Search results for "REDUCTASE"

showing 10 items of 798 documents

Studies on the Biosynthesis of Microsomal Membrane Proteins. Site of Synthesis and Mode of Insertion of Cytochrome b5, Cytochrome b5 Reductase, Cytoc…

1982

The site of synthesis and mechanism of insertion into membranes of several microsomal polypeptides was studied using translation system programmed in vitro with polysomes or with mRNA extracted from free and membrane-bound rat liver polysomes. Primary translation products of cytochrome b5, NADH: cytochrome b5 oxidoreductase, NADPH: cytochrome P-450 oxidoreductase and epoxide hydrolase were isolated by specific immunoprecipitation and compared with the mature proteins. The following observations were made: 1 While cytochrome b5 and NADH: cytochrome b5 oxidoreductase are synthesized in free polysomes, NADPH: cytochrome P-450 oxidoreductase and epoxide hydrolase are made in membrane-bound poly…

MaleImmunodiffusionTime FactorsCytochromeBiochemistryElectron TransportCytochrome b5AnimalsCytochrome P450 family 1 member A1Epoxide hydrolaseCytochrome ReductasesCytochrome b5 reductaseNADPH-Ferrihemoprotein ReductaseEpoxide HydrolasesbiologyCytochrome bMembrane ProteinsCytochrome P450 reductaseRats Inbred StrainsMolecular biologyRatsCytochromes b5BiochemistryEnzyme InductionPhenobarbitalProtein BiosynthesisCoenzyme Q – cytochrome c reductaseMicrosomes Liverbiology.proteinCytochromesRabbitsCytochrome-B(5) ReductaseEuropean Journal of Biochemistry
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Effect of hypolipidemic treatment on emerging risk factors in mixed dyslipidemia: a randomized pilot trial

2012

Background The effects of different hypolipidemic treatment strategies on emerging atherosclerosis risk factors remain unknown. Materials and methods This is a prespecified analysis of a prospective, randomized, open-label, blinded end point (PROBE) study (ClinicalTrials.gov identifier: NCT01010516). Patients (n = 100) with mixed dyslipidaemia on a standard statin dose who had not achieved lipid targets were randomized to switch to the highest dose of rosuvastatin (40 mg/day) or to add-on-statin extended release nicotinic acid (ER-NA)/laropiprant (LRPT) or to add-on-statin micronized fenofibrate for a total of 3 months. Results Following 3 months of treatment, low-density lipoprotein (LDL) …

MaleIndolesTime FactorsClinical BiochemistryPilot ProjectsPharmacologyBiochemistryGastroenterologychemistry.chemical_compoundFenofibrateRisk FactorsProspective StudiesRosuvastatin CalciumHypolipidemic AgentsSulfonamidesFenofibratebiologyGeneral MedicineMiddle AgedRosuvastatin CalciumC-Reactive ProteinCardiovascular DiseasesDrug Therapy CombinationFemalelipids (amino acids peptides and proteins)Laropiprantmedicine.drugAdultmedicine.medical_specialtyStatinmedicine.drug_classNiacinInternal medicinemedicineHumansRosuvastatinAgedApolipoproteins BDyslipidemiasbusiness.industryCholesterolC-reactive proteinnutritional and metabolic diseasesCholesterol LDLAtherosclerosismedicine.diseaseFluorobenzenesPyrimidineschemistry1-Alkyl-2-acetylglycerophosphocholine Esterasebiology.proteinHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessDyslipidemiaEuropean Journal of Clinical Investigation
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Linkage disequilibrium of MTHFR genotypes 677C/T-1298A/C in the German population and association studies in probands with neural tube defects(NTD).

1999

A number of studies have demonstrated that the common polymorphism 677CT in the gene encoding 5, 10-methylenetetrahydrofolate reductase (MTHFR) leads to a thermolabile variant with decreased enzyme activity and to mildly elevated plasma homocysteine. 677TT homozygosity was shown to be more frequent in NTD probands compared with controls in some studies. Recently, another polymorphism, 1298AC, in the MTHFR gene was described and combined heterozygosity 677CT/1298AC was suggested to be an additional risk factor for NTD. The present study examines the genotype and haplotype distribution of the two polymorphisms in the German population and evaluates the impact on NTD individuals and their rela…

MaleLinkage disequilibriumGenotypePopulationLinkage DisequilibriumFetusGene FrequencyGermanyHumansNeural Tube DefectseducationAllele frequencyGenetics (clinical)AllelesMethylenetetrahydrofolate Reductase (NADPH2)Genetic associationGeneticsFamily Healtheducation.field_of_studyOxidoreductases Acting on CH-NH Group DonorsPolymorphism GeneticbiologyHaplotypeTransmission disequilibrium testDNAGenotype frequencyPedigreeHaplotypesMethylenetetrahydrofolate reductaseCase-Control StudiesPopulation SurveillanceMutationbiology.proteinFemaleAmerican journal of medical genetics
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Long-Term Clinical Outcomes According to Previous Manifestations of Atherosclerotic Disease (from the FAST-MI 2010 Registry)

