Search results for "Phenotype"

showing 10 items of 1875 documents

Additive effect of mutations in LDLR and PCSK9 genes on the phenotype of familial hypercholesterolemia.

2006

Patients homozygous or Compound heterozygous for LDLR mutations or double heterozygous for LDLR and apo B R3500Q mutation have higher LDL-C levels. more extensive xanthomatosis and more severe premature coronary disease (pCAD) than simple heterozygotes for mutations in either these genes or for missense mutations in PCSK9 gene. It is not known whether combined mutations in LDLR and PKCS9 are associated with such a severe phenotype. We sequenced Apo B and PCSK9 genes in two patients with the clinical diagnosis of homozygous FH who were heterozygous for LDLR gene mutations. Proband Z.P. (LDL-C 13.39 mmol/L and pCAD) was heterozygous for an LDLR mutation (p.E228K) inherited from her father (LD…

ProbandLDLR geneAdultMaleSettore MED/09 - Medicina InternaApolipoprotein BFamilial hypercholesterolemia (FH); Autosomal dominant hypercholesterolemia 3 (ADH3); LDLR gene; PCSK9 gene; Premature coronary artery diseasePremature coronary artery diseaseLDLR PCSK9Mutation MissenseFamilial hypercholesterolemiaCompound heterozygositymedicine.disease_causeHyperlipoproteinemia Type IIFamilial hypercholesterolemia (FH) Autosomal dominant hypercholesterolemia 3 (ADH3) LDLR gene PCSK9 gene Premature coronary artery diseaseFamilial hypercholesterolemia (FH)medicineMissense mutationHumansCells CulturedGeneticsMutationbiologybusiness.industrySerine EndopeptidasesHeterozygote advantageMiddle Agedmedicine.diseaseAutosomal dominant hypercholesterolemia 3 (ADH3)PedigreePhenotypeSettore MED/03 - Genetica MedicaAmino Acid SubstitutionReceptors LDLPCSK9 geneLDL receptorbiology.proteinlipids (amino acids peptides and proteins)FemaleProprotein ConvertasesProprotein Convertase 9Cardiology and Cardiovascular MedicinebusinessAtherosclerosis
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BBS1 Mutations in a Wide Spectrum of Phenotypes Ranging From Nonsyndromic Retinitis Pigmentosa to Bardet-Biedl Syndrome

2012

OBJECTIVE: To investigate the involvement of the Bardet-Biedl syndrome (BBS) gene BBS1 p.M390R variant in nonsyndromic autosomal recessive retinitis pigmentosa (RP). METHODS: Homozygosity mapping of a patient with isolated RP was followed by BBS1 sequence analysis. We performed restriction fragment length polymorphism analysis of the p.M390R allele in 2007 patients with isolated RP or autosomal recessive RP and in 1824 ethnically matched controls. Patients with 2 BBS1 variants underwent extensive clinical and ophthalmologic assessment. RESULTS: In an RP proband who did not fulfill the clinical criteria for BBS, we identified a large homozygous region encompassing the BBS1 gene, which carrie…

ProbandMaleBBS1Genetics and epigenetic pathways of disease [NCMLS 6]DNA Mutational AnalysisEvaluation of complex medical interventions Genomic disorders and inherited multi-system disorders [NCEBP 2]GenotypeEthnicityPrevalenceIsraelGeneticseducation.field_of_studyRetinitis Pigmentosa/diagnosisMiddle AgedDisease gene identificationPedigreeEuropePhenotypeFemaleMicrotubule-Associated ProteinsRetinitis PigmentosaAdultcongenital hereditary and neonatal diseases and abnormalitiesCanadaPopulationCanada/epidemiologyMicroscopy AcousticMutation MissenseEthnic GroupsDNA/geneticsBiologyEurope/epidemiologyGenomic disorders and inherited multi-system disorders [IGMD 3]Bardet-Biedl Syndrome/diagnosisBardet–Biedl syndromeRetinitis pigmentosamedicineElectroretinographyHumansAlleleeducationBardet-Biedl SyndromeIsrael/epidemiologyAllelesDNAMicrotubule-Associated Proteins/geneticsmedicine.diseaseOphthalmoscopyOphthalmologyGenetics and epigenetic pathways of disease Genomic disorders and inherited multi-system disorders [NCMLS 6]
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Separation of Cognitive Impairments in Attention-Deficit/Hyperactivity Disorder Into 2 Familial Factors

