Search results for "Phenotype"

showing 10 items of 1875 documents

Extra collagen overlay prolongs the differentiated phenotype in sandwich-cultured rat hepatocytes

2018

INTRODUCTION: Sandwich-cultured rat hepatocytes (SCRH) have become an invaluable in vitro model to study hepatic drug disposition. SCRH are maintained between two layers of extracellular matrix. In this configuration, culture periods of 4days are typically applicable. The aim of the present study was to modify conventional SCRH by applying an additional collagen overlay to prolong the hepatic phenotype in SCRH and thus to extend the applicability of the model. METHODS: The cultures receiving an extra top layer ('SCRH-plus' cultures) were compared with the conventional SCRH by testing the morphology, cell functionality, metabolic capacity and Mrp2-activity. RESULTS: In the SCRH-plus cultures…

Male0301 basic medicineGlucuronosyltransferaseCellular differentiationCellCell Culture TechniquesToxicologyExtracellular matrix03 medical and health sciencesBile canaliculiMethodsmedicineAnimalsBileGlucuronosyltransferaseRats WistarCells CulturedPharmacologybiologyCell DifferentiationMetabolismPhenotypeExtracellular MatrixRatsCell biologyPhenotype030104 developmental biologymedicine.anatomical_structureLiverBiochemistryCell cultureToxicityHepatocytesbiology.proteinHepatic drug dispositionCollagenSandwich-cultured hepatocytesJournal of Pharmacological and Toxicological Methods
researchProduct

Heterozygous HMGB1 loss-of-function variants are associated with developmental delay and microcephaly

2021

International audience; 13q12.3 microdeletion syndrome is a rare cause of syndromic intellectual disability. Identification and genetic characterization of patients with 13q12.3 microdeletion syndrome continues to expand the phenotypic spectrum associated with it. Previous studies identified four genes within the approximately 300 Kb minimal critical region including two candidate protein coding genes: KATNAL1 and HMGB1. To date, no patients carrying a sequence-level variant or a single gene deletion in HMGB1 or KATNAL1 have been described. Here we report six patients with loss-of-function variants involving HMGB1 and who had phenotypic features similar to the previously described 13q12.3 m…

Male0301 basic medicineHeterozygoteMicrocephalyAdolescentDNA Copy Number VariationsLanguage delay[SDV]Life Sciences [q-bio]KaryotypeInheritance Patternschemical and pharmacologic phenomena030105 genetics & heredityBiologydysmorphic featuresloss of function mutation03 medical and health sciencesExome SequencingIntellectual disabilityGeneticsmedicineHumansGenetic Predisposition to DiseaseHMGB1 ProteinChildGeneGenetic Association StudiesIn Situ Hybridization FluorescenceGenetics (clinical)Loss functionGeneticsHMGB1FaciesExonsdevelopmental disabilitiesMicrodeletion syndromemedicine.diseasePhenotypePhenotype030104 developmental biologyChild PreschoolMicrocephalyFemaleHaploinsufficiency
researchProduct

PD-1, PD-L1, and CD163 in pancreatic undifferentiated carcinoma with osteoclast-like giant cells: A expression patterns and clinical implications

2018

Undifferentiated carcinoma with osteoclast-like giant cells (UCOGC), a variant of pancreatic ductal adenocarcinoma (PDAC), has a striking genetic similarity to PDAC but a significantly improved overall survival. We hypothesize that this difference could be due to the immune response to the tumor, and as such, we investigated the expression of PD-1, PD-L1, and CD163 in a series of UCOGC. To this aim, 27 pancreatic UCOGCs (11 pure and 16 PDAC-associated), 5 extrapancreatic tumors with osteoclast-like giant cells and 10 pancreatic anaplastic carcinomas were immunostained using antibodies against PD-1, PD-L1, and CD163. In pancreatic UCOGCs, PD-L1 was expressed in neoplastic cells of 17 (63%) o…

