Search results for "CANDIDA"

showing 10 items of 844 documents

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
researchProduct

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
researchProduct

Mutations in LCA5, encoding the ciliary protein lebercilin, cause Leber congenital amaurosis

2007

Contains fulltext : 53618.pdf (Publisher’s version ) (Closed access) Leber congenital amaurosis (LCA) causes blindness or severe visual impairment at or within a few months of birth. Here we show, using homozygosity mapping, that the LCA5 gene on chromosome 6q14, which encodes the previously unknown ciliary protein lebercilin, is associated with this disease. We detected homozygous nonsense and frameshift mutations in LCA5 in five families affected with LCA. In a sixth family, the LCA5 transcript was completely absent. LCA5 is expressed widely throughout development, although the phenotype in affected individuals is limited to the eye. Lebercilin localizes to the connecting cilia of photore…

MaleCandidate geneGenetics and epigenetic pathways of disease [NCMLS 6]genetic structuresMolecular Sequence DataOptic Atrophy Hereditary LeberNeuroinformatics [DCN 3]Biologymedicine.disease_causeCiliopathiesJoubert syndromeCell LineFrameshift mutationGenomic disorders and inherited multi-system disorders [IGMD 3]MiceTranslational research [ONCOL 3]Chlorocebus aethiopsPerception and Action [DCN 1]GeneticsmedicineNeurosensory disorders [UMCN 3.3]AnimalsHumansCiliaRats WistarEye ProteinsFrameshift MutationRenal disorder [IGMD 9]GeneticsMutationCiliumDisease gene identificationmedicine.diseasePhenotypeeye diseasesPedigreeRatsMice Inbred C57BLGenetic defects of metabolism [UMCN 5.1]Codon NonsenseCOS CellsFemalesense organsFunctional Neurogenomics [DCN 2]Microtubule-Associated ProteinsNature Genetics
researchProduct

A polymorphic locus in the intron 16 of the human angiotensin-converting enzyme (ACE) gene is not correlated with complex regional pain syndrome I (C…

2004

Exaggerated neurogenic inflammation has been recognized to be one reason for many CRPS symptoms. Since angiotensin-converting enzyme (ACE) is a key enzyme for the termination of neurogenic inflammation, it has been selected as a candidate gene for CRPS predisposition. A previous report of an insertion/deletion (I/D) polymorphism in intron 16 within the ACE gene implicated an increased risk to develop CRPS I associated with the D allele. However, in the present study the D allele frequency was not increased in CRPS I cases (0.51 for D allele, 0.49 for I allele). Furthermore, there was no co-segregation of any genotype (DD, ID, II) with the CRPS phenotype in 12 selected familial CRPS I cases …

MaleCandidate geneGenotypeDNA Mutational AnalysisPeptidyl-Dipeptidase Amedicine.disease_causeGene FrequencyPolymorphism (computer science)GenotypemedicineHumansGenetic Predisposition to DiseaseGenetic TestingAlleleAllele frequencyGeneticsMutationPolymorphism GeneticbiologyNeuropeptidesAngiotensin-converting enzymemedicine.diseaseIntronsPedigreeReflex Sympathetic DystrophyAnesthesiology and Pain MedicineComplex regional pain syndromePhenotypeImmunologyMutationbiology.proteinFemaleEuropean journal of pain (London, England)
researchProduct

A genome scan for developmental dyslexia confirms linkage to chromosome 2p11 and suggests a new locus on 7q32

2003

Developmental dyslexia is a distinct learning disability with unexpected difficulty in learning to read despite adequate intelligence, education, and environment, and normal senses. The genetic aetiology of dyslexia is heterogeneous and loci on chromosomes 2, 3, 6, 15, and 18 have been repeatedly linked to it. We have conducted a genome scan with 376 markers in 11 families with 38 dyslexic subjects ascertained in Finland. Linkage of dyslexia to the vicinity of DYX3 on 2p was confirmed with a non-parametric linkage (NPL) score of 2.55 and a lod score of 3.01 for a dominant model, and a novel locus on 7q32 close to the SPCH1 locus was suggested with an NPL score of 2.77. The SPCH1 locus has p…

MaleCandidate geneGenotypeDNA Mutational AnalysisShort ReportLocus (genetics)BiologyDyslexia03 medical and health sciences0302 clinical medicineCommunication disorderDCDC2mental disordersGeneticsmedicineHumansLanguage disorderFinlandGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesGenome HumanDyslexiaChromosome MappingForkhead Transcription FactorsFOXP2medicine.diseasePedigreeRepressor ProteinsChromosomes Human Pair 2Learning disabilityFemaleLod Scoremedicine.symptomChromosomes Human Pair 7030217 neurology & neurosurgeryTranscription FactorsJournal of Medical Genetics
researchProduct

