Search results for "MUTATION"

showing 10 items of 2830 documents

Transmission of HIV Drug Resistance and the Predicted Effect on Current First-line Regimens in Europe

2016

Transmitted human immunodeficiency virus drug resistance in Europe is stable at around 8%. The impact of baseline mutation patterns on susceptibility to antiretroviral drugs should be addressed using clinical guidelines. The impact on baseline susceptibility is largest for nonnucleoside reverse transcriptase inhibitors.

MaleHuman immunodeficiency virus 1EtravirineRNA directed DNA polymerase inhibitordarunavirHIV InfectionsSettore MED/42 - Igiene Generale E Applicata:Disciplines and Occupations::Health Occupations::Medicine::Public Health [Medical Subject Headings]:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]Salud públicageneticsInhibidores de proteasas:Analytical Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Data Collection::Vital Statistics::Morbidity::Prevalence [Medical Subject Headings]atazanavirmedia_commontransmission:Geographicals::Geographic Locations::Europe [Medical Subject Headings]3. Good healthmicrobial sensitivity testpriority journalEurope ; HIV-1 ; antiretroviral therapy ; drug resistance ; transmissionHIV/AIDSlamivudineReverse Transcriptase Inhibitors/pharmacologyanti human immunodeficiency virus agentDrugMicrobiology (medical)medicine.medical_specialtyantiviral susceptibility:Phenomena and Processes::Genetic Phenomena::Genetic Variation::Mutation [Medical Subject Headings]media_common.quotation_subjectantiretroviral therapy030106 microbiologyHIV Infections/drug therapy:Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Therapeutic Uses::Anti-Infective Agents::Antiviral Agents::Anti-Retroviral Agents::Reverse Transcriptase Inhibitors [Medical Subject Headings]Microbial Sensitivity TestsRILPIVIRINEArticleEFAVIRENZ03 medical and health sciencestransmitted drug resistanceSDG 3 - Good Health and Well-beingHumansTransmissionhuman:Phenomena and Processes::Physiological Phenomena::Pharmacological Phenomena::Drug Resistance [Medical Subject Headings]REVERSE-TRANSCRIPTASE INHIBITORSRilpivirinaINTEGRASEMUTATIONSabacavirmajor clinical studyVirologyInfecciones por VIHRegimenAntiretroviral therapy; Drug resistance; Europe; HIV-1; Transmission; Medicine (all); Microbiology (medical); Infectious DiseaseschemistryDrug resistance:Chemicals and Drugs::Heterocyclic Compounds::Heterocyclic Compounds 1-Ring::Oxazines::Benzoxazines [Medical Subject Headings]MutationHIV-10301 basic medicinenevirapineDrug resistanceCommunicable diseases:Analytical Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Statistics as Topic::Confidence Intervals [Medical Subject Headings]chemistry.chemical_compoundantiviral therapyINFECTIONMedicine and Health SciencesPrevalence:Analytical Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Data Collection::Surveys and Questionnaires [Medical Subject Headings]ViralNon-U.S. Gov'tReverse-transcriptase inhibitorantiretrovirus agentResearch Support Non-U.S. Gov'tMedicine (all)Human immunodeficiency virus infected patientMiddle AgedvirologyPREVALENCEAntiretroviral therapyEncuestas y CuestionariosANTIRETROVIRAL TREATMENTEuropeInfectious DiseasesHIV-1/drug effectsHIV Protease Inhibitors/pharmacologyRilpivirineReverse Transcriptase Inhibitors:Diseases::Immune System Diseases::Immunologic Deficiency Syndromes::HIV Infections [Medical Subject Headings]FemaleHIV drug resistancemedicine.drugAdultHuman immunodeficiency virus proteinase inhibitor:Chemicals and Drugs::Organic Chemicals::Nitriles::Rilpivirine [Medical Subject Headings]EfavirenzAnti-HIV AgentsResearch SupportResistencia a medicamentosSettore MED/17 - MALATTIE INFETTIVEantiviral resistanceInternal medicineAnti-HIV Agents/pharmacologyDrug Resistance ViralJournal Articlemedicine:Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Molecular Mechanisms of Pharmacological Action::Enzyme Inhibitors::Protease Inhibitors [Medical Subject Headings]abacavir plus lamivudineEuropa (Continente)Antiretroviral therapy; Drug resistance; Europe; HIV-1; Transmission; Adult; Anti-HIV Agents; Drug Resistance Viral; Europe; Female; HIV Infections; HIV Protease Inhibitors; HIV-1; Humans; Male; Microbial Sensitivity Tests; Middle Aged; Mutation; Prevalence; Reverse Transcriptase Inhibitors; Microbiology (medical); Infectious DiseasesemtricitabinenonhumanIntervalos de confianzadrug resistanceMutaciónAntiretroviral therapy; Drug resistance; Europe; HIV-1; Transmissionbusiness.industryHIVpredictionInhibidores de la transcriptasa inversaHIV Protease InhibitorsHuman immunodeficiency virus 1 infectiontenofovirINDIVIDUALSDrug Resistance Viral/geneticsBenzoxazinasETRAVIRINEdrug effects3121 General medicine internal medicine and other clinical medicinePrevalenciabusiness
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Novel SCNN1A gene splicing-site mutation causing autosomal recessive pseudohypoaldosteronism type 1 (PHA1) in two Italian patients belonging to the s…

