavior and SystematicsGenetic Association StudiesCardiovascular Disease EpidemiologyAlleles030304 developmental biologyAged0604 GeneticsScience & TechnologyCase-control studyGenetic VariationHuman GeneticsOdds ratiolarge-scale gene analysiscoronary artery disease; large-scale gene analysislcsh:GeneticsLIPOPROTEINMYOCARDIAL-INFARCTIONATHEROSCLEROSISCase-Control StudiesGenetics of DiseaseIBC 50K CAD ConsortiumDevelopmental BiologyGenome-Wide Association Study
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Gene–alcohol interactions in the metabolic syndrome

2007

Abstracts Aims Recent studies have reported that moderate alcohol consumption is associated with a lesser prevalence of the metabolic syndrome (MetS). However, this relationship is still confusing and the presence of gene–environment interactions has been suggested. Our aim is to summarize evidence for gene–alcohol interactions in the MetS. Data synthesis Research in gene–alcohol interactions applied to MetS is very complex due to the difficulties surrounding the definition of phenotype, environment and genotype, as well as in estimating the influence of the social context. In the MetS there is a constellation of metabolic disturbances the definition of which is still changing. Thus, most s…

MaleCandidate geneAlcohol DrinkingGenotypeEndocrinology Diabetes and MetabolismMedicine (miscellaneous)AlcoholBiologySocial EnvironmentBioinformaticsSensitivity and Specificitychemistry.chemical_compoundRisk FactorsGenotypePrevalencemedicineHumansGenetic Predisposition to DiseaseEthanol metabolismGeneMetabolic SyndromeNutrition and Dieteticsbusiness.industryGenetic VariationSocial environmentGenomicsmedicine.diseasePhenotypeBiotechnologyPhenotypechemistryFemaleMetabolic syndromeCardiology and Cardiovascular MedicinebusinessNutrition, Metabolism and Cardiovascular Diseases
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Association of a functional deficit of the BKCa channel, a synaptic regulator of neuronal excitability, with autism and mental retardation

2006

International audience; Objective: Autism is a complex, largely genetic psychiatric disorder. In the majority of cases, the cause of autism is not known, but there is strong evidence for a genetic etiology. To identify candidate genes, the physical mapping of balanced chromosomal aberrations is a powerful strategy, since several genes have been characterized in numerous disorders. In this study, the authors analyzed a balanced reciprocal translocation arising de novo in a subject with autism and mental retardation. Method: The authors performed the physical mapping of the balanced 9q23/ 10q22 translocation by fluorescent in situ hybridization experiments using bacterial artificial chromosom…

MaleCandidate geneChromosomes Artificial BacterialIndolesDNA Mutational AnalysisRegulatorChromosomal translocationautism mental retardation KCNMA1 genelarge conductance Ca(2+)-activated K(+) (BK(Ca)) channel synaptic transmission chromosomal translocationSynaptic TransmissionTranslocation GeneticPair 10CA2+-ACTIVATED K+ CHANNELSCloning MolecularChildLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMUTATIONIn Situ HybridizationIn Situ Hybridization FluorescenceReverse Transcriptase Polymerase Chain ReactionBacterialChromosome MappingETIOLOGYPsychiatry and Mental healthArtificialKCNMA1 Gene[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]HaploinsufficiencyPsychologyChromosomes Human Pair 9POTASSIUM CHANNELSHumanPair 9Autistic Disorder; Child; Chromosome Aberrations; Chromosome Mapping; Chromosomes; Artificial; Bacterial; Chromosomes; Human; Pair 10; Chromosomes; Human; Pair 9; Cloning; Molecular; DNA Mutational Analysis; Humans; In Situ Hybridization; Fluorescence; Indoles; Intellectual Disability; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; Male; Reverse Transcriptase Polymerase Chain Reaction; Synaptic Transmission; Translocation; GeneticTranslocationNeurotransmissionChromosomesFluorescenceGeneticIntellectual DisabilitymedicineHumansAutistic DisorderRELEASEChromosome AberrationsCOMPLEXChromosomes Human Pair 10MolecularAutistic Disorder; Child; Chromosome Aberrations; Chromosome Mapping; Chromosomes Artificial Bacterial; Chromosomes Human Pair 10; Chromosomes Human Pair 9; Cloning Molecular; DNA Mutational Analysis; Humans; In Situ Hybridization Fluorescence; Indoles; Intellectual Disability; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; Male; Reverse Transcriptase Polymerase Chain Reaction; Synaptic Transmission; Translocation GeneticPERVASIVE DEVELOPMENTAL DISORDERSmedicine.diseaseDevelopmental disorderINDIVIDUALSLARGE-CONDUCTANCEAutismSCREENNeuroscience[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyCloning
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Nonradioactive Detection of Differentially Expressed Genes Using Complex RNA or DNA Hybridization Probes

