Search results for "gene mutation"

showing 10 items of 187 documents

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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Analysis of thiamine transporter genes in sporadic beriberi

2014

Abstract Objective Thiamine or vitamin B 1 deficiency diminishes thiamine-dependent enzymatic activity, alters mitochondrial function, impairs oxidative metabolism, and causes selective neuronal death. We analyzed for the first time, the role of all known mutations within three specific thiamine carrier genes, SLC19 A2, SLC19 A3 , and SLC25 A19 , in a patient with atrophic beriberi, a multiorgan nutritional disease caused by thiamine deficiency. Methods A 44-year-old male alcoholic patient from Morocco developed massive bilateral leg edema, a subacute sensorimotor neuropathy, and incontinence. Despite normal vitamin B 1 serum levels, his clinical picture was rapidly reverted by high-dose in…

AdultMalemedicine.medical_specialtySLC19 A- SLC25 A19SLC19 AEndocrinology Diabetes and MetabolismGene mutationBeriberimedicine.disease_causeMitochondrial Membrane Transport Proteinslaw.inventionBeriberilawInternal medicineGenotypemedicineThiamine transporterObjective: Thiamine or vitamin B1 deficiency diminishes thiamine-dependent enzymatic activity alters mitochondrial function impairs oxidative metabolism and causes selective neuronal death. We analyzed for the first time the role of all known mutations within three specific thiamine carrier genes SLC19 A2 SLC19 A3 and SLC25 A19 in a patient with atrophic beriberi a multiorgan nutritional disease caused by thiamine deficiency. Methods: A 44-year-old male alcoholic patient from Morocco developed massive bilateral leg edema a subacute sensorimotor neuropathy and incontinence. Despite normal vitamin B1 serum levels his clinical picture was rapidly reverted by high-dose intramuscular thiamine treatment suggesting a possible genetic resistance. We used polymerase chain reaction followed by amplicon sequencing to study all the known thiamine-related gene mutations identified within the Human Gene Mutation Database. Results: Thirty-seven mutations were tested: 29 in SLC19 A2 6 in SLC19 A3 and 2 in SLC25 A19. Mutational analyses showed a wild-type genotype for all sequences investigated. Conclusion: This is the first genetic study in beriberi disease. We did not detect any known mutation in any of the three genes in a sporadic dry beriberi patient. We cannot exclude a role for other known or unknown mutations in the same genes or in other thiamine-associated genes in the occurrence of this nutritional neuropathy.HumansThiamineGenePolymerase chain reactionGeneticsMutationNutrition and DieteticsbiologyMembrane Transport ProteinsThiamine Deficiencymedicine.diseaseAlcoholismEndocrinologyMutationbiology.proteinThiamineMutations
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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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Primary HBB gene mutation severity and long-term outcomes in a global cohort of β-thalassaemia

2021

In β-thalassaemia, the severity of inherited β-globin gene mutations determines the severity of the clinical phenotype at presentation and subsequent transfusion requirements. However, data on associated long-term outcomes remain limited. We analysed data from 2109 β-thalassaemia patients with available genotypes in a global database. Genotype severity was grouped as β0 /β0 , β0 /β+ , β+ /β+ , β0 /β++ , β+ /β++ , and β++ /β++ . Patients were followed from birth until death or loss to follow-up. The median follow-up time was 34·1 years. Mortality and multiple morbidity outcomes were analyzed through five different stratification models of genotype severity groups. Interestingly, β0 and β+ mu…

AdultMalemedicine.medical_specialtyphenotypegenotypemorbidityKaplan-Meier Estimatebeta-GlobinsGene mutationβ thalassaemiaGlobal HealthGastroenterologySeverity of Illness IndexsurvivalCohort StudiesYoung AdultInternal medicineGenotypemedicineLong term outcomesOdds RatioHumansAllelesgenotype; morbidity; mortality; phenotype; survivalProportional Hazards Modelsbusiness.industrybeta-ThalassemiaDisease ManagementHematologyPrognosisPhenotypemortalityConfidence intervalPopulation SurveillanceCohortMutationFemaleRisk of deathbusinessFollow-Up Studies
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Six novel mutations of the LDL receptor gene in FH kindred of Sicilian and Paraguayan descent

