Search results for "Mutation testing"

showing 10 items of 21 documents

Familial hemiplegic migraine type 2 is linked to 0.9Mb region on chromosome 1q23

2003

Familial hemiplegic migraine (FHM) is a rare autosomal dominant disorder characterized by episodes of transient hemiparesis followed by headache. Two chromosomal loci are associated to FHM: FHM1 on chromosome 19 and FHM2 on chromosome 1q21-23. Mutations of the alpha-1A subunit of the voltage gated calcium channel (CACNA1A) are responsible for FHM1. FHM2 critical region spans 28 cM, hence hampering the identification of the responsible gene. Here, we report the FHM2 locus refining by linkage analysis on two large Italian families affected by pure FHM. The new critical region covers a small area of 0.9Mb in 1q23 and renders feasible a positional candidate approach. By mutation analysis, we ex…

AdultMaleAdolescentGenetic LinkageMigraine with AuraLocus (genetics)Genetic determinismGenetic linkageATP1A2Chromosome 19HumansMedicineChildFamilial hemiplegic migraineAgedAged 80 and overGeneticsbusiness.industryChromosome MappingChromosomeMiddle Agedmedicine.diseasePedigreeNeurologyChromosomes Human Pair 1MutationMutation testingFemaleNeurology (clinical)Lod ScorebusinessNeuroscienceAnnals of Neurology
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Mutation analysis in myophosphorylase deficiency (McArdle's disease).

1998

Inherited deficiency of myophosphorylase leads to glycogen storage disease type V (McArdle's disease). We performed mutation analysis in 9 patients of eight unrelated families from Germany with typical cliniclal presentation of myophos-phorylase deficiency. Beside previously described mutations we identified four novel mutations in the myophorsphorylase gene. Four patients were homozygous for a nonsense mutation Arg49Stop that has been reported to be the most common mutation in white patients. Two affected siblings were compound heterozygotes for a novel missense mutation Gly685Arg and the nonsense mutation Arg49Stop. One patient carried a novel nonsense mutation Arg575Stop and a previously…

AdultMaleAdolescentNonsense mutationDNA Mutational AnalysisBiologyCompound heterozygosityPolymerase Chain ReactionmedicineMissense mutationHumansAmino Acid SequenceChildCodonAgedGeneticsTransition (genetics)Base SequenceHomozygoteMiddle Agedmedicine.diseaseNeurologyMyophosphorylaseMutation (genetic algorithm)MutationMutation testingGlycogen Storage Disease Type VFemaleNeurology (clinical)Glycogen storage disease type VPolymorphism Restriction Fragment LengthAnnals of neurology
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Recessive multiple epiphyseal dysplasia (rMED): phenotype delineation in eighteen homozygotes for DTDST mutation R279W.

2003

Multiple epiphyseal dysplasia (MED) is a generalised skeletal dysplasia that although relatively mild is associated with significant morbidity. Joint pain, joint deformity, waddling gait, and short stature are the main clinical signs and symptoms. In the past, the disorder was subdivided into the milder Ribbing type, usually with flattened epiphyses,1 and the more severe Fairbank type with round epiphyses,2 but many cases were not classifiable as clearly either type.3 MED can be caused by mutations in at least six separate genes: COMP ,4–7 collagen IX ( COL9A1 , COL9A2 , and COL9A3 ),8–13 matrilin 3 ( MATN3 ),15 and the sulphate transporter, DTDST ( DTDST/SLC26A2 ). We have previously repor…

AdultMalePathologymedicine.medical_specialtyAdolescentAnion Transport ProteinsGenes RecessiveBiologySLC26A2ArginineOsteochondrodysplasiasShort statureMultiple epiphyseal dysplasiaGeneticsmedicineHumansChildGenetics (clinical)GeneticsAchondrogenesisSulfatesPoint mutationHomozygoteTryptophanChromosome MappingMembrane Transport ProteinsBiological TransportMiddle Agedmedicine.diseasePhenotypeGenetic defects of metabolism [UMCN 5.1]Amino Acid SubstitutionDysplasiaSulfate TransportersMutation (genetic algorithm)MutationMutation testingbiology.proteinFemalemedicine.symptomCarrier ProteinsLetter to JMGJournal of medical genetics
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21-Hydroxylase and 11beta-hydroxylase mutations in Romanian patients with classic congenital adrenal hyperplasia.

