Search results for " Sequencing"

showing 10 items of 976 documents

Aging and serum exomiR content in women-effects of estrogenic hormone replacement therapy.

2017

AbstractExosomes participate in intercellular messaging by transporting bioactive lipid-, protein- and RNA-molecules and -complexes. The contents of the exosomes reflect the physiological status of an individual making exosomes promising targets for biomarker analyses. In the present study we extracted exosome microRNAs (exomiRs) from serum samples of premenopausal women (n = 8) and monozygotic postmenopausal twins (n = 10 female pairs), discordant for the use of estrogenic hormone replacement therapy (HRT), in order to see whether the age or/and the use of HRT associates with exomiR content. A total of 241 exomiRs were detected by next generation sequencing, 10 showing age, 14 HRT and 10 a…

0301 basic medicineMICRORNASTranscriptomeMedicineGene Regulatory NetworksMultidisciplinaryEstradiolmicroRNAEstrogen Replacement TherapyEndocrine system and metabolic diseasesHigh-Throughput Nucleotide Sequencingta3141Middle AgedMenopausePostmenopauseDISCORDANTPOSTMENOPAUSAL WOMENTransgender hormone therapymiRNAsBiomarker (medicine)SKELETAL-MUSCLEFemaleAdultEXPRESSIONmedicine.medical_specialtyMENOPAUSEBODY-COMPOSITIONexosomesta3111ExosomeArticleestrogenic hormone replacement therapy03 medical and health sciencesBreast cancerInternal medicineHumansBREAST-CANCERbusiness.industryta1184Gene Expression ProfilingReproducibility of Resultsbiomarkersmedicine.diseaseGene expression profilingMONOZYGOTIC TWIN PAIRS030104 developmental biologyEndocrinologyPremenopauseCELLSNext-generation sequencing3111 Biomedicinemikro-RNAbusinessTranscriptomeHormone
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Further delineation of the clinical spectrum of de novo TRIM8 truncating mutations.

2018

IF 2.264; International audience; De novo mutations of the TRIM8 gene, which codes for a tripartite motif protein, have been identified using whole exome sequencing (WES) in two patients with epileptic encephalopathy (EE), but these reports were not sufficient to conclude that TRIM8 was a novel gene responsible for EE. Here we report four additional patients presenting with EE and de novo truncating mutations of TRIM8 detected by WES, and give further details of the patient previously reported by the Epi4K consortium. Epilepsy of variable severity was diagnosed in children aged 2 months to 3.5 years of age. All patients had developmental delay of variable severity with no or very limited la…

0301 basic medicineMaleAdolescentNerve Tissue ProteinsBioinformaticswhole exome sequencing03 medical and health sciencesEpilepsyTripartite MotifGeneticsmedicineHumansTRIM8Amino Acid SequenceChildGeneGenetics (clinical)De novo mutationsExome sequencingbusiness.industrynephrotic syndromeEpileptic encephalopathyInfant NewbornInfantmedicine.diseasePhenotype3. Good health030104 developmental biologyepileptic encephalopathy[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolMutationFemalebusinessCarrier ProteinsNephrotic syndromeAmerican journal of medical genetics. Part A
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Gut microbiota differs between children with Inflammatory Bowel Disease and healthy siblings in taxonomic and functional composition: a metagenomic a…

2017

Current treatment for pediatric inflammatory bowel disease (IBD) patients is often ineffective, with serious side effects. Manipulating the gut microbiota via fecal microbiota transplantation (FMT) is an emerging treatment approach but remains controversial. We aimed to assess the composition of the fecal microbiome through a comparison of pediatric IBD patients to their healthy siblings, evaluating risks and prospects for FMT in this setting. A case-control (sibling) study was conducted analyzing fecal samples of six children with Crohn’s disease (CD), six children with ulcerative colitis (UC) and 12 healthy siblings by metagenomic sequencing. In addition, lifetime antibiotic intake was r…

0301 basic medicineMaleAdolescentPhysiologyGut floraMicrobial dysbiosisInflammatory bowel disease03 medical and health sciencesFecesYoung Adult0302 clinical medicinePhysiology (medical)medicineHumansMicrobiomeSiblingIntestinal MucosaChildHepatologybiologyShotgun sequencingSiblingsGastroenterologymedicine.diseasebiology.organism_classification16S ribosomal RNAInflammatory Bowel DiseasesGastrointestinal Microbiome030104 developmental biologyMetagenomicsCardiovascular and Metabolic DiseasesImmunologyMetagenome030211 gastroenterology & hepatologyFemaleAmerican journal of physiology. Gastrointestinal and liver physiology
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Exome-wide somatic mutation characterization of small bowel adenocarcinoma