2006

Familial hypercholesterolemia (FH) is an autosomal dominant inherited disease caused by mutations in the gene coding for the low density lipoprotein receptor (LDL-R). It is characterized by a high concentration of low density lipoprotein (LDL), which frequently gives rise to premature coronary artery disease. We studied the probands of five FH Sicilian families with 'definite' FH and one proband of Paraguayan descent with homozygous FH who has been treated with an effective living-donor liver transplantation. In order to seek the molecular defect in these six families, we used direct sequencing to define the molecular defects of the LDL-R gene responsible for the disease. We described three…

AdultProbandhypercholesterolemia LDL receptor gene mutation analysis direct sequencing splicing living-donor transplantationSettore MED/09 - Medicina InternaDNA Mutational AnalysisDirect sequencingHypercholesterolemiaFamilial hypercholesterolemiaBiologyGene mutationSplicingmedicine.disease_causeFrameshift mutationHyperlipoproteinemia Type IIExonGeneticsmedicineHumansMissense mutationRNA MessengerChildSicilyCells CulturedLiving-donor transplantationLDL receptor geneGeneticsMutationIntronExonsGeneral MedicineMiddle Agedmedicine.diseaseLipidsMolecular biologyPedigreeDirect sequencing; Hypercholesterolemia; LDL receptor gene; Living-donor transplantation; Mutation analysis; SplicingMutation analysisReceptors LDLParaguayChild PreschoolMutationBiological Assay
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Refractory Acne and 21-Hydroxylase Deficiency in a Selected Group of Female Patients.

2009

<i>Background:</i> Excessive androgen production, suspected in women when acne is accompanied by hirsutism and menstrual irregularities, may be due to congenital adrenal hyperplasia. This inherited disorder of cortisol biosynthesis is caused in more than 90–95% of all cases by 21-hydroxylase deficiency (21-OHD). The steroid 21-hydroxylase gene <i>(CYP21)</i> has a high degree of variability. <i>Objective:</i> This study was conducted to evaluate <i>CYP21 </i>gene mutations in a selected group of women with papulopustular and comedonal acne refractory to treatment, irregular menses and hirsutism. <i>Methods:</i> 30 out of 61 women e…

Adultmedicine.medical_specialtyAdolescentDrug ResistancePhysiologyDermatologyAdrenocorticotropic hormoneYoung AdultSettore MED/38 - Pediatria Generale E SpecialisticaPapulopustularInternal medicineAcne VulgarismedicineHumansPoint MutationCongenital adrenal hyperplasiaGenetic TestingRefractory acne Excessive androgen production Non-classical 21-hydroxylase deficiency CYP21 gene mutations.AcnehirsutismAdrenal Hyperplasia Congenitalmedicine.diagnostic_testbiologybusiness.industry17-alpha-HydroxyprogesteroneACTH stimulation test21-Hydroxylasemedicine.diseasePolycystic ovaryEndocrinologybiology.proteinFemaleSteroid 21-HydroxylaseHyperandrogenismbusinessPolycystic Ovary Syndrome
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Comparison of the rates of joint arthroplasty in patients with severe factor VIII and IX deficiency: an index of different clinical severity of the 2…

2009

AbstractData from the Italian Hemophilia Centres were collected to perform a retrospective survey of joint arthroplasty in patients with severe hemophilia. Twenty-nine of 49 hemophilia centers reported that 328 of the 347 operations were carried out in 253 patients with severe hemophilia A (HA) and 19 in 15 patients with severe hemophilia B (HB). When results were normalized to the whole Italian hemophilia population (1770 severe HA and 319 severe HB), patients with HA had a 3-fold higher risk of undergoing joint arthroplasty (odds ratio [OR], 3.38; 95% confidence interval [CI], 1.97-5.77; P < .001). These results were confirmed after adjustment for age, HIV, hepatitis C virus (HCV), and…

