Search results for "HETEROGENEITY"

showing 10 items of 402 documents

Genotyping and antifungal susceptibility of human subgingival Candida albicans isolates.

2002

Subgingival colonization by Candida albicans has been described in human immunodeficiency virus (HIV)-infected individuals, but subgingival isolates have scarcely been characterized, particularly with respect to genotype and antifungal susceptibility. A series of 29 subgingival strains of C. albicans isolated from nine HIV-infected individuals was typed by electrophoretic karyotyping and tested for susceptibility to fluconazole, itraconazole, the new investigational triazole posaconazole and amphotericin B. DNA typing showed genetic heterogeneity within subgingival isolates, as almost every individual harbored his/her own specific isolate. Genetic identity was usually demonstrated within or…

AdultMalePosaconazoleAntifungal AgentsItraconazoleDental PlaqueHIV InfectionsMicrobial Sensitivity TestsMicrobiologyPeriodontal pathogenGenetic HeterogeneityDrug Resistance FungalAmphotericin BGenotypeCandida albicansmedicineHumansCandida albicansDNA FungalMycological Typing TechniquesGeneral DentistryGenotypingFluconazolebiologyCell BiologyGeneral MedicineTriazolesbiology.organism_classificationVirologyCorpus albicansOtorhinolaryngologyKaryotypingFemaleItraconazoleFluconazolemedicine.drugArchives of oral biology
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The HLA locus and multiple sclerosis in Sicily

2005

The authors report the analysis of HLA-class II allelic heterogeneity in a well characterized multiple sclerosis (MS) Sicilian dataset. Family-based association analysis revealed evidence for excess transmission to affected individuals for alleles HLA-DRB1*1501, DRB1*04, and DQB1*0302. When analyzed as haplotypes, the authors observed excess transmission for the DRB1*0400-DQB1*0302 haplotype. Sicilian patients share the HLA-DRB1*1501 susceptibility allele with affecteds living in continental Italy, but also display the allelic heterogeneity that characterizes Mediterranean populations.

AdultMaleRiskmusculoskeletal diseasesMultiple SclerosisAdolescentGenes MHC Class IILocus (genetics)Human leukocyte antigenBiologySeverity of Illness IndexLinkage DisequilibriumCohort StudiesDisability EvaluationGene Frequencyimmune system diseasesMultiple Sclerosis/epidemiologyPrevalencemedicineHumansGenetic Predisposition to DiseaseAge of OnsetAlleleskin and connective tissue diseasesSicilyAllelesGenetic associationGeneticsHLA-D AntigensIncidenceMultiple sclerosisHaplotypeGene Poolmedicine.diseaselanguage.human_languageSettore BIO/18 - GeneticaHaplotypeslanguageFemaleAllelic heterogeneitySettore MED/26 - NeurologiaNeurology (clinical)Sicilian
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Phenotypic variability in patients with generalised resistance to thyroid hormone.

1995

Genetic linkage of generalised resistance to thyroid hormone (GRTH) to the human thyroid receptor beta 1 gene has been identified. To date 38 different mutations in several kindreds have been documented. We report on a family with GRTH displaying an adenine for guanine substitution at nucleotide 1234 resulting in a threonine for alanine substitution at codon 317 of exon 9. This mutation has been described for different phenotypes, suggesting that the heterogeneity in GRTH may be the result of multiple genetic factors.

AdultMaleThyroid Hormone Resistance SyndromeThyroid Hormonesmedicine.medical_specialtyGenetic LinkageMolecular Sequence DataThyroid Function TestsBiologymedicine.disease_causeThyroid function testsGenetic HeterogeneityExonGenetic linkageInternal medicineGeneticsmedicineHumansPoint MutationAmino Acid SequenceChildGeneGenetics (clinical)GeneticsMutationReceptors Thyroid HormoneBase Sequencemedicine.diagnostic_testGenetic heterogeneityPoint mutationThyroidPedigreePhenotypemedicine.anatomical_structureEndocrinologyChild PreschoolFemaleResearch ArticleJournal of Medical Genetics
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MFAP5 Loss-of-Function Mutations Underscore the Involvement of Matrix Alteration in the Pathogenesis of Familial Thoracic Aortic Aneurysms and Dissec…

2014

Thoracic aortic aneurysm and dissection (TAAD) is an autosomal-dominant disorder with major life-threatening complications. The disease displays great genetic heterogeneity with some forms allelic to Marfan and Loeys-Dietz syndrome, and an important number of cases still remain unexplained at the molecular level. Through whole-exome sequencing of affected members in a large TAAD-affected family, we identified the c.472CT (p.Arg158(∗)) nonsense mutation in MFAP5 encoding the extracellular matrix component MAGP-2. This protein interacts with elastin fibers and the microfibrillar network. Mutation screening of 403 additional probands identified an additional missense mutation of MFAP5 (c.62GT …