2021

Abstract Introduction Pseudohypoaldosteronism type 1 (PHA1) is a rare genetic disease due to the peripheral resistance to aldosterone. Its clinical spectrum includes neonatal salt loss syndrome with hyponatremia and hypochloraemia, hyperkalemia, metabolic acidosis and increased plasmatic levels of aldosterone. Two genetically distinct forms of disease, renal and systemic, have been described, showing a wide clinical expressivity. Mutations in the genes encoding for the subunits of the epithelial sodium channels (ENaC) are responsible for generalized PHA1. Patients’ presentation We hereby report on two Italian patients with generalized PHA1, coming from the same small town in the center of S…

MaleHyperkalemiaPseudohypoaldosteronismENaCCase ReportGene mutationBioinformaticsPediatricsRJ1-570chemistry.chemical_compoundConsanguinityYoung AdultNext generation sequencingmedicineHumansFamily historyEpithelial Sodium ChannelsSicilyENaC Next generation sequencing SCNN1A gene Splicing mutation Consanguinity Epithelial Sodium Channels Female Humans Infant Newborn Male Mutation Pseudohypoaldosteronism Sicily Young AdultAldosteronebusiness.industryInfant NewbornPseudohypoaldosteronismmedicine.diseasechemistrySCNN1A geneMutation (genetic algorithm)MutationFemalemedicine.symptombusinessHyponatremiaSplicing mutationAuntItalian Journal of Pediatrics
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Novel mutations of CETP gene in Italian subjects with hyeralphalipoproteinemia

2009

Abstract Cholesteryl ester transfer protein (CETP) is a plasma glycoprotein that catalyses the transfer of cholesteryl esters from HDL to the other plasma lipoproteins. Genetic deficiency of CETP is one of the known causes of elevation of plasma HDL-C (primary hyperalphalipoproteinemia, HALP). We sequenced CETP gene in a group of 24 Italian subjects with primary HALP (HDL-C>80 mg/dl) suspected to have CETP deficiency. Two unrelated subjects both coming from the same geographical district, were found to be heterozygous for a nucleotide substitution in exon 6 (c.544C>T) and another subject was found to be heterozygous for a C>T transition in exon 9 (c.802C>T). Both mutations introduce a prema…

MaleHyperlipoproteinemiasMessengerDNA Mutational Analysismedicine.disease_causeExonFamilial hyperalphalipoproteinemiaChlorocebus aethiopsCETP activity; CETP gene mutations; Familial hyperalphalipoproteinemia; HDL size; Adolescent; Adult; Aged; Animals; Biomarkers; COS Cells; Cercopithecus aethiops; Cholesterol Ester Transfer Proteins; Cholesterol HDL; DNA Mutational Analysis; European Continental Ancestry Group; Female; Humans; Hyperlipoproteinemias; Italy; Male; Middle Aged; Phenotype; RNA Messenger; Transfection; Up-Regulation; Young Adult; Mutation; Cardiology and Cardiovascular MedicineGeneticsMutationTransition (genetics)biologyCETP activityMiddle AgedUp-RegulationCholesterolPhenotypeItalyCOS CellsRNA splicingFemaleFamilial hyperalphalipoproteinemia; CETP gene mutations; CETP activity; HDL sizelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineAdultHDLAdolescentEuropean Continental Ancestry GroupSocio-culturaleHDL sizeTransfectionWhite PeopleCercopithecus aethiopsYoung AdultCETP gene mutationsCholesterylester transfer proteinmedicineAnimalsHumansRNA MessengerGeneAgedCholesterol HDLIntroncetpCholesterol Ester Transfer Proteinscarbohydrates (lipids)biology.proteinRNAmutationBiomarkersMinigene
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Novel LRPPRC compound heterozygous mutation in a child with early-onset Leigh syndrome French-Canadian type: Case report of an Italian patient