Adultmedicine.medical_specialtyAdolescentmedicine.medical_treatmentImmunologyPopulationmacromolecular substancesGene mutationHemophilia AHemophilia BSeverity of Illness IndexBiochemistryArthroplastySettore MED/15 - Malattie Del SangueCohort StudiesYoung AdultRisk Factorshemic and lymphatic diseasesInternal medicineSeverity of illnessmedicineCoagulopathyHumansChildeducationRetrospective Studieseducation.field_of_studyHematologyhamophilia arthroplastybusiness.industryRetrospective cohort studyCell BiologyHematologyOdds ratioBlood Coagulation DisordersMiddle Agedmedicine.diseaseArthroplastySurgeryItalyJoint DiseasesbusinessAlgorithms
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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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Genetic polymorphisms affecting the phenotypic expression in familial hypercholesterolemia

2004

The clinical expression of heterozygous familial hypercholesterolemia (FH) is highly variable even in patients carrying the same LDL receptor (LDL-R) gene mutation. This variability might be due to environmental factors as well as to modifying genes affecting lipoprotein metabolism. We investigated Apo E (2, 3, 4), MTP (-493G/T), Apo B (-516C/T), Apo A-V (-1131T/C), HL (-514C/T and -250G/A), FABP-2 (A54T), LPL (D9N, N291S, S447X) and ABCA1 (R219K) polymorphisms in 221 unrelated FH index cases and 349 FH relatives with defined LDL-R gene mutations. We found a significant and independent effect of the following polymorphisms on: (i) plasma LDL-C (Apo E, MTP and Apo B); (ii) plasma HDL-C (HL, …

Apolipoprotein EMaleSettore MED/09 - Medicina InternaApolipoprotein BFamilial hypercholesterolemiaGene mutationPolymerase Chain ReactionCoronary artery diseasecoronary artery disease; familial hypercholesterolemia; genetic polymorphisms; plasma lipidsCohort Studieschemistry.chemical_compoundGenotypePlasma lipidsOdds RatiobiologyFamilial hypercholesterolemia Plasma lipids Genetic polymorphisms Coronary artery diseaseIncidenceMiddle AgedPhenotypelipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineAdultmedicine.medical_specialtyMolecular Sequence DataFamilial hypercholesterolemiaPlasma lipidGenetic polymorphismsRisk AssessmentHyperlipoproteinemia Type IIFamilial hypercholesterolemia; Plasma lipids; Genetic polymorphisms; Coronary artery diseasePredictive Value of TestsInternal medicinemedicineConfidence IntervalsHumansGenetic Predisposition to DiseaseGenetic polymorphismPolymorphism GeneticBase SequenceCholesterolCholesterol HDLCase-control studyCholesterol LDLmedicine.diseaseEndocrinologyApolipoproteinschemistrySettore MED/03 - Genetica MedicaGene Expression RegulationReceptors LDLCase-Control StudiesLDL receptorbiology.protein
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Azole-resistant Aspergillus fumigatus: A global phenomenon originating in the environment?

2019

Abstract Aspergillus fumigatus is the predominant etiological agent of invasive aspergillosis (IA), a difficult-to-manage fungal disease associated with a high case fatality rate. Azole antifungals, particularly voriconazole, have significantly improved the survival rate of patients with IA. However, the clinical advances made possible through the use of medical azoles could be threatened by the emergence of azole-resistant strains which has been reported in an ever-increasing number of countries over the last 10 years. The major resistance mechanism, that combines point mutation(s) in the coding sequence of cyp51A gene and an insertion of a tandem repeat in the promoter region of this gene…

AzolesAntifungal AgentsGenotypeMicrobial Sensitivity TestsGene mutationAspergillosisAspergillus fumigatusMicrobiologyFungal Proteins03 medical and health sciencesDrug Resistance FungalmedicineAspergillosisHumansGeneComputingMilieux_MISCELLANEOUSchemistry.chemical_classificationVoriconazole[SDV.EE.SANT]Life Sciences [q-bio]/Ecology environment/Health0303 health sciencesbiology030306 microbiologyPoint mutationAspergillus fumigatusbiology.organism_classificationmedicine.disease3. Good healthInfectious DiseaseschemistryAzoleEffluxVoriconazolemedicine.drug
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