2017

IF 3.398; International audience; The prognosis of patients with acute myocardial infarction (AMI) has notably improved in the past 20 years. Using the French Registry of ST-Elevation and Non-ST-elevation Myocardial Infarction (FAST-MI) 2010 registry, we investigated whether previous manifestations of atherosclerotic disease (i.e., previous MI, or a history of any form of atherosclerotic disease) are at truly increased risk compared with those in whom AMI is the first manifestation of the disease. FAST-MI 2010 is a nationwide French registry including 3,079 patients with AMI, among whom 1,062 patients had a history of cardiovascular atherosclerotic disease and 498 patients had a history of …

MaleMESH : Atherosclerosismedicine.medical_treatmentMESH : MortalityMyocardial InfarctionMESH : AgedMESH : Prospective StudiesAngiotensin-Converting Enzyme InhibitorsCoronary Artery DiseaseDiseaseMESH : Cerebrovascular Disorders0302 clinical medicineMedicineLongitudinal StudiesProspective StudiesMESH: Coronary Artery DiseaseMyocardial infarctionCoronary Artery BypassMESH: Treatment OutcomeCause of deathAged 80 and overeducation.field_of_studyMESH: Middle AgedHazard ratioMESH : Platelet Aggregation InhibitorsPrognosisMESH: Case-Control Studies3. Good healthMESH: Myocardial InfarctionMESH: Angiotensin Receptor AntagonistsMESH : Angiotensin-Converting Enzyme InhibitorsCardiology and Cardiovascular MedicineMESH: Percutaneous Coronary InterventionMESH : Case-Control Studiesmedicine.medical_specialtyMESH : Angiotensin Receptor AntagonistsMESH: Prognosis03 medical and health sciencesPercutaneous Coronary Intervention[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemHumansMESH : Middle AgedMESH : Coronary Artery DiseaseMESH : Aged 80 and overMESH: Hydroxymethylglutaryl-CoA Reductase InhibitorseducationMESH: Age DistributionAgedMESH: HumansMESH: MortalityProportional hazards modelMESH: Coronary Artery BypassMESH : HumansCase-control studyMESH : Proportional Hazards Modelsmedicine.diseaseMESH : Coronary Artery BypassCase-Control StudiesMESH: FemaleMESH: RegistriesMESH : Age Distribution030204 cardiovascular system & hematologyMESH: AtherosclerosisMESH: Proportional Hazards ModelsMESH: Cause of DeathMESH: Aged 80 and overMESH : Percutaneous Coronary InterventionRisk FactorsMESH: Risk FactorsCause of DeathMESH : FemaleRegistries030212 general & internal medicineMESH: Longitudinal StudiesMESH : Longitudinal StudiesMESH: AgedMESH : PrognosisMESH: Angiotensin-Converting Enzyme InhibitorsMESH: Adrenergic beta-AntagonistsMiddle Aged[ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemMESH : Risk FactorsTreatment OutcomeMESH: Platelet Aggregation InhibitorsCardiologyFemaleMESH: Cerebrovascular DisordersFranceMESH : MaleAdrenergic beta-AntagonistsMESH : Adrenergic beta-AntagonistsPopulationMESH : Treatment OutcomeMESH: Multivariate AnalysisAngiotensin Receptor AntagonistsAge DistributionInternal medicineMortalityMESH : FranceProportional Hazards ModelsMESH : Cause of Deathbusiness.industryMESH : Hydroxymethylglutaryl-CoA Reductase InhibitorsMESH : Multivariate AnalysisPercutaneous coronary interventionAtherosclerosisMESH: MaleMESH: Prospective StudiesMESH: FranceCerebrovascular DisordersMultivariate AnalysisHydroxymethylglutaryl-CoA Reductase InhibitorsMESH : Myocardial InfarctionbusinessPlatelet Aggregation InhibitorsMESH : RegistriesThe American Journal of Cardiology
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Phenotypic and biochemical analysis of an international cohort of individuals with variants in NAA10 and NAA15.