1999

The analysis of differential gene expression has become increasingly important in recent years. Typically, differentially expressed genes are identified in a primary screening procedure, yielding candidate genes whose differential expression has to be verified. We provide a highly sensitive, efficient and nonradioactive differential screening procedure to analyze numerous candidate genes in a single step. This comprises labeling of poly(A)+ RNA of the cell types analyzed with DIG Chem-Link and differential hybridization to the candidate genes fixed on dot blots. DIG Chem-Link allows, to our knowledge, for the first time efficient and direct nonradioactive labeling of RNA in vitro. Advantag…

MaleCandidate geneDNA ComplementaryMolecular Probe TechniquesBiologySensitivity and SpecificityGeneral Biochemistry Genetics and Molecular BiologyMiceDigGene expressionAnimalsHumansGeneGenomic LibraryMice Inbred BALB CMessenger RNADNA–DNA hybridizationNucleic Acid HybridizationRNARNA ProbesMolecular biologyGene Expression RegulationGenesLangerhans CellsLuminescent MeasurementsFemaleMolecular probeDigoxigeninBiotechnologyBioTechniques
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The DYRK1A gene is a cause of syndromic intellectual disability with severe microcephaly and epilepsy.

2012

Background DYRK1A plays different functions during development, with an important role in controlling brain growth through neuronal proliferation and neurogenesis. It is expressed in a gene dosage dependent manner since dyrk1a haploinsufficiency induces a reduced brain size in mice, and DYRK1A overexpression is the candidate gene for intellectual disability (ID) and microcephaly in Down syndrome. We have identified a 69 kb deletion including the 5′ region of the DYRK1A gene in a patient with growth retardation, primary microcephaly, facial dysmorphism, seizures, ataxic gait, absent speech and ID. Because four patients previously reported with intragenic DYRK1A rearrangements or 21q22 microd…

MaleCandidate geneDown syndromeMicrocephalyAdolescentGenotypeBiologyProtein Serine-Threonine KinasesBioinformaticsFrameshift mutationEpilepsyAngelman syndromeIntellectual DisabilityGene OrderGeneticsmedicineHumansChildGenetics (clinical)GeneticsEpilepsyBase SequenceFaciesElectroencephalographySyndromeProtein-Tyrosine Kinasesmedicine.diseasePhenotypeChild PreschoolSpeech delayMutationMicrocephalyFemalemedicine.symptomHaploinsufficiencyJournal of medical genetics
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Mutations in the mu heavy-chain gene in patients with agammaglobulinemia.

1996

Most patients with congenital hypogammaglobulinemia and absent B cells are males with X-linked agammaglobulinemia, which is caused by mutations in the gene for Bruton's tyrosine kinase (Btk); however, there are females with a similar disorder who do not have mutations in this gene. We studied two families with autosomal recessive defects in B-cell development and patients with presumed X-linked agammaglobulinemia who did not have mutations in Btk.A series of candidate genes that encode proteins involved in B-cell signal-transduction pathways were analyzed by linkage studies and mutation screening.Four different mutations were identified in the mu heavy-chain gene on chromosome 14. In one fa…

MaleCandidate geneGenetic LinkageDNA Mutational AnalysisConsanguinitymedicine.disease_causeConsanguinityGenetic linkageAgammaglobulinemiahemic and lymphatic diseasesmedicineBruton's tyrosine kinaseHumansLymphocyte CountGeneGeneticsChromosomes Human Pair 14MutationB-LymphocytesbiologyImmunoglobulin mu-ChainsChromosomeGeneral MedicinePedigreeRNA splicingMutationbiology.proteinFemaleThe New England journal of medicine
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Genome-wide association scan of quantitative traits for attention deficit hyperactivity disorder identifies novel associations and confirms candidate…