2020

Abstract Background Mitochondrial diseases, also known as oxidative phosphorylation (OXPHOS) disorders, with a prevalence rate of 1:5000, are the most frequent inherited metabolic diseases. Leigh Syndrome French Canadian type (LSFC), is caused by mutations in the nuclear gene (2p16) leucine-rich pentatricopeptide repeat-containing (LRPPRC). It is an autosomal recessive neurogenetic OXPHOS disorder, phenotypically distinct from other types of Leigh syndrome, with a carrier frequency up to 1:23 and an incidence of 1:2063 in the Saguenay-Lac-St Jean region of Quebec. Recently, LSFC has also been reported outside the French-Canadian population. Patient presentation We report a male Italian (Sic…

MaleHypotonia - developmental delayPediatricsmedicine.medical_specialtyPopulationEncephalopathyCytochrome-c Oxidase DeficiencyCase ReportHypotoniaCompound heterozygosityDiagnosis Differential03 medical and health sciences0302 clinical medicineWhole-genome-sequencingHypotonia; developmental delay; Mitochondrial disease; Whole-exome sequencing; CCT5030225 pediatricsmedicineMissense mutationHumansGlobal developmental delayeducationeducation.field_of_studyComparative Genomic Hybridizationbusiness.industrylcsh:RJ1-570Infant Newbornlcsh:Pediatricsmedicine.diseaseHypotoniaHypoplasiaMitochondrial diseaseNeoplasm Proteinsdevelopmental delayNeonatal hypotoniaPhenotypeItalyWhole-exome sequencingMutationLSFCmedicine.symptomLeigh DiseaseCCT5business030217 neurology & neurosurgeryInfant Premature
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PBX1 acts as terminal selector for olfactory bulb dopaminergic neurons

2020

15 páginas, 8 figuras. Supplementary information available online at http://dev.biologists.org/lookup/doi/10.1242/dev.186841.supplemental

MaleInterneuronCell SurvivalNeurogenesisRNA SplicingNeuron differentiationMitosisBiologyAdult neurogenesis03 medical and health sciencesOlfactory bulb0302 clinical medicineNeuroblastInterneuronsmedicineAnimalsProtein IsoformsCell LineageProgenitor cellTerminal selector10. No inequalityMolecular BiologyTranscription factorBody Patterning030304 developmental biologyMice KnockoutDopaminergic neuron0303 health sciencesDopaminergic NeuronsPre-B-Cell Leukemia Transcription Factor 1fungiNeurogenesisDopaminergicCell DifferentiationExonsEmbryo Mammalian3. Good healthOlfactory bulbmedicine.anatomical_structureMutationNeuron differentiationNeuroscience030217 neurology & neurosurgeryTranscription FactorsAlternative splicingDevelopmental BiologyDevelopment
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Friedreich's Ataxia: Autosomal Recessive Disease Caused by an Intronic GAA Triplet Repeat Expansion

1996

International audience; Friedreich's ataxia (FRDA) is an autosomal recessive, degenerative disease that involves the central and peripheral nervous systems and the heart. A gene, X25, was identified in the critical region for the FRDA locus on chromosome 9q13. This gene encodes a 210-amino acid protein, frataxin, that has homologs in distant species such as Caenorhabditis elegans and yeast. A few FRDA patients were found to have point mutations in X25, but the majority were homozygous for an unstable GAA trinucleotide expansion in the first X25 intron.