Male0301 basic medicineIndianaProgrammed Cell Death 1 ReceptorOsteoclast; PDAC; Pancreatic Cancer; Tumor-Associated Macrophages; UCOGCOsteoclastsGiant CellsB7-H1 Antigen0302 clinical medicineTumor-Associated MacrophagesTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]LymphocytesAged 80 and overbiologyTumor-associated macrophagesCell DifferentiationMiddle AgedOsteoclast; Pancreatic cancer; PDAC; Tumor-associated macrophages; UCOGC; 2734ImmunohistochemistryEuropePhenotypemedicine.anatomical_structure030220 oncology & carcinogenesisOsteoclastFemaleAntibodyCarcinoma Pancreatic DuctalAdult2734Antigens Differentiation MyelomonocyticReceptors Cell SurfaceUCOGCPathology and Forensic MedicinePancreatic Cancer03 medical and health sciencesImmune systemAll institutes and research themes of the Radboud University Medical CenterAntigens CDOsteoclastPD-L1Pancreatic cancerBiomarkers TumormedicineHumansHistiocyteAgedNeoplasm StagingPDACHistiocytesPancreatic cancermedicine.diseasePancreatic Neoplasms030104 developmental biologyGiant cellCancer researchbiology.proteinCD163
researchProduct

Direct conversion of human fibroblast to hepatocytes using a single inducible polycistronic vector

2019

Abstract Background Human fibroblasts can be reprogrammed into induced hepatocyte-like cells through the expression of a set of transcription factors. Although the generation of induced hepatocyte-like cells by HNF4A, HNF1A, and FOXA3 expression has proven to be a robust experimental strategy, using multiple lentivirus results in a highly variable heterogeneous population. Methods We designed and implemented a novel approach based on the delivery of reprogramming factors and green fluorescent protein in a single doxycycline-inducible lentiviral vector using 2A self-cleaving peptides. Results Fibroblasts infected with the lentiviral vector can be amplified in basic fibroblast culture media i…

Male0301 basic medicineInducibleGenetic VectorsGreen Fluorescent ProteinsMedicine (miscellaneous)Biochemistry Genetics and Molecular Biology (miscellaneous)Cell LineViral vectorGreen fluorescent proteinlcsh:BiochemistryMice03 medical and health sciences0302 clinical medicinePolycistronic vectorsmedicineAnimalsHumanslcsh:QD415-436TransgenesFibroblastGeneTranscription factorlcsh:R5-920ChemistryResearchReprogrammingDermisCell BiologyFibroblastsCellular ReprogrammingCell biologyInduced hepatocyte-like cellsiHEPPhenotype030104 developmental biologymedicine.anatomical_structureGenes030220 oncology & carcinogenesisDoxycyclineHepatocytesMolecular MedicineFOXA3Stem celllcsh:Medicine (General)ReprogrammingStem Cell Research & Therapy
researchProduct

A novel mutation of WDR62 gene associated with severe phenotype including infantile spasm, microcephaly, and intellectual disability

2017

Abstract The autosomal recessive form of primary microcephaly (MCPH) is a rare disorder characterized by head circumference of at least 3 standard deviation below the mean. The MCPH exhibits genetic heterogeneity with thirteen loci (MCPH1-MCPH13) identified, and associated with variable degree of intellectual disability. It has been reported that WDR62 is the second causative gene of autosomal recessive microcephaly (MCPH2) playing a significant role in spindle formation and the proliferation of neuronal progenitor cells. We report a clinical feature, electroclinical findings, and clinical course of a patient with a severe phenotype of MCPH2 including microcephaly, refractory infantile spas…

Male0301 basic medicineMicrocephalyAdolescentMutation MissenseIntellectual disabilityCell Cycle ProteinsNerve Tissue ProteinsGenetic analysisReceptors G-Protein-CoupledConsanguinity03 medical and health sciences0302 clinical medicineDevelopmental NeuroscienceSettore M-PSI/08 - Psicologia ClinicaIntellectual disabilityHumansMedicineMissense mutationGeneWDR62GeneticsMCPHEpilepsybusiness.industryGenetic heterogeneityInfantGeneral MedicineInfantile Spasmmedicine.diseaseSettore MED/39 - Neuropsichiatria InfantilePedigreePhenotype030104 developmental biologyGPR56MutationPediatrics Perinatology and Child HealthMicrocephalyInfantile spasmNeurology (clinical)businessSpasms Infantile030217 neurology & neurosurgeryBrain and Development
researchProduct

Inheritance patterns of ATCCT repeat interruptions in spinocerebellar ataxia type 10 (SCA10) expansions

2017

Spinocerebellar ataxia type 10 (SCA10), an autosomal dominant cerebellar ataxia disorder, is caused by a non-coding ATTCT microsatellite repeat expansion in the ataxin 10 gene. In a subset of SCA10 families, the 5'-end of the repeat expansion contains a complex sequence of penta- and heptanucleotide interruption motifs which is followed by a pure tract of tandem ATCCT repeats of unknown length at its 3'-end. Intriguingly, expansions that carry these interruption motifs correlate with an epileptic seizure phenotype and are unstable despite the theory that interruptions are expected to stabilize expanded repeats. To examine the apparent contradiction of unstable, interruption-positive SCA10 e…

