Search results for "Phenotype"

showing 10 items of 1875 documents

Clinical and biochemical characteristics of individuals with low cholesterol syndromes: A comparison between familial hypobetalipoproteinemia and fam…

2017

Background The most frequent monogenic causes of low plasma cholesterol are familial hypobetalipoproteinemia (FHBL1) because of truncating mutations in apolipoprotein B coding gene (APOB) and familial combined hypolipidemia (FHBL2) due to loss-of-function mutations in ANGPTL3 gene. Objective A direct comparison of lipid phenotypes of these 2 conditions has never been carried out. In addition, although an increased prevalence of liver steatosis in FHBL1 has been consistently reported, the hepatic consequences of FHBL2 are not well established. Methods We investigated 350 subjects, 67 heterozygous carriers of APOB mutations, 63 carriers of the p.S17* mutation in ANGPTL3 (57 heterozygotes and …

0301 basic medicineMaleHepatic steatosisSettore MED/09 - Medicina InternaApolipoprotein BEndocrinology Diabetes and Metabolism030204 cardiovascular system & hematologymedicine.disease_causeANGPTL3 gene; APOB gene; Familial combined hypolipidemia; Familial hypobetalipoproteinemia; HDL cholesterol; Hepatic steatosis; Low cholesterol syndromesHypobetalipoproteinemiasExon0302 clinical medicineHDL cholesterolANGPTL3Nutrition and DieteticFamilial hypobetalipoproteinemiaGeneticsMutationNutrition and Dieteticsbiologyhepatic steatosisHomozygoteANGPTL3 geneMiddle AgedLow cholesterol syndromesPhenotypePhenotypelipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineANGPTL3 gene; APOB gene; familial combined hypolipidemia; familial hypobetalipoproteinemia; HDL cholesterol; hepatic steatosis; low cholesterol syndromesmedicine.medical_specialtyHeterozygoteLow cholesterol syndromeHepatic steatosi03 medical and health sciencesInternal medicineInternal MedicinemedicineHumansAPOB geneFamilial combined hypolipidemiaGeneAgedAngiopoietin-Like Protein 3Apolipoproteins Bbusiness.industryHeterozygote advantagemedicine.disease030104 developmental biologyEndocrinologyAngiopoietin-like ProteinsMutationbiology.proteinlow cholesterol syndromesSteatosisbusiness
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Functional Interactions between Gut Microbiota Transplantation, Quercetin, and High-Fat Diet Determine Non-Alcoholic Fatty Liver Disease Development …

2019

Scope Modulation of intestinal microbiota has emerged as a new therapeutic approach for non-alcoholic fatty liver disease (NAFLD). Herein, it is addressed whether gut microbiota modulation by quercetin and intestinal microbiota transplantation can influence NAFLD development. Methods and results Gut microbiota donor mice are selected according to their response to high-fat diet (HFD) and quercetin in terms of obesity and NAFLD-related biomarkers. Germ-free recipients displayed metabolic phenotypic differences derived from interactions between microbiota transplanted, diets, and quercetin. Based on the evaluation of hallmark characteristics of NAFLD, it is found that gut microbiota transplan…

0301 basic medicineMaleInflammasomesmedicine.medical_treatmentBiologyGut floraDiet High-Fatdigestive system03 medical and health scienceschemistry.chemical_compoundVerrucomicrobiaNon-alcoholic Fatty Liver DiseasemedicineAnimalsObesity030109 nutrition & dieteticsPrebioticdigestive oral and skin physiologyFatty livernutritional and metabolic diseasesAkkermansiaFecal Microbiota Transplantationbiology.organism_classificationmedicine.diseaseFatty Acids VolatileObesityPhenotypedigestive system diseasesEndotoxemiaGastrointestinal MicrobiomeTransplantationMice Inbred C57BL030104 developmental biologychemistryLiverImmunologyQuercetinInsulin ResistanceQuercetinFood ScienceBiotechnologyMolecular nutritionfood research
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The oculoauriculofrontonasal syndrome: Further clinical characterization and additional evidence suggesting a nontraditional mode of inheritance