2008

Contains fulltext : 70192.pdf (Publisher’s version ) (Closed access) Attention deficit hyperactivity disorder (ADHD) is a complex condition with environmental and genetic etiologies. Up to this point, research has identified genetic associations with candidate genes from known biological pathways. In order to identify novel ADHD susceptibility genes, 600,000 SNPs were genotyped in 958 ADHD proband-parent trios. After applying data cleaning procedures we examined 429,981 autosomal SNPs in 909 family trios. We generated six quantitative phenotypes from 18 ADHD symptoms to be used in genome-wide association analyses. With the PBAT screening algorithm, we identified 2 SNPs, rs6565113 and rs5526…

MaleCandidate geneGenetics and epigenetic pathways of disease [NCMLS 6]2804 Cellular and Molecular NeuroscienceMedizinGenome-wide association studyNeuroinformatics [DCN 3]Genome2738 Psychiatry and Mental Health0302 clinical medicinePerception and Action [DCN 1]Cluster AnalysisGenetics(clinical)Genetics (clinical)Genetics0303 health sciences10058 Department of Child and Adolescent PsychiatryCadherinsPedigreePsychiatry and Mental healthFemaleFunctional Neurogenomics [DCN 2]CDH13AlgorithmsGenetic Markers2716 Genetics (clinical)GenotypeQuantitative Trait Loci610 Medicine & healthSingle-nucleotide polymorphismBiologyQuantitative trait locusPolymorphism Single NucleotideMental health [NCEBP 9]Genetic determinismGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular NeuroscienceCognitive neurosciences [UMCN 3.2]medicineADHDAttention deficit hyperactivity disorderHumansGenetic Predisposition to Diseaseddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersGene030304 developmental biologyProbabilityModels GeneticGenome Humancandidate genefamily-based associationmedicine.diseaseIntronsHaplotypesGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with Hyperactivitygenome-wide association030217 neurology & neurosurgeryGenome-Wide Association StudyAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics
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Genome-wide association scan of the time to onset of attention deficit hyperactivity disorder.

2008

Contains fulltext : 70149.pdf (Publisher’s version ) (Closed access) A time-to-onset analysis for family-based samples was performed on the genomewide association (GWAS) data for attention deficit hyperactivity disorder (ADHD) to determine if associations exist with the age at onset of ADHD. The initial dataset consisted of 958 parent-offspring trios that were genotyped on the Perlegen 600,000 SNP array. After data cleaning procedures, 429,981 autosomal SNPs and 930 parent-offspring trios were used found suitable for use and a family-based logrank analysis was performed using that age at first ADHD symptoms as the quantitative trait of interest. No SNP achieved genome-wide significance, and…

MaleCandidate geneGenetics and epigenetic pathways of disease [NCMLS 6]2804 Cellular and Molecular NeuroscienceMedizinGenome-wide association studyNeuroinformatics [DCN 3]Linkage Disequilibrium2738 Psychiatry and Mental Health0302 clinical medicinePerception and Action [DCN 1]Genetics(clinical)Age of OnsetChildGenetics (clinical)Genetics0303 health sciences10058 Department of Child and Adolescent PsychiatryPedigreePsychiatry and Mental healthChild PreschoolFemaleFunctional Neurogenomics [DCN 2]SNP arrayGenetic Markers2716 Genetics (clinical)Sodium-Hydrogen ExchangersAdolescentQuantitative Trait Loci610 Medicine & healthSingle-nucleotide polymorphismBiologyQuantitative trait locusMental health [NCEBP 9]Polymorphism Single NucleotideArticleGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular NeuroscienceCognitive neurosciences [UMCN 3.2]medicineAttention deficit hyperactivity disorderSNPHumansGenetic Predisposition to Diseaseddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und Jugendalters030304 developmental biologyProbabilityRetrospective StudiesGenome Humanmedicine.diseaseGenetic defects of metabolism [UMCN 5.1]HaplotypesAttention Deficit Disorder with HyperactivityAge of onset030217 neurology & neurosurgeryGenome-Wide Association Study
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