Search results for "MUTATION"

showing 10 items of 2830 documents

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
researchProduct

Afatinib versus cisplatin-based chemotherapy for EGFR mutation-positive lung adenocarcinoma (LUX-Lung 3 and LUX-Lung 6): analysis of overall survival…

2015

Summary Background We aimed to assess the effect of afatinib on overall survival of patients with EGFR mutation-positive lung adenocarcinoma through an analysis of data from two open-label, randomised, phase 3 trials. Methods Previously untreated patients with EGFR mutation-positive stage IIIB or IV lung adenocarcinoma were enrolled in LUX-Lung 3 (n=345) and LUX-Lung 6 (n=364). These patients were randomly assigned in a 2:1 ratio to receive afatinib or chemotherapy (pemetrexed-cisplatin [LUX-Lung 3] or gemcitabine-cisplatin [LUX-Lung 6]), stratified by EGFR mutation (exon 19 deletion [del19], Leu858Arg, or other) and ethnic origin (LUX-Lung 3 only). We planned analyses of mature overall sur…

AdultMalemedicine.medical_specialtyGuanineLung NeoplasmsAfatinibPopulationMedizinPemetrexedNeutropeniaAdenocarcinomaAfatinibGastroenterologyDeoxycytidineGlutamatesInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineMucositisHumansRociletinibeducationLung cancerSurvival rateAgedNeoplasm StagingAged 80 and overeducation.field_of_studybusiness.industryMiddle Agedmedicine.diseasePrognosisGemcitabineSurgeryErbB ReceptorsSurvival RatePemetrexedOncologyMutationQuinazolinesFemaleCisplatinbusinessmedicine.drugFollow-Up StudiesThe Lancet. Oncology
researchProduct

Association of C677T polymorphism in MTHFR gene, high homocysteine and low HDL cholesterol plasma values in heterozygous familial hypercholesterolemi…

2010

Aim: to investigate the association of C677T polymorphism in the methylene tetrahydrofolate reductase (MTHFR) gene, homocysteine plasma values (Hcy), and plasma HDL cholesterol in heterozy-gous familial hypercholesterolemia (hFH).Methods: One hundred and twenty-five hFH subjects were studied. Plasma lipid, lipoprotein, vitamin B12, folic acid and Hcy values were determined. C677T polymorphism in the MTHFR gene was detected by SSCP-PCR. Genetic diagnosis of FH was determined by a three-step protocol using SSCP-PCR, Southern blot, long PCR and automatic sequencing.Results: We found significant differences in plasma HDL-C (CC 1.39±0.34, CT 1.33±0.39 and TT 1.14±0.26 mmol/L, p=0.028) between th…

AdultMalemedicine.medical_specialtyHeterozygoteApolipoprotein BHomocysteineHypercholesterolemiaFamilial hypercholesterolemiaPolymerase Chain Reactionchemistry.chemical_compoundInternal medicineGenotypeInternal MedicinemedicineHumansVitamin B12HomocysteineMethylenetetrahydrofolate Reductase (NADPH2)Polymorphism Single-Stranded ConformationalApolipoproteins BGeneticsPolymorphism GeneticbiologyCholesterolbusiness.industryBiochemistry (medical)Cholesterol HDLMiddle Agedmedicine.diseaseEndocrinologychemistryReceptors LDLMethylenetetrahydrofolate reductaseMutationbiology.proteinFemaleCardiology and Cardiovascular MedicinebusinessLipoproteinJournal of atherosclerosis and thrombosis
researchProduct

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
researchProduct

Genetic predisposition to thrombophilia in inflammatory bowel disease

2011

BACKGROUND Inflammatory bowel disease (IBD) is linked to a definite risk of thromboembolic events (TE), but data on the role of prothrombotic genetic mutations are conflicting. STUDY Fourteen genetic factors involved in TE pathogenesis were investigated in a homogeneous cohort of Sicilian patients with IBD with and without history of TE and in healthy controls. Forty IBD patients (21 CD, 19 UC) and 20 healthy individuals were enrolled. Genetic testing was based on the reverse hybridization principle by a commercial assay that analyzes 14 polymorphisms involved in thrombophilia and cholesterol metabolism. The rate of genetic polymorphisms and mutations was compared between IBD patients and h…

AdultMalemedicine.medical_specialtyIBDAngiotensinogenPeptidyl-Dipeptidase AThrombophiliaInflammatory bowel diseaseGastroenterologyPolymorphism (computer science)Risk FactorsInternal medicineDiabetes mellitusGenotypeGenetic predispositionmedicineHumansThrombophiliaGenetic Predisposition to DiseaseAllele frequencySicilyGenetic testingAgedPolymorphism Geneticmedicine.diagnostic_testbusiness.industryGastroenterologyMiddle Agedmedicine.diseaseInflammatory Bowel Diseasesdigestive system diseasesMutationFemalebusiness
researchProduct

