Search results for "Mutational analysis"

showing 10 items of 245 documents

Clinical characteristics and determinants of the phenotype in TMEM43 arrhythmogenic right ventricular cardiomyopathy type 5.

2020

Arrhythmogenic right ventricular cardiomyopathy type V (ARVC-5) is the most aggressive heterozygous form of ARVC. It is predominantly caused by a fully penetrant mutation (p.S358L) in the nondesmosomal gene TMEM43-endemic to Newfoundland, Canada. To date, all familial cases reported worldwide share a common ancestral haplotype. It is unknown whether the p.S358L mutation by itself causes ARVC-5 or whether the disease is influenced by genetic or environmental factors. The purpose of this study was to examine the phenotype, clinical course, and the impact of exercise on patients with p.S358L ARVC-5 without the Newfoundland genetic background. We studied 62 affected individuals and 73 noncarrie…

AdultMalemedicine.medical_specialtyDNA Mutational AnalysisMutation MissenseDisease030204 cardiovascular system & hematologyVentricular Function LeftRight ventricular cardiomyopathySudden cardiac deathElectrocardiography03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicinemedicineGeneticsHumans030212 general & internal medicineExerciseArrhythmogenic Right Ventricular DysplasiaEjection fractionTMEM43business.industryIncidence (epidemiology)HaplotypeMembrane ProteinsStroke VolumeDNAmedicine.diseasePhenotypePedigree3. Good healthPhenotypeMutation (genetic algorithm)CardiologyFemaleCardiology and Cardiovascular MedicinebusinessArrhythmogenic right ventricular cardiomyopathyArrhythmia
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Norepinephrine transporter gene polymorphism is not associated with susceptibility to alcohol dependence

2002

Abnormalities in monoamine neurotransmission have been implicated in the pathogenesis of alcoholism, mood disorders and schizophrenia. Murine norepinephrine transporter gene (NET) has been mapped to a region on chromosome 8 where a quantitative trait locus for ethanol sensitivity. Therefore we tested whether norepinephrine transporter (NET) gene variants confer susceptibility to either alcohol dependence or severe alcohol withdrawal symptoms. There is a highly polymorphic silent G1287A mutation in the NET gene. In our study 157 alcoholics and 185 healthy unrelated matched control subjects were analyzed for a silent G1287A mutation. No significant differences in allele and genotype distribut…

AdultMalemedicine.medical_specialtyGenotypeDNA Mutational AnalysisMolecular Sequence DataAlcohol Withdrawal DeliriumGene FrequencyPolymorphism (computer science)Internal medicineGenotypemedicineHumansGenetic Predisposition to DiseaseRNA MessengerAlleleAllelesBiological PsychiatryGeneticsNorepinephrine Plasma Membrane Transport ProteinsPolymorphism GeneticSymportersbiologybusiness.industryAlcohol dependenceExonsMiddle Agedmedicine.diseaseAlcoholismPsychiatry and Mental healthMonoamine neurotransmitterEndocrinologyMood disordersNorepinephrine transporterbiology.proteinFemaleGene polymorphismbusinessPolymorphism Restriction Fragment LengthPsychiatry Research
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Inflammation, genetics, and longevity: further studies on the protective effects in men of IL-10 -1082 promoter SNP and its interaction with TNF-alph…

2003

Ageing is associated with chronic, low grade inflammatory activity leading to long term tissue damage, and systemic chronic inflammation has been found to be related to mortality risk from all causes in older persons.1 Also, the genetic constitution of the organism interacting with systemic inflammation may cause defined organ specific illnesses. Thus, age related diseases such as Alzheimer’s disease (AD), Parkinson’s disease, atherosclerosis, type 2 diabetes, sarcopenia, and osteoporosis, are initiated or worsened by systemic inflammation, suggesting the critical importance of unregulated systemic inflammation in the shortening of survival in humans.1–3 Accordingly, proinflammatory cytokin…

