Search results for "Disposition"

showing 10 items of 832 documents

Exonic Mosaic Mutations Contribute Risk for Autism Spectrum Disorder

2017

AbstractGenetic risk factors for autism spectrum disorder (ASD) have yet to be fully elucidated. Postzygotic mosaic mutations (PMMs) have been implicated in several neurodevelopmental disorders and overgrowth syndromes. We systematically evaluated PMMs by leveraging whole-exome sequencing data on a large family-based ASD cohort, the Simons Simplex Collection. We found evidence that 11% of published single nucleotide variant (SNV)de novomutations are potentially PMMs. We then developed a robust SNV PMM calling approach that leverages complementary callers, logistic regression modeling, and additional heuristics. Using this approach, we recalled SNVs and found that 22% ofde novomutations like…

Male0301 basic medicineProbandZygoteautism spectrum disorderSYNGAP1Biologypostzygoticmedicine.disease_causeArticleGermlineCohort Studies03 medical and health sciencessplicing0302 clinical medicineNeurodevelopmental disorderGermline mutationDatabases GeneticGeneticsmedicineHumansMissense mutationGenetic Predisposition to DiseaseChild[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesMutationneurodevelopmentsomaticGenetic VariationExonsmedicine.disease030104 developmental biologymosaicism[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutism spectrum disorderCHD2AutismFemalemutation030217 neurology & neurosurgeryexome
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Gluten Degrading Enzymes for Treatment of Celiac Disease

2020

Celiac disease (CeD) affects about 1% of most world populations. It presents a wide spectrum of clinical manifestations, ranging from minor symptoms to mild or severe malabsorption, and it may be associated with a wide variety of autoimmune diseases. CeD is triggered and maintained by the ingestion of gluten proteins from wheat and related grains. Gluten peptides that resist gastrointestinal digestion are antigenically presented to gluten specific T cells in the intestinal mucosa via HLA-DQ2 or HLA-DQ8, the necessary genetic predisposition for CeD. To date, there is no effective or approved treatment for CeD other than a strict adherence to a gluten-free diet, which is difficult to maintain…

Male0301 basic medicineProteasesGlutensDrug CompoundingT-Lymphocytesenzyme therapylcsh:TX341-641ReviewBiologyDiet Gluten-Free03 medical and health sciences0302 clinical medicineAntigenIntestinal mucosaglutenasewheatHLA-DQ AntigensEnzyme StabilityGenetic predispositionHumansGenetic Predisposition to Diseaseenteric coatingSubtilisinsendopeptidasechemistry.chemical_classificationNutrition and Dieteticstreatmentfungiautoimmunitynutritional and metabolic diseasesGlutendigestive system diseasesGlutamine030104 developmental biologyEnzymeBiochemistrychemistryglutenProteolysisFemale030211 gastroenterology & hepatologyProlyl OligopeptidasesSubtilisinslcsh:Nutrition. Foods and food supplyceliac diseaseFood ScienceNutrients
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Proprotein Convertase Subtilisin Kexin Type 9 Inhibition for Autosomal Recessive Hypercholesterolemia—Brief Report

2016

Objective— Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors lower low-density lipoprotein (LDL) cholesterol in the vast majority of patients with autosomal dominant familial hypercholesterolemia. Will PCSK9 inhibition with monoclonal antibodies, in particular alirocumab, be of therapeutic value for patients with autosomal recessive hypercholesterolemia (ARH)? Approach and Results— Primary lymphocytes were obtained from 28 genetically characterized ARH patients and 11 controls. ARH lymphocytes treated with mevastatin were incubated with increasing doses of recombinant PCSK9 with or without saturating concentrations of alirocumab. Cell surface LDL receptor expression measured…

