Search results for "Genetic Testing"

showing 10 items of 193 documents

A novel DFNB1 deletion allele supports the existence of a distant cis-regulatory region that controls GJB2 and GJB6 expression

2010

Contains fulltext : 87760_1.pdf (author's version ) (Open Access) Contains fulltext : 87760_2.pdf (Publisher’s version ) (Closed access) Eleven affected members of a large German-American family segregating recessively inherited, congenital, non-syndromic sensorineural hearing loss (SNHL) were found to be homozygous for the common 35delG mutation of GJB2, the gene encoding the gap junction protein Connexin 26. Surprisingly, four additional family members with bilateral profound SNHL carried only a single 35delG mutation. Previously, we demonstrated reduced expression of both GJB2 and GJB6 mRNA from the allele carried in trans with that bearing the 35delG mutation in these four persons. Usin…

MaleGenetics and epigenetic pathways of disease [NCMLS 6][SDV]Life Sciences [q-bio]PenetranceMESH: Base SequenceRegulatory Sequences Nucleic Acidsensorineural hearing lossConnexinsMESH: GenotypeMESH: Hearing Loss Sensorineural/diagnosisMESH: PenetranceGenotypeCopy-number variationGenetics (clinical)Sequence DeletionGeneticsComparative Genomic Hybridization0303 health sciencesMESH: Genetic TestingMESH: Gene Expression Regulation*030305 genetics & heredityPenetranceGJB2PedigreeConnexin 26MESH: Sequence Deletion*MESH: Hearing Loss Sensorineural/geneticsFemaleChromosome DeletionFunctional Neurogenomics [DCN 2]GJB6GenotypeMESH: PedigreeMESH: Chromosome DeletionHearing Loss SensorineuralMolecular Sequence Dataconnexin 26connexin 30DFNB1gene expression regulationGJB2GJB6sensorineural hearing losssequence deletionBiologyMESH: Connexin 30MESH: Connexins/genetics*MESH: Sequence Homology Nucleic AcidArticleGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesMonoallelic MutationGJB6MESH: Connexin 26Sequence Homology Nucleic AcidConnexin 30otorhinolaryngologic diseasesGeneticsHumansGenetic TestingAlleleGeneMESH: Regulatory Sequences Nucleic Acid/genetics*AllelesDFNB1030304 developmental biologyFamily HealthMESH: HumansMESH: Molecular Sequence DataBase SequenceChromosomes Human Pair 13MESH: AllelesBreakpointMESH: MaleMESH: Comparative Genomic HybridizationGene Expression RegulationMESH: Family Healthbiology.proteinHuman medicineMESH: Chromosomes Human Pair 13/geneticsMESH: FemaleClinical Genetics
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Bayesian model to detect phenotype-specific genes for copy number data

2012

Abstract Background An important question in genetic studies is to determine those genetic variants, in particular CNVs, that are specific to different groups of individuals. This could help in elucidating differences in disease predisposition and response to pharmaceutical treatments. We propose a Bayesian model designed to analyze thousands of copy number variants (CNVs) where only few of them are expected to be associated with a specific phenotype. Results The model is illustrated by analyzing three major human groups belonging to HapMap data. We also show how the model can be used to determine specific CNVs related to response to treatment in patients diagnosed with ovarian cancer. The …

MaleGenotypeGene DosageHapMap ProjectBiologylcsh:Computer applications to medicine. Medical informaticsPopulation stratificationBayesian inferencePolymorphism Single NucleotideBiochemistry03 medical and health sciencesBayes' theorem0302 clinical medicineStructural BiologymedicineHumansComputer SimulationGenetic Predisposition to DiseaseGenetic TestingCopy-number variationInternational HapMap Projectlcsh:QH301-705.5Molecular Biology030304 developmental biologyGenetic testingGenetics0303 health sciencesModels StatisticalModels Geneticmedicine.diagnostic_testMethodology ArticleApplied MathematicsConfoundingBayes Theorem3. Good healthComputer Science ApplicationsPhenotypelcsh:Biology (General)030220 oncology & carcinogenesislcsh:R858-859.7FemaleDNA microarrayAlgorithmsBMC Bioinformatics
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Assessment of Susceptibility Risk Factors for ADHD in Imaging Genetic Studies