2005

Congenital adrenal hyperplasia (CAH) comprises autosomal recessive disorders mainly due to defects in the 21-hydroxylase (CYP21) gene.The study aimed to perform molecular characterization in 43 Romanian patients with classical CAH forms diagnosed at the Center for Genetic Diseases of the Pediatric Clinic/University Cluj (38 with 21-hydroxylase deficiency, five with 11beta-hydroxylase deficiency), to determine the frequency of mutations in the CYP21A2 gene and attempt a genotype-phenotype correlation in patients with 21-hydroxylase deficiency.Molecular analysis was performed by direct sequencing of PCR amplified products of the CYP21A2 and CYP11B1 genes.The most frequent mutation in Romanian…

AdultMalemedicine.medical_specialtyAdolescentGenotypeEndocrinology Diabetes and MetabolismClinical BiochemistryContext (language use)Biologymedicine.disease_causeBiochemistryEndocrinologyGene FrequencyInternal medicineGenotypemedicineHumansCongenital adrenal hyperplasiaSteroid 11-beta-hydroxylaseChildAllelesMutationAdrenal Hyperplasia CongenitalRomaniaBiochemistry (medical)Genetic disorder21-HydroxylaseInfantmedicine.diseaseEndocrinologyChild PreschoolMutationbiology.proteinMutation testingSteroid 11-beta-HydroxylaseFemaleSteroid 21-HydroxylaseThe Journal of clinical endocrinology and metabolism
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Mutation Analysis of Core Binding Factor A1 in Patients with Cleidocranial Dysplasia

1999

SummaryCleidocranial dysplasia (CCD) is a dominantly inherited disorder characterized by patent fontanelles, wide cranial sutures, hypoplasia of clavicles, short stature, supernumerary teeth, and other skeletal anomalies. We recently demonstrated that mutations in the transcription factor CBFA1, on chromosome 6p21, are associated with CCD. We have now analyzed the CBFA1 gene in 42 unrelated patients with CCD. In 18 patients, mutations were detected in the coding region of the CBFA1 gene, including 8 frameshift, 2 nonsense, and 9 missense mutations, as well as 2 novel polymorphisms. A cluster of missense mutations at arginine 225 (R225) identifies this residue as crucial for CBFA1 function. …

Core binding factorRecombinant Fusion ProteinsDNA Mutational AnalysisGreen Fluorescent ProteinsMolecular Sequence DataMutation MissenseHuman malformation syndromeCore Binding Factor Alpha 1 SubunitBiologyTransfectionmedicine.disease_causeBone and BonesCleidocranial dysplasiaCell LineFrameshift mutationCBFA1GeneticsmedicineHumansMissense mutationGenetics(clinical)SupernumeraryFrameshift MutationGenetics (clinical)Sequence DeletionGeneticsMutationPolymorphism GeneticCleidocranial DysplasiaCore Binding FactorsArticlesmedicine.diseaseOsteochondrodysplasiaNeoplasm ProteinsRadiographyNuclear localizationLuminescent ProteinsPhenotypeMicroscopy FluorescenceMutation testingTranscription factorHaploinsufficiencyToothTranscription FactorsThe American Journal of Human Genetics
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Large-scale network functional interactions during distraction and reappraisal in remitted bipolar and unipolar patients.

2017

Objectives The human brain is organized into large-scale networks that dynamically interact with each other. Extensive evidence has shown characteristic changes in certain large-scale networks during transitions from internally directed to externally directed attention. The aim of the present study was to compare these context-dependent network interactions during emotion regulation and to examine potential alterations in remitted unipolar and bipolar disorder patients. Methods We employed a multi-region generalized psychophysiological interactions analysis to quantify connectivity changes during distraction vs reappraisal pair-wise across 90 regions placed throughout the four networks of i…

DorsumAdultMaleBipolar DisorderEmotions050105 experimental psychologyDevelopmental psychology03 medical and health sciences0302 clinical medicineCognitionSalience (neuroscience)DistractionmedicinePermutation testingConnectomeHumans0501 psychology and cognitive sciencesAttentionBipolar disorderBiological PsychiatryNeuronal PlasticityLarge scale network05 social sciencesHealthy subjectsBrainCognitionmedicine.diseasePsychiatry and Mental healthFemaleNerve NetPsychologyNeuroscience030217 neurology & neurosurgeryBipolar disorders
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Mutations in Myosin VIIA (MYO7A) and Usherin (USH2A) in Spanish patients with usher syndrome types I and II, respectively

