Search results for "ERAS"

showing 10 items of 4431 documents

Glutathione S-transferase T1 and M1 gene defects in ovarian carcinoma

1998

Glutathione S-transferases (GSTs) M1 and T1 are known to be polymorphic in humans. Both polymorphisms are due to gene deletions, which are responsible for the existence of null genotypes. The gene defect of GSTT1 has been reported to be associated with an increased risk of myelodysplastic syndromes, astrocytoma and meningioma. A lack of GSTM1 was associated with tobacco smoke-induced lung and bladder cancer. In this study we examined whether the GSTT1 and/or GSTM1 homozygous null genotypes were associated with an increased risk of ovarian cancer using a multiplex polymerase chain reaction protocol. The GSTT1 null genotype was observed in 14% of the control subjects that had never suffered f…

AdultGenetic MarkersCancer Researchmedicine.medical_specialty10050 Institute of Pharmacology and Toxicology610 Medicine & healthGastroenterologyInternal medicineOvarian carcinomaGenotypemedicineCarcinomaHumans1306 Cancer ResearchFamily historyneoplasmsAgedGlutathione TransferaseAged 80 and overOvarian NeoplasmsPolymorphism GeneticBladder cancerbiologyAge FactorsAstrocytomaMiddle Agedmedicine.diseaseNeoplasm ProteinsGlutathione S-transferaseEndocrinologyOncologybiology.protein570 Life sciences; biologyFemale2730 OncologyOvarian cancerCancer Letters
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Causal relationship of hepatic fat with liver damage and insulin resistance in nonalcoholic fatty liver

2017

Abstract Background and Aims Nonalcoholic fatty liver disease is epidemiologically associated with hepatic and metabolic disorders. The aim of this study was to examine whether hepatic fat accumulation has a causal role in determining liver damage and insulin resistance. Methods We performed a Mendelian randomization analysis using risk alleles in PNPLA3, TM6SF2, GCKR and MBOAT7, and a polygenic risk score for hepatic fat, as instruments. We evaluated complementary cohorts of at‐risk individuals and individuals from the general population: 1515 from the liver biopsy cohort (LBC), 3329 from the Swedish Obese Subjects Study (SOS) and 4570 from the population‐based Dallas Heart Study (DHS). Re…

AdultGenetic MarkersLiver CirrhosisMalenonalcoholic fatty liver diseaseNon-alcoholic Fatty Liver Diseaseinsulin resistanceHumansgeneticsProspective StudiesAdaptor Proteins Signal TransducingSettore MED/12 - GastroenterologiafibrosisMembrane ProteinsOriginal ArticlesLipaseMendelian Randomization AnalysisAdipose TissueDiabetes Mellitus Type 2Chronic Diseasemendelian randomizationOriginal ArticleFemaletype 2 diabetesgeneticfibrosiAcyltransferases
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A 588-gene microarray analysis of the peripheral blood mononuclear cells of spondyloarthropathy patients

2002

OBJECTIVES: To identify genes which are more highly expressed in the peripheral blood mononuclear cells (PBMC) of patients with spondyloarthropathy (SpA), rheumatoid arthritis (RA) and psoriatic arthritis (PsA), in comparison to normal subjects. METHODS: A 588-gene microarray was used as a screening tool to select a panel of such genes from PBMC of these subjects and of normal subjects. Results were then validated by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The following genes were more highly expressed in arthritis patients than in normal subjects: macrophage differentiation marker MNDA (myeloid nuclear differentiation antigen), MRP8 and MRP14 (migratory inhibitor…

AdultGenetic MarkersMaleCCR1Receptors CXCR4AdolescentSpondyloarthropathyArthritisPeripheral blood mononuclear cellArthritis RheumatoidPsoriatic arthritisRheumatologymedicineHumansSpondylitis AnkylosingPharmacology (medical)AgedOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain Reactionbusiness.industryJanus kinase 3Arthritis PsoriaticSynovial MembraneMNDAInterleukinDNAMiddle Agedmedicine.diseaseAntigens DifferentiationChemokine CXCL12ImmunologyLeukocytes MononuclearFemalebusinessChemokines CXCRheumatology (Oxford, England)
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Association between C1019T polymorphism of connexin37 and acute myocardial infarction: a study in patients from Sicily

2003

Abstract During atherogenesis, a critical role is played by intercellular communication via gap junctions, cell membrane channels linking the cytoplasmic compartments of adjacent cells. The component protein subunits of these channels, called connexin (Cx), belong to a multigene family. Cx37 is involved in growth, regeneration after injury and ageing of the endothelial cells, suggesting its role in atherosclerosis. The C1019 single nucleotide polymorphism (SNP) of Cx37 gene was associated with thickening of the carotid intima in Swedish men and was also associated with coronary artery disease in a Taiwanese population. On the other hand, in two more recent studies performed in male Japanese…