2019

Objective: ADHD consists of a count of symptoms that often presents heterogeneity due to overdispersion and excess of zeros. Statistical inference is usually based on a dichotomous outcome that is underpowered. The main goal of this study was to determine a suited probability distribution to analyze ADHD symptoms in Imaging Genetic studies. Method: We used two independent population samples of children to evaluate the consistency of the standard probability distributions based on count data for describing ADHD symptoms. Results: We showed that the zero-inflated negative binomial (ZINB) distribution provided the best power for modeling ADHD symptoms. ZINB reveals a genetic variant, rs273342…

MaleGenotypeImaging geneticsPopulationNegative binomial distributionPolymorphism Single NucleotideADHD symptomsImaging Genetics03 medical and health sciencesImaging Three-Dimensional0302 clinical medicineOverdispersionRisk FactorsStatisticsmental disordersDevelopmental and Educational PsychologyStatistical inferenceHumansGenetic Predisposition to Disease0501 psychology and cognitive sciencesGenetic TestingLongitudinal StudiesPoisson DistributionProspective Studiesp-valueMAPRE2Childeducationchildhoodzero-inflated negative binomialeducation.field_of_studyModels Statisticalbasal ganglia perivascular volumes05 social sciencesMagnetic Resonance Imagingcount dataVirchow-Robin spaceBinomial DistributionClinical PsychologyAttention Deficit Disorder with HyperactivityChild PreschoolProbability distributionFemalePsychology030217 neurology & neurosurgery050104 developmental & child psychologyCount data
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A novel KCNQ3 mutation in familial epilepsy with focal seizures and intellectual disability

2015

Mutations in the KCNQ2 gene encoding for voltage-gated potassium channel subunits have been found in patients affected with early onset epilepsies with wide phenotypic heterogeneity, ranging from benign familial neonatal seizures (BFNS) to epileptic encephalopathy with cognitive impairment, drug resistance, and characteristic electroencephalography (EEG) and neuroradiologic features. By contrast, only few KCNQ3 mutations have been rarely described, mostly in patients with typical BFNS. We report clinical, genetic, and functional data from a family in which early onset epilepsy and neurocognitive deficits segregated with a novel mutation in KCNQ3 (c.989G>T; p.R330L). Electrophysiological stu…

MaleGenotype-phenotype correlationmedicine.medical_specialtyNeurologyBenign familial neonatal seizuresMutantGenotype-phenotype correlationsmedicine.disease_causeMutagenesiKCNQ3 Potassium ChannelEpilepsyKCNQBenign Familial Neonatal Seizures KCNQ cognitive impairment voltage-gated potassium channels epilepsy mutagenesis genotype-phenotype correlationsSeizuresSettore M-PSI/08 - Psicologia ClinicaIntellectual DisabilityIntellectual disabilitymedicineHumansKCNQ2 Potassium ChannelVoltage-gated potassium channelBenign familial neonatal seizuresGenetic Predisposition to DiseaseGenetic TestingChildGenetic testingGeneticsMutationEpilepsymedicine.diagnostic_testGenetic heterogeneitybusiness.industryMedicine (all)Benign familial neonatal seizures; Cognitive impairment; Epilepsy; Genotype-phenotype correlations; KCNQ; Mutagenesis; Voltage-gated potassium channels; Child; Female; Genetic Testing; Humans; Intellectual Disability; KCNQ2 Potassium Channel; KCNQ3 Potassium Channel; Male; Mutation; Pedigree; Seizures; Genetic Predisposition to Disease; Neurology (clinical); Neurology; Medicine (all)Benign familial neonatal seizuremedicine.diseaseSeizureSettore MED/39 - Neuropsichiatria InfantilePedigreeCognitive impairmentNeurologyMutagenesisMutationFemaleNeurology (clinical)businessVoltage-gated potassium channelsHuman
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Preconception genome medicine: current state and future perspectives to improve infertility diagnosis and reproductive and health outcomes based on i…

2021

Abstract BACKGROUND Our genetic code is now readable, writable and hackable. The recent escalation of genome-wide sequencing (GS) applications in population diagnostics will not only enable the assessment of risks of transmitting well-defined monogenic disorders at preconceptional stages (i.e. carrier screening), but also facilitate identification of multifactorial genetic predispositions to sub-lethal pathologies, including those affecting reproductive fitness. Through GS, the acquisition and curation of reproductive-related findings will warrant the expansion of genetic assessment to new areas of genomic prediction of reproductive phenotypes, pharmacogenomics and molecular embryology, fur…