2002

Usher syndrome is an autosomal recessive disorder characterized by congenital hearing impairment and retinitis pigmentosa. Three clinical types are known (USH1, USH2 and USH3), and there is an extensive genetic heterogeneity, with at least ten genes implicated. The most frequently mutated genes are MYO7A, which causes USH1B, and usherin, which causes USH2A. We carried out a mutation analysis of these two genes in the Spanish population. Analysis of the MYO7A gene in patients from 30 USH1 families and sporadic cases identified 32% of disease alleles, with mutation Q821X being the most frequent. Most of the remaining variants are private mutations. With regard to USH2, mutation 2299delG was d…

GeneticsMutationMYO7AGenetic heterogeneityUsher syndromeBiologymedicine.disease_causemedicine.diseaseRetinitis pigmentosaotorhinolaryngologic diseasesGeneticsmedicineMutation testingAlleleGeneGenetics (clinical)Human Mutation
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Novel mutations including deletions of the entire OFD1 gene in 30 families with type 1 orofaciodigital syndrome : a study of the extensive clinical v…

2012

OFD1, now recognized as a ciliopathy, is characterized by malformations of the face, oral cavity and digits, and is transmitted as an X-linked condition with lethality in males. Mutations in OFD1 also cause X-linked Joubert syndrome (JBTS10) and Simpson-Golabi-Behmel syndrome type 2 (SGBS2). We have studied 55 sporadic and six familial cases of suspected OFD1. Comprehensive mutation analysis in OFD1 revealed mutations in 37 female patients from 30 families; 22 mutations have not been previously described including two heterozygous deletions spanning OFD1 and neighbouring genes. Analysis of clinical findings in patients with mutations revealed that oral features are the most reliable diagnos…

GeneticsMutationMedizinBiologymedicine.diseasemedicine.disease_causePhenotypeX-inactivationJoubert syndromeCiliopathyGeneticsmedicineMutation testingAgenesis of the corpus callosumGenetics (clinical)Ventriculomegaly
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Identification of Novel Wsf1 Mutations in a Sicilian Child with Wolfram Syndrome

2014

Wolfram Syndrome (WS) is a rare hereditary disease with autosomal recessive inheritance with incomplete penetrance. It is characterized by diabetes mellitus associated with progressive optic atrophy. The diagnosis is essentially clinical and mutation analysis is used to confirm the diagnosis. In the present study we describe the clinical and molecular features of a diabetic child carrying two novel WFS1 mutations. The Sicilian proband and his non-affected family were studied. Ophthalmologic examination included: visual acuity determination and funduscopy, optical coherent tomography, retinal fluorangiography, perimetry and electroretinogram. Molecular methods: automatic sequencing of PCR am…

GeneticsProbandMutationWolfram syndromebusiness.industryWolfram syndromeDiabetesWFS1medicine.disease_causemedicine.diseasePenetranceSettore MED/13 - EndocrinologiaAtrophyDIDMOADDiabetes mellitusMutation testingMedicineAllelebusinessJournal of Genetic Syndromes & Gene Therapy
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Novel <b><i>VANGL1</i></b> Gene Mutations in 144 Slovakian, Romanian and German Patients with Neural Tube Defects

2012

Neural tube defects (NTDs) are a group of congenital malformations of the central nervous system occurring at an average rate of 1 per 1,000 human pregnancies worldwide. Numerous genetic and environmental factors are discussed to be relevant in their etiology. In mice, mutants in >200 genes including the planar cell polarity (PCP) pathway are known to cause NTDs, and recently, heterozygous mutations in the human <i>VANGL1</i> gene have been described in a small subset of patients with NTDs. We performed a <i>VANGL1</i> mutation analysis in 144 unrelated individuals with NTDs from Slovakia, Romania and Germany and identified 3 heterozygous missense mutations: c.613…

Geneticscongenital hereditary and neonatal diseases and abnormalitiesMutationbusiness.industryMutantCentral nervous systemNeural tubeGene mutationmedicine.disease_causemedicine.anatomical_structureGeneticsMutation testingmedicineMissense mutationbusinessGeneGenetics (clinical)Molecular Syndromology
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