AdultGenetic MarkersMalemedicine.medical_specialtyPathologyGenotypeHeart diseasePopulationMyocardial InfarctionSingle-nucleotide polymorphismPolymerase Chain ReactionPolymorphism Single NucleotideGastroenterologyConnexinsCoronary artery diseaseGene FrequencyRisk FactorsInternal medicineOdds RatioHumansMedicineSNPMyocardial infarctioneducationSicilyRetrospective Studieseducation.field_of_studybusiness.industryIncidenceCase-control studyDNAOdds ratioMiddle Agedmedicine.diseasePhenotypeCardiology and Cardiovascular MedicinebusinessInternational Journal of Cardiology
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Genome-wide analysis reveals DNA methylation markers that vary with both age and obesity

2014

AbstractThe combination of the obesity epidemic and an aging population presents growing challenges for the healthcare system. Obesity and aging are major risk factors for a diverse number of diseases and it is of importance to understand their interaction and the underlying molecular mechanisms. Herein the authors examined the methylation levels of 27578 CpG sites in 46 samples from adult peripheral blood. The effect of obesity and aging was ascertained with general linear models. More than one hundred probes were correlated to aging, nine of which belonged to the KEGG group map04080. Additionally, 10 CpG sites had diverse methylation profiles in obese and lean individuals, one of which wa…

AdultGenetic Markersmedicine.medical_specialtyAgingAlpha-Ketoglutarate-Dependent Dioxygenase FTOGenome-wide association studyBiologyMicroarrayBioinformaticsEpigenesis GeneticGeneticsmedicineHumansEpigeneticsObesityKEGGTelomeraseAgedMedicinsk genetikGeneticsProteinsGeneral MedicineMethylationDNA MethylationMiddle Agedmedicine.diseaseObesityCpG siteDNA methylationMedical geneticsCpG IslandsFemaleEpigeneticsMedical GeneticsGenome-Wide Association Study
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Prevention of ischemic-type biliary lesions by arterial back-table pressure perfusion

2003

Abstract Ischemic-type biliary lesions (ITBLs) lead to considerable morbidity after orthotopic liver transplantation (OLT). The exact pathogenesis is unknown. We tested the hypothesis that insufficient perfusion of biliary arterial vessels might be responsible for ITBLs. This could be prevented by improved perfusion techniques. Since February 2000, we performed a controlled study using arterial back-table pressure perfusion (AP) to achieve reliable perfusion of the biliary-tract capillary system, which may be impaired by the high viscosity of University of Wisconsin solution. We retrospectively analyzed 190 OLTs performed between September 1997 and July 2002 with regard to ITBLs. One hundre…

AdultGraft Rejectionmedicine.medical_specialtyAdenosineOrthotopic liver transplantationAllopurinolmedicine.medical_treatmentOrgan Preservation SolutionsUrologyLiver transplantationPathogenesisPostoperative ComplicationsRaffinosePressuremedicineHumansInsulinViaspanAlanine aminotransferaseAgedRetrospective StudiesTransplantationHepatologyViscositybusiness.industryLiver DiseasesGraft SurvivalImmunosuppressionMiddle AgedGlutathioneStandard techniqueLiver TransplantationSurgeryPerfusionSurvival RateReperfusion InjurySurgeryBile DuctsbusinessPerfusionImmunosuppressive AgentsLiver Transplantation
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Transient CD15-positive endothelial phenotype in the human placenta correlates with physiological and pathological fetoplacental immaturity

2013

Abstract Objective Placental growth and villous maturation are critical parameters of placental function at the end of pregnancy. A failure in these processes leads to the development of placental dysfunction, as well as fetal and neonatal mortality and morbidity. The aim of the study was to determine the relevant diagnostic markers associated with pathological placental development. Study design Forty tissue samples from normal placentas of different gestational age and 68 pathological term placentas with defective villous maturation (GDM, idiopathic IUFD, preeclamsia, HELLP syndrome) comprised the comparative immunohistochemical study (CD15, CD45 and CD34). Positive immunohistochemical re…

AdultHELLP SyndromePathologymedicine.medical_specialtyStromal cellEndotheliumHELLP syndromePlacentaCD34Lewis X AntigenAntigens CD34Gestational AgePre-EclampsiaPregnancymedicineHumansPathologicalPregnancyFetusFetal Growth Retardationbusiness.industryEndothelial CellsObstetrics and GynecologyFucosyltransferasesmedicine.diseaseImmunohistochemistryPlacentationDiabetes Gestationalmedicine.anatomical_structureReproductive MedicineCase-Control Studiesembryonic structuresLeukocyte Common AntigensImmunohistochemistryFemalebusinessEuropean Journal of Obstetrics & Gynecology and Reproductive Biology
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HLA-DRB1*1301 AND *1302 protect against chronic hepatitis B