MaleInfertilitymedicine.medical_specialtyPopulationReproductive medicineGenome-wide association studyBioinformaticspolygenic medicinegenetic diagnosis03 medical and health sciences0302 clinical medicinePregnancyreproductive geneticsOutcome Assessment Health CaremedicineGenetic predispositionHumanswhole-exome sequencingProspective StudieseducationIVF/ICSI outcomesExome sequencing030304 developmental biologyReproductive healthGenetic testing0303 health scienceseducation.field_of_study030219 obstetrics & reproductive medicinemedicine.diagnostic_testoocyte and embryo genetic defectsbusiness.industryObstetrics and GynecologyGenomicsmedicine.disease3. Good healthReproductive Medicinewhole-genome sequencingInfertilitygenomic sequencingpreconception carrier screeningFemaleinfertilitybusinessGenome-Wide Association StudyHuman Reproduction Update
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A whole genome screen for linkage disequilibrium in multiple sclerosis performed in a continental Italian population

2003

We have systematically screened the genome for evidence of linkage disequilibrium (LD) with multiple sclerosis (MS) by typing 6000 microsatellite markers in case-control and family based (AFBAC) cohorts from the Italian population. DNA pooling was used to reduce the genotyping effort involved. Four DNA pools were considered: cases (224 Italian MS patients), controls (231 healthy Italians), index (185 index cases from trio families) and parents (the 370 parents of the patient included in the Index pool), respectively. After refining analysis of the most promising 14 markers to emerge from this screening process, only marker D2S367 retained evidence for association. © 2003 Elsevier B.V. All r…

MaleLinkage disequilibriumMultiple SclerosisGenotypeInternational CooperationImmunologyBiologyGenomeLinkage DisequilibriumWhole genome linkage disequilibriumGene FrequencyGenotypemedicineHumansImmunology and AllergyGenetic Predisposition to DiseaseMultiple sclerosiGenetic TestingGenotypingAllele frequencyAllelesGenetic testingGeneticsmedicine.diagnostic_testGenome HumanRacial GroupsDNA poolMicrosatelliteSettore BIO/18 - GeneticaItalyNeurologyCase-Control StudiesMicrosatelliteHuman genomeFemaleSettore MED/26 - NeurologiaNeurology (clinical)Microsatellite Repeats
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Identifying loci for the overlap between attention-deficit/hyperactivity disorder and autism spectrum disorder using a genome-wide QTL linkage approa…

2010

Contains fulltext : 88211.pdf (Publisher’s version ) (Closed access) OBJECTIVE: The genetic basis for autism spectrum disorder (ASD) symptoms in children with attention-deficit/hyperactivity disorder (ADHD) was addressed using a genome-wide linkage approach. METHOD: Participants of the International Multi-Center ADHD Genetics study comprising 1,143 probands with ADHD and 1,453 siblings were analyzed. The total and subscale scores of the Social Communication Questionnaire (SCQ) were used as quantitative traits for multipoint regression-based linkage analyses on 5,407 autosomal single-nucleotide polymorphisms applying MERLIN-regress software, both without and with inclusion of ADHD symptom sc…

MaleMedizinGenome-wide association studyComorbidityPersonality Assessment0302 clinical medicineDevelopmental and Educational PsychologyPerception and Action [DCN 1]GENETIC INFLUENCESChildGENERAL-POPULATION0303 health sciencesMental Health [NCEBP 9]CommunicationChromosome MappingPsychiatry and Mental healthcomorbidityAutism spectrum disorderFemalePsychologylinkageFunctional Neurogenomics [DCN 2]TRAITSmedicine.medical_specialtyAdolescentPsychometricsSUSCEPTIBILITY LOCIDEFICIT HYPERACTIVITY DISORDERQuantitative Trait Lociautism spectrum disorderQuantitative trait locusPolymorphism Single Nucleotidebehavioral disciplines and activitiesArticleTWIN SAMPLEGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesGenetic linkagemental disordersmedicinePervasive developmental disorderAttention deficit hyperactivity disorderADHDHumansGenetic Predisposition to DiseaseGenetic TestingSOCIAL-BEHAVIORPsychiatrySocial Behavior030304 developmental biologyChromosome AberrationsChromosomes Human Pair 15PERVASIVE DEVELOPMENTAL DISORDERSmedicine.diseaseHOMEOBOX-TRANSCRIPTION-FACTORDevelopmental disorderAttention Deficit Disorder with HyperactivityChild Development Disorders PervasiveAutismLod ScoreChromosomes Human Pair 18030217 neurology & neurosurgeryChromosomes Human Pair 16SCANGenome-Wide Association Study
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Phenotypic and biochemical analysis of an international cohort of individuals with variants in NAA10 and NAA15.

