Search results for "NHE"

showing 10 items of 1058 documents

The role of parental affection and psychological control in adolescent athletes' symptoms of school and sport burnout during the transition to upper …

2018

Abstract Introduction The transition from compulsory school to upper secondary school is a challenging period for adolescents. Especially challenging it can be for adolescents who aim to integrate two domains of achievement, such as an athletic career and academic education. The pressure from two intertwined achievement domains may make student-athletes vulnerable to symptoms of burnout. The study examined the role of mothers' and fathers’ affection and psychological control as possible risk or protective factors in the symptoms of school and sport burnout among 15–16 year olds adolescent athletes in Finland. Methods The adolescents’ (n = 391) burnout symptoms in the two domains were measur…

MaleAdolescent athletesBurnoutkoulu-uupumus0302 clinical medicinePsychological controlparentingSurveys and Questionnairessport burnoutDevelopmental and Educational PsychologyParent-Child Relationsta515Finlandmedia_commonSecondary levelSchoolsbiologyParenting05 social sciencesYouth Sportsschool burnoutlukioPsychiatry and Mental healthvanhemmatkontrolliupper secondary schoolFemalePsychology050104 developmental & child psychologyClinical psychologypsychological controlSocial PsychologyAdolescentvanhemmuusmedia_common.quotation_subjecteducationMothersBurnout Psychologicaluupumus03 medical and health sciencesAffectionHumans0501 psychology and cognitive sciencesAcademic educationAthletes030229 sport sciencesbiology.organism_classificationAthletesPediatrics Perinatology and Child HealthurheilijatJournal of adolescence
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Linkage to chromosome 1p36 for attention-deficit/hyperactivity disorder traits in school and home settings.

2008

Contains fulltext : 69485.pdf (Publisher’s version ) (Closed access) BACKGROUND: Limited success has been achieved through previous attention-deficit/hyperactivity disorder (ADHD) linkage scans, which were all designed to map genes underlying the dichotomous phenotype. The International Multi-centre ADHD Genetics (IMAGE) project performed a whole genome linkage scan specifically designed to map ADHD quantitative trait loci (QTL). METHODS: A set of 1094 single selected Caucasian ADHD nuclear families was genotyped on a highly accurate and informative single nucleotide polymorphism (SNP) panel. Two quantitative traits measuring the children's symptoms in home and school settings were collecte…

MaleAdolescentGenetics and epigenetic pathways of disease [NCMLS 6]Genetic LinkageMedizin610 Medicine & healthSingle-nucleotide polymorphismLocus (genetics)Quantitative trait locusNeuroinformatics [DCN 3]Social EnvironmentMental health [NCEBP 9]ArticleWhite PeopleDyslexiaGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciences0302 clinical medicineCognitive neurosciences [UMCN 3.2]Genetic linkagemental disordersmedicinePerception and Action [DCN 1]HumansAttention deficit hyperactivity disorderddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersChildBiological PsychiatryGenetics0303 health sciencesSchools030305 genetics & heredityDyslexia10058 Department of Child and Adolescent PsychiatryHeritabilitymedicine.disease030227 psychiatryPhenotypeGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with HyperactivityChromosomes Human Pair 1Child PreschoolTraitFemalePsychology2803 Biological PsychiatryFunctional Neurogenomics [DCN 2]
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Twelve Variants Polygenic Score for Low-Density Lipoprotein Cholesterol Distribution in a Large Cohort of Patients With Clinically Diagnosed Familial…

2022

: Background A significant proportion of individuals clinically diagnosed with familial hypercholesterolemia (FH), but without any disease-causing mutation, are likely to have polygenic hypercholesterolemia. We evaluated the distribution of a polygenic risk score, consisting of 12 low-density lipoprotein cholesterol (LDL-C)-raising variants (polygenic LDL-C risk score), in subjects with a clinical diagnosis of FH. Methods and Results Within the Lipid Transport Disorders Italian Genetic Network (LIPIGEN) study, 875 patients who were FH-mutation positive (women, 54.75%; mean age, 42.47±15.00 years) and 644 patients who were FH-mutation negative (women, 54.21%; mean age, 49.73±13.54 years) wer…