A Pilot Study on Prostate Cancer Risk and Pro-Inflammatory Genotypes: Pathophysiology and Therapeutic Implications

2010

Host genetic factors are crucial risk determinants for many human cancers. In this framework, an interesting model is represented by prostate cancer (PC), which is featured by a complex pathophysiology with a strong genetic component. Multiple genes seem to influence PC risk and several single nucleotide polymorphisms (SNPs) of candidate genes modifying PC susceptibility have been identified. It is noteworthy the potential association of common SNPs in pro-inflammatory genes with PC risk, since chronic inflammation is assumed to play a key role in prostate carcinogenesis. With the aim to identify candidate genes as an experimental basis to develop new strategies for both prevention and trea…

MaleCandidate geneGenotypePilot ProjectsSingle-nucleotide polymorphismBioinformaticsPolymorphism Single NucleotideProstate cancerRisk FactorsDrug DiscoveryGenotypemedicineHumansSNPSettore MED/05 - Patologia ClinicaGeneAgedAged 80 and overInflammationPharmacologySettore MED/04 - Patologia Generalebusiness.industryProstatic NeoplasmsCancerMiddle AgedProstate cancer (PC) inflammation genetics TLR4 TLR2 PTGS2 5-LO SNP.medicine.diseaseImmunologyTLR4Inflammation Mediatorsbusiness
researchProduct

Homozygous disruption of PDZD7 by reciprocal translocation in a consanguineous family: a new member of the Usher syndrome protein interactome causing…

2008

A homozygous reciprocal translocation, 46,XY,t(10;11),t(10;11), was detected in a boy with non-syndromic congenital sensorineural hearing impairment. Both parents and their four other children were heterozygous translocation carriers, 46,XX,t(10;11) and 46,XY,t(10;11), respectively. Fluorescence in situ hybridization of region-specific clones to patient chromosomes was used to localize the breakpoints within bacterial artificial chromosome (BAC) RP11-108L7 on chromosome 10q24.3 and within BAC CTD-2527F12 on chromosome 11q23.3. Junction fragments were cloned by vector ligation and sequenced. The chromosome 10 breakpoint was identified within the PDZ domain containing 7 (PDZD7) gene, disrupti…

MaleCandidate geneHeterozygoteUsher syndromePDZ domainMolecular Sequence DataChromosomal translocationBiologyTranslocation GeneticConsanguinityotorhinolaryngologic diseasesGeneticsmedicineHumansAmino Acid SequenceHearing LossMolecular BiologyGenetics (clinical)GeneticsGene RearrangementBacterial artificial chromosomemedicine.diagnostic_testBase SequenceChromosomes Human Pair 10Chromosomes Human Pair 11BreakpointHomozygoteChromosomeGeneral Medicinemedicine.diseaseMolecular biologyPedigreeChild PreschoolEar InnerFemaleUsher SyndromesFluorescence in situ hybridizationHuman molecular genetics
researchProduct

Functional Inactivation of the Genome-Wide Association Study Obesity Gene Neuronal Growth Regulator 1 in Mice Causes a Body Mass Phenotype

2012

To date, genome-wide association studies (GWAS) have identified at least 32 novel loci for obesity and body mass-related traits. However, the causal genetic variant and molecular mechanisms of specific susceptibility genes in relation to obesity are yet to be fully confirmed and characterised. Here, we examined whether the candidate gene NEGR1 encoding the neuronal growth regulator 1, also termed neurotractin or Kilon, accounts for the obesity association. To characterise the function of NEGR1 for body weight control in vivo, we generated two novel mutant mouse lines, including a constitutive NEGR1-deficient mouse line as well as an ENU-mutagenised line carrying a loss-of-function mutation …