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
researchProduct

Virological efficacy and emergence of drug resistance in adults on antiretroviral treatment in rural Tanzania

2009

Background Virological response to antiretroviral treatment (ART) in rural Africa is poorly described. We examined virological efficacy and emergence of drug resistance in adults receiving first-line ART for up to 4 years in rural Tanzania. Methods Haydom Lutheran Hospital has provided ART to HIV-infected patients since October 2003. A combination of stavudine or zidovudine with lamivudine and either nevirapine or efavirenz is the standard first-line regimen. Nested in a longitudinal cohort study of patients consecutively starting ART, we carried out a cross-sectional virological efficacy survey between November 2007 and June 2008. HIV viral load was measured in all adults who had completed…

AdultMalemedicine.medical_specialtyNevirapineEfavirenzTime FactorsAnti-HIV AgentsHIV InfectionsVDP::Medical disciplines: 700::Clinical medical disciplines: 750::Communicable diseases: 776Drug resistanceTanzanialcsh:Infectious and parasitic diseasesCohort StudiesZidovudinechemistry.chemical_compoundInternal medicineDrug Resistance ViralmedicineHumanslcsh:RC109-216Viremiabusiness.industryStavudineLamivudineResistance mutationVirologyInfectious DiseasesCross-Sectional StudieschemistryHIV-1FemalebusinessViral loadmedicine.drugResearch Article
researchProduct

A Novel Loss of Function Mutation of PCSK9 Gene in White Subjects With Low-Plasma Low-Density Lipoprotein Cholesterol

2007

Objectives— The PCSK9 gene, encoding a pro-protein convertase involved in posttranslational degradation of low-density lipoprotein receptor, has emerged as a key regulator of plasma low-density lipoprotein cholesterol. In African-Americans two nonsense mutations resulting in loss of function of PCSK9 are associated with a 30% to 40% reduction of plasma low-density lipoprotein cholesterol. The aim of this study was to assess whether loss of function mutations of PCSK9 were a cause of familial hypobetalipoproteinemia and a determinant of low-plasma low-density lipoprotein cholesterol in whites. Methods and Results— We sequenced PCSK9 gene in 18 familial hypobetalipoproteinemia subjects and i…

AdultMalemedicine.medical_specialtyNonsense mutationBiologymedicine.disease_causePolymorphism Single NucleotideRisk AssessmentSensitivity and SpecificityStatistics NonparametricWhite Peopleloss of function mutationHypobetalipoproteinemiaschemistry.chemical_compoundPCSK9 GeneGene FrequencyInternal medicinemedicineHumansGenetic Predisposition to DiseaseMutationhypocholesterolemiaCholesterolIncidencePCSK9Serine EndopeptidasesCholesterol LDLmedicine.diseaseHypocholesterolemiaEndocrinologyfamilial hypobetalipoproteinemiachemistryCodon NonsensePCSK9 geneCase-Control Studiesfamilial hypobetalipoproteinemia hypocholesterolemia loss of function mutation PCSK9 genefamilial hypobetalipoproteinemia; hypocholesterolemia; loss of function mutation; PCSK9 gene.FemaleProprotein ConvertasesHypobetalipoproteinemiaProprotein Convertase 9Cardiology and Cardiovascular MedicineLipoprotein
researchProduct

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
researchProduct

Incidence of Crohn's disease and CARD15 mutation in a small township in Sicily.

2006

Background: The incidence of Crohn's disease (CD) has been shown to be lower in Southern than in Northern Europe. Data on the frequency of the NOD2/CARD15 mutations for Mediterranean area are very scant. Aim: To determine the incidence of CD from 1979 to 2002 in a township in Sicily together with the allele frequency of NOD2/CARD15 mutations in patients, family members and controls, and to determine the allele frequency of these mutations in sporadic CD from other areas of Sicily in comparison with a control population. Methods: Casteltermini is a small town close to Agrigento (Sicily) with a population of 9,130 inhabitants. All the diagnoses of inflammatory bowel disease (IBD) made from 19…

AdultMalemedicine.medical_specialtyPathologyAdolescentEpidemiologyPopulationNod2 Signaling Adaptor ProteinInflammatory bowel diseaseGastroenterologyCrohn DiseaseGene FrequencyInternal medicineEpidemiologyPrevalencemedicineHumansGenetic Predisposition to DiseaseRisk factoreducationAllele frequencySicilyNOD2/CARD15Crohn's diseaseeducation.field_of_studybusiness.industryIncidence (epidemiology)IncidenceMiddle Agedmedicine.diseaseUlcerative colitisdigestive system diseasesCrohn's diseaseMutationColitis UlcerativeFemalebusinessEuropean journal of epidemiology
researchProduct