AdultMalemedicine.medical_specialtyGenotypemedicine.medical_treatmentDNA Mutational AnalysisLongevityInflammationSingle-nucleotide polymorphismBiologySystemic inflammationPolymorphism Single NucleotideProinflammatory cytokineGene FrequencyInternal medicineGeneticsmedicineHumansAllelePromoter Regions GeneticGenetics (clinical)AgedGeneticsAged 80 and overInflammationTumor Necrosis Factor-alphaAge FactorsDNAMiddle AgedInterleukin-10Interleukin 10CytokineEndocrinologyImmunologyFemalemedicine.symptomCentenarianLetter to JMGJournal of medical genetics
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Mutations in the skeletal muscle alpha-actin gene in patients with actin myopathy and nemaline myopathy

1999

Muscle contraction results from the force generated between the thin filament protein actin and the thick filament protein myosin, which causes the thick and thin muscle filaments to slide past each other. There are skeletal muscle, cardiac muscle, smooth muscle and non-muscle isoforms of both actin and myosin. Inherited diseases in humans have been associated with defects in cardiac actin (dilated cardiomyopathy and hypertrophic cardiomyopathy), cardiac myosin (hypertrophic cardiomyopathy) and non-muscle myosin (deafness). Here we report that mutations in the human skeletal muscle alpha-actin gene (ACTA1) are associated with two different muscle diseases, 'congenital myopathy with excess o…

AdultMalemedicine.medical_specialtyMyofilamentAdolescentDNA Mutational AnalysisMolecular Sequence Datamacromolecular substancesBiologyMyopathies NemalineTPM203 medical and health sciences0302 clinical medicineNemaline myopathyMuscular DiseasesInternal medicineMyosinGeneticsmedicineHumansPoint MutationAmino Acid SequenceChildMuscle SkeletalPolymorphism Single-Stranded ConformationalActin030304 developmental biologyFamily Health0303 health sciencesPolymorphism GeneticBase SequenceSequence Homology Amino AcidInfantSkeletal muscleDNASequence Analysis DNAmedicine.diseaseCongenital myopathyActins3. Good healthEndocrinologymedicine.anatomical_structureAmino Acid SubstitutionChild PreschoolMutationFemaleMYH7030217 neurology & neurosurgery
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Myocardial 123metaiodobenzylguanidine uptake in genetic Parkinson's disease.

2008

Myocardial (123)Metaiodobenzylguanidine (MIBG) enables the assessment of postganglionic sympathetic cardiac innervation. MIBG uptake is decreased in nearly all patients with Parkinson's disease (PD). Our objective was to evaluate MIBG uptake in patients with genetic PD. We investigated MIBG uptake in 14 patients with PD associated with mutations in different genes (Parkin, DJ-1, PINK], and leucine-rich repeat kinase 2 -LRRK2), in 15 patients with idiopathic PD, and 10 control subjects. The myocardial MIGB uptake was preserved in 3 of the 4 Parkin-associated Parkinsonisms, in I of the 2 patients with DJ-1 mutations, in 1 of the 2 brothers with PINK] mutations, in 3 of the 6 unrelated patient…

AdultMalemedicine.medical_specialtyParkinson's diseaseGenotypeUbiquitin-Protein LigasesDNA Mutational AnalysisProtein Deglycase DJ-1PINK1Gene mutationProtein Serine-Threonine Kinasesmedicine.disease_causeLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Severity of Illness IndexParkinCentral nervous system diseaseDiagnosis DifferentialDegenerative diseaseParkinsonian DisordersInternal medicineSurveys and QuestionnairesmedicineHumansPoint MutationPromoter Regions GeneticGenetic PD Myocardial scintigraphyOncogene ProteinsTomography Emission-Computed Single-PhotonMutationMovement Disordersbusiness.industryMyocardiumIntracellular Signaling Peptides and ProteinsParkinson DiseaseGalvanic Skin ResponseMiddle Agedmedicine.diseaseLRRK2nervous system diseases3-IodobenzylguanidineEndocrinologyNeurologySettore MED/26 - NeurologiaFemaleNeurology (clinical)RadiopharmaceuticalsbusinessProtein KinasesMovement disorders : official journal of the Movement Disorder Society
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Lattice Corneal Dystrophy Type 1