2018

IF 2.264; International audience; The oculoauriculofrontonasal syndrome (OAFNS) is a rare disorder characterized by the association of frontonasal dysplasia (widely spaced eyes, facial cleft, and nose abnormalities) and oculo-auriculo-vertebral spectrum (OAVS)-associated features, such as preauricular ear tags, ear dysplasia, mandibular asymmetry, epibulbar dermoids, eyelid coloboma, and costovertebral anomalies. The etiology is unknown so far. This work aimed to identify molecular bases for the OAFNS. Among a cohort of 130 patients with frontonasal dysplasia, accurate phenotyping identified 18 individuals with OAFNS. We describe their clinical spectrum, including the report of new features…

0301 basic medicineMaleInheritance Patterns030105 genetics & heredityfrontonasal dysplasiawhole exome sequencingCraniofacial Abnormalities0302 clinical medicinePolymicrogyriaEye AbnormalitiesEar External10. No inequalityChildGenetics (clinical)Exome sequencingwhole genome sequencingThyroid agenesisHypoplasiaDNA-Binding ProteinsPhenotypeChild PreschoolFemaleRespiratory System Abnormalitiesmedicine.medical_specialtyAdolescentQuantitative Trait LociOculoauriculofrontonasal syndrome03 medical and health sciencesExome SequencingGeneticsmedicineHumansGenetic Predisposition to DiseaseFrontonasal dysplasiaGenetic Association StudiesWhole genome sequencingHomeodomain Proteinsbusiness.industryFacial cleftSkullInfant NewbornFaciesInfant030206 dentistrymedicine.diseaseDermatologySpine[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsDysplasiabusinessTomography Spiral ComputedTranscription Factors
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De Novo and Inherited Pathogenic Variants in KDM3B Cause Intellectual Disability, Short Stature, and Facial Dysmorphism

2019

Contains fulltext : 202646.pdf (Publisher’s version ) (Open Access) By using exome sequencing and a gene matching approach, we identified de novo and inherited pathogenic variants in KDM3B in 14 unrelated individuals and three affected parents with varying degrees of intellectual disability (ID) or developmental delay (DD) and short stature. The individuals share additional phenotypic features that include feeding difficulties in infancy, joint hypermobility, and characteristic facial features such as a wide mouth, a pointed chin, long ears, and a low columella. Notably, two individuals developed cancer, acute myeloid leukemia and Hodgkin lymphoma, in childhood. KDM3B encodes for a histone …

0301 basic medicineMaleJumonji Domain-Containing Histone DemethylasesDevelopmental DisabilitiesWEAVER SYNDROMEPROTEINHaploinsufficiencyCraniofacial AbnormalitiesHistones0302 clinical medicineIntellectual disabilityTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]Missense mutationDEMETHYLASE KDM3BExomeChildGenetics (clinical)Exome sequencingGeneticsRUBINSTEIN-TAYBI SYNDROMEMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]Phenotype030220 oncology & carcinogenesisFemalemedicine.symptomHaploinsufficiencyRare cancers Radboud Institute for Health Sciences [Radboudumc 9]Joint hypermobilityGENETICSJMJD1CMutation MissenseDwarfismBiologyShort statureKdm3b ; Cancer Predisposition ; Developmental Delay ; Facial Recognition ; Intellectual Disability ; Leukemia ; Lymphoma ; Short Stature03 medical and health sciencesReportIntellectual DisabilitymedicineHumansMYELOID-LEUKEMIAGenetic Association StudiesGerm-Line MutationWeaver syndromeNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Rubinstein–Taybi syndromeMUTATIONSDELETIONGenetic Variationmedicine.diseaseBody HeightMusculoskeletal AbnormalitiesINDIVIDUALS030104 developmental biologyFaceNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]American Journal of Human Genetics
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Increased PD-1 Expression and Altered T Cell Repertoire Diversity Predict Mortality in Patients with Septic Shock: A Preliminary Study

2017

Sepsis causes impairment of innate and adaptive immunity by multiple mechanisms, including depletion of immune effector cells and T cell exhaustion. Although lymphocyte dysfunction is associated with increased mortality and potential reactivation of latent viral infection in patients with septic shock, the relation between viral reactivation and lymphocyte dysfunction is obscure. The objectives of this study were 1) to determine the relation of lymphocyte dysfunction to viral reactivation and mortality, and 2) to evaluate recovery of lymphocyte function during septic shock, including T cell receptor (TCR) diversity and the expression of programmed death 1 (PD-1). In 18 patients with septic …

