Search results for " dominant"

showing 10 items of 139 documents

A dominant gene for developmental dyslexia on chromosome 3.

2001

Developmental dyslexia is a neurofunctional disorder characterised by an unexpected difficulty in learning to read and write despite adequate intelligence, motivation, and education. Previous studies have suggested mostly quantitative susceptibility loci for dyslexia on chromosomes 1, 2, 6, and 15, but no genes have been identified yet. We studied a large pedigree, ascertained from 140 families considered, segregating pronounced dyslexia in an autosomal dominant fashion. Affected status and the subtype of dyslexia were determined by neuropsychological tests. A genome scan with 320 markers showed a novel dominant locus linked to dyslexia in the pericentromeric region of chromosome 3 with a m…

AdultMaleReading disabilityAdolescentLocus (genetics)Biologybehavioral disciplines and activitiesDyslexia03 medical and health sciences0302 clinical medicineGenetic linkageDCDC2Memorymental disordersGeneticsmedicineHumansChildGenetics (clinical)Finland030304 developmental biologyAgedGenes DominantGenetics0303 health sciencesAnalysis of VariancePsychological TestsRadiation Hybrid MappingReceptors Dopamine D2HaplotypeDyslexiaReceptors Dopamine D3Chromosome MappingOriginal ArticlesMiddle Agedmedicine.diseasePedigreeDevelopmental disorderChromosome 3HaplotypesReadingReceptors SerotoninFemaleChromosomes Human Pair 3Lod Score030217 neurology & neurosurgeryJournal of medical genetics
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Gly114Asp mutation of rhodopsin in autosomal dominant retinitis pigmentosa

1995

Two autosomal dominant retinitis pigmentosa families of different origin were screened for rhodopsin mutations using the method of single strand conformation polymorphism and direct sequencing. We found a CGG-CAG substitution in codon 114 of rhodopsin in both families. This change predicted the replacement of a glycine by an aspartic acid and suggested that this change is the cause of the disease in these families.

AdultMaleRhodopsincongenital hereditary and neonatal diseases and abnormalitiesAdolescentgenetic structuresMolecular Sequence DataGlycinemedicine.disease_causeAutosomal dominant retinitis pigmentosaRetinitis pigmentosaAspartic acidmedicineHumansPoint MutationAmino Acid SequenceCodonMolecular BiologyGenes DominantGeneticsAspartic AcidMutationPolymorphism GeneticBase SequencebiologyDirect sequencingSingle-strand conformation polymorphismCell BiologyMiddle Agedmedicine.diseasePedigreeRhodopsinGlycinebiology.proteinFemalesense organsRetinitis PigmentosaMolecular and Cellular Probes
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Hereditary angioedema with normal C1-inhibitor activity in women.

2000

Summary Background Hereditary angioedema (HAE) is a well defined autosomal dominant disease (Mendelian Inheritance in Man #106100) that results from an inherited deficiency of C1 (the activated first component of complement) inhibitor function. We report an unusual variant of HAE with normal biochemical C1-inhibitor function, occurring only in women. Methods We screened 574 patients with recurrent angioedema of the skin for presence of HAE. 283 patients were selected, in whom angioedema was associated with abdominal pain attacks or recurrent life-threatening episodes of upper-airway obstruction, or both, rather than with urticaria. We measured C1-inhibitor concentration and functional activ…

AdultMaleX ChromosomeAdolescentGenetic LinkageComplement C1 Inactivator ProteinsC1-inhibitorEcallantideSex FactorsRecurrenceTerminology as TopicmedicineHumansHereditary Angioedema Type IIISex RatioFamily historyAngioedemaChildDominance (genetics)Genes DominantAngioedemabiologybusiness.industryAutosomal dominant traitComplement C4General MedicineMiddle Agedmedicine.diseaseAbdominal PainPedigreeAirway ObstructionImmunologyHereditary angioedemaMutationbiology.proteinFemalemedicine.symptombusinessmedicine.drugLancet (London, England)
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Increased sensitivity of the neuronal nicotinic receptor alpha-2 subunit causes familial epilepsy with nocturnal wandering and ictal fear

2006

Sleep has traditionally been recognized as a precipitating factor for some forms of epilepsy, although differential diagnosis between some seizure types and parasomnias may be difficult. Autosomal dominant frontal lobe epilepsy is characterized by nocturnal seizures with hyperkinetic automatisms and poorly organized stereotyped movements and has been associated with mutations of the α4 and β2 subunits of the neuronal nicotinic acetylcholine receptor. We performed a clinical and molecular genetic study of a large pedigree segregating sleep-related epilepsy in which seizures are associated with fear sensation, tongue movements, and nocturnal wandering, closely resembling nightmares and sleep …

