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showing 10 items of 10618 documents

Benign nocturnal alternating hemiplegia of childhood

2018

Objective: To describe the clinical spectrum of benign nocturnal alternating hemiplegia of childhood (BNAHC) including long-term follow-up data of previously published cases and to propose an underlying genetic cause of this disorder. Methods: We studied the medical data of two novel patients, reviewed the literature on BNAHC, and gathered information of the most recent follow-up of published cases regarding the course of episodes, further development, attempted drugs, ancillary investigations, and sequelae. Results: All patients, i.e. two novel cases and twelve patients identified in the literature (13 boys, 1 girl, age at onset four months to three years), experienced episodes of hemipleg…

0301 basic medicineMaleExome sequencingPediatricsmedicine.medical_specialtyHeterozygoteHemiplegiaNerve Tissue ProteinsPATIENTSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]03 medical and health sciences0302 clinical medicinePRRT2 MUTATIONSmedicineHumansIctalPAROXYSMAL KINESIGENIC DYSKINESIAFamily historyPRRT2 geneExome sequencingCryingbusiness.industryAlternating hemiplegia of childhoodInfantMembrane ProteinsGeneral MedicineParoxysmal dyskinesiamedicine.diseaseDisorders of movement Donders Center for Medical Neuroscience [Radboudumc 3]GENESleep deprivation030104 developmental biologyPhenotypeTreatment OutcomeSYNAPTIC-TRANSMISSIONMigraineMIGRAINEChild PreschoolPediatrics Perinatology and Child HealthDisease ProgressionNeurology (clinical)medicine.symptombusinessINFANTILE CONVULSIONS030217 neurology & neurosurgeryGene DeletionBenign nocturnal alternating hemiplegia of childhoodEuropean Journal of Paediatric Neurology
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The Commensal Microbiota Enhances ADP-Triggered Integrin αIIbβ3 Activation and von Willebrand Factor-Mediated Platelet Deposition to Type I Collagen

2020

The commensal microbiota is a recognized enhancer of arterial thrombus growth. While several studies have demonstrated the prothrombotic role of the gut microbiota, the molecular mechanisms promoting arterial thrombus growth are still under debate. Here, we demonstrate that germ-free (GF) mice, which from birth lack colonization with a gut microbiota, show diminished static deposition of washed platelets to type I collagen compared with their conventionally raised (CONV-R) counterparts. Flow cytometry experiments revealed that platelets from GF mice show diminished activation of the integrin αIIbβ3 (glycoprotein IIbIIIa) when activated by the platelet agonist adenosine diphosphate (ADP). Fu…

0301 basic medicineMaleGene Expression030204 cardiovascular system & hematologyvon Willebrand factorlcsh:Chemistrychemistry.chemical_compoundMice0302 clinical medicinePlateletToll-like receptor-2lcsh:QH301-705.5SpectroscopyMice KnockoutbiologyChemistryBrief ReportαIIbβ3General MedicineArteriesComputer Science ApplicationsCell biologyAdenosine DiphosphatePlatelet Glycoprotein GPIb-IX Complexgerm-freeplateletsFemaleType I collagenBlood PlateletsIntegrinPrimary Cell CulturePlatelet Glycoprotein GPIIb-IIIa ComplexCatalysisCollagen Type IInorganic Chemistry03 medical and health sciencesVon Willebrand factormedicineCell AdhesionmicrobiotaAnimalsGerm-Free LifeHumansPhysical and Theoretical ChemistryThrombusSymbiosisMolecular Biologyα<sub>IIb</sub>β<sub>3</sub>Innate immune systemOrganic ChemistryThrombosismedicine.diseaseImmunity InnateToll-Like Receptor 2Gastrointestinal MicrobiomeMice Inbred C57BLAdenosine diphosphateTLR2030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinInternational Journal of Molecular Sciences
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Retrotransposon insertions can initiate colorectal cancer and are associated with poor survival