2014

PURPOSE To evaluate the question whether lattice corneal dystrophy type 1 (LCD1) is of epithelial or stromal origin. METHODS The landmark of advanced LCD1 shows central superficial haze and paracentral stromal lattice lines. In 16 eyes of 8 affected individuals of 2 families, a penetrating keratoplasty was performed. The follow-up was 8 to 16 years after penetrating keratoplasty. Slit-lamp documentation of the patients was evaluated in direct and indirect illumination with dilated pupil to assess the horizontal and vertical pattern of new deposits on the corneal graft. Three affected patients of 2 families are demonstrated in detail. A DNA analysis was performed. RESULTS Gene identification…

AdultMalemedicine.medical_specialtyStromal cellCorneal StromaDNA Mutational AnalysisCorneal graftCorneal KeratocytesCorneal erosionDirect illuminationTransforming Growth Factor betaOphthalmologyTGFBI genemedicineHumansCorneal Dystrophies HereditaryExtracellular Matrix Proteinsbusiness.industryEpithelium Cornealmedicine.diseaseeye diseasesOphthalmologyMutationLattice corneal dystrophyFemalebusinessKeratoplasty PenetratingTGFBICornea
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Clinical and genetic characteristics of congenital hypothyroidism due to mutations in the thyroid peroxidase (TPO) gene in Israelis

2007

Summary Objectives  Iodide organification defect (IOD) is characterized by a reduced ability of the thyroid gland to retain iodide and results in hypothyroidism. Mutations in the thyroid peroxidase (TPO) gene are a frequent cause of IOD. While TPO mutations have been identified in various populations, none have been reported in Israeli patients with IOD. The objectives of this study were to characterize the molecular basis of IOD in an Israeli Arab-Muslim population and to analyse the clinical, neurological and imaging data of patients with TPO mutations followed for up to 29 years. Patients  Twenty-two patients from six core families with congenital hypothyroidism (CH) and IOD living in th…

AdultMalemedicine.medical_specialtyendocrine systemAdolescentEndocrinology Diabetes and MetabolismPopulationDNA Mutational AnalysisConsanguinityGene mutationmedicine.disease_causeIodide PeroxidaseIslamConsanguinityEndocrinologyThyroid peroxidaseInternal medicinemedicineCongenital HypothyroidismHumansGenetic TestingIsraeleducationChildMutationeducation.field_of_studybiologybusiness.industryThyroidPrimary hypothyroidismExonsmedicine.diseaseCongenital hypothyroidismArabsmedicine.anatomical_structureEndocrinologyHaplotypesChild PreschoolMutationbiology.proteinFemalebusinessPolymorphism Restriction Fragment Length
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Detection of a germline mutation and somatic homozygous loss of the von Hippel-Lindau tumor-suppressor gene in a family with a de novo mutation

1996

von Hippel-Lindau (VHL) disease is a pleiotropic disorder featuring a variety of malignant and benign tumors of the eye, central nervous system, kidney, and adrenal gland. Recently the VHL gene has been identified in the chromosomal region 3p25-26. Prognosis and successful management of VHL patients and their descendants depend on unambiguous diagnosis. Due to recurrent hemangioblastomas, a29-year-old patient without familial history of VHL disease was diagnosed to be at risk for the disease. Histopathological examination of a small renal mass identified a clear cell tumor with a G1 grading. Genetic characterization of the germline and of the renal tumor was performed. Polymerase chain reac…