AdultMalemedicine.medical_specialtyAdolescentSomnambulismMolecular Sequence DataMutation MissenseAutosomal dominant nocturnal frontal lobe epilepsyReceptors NicotinicBiologymedicine.disease_causeLigandsNicotinicArticleEpilepsyBIO/09 - FISIOLOGIAInternal medicineAcetylcholine; Adolescent; Adult; Aged; Aged 80 and over; Amino Acid Sequence; Epilepsy; Female; Humans; Ligands; Male; Molecular Sequence Data; Mutation Missense; Neurons; Pedigree; Receptors Nicotinic; Somnambulism; FearReceptorsmedicine80 and overGeneticsHumansIctalGenetics(clinical)Amino Acid SequenceGenetics (clinical)Acetylcholine receptorAgedAged 80 and overNeuronsMutationEpilepsySeizure typesFearmedicine.diseaseAcetylcholinePedigreeNicotinic acetylcholine receptorNicotinic agonistEndocrinologyMutationnAChR patch-clamp ADNFLE sleep-related epilepsy M1 TM1 ACh nicotineSettore MED/26 - NeurologiaFemaleMissense
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Left ventricular Myocardial dysfunction in arrhythmogenic cardiomyopathy with left ventricular involvement: A door to improving diagnosis.

2018

[EN] Background: Diagnostic Task Force Criteria (TFC) for arrhythmogenic cardiomyopathy (AC) exhibit poor performance for left dominant forms. TFC only include right ventricular (RV) dysfunction (akinesia, dyssynchrony, volumes and ejection fraction). Moreover, cardiac magnetic resonance imaging (CMRI) assessment of left ventricular (LV) dyssynchrony has hitherto not been described. Thus, we aimed to comprehensively characterize LVCMRI behavior in AC patients. Methods: Thirty-five AC patients with LV involvement and twenty-three non-affected family members (controls) were enrolled. Feature-tracking analysis was applied to cine CMRI to assess LV ejection fraction (LVEF), LV end-systolic and …

AdultMalemedicine.medical_specialtyHeart VentriclesCardiomyopathyMagnetic Resonance Imaging Cine030204 cardiovascular system & hematologyVentricular Function LeftStrainTECNOLOGIA ELECTRONICA03 medical and health sciencesVentricular Dysfunction Left0302 clinical medicineCardiac magnetic resonance imagingDiastoleInternal medicinemedicineLate gadolinium enhancementHumansCor030212 general & internal medicineLeft ventricular involvementVentricular dysfunctionCardiac magnetic resonance imagingArrhythmogenic Right Ventricular DysplasiaEjection fractionmedicine.diagnostic_testTask forcebusiness.industryLeft ventricular arrhythmogenic cardiomyopathyReproducibility of ResultsStroke VolumeMiddle Agedmedicine.diseasePatologiaDyssynchronyLv dyssynchronyCardiologyFemaleCardiology and Cardiovascular MedicineLEFT DOMINANTbusiness
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Sympathetic Activity and Blood Pressure Pattern in Autosomal Dominant Polycystic Kidney Disease Hypertensives

1998

To study the potential role of sympathetic activity in the pathogenesis of arterial hypertension associated with autosomal dominant polycystic kidney disease (ADPKD) and to analyze its relationship with 24-hour blood pressure pattern, plasma catecholamines and 24-hour ambulatory blood pressure monitoring were evaluated in 30 ADPKD hypertensive patients (of which 17 without and 13 with renal failure) and in 50 essential hypertensives. The groups were matched for sex, body mass index, known duration of hypertension, and clinic blood pressure. Plasma catecholamines, determined in resting position, were higher in ADPKD patients without renal failure than in essential hypertensives. Nighttime di…

AdultMalemedicine.medical_specialtyHypertension RenalSympathetic Nervous SystemAmbulatory blood pressureAutosomal dominant polycystic kidney diseaseRenal functionHemodynamicsBlood Pressureurologic and male genital diseasesEssential hypertensionCatecholaminesInternal medicineReninmedicineHumansbusiness.industryBlood Pressure Monitoring AmbulatoryMiddle AgedPolycystic Kidney Autosomal Dominantmedicine.diseaseCircadian RhythmMean blood pressureBlood pressureEndocrinologyNephrologyCreatinineHypertensionCardiologyKidney Failure ChronicFemalebusinessKidney diseaseAmerican Journal of Nephrology
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Desmin-related myopathies

1997

Desmin-related myopathies are marked by accumulation of desmin, which is often familial and associated with cardiomyopathy. When multifocal this excess is characterized by inclusions such as cytoplasmic or spheroid bodies, when disseminated the excess is called granulofilamentous material. Excess of desmin might represent an abnormal type of protein metabolism.

AdultPathologymedicine.medical_specialtyGranulofilamentous materialCardiomyopathyChromosome DisordersGenes Recessivemacromolecular substancesBiologyDesminMuscular DiseasesmedicineHumansChildMuscle SkeletalGenotype-Phenotype CorrelationsGenes DominantChromosome AberrationsInclusion BodiesDESMIN-RELATED MYOPATHYMyocardiumMolecular pathogenesismusculoskeletal systemmedicine.diseaseActin CytoskeletonNeurologyCytoplasmDesminNeurology (clinical)CardiomyopathiesCurrent Opinion in Neurology
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Spectrum of mutations and phenotypic expression in patients with autosomal dominant hypercholesterolemia identified in Italy.