2010

Contains fulltext : 89304.pdf (Publisher’s version ) (Open Access) CONTEXT: Attention-deficit/hyperactivity disorder (ADHD) is associated with widespread cognitive impairments, but it is not known whether the apparent multiple impairments share etiological roots or separate etiological pathways exist. A better understanding of the etiological pathways is important for the development of targeted interventions and for identification of suitable intermediate phenotypes for molecular genetic investigations. OBJECTIVES: To determine, by using a multivariate familial factor analysis approach, whether 1 or more familial factors underlie the slow and variable reaction times, impaired response inhi…

ProbandMaleMedizinComorbidityNeuropsychological TestsChoice BehaviorDevelopmental psychology2738 Psychiatry and Mental HealthMOLECULAR-GENETICS0302 clinical medicinePerception and Action [DCN 1]GENETIC INFLUENCES10. No inequalityChildMental Health [NCEBP 9]Cognitive disorderCognition10058 Department of Child and Adolescent PsychiatryPedigreePsychiatry and Mental healthPhenotype1201 Arts and Humanities (miscellaneous)Femalemedicine.symptomPsychologyFunctional Neurogenomics [DCN 2]AdolescentDEFICIT HYPERACTIVITY DISORDERContext (language use)610 Medicine & healthImpulsivityArticleREACTION-TIME PERFORMANCE03 medical and health sciencesArts and Humanities (miscellaneous)medicineReaction TimeAttention deficit hyperactivity disorderHumansINTRA-SUBJECT VARIABILITYFamilyINHIBITORY CONTROLGENOME-WIDE ASSOCIATIONDELAY AVERSIONSiblingsSocial environmentmedicine.diseaseComorbidity030227 psychiatryAttention Deficit Disorder with HyperactivityImpulsive BehaviorRESPONSE VARIABILITYSUSTAINED ATTENTIONCognition DisordersFactor Analysis Statistical030217 neurology & neurosurgery
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Exclusion of PAX9 and MSX1 mutation in six families affected by tooth agenesis. A genetic study and literature review

2013

Objectives: In the present study, it is described the phenotypical analysis and the mutational screening, for genes PAX9 and MSX1, of six families affected by severe forms of tooth agenesis associated with other dental anomalies and systemic entities. Study Design: Six families affected by severe tooth agenesis associated with other dental anomalies and systemic entities were included. Oral exploration, radiological examination, medical antecedents consideration and mutational screening for PAX9 and MSX1 were carried out. Results: No mutations were discovered despite the fact that numerous teeth were missing. An important phenotypical variability was observed within the probands, not being …

ProbandMaleNonsense mutationOdontologíaGene mutationmedicine.disease_causeGene dosageAnodontiaGenetic transformationstomatognathic systemDental abnormalitiesmedicineMalalties hereditàriesMissense mutationHumansGeneral DentistryGenetic Association StudiesAnodontiaGeneticsMSX1 Transcription FactorMutationOral Medicine and Pathologybusiness.industryResearchmedicine.disease:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludFenotipstomatognathic diseasesPhenotypeOtorhinolaryngologyGenesUNESCO::CIENCIAS MÉDICASMutationSurgeryFemalePAX9 Transcription FactorbusinessMalformacions dentalsTransformació genèticaPAX9GensGenetic diseases
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Inheritance and variable expression in Rubinstein-Taybi syndrome.