Male0301 basic medicineSettore MED/09 - Medicina Interna[SDV]Life Sciences [q-bio]receptorsalirocumabFamilial hypercholesterolemia030204 cardiovascular system & hematologyproprotein convertase subtilisin kexin type 90302 clinical medicinetherapeuticsLymphocytesCells CulturedhypercholesterolemiaAnticholesteremic AgentsPCSK9 InhibitorsAntibodies MonoclonalMiddle Aged3. Good healthPhenotypeAutosomal Recessive HypercholesterolemiaKexinDrug Therapy CombinationFemalelipids (amino acids peptides and proteins)LovastatinProprotein Convertase 9Cardiology and Cardiovascular Medicinemedicine.drugAdultmedicine.medical_specialtySerine Proteinase InhibitorsAdolescentBiologyAntibodies Monoclonal HumanizedLDLYoung Adult03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseLovastatinAdaptor Proteins Signal TransducingAlirocumabPCSK9receptors LDLCholesterol LDLmedicine.diseaseProprotein convertasetherapeutic030104 developmental biologyEndocrinologyCase-Control Studiesalirocumab; hypercholesterolemia; proprotein convertase subtilisin kexin type 9; receptors LDL; therapeutics; Cardiology and Cardiovascular MedicineMutationLDL receptorHydroxymethylglutaryl-CoA Reductase InhibitorsArteriosclerosis, Thrombosis, and Vascular Biology
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CLOCK gene variation is associated with incidence of type‑2 diabetes and cardiovascular diseases in type‑2 diabetic subjects: dietary modulation in t…

2016

Background: Circadian rhythms regulate key biological processes influencing metabolic pathways. Disregulation is associated with type 2 diabetes (T2D) and cardiovascular diseases (CVD). Circadian rhythms are generated by a transcriptional autoregulatory feedback loop involving core clock genes. CLOCK (circadian locomotor output cycles protein kaput), one of those core genes, is known to regulate glucose metabolism in rodent models. Cross-sectional studies in humans have reported associations between this locus and obesity, plasma glucose, hypertension and T2D prevalence, supporting its role in cardiovascular risk. However, no longitudinal study has investigated the association between CLOCK…

Male0301 basic medicineTime Factorsmodelos de riesgos proporcionalesEndocrinology Diabetes and MetabolismhumanosCLOCK ProteinsType 2 diabetesKaplan-Meier Estimatefrecuencia génica030204 cardiovascular system & hematologyDiet Mediterranean0302 clinical medicineGene FrequencyRisk Factorsevaluación de riesgosLongitudinal Studiesmediana edadOriginal InvestigationAged 80 and overancianoDiabetishomocigotodietaIncidenceresultado del tratamientoHomozygoteDiabetesdistribución de la ji al cuadradoMiddle AgedCircadian RhythmCLOCKStrokePhenotypeTreatment OutcomeCardiovascular diseasesinteracción gen-ambientediabetes mellitusfenotipoCardiology and Cardiovascular Medicineestimación de Kaplan-Meiermedicine.medical_specialtyHeterozygoteenfermedades cardiovascularesSingle-nucleotide polymorphism:Ciencias de la Salud::Nutrición y dietética [Materias Investigacion]Polymorphism Single NucleotideRisk Assessmentincidencia03 medical and health sciencesInsulin resistanceMediterranean cookingfactores de tiempo:Ciencias de la Salud::Medicina preventiva [Materias Investigacion]Diabetes mellitusInternal medicineSistema cardiovascular -- Malalties -- Aspectes genèticsMediterranean dietCuina mediterràniamedicineSNPHumansproteínas CLOCKfactores de riesgoGenetic Predisposition to DiseaseCircadian rhythmanálisis multifactorialDieta -- Mediterrània Regió de laAgedProportional Hazards ModelsChi-Square DistributionCLOCK genebusiness.industryMalalties cardiovascularspredisposición genética a la enfermedadProtective Factorsmedicine.diseaseObesityDiet030104 developmental biologyEndocrinologyritmo circadianoDiabetes Mellitus Type 2SpainMultivariate Analysisestudios longitudinalesGene-Environment Interactionbusiness:Ciencias de la Salud::Endocrinología [Materias Investigacion]heterocigoto
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Genome-wide Association Studies Identify Genetic Loci Associated with Albuminuria in Diabetes

2016

Elevated concentrations of albumin in the urine, albuminuria, are a hallmark of diabetic kidney disease and are associated with an increased risk for end-stage renal disease and cardiovascular events. To gain insight into the pathophysiological mechanisms underlying albuminuria, we conducted meta-analyses of genome-wide association studies and independent replication in up to 5,825 individuals of European ancestry with diabetes and up to 46,061 without diabetes, followed by functional studies. Known associations of variants in CUBN, encoding cubilin, with the urinary albumin-to-creatinine ratio (UACR) were confirmed in the overall sample (P = 2.4 × 10−10). Gene-by-diabetes interactions were…