2018

Small bowel adenocarcinoma (SBA) is an aggressive disease with limited treatment options. Despite previous studies, its molecular genetic background has remained somewhat elusive. To comprehensively characterize the mutational landscape of this tumor type, and to identify possible targets of treatment, we conducted the first large exome sequencing study on a population-based set of SBA samples from all three small bowel segments. Archival tissue from 106 primary tumors with appropriate clinical information were available for exome sequencing from a patient series consisting of a majority of confirmed SBA cases diagnosed in Finland between the years 2003–2011. Paired-end exome sequencing was…

0301 basic medicineMaleCancer ResearchMICROSATELLITE INSTABILITYColorectal canceroncogenesReceptor ErbB-2medicine.disease_causeCOLORECTAL-CANCERACTIVATIONCohort Studies0302 clinical medicineAnimal CellsAdenocarcinomasMedicine and Health SciencesExomeFrameshift MutationExomeGenetics (clinical)Exome sequencingAged 80 and overSMALL-INTESTINEeducation.field_of_study1184 Genetics developmental biology physiologyCELIAC-DISEASENonsense MutationMiddle Aged3. Good healthsyöpägeenitOncology030220 oncology & carcinogenesissyöpätauditFemaleSIGNALING PATHWAYKRASCellular TypesResearch ArticleAdultProto-Oncogene Proteins B-raflcsh:QH426-470SEQUENCING DATAImmune CellsNonsense mutationPopulationImmunologyAntigen-Presenting CellsComputational biologysuolistosyövätBiologyAdenocarcinomata3111CarcinomasFrameshift mutation03 medical and health sciencesGermline mutationQUALITY-CONTROLGenetiikka kehitysbiologia fysiologia - Genetics developmental biology physiologySyöpätaudit - CancersIntestinal NeoplasmsmedicineGeneticsPoint MutationHumanseducationMolecular BiologyEcology Evolution Behavior and SystematicsAgedColorectal CancerBiology and Life SciencesCancers and Neoplasmscancerous diseasesCell Biologymedicine.diseaseta3122mutationsCOMPREHENSIVE MOLECULAR CHARACTERIZATIONlcsh:Genetics030104 developmental biologyMutationSomatic Mutationbowel cancer3111 BiomedicinemutaatiotHIGH-RESOLUTIONPLoS Genetics
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Investigation of SOSTDC1 gene in non-syndromic patients with supernumerary teeth

2018

WOS: 000443304400005 PubMed: 30148467 Background: The etiology of supernumerary teeth is still unclear however heredity is believed to be a major factor and this idea was supported by several case reports. Recently, a relationship between supernumerary tooth formation and deficiency of Uterine Sensitization Associated Gene-1 (Usag-1), a rat gene that is expressed in sensitized endometrium, was reported in mice. The human homolog gene for Usag-1, Sclerostin Domain Containing 1 (SOSTDC1), shows 85% identity with mouse Usag-1. The present study aimed to investigate SOSTDC1 coding regions in non-syndromic patients with one or more supernumerary teeth. Material and Methods: Twenty-five non-syndr…

0301 basic medicineMaleCandidate geneAdolescentBiologymesiodensmedicine.disease_cause03 medical and health sciences0302 clinical medicineHeredityGeneticsmedicineCoding regionHumansSupernumeraryDNA sequencingChildGeneral DentistryGeneAdaptor Proteins Signal TransducingGeneticsOral Medicine and PathologyResearchIntracellular Signaling Peptides and ProteinsProteins030206 dentistry:CIENCIAS MÉDICAS [UNESCO]Phenotypepediatric dentistryPCR030104 developmental biologyOtorhinolaryngologyTooth SupernumeraryUsag-1Child PreschoolUNESCO::CIENCIAS MÉDICASEtiologySurgeryHuman genomeFemaleMedicina Oral, Patología Oral y Cirugía Bucal
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Exome sequencing in congenital ataxia identifies two new candidate genes and highlights a pathophysiological link between some congenital ataxias and…

2019

To investigate the genetic basis of congenital ataxias (CAs), a unique group of cerebellar ataxias with a nonprogressive course, in 20 patients from consanguineous families, and to identify new CA genes. Singleton -exome sequencing on these 20 well-clinically characterized CA patients. We first checked for rare homozygous pathogenic variants, then, for variants from a list of genes known to be associated with CA or very early-onset ataxia, regardless of their mode of inheritance. Our replication cohort of 180 CA patients was used to validate the new CA genes. We identified a causal gene in 16/20 families: six known CA genes (7 patients); four genes previously implicated in another neurologi…

