Search results for "genetic association studie"

showing 10 items of 166 documents

Association of Monocarboxylate Transporter-1 (MCT1) A1470T Polymorphism (rs1049434) with Forward Football Player Status.

2018

AbstractThe aim of this study was to investigate the association between the MCT1 (monocarboxylate transporter 1) A1470T polymorphism and positional roles in a large cohort of professional football players from five different countries. We compared genotype distributions of the MCT1 A1470T polymorphism between football players (n=694) and non-athlete controls (n=781) from Italy, Poland, Lithuania, Ukraine and Malta, and we analyzed the MCT1 genotype distributions with respect to the players’ positions in the field (e. g. forwards, midfielders, defenders and goalkeepers). Genomic DNA was extracted from either buccal epithelium or peripheral blood using a standard protocol. In the pooled coho…

MaleMonocarboxylic Acid TransportersGenotypePhysical Therapy Sports Therapy and RehabilitationFootball030204 cardiovascular system & hematology03 medical and health sciences0302 clinical medicineGene FrequencySoccerGenotypeHumansOrthopedics and Sports MedicineGenetic differences lactate monocarboxylate transporter-1 repeated sprint ability soccerAlleleAllele frequencyAllelesGenetic Association StudiesPolymorphism GeneticSymportersbiology030229 sport sciencesPeripheral bloodMonocarboxylate transporter 1CohortStandard protocolbiology.proteinDemography
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Longitudinal heritability of childhood aggression

2016

The genetic and environmental contributions to the variation and longitudinal stability in childhood aggressive behavior were assessed in two large twin cohorts, the Netherlands Twin Register (NTR), and the Twins Early Development Study (TEDS; United Kingdom). In NTR, maternal ratings on aggression from the Child Behavior Checklist (CBCL) were available for 10,765 twin pairs at age 7, for 8,557 twin pairs at age 9/10, and for 7,176 twin pairs at age 12. In TEDS, parental ratings of conduct disorder from the Strength and Difficulty Questionnaire (SDQ) were available for 6,897 twin pairs at age 7, for 3,028 twin pairs at age 9 and for 5,716 twin pairs at age 12. In both studies, stability and…

MaleParentsNetherlands Twin Register (NTR)0301 basic medicinePersonality InventoryPoison controlCBCLheritability0302 clinical medicineLongitudinal StudiesChildChild Behavior Checklistta515Genetics (clinical)NetherlandsaggressionAge Factorsta3142Justice and Strong InstitutionsPsychiatry and Mental healthConduct disorderFemalePersonality Assessment Inventorymedicine.symptomPsychologyTwins Early Development StudySDG 16 - PeaceAdolescentlongitudinalEnvironment03 medical and health sciencesCellular and Molecular NeuroscienceSex FactorsDiseases in Twins/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_medicineHumansGenetic Association StudiesAggressionta1184SDG 16 - Peace Justice and Strong InstitutionsstabilityHeritabilitymedicine.diseasegenetic architecture/dk/atira/pure/sustainabledevelopmentgoals/peace_justice_and_strong_institutionsUnited Kingdomta3124030104 developmental biologyGene-Environment Interaction030217 neurology & neurosurgeryDemographyAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics
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A multi-centre clinico-genetic analysis of the VPS35 gene in Parkinson disease indicates reduced penetrance for disease-associated variants

2012

Abstract: Background Two recent studies identified a mutation (p.Asp620Asn) in the vacuolar protein sorting 35 gene as a cause for an autosomal dominant form of Parkinson disease. Although additional missense variants were described, their pathogenic role yet remains inconclusive. Methods and results We performed the largest multi-center study to ascertain the frequency and pathogenicity of the reported vacuolar protein sorting 35 gene variants in more than 15,000 individuals worldwide. p.Asp620Asn was detected in 5 familial and 2 sporadic PD cases and not in healthy controls, p.Leu774Met in 6 cases and 1 control, p.Gly51Ser in 3 cases and 2 controls. Overall analyses did not reveal any sig…

MaleParkinson's diseasePopulationVesicular Transport ProteinsLocus (genetics)DiseaseBiologyVPS35 protein humanBioinformaticsgenetics [Vesicular Transport Proteins]genetics [Parkinson Disease]Risk Factorsmedicinemetabolism [Vesicular Transport Proteins]GeneticsMissense mutationVPS35 GeneHumansGenetic epidemiologyGenetic Predisposition to Diseaseddc:6101506Genome-wideeducationGenetics (clinical)Genetic Association StudiesGeneticsVacuolar protein sortingeducation.field_of_studyGenotype-Phenotype CorrelationsParkinson DiseaseComplex traitsmedicine.diseasePenetranceddc:MutationFemaleHuman medicineParkinson-s diseaseJournal of Medical Genetics
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Clinical and molecular spectrum of renal malformations in Kabuki syndrome.