MaleAdultMultifactorial InheritanceSettore MED/09 - Medicina Internafamilial hypercholesterolemia; molecular diagnosis; polygenic risk score; Adult; Cholesterol LDL; Female; Humans; Middle Aged; Multifactorial Inheritance; Mutation; Gene Regulatory Networks; Hyperlipoproteinemia Type IIfamilial hypercholesterolemiaCholesterol LDLMiddle AgedLDLHyperlipoproteinemia Type IICholesterolmolecular diagnosispolygenic risk scoreMutationHumansFemaleGene Regulatory Networksmolecular diagnosifamilial hypercholesterolemia; molecular diagnosis; polygenic risk score
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Loss-of-function maternal-effect mutations of PADI6 are associated with familial and sporadic Beckwith-Wiedemann syndrome with multi-locus imprinting…

2020

Abstract Background PADI6 is a component of the subcortical maternal complex, a group of proteins that is abundantly expressed in the oocyte cytoplasm, but is required for the correct development of early embryo. Maternal-effect variants of the subcortical maternal complex proteins are associated with heterogeneous diseases, including female infertility, hydatidiform mole, and imprinting disorders with multi-locus imprinting disturbance. While the involvement of PADI6 in infertility is well demonstrated, its role in imprinting disorders is less well established. Results We have identified by whole-exome sequencing analysis four cases of Beckwith-Wiedemann syndrome with multi-locus imprintin…

MaleBeckwith-Wiedemann SyndromeGenomic imprintingMulti-locus imprinting disturbanceBeckwith–Wiedemann syndromeWhole Exome SequencingProtein-Arginine Deiminase Type 60302 clinical medicinePregnancyImprinting (psychology)ChildGenetics (clinical)Genetics0303 health sciencesDNA methylationPADI6Beckwith-Wiedemann syndrome; DNA methylation; Genomic imprinting; Infertility; Maternal-effect variants; Multi-locus imprinting disturbance; PADI6; Subcortical maternal complex; Adolescent; Adult; Beckwith-Wiedemann Syndrome; Child Preschool; DNA Methylation; Female; Genomic Imprinting; Heterozygote; Humans; Hydatidiform Mole; Infant; Infertility Female; Male; Maternal Inheritance; Mutation; Oocytes; Pedigree; Phenotype; Pregnancy; Protein-Arginine Deiminase Type 6; Siblings; Whole Exome SequencingFemale infertilityMaternal effectHydatidiform MolePedigreePhenotypeChild Preschool030220 oncology & carcinogenesisDNA methylationFemaleMaternal InheritanceInfertility FemaleAdultHeterozygoteAdolescentSubcortical maternal complexBiology03 medical and health sciencesExome SequencingGeneticsmedicineHumansMaternal-effect variantsPreschoolMolecular BiologyLoss function030304 developmental biologyMaternal-effect variantResearchSiblingsInfantmedicine.diseaseHuman geneticsInfertilityMutationOocytesGenomic imprintingDevelopmental BiologyClinical Epigenetics
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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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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
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Molecular diagnosis of hypobetalipoproteinemia: an ENID review.

2007

Abstract Primary hypobetalipoproteinemia (HBL) includes a group of genetic disorders: abetalipoproteinemia (ABL) and chylomicron retention disease (CRD), with a recessive transmission, and familial hypobetalipoproteinemia (FHBL) with a co-dominant transmission. ABL and CRD are rare disorders due to mutations in the MTP and SARA2 genes, respectively. Heterozygous FHBL is much more frequent. FHBL subjects often have fatty liver and, less frequently, intestinal fat malabsorption. FHBL may be linked or not to the APOB gene. Most mutations in APOB gene cause the formation of truncated forms of apoB which may or may be not secreted into the plasma. Truncated apoBs with a size below that of apoB-3…