2013

Abstract Objective To determine the spectrum of gene mutations and the genotype–phenotype correlations in patients with Autosomal Dominant Hypercholesterolemia (ADH) identified in Italy. Methods The resequencing of LDLR , PCSK9 genes and a selected region of APOB gene were conducted in 1018 index subjects clinically heterozygous ADH and in 52 patients clinically homozygous ADH. The analysis was also extended to 1008 family members of mutation positive subjects. Results Mutations were detected in 832 individuals: 97.4% with LDLR mutations, 2.2% with APOB mutations and 0.36% with PCSK9 mutations. Among the patients with homozygous ADH, 51 were carriers of LDLR mutations and one was an LDLR / …

Adultmedicine.medical_specialtyHeterozygoteSettore MED/09 - Medicina InternaApolipoprotein BCoronary DiseaseBiologyGene mutationmedicine.disease_causeHyperlipoproteinemia Type IITendonschemistry.chemical_compoundReference ValuesInternal medicinemedicineXanthomatosisHumansGeneAllelesGenetic Association StudiesAgedGeneticsMutationCholesterolPCSK9Cholesterol HDLSerine EndopeptidasesSmokingAlcohol Dehydrogenasenutritional and metabolic diseasesCholesterol LDLMiddle AgedEndocrinologyPhenotypechemistryItalyLDL receptorMutationbiology.proteinAutosomal dominanthypercholesterolemia LDL receptor Apolipoprotein B PCSK9 Mutationslipids (amino acids peptides and proteins)Allelic heterogeneityFemaleProprotein ConvertasesProprotein Convertase 9Cardiology and Cardiovascular MedicineAtherosclerosis
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Influence of microsomal triglyceride transfer protein promoter polymorphism -493 GT on fasting plasma triglyceride values and interaction with treatm…

2005

Familial hypercholesterolaemia (FH) is an autosomal dominant disease characterized by elevated levels of low-density lipoprotein-cholesterol (LDL-C). Phenotypic expression is highly variable, being influenced by diet, age, gender, body mass index, apolipoprotein E genotype and type of LDL-receptor gene mutation. Microsomal triglyceride (TG) transfer protein (MTP) is a protein involved in lipid metabolism. Polymorphism MTP -493 GT has been shown to modulate lipid levels in several populations. To analyse the effect of this polymorphism in the lipid phenotype expression of FH and treatment response, we studied a sample of 222 Spanish FH patients, of whom 147 were studied before and after trea…

Apolipoprotein EMaleAtorvastatinPolymerase Chain ReactionMicrosomal triglyceride transfer proteinBody Mass Indexchemistry.chemical_compoundAtorvastatinGeneral Pharmacology Toxicology and PharmaceuticsPromoter Regions GeneticGenetics (clinical)Polymorphism Single-Stranded ConformationalGeneticsbiologyAutosomal dominant traitFastingLipoproteins LDLCholesterolPhenotypeMolecular Medicinelipids (amino acids peptides and proteins)Femalemedicine.drugmedicine.medical_specialtyHeterozygoteGenotypeLipoproteinsHyperlipoproteinemia Type IIApolipoproteins ESex FactorsInternal medicineGeneticsmedicineHumansPyrrolesMolecular BiologyAllelesTriglyceridesPolymorphism GeneticTriglycerideCholesterolGenetic VariationCholesterol LDLDNALipid MetabolismEndocrinologychemistryHeptanoic AcidsPharmacogeneticsMutationbiology.proteinHydroxymethylglutaryl-CoA Reductase InhibitorsCarrier ProteinsBody mass indexPharmacogeneticsPharmacogenetics and genomics
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Sensory neuropathy with bone destruction due to a mutation in the membrane-shaping atlastin GTPase 3.

2014

Many neurodegenerative disorders present with sensory loss. In the group of hereditary sensory and autonomic neuropathies loss of nociception is one of the disease hallmarks. To determine underlying factors of sensory neurodegeneration we performed whole-exome sequencing in affected individuals with the disorder. In a family with sensory neuropathy with loss of pain perception and destruction of the pedal skeleton we report a missense mutation in a highly conserved amino acid residue of atlastin GTPase 3 (ATL3), an endoplasmic reticulum-shaping GTPase. The same mutation (p.Tyr192Cys) was identified in a second family with similar clinical outcome by screening a large cohort of 115 patients …

AtlastinAdultMaleIntracellular SpaceMutation MissenseSensory systemBiologymedicine.disease_causeEndoplasmic ReticulumGTP PhosphohydrolasesCohort StudiesFractures BoneYoung AdultmedicineMissense mutationHumansExomenociceptionAxonAge of OnsetHereditary Sensory and Autonomic NeuropathiesGenes DominantaxonGeneticsMutationEndoplasmic reticulumNeurodegenerationneurodegenerationmedicine.diseasePenetrancePedigreeHSANsensory neuronsmedicine.anatomical_structurePhenotypeCoughHaplotypesMutationGastroesophageal RefluxFemaleNeurology (clinical)Human medicineBone DiseasesNeuroscienceBrain : a journal of neurology
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