2010

Familial Rubinstein-Taybi syndrome (RTS) is very rare. Here we report on the 6th and 7th case of inherited RTS. Family 1 presents with incomplete or mild RTS over three generations; a 13-year-old girl (proband 1) with mild but typical facial features and learning disabilities, her very mildly affected mother (proband 2), and the maternal grandmother (proband 3). Family 2 includes three females with classical RTS (probands 4-6) and their father (proband 7) with broad thumbs and halluces. Proband 5 also had a brain tumor (ganglioglioma) at the age of 3 years. In probands 1-3, direct sequencing identified a novel CREBBP missense mutation, c.2728A > G (predicting p.Thr910Ala), that was absent i…

ProbandMaleRiskAdolescentDNA Mutational AnalysisMutation MissenseBiologyVariable ExpressionGenetic HeterogeneityGeneticsmedicineMissense mutationHumansPoint MutationFamilyAlleleGenetics (clinical)GeneticsRubinstein-Taybi SyndromeRubinstein–Taybi syndromeGenetic heterogeneityMosaicismPoint mutationmedicine.diseaseCREB-Binding ProteinPedigreePhenotypeChild PreschoolMutation (genetic algorithm)FemaleAmerican journal of medical genetics. Part A
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The impact of the endogenous subtype on the familial aggregation of unipolar depression.

1991

The endogenous/non-endogenous distinction of unipolar major depression is widely accepted, as is the family study approach to the validation of diagnostic distinctions. Rates of affective disorders were examined in 689 first-degree relatives of 184 patients with unipolar major depression and were compared with 312 first-degree relatives of 80 healthy controls. Only unipolar depression and alcoholism were more common in families of depressed probands compared with families of healthy controls. As a variety of diagnostic definitions of endogenous depression have been proposed, probands and relatives were diagnosed in a polydiagnostic manner. None of the five diagnostic definitions of endogeno…

ProbandMalemedicine.medical_specialtyEndogenybehavioral disciplines and activitiesDelusionsArousalDiagnosis DifferentialChild of Impaired ParentsRisk Factorsmental disordersmedicineHumansPharmacology (medical)PsychiatryBiological PsychiatryDepression (differential diagnoses)Depressive DisorderGeneral NeuroscienceMental DisordersFamily aggregationGeneral MedicineFamilial riskMiddle AgedCircadian RhythmPsychiatry and Mental healthNeuropsychology and Physiological PsychologyPhenotypeEndogenous depressionFemalePsychologyArousalClinical psychologyEuropean archives of psychiatry and clinical neuroscience
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High efficiency and clinical relevance of exome sequencing in the daily practice of neurogenetics

2021

ObjectiveTo assess the efficiency and relevance of clinical exome sequencing (cES) as a first-tier or second-tier test for the diagnosis of progressive neurological disorders in the daily practice of Neurology and Genetic Departments.MethodsSixty-seven probands with various progressive neurological disorders (cerebellar ataxias, neuromuscular disorders, spastic paraplegias, movement disorders and individuals with complex phenotypes labelled ‘other’) were recruited over a 4-year period regardless of their age, gender, familial history and clinical framework. Individuals could have had prior genetic tests as long as it was not cES. cES was performed in a proband-only (60/67) or trio (7/67) st…

ProbandPediatricsmedicine.medical_specialtyMovement disordersNeurologyNeurodegeneration with brain iron accumulation[SDV]Life Sciences [q-bio]EncephalopathyNeurogenetics03 medical and health sciences0302 clinical medicineExome SequencingGeneticsHumansMedicineExomeClinical significance030212 general & internal medicineGenetic TestingGenetics (clinical)Exome sequencingComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciencesbusiness.industrymedicine.diseasePhenotypeNeurology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Neurology (clinical)Nervous System Diseasesmedicine.symptombusiness030217 neurology & neurosurgery
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The impact of study design and diagnostic approach in a large multi-centre ADHD study: Part 2: Dimensional measures of psychopathology and intelligen…