MaleCandidate geneSettore MED/09 - Medicina InternaApolipoprotein BGenotypeLocus (genetics)BiologyPolymorphism Single NucleotidePCSK9 GenemedicineHumansFamilial hypobetalipoproteinemiaGenetic TestingAPOB geneApolipoproteins BGeneticsPCSK9AbetalipoproteinemiaChylomicron retention diseasemedicine.diseaseEuropean Network for Inherited Dyslipidemia (ENID)AbetalipoproteinemiaPhenotypePCSK9 geneHypobetalipoproteinemia Familial Apolipoprotein BMutationbiology.proteinlipids (amino acids peptides and proteins)FemaleHypobetalipoproteinemiaMTP geneCardiology and Cardiovascular MedicineCarrier Proteinsuropean Network for Inherited Dyslipidemia (ENID)European Network for Inherited Dyslipidemia (ENID) Familial hypobetalipoproteinemia Abetalipoproteinemia Chylomicron retention disease.Chylomicron retention diseaseAtherosclerosis
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Intergenerational transmission of the positive effects of physical exercise on brain and cognition

2019

Physical exercise has positive effects on cognition, but very little is known about the inheritance of these effects to sedentary offspring and the mechanisms involved. Here, we use a patrilineal design in mice to test the transmission of effects from the same father (before or after training) and from different fathers to compare sedentary- and runner-father progenies. Behavioral, stereological, and whole-genome sequence analyses reveal that paternal cognition improvement is inherited by the offspring, along with increased adult neurogenesis, greater mitochondrial citrate synthase activity, and modulation of the adult hippocampal gene expression profile. These results demonstrate the inher…

MaleCognition traitsOffspringGene ExpressionPhysical exerciseHippocampal formationintergenerational inheritanceGermlineRunningFathersMice03 medical and health sciencesCognition0302 clinical medicinePregnancyAnimalsCitrate synthase030304 developmental biology0303 health sciencesMultidisciplinaryexercisebiologyNeurogenesisInheritance (genetic algorithm)BrainCognition3. Good healthmitochondriaPNAS PlusPaternal Inheritancebiology.proteinAdult hippocampal neurogenesisFemaleNeurosciencemoderate physical exercisemoderate physical030217 neurology & neurosurgeryProceedings of the National Academy of Sciences
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A high-density SNP linkage scan with 142 combined subtype ADHD sib pairs identifies linkage regions on chromosomes 9 and 16

2008

As part of the International Multi-centre ADHD Gene (IMAGE) project we have completed an affected sibling pair study of 142 narrowly defined DSM-IV combined type ADHD proband-sibling pairs. We found suggestive linkage on chromosomes 9 and 16 with non-parametric multipoint peak LOD scores of 2.13 and 3.1 respectively. There have been several previous ADHD linkage scans. The UCLA study (Fisher et al. 2002; Ogdie et al. 2004; Ogdie et al. 2003), the Dutch study (Bakker et al. 2003), the German study (Hebebrand et al. 2006) and the MGH Study (Faraone et al., submitted) applied the affected sib pair (ASP) strategy; the Columbian study used extended pedigrees ascertained from a population isolate…

MaleGenetics and epigenetic pathways of disease [NCMLS 6]GENOMEWIDE SCANMedizin2804 Cellular and Molecular NeuroscienceCHILDRENComorbidityNeuroinformatics [DCN 3]Severity of Illness IndexDevelopmental psychology2738 Psychiatry and Mental Health0302 clinical medicinePerception and Action [DCN 1]HETEROGENEITYIsraelChildGeneticsObserver Variation0303 health sciencesATTENTION-DEFICIT/HYPERACTIVITY DISORDERPSYCHIATRIC-DISORDERSDOPAMINE TRANSPORTER GENEASSOCIATION10058 Department of Child and Adolescent PsychiatryEuropePsychiatry and Mental healthFemalePsychologyChromosomes Human Pair 9linkageFunctional Neurogenomics [DCN 2]GenotypeDEFICIT HYPERACTIVITY DISORDER610 Medicine & healthPolymorphism Single NucleotideMental health [NCEBP 9]Genetic determinismWhite PeopleGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular NeuroscienceCognitive neurosciences [UMCN 3.2]Genetic linkage1312 Molecular BiologymedicineSNPAttention deficit hyperactivity disorderHumansADHDSiblingMolecular Biology030304 developmental biologyLinkage (software)SiblingsChromosomemedicine.diseaseSib pairsUnited Statesaffected sib pairsGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with HyperactivityCONDUCT DISORDERLod ScoreDISEQUILIBRIUM030217 neurology & neurosurgeryChromosomes Human Pair 16
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