Search results for "ALLELES"

showing 10 items of 478 documents

Two Italian kindreds carrying the Arg136--Ser mutation of the Apo E gene: development of premature and severe atherosclerosis in the presence of epsi…

2003

Abstract Background and Aims: Type III hyperlipoproteinemia, or dysbetalipoproteinemia, is commonly associated with apolipoprotein E2 homozygosity (Cy Background and Aims: 12, Cy Background and Aims: 58). Apo E2-Christchurch (Arg136→Ser), a rare mutation of the Apo E gene, located in the receptor-binding domain of the protein, has been found to be associated in the vast majority of cases of dysbetalipoproteinemia. Methods and Results: This is the first report of two Italian kindreds carrying the Arg136→Ser mutation. One family is a four-generation kindred from Genoa (Liguria, Italy) with a high rate of mortality due to coronary artery disease: the proband was a 51-year-old woman with previo…

Apolipoprotein EProbandMaleSettore MED/09 - Medicina InternaGenotypeApolipoprotein E2ArteriosclerosisEndocrinology Diabetes and MetabolismMedicine (miscellaneous)Sequence HomologyBiologyArteriosclerosiPolymerase Chain ReactionCoronary artery diseaseApolipoproteins EGenotypeHyperlipoproteinemia Type IIImedicineHaplotypeHumansAlleleGenotypingAllelesGeneticsAlleleNutrition and DieteticsBase SequenceHaplotypeLipidMiddle Agedmedicine.diseaseLipidsPedigreeSettore MED/03 - Genetica MedicaHaplotypesMutationFemaleCardiology and Cardiovascular MedicineApolipoprotein E2HumanNutrition, metabolism, and cardiovascular diseases : NMCD
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On the geographical distribution of pseudocholinesterase variants.

1975

The incidence of pseudocholinesterase (PCHE equals E.C. 3.1.1.8) variants in samples of 8 different population (total of 2218 individuals) is reported. Together with previously mentioned data from the literature, a general survey on the geographical distribution of PCHE isoenzymes is given. Possible reasons for present-day heterogeneity of their distribution are also discussed. Concerning the incidence of the C5 variant, it is pointed out that the validity of applying population genetic models depends upon the accuracy of the genetic basis.

AsiaNative Hawaiian or Other Pacific IslanderGenotypePopulationDistribution (economics)IndiaBiologyGene FrequencyGenetic modelStatisticsGenetic variationCholinesterasesHumansAlleleeducationBulgariaAllele frequencyMolecular BiologyAlleleseducation.field_of_studybusiness.industryIncidence (epidemiology)Racial GroupsGermany WestGenetic VariationGeneral MedicineEuropeGenetics PopulationButyrylcholinesteraseAfricaAmericasbusinessHumangenetik
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Pathogenesis of autoimmune diseases associated with 8.1 ancestral haplotype: effect of multiple gene interactions.

2003

Genetic studies have shown that individuals with certain HLA alleles have a higher risk of specific autoimmune disease than those without these alleles. Particularly, the association in all Caucasian populations of an impressive number of autoimmune diseases with genes from the HLA-B8,DR3 haplotype that is part of the ancestral haplotype (AH) 8.1 HLA-A1, Cw7, B8, TNFAB*a2b3, TNFN*S, C2*C, Bf*s, C4A*Q0, C4B*1, DRB1*0301, DRB3*0101, DQA1*0501, DQB1*0201 has been reported by different research groups. This haplotype, the more common one in northern Europe, is also associated in healthy subjects with a number of immune system dysfunctions. It has been proposed that a small number of genes withi…

Autoimmune diseaseGeneticsHeterozygotebiologyImmunologyHaplotypeC4AHuman leukocyte antigenmedicine.diseaseMajor histocompatibility complexAutoimmune DiseasesImmune systemHaplotypesHLA AntigensImmunologymedicinebiology.proteinImmunology and AllergyAnimalsCytokinesHumansAlleleGeneAllelesAutoimmunity reviews
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Further studies on associations between leprosy and genetic markers in human serum.

1973

Seven serum proteins were typed on a sample of 910 individuals from Angola, Africa. The sample consisted of both leprosy patients and healthy controls from the same geographical area. Significant associations with leprosy were found for the Hp and Pi systems. The results are discussed.