2019

Abstract N-alpha-acetylation is one of the most common co-translational protein modifications in humans and is essential for normal cell function. NAA10 encodes for the enzyme NAA10, which is the catalytic subunit in the N-terminal acetyltransferase A (NatA) complex. The auxiliary and regulatory subunits of the NatA complex are NAA15 and Huntington-interacting protein (HYPK), respectively. Through a genotype-first approach with exome sequencing, we identified and phenotypically characterized 30 individuals from 30 unrelated families with 17 different de novo or inherited, dominantly acting missense variants in NAA10 or NAA15. Clinical features of affected individuals include variable levels…

MaleModels Molecular0301 basic medicineProtein ConformationMicrophthalmia0302 clinical medicineEnzyme StabilityMissense mutationN-Terminal Acetyltransferase EChildN-Terminal Acetyltransferase AExome sequencingGenetics (clinical)GeneticsbiologyGeneral MedicinePhenotypeRecombinant ProteinsChemistryPhenotypeChild PreschoolHMG-CoA reductaseCohortFemaleGeneral ArticleCorrigendumAdultNatA complexmedicine.medical_specialtyAdolescentGenotypeFrameshift mutationStructure-Activity RelationshipYoung Adult03 medical and health sciencesMolecular geneticsGeneticsmedicineHumansGenetic Predisposition to DiseaseGenetic TestingAlleleBiologyMolecular BiologyAllelesGenetic Association StudiesComputational BiologyFaciesGenetic VariationInfantmedicine.diseaseEnzyme ActivationLenz microphthalmia syndrome030104 developmental biologyGenetic LociMutationbiology.proteinHuman medicineBiomarkers030217 neurology & neurosurgeryNAA15Human molecular genetics
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Is it wrong to deliberately conceive or give birth to a child with mental retardation?

2002

This paper discusses the issues of deciding to have a child with mental retardation, and of terminating a pregnancy when the future child is known to have the same disability. I discuss these problems by criticizing a utilitarian argument, namely, that one should act in a way that results in less suffering and less limited opportunity in the world. My argument is that future parents ought to assume a strong responsibility towards the well-being of their prospective children when they decide to reproduce. The moral point in cases in which our acts affect the well-being of future children should be expressed strictly in terms of parents' culpability. Future children thus do not have current m…

MaleMoral ObligationsParentsHealth Knowledge Attitudes PracticeWrongful LifeAbortionArgumentPregnancyIntellectual DisabilityEugenicsmedicineWrongful lifeHumansSociologyBioethical IssuesGenetic TestingChildPhilosophical methodologySocial ResponsibilityGeneral MedicineMental illnessmedicine.diseasehumanitiesDisabled ChildrenPhilosophyIssues ethics and legal aspectsFemaleEthical TheorySocial responsibilitySocial psychologyAbortion EugenicCulpabilityThe Journal of medicine and philosophy
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Complexity of the Hereditary Motor and Sensory Neuropathies

2015

Early-onset hereditary motor and sensory neuropathies are rare diseases representing a broad clinical and genetic spectrum. Without a notable familial history, the clinical diagnosis is complicated because acquired causes of peripheral neuropathy, such as inflammatory neuropathies, neuropathies with toxic causes, and nutritional deficiencies, must be considered. We examined the clinical, electrophysiological, and pathologic manifestations of a boy with an initial diagnosis of chronic inflammatory demyelinating polyneuropathy. The progression of the disease despite treatment led to a suspicion of hereditary motor and sensory neuropathy. Genetic testing revealed the presence of the MPZ p.D90…

MalePathologymedicine.medical_specialtyChronic inflammatory demyelinating polyneuropathySensory systemDiseaseBioinformaticsSural NervemedicineHumansGenetic testingmedicine.diagnostic_testbusiness.industrymedicine.diseasePhenotypePeripheral neuropathyChild PreschoolClinical diagnosisMutationPediatrics Perinatology and Child HealthMutation (genetic algorithm)Disease ProgressionNeurology (clinical)Hereditary Sensory and Motor NeuropathybusinessHereditary motor and sensory neuropathyMyelin P0 ProteinHeLa CellsJournal of Child Neurology
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