2013

International audience; OBJECTIVE: To determine the frequency and types of renal malformations, and to evaluate renal function in a cohort of patients with Kabuki syndrome (KS). STUDY DESIGN: Renal ultrasound scans and plasma creatinine measurements were collected from a French cohort of 94 patients with genotyped KS. Renal function was evaluated based on the estimated glomerular filtration rate. A genotype-phenotype study was conducted for renal and urinary tract malformations. RESULTS: Renal malformations were present in 22% of cases, and urinary tract anomalies were present in 15%. Renal malformations were observed in 28% of the MLL2 mutation-positive group and in 0% of the MLL2 mutation…

MalePathologyGenotyping Techniquesurologic and male genital diseasesKidneyCohort Studieschemistry.chemical_compoundChildUltrasonographyHistone Demethylases0303 health sciencesKidney030305 genetics & heredityNuclear ProteinsHypoplasia3. Good healthNeoplasm ProteinsDNA-Binding Proteinsmedicine.anatomical_structureVestibular DiseasesChild PreschoolCreatinineBiological MarkersFemaleFranceAbnormalitiesMultipleCohort studyGlomerular Filtration RateAdultGenetic Markersmedicine.medical_specialtyAdolescentUrinary systemUrologyRenal function03 medical and health sciencesYoung AdultmedicineHumansAbnormalities MultiplePreschoolGenetic Association Studies030304 developmental biologyRetrospective StudiesCreatinine[SDV.GEN]Life Sciences [q-bio]/Geneticsbusiness.industryInfantRetrospective cohort studymedicine.diseaseHematologic DiseaseschemistryFacePediatrics Perinatology and Child Healthbusiness[ SDV.GEN ] Life Sciences [q-bio]/GeneticsKabuki syndromeBiomarkersThe Journal of pediatrics
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Further delineation of eye manifestations in homozygous 15q13.3 microdeletions including TRPM1: a differential diagnosis of ceroid lipofuscinosis.

2014

The 15q13.3 heterozygous microdeletion is a fairly common microdeletion syndrome with marked clinical variability and incomplete penetrance. The average size of the deletion, which comprises six genes including CHRNA7, is 1.5 Mb. CHRNA7 has been identified as the gene responsible for the neurological phenotype in this microdeletion syndrome. Only seven patients with a homozygous microdeletion that includes at least CHRNA7, and is inherited from both parents have been described in the literature. The aim of this study was to further describe the distinctive eye manifestations from the analysis in the three French patients diagnosed with the classical 1.5 Mb homozygous microdeletion. Patients…

MalePathologymedicine.medical_specialtygenetic structuresalpha7 Nicotinic Acetylcholine ReceptorEncephalopathyTRPM Cation ChannelsChromosome DisordersBiologyBlindnessEyePupilNeuronal Ceroid-LipofuscinosesNight BlindnessSeizuresIntellectual DisabilityRetinal DystrophiesGeneticsmedicineElectroretinographyMyopiaHumansEye AbnormalitiesChildGenetics (clinical)TRPM1Genetic Association StudiesCongenital stationary night blindnessGeneticsChromosomes Human Pair 15DystrophyEye Diseases HereditaryGenetic Diseases X-LinkedOptic NerveMicrodeletion syndromemedicine.diseasePenetranceChild PreschoolFemalesense organsDifferential diagnosisChromosome DeletionAmerican journal of medical genetics. Part A
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Transient Receptor Potential Channel Polymorphisms Are Associated with the Somatosensory Function in Neuropathic Pain Patients

2011

Transient receptor potential channels are important mediators of thermal and mechanical stimuli and play an important role in neuropathic pain. The contribution of hereditary variants in the genes of transient receptor potential channels to neuropathic pain is unknown. We investigated the frequency of transient receptor potential ankyrin 1, transient receptor potential melastin 8 and transient receptor potential vanilloid 1 single nucleotide polymorphisms and their impact on somatosensory abnormalities in neuropathic pain patients. Within the German Research Network on Neuropathic Pain (Deutscher Forscbungsverbund Neuropathischer Schmerz) 371 neuropathic pain patients were phenotypically ch…