Male0301 basic medicinediabetes geneEndocrinology Diabetes and MetabolismGenome-wide association studyKidneyGLOMERULAR-FILTRATION-RATECathepsin CGene Knockout TechniquescubilinSettore MED/14 - NEFROLOGIADiabetic NephropathiesMODULATES PROTEINURIAddc:616HERITABILITYDiabetesGenetics/Genomes/Proteomics/MetabolomicsMiddle AgedRISK POPULATION COHORTS3. Good healthINSIGHTSKidney TubulesFemaleSulfotransferasesmedicine.symptomRAB38AdultEXPRESSIONmedicine.medical_specialtyRenal functionReceptors Cell Surface610 Medicine & healthSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotidealbuminuriaDiabetes Mellitus Experimental03 medical and health sciencesDiabetes mellitusInternal medicineInternal MedicinemedicineAnimalsHumansGenetic Predisposition to DiseaseAgedMORTALITYKIDNEY-DISEASEmedicine.diseaseCubilinRatsMinor allele frequency030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2rab GTP-Binding ProteinsCOLLABORATIVE METAANALYSISAlbuminuria570 Life sciences; biologyalbuminuria diabetes cubilinGenome-Wide Association StudyKidney disease
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CNTN6 mutations are risk factors for abnormal auditory sensory perception in autism spectrum disorders

2017

International audience; Contactin genes CNTN5 and CNTN6 code for neuronal cell adhesion molecules that promote neurite outgrowth in sensory-motor neuronal pathways. Mutations of CNTN5 and CNTN6 have previously been reported in individuals with autism spectrum disorders (ASDs), but very little is known on their prevalence and clinical impact. In this study, we identified CNTN5 and CNTN6 deleterious variants in individuals with ASD. Among the carriers, a girl with ASD and attention-deficit/hyperactivity disorder was carrying five copies of CNTN5. For CNTN6, both deletions (6/1534 ASD vs 1/8936 controls; P=0.00006) and private coding sequence variants (18/501 ASD vs 535/33480 controls; P=0.000…

Male0301 basic medicinegenetic structuresAutism Spectrum Disorder[ SDV.MHEP.PSM ] Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental health[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[SDV.MHEP.PSM] Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental healthmedicine.disease_causeChild[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGeneticsMutationPsychiatry and Mental healthSchizophrenia[ SDV.NEU.NB ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology[ SCCO.NEUR ] Cognitive science/NeuroscienceAuditory PerceptionMedical geneticsOriginal ArticleFemalePsychopharmacologymedicine.symptomPsychologyAdultmedicine.medical_specialtyAdolescentDNA Copy Number Variations[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsPolymorphism Single Nucleotidebehavioral disciplines and activities03 medical and health sciencesCellular and Molecular NeuroscienceContactinsmental disordersmedicineHumansDementiaGenetic Predisposition to DiseaseMolecular Biology[SCCO.NEUR]Cognitive science/Neuroscience[SCCO.NEUR] Cognitive science/NeuroscienceHyperacusis[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[ SDV.SP.PHARMA ] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacologymedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAttention Deficit Disorder with Hyperactivity[SDV.MHEP.PSM]Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental healthMutationBehavioral medicine[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyAutismNeuroscienceMolecular Psychiatry
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Genetic contribution to the relationship between personality and depressive symptoms among older women.

2009

BackgroundPrior studies suggest that certain types of personality are at higher risk for developing depressive disorders. This study examined the relationship between old age depressive symptoms and two middle-age personality dimensions, neuroticism and extraversion.MethodThe present study is part of the Finnish Twin Study on Aging, where altogether 409 female twins who had completed the Eysenck Personality Inventory at the age of 38–51 years were studied for depressive symptoms 28 years later using Center for the Epidemiologic Studies Depression Scale. Logistic regression analysis suitable for dependent data and univariate and Cholesky models for decomposing the genetic and environmental f…

Male050103 clinical psychologyCharacterNeurotic Disordersmedia_common.quotation_subjectStatistics as TopicModels PsychologicalLogistic regressionDevelopmental psychologyCohort StudiesExtraversion Psychological03 medical and health sciences0302 clinical medicineRisk FactorsTwins DizygoticPersonalityHumans0501 psychology and cognitive sciencesGenetic Predisposition to DiseaseApplied PsychologyDepressive symptomsFinlandmedia_commonDepressive DisorderExtraversion and introversion05 social sciencesAge FactorsGender IdentityTwins MonozygoticNeuroticismTwin studyEysenck Personality QuestionnaireMiddle age030227 psychiatryPsychiatry and Mental healthCross-Sectional StudiesFemalePsychologyClinical psychologyPsychological medicine
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Combination of KIR 2DL2 and HLA-C1 (Asn 80) confers susceptibility to type 1 diabetes in Latvians.