MaleIron-sulfur cluster assemblyPolymerase Chain Reaction0302 clinical medicineTrinucleotide RepeatsIron-Binding ProteinsGenetics0303 health sciencesMultidisciplinaryAutosomal recessive cerebellar ataxiaPedigree3. Good healthFemalemedicine.symptomChromosomes Human Pair 9HumanPair 9Heterozygotecongenital hereditary and neonatal diseases and abnormalitiesAtaxiaMolecular Sequence DataGenes RecessiveLocus (genetics)BiologyChromosomes03 medical and health sciencesGene mappingAlleles; Amino Acid Sequence; Base Sequence; Chromosomes Human Pair 9; DNA Primers; Female; Friedreich Ataxia; Genes Recessive; Heterozygote; Humans; Male; Molecular Sequence Data; Pedigree; Point Mutation; Polymerase Chain Reaction; Proteins; Sequence Alignment; Introns; Iron-Binding Proteins; Trinucleotide RepeatsmedicineRecessiveHumansPoint MutationAmino Acid SequenceAlleleAllelesDNA Primers030304 developmental biologyBase SequencePoint mutationProteins[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologymedicine.diseaseMolecular biologyIntronsGenes[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsFriedreich AtaxiaFrataxinbiology.proteinSequence Alignment030217 neurology & neurosurgeryScience
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A de novo heterozygous mutation in KCNC2 gene implicated in severe developmental and epileptic encephalopathy

2020

Abstract An increasing number of developmental and epileptic encephalopathies have been correlated with variants of ion channel genes, and in particular of potassium channels genes, such as KCNA1, KCNA2, KCNB1, KCNQ2, KCTD7 and KCNT1. Here we report a child with an early severe developmental and epileptic encephalopathy, spastic tetraplegia, opisthotonos attacks. The whole exome sequencing showed the de novo heterozygous variant c.1411G > C (p.Val471Leu) in the KCNC2 gene. Although this is, to our knowledge, the first case of encephalopathy associated with a KCNC2 gene variant, and further confirmatory studies are needed, previous preclinical and clinical evidence seems to suggest that KCNC…

MaleKCNC2 geneKCTD7EncephalopathyBiologyEpilepsyGeneticsmedicineHumansExomeEEGChildGeneExomeSpastic tetraplegiaGenetics (clinical)Exome sequencingGeneticsEpilepsyKv3.2ElectroencephalographyDevelopmental and epileptic encephalopathieGeneral Medicinemedicine.diseaseKCNC2Shaw Potassium ChannelsNGSMutationEuropean Journal of Medical Genetics
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GERMLINE PROKINETICIN RECEPTOR 2 (PROKR2) VARIANTS ASSOCIATED WITH CENTRAL HYPOGONADISM CAUSE DIFFERENTAL MODULATION OF DISTINCT INTRACELLULAR PATHWA…

2013

INTRODUCTION: Defects of prokineticin pathway affect the neuroendocrine control of reproduction, but their role in the pathogenesis of central hypogonadism remains undefined, and the functional impact of the missense PROKR2 variants has been incompletely characterized. MATERIAL AND METHODS: In a series of 246 idiopathic central hypogonadism patients, we found three novel (p.V158I, p.V334M, and p.N15TfsX30) and six already known (p.L173R, p.T260M, p.R268C, p.V274D, p.V331M, and p.H20MfsX23) germline variants in the PROKR2 gene. We evaluated the effects of seven missense alterations on two different prokineticin receptor 2 (PROKR2)-dependent pathways: inositol phosphate-Ca(2+) (Gq coupling) a…

MaleKallmann syndromeEndocrinology Diabetes and MetabolismClinical BiochemistryInositol Phosphatemedicine.disease_causeBiochemistryHypogonadotropic hypogonadismGermlineReceptors G-Protein-CoupledCohort StudiesEndocrinologySettore MED/38 - Pediatria Generale E SpecialisticaAdolescent; Adult; Child; Cohort Studies; Cyclic AMP; Female; Genetic Association Studies; Humans; Hypogonadism; Inositol Phosphates; Male; Middle Aged; Mutation Missense; Receptors G-Protein-Coupled; Receptors Peptide; Signal Transduction; Young Adult; Germ-Line MutationReceptorsCyclic AMPmutations; Kallmann syndrome; septo-optic dysplasiaMissense mutationReceptorChildMutationMiddle AgedProkineticinPeptideFemaleHumanSignal TransductionAdultmedicine.medical_specialtyReceptors PeptideAdolescentAdolescent Adult Child Cohort Studies Cyclic AMP; metabolism Female Genetic Association Studies Germ-Line Mutation Humans Hypogonadism; epidemiology/genetics Inositol Phosphates; metabolism Male Middle Aged Missense Receptors; G-Protein-Coupled; genetics Receptors; Peptide; genetics Signal Transduction; genetics Young AdultInositol PhosphatesMutation MissenseGenetic Association StudieBiologyG-Protein-CoupledYoung AdultGermline mutationInternal medicinesepto-optic dysplasiamedicineHumansGenetic Association StudiesGerm-Line MutationHypogonadismBiochemistry (medical)Kallmann syndromeProkineticin receptor 2medicine.diseasePROKR2 hypogonadism prokineticinmutationsAdolescent; Adult; Child; Cohort Studies; Cyclic AMP; Female; Genetic Association Studies; Humans; Hypogonadism; Inositol Phosphates; Male; Middle Aged; Mutation; Missense; Receptors; G-Protein-Coupled; Peptide; Signal Transduction; Young Adult; Germ-Line MutationEndocrinologyMutationCohort StudieMissense
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Gitelman-Like Syndrome Caused by Pathogenic Variants in mtDNA