MalePharmacologyTransient receptor potential channelTransient Receptor Potential ChannelsAnesthesiologyMolecular Cell BiologyMembrane Receptor SignalingMultidisciplinaryQRMiddle AgedNeurologyHyperalgesiaNeuropathic painMedicineFemaleSensory Perceptionmedicine.symptomResearch ArticleSignal TransductionAdultAnkyrinsGenotypeScienceMedizinische Fakultät -ohne weitere Spezifikation-Receptor potential610TRPV Cation ChannelsSensory systemSingle-nucleotide polymorphism-Polymorphism Single NucleotidemedicineGeneticsHumansPain ManagementGenetic Predisposition to Diseaseddc:610BiologyGenetic Association StudiesAgedHypoalgesiaPolymorphism GeneticPopulation Biologybusiness.industryHuman Geneticsmedicine.diseaseNeuralgiaGenetic PolymorphismNeuralgiabusinessPopulation GeneticsNeuroscience
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Disruption of the ASTN2 / TRIM32 locus at 9q33.1 is a risk factor in males for Autism Spectrum Disorders, ADHD and other neurodevelopmental phenotypes

2014

Rare copy number variants (CNVs) disrupting ASTN2 or both ASTN2 and TRIM32 have been reported at 9q33.1 by genome-wide studies in a few individuals with neurodevelopmental disorders (NDDs). The vertebrate-specific astrotactins, ASTN2 and its paralog ASTN1, have key roles in glial-guided neuronal migration during brain development. To determine the prevalence of astrotactin mutations and delineate their associated phenotypic spectrum, we screened ASTN2/TRIM32 and ASTN1 (1q25.2) for exonic CNVs in clinical microarray data from 89 985 individuals across 10 sites, including 64 114 NDD subjects. In this clinical dataset, we identified 46 deletions and 12 duplications affecting ASTN2. Deletions o…

MaleReceptors Cell Surface/geneticsAutismChild Development Disorders Pervasive/geneticsGene ExpressionGenome-wide association studyMedical and Health SciencesTripartite Motif ProteinsRisk FactorsReceptors2.1 Biological and endogenous factorsProtein IsoformsNerve Tissue Proteins/geneticsCopy-number variationAetiologyChildGenetics (clinical)Sequence DeletionPediatricGenetics & HeredityGeneticseducation.field_of_studySingle NucleotideArticlesGeneral MedicineExonsBiological SciencesMental HealthPhenotypeAutism spectrum disorderOrgan SpecificityCerebellar cortexChild PreschoolCell SurfaceSpeech delayFemalemedicine.symptomTranscription Initiation SiteAttention Deficit Disorder with Hyperactivity/geneticsChromosomes Human Pair 9HumanPair 9AdultPediatric Research InitiativeChild Development DisordersAdolescentDNA Copy Number VariationsIntellectual and Developmental Disabilities (IDD)Ubiquitin-Protein LigasesPopulationTranscription Factors/geneticsNerve Tissue ProteinsReceptors Cell SurfaceBiologyPolymorphism Single NucleotideChromosomesYoung AdultClinical ResearchProtein Isoforms/geneticsBehavioral and Social ScienceGeneticsmedicineAttention deficit hyperactivity disorderHumansGenetic Predisposition to DiseasePolymorphismPreschooleducationMolecular BiologyGenetic Association StudiesPervasiveGlycoproteinsHuman GenomeNeurosciencesInfant NewbornGlycoproteins/geneticsInfantNewbornmedicine.diseaseBrain DisordersAttention Deficit Disorder with HyperactivityChild Development Disorders PervasiveCase-Control StudiesAutismTranscription Factors
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TRIB1 constitutes a molecular link between regulation of sleep and lipid metabolism in humans.

2012

Epidemiological studies show association between sleep duration and lipid metabolism. In addition, inactivation of circadian genes induces insulin resistance and hyperlipidemia. We hypothesized that sleep length and lipid metabolism are partially controlled by the same genes. We studied the association of total sleep time (TST) with 60 genetic variants that had previously been associated with lipids. The analyses were performed in a Finnish population-based sample (N = 6334) and replicated in 2189 twins. Finally, RNA expression from mononuclear leucocytes was measured in 10 healthy volunteers before and after sleep restriction. The genetic analysis identified two variants near TRIB1 gene th…