2011

Contains fulltext : 97437.pdf (Publisher’s version ) (Open Access) BACKGROUND: The International Multi-centre ADHD Genetics (IMAGE) project with 11 participating centres from 7 European countries and Israel has collected a large behavioural and genetic database for present and future research. Behavioural data were collected from 1068 probands with ADHD and 1446 unselected siblings. The aim was to describe and analyse questionnaire data and IQ measures from all probands and siblings. In particular, to investigate the influence of age, gender, family status (proband vs. sibling), informant, and centres on sample homogeneity in psychopathological measures. METHODS: Conners' Questionnaires, St…

ProbandResearch designMale110 012 Social cognition of verbal communicationIntelligencePerception and Actions Mental Health [DCN 1]MedizinSocial Sciencescentre effectsDevelopmental psychology2738 Psychiatry and Mental Health0302 clinical medicinelcsh:PsychiatryMulticenter Studies as Topicsibling designChildATTENTION-DEFICIT/HYPERACTIVITY DISORDERMental DisordersWechsler ScalesWechsler Adult Intelligence Scale10058 Department of Child and Adolescent PsychiatryDiagnostic and Statistical Manual of Mental DisordersPsychiatry and Mental healthPhenotypeConduct disorderResearch DesignRELIABILITYFemaleFamily RelationsPsychologyClinical psychologyPsychopathologyResearch ArticleAdultlcsh:RC435-571DEFICIT HYPERACTIVITY DISORDERTWIN610610 Medicine & health150 000 MR Techniques in Brain Function03 medical and health sciencesmulti-centre studyADHD multi-centre studymedicineCriterion validityAttention deficit hyperactivity disorderHumansADHDGenetic Predisposition to Diseaseddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersSiblingMETAANALYSISFamily HealthPsychiatric Status Rating ScalesCHILD PSYCHIATRIC-PATIENTSSiblingsPARENTmedicine.disease030227 psychiatryAttention Deficit Disorder with HyperactivityCONDUCT DISORDERCRITERION VALIDITY030217 neurology & neurosurgery
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Hypoxia inducible factor-1alpha inactivation unveils a link between tumor cell metabolism and hypoxia-induced cell death.

2008

Hypoxia and the acquisition of a glycolytic phenotype are intrinsic features of the tumor microenvironment. The hypoxia inducible factor-1alpha (HIF-1alpha) pathway is activated under hypoxic conditions and orchestrates a complex transcriptional program that enhances cell survival. Although the consequences of HIF-1alpha inactivation in cancer cells have been widely investigated, only a few studies have addressed the role of HIF-1alpha in the survival of cancer cells endowed with different glycolytic capacities. In this study, we investigated this aspect in ovarian cancer cells. Hypoxia-induced toxicity was increased in highly glycolytic cells compared with poorly glycolytic cells; it was a…

Programmed cell deathMice SCIDBiologyPathology and Forensic MedicineMiceCell Line TumormedicineAnimalsHumansGene SilencingRNA Small InterferingCell ProliferationOvarian NeoplasmsTumor microenvironmentCell DeathCell growthLentivirusHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaCell biologyPhenotypeHypoxia-inducible factorsApoptosisCell cultureCancer cellFemalemedicine.symptomRegular ArticlesThe American journal of pathology
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Selective loss of regulatory T cells in thymomas

2004

Myasthenia gravis (MG) is the prime autoimmune manifestation of thymomas. We investigated the generation of T cells with a regulatory phenotype (T(R)) in thymomas with and without associated MG. In patients with MG(+) thymomas, maturation and export of T(R) cells but not of other T-cell subsets was significantly reduced. We conclude that imbalance between effector and regulatory T cells in thymomas may be involved in modulation of onset and/or severity of MG.

Programmed cell deathThymomabusiness.industryEffectorCellular differentiationchemical and pharmacologic phenomenaT lymphocytemedicine.diseasePhenotypeClonal deletionMyasthenia gravissurgical procedures operativeNeurologyhemic and lymphatic diseasesImmunologyCancer researchMedicineNeurology (clinical)businessneoplasmsAnnals of Neurology
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