2008

Summary Killer immunoglobulin-like receptors (KIRs) are known to modulate natural killer (NK) and NK T-cell function by interacting with human leucocyte antigen (HLA) class I ligands on target cells. The aim of our study was to investigate the influence of KIR2D genes with their HLA-C ligands in susceptibility to type 1 diabetes. A total of 98 type 1 diabetes patients and 70 healthy subjects from Latvia were typed for KIR genes and HLA-C ligands using polymerase chain reaction-based genotyping. The HLA C1+/C2+ combination was positively, and C1–/C2+ combination was negatively, associated with type 1 diabetes. Stratification analysis of KIR/HLA-C ligand combinations showed 2DL2+/C1+, 2DL3+/C…

MaleAdolescentGenotypeImmunologyHuman leukocyte antigenHLA-C AntigensBiologyWhite Peoplelaw.inventionImmune systemGene FrequencylawGeneticsmedicineHumansGenetic Predisposition to DiseaseReceptorChildMolecular BiologyGenotypingGeneGenetics (clinical)Polymerase chain reactionType 1 diabetesInfant NewbornInfantGeneral Medicinemedicine.diseaseLatviaDiabetes Mellitus Type 1Child PreschoolReceptors KIR2DL2ImmunologyFemaleFunction (biology)International journal of immunogenetics
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Childhood gene-environment interactions and age-dependent effects of genetic variants associated with refractive error and myopia: The CREAM Consorti…

2018

Myopia, currently at epidemic levels in East Asia, is a leading cause of untreatable visual impairment. Genome-wide association studies (GWAS) in adults have identified 39 loci associated with refractive error and myopia. Here, the age-of-onset of association between genetic variants at these 39 loci and refractive error was investigated in 5200 children assessed longitudinally across ages 7-15 years, along with gene-environment interactions involving the major environmental risk-factors, nearwork and time outdoors. Specific variants could be categorized as showing evidence of: (a) early-onset effects remaining stable through childhood, (b) early-onset effects that progressed further with i…

MaleAdolescentRefractive ErrorsPolymorphism Single NucleotideArticleWhite PeopleAsian PeopleMyopiaHumansFemaleGene-Environment InteractionGenetic Predisposition to DiseaseLongitudinal StudiesAge of OnsetChildGenome-Wide Association Study
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Genetic and environmental influences on psychological traits and eating attitudes in a sample of Spanish schoolchildren.

2014

Introduction: The heritability of eating disorders has been estimated to range from 22% to over 62%.The aim of this study is to determine the relative influence of genetics and environment that contribute to the drive for thinness, body dissatisfaction, perfectionism, and ineffectiveness, by evaluating sex differences in a sample of adolescent twins from Valencia, Spain. Material and methods: Five hundred eighty-four pairs of adolescent twins between 13 and 18 years of age completed the study. To determine zygosity, teachers responded to a questionnaire on physical similarity. Psychological traits of eating disorders were assessed with four sub-scales of the Eating Disorder Inventory (EDI);…

MaleAdolescentTwinsSample (statistics)Environmentmedicine.disease_causeAdolescentsDevelopmental psychologyFeeding and Eating Disorders03 medical and health sciences0302 clinical medicineSex FactorsRisk FactorsmedicineGeneticsBody ImageHumansGenetic Predisposition to DiseaseEating attitudesGeneral MedicinePerfectionism (psychology)Heritabilitymedicine.diseaseEating Disorder InventoryZygositySelf Efficacy030227 psychiatryEating disordersCross-Sectional StudiesSpainPsychological traitsEating disordersFemalePerfectionismPsychology030217 neurology & neurosurgeryBody dissatisfactionClinical psychologyRevista de psiquiatria y salud mental
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