MaleCandidate geneMutantlcsh:MedicineGenome-wide association studymedicine.disease_causeEndoplasmic ReticulumEatingGene Knockout TechniquesMice0302 clinical medicineEndocrinologylcsh:ScienceObesity; NEGR1; GWAS; body weight control2. Zero hungerGenetics0303 health sciencesMutationMultidisciplinaryNeuronal growth regulator 1GenomicsPhenotypePhenotypeMedicineFemaleFunction and Dysfunction of the Nervous SystemResearch ArticleGenotypeHypothalamusNerve Tissue ProteinsBiologyMotor ActivityDiet High-FatCell Line03 medical and health sciencesGenetic MutationGenome Analysis ToolsmedicineGeneticsGenome-Wide Association StudiesCell AdhesionNeuritesAnimalsHumansObesityGene SilencingGeneBiologyAlleles030304 developmental biologyNutritionlcsh:RBody WeightMembrane ProteinsHuman GeneticsNeuroendocrinologyBody HeightMetabolic DisordersGenetics of DiseaseLean body masslcsh:QEnergy Metabolism030217 neurology & neurosurgeryGenome-Wide Association StudyPLoS ONE
researchProduct

The genomic and clinical landscape of fetal akinesia

2020

International audience; Fetal akinesia has multiple clinical subtypes with over 160 gene associations, but the genetic etiology is not yet completely understood.Methods: In this study, 51 patients from 47 unrelated families were analyzed using next-generation sequencing (NGS) techniques aiming to decipher the genomic landscape of fetal akinesia (FA).Results: We have identified likely pathogenic gene variants in 37 cases and report 41 novel variants. Additionally, we report putative pathogenic variants in eight cases including nine novel variants. Our work identified 14 novel disease-gene associations for fetal akinesia: ADSSL1, ASAH1, ASPM, ATP2B3, EARS2, FBLN1, PRG4, PRICKLE1, ROR2, SETBP1…

MaleCandidate geneMyopathyVARIANTSFetal akinesiaMESH: Ryanodine Receptor Calcium Release Channel0302 clinical medicineMESH: ChildGuanine Nucleotide Exchange FactorsMESH: Guanine Nucleotide Exchange FactorsExomeCopy-number variationChildExomeMESH: High-Throughput Nucleotide SequencingGenetics (clinical)GeneticsArthrogryposisArthrogryposis0303 health sciencesMESH: Infant NewbornMESH: Genetic Predisposition to DiseaseHigh-Throughput Nucleotide SequencingRNA-Binding ProteinsMESH: Infant3. Good healthFetal DiseasesCopy-number variationMESH: Fetal DiseasesMESH: Young AdultChild PreschoolASAH1FemaleMESH: DNA Copy Number Variationsmedicine.symptomAdultGENETICSAdolescentDNA Copy Number VariationsMESH: Trans-ActivatorsMESH: ArthrogryposisBiologyASPMYoung Adult03 medical and health sciencesMuscular DiseasesmedicineHumansGenetic Predisposition to DiseaseGene030304 developmental biologyMESH: Adolescent[SDV.MHEP.PED]Life Sciences [q-bio]/Human health and pathology/PediatricsMESH: HumansMUTATIONSMESH: Child PreschoolInfant NewbornMESH: Muscular DiseasesInfantNEMALINE MYOPATHYRyanodine Receptor Calcium Release ChannelMESH: Adultmedicine.diseaseCongenital myopathyMESH: MaleMESH: RNA-Binding Proteins[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsDISTAL ARTHROGRYPOSISTrans-ActivatorsMESH: Female030217 neurology & neurosurgery
researchProduct

Genome-wide association study of PR interval.

2009

The electrocardiographic PR interval reflects atrial and atrioventricular nodal conduction, disturbances of which increase risk of atrial fibrillation (AF). To identify underlying common genetic variation, we meta-analyzed genome-wide association results for PR interval from seven community-based studies of European-ancestry individuals in the CHARGE consortium: AGES, ARIC, CHS, FHS, KORA, Rotterdam Study, and SardiNIA (N=28,517). Statistically significant loci (P<5×10-8) were tested for association with AF (N=5,741 cases). We identified nine loci associated with PR interval. At chromosome 3p22.2, we observed two independent associations in voltage gated sodium channel genes SCN10A and SCN5…

MaleCandidate genePopulationvoltage gated sodium channelGenome-wide association studyLocus (genetics)030204 cardiovascular system & hematologyBiologyArticleCohort Studiesquantitative trait03 medical and health sciencesRotterdam StudyElectrocardiography0302 clinical medicineMeta-Analysis as TopicHeart Conduction SystemAtrial FibrillationGeneticsmedicineHumansGenetic Predisposition to Diseasecardiovascular diseasesPR intervaleducation030304 developmental biologyGenetic associationAgedGeneticsdevelopmental genes0303 health scienceseducation.field_of_studygenome-wide association studyPQ intervalAtrial fibrillationmedicine.diseaseGenetic Locicardiovascular systemPR intervalFemaleNature genetics
researchProduct