0301 basic medicineMaleLymphocyteReceptor expressionProgrammed Cell Death 1 Receptorlcsh:MedicineCytomegalovirusGene ExpressionArtificial Gene Amplification and ExtensionPathology and Laboratory MedicineImmune ReceptorsBiochemistryPolymerase Chain ReactionMonocytesWhite Blood Cells0302 clinical medicineSpectrum Analysis TechniquesAnimal CellsT-Lymphocyte SubsetsMedicine and Health SciencesLymphocyteslcsh:ScienceAged 80 and overMultidisciplinaryImmune System ProteinsT CellsMiddle AgedAcquired immune systemFlow CytometryPrognosisShock Septicmedicine.anatomical_structurePhenotypeSpectrophotometryShock (circulatory)Cytomegalovirus InfectionsFemaleCytophotometrymedicine.symptomCellular TypesResearch ArticleSignal TransductionT cellImmune CellsImmunologyReceptors Antigen T-CellBiologyResearch and Analysis MethodsMicrobiologyImmunophenotypingSepsis03 medical and health sciencesImmune systemSigns and SymptomsDiagnostic MedicineSepsisVirologymedicineHumansMolecular Biology TechniquesMolecular BiologyAgedBlood CellsSeptic shocklcsh:RBiology and Life SciencesProteins030208 emergency & critical care medicineCell BiologyHLA-DR Antigensmedicine.diseaseViral ReplicationT Cell Receptors030104 developmental biologyCase-Control StudiesImmunologylcsh:QBiomarkersPLoS ONE
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Dominant variants in the splicing factor PUF60 cause a recognizable syndrome with intellectual disability, heart defects and short stature

2016

Item does not contain fulltext Verheij syndrome, also called 8q24.3 microdeletion syndrome, is a rare condition characterized by ante- and postnatal growth retardation, microcephaly, vertebral anomalies, joint laxity/dislocation, developmental delay (DD), cardiac and renal defects and dysmorphic features. Recently, PUF60 (Poly-U Binding Splicing Factor 60 kDa), which encodes a component of the spliceosome, has been discussed as the best candidate gene for the Verheij syndrome phenotype, regarding the cardiac and short stature phenotype. To date, only one patient has been reported with a de novo variant in PUF60 that probably affects function (c.505C>T leading to p.(His169Tyr)) associated wi…

0301 basic medicineMaleMESH: Heart Defects Congenital / physiopathologyMicrocephalyPathologyMESH: Heart Defects Congenital / geneticsMESH: Exome / genetics030105 genetics & heredityMESH: RNA Splicing / geneticsMicrophthalmia[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesMESH: ChildExomeMESH: RNA Splicing Factors / geneticsChildFrameshift MutationMESH: High-Throughput Nucleotide SequencingGenetics (clinical)Exome sequencingColobomaMESH: Frameshift MutationHigh-Throughput Nucleotide SequencingMicrodeletion syndromeMicrocephaly Verheij syndrome PUF60ChemistryPhenotypeChild PreschoolDISEASESMicrocephalyMedical geneticsFemaleRNA Splicing Factorsmedicine.symptomChromosome DeletionChromosomes Human Pair 8MESH: Dwarfism / genetics*Heart Defects Congenitalmedicine.medical_specialtyGENESAdolescentRNA SplicingMESH: Chromosome DeletionDwarfismBiologyMESH: PhenotypeShort statureArticlePUF6003 medical and health sciencesInternal medicineIntellectual Disability[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineHumansCraniofacialBiologyMESH: AdolescentNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]MESH: HumansMESH: Child Preschoolmedicine.diseaseMESH: Repressor Proteins / geneticsMESH: MaleRepressor Proteins030104 developmental biologyEndocrinologyMESH: Chromosomes Human Pair 8 / geneticsMESH: Dwarfism / physiopathologyMESH: Intellectual Disability / physiopathologyHuman medicineMESH: Intellectual Disability / geneticsVerheij syndromeMESH: Female[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Mutation-specific pathophysiological mechanisms define different neurodevelopmental disorders associated with SATB1 dysfunction