1997

Abstract Background/Aims: The outcome of acute hepatitis B infection may be influenced by host factors like the major histocompatibility complex (MHC). We have investigated MHC class I and class II antigens in patients with chronic hepatitis B compared to a healthy control population. To confirm the findings of this first study we performed a second study in a group of subjects who had spontaneously recovered from acute hepatitis B infection. Methods: Frequencies of MHC class I and class II antigens were analyzed in patients with chronic hepatitis B virus infection and in control subjects. MHC class I typing was done by standard microlymphocytotoxicity assays. DRB1 and DQA1 genotypes were d…

AdultHepatitis B virusRemission SpontaneousPopulationEnzyme-Linked Immunosorbent AssayMajor histocompatibility complexmedicine.disease_causePolymerase Chain ReactionHLA-DQ alpha-ChainsVirusHLA-DQ AntigensMHC class ImedicineHumansSerologic TestsProspective StudiesHepatitis B AntibodieseducationHLA-DRB1AllelesHepatitis B viruseducation.field_of_studyMHC class IIHepatitis B Surface AntigensHepatologybiologyHLA-DR AntigensHepatitis BVirologyChronic infectionImmunoglobulin GChronic DiseaseDNA ViralImmunologybiology.proteinHLA-DRB1 ChainsJournal of Hepatology
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AISF update on the diagnosis and management of adult-onset lysosomal storage diseases with hepatic involvement.

2020

Lysosomal storage diseases (LSDs) are a heterogeneous group of inherited disorders caused by loss-of-function mutations in genes encoding for lysosomal enzymes/proteins. The consequence is a progressive accumulation of substrates in these intracellular organelles, resulting in cellular and tissue damage. The overall incidence is about 1/8000 live births, but is likely underestimated. LSDs are chronic progressive multi-systemic disorders, generally presenting with visceromegaly, and involvement of the central nervous system, eyes, the skeleton, and the respiratory and cardiovascular systems. The age at onset and phenotypic expression are highly variable, according to the specific enzymatic d…

AdultHepatosplenomegalyLysosomal acid lipase deficiencyBioinformaticsOrganomegaly03 medical and health sciencesLiver disease0302 clinical medicinemedicineCholesteryl ester storage disease Enzyme replacement therapy Gaucher disease Lysosomal acid lipase Niemann–Pick disease deficiency Substrate reduction therapyHumansSubstrate reduction therapyEnzyme Replacement TherapySocieties MedicalNiemann-Pick DiseasesAcid sphingomyelinase deficiencyGaucher DiseaseHepatologybusiness.industryGastroenterologyWolman DiseaseEnzyme replacement therapymedicine.diseaseLysosomal Storage DiseasesSphingomyelin PhosphodiesteraseItaly030220 oncology & carcinogenesis030211 gastroenterology & hepatologymedicine.symptombusinessNiemann–Pick diseaseLysosomesVisceromegalyDigestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
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Genotype and phenotype analysis of Friedreich's ataxia compound heterozygous patients

2000

Friedreich's ataxia is caused by mutations in the FRDA gene that encodes frataxin, a nuclear-encoded mitochondrial protein. Most patients are homozygous for the expansion of a GAA triplet repeat within the FRDA gene, but a few patients show compound heterozygosity for a point mutation and the GAA-repeat expansion. We analyzed DNA samples from a cohort of 241 patients with autosomal recessive or isolated spinocerebellar ataxia for the GAA triplet expansion. Patients heterozygous for the GAA expansion were screened for point mutations within the FRDA coding region. Molecular analyses included the single-strand conformation polymorphism analysis, direct sequencing, and linkage analysis with FR…

AdultHeterozygotecongenital hereditary and neonatal diseases and abnormalitiesAtaxiaGenotypeGenetic LinkageDNA Mutational AnalysisGenes RecessiveCompound heterozygosityLoss of heterozygosityTrinucleotide RepeatsIron-Binding ProteinsGenotypeGeneticsmedicineHumansPoint MutationAge of OnsetAlleleChildAllelesPolymorphism Single-Stranded ConformationalGenetics (clinical)Family HealthGeneticsbiologynutritional and metabolic diseasesmedicine.diseasePedigreePhosphotransferases (Alcohol Group Acceptor)PhenotypeFriedreich AtaxiaChild PreschoolFrataxinbiology.proteinSpinocerebellar ataxiamedicine.symptomTrinucleotide Repeat ExpansionTrinucleotide repeat expansionMicrosatellite Repeats
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