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesAdolescentExtracellular matrix componentNonsense mutationHaploinsufficiencyThoracic aortic aneurysmPathogenesisContractile ProteinsReportGeneticsmedicineHumansMissense mutationGenetics(clinical)ExomeChildGenetics (clinical)AgedGlycoproteinsAged 80 and overGeneticsAortic Aneurysm ThoracicbiologyGenetic heterogeneitySequence Analysis DNAFibroblastsMiddle Agedmedicine.diseasePedigree3. Good healthAortic DissectionAmino Acid SubstitutionCodon Nonsensebiology.proteinIntercellular Signaling Peptides and ProteinsFemaleHaploinsufficiencyElastinThe American Journal of Human Genetics
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Intragenic KANSL1 mutations and chromosome 17q21.31 deletions: broadening the clinical spectrum and genotype-phenotype correlations in a large cohort…

2015

Background The 17q21.31 deletion syndrome phenotype can be caused by either chromosome deletions or point mutations in the KANSL1 gene. To date, about 60 subjects with chromosome deletion and 4 subjects with point mutation in KANSL1 have been reported. Prevalence of chromosome deletions compared with point mutations, genotype–phenotype correlations and phenotypic variability have yet to be fully clarified. Methods We report genotype–phenotype correlations in 27 novel subjects with 17q21.31 deletion and in 5 subjects with KANSL1 point mutation , 3 of whom were not previously reported. Results The prevalence of chromosome deletion and KANSL1 mutation was 83% and 17%, respectively. All patient…

AdultMalemedicine.medical_specialtyAdolescentgenotype-phenotype correlationsKoolen De Vries syndromeKANSL1 mutationHaploinsufficiencyBiologySettore MED/03 - GENETICA MEDICASeverity of Illness IndexCraniofacial AbnormalitiesYoung AdultSeizuresMolecular geneticsGeneticsmedicineHumansAbnormalities MultipleLanguage Development DisordersChildGenetics (clinical)Genetic Association StudiesGeneticsOptic nerve hypoplasiaFetal Growth RetardationPoint mutationMacrocephalyInfantNuclear ProteinsSyndromeclinical heterogeneitySmith–Magenis syndromemedicine.diseaseChild PreschoolSpeech delayFemalemedicine.symptomChromosome DeletionSmith-Magenis SyndromeHaploinsufficiencyChromosomes Human Pair 1717q21.31 deletion
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High cognitive reserve in bipolar disorders as a moderator of neurocognitive impairment

2017

BackgroundCognitive reserve (CR) reflects the capacity of the brain to endure neuropathology, minimize clinical manifestations and successfully complete cognitive tasks. The present study aims to determine whether high CR may constitute a moderator of cognitive functioning in bipolar disorder (BD).MethodsOne hundred and two patients with BD and 32 healthy controls were enrolled. All patients met DSM-IV criteria for I or II BD and were euthymic (YMRS ≤ 6 and HDRS ≤ 8) during a 6-month period. All participants were tested with a comprehensive neuropsychological battery, and a Cerebral Reserve Score (CRS) was estimated. Subjects with a CRS below the group median were classified as having low C…

AdultMalemedicine.medical_specialtyElementary cognitive taskBipolar DisorderBipolar disorderCognitive reserveNeuropsychological TestsAudiologyYoung Adult03 medical and health sciences0302 clinical medicineCognitive ReservemedicineHumansVerbal fluency testCognitive skillBipolar disorderPsychiatryNeurocognitionCognitive reserveCalifornia Verbal Learning TestBipolar disorder Cognitive heterogeneity Cognitive reserve NeurocognitionMiddle Agedmedicine.diseaseCyclothymic Disorder030227 psychiatryDiagnostic and Statistical Manual of Mental DisordersPsychiatry and Mental healthClinical PsychologyCross-Sectional StudiesCognitive remediation therapyFemaleCuesVerbal memoryCognition DisordersPsychologyNeurocognitive030217 neurology & neurosurgeryCognitive heterogeneityJournal of Affective Disorders
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Familial HDL deficiency due to ABCA1 gene mutations with or without other genetic lipoprotein disorders