Black PeopleBiologyLeprosyGeneticsmedicineHumansGenetics (clinical)AllelesGeneticsPolymorphism GeneticHaptoglobinsTransferrinCeruloplasminBlood Proteinsmedicine.diseaseMolecular medicineBlood proteinsHuman geneticsGenetics PopulationPhenotypeAngolaGenetic markerImmunologyLeprosygamma-GlobulinsPeptide HydrolasesHumangenetik
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Identification of NY-ESO-1 epitopes presented by human histocompatibility antigen (HLA)-DRB4*0101-0103 and recognized by CD4(+) T lymphocytes of pati…

2000

NY-ESO-1 is a member of the cancer-testis family of tumor antigens that elicits strong humoral and cellular immune responses in patients with NY-ESO-1–expressing cancers. Since CD4+ T lymphocytes play a critical role in generating antigen-specific cytotoxic T lymphocyte and antibody responses, we searched for NY-ESO-1 epitopes presented by histocompatibility leukocyte antigen (HLA) class II molecules. Autologous monocyte-derived dendritic cells of cancer patients were incubated with recombinant NY-ESO-1 protein and used in enzyme-linked immunospot (ELISPOT) assays to detect NY-ESO-1–specific CD4+ T lymphocyte responses. To identify possible epitopes presented by distinct HLA class II allele…

CD4-Positive T-LymphocytesImmunologyMolecular Sequence DataAntigen-Presenting Cells10050 Institute of Pharmacology and Toxicology610 Medicine & healthHuman leukocyte antigenBiologyEpitopeCell LineAntigenAntigens NeoplasmImmunology and AllergyCytotoxic T cellHumansAmino Acid SequenceAntigen-presenting cellMelanomaHLA-DRB4Alleles2403 ImmunologyHLA class II–restricted NY-ESO-1 epitopesMembrane ProteinsProteinsT lymphocyteDendritic CellsHLA-DR AntigensVirologyRecombinant ProteinsHistocompatibilityImmunologyCD4+ T cell recognition2723 Immunology and Allergy570 Life sciences; biologyOriginal ArticleHLA-DRB4 Chains
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Role of genetic factors on the effect of additional loading doses and two maintenance doses used to overcome clopidogrel hyporesponsiveness.

2014

Background and objective: Additional loading doses and higher maintenance doses (MDs) have been used to overcome hyporesponsiveness of clopidogrel. We aimed to investigate whether genetic polymorphisms of two cytochromes (CYP2C19 and CYP2C9) and ABCB1 modify effect of such dose-adjustment strategy.Materials and methods: We enrolled 118 patients undergoing elective or acute percutaneous coronary intervention (PCI) with drug eluting stent (DES). Platelet reactivity index (PRI) was measured using the vasodilator-stimulated phosphoprotein (VASP) index and a cut-off value of ≥60% was defined as hyporesponsiveness. Polymorphism of two cytochromes (CYP2C19, CYP2C9) and gene ABCB1 were determined. …

CYP2C9MaleMedicine (General)ATP Binding Cassette Transporter Subfamily BTiclopidinemedicine.medical_treatmentCYP2C19PharmacologyR5-920Percutaneous Coronary InterventionmedicinePotencyHumansProspective StudiesCYP2C19AlleleCYP2C9AllelesAgedCytochrome P-450 CYP2C9Medicine(all)Polymorphism GeneticDose-Response Relationship Drugbusiness.industryClopidogrel resistanceMicrofilament ProteinsPercutaneous coronary interventionABCB1Drug-Eluting StentsVASPMiddle AgedClopidogrelPhosphoproteinsClopidogrelCytochrome P-450 CYP2C19Drug-eluting stentPharmacogeneticsAutomotive EngineeringConventional PCIFemalebusinessCell Adhesion MoleculesPlatelet Aggregation InhibitorsClopidogrel resistance; VASP; CYP2C19; ABCB1; CYP2C9medicine.drugMedicina (Kaunas, Lithuania)
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Genetic evolution of T-cell resistance in the course of melanoma progression

2014

Abstract Purpose: CD8+ T lymphocytes can kill autologous melanoma cells, but their activity is impaired when poorly immunogenic tumor phenotypes evolve in the course of disease progression. Here, we analyzed three consecutive melanoma lesions obtained within one year of developing stage IV disease for their recognition by autologous T cells. Experimental Design: One skin (Ma-Mel-48a) and two lymph node (Ma-Mel-48b, Ma-Mel-48c) metastases were analyzed for T-cell infiltration. Melanoma cell lines established from the respective lesions were characterized, determining the T-cell–stimulatory capacity, expression of surface molecules involved in T-cell activation, and specific genetic alteratio…

Cancer ResearchB7 Antigensmedicine.medical_treatmentMedizinGene ExpressionT-Lymphocyte Subsetshemic and lymphatic diseasesCluster AnalysisLymphocytesNeoplasm MetastasisLymph nodeMelanomaTumorImmunogenicityMelanomaSingle Nucleotidemedicine.anatomical_structurePhenotypeButorphanolOncologyDisease ProgressionCytokinesEvolutionT cellHuman leukocyte antigenBiologyPolymorphism Single NucleotideArticleCell LineEvolution MolecularLymphocytes Tumor-InfiltratingCell Line TumormedicineHumansGenetic Predisposition to DiseaseTumor-InfiltratingAllelePolymorphismneoplasmsAllelesNeoplasm StagingHistocompatibility Antigens Class IMolecularImmunotherapymedicine.diseaseAlleles; B7 Antigens; Butorphanol; Cell Line Tumor; Cluster Analysis; Cytokines; Disease Progression; Gene Expression; Genetic Predisposition to Disease; Histocompatibility Antigens Class I; Humans; Lymphocytes Tumor-Infiltrating; Melanoma; Mutation; Neoplasm Metastasis; Neoplasm Staging; Phenotype; Polymorphism Single Nucleotide; T-Lymphocyte Subsets; beta 2-Microglobulin; Evolution Molecular; Oncology; Cancer ResearchImmunologyMutationbeta 2-MicroglobulinCD8
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Stochastic Loss of Silencing of the Imprinted Ndn/NDN Allele, in a Mouse Model and Humans with Prader-Willi Syndrome, Has Functional Consequences