2019

Abstract N-alpha-acetylation is one of the most common co-translational protein modifications in humans and is essential for normal cell function. NAA10 encodes for the enzyme NAA10, which is the catalytic subunit in the N-terminal acetyltransferase A (NatA) complex. The auxiliary and regulatory subunits of the NatA complex are NAA15 and Huntington-interacting protein (HYPK), respectively. Through a genotype-first approach with exome sequencing, we identified and phenotypically characterized 30 individuals from 30 unrelated families with 17 different de novo or inherited, dominantly acting missense variants in NAA10 or NAA15. Clinical features of affected individuals include variable levels…

MaleModels Molecular0301 basic medicineProtein ConformationMicrophthalmia0302 clinical medicineEnzyme StabilityMissense mutationN-Terminal Acetyltransferase EChildN-Terminal Acetyltransferase AExome sequencingGenetics (clinical)GeneticsbiologyGeneral MedicinePhenotypeRecombinant ProteinsChemistryPhenotypeChild PreschoolHMG-CoA reductaseCohortFemaleGeneral ArticleCorrigendumAdultNatA complexmedicine.medical_specialtyAdolescentGenotypeFrameshift mutationStructure-Activity RelationshipYoung Adult03 medical and health sciencesMolecular geneticsGeneticsmedicineHumansGenetic Predisposition to DiseaseGenetic TestingAlleleBiologyMolecular BiologyAllelesGenetic Association StudiesComputational BiologyFaciesGenetic VariationInfantmedicine.diseaseEnzyme ActivationLenz microphthalmia syndrome030104 developmental biologyGenetic LociMutationbiology.proteinHuman medicineBiomarkers030217 neurology & neurosurgeryNAA15Human molecular genetics
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Rosiglitazone evaluated for cardiovascular outcomes in oral agent combination therapy for type 2 diabetes (RECORD): a multicentre, randomised, open-l…

2009

Udgivelsesdato: 2009-Jun-20 BACKGROUND: Rosiglitazone is an insulin sensitiser used in combination with metformin, a sulfonylurea, or both, for lowering blood glucose in people with type 2 diabetes. We assessed cardiovascular outcomes after addition of rosiglitazone to either metformin or sulfonylurea compared with the combination of the two over 5-7 years of follow-up. We also assessed comparative safety. METHODS: In a multicentre, open-label trial, 4447 patients with type 2 diabetes on metformin or sulfonylurea monotherapy with mean haemoglobin A(1c) (HbA(1c)) of 7.9% were randomly assigned to addition of rosiglitazone (n=2220) or to a combination of metformin and sulfonylurea (active con…

MaleMyocardial InfarctionAdministration OralType 2 diabeteslaw.inventionFractures BoneRandomized controlled triallawNeoplasmsClinical endpointMyocardial infarctionrosiglitazone; cardiovascular outcomesProspective StudiesDiureticsGeneral MedicineMiddle AgedMetforminMetforminHospitalizationStrokeDrug Therapy CombinationFemaleRosiglitazonemedicine.drugmedicine.medical_specialtyRosiglitazoneSex FactorsInternal medicineDiabetes mellitusmedicineHumansHypoglycemic AgentsAngina UnstableDiabetes Rosiglitazone Cardiovascular RiskHemoglobin A GlycosylatedGlycated HemoglobinHeart FailureIntention-to-treat analysisbusiness.industryBody WeightCholesterol HDLCholesterol LDLtype 2 diabetes; rosiglitazonemedicine.diseaseDrug UtilizationSurgerySulfonylurea CompoundsDiabetes Mellitus Type 2ThiazolidinedionesHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessLancet (London, England)
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Nitric oxide is involved in non-adrenergic, non-cholinergic inhibitory neurotransmission in rat duodenum

1995

1. In rat duodenum, electrical field stimulation (EFS) induced a relaxation due to activation of non-adrenergic, non-cholinergic (NANC) inhibitory intramural neurones. 2. Nitric oxide synthase (NOS) inhibitors, N omega-nitro-L-arginine (L-NNA) and N omega-nitro-L-arginine methyl ester (L-NAME), caused a dose-dependent reduction in amplitude of the NANC relaxation. Responses to low frequencies of stimulation were more sensitive to NOS inhibitors than those to high frequencies. 3. Effects induced by NOS inhibitors were stereospecific since D-NNA and D-NAME did not affect NANC relaxation. L-arginine, but not D-arginine, partially prevented the effects induced by NOS inhibitors on NANC relaxati…

MaleNitroprussidemedicine.medical_specialtyDuodenumMuscle RelaxationStimulationIn Vitro TechniquesArginineAutonomic Nervous SystemNitric OxideNitroarginineSynaptic TransmissionNitric oxidechemistry.chemical_compoundNitroarginineInternal medicineMedicineAnimalsChymotrypsinRats WistarPharmacologybiologybusiness.industrymusculoskeletal neural and ocular physiologyGeneral NeuroscienceMuscle SmoothElectric StimulationRatsNitric oxide synthaseMuscle relaxationEndocrinologyNG-Nitroarginine Methyl EsterchemistryTetrodotoxinbiology.proteinSodium nitroprussideAmino Acid OxidoreductasesNitric Oxide SynthasebusinessNitrovasodilatormedicine.drug
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Liver subcellular fractions from rats treated by organosulfur compounds from Allium modulate mutagen activation