2019

Genomic instability pathways in colorectal cancer (CRC) have been extensively studied, but the role of retrotransposition in colorectal carcinogenesis remains poorly understood. Although retrotransposons are usually repressed, they become active in several human cancers, in particular those of the gastrointestinal tract. Here we characterize retrotransposon insertions in 202 colorectal tumor whole genomes and investigate their associations with molecular and clinical characteristics. We find highly variable retrotransposon activity among tumors and identify recurrent insertions in 15 known cancer genes. In approximately 1% of the cases we identify insertions in APC, likely to be tumor-initi…

0301 basic medicineMaleGenome instabilityMICROSATELLITE INSTABILITYHYPOMETHYLATIONCarcinogenesisColorectal cancergenetic processestransposonitGeneral Physics and AstronomyRetrotransposon02 engineering and technologyKaplan-Meier EstimateGenome0302 clinical medicineCancer genomicslcsh:ScienceGenetics0303 health sciencesGastrointestinal tractMultidisciplinaryQISLAND METHYLATOR PHENOTYPEGastroenterologyfood and beveragesgenomiikkaMiddle Aged021001 nanoscience & nanotechnology3. Good healthGene Expression Regulation NeoplasticCpG sitesyöpägeenit030220 oncology & carcinogenesisDNA methylationAllelic ImbalanceWHOLE-GENOMEFemaleSVA ELEMENTS0210 nano-technologyColorectal NeoplasmsScience3122 Cancersinformation scienceGenomicssuolistosyövätBiologyGeneral Biochemistry Genetics and Molecular BiologyArticleGenomic Instability03 medical and health sciencesCell Line TumormedicineHumansAged030304 developmental biologySOMATIC L1 RETROTRANSPOSITIONCpG Island Methylator PhenotypeGene Expression ProfilingfungiMicrosatellite instabilityGeneral ChemistryDNA Methylationmedicine.diseaseGENEMutagenesis Insertional030104 developmental biologyLong Interspersed Nucleotide ElementsCPGhealth occupationsCancer researchlcsh:QCpG Islands3111 BiomedicineCaco-2 Cells
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IQSEC2-related encephalopathy in males and females: a comparative study including 37 novel patients.

2019

Variants in IQSEC2, escaping X inactivation, cause X-linked intellectual disability with frequent epilepsy in males and females. We aimed to investigate sex-specific differences.

0301 basic medicineMaleGénétique clinique[SDV]Life Sciences [q-bio]MedizinPhysiology030105 genetics & hereditySeizures/epidemiologyEpilepsyBrain Diseases/epidemiologyX-linked inheritanceIntellectual disabilityGuanine Nucleotide Exchange FactorsProtein IsoformsMissense mutationGenetics(clinical)10. No inequalityNon-U.S. Gov'tGenetics (clinical)X-linked recessive inheritanceComputingMilieux_MISCELLANEOUSBrain DiseasesSex CharacteristicsResearch Support Non-U.S. Gov'tBrainSciences bio-médicales et agricoles3. Good healthPedigreePhenotypeintellectual disabilityFemaleBrain/growth & developmentSex characteristicsGénétique moléculaireGuanine Nucleotide Exchange Factors/geneticsEncephalopathyResearch SupportX-inactivationArticle03 medical and health sciencesSeizuresProtein Isoforms/geneticsmedicineJournal ArticleIQSEC2HumansIntellectual Disability/epidemiology[SDV.GEN]Life Sciences [q-bio]/Geneticsbusiness.industryInfant NewbornisoformsCorrectionInfantmedicine.diseaseNewbornHuman genetics030104 developmental biologyMutationepilepsyHuman medicinebusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Interferon-γ-Driven iNOS: A Molecular Pathway to Terminal Shock in Arenavirus Hemorrhagic Fever

2017

Arenaviruses such as Lassa virus (LASV) cause hemorrhagic fever. Terminal shock is associated with a systemic cytokine storm, but the mechanisms are ill defined. Here we used HLA-A2-expressing mice infected with a monkey-pathogenic strain of lymphocytic choriomeningitis virus (LCMV-WE), a close relative of LASV, to investigate the pathophysiology of arenavirus hemorrhagic fever (AHF). AHF manifested as pleural effusions, edematous skin swelling, and serum albumin loss, culminating in hypovolemic shock. A characteristic cytokine storm included numerous pro-inflammatory cytokines and nitric oxide (NO) metabolites. Edema formation and terminal shock were abrogated in mice lacking inducible nit…