2004

Mutations in ABCA1 have been shown to be the cause of Tangier disease (TD) and some forms of familial hypoalphalipoproteinemia (HA), two genetic disorders characterized by low plasma HDL levels. Here we report six subjects with low HDL, carrying seven ABCA1 mutations, six of which are previously unreported. Two mutations (R557X and H160FsX173) were predicted to generate short truncated proteins; two mutations (E284K and Y482C) were located in the first extracellular loop and two (R1901S and Q2196H) in the C-terminal cytoplasmic domain of ABCA1. Two subjects found to be compound heterozygotes for ABCA1 mutations did not have overt clinical manifestations of TD. Three subjects, all with prema…

AdultMalemedicine.medical_specialtyHeterozygoteSettore MED/09 - Medicina InternaApolipoprotein BAdolescentPremature coronary artery diseaseTangier diseaseCoronary DiseaseBiologyGene mutationmedicine.disease_causeCompound heterozygosityTangier diseaseInternal medicineGenotypeABCA1 genemedicineHumansChildHypoalphalipoproteinemiaSelection BiasAgedApolipoproteins BGeneticsMutationFamilial defective Apo B (FDB)Apolipoprotein A-ICholesterol HDLnutritional and metabolic diseasesMiddle Agedmedicine.diseaseLipoprotein lipaseTangier disease; Familial HDL deficiency; ABCA1 gene; Familial defective Apo B (FDB); Lipoprotein lipase; Premature coronary artery diseaseEndocrinologyChild PreschoolMutationbiology.proteinlipids (amino acids peptides and proteins)Allelic heterogeneityATP-Binding Cassette TransportersFemaleCardiology and Cardiovascular MedicineFamilial HDL deficiencyATP Binding Cassette Transporter 1
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Human cooperation in groups: variation begets variation

2015

Open Access Published: 04 November 2015 Human cooperation in groups: variation begets variation Pieter van den Berg, Lucas Molleman, Jaakko Junikka, Mikael Puurtinen & Franz J. Weissing Scientific Reports volume 5, Article number: 16144 (2015) Cite this article 383 Accesses 4 Citations 6 Altmetric Metricsdetails Abstract Many experiments on human cooperation have revealed that individuals differ systematically in their tendency to cooperate with others. It has also been shown that individuals condition their behaviour on the overall cooperation level of their peers. Yet, little is known about how individuals respond to heterogeneity in cooperativeness in their neighbourhood. Here, we presen…

AdultMaleta520genetic structuresPREFERENCESBioinformaticsINDIVIDUAL-DIFFERENCESArticleYoung AdultGame Theorypublic goods gamePublic goods gameHumansMedicineCooperative BehaviorNeighbourhood (mathematics)cooperation tendencyMultidisciplinarybusiness.industryCooperativenesshuman cooperationPrisoner's dilemmaPublic goodPERSONALITY-DIFFERENCESEVOLUTIONSOCIAL VALUE ORIENTATIONVariation (linguistics)Group selectionGROUP SELECTIONCooperation Heterogeneity Public goods Behavioural experimentANIMAL PERSONALITIESheterogeneous behaviourPRISONERS-DILEMMAta1181FemaleHUMAN ALTRUISMbusinessSocial psychologyGame theoryBEHAVIOR
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Genetic variability of hepatitis C virus non-structural protein 3 and virus-specific CD8+ response in patients with chronic hepatitis C.

2004

Hepatitis C virus (HCV) variation in specific T-cell epitopes may represent a mechanism of viral persistence in chronic infection. We examined the HCV non-structural protein 3 (NS3), including the immunologically relevant epitopes HCV NS3-2 KLVALGINAV (human leukocyte antigen [HLA]-A2-restricted) and HCV NS3-1391 LIFCHSKKK (HLA-A3-restricted), in 22 HLA-A2+ patients with chronic infection. Significant amino acid variation was found in HCV NS3-2 epitope sequences when compared to the HCV-1 prototype virus. Six of the nine different HCV NS3-2 peptide variants were identified in patients with HCV NS3-2-specific CD8+ cells, detected with an HLA-A2 tetramer made with the HCV-1 prototype peptide.…

AdultMalevirusesHepacivirusHepatitis C virusMolecular Sequence DataEpitopes T-LymphocyteHuman leukocyte antigenHepacivirusCD8-Positive T-LymphocytesHLA-A3 AntigenViral Nonstructural Proteinsmedicine.disease_causeEpitopeVirusFlaviviridaeVirologySequence Homology Nucleic AcidHLA-A2 AntigenmedicineHumansAmino Acid SequencePhylogenyAgedNS3Polymorphism GeneticbiologyGenetic heterogeneityReverse Transcriptase Polymerase Chain Reactionvirus diseasesGenetic VariationHepatitis C ChronicMiddle Agedbiology.organism_classificationVirologydigestive system diseasesInfectious DiseasesImmunologyRNA ViralFemaleHepatitis C AntigensJournal of medical virology
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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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