2013

Genomic imprinting is a process that causes genes to be expressed from one allele only according to parental origin, the other allele being silent. Diseases can arise when the normally active alleles are not expressed. In this context, low level of expression of the normally silent alleles has been considered as genetic noise although such expression has never been further studied. Prader-Willi Syndrome (PWS) is a neurodevelopmental disease involving imprinted genes, including NDN, which are only expressed from the paternally inherited allele, with the maternally inherited allele silent. We present the first in-depth study of the low expression of a normally silent imprinted allele, in path…

Cancer ResearchHeterozygotelcsh:QH426-470Apnea[SDV]Life Sciences [q-bio]Nerve Tissue ProteinsBiologyEpigenesis Genetic03 medical and health sciencesGenomic ImprintingMice0302 clinical medicineGeneticsAnimalsHumansEpigeneticsAlleleImprinting (psychology)Promoter Regions GeneticMolecular BiologyGeneGenetics (clinical)Ecology Evolution Behavior and SystematicsAlleles030304 developmental biologyGeneticsMice Knockout0303 health sciencesBrainNuclear ProteinsPhenotypeAllelic exclusionDisease Models Animallcsh:GeneticsGene Expression RegulationDNA methylationGenomic imprintingPrader-Willi Syndrome030217 neurology & neurosurgeryResearch Article
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The BCL6 gene in B-cell lymphomas with 3q27 translocations is expressed mainly from the rearranged allele irrespective of the partner gene

2003

The BCL6 gene, which functions as a transcription repressor, is the target of multiple chromosomal translocations in non-Hodgkin's lymphomas (NHL). These translocations occur in the nontranslated region of the BCL6 gene, juxtaposing regulatory sequences of the diverse partner genes to the open reading frame of the BCL6 gene and thus are thought to deregulate BCL6 gene expression. The levels of expression of the BCL6 gene and protein have been demonstrated to predict the clinical outcome of diffuse large B-cell lymphomas. By contrast, the prognostic significance of BCL6 gene translocations is unclear. In this study we have sought an explanation for this apparent discrepancy. We examined tumo…

Cancer ResearchLymphoma B-CellBiologyTranslocation Geneticimmune system diseasesProto-Oncogene Proteinshemic and lymphatic diseasesGene expressionTumor Cells CulturedHumansRNA MessengerAllelePromoter Regions GeneticGeneAllelesGene RearrangementGeneticsRegulation of gene expressionPromoterHematologyGene rearrangementBCL6Neoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticRepressor ProteinsOncologyRegulatory sequenceMutationProto-Oncogene Proteins c-bcl-6Cancer researchChromosomes Human Pair 3Transcription FactorsLeukemia
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Acute myeloid leukemia (AML)-reactive cytotoxic T lymphocyte clones rapidly expanded from CD8(+) CD62L((high)+) T cells of healthy donors prevent AML…

2008

Objective Current in vitro techniques for isolating leukemia-reactive cytotoxic T lymphocytes (CTLs) from healthy donors are of relatively low efficiency and yield responder populations with unknown biological significance. This study aimed at the development of a more reliable approach, allowing generation and expansion of acute myeloid leukemia (AML)-reactive CTLs using primary in vitro stimulation. Materials and Methods We established allogeneic mini-mixed lymphocyte-leukemia cultures (mini-MLLCs) by stimulating donor CD8 + T cells with human leukocyte antigen (HLA) class I–matched AML blasts in microtiter plates. Before culture, CD8 + T cells were separated into CD62L (high)+ and CD62L …

Cancer ResearchMyeloidGenes MHC Class Ichemical and pharmacologic phenomenaHuman leukocyte antigenMice SCIDBiologyCD8-Positive T-LymphocytesMiceImmune systemMice Inbred NODhemic and lymphatic diseasesGeneticsmedicineCytotoxic T cellAnimalsHumansL-SelectinMolecular BiologyAllelesCells CulturedMice KnockoutMyeloid leukemiahemic and immune systemsCell BiologyHematologyReference Standardsmedicine.diseaseCytotoxicity Tests ImmunologicClone CellsCTL*LeukemiaLeukemia Myeloid Acutemedicine.anatomical_structureImmunologyCD8Neoplasm TransplantationInterleukin Receptor Common gamma SubunitT-Lymphocytes CytotoxicExperimental hematology
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