2021

AbstractWhereas large-scale statistical analyses can robustly identify disease-gene relationships, they do not accurately capture genotype-phenotype correlations or disease mechanisms. We use multiple lines of independent evidence to show that different variant types in a single gene,SATB1, cause clinically overlapping but distinct neurodevelopmental disorders. Clinical evaluation of 42 individuals carryingSATB1variants identified overt genotype-phenotype relationships, associated with different pathophysiological mechanisms, established by functional assays. Missense variants in the CUT1 and CUT2 DNA-binding domains result in stronger chromatin binding, increased transcriptional repression…

0301 basic medicineMaleModels MolecularMISSENSE MUTATIONSCHROMATINTranscription GeneticCellMedizinDiseaseHaploinsufficiencymedicine.disease_cause0302 clinical medicineMissense mutationde novo variantsGenetics (clinical)INTERLEUKIN-2seizuresGenetics0303 health sciencesMutationChromatin bindingneurodevelopmental disordersMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]SATB1Phenotypemedicine.anatomical_structureintellectual disabilityFemaleHaploinsufficiencyteeth abnormalitiesProtein BindingNeuroinformaticsEXPRESSIONGENESMutation MissenseBiologyBINDING PROTEINREGION03 medical and health sciencesSATB1Protein DomainsReportGeneticsmedicineHPO-based analysisHumansGenetic Association StudiesHpo-based Analysis ; Satb1 ; Cell-based Functional Assays ; De Novo Variants ; Intellectual Disability ; Neurodevelopmental Disorders ; Seizures ; Teeth Abnormalities030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Matrix Attachment Region Binding Proteins030104 developmental biologyNeurodevelopmental DisordersMutationNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]030217 neurology & neurosurgerycell-based functional assays
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Expanding the Phenotype Associated with NAA10-Related N-Terminal Acetylation Deficiency

2016

International audience; N-terminal acetylation is a common protein modification in eukaryotes associated with numerous cellular processes. Inherited mutations in NAA10, encoding the catalytic subunit of the major N-terminal acetylation complex NatA have been associated with diverse, syndromic X-linked recessive disorders, whereas de novo missense mutations have been reported in one male and one female individual with severe intellectual disability but otherwise unspecific phenotypes. Thus, the full genetic and clinical spectrum of NAA10 deficiency is yet to be delineated. We identified three different novel and one known missense mutation in NAA10, de novo in 11 females, and due to maternal…

0301 basic medicineMaleModels MolecularMicrocephalyMutation MissenseBiologyGermlineKEY WORDS: NAA1003 medical and health sciencesGermline mutationGenes X-LinkedIntellectual disabilityGeneticsmedicineMissense mutationHumansGenetic Predisposition to DiseaseN-Terminal Acetyltransferase EGenetics (clinical)Genetic Association StudiesGerm-Line MutationN-Terminal Acetyltransferase AResearch ArticlesGeneticsX-linked[SDV.GEN]Life Sciences [q-bio]/GeneticsRegional Council of BurgundyMosaicismN-terminal acetylationAcetylationmedicine.diseasePhenotypePedigreeOgden SyndromeX‐linked030104 developmental biologyNAA10intellectual disabilityN‐terminal acetylationContract grant sponsors: Dijon University HospitalFemale[ SDV.GEN ] Life Sciences [q-bio]/GeneticsNAA15Research ArticleHuman Mutation
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Characterization of the Clinical and Immunologic Phenotype and Management of 157 Individuals with 56 Distinct Heterozygous NFKB1 Mutations

2020

Contains fulltext : 229571.pdf (Publisher’s version ) (Closed access) BACKGROUND: An increasing number of NFKB1 variants are being identified in patients with heterogeneous immunologic phenotypes. OBJECTIVE: To characterize the clinical and cellular phenotype as well as the management of patients with heterozygous NFKB1 mutations. METHODS: In a worldwide collaborative effort, we evaluated 231 individuals harboring 105 distinct heterozygous NFKB1 variants. To provide evidence for pathogenicity, each variant was assessed in silico; in addition, 32 variants were assessed by functional in vitro testing of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) signaling. RESU…