AdultMalemedicine.medical_specialtyvon Hippel-Lindau DiseaseTumor suppressor geneDNA Mutational AnalysisMolecular Sequence Dataurologic and male genital diseasesPolymerase Chain ReactionGermlineGermline mutationVon Hippel–Lindau tumor suppressorGeneticsmedicineHumansGenes Tumor SuppressorSpinal Cord NeoplasmsVon Hippel–Lindau diseaseGerm-Line MutationPolymorphism Single-Stranded ConformationalGenetics (clinical)Sequence Deletionbiologymedicine.diagnostic_testHomozygoteCytogeneticsExonsmedicine.diseaseKidney Neoplasmsfemale genital diseases and pregnancy complicationsHemangioblastomaPedigreeKaryotypingChromosomal regionbiology.proteinCancer researchFemaleChromosomes Human Pair 3Chromosome DeletionFluorescence in situ hybridizationHuman Genetics
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A Novel Loss-of-Function Mutation (N48K) in the PTEN Gene in a Spanish Patient with Cowden Disease

2003

Cowden disease, also known as multiple hamartoma syndrome, is a rare disease inherited in an autosomal dominant pattern, which confers a high risk of developing breast and thyroid carcinomas. Mutations in PTEN, a tumor suppressor gene located on chromosome 10q23, have been identified in patients with Cowden disease. In this work, the direct sequencing of all coding regions of the PTEN gene led us to the identification of N48K, a new germline PTEN missense mutation, in a patient suffering from Cowden disease. The genetic analysis of 200 chromosomes from healthy individuals revealed that the variant was not common in our population. Moreover, by functional analysis we found that the ability o…

AdultPTENcongenital hereditary and neonatal diseases and abnormalitiesTumor suppressor geneDNA Mutational AnalysisMolecular Sequence DataLoss of Heterozygositygenetic analysisDermatologyProtein Serine-Threonine Kinasesmedicine.disease_causeProto-Oncogene MasBiochemistryGenètica molecularfunctional analysisLoss of heterozygosityStructure-Activity RelationshipProto-Oncogene ProteinsmedicineLeukocytesMissense mutationPTENHumansPoint MutationCowden diseaseAmino Acid SequenceMolecular BiologyTumorsGeneticsMutationbiologySequence Homology Amino AcidPoint mutationTumor Suppressor ProteinsPTEN PhosphohydrolaseMultiple hamartoma syndromeCowden syndromeCell Biologymedicine.diseasePhosphoric Monoester HydrolasesN48KSpainbiology.proteinCancer researchFemaleHamartoma Syndrome MultipleProto-Oncogene Proteins c-akt
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Congenital neutropenia with retinopathy, a new phenotype without intellectual deficiency or obesity secondary toVPS13Bmutations

2013

Over one hundred VPS13B mutations are reported in Cohen syndrome (CS). Most cases exhibit a homogeneous phenotype that includes intellectual deficiency (ID), microcephaly, facial dysmorphism, slender extremities, truncal obesity, progressive chorioretinal dystrophy, and neutropenia. We report on a patient carrying two VPS13B splicing mutations with an atypical phenotype that included microcephaly, retinopathy, and congenital neutropenia, but neither obesity nor ID. RNA analysis of the IVS34+2T_+3AinsT mutation did not reveal any abnormal splice fragments but mRNA quantification showed a significant decrease in VPS13B expression. RNA sequencing analysis up- and downstream from the IVS57+2T>C…

AdultPathologymedicine.medical_specialtyMicrocephalyNeutropeniaDNA Mutational AnalysisVesicular Transport ProteinsNeutropeniamedicine.disease_causeRetinal DiseasesIntellectual DisabilityGene OrderGeneticsmedicineCongenital Bone Marrow Failure SyndromesHumansObesityCongenital NeutropeniaGenetics (clinical)GeneticsMutationCohen syndromebusiness.industryFaciesSyndromemedicine.diseasePhenotypePedigreeVPS13BPhenotypeMutationFemalebusinessRetinopathyAmerican Journal of Medical Genetics Part A
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