Male0301 basic medicineMolecular biologyInheritance Patternslcsh:MedicineGene ExpressionArtificial Gene Amplification and ExtensionPolymerase Chain ReactionDatabase and Informatics MethodsSequencing techniquesAutosomal dominant cerebellar ataxiaMedicine and Health SciencesDNA sequencinglcsh:ScienceGeneticsMovement DisordersMultidisciplinaryNeurodegenerative DiseasesGenomicsPedigreePhenotypeNeurologyMutation (genetic algorithm)Spinocerebellar ataxiaFemaleSequence AnalysisResearch ArticleBioinformaticsBiologyAtaxin-1003 medical and health sciencesSequence Motif AnalysisMicrosatellite RepeatGeneticsmedicineHumansSpinocerebellar AtaxiasRepeated SequencesAlleleAllelesSequence (medicine)EpilepsyBase SequenceBiology and life scienceslcsh:RDideoxy DNA sequencingGenetic Variationmedicine.diseaseResearch and analysis methodsMolecular biology techniques030104 developmental biologyTandem Repeat Sequence AnalysisAtaxinMutationlcsh:QAtaxiaTrinucleotide repeat expansionMicrosatellite RepeatsPLOS ONE
researchProduct

Incorporating Functional Genomic Information to Enhance Polygenic Signal and Identify Variants Involved in Gene-by-Environment Interaction for Young …

2018

BACKGROUND: Characterizing aggregate genetic risk for alcohol misuse and identifying variants involved in gene-by-environment (G × E) interaction effects has so far been a major challenge. We hypothesized that functional genomic information could be used to enhance detection of polygenic signal underlying alcohol misuse and to prioritize identification of single nucleotide polymorphisms (SNPs) most likely to exhibit G × E effects.METHODS: We examined these questions in the young adult FinnTwin12 sample (n = 1,170). We used genomewide association estimates from an independent sample to derive 2 types of polygenic scores for alcohol problems in FinnTwin12. Genomewide polygenic scores included…

Male0301 basic medicineMultifactorial InheritanceTwinsMedicine (miscellaneous)AlcoholToxicologyBioinformaticschemistry.chemical_compound0302 clinical medicineGene–environment interactionYoung adultta515FinlandGeneticsalcoholta3142GenomicsgenomiikkaPhenotypeAlcoholismPsychiatry and Mental health/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFemaleGenomic informationgeneettiset tekijätfunctional genomicsFunctional genomicsAdultympäristötekijätSingle-nucleotide polymorphismBiologyta3111Polymorphism Single NucleotideArticleYoung Adult03 medical and health sciencesSDG 3 - Good Health and Well-beingHumansGenetic Predisposition to Diseasenuoret aikuisetGenetic Variationalkoholiongelmatpolygenic scores030104 developmental biologychemistryGenomewide associationgene-environment interplayGene-Environment Interaction030217 neurology & neurosurgeryGenome-Wide Association StudyAlcoholism, Clinical and Experimental Research
researchProduct

Genome-wide associations for birth weight and correlations with adult disease

2016

Birth weight (BW) has been shown to be influenced by both fetal and maternal factors and in observational studies is reproducibly associated with future risk of adult metabolic diseases including type 2 diabetes (T2D) and cardiovascular disease. These life-course associations have often been attributed to the impact of an adverse early life environment. Here, we performed a multi-ancestry genome-wide association study (GWAS) meta-analysis of BW in 153,781 individuals, identifying 60 loci where fetal genotype was associated with BW (P < 5 × 10(-8)). Overall, approximately 15% of variance in BW was captured by assays of fetal genetic variation. Using genet…

Male0301 basic medicineNetherlands Twin Register (NTR)AgingDatasets as TopicPhysiologyBlood PressureGenome-wide association studyCoronary Artery DiseaseType 2 diabetesBioinformaticsCHARGE Consortium Hematology Working GroupCohort Studies0302 clinical medicineBirth WeightInsulinGlucose homeostasis030212 general & internal medicineeducation.field_of_studyMultidisciplinaryAnthropometry3. Good healthPhenotype/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFemaleGlycogenSignal TransductionAdulthypertensionGenotypeGeneral Science & TechnologyBirth weightintrauterine growthPopulationQuantitative trait locusBiologyArticlequantitative traitGenomic Imprinting03 medical and health sciencesFetusSDG 3 - Good Health and Well-beingEarly Growth Genetics (EGG) ConsortiumMD MultidisciplinaryGenetic variation/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_medicineHumansmetabolic disordersGenetic Predisposition to DiseaseeducationgenomeGenetic associationGenetic Variationbirth weightta3121Chromatin Assembly and Disassemblymedicine.diseaseta3123Glucose030104 developmental biologyDiabetes Mellitus Type 2Genetic Locigenome-wide association studiesadult diseaseGenome-Wide Association Study
researchProduct