0301 basic medicineMaleNF-KAPPA-BMedizinlnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Fluorescent Antibody TechniqueAutoimmunityDiseaseNUCLEAR-FACTORKaplan-Meier Estimatemedicine.disease_causeHypogammaglobulinemia0302 clinical medicineNFKB1 variants and mutations; autosomal dominant inheritance; common variable immunodeficiency; reduced penetrance; variable expressivityHDE PEDImmunology and Allergyvariants and mutationsNF-κB1-related phenotypeImmunodeficiencyIMMUNODEFICIENCY*NF-?B1-related phenotypeNFKB1 variants and mutations1184 Genetics developmental biology physiologycommon variable immunodeficiencyDisease ManagementMiddle AgedNF-kappa B1-related phenotypereduced penetrancePrognosisPenetranceImmunohistochemistryMagnetic Resonance Imaging3. Good healthPhenotypeNFKB1 variant*NFKB1 variant*common variable immunodeficiencyFemaleHaploinsufficiency*reduced penetranceNFKB1 mutationAdultHeterozygote*NFKB1 mutationImmunologyHAPLOINSUFFICIENCYArticle03 medical and health sciencesvariable expressivityautosomal dominantmedicineHumansGenetic Predisposition to DiseaseGenetic Association StudiesAgedbusiness.industryCommon variable immunodeficiencyNF-kappa B p50 SubunitNF-KAPPA-B1Immune dysregulationmedicine.diseaseautosomal dominant inheritance030104 developmental biologyBiological Variation PopulationImmunologyCELLSMutation*autosomal dominantPrimary immunodeficiency3111 BiomedicinebusinessTomography X-Ray ComputedBiomarkers030215 immunology
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Maternal Inheritance of a Recessive RBP4 Defect in Canine Congenital Eye Disease

2018

SUMMARY Maternally skewed transmission of traits has been associated with genomic imprinting and oocyte-derived mRNA. We report canine congenital eye malformations, caused by an amino acid deletion (K12del) near the N terminus of retinol-binding protein (RBP4). The disease is only expressed when both dam and offspring are deletion homozygotes. RBP carries vitamin A (retinol) from hepatic stores to peripheral tissues, including the placenta and developing eye, where it is required to synthesize retinoic acid. Gestational vitamin A deficiency is a known risk factor for ocular birth defects. The K12del mutation disrupts RBP folding in vivo, decreasing its secretion from hepatocytes to serum. T…

0301 basic medicineMaleNon-Mendelian inheritanceProtein Foldingcongenital eye defectEye Diseasesgenetic structuresNATIVE DISULFIDE BONDSMedical PhysiologyRetinoic acidReproductive health and childbirth413 Veterinary scienceMicrophthalmiavitamin Achemistry.chemical_compoundPlasmaA-vitamiini2.1 Biological and endogenous factorsMicrophthalmosPrealbuminCRYSTAL-STRUCTUREAetiologyBase Pairinglcsh:QH301-705.5Sequence DeletionPediatricwhole genome sequencingVITAMIN-A-DEFICIENCYANOPHTHALMIAPenetrancePedigreemedicine.anatomical_structurePhenotypeFemalemedicine.medical_specialtyGenotypeENDOPLASMIC-RETICULUMGenes RecessiveMETABOLISMBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesDogscanine geneticsInternal medicinePlacentaRETINOL-BINDING-PROTEINGeneticsmedicineAnimalsHumansRecessiveMALFORMATIONSBIOCHEMICAL BASISAmino Acid SequenceAlleleEye Disease and Disorders of VisionNutritiongenome-wide association study030102 biochemistry & molecular biologywestern blottingMUTATIONSta1184RBP4maternal inheritancemedicine.diseaseRetinol-Binding ProteinsRetinol binding proteinnuclear magnetic resonance030104 developmental biologyEndocrinologychemistryGeneslcsh:Biology (General)microphthalmiaGenetic LociHela Cells1182 Biochemistry cell and molecular biologyCongenital Structural Anomalies3111 BiomedicineBiochemistry and Cell BiologyDigestive DiseasesGenomic imprintingRetinol-Binding Proteins PlasmaHeLa Cells
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