2022

Contains fulltext : 248375.pdf (Publisher’s version ) (Closed access) BACKGROUND: Gitelman syndrome is the most frequent hereditary salt-losing tubulopathy characterized by hypokalemic alkalosis and hypomagnesemia. Gitelman syndrome is caused by biallelic pathogenic variants in SLC12A3, encoding the Na(+)-Cl(-) cotransporter (NCC) expressed in the distal convoluted tubule. Pathogenic variants of CLCNKB, HNF1B, FXYD2, or KCNJ10 may result in the same renal phenotype of Gitelman syndrome, as they can lead to reduced NCC activity. For approximately 10 percent of patients with a Gitelman syndrome phenotype, the genotype is unknown. METHODS: We identified mitochondrial DNA (mtDNA) variants in th…

MaleKidneyDISEASEion transportGenotypeSolute Carrier Family 12 Member 3Gitelman-s syndromeCHANNEL GENEChildRNA Transfer IlePHOSPHORYLATIONNCCbiologygenetic renal diseaseblood pressureMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]General MedicineMiddle Agedchronic kidney failureTUBULENa transportPedigreemitochondriaBARTTER-SYNDROMEPhenotypemedicine.anatomical_structureMitochondrial respiratory chainMAGNESIUMNephrologyChild Preschoolepithelial sodium transportFemaleGitelman SyndromeAdultMitochondrial DNAAdolescentGenotypehuman geneticsKCNJ10DNA MitochondrialModels BiologicalPolymorphism Single NucleotideRNA Transfer PheYoung AdultTubulopathymedicineHumansDistal convoluted tubuleHYPOMAGNESEMIAAgedCLCNKBNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]MITOCHONDRIAL-DNA MUTATIONBase SequenceInfantGitelman syndromemedicine.diseaseMolecular biologySODIUM-CHLORIDE COTRANSPORTERHEK293 CellsRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]Basic ResearchMutationbiology.proteinNucleic Acid Conformationchronic kidney disease
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Mutant K-ras2 in serum

2003

Mutant tumour derived DNA has been detected in the sera of colorectal cancer patients. We investigated if mutant serum KRAS2 was detectable preoperatively in a large group of patients with colorectal neoplasia. A prospective study of 94 patients who underwent putative curative resection for colorectal carcinoma (CRC) was performed to ascertain if serum mutant KRAS2 could be used postoperatively as a disease marker.Preoperative sera from 78 patients were analysed (group A). Sera from 94 patients were obtained three monthly for up to three years during the postoperative period (group B). Codon 12 and 13 KRAS2 mutations were analysed in matched tumour and serum samples.In the preoperative grou…

MaleLetterColorectal cancervirusesMutantDNA Mutational AnalysisBioinformaticsProto-Oncogene Proteins p21(ras)03 medical and health sciencesCollaborative group0302 clinical medicineProto-Oncogene ProteinsMedicineHumansRas2neoplasmsGene030304 developmental biologyAged0303 health sciencesbusiness.industryPoint mutationGastroenterologyDNA NeoplasmMiddle Agedmedicine.diseasePrognosis3. Good healthProto-Oncogene Proteins p21(ras)Molecular analysisCarcinoembryonic AntigenEpidemiologic Studies030220 oncology & carcinogenesisCancer researchras ProteinsFemaleNeoplasm Recurrence LocalbusinessColorectal NeoplasmsBiomarkers
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