Association of Common Polymorphisms in the Nicotinic Acetylcholine Receptor Alpha4 Subunit Gene with an Electrophysiological Endophenotype in a Large…

2016

PLoS one 11(4), e0152984 (2016). doi:10.1371/journal.pone.0152984

Male0301 basic medicineNicotinic Acetylcholine ReceptorsPhysiologyEvent-Related Potentialslcsh:MedicineReceptors NicotinicElectroencephalography600 Technik Medizin angewandte Wissenschaften::610 Medizin und GesundheitBiochemistryExonCognitionMathematical and Statistical Techniques0302 clinical medicineMedizinische FakultätGermanyMedicine and Health Scienceslcsh:ScienceCerebral CortexClinical NeurophysiologyGeneticsBrain MappingN100education.field_of_studyMultidisciplinarymedicine.diagnostic_testSmokingBrainElectroencephalographyTobacco Use DisorderTemporal LobeFrontal LobeElectrophysiologyNicotinic acetylcholine receptorBioassays and Physiological AnalysisBrain ElectrophysiologyPhysical SciencesRegression AnalysisFemaleAnatomyFunction and Dysfunction of the Nervous SystemStatistics (Mathematics)Research ArticleSignal TransductionAdultTransmembrane ReceptorsImaging TechniquesEndophenotypesCognitive NeurosciencePopulation610NeurophysiologyNeuroimagingSingle-nucleotide polymorphism-Linear Regression AnalysisBiologyResearch and Analysis MethodsPolymorphism Single Nucleotide03 medical and health sciencesDiagnostic MedicineEvent-related potentialReaction TimemedicineHumansddc:610Statistical MethodseducationElectrophysiological Techniqueslcsh:RBiology and Life SciencesProteinsCell BiologyElectrophysiological Phenomena030104 developmental biologyAcetylcholine ReceptorsEndophenotypeCognitive Sciencelcsh:QMathematics030217 neurology & neurosurgeryNeuroscience
researchProduct

Homozygous Familial Hypercholesterolemia in Spain Prevalence and Phenotype-Genotype Relationship

2016

Background— Homozygous familial hypercholesterolemia (HoFH) is a rare disease characterized by elevated plasma levels of low-density lipoprotein cholesterol (LDL-C) and extremely high risk of premature atherosclerotic cardiovascular disease. HoFH is caused by mutations in several genes, including LDL receptor ( LDLR ), apolipoprotein B ( APOB ), proprotein convertase subtilisin/kexin type 9 ( PCSK9 ), and LDL protein receptor adaptor 1 ( LDLRAP1 ). No epidemiological studies have assessed HoFH prevalence or the clinical and molecular characteristics of this condition. Here, we aimed to characterize HoFH in Spain. Methods and Results— Data were collected from the Spanish Dyslipidemia Regist…

Male0301 basic medicineOncologyLdl receptor geneApolipoprotein BLipid-lowering therapyFamilial hypercholesterolemia030204 cardiovascular system & hematologyCompound heterozygosity0302 clinical medicineAutosomal-dominant hypercholesterolemiaRisk FactorsEpidemiologyPrevalenceDiseaseRegistriesGenetics (clinical)Molecular EpidemiologybiologyhypercholesterolemiaHomozygoteDouble-blindMiddle AgedPhenotypeCardiovascular DiseasesApolipoprotein B-100allelesFemalelipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineMutationsAdultGenetic MarkersHeterozygotemedicine.medical_specialtyInhibitorAdolescentPlacebo-controlled trialHyperlipoproteinemia Type IIlipidsYoung Adult03 medical and health sciencesInternal medicineGeneticsmedicineHumansGenetic Predisposition to DiseaseAlleleAdaptor Proteins Signal TransducingRecessive hypercholesterolemiaPCSK9registriesCholesterol LDLApolipoprotein-bmedicine.disease030104 developmental biologyEndocrinologyReceptors LDLSpainMutationLDL receptorbiology.proteinmutationDyslipidemia
researchProduct