2000

The effects of in vivo administration of naturally occurring organosulfur compounds (OSCs) from Allium species were studied on the activation of several mutagens. Male SPF Wistar rats were given p.o. one of either diallyl sulfide (DAS), diallyl disulfide (DADS), dipropyl sulfide (DPS) or dipropyl disulfide (DPDS) during 4 consecutive days and the ability of hepatic S9 and microsomes from treated rats to activate benzo[a]pyrene (BaP), cyclophosphamide (CP), dimethylnitrosamine (DMN), N-nitrosopiperidine (N-PiP) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) was determined in the Ames test. Administration of DAS, DPS and DPDS resulted in a significant increase of the activation of…

MaleNitrosaminesHealth Toxicology and Mutagenesis[SDV]Life Sciences [q-bio]MutagenSulfidesmedicine.disease_causeIsozymeAlliumDimethylnitrosamineAmes testPropane03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCytochrome P-450 Enzyme SystemBenzo(a)pyreneCytochrome P-450 CYP1A1GeneticsmedicineAnimalsDisulfidesRats WistarCyclophosphamideComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciencesDose-Response Relationship DrugMutagenicity TestsDiallyl disulfideImidazolesCytochrome P-450 CYP2E1CYP2E1RatsAllyl Compounds[SDV] Life Sciences [q-bio]Dose–response relationshipBiochemistrychemistry030220 oncology & carcinogenesisCytochrome P-450 CYP2B1ToxicityMicrosomes LiverMicrosomeLiver ExtractsOxidoreductasesMutagensSubcellular Fractions
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Dihydrodiol dehydrogenase activities of rabbit liver are associated with hydroxysteroid dehydrogenases and aldo-keto reductases.

1992

1. Dihydrodiol dehydrogenase activities were investigated in rabbit liver. Using a five-step purification scheme, eight isoenzymes of dihydrodiol dehydrogenase with isoelectric points of 5.55-9.3 and promoter molecular masses of 34-35 kDa were purified to apparent homogeneity and designated CF-1 to CF-6, CM-1 and CM-2. 2. CF-1 and CF-2 had near-neutral isoelectric points of 7.4 and 6.8 and molecular masses of about 125 kDa in the native state. Both enzymes readily accepted NAD+ as well as NADP+ as coenzymes, had relatively low Km values of 0.33 mM and 0.47 mM for benzene dihydrodiol and resembled previously described carbonyl reductases in their substrate specificity towards ketones and qui…

MaleOxidoreductases Acting on CH-CH Group DonorsCarbonyl ReductaseStereochemistryAldo-Keto ReductasesDehydrogenaseReductaseBiochemistryCofactorCatalysisSubstrate SpecificityAldehyde Reductasepolycyclic compoundsAnimalsTissue DistributionIsoelectric PointAldehyde ReductaseAldo-keto reductasebiologyChemistryHydroxysteroid DehydrogenasesAntibodies MonoclonalHydroxysteroid DehydrogenasesIsoenzymesMolecular WeightAlcohol OxidoreductasesBiochemistryLiverbiology.proteinElectrophoresis Polyacrylamide GelNAD+ kinaseRabbitsOxidoreductasesEuropean journal of biochemistry
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Portal Vein Thrombosis in a Preterm Newborn with Mutation of the MTHFR and PAI-1 Genes and Sepsis by Candida parapsilosis

2016

Objective This report discusses the role of both congenital and acquired risk factors in the pathogenesis of portal vein thrombosis (PVT). Study Design We describe the clinical management and treatment of PVT in a preterm newborn with a homozygous mutation of the methylenetetrahydrofolate reductase (MTHFR) and plasminogen activator inhibitor-1 (PAI-1) genes and sepsis by Candida parapsilosis. Results Although literature data suggest a minor role of genetic factors in thrombophilia in the case of only one mutation, we hypothesize that combined thrombophilic genetic defects may have a cumulative effect and significantly increase the thrombotic risk. Conclusion It could be appropriate to incl…

MalePathologymedicine.medical_specialtyCandida parapsilosis030204 cardiovascular system & hematologyBioinformaticsCandida parapsilosisThrombophiliaSepsisPathogenesis03 medical and health sciences0302 clinical medicineSepsis030225 pediatricsPlasminogen Activator Inhibitor 1medicineHumansMethylenetetrahydrofolate Reductase (NADPH2)Venous ThrombosisPolymorphism GeneticbiologyPortal Veinbusiness.industryCandidiasisInfant NewbornAnticoagulantsFactor VObstetrics and Gynecologyportal thrombosis fungal infection gene polymorphismmedicine.diseasebiology.organism_classificationPortal vein thrombosisSurgical Procedures OperativeMethylenetetrahydrofolate reductaseMutationPediatrics Perinatology and Child Healthbiology.proteinGene polymorphismbusinessPlasminogen activatorAmerican Journal of Perinatology
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