0301 basic medicineMaleHemorrhagic Fevers ViralNitric Oxide Synthase Type IIBiologyLymphocytic Choriomeningitisddc:616.07Lymphocytic choriomeningitismedicine.disease_causeNitric OxideMicrobiologyViral hemorrhagic fever03 medical and health sciencesInterferon-gammaMice0302 clinical medicineVirologymedicineAnimalsHumansLymphocytic choriomeningitis virusLassa feverArenavirusddc:617medicine.diseasebiology.organism_classification3. Good healthNitric oxide synthaseMice Inbred C57BLDisease Models Animal030104 developmental biologyLassa virus030220 oncology & carcinogenesisShock (circulatory)Immunologybiology.proteinParasitologyFemalemedicine.symptomCytokine storm
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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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Expression quantitative trait loci for PAX8 contributes to the prognosis of hepatocellular carcinoma

2017

Paired-box family member PAX8 encodes a transcription factor that has a role in cell differentiation and cell growth and may participate in the prognosis of hepatocellular carcinoma (HCC). By bioinformatics analysis, we identified several single nucleotide polymorphisms (SNPs) within a newly identified long non-coding RNA (lncRNA) AC016683.6 as expression quantitative trait loci (eQTLs) for PAX8. Hence, we hypothesized that PAX8eQTLs in lncRNA AC016683.6 may influence the HCC prognosis. We then performed a case-only study to assess the association between the two SNPs as well as the prognosis of HCC in 331 HBV-positive HCC patients without surgical treatment. Cox proportional hazard models …

0301 basic medicineMaleHeredityPaired BoxCancer Treatmentlcsh:MedicineBiochemistry0302 clinical medicineMathematical and Statistical TechniquesMedicine and Health Scienceslcsh:ScienceMultidisciplinaryPharmaceuticsLiver DiseasesLiver NeoplasmsMiddle AgedPrognosisNucleic acidsSurvival RateGenetic MappingOncology030220 oncology & carcinogenesisHepatocellular carcinomaPhysical SciencesRegression AnalysisFemaleLiver cancerStatistics (Mathematics)Research ArticleCarcinoma HepatocellularGenotypeQuantitative Trait LociSingle-nucleotide polymorphismVariant GenotypesGastroenterology and HepatologyResearch and Analysis MethodsCarcinomasPolymorphism Single Nucleotide03 medical and health sciencesPAX8 Transcription FactorProtein DomainsDrug TherapyDiagnostic MedicineGastrointestinal TumorsCarcinomamedicineGeneticsChemotherapyHumansGenetic Predisposition to DiseaseAlleleStatistical MethodsNon-coding RNASurvival rateSurvival analysisAllelesbusiness.industrylcsh:RCancers and NeoplasmsBiology and Life SciencesProteinsHepatocellular Carcinomamedicine.disease030104 developmental biologyExpression quantitative trait lociCancer researchLong non-coding RNAsRNAlcsh:QbusinessMathematicsPLoS ONE
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Generation of a disease-specific iPS cell line derived from a patient with Charcot-Marie-Tooth type 2K lacking functional GDAP1 gene

2016

Human CMT2-FiPS4F1 cell line was generated from fibroblasts of a patient with Charcot-Marie-Tooth disease harbouring the following mutations in the GDAP1 gene in heterozygosis: p.Q163X/p.T288NfsX3. This patient did not present mutations in the PM22, MPZ or GJB genes. Human reprogramming factors OCT3/4, KLF4, SOX2 and C-MYC were delivered using a non-integrative methodology that involves the use of Sendai virus.