MaleTwinsBlood lipidsGene ExpressionCohort Studies0302 clinical medicineGene FrequencySleep and metabolismHomeostasisgeneticsta515FinlandSlow-wave sleepSleep restriction2. Zero hunger0303 health sciencesIntracellular Signaling Peptides and Proteinsta3141Middle AgedSleep in non-human animals3142 Public health care science environmental and occupational health3. Good healthPsychiatry and Mental healthFemaleOriginal Articleepidemiologymedicine.symptomAdultmedicine.medical_specialtyGenotypeSNPDisorders of Excessive SomnolenceBiologyProtein Serine-Threonine Kinasesta3111Polymorphism Single Nucleotidelipids03 medical and health sciencesCellular and Molecular NeuroscienceInternal medicinemedicineHumansCircadian rhythmsleepBiological PsychiatryAllelesGenetic Association StudiesTriglycerides030304 developmental biologyAgedCholesterol HDLGenetic VariationLipid metabolismCholesterol LDLLipid Metabolismta3124Sleep deprivationEndocrinologySleep Deprivationmetabolism030217 neurology & neurosurgeryTranslational psychiatry
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Novel association of the obesity risk-allele near Fas Apoptotic Inhibitory Molecule 2 (FAIM2) gene with heart rate and study of its effects on myocar…

2014

[Background] The Fas apoptotic pathway has been implicated in type 2 diabetes and cardiovascular disease. Although a polymorphism (rs7138803; G > A) near the Fas apoptotic inhibitory molecule 2 (FAIM2) locus has been related to obesity, its association with other cardiovascular risk factors and disease remains uncertain.

MalealelosEndocrinology Diabetes and MetabolismhumanosLOCIMyocardial Infarctionproteínas reguladoras de la apoptosisApoptosisType 2 diabetesVARIANTSDiet Mediterraneanestudios de seguimientoCoronary artery diseaseClinical trialsRisk FactorsMyocardial infarctionLongitudinal Studiesmediana edadOriginal Investigationeducation.field_of_studyancianoDiabetisdietaHàbits alimentarisCAUSE MORTALITYDiabetesSOLUBLE FASMiddle Agedestudios de asociación genéticaMEDITERRANEAN DIETCARDIOVASCULAR-DISEASECORONARY-ARTERY-DISEASEObesitatFemaleCardiology and Cardiovascular Medicinemedicine.medical_specialtyFood habitsPopulationHeart rateproteínas de membranasMediterranean cookingDiabetes mellitusInternal medicineCuina mediterràniamedicineDiabetes MellitusHumansfactores de riesgoJAPANESE POPULATIONGenetic Predisposition to DiseaseObesityGENOME-WIDE ASSOCIATIONeducationobesidadAllelesGenetic Association Studiesinfarto de miocardioAgedPolymorphism Geneticbusiness.industryMembrane Proteinspredisposición genética a la enfermedadmedicine.diseaseObesityFAIM2DietBODY-MASS INDEXInfart de miocardiMyocardial infarctionEndocrinologyBlood pressureDiabetes Mellitus Type 2frecuencia cardíacaestudios longitudinalesbusinessApoptosis Regulatory ProteinsBody mass indexFollow-Up StudiesAssaigs clínics
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Novel deletion of the E3A ubiquitin protein ligase gene detected by multiplex ligation-dependent probe amplification in a patient with Angelman syndr…

2010

Angelman syndrome (AS) is a severe neurobehavioural disorder caused by failure of expression of the maternal copy of the imprinted domain located on 15q11-q13. There are different mechanisms leading to AS: maternal microdeletion, uniparental disomy, defects in a putative imprinting centre, mutations of the E3 ubiquitin protein ligase (UBE3A) gene. However, some of suspected cases of AS are still scored negative to all the latter mutations. Recently, it has been shown that a proportion of negative cases bear large deletions overlapping one or more exons of the UBE3A gene. These deletions are difficult to detect by conventional gene-scanning methods due to the masking effect by the non-delete…

Malecongenital hereditary and neonatal diseases and abnormalitiesClinical Biochemistrygene dosageBiochemistryGene dosageExonSettore BIO/13 - Biologia ApplicataAngelman syndromemedicineUBE3AHumansMultiplexGenetic TestingMultiplex ligation-dependent probe amplificationChildMolecular BiologyGeneticsbiologyubiquitin-protein ligasesgenetic association studiemedicine.diseaseMolecular biologyUniparental disomyUbiquitin ligaseAngelman syndromebiology.proteinMolecular MedicineOriginal ArticleFemaleGene Deletion
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