0301 basic medicineMaleCandidate geneAtaxiaAdolescentCerebellar AtaxiaGenotype[SDV]Life Sciences [q-bio]Consanguinity030105 genetics & heredityBiologyPathophysiologyCohort Studies03 medical and health sciencesGenetic HeterogeneityYoung AdultmedicineSTXBP1HumansExomeGenetic Predisposition to DiseaseChildGenetics (clinical)Exome sequencingGeneticsEarly infantile epileptic encephalopathies[SDV.GEN]Life Sciences [q-bio]/GeneticsBRAT1Genetic heterogeneityPhenotype3. Good health030104 developmental biologyPhenotype[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolMutationCerebellar atrophyCongenital ataxiaAtaxiaFemaleFrancemedicine.symptomSpasms Infantileexome sequencing
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Bi-allelic JAM2 Variants Lead to Early-Onset Recessive Primary Familial Brain Calcification

2020

International audience; Primary familial brain calcification (PFBC) is a rare neurodegenerative disorder characterized by a combination of neurological, psychiatric, and cognitive decline associated with calcium deposition on brain imaging. To date, mutations in five genes have been linked to PFBC. However, more than 50% of individuals affected by PFBC have no molecular diagnosis. We report four unrelated families presenting with initial learning difficulties and seizures and later psychiatric symptoms, cerebellar ataxia, extrapyramidal signs, and extensive calcifications on brain imaging. Through a combination of homozygosity mapping and exome sequencing, we mapped this phenotype to chromo…

0301 basic medicineMaleCerebellumPathology[SDV]Life Sciences [q-bio]recessive brain calcificationMice0302 clinical medicineCognitive declineAge of OnsetChildGenetics (clinical)Exome sequencingComputingMilieux_MISCELLANEOUSBrain Diseasesprimary familial brain calcificationMalalties neurodegenerativesBrainFahr diseaseCalcinosisOCLNNeurodegenerative DiseasesHuman brainMiddle AgedPedigree[SDV] Life Sciences [q-bio]medicine.anatomical_structureKnockout mouseFemalemedicine.symptomAdultmedicine.medical_specialtyAdolescentGenes RecessiveNeuropathologyBiologyCalcificacióCalcification03 medical and health sciencesBasal Ganglia DiseasesReportGeneticsmedicineAnimalsHumansAllelesSLC20A2Cerebellar ataxiaknock out mouse modelmedicine.diseaseJAM2030104 developmental biologyFahr disease; familial idiopathic basal ganglia calcification; JAM2; JAM3; knock out mouse model; MYORG; OCLN; primary familial brain calcification; recessive brain calcification; SLC20A2familial idiopathic basal ganglia calcificationJAM3MYORGXenotropic and Polytropic Retrovirus ReceptorCell Adhesion Molecules030217 neurology & neurosurgeryCalcification
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Assessment of Targeted Next-Generation Sequencing as a Tool for the Diagnosis of Charcot-Marie-Tooth Disease and Hereditary Motor Neuropathy

2016

Charcot-Marie-Tooth disease is characterized by broad genetic heterogeneity with >50 known disease-associated genes. Mutations in some of these genes can cause a pure motor form of hereditary motor neuropathy, the genetics of which are poorly characterized. We designed a panel comprising 56 genes associated with Charcot-Marie-Tooth disease/hereditary motor neuropathy. We validated this diagnostic tool by first testing 11 patients with pathological mutations. A cohort of 33 affected subjects was selected for this study. The DNAJB2 c.352+1G>A mutation was detected in two cases; novel changes and/or variants with low frequency (50 known disease-associated genes. Mutations in some of these gene…

0301 basic medicineMaleDiseaseBioinformaticsDNA sequencingPathology and Forensic Medicine03 medical and health sciences0302 clinical medicineCharcot-Marie-Tooth DiseaseMedicineHumansGeneGeneticsbusiness.industryGenetic heterogeneityHaplotypeCase-control studyHigh-Throughput Nucleotide SequencingReproducibility of ResultsHSP40 Heat-Shock Proteins030104 developmental biologyHaplotypesCase-Control StudiesMutation (genetic algorithm)MutationMolecular MedicineFemalebusinessHereditary Sensory and Motor Neuropathy030217 neurology & neurosurgeryFounder effectMolecular Chaperones
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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 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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