0301 basic medicineMaleHeterozygoteCellular differentiationCèl·lulesDNA Mutational AnalysisGenetic VectorsInduced Pluripotent Stem CellsKaryotypeNerve Tissue ProteinsBiologyPolymorphism Single NucleotideSendai virusCell Line03 medical and health sciencesKruppel-Like Factor 4stomatognathic systemCharcot-Marie-Tooth DiseaseHumansInduced pluripotent stem cellGeneTranscription factorMedicine(all)GeneticsBase SequenceHeterozygote advantageCell DifferentiationCell BiologyGeneral MedicineFibroblastsbiology.organism_classificationCellular ReprogrammingSendai virus030104 developmental biologyMicroscopy FluorescenceKLF4embryonic structuresSistema nerviós MalaltiesReprogrammingDevelopmental BiologyTranscription Factors
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The Effect of a Novel c.820C>T (Arg274Trp) Mutation in the Mitofusin 2 Gene on Fibroblast Metabolism and Clinical Manifestation in a Patient

2017

Charcot-Marie-Tooth disease type 2A (CMT2A) is an autosomal dominant axonal peripheral neuropathy caused by mutations in the mitofusin 2 gene (MFN2). Mitofusin 2 is a GTPase protein present in the outer mitochondrial membrane and responsible for regulation of mitochondrial network architecture via the fusion of mitochondria. As that fusion process is known to be strongly dependent on the GTPase activity of mitofusin 2, it is postulated that the MFN2 mutation within the GTPase domain may lead to impaired GTPase activity, and in turn to mitochondrial dysfunction. The work described here has therefore sought to verify the effects of MFN2 mutation within its GTPase domain on mitochondrial and e…

0301 basic medicineMaleHydrolasesMutantMFN2lcsh:MedicineGTPaseMitochondrionmedicine.disease_causeEndoplasmic ReticulumBiochemistryGTP Phosphohydrolases0302 clinical medicineMental RetardationAnimal CellsCharcot-Marie-Tooth DiseaseMedicine and Health SciencesMissense mutationlcsh:ScienceEnergy-Producing OrganellesCells CulturedConnective Tissue CellsGeneticsMutationMultidisciplinarySecretory PathwayOrganic CompoundsMonosaccharidesTryptophanMitochondrial DNACell biologyMitochondriaEnzymesNucleic acidsChemistryNeurologyConnective TissueCell ProcessesPhysical SciencesCellular Structures and OrganellesCellular TypesAnatomyResearch ArticleForms of DNACarbohydratesMutation MissenseBiologyBioenergeticsArgininePolymorphism Single NucleotideMitochondrial Proteins03 medical and health sciencesMitofusin-2Young AdultmedicineGeneticsHumansEndoplasmic reticulumlcsh:ROrganic ChemistryChemical CompoundsBiology and Life SciencesProteinsCell BiologyDNAFibroblastsGuanosine Triphosphatase030104 developmental biologyBiological TissueGlucoseAmino Acid SubstitutionCase-Control StudiesMutationEnzymologylcsh:Q030217 neurology & neurosurgeryPLoS ONE
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Protective and causative killer Ig-like receptor (KIR) and metalloproteinase genetic patterns associated with Herpes simplex virus 1 (HSV-1) encephal…

2020

Abstract Background The cerebral innate immune system has a critical role in control processes of viral replication in the brain after primary infactivo and immunologic disregulation and inflammation has been reported as a primary determinant of pathogenesis and prognosis of subsequent HSV-1 related encephalitis (HSE). Interaction linking LTR3-activated DCs is also represented by the killer Ig-like receptor (KIR) + pathways on NK cells. Only a few studies analyzed the role of of MMP-9 activity regulating genetic polymorphism on clinical outcome of viral infections. Susceptibility to symptomatic encephalitis depends on SNC viral invasion and BBB disruption. We hypothesize that certain KIR ge…

0301 basic medicineMaleImmunologyHuman leukocyte antigenHerpesvirus 1 Humanmedicine.disease_causePathogenesisCohort StudiesMetalloprotease03 medical and health sciences0302 clinical medicineReceptors KIRHLA AntigensEncephalitiGenotypemedicineImmunology and AllergyHumansEncephalitis ViralHLA AntigenAllele frequencyAgedbusiness.industryHaplotypeHerpes SimplexMiddle Agedmedicine.diseaseHSV-1KIR030104 developmental biologyHerpes simplex virusNeurologyViral replicationMatrix Metalloproteinase 9ImmunologyMetalloproteasesFemaleNeurology (clinical)Cohort StudiebusinessInfectionMMP-9030217 neurology & neurosurgeryEncephalitis
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