Search results for "DPH"

showing 10 items of 361 documents

Impact of NADPH oxidase functional polymorphisms in acute myeloid leukemia induction chemotherapy.

2016

Efficacy and toxicity of anthracycline treatment in acute myeloid leukemia (AML) is mediated by reactive oxygen species (ROS). NADPH oxidase is the major endogenous source of ROS and a key mediator of oxidative cardiac damage. The impact of NADPH oxidase polymorphisms (CYBA:rs4673, NCF4:rs1883112, RAC2:rs13058338) was evaluated in 225 adult de novo AML patients. Variant alleles of NCF4 and RAC2 were related to higher complete remission (P=0.035, P=0.016), and CYBA homozygous variant showed lower overall survival with recessive model (P=0.045). Anthracycline-induced cardiotoxicity was associated to NCF4 homozygous variant (P=0.012) and CYBA heterozygous genotype (P=0.027). Novel associations…

0301 basic medicineMaleAnthracyclinePharmacologyBiologyPolymorphism Single NucleotideNephrotoxicity03 medical and health sciences0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsGeneticsHumansAgedRetrospective StudiesPharmacologychemistry.chemical_classificationReactive oxygen speciesCardiotoxicityNADPH oxidaseRemission InductionMyeloid leukemiaNADPH OxidasesInduction ChemotherapyMiddle Agedrac GTP-Binding ProteinsRac GTP-Binding ProteinsLeukemia Myeloid Acute030104 developmental biologychemistry030220 oncology & carcinogenesisToxicitybiology.proteinMolecular MedicineFemaleReactive Oxygen SpeciesThe pharmacogenomics journal
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Homocysteine concentration in coronary artery disease: Influence of three common single nucleotide polymorphisms.

2017

Whether single nucleotide polymorphisms (SNPs) of homocysteine metabolism enzymes influence the rate of cardiovascular (CV) events in coronary artery disease (CAD) patients remains controversial.In this analysis, 1126 subjects from the AtheroGene study with CAD and 332 control subjects without known CAD were included. The following SNPs were investigated: methylentetrahydrofolate reductase (MTHFR-C667T), methionin synthetase (MS-D919G), and cystathionin beta synthetase (CBS-I278T). The endpoint was the combination of cardiovascular death, stroke, and non-fatal myocardial infarction (N = 286). The median follow-up time was 6.4 years. Kaplan-Meier curve analysis showed an increasing event rat…

0301 basic medicineMaleTime FactorsHomocysteineEndocrinology Diabetes and MetabolismMyocardial InfarctionMedicine (miscellaneous)Coronary Artery DiseaseKaplan-Meier Estimate030204 cardiovascular system & hematologyReductaseGastroenterology5-Methyltetrahydrofolate-Homocysteine S-MethyltransferaseCoronary artery diseasechemistry.chemical_compound0302 clinical medicineGene FrequencyRisk FactorsMyocardial infarctionStrokeHomocysteineGeneticsNutrition and DieteticsbiologyHomozygoteMiddle AgedStrokePhenotypeArea Under CurveDisease ProgressionFemaleCardiology and Cardiovascular Medicinemedicine.medical_specialtyHeterozygoteCystathionine beta-SynthaseSingle-nucleotide polymorphismPolymorphism Single NucleotideRisk Assessment03 medical and health sciencesPredictive Value of TestsInternal medicinemedicineHumansGenetic Predisposition to DiseaseGenetic Association StudiesMethylenetetrahydrofolate Reductase (NADPH2)AgedProportional Hazards ModelsChi-Square DistributionCurve analysismedicine.disease030104 developmental biologychemistryROC CurveMethylenetetrahydrofolate reductaseCase-Control Studiesbiology.proteinBiomarkersNutrition, metabolism, and cardiovascular diseases : NMCD
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Silver nanoparticle based coatings enhance adipogenesis compared to osteogenesis in human mesenchymal stem cells through oxidative stress.

2020

Silver nanoparticle (AgNP) based antibacterial surfaces were fabricated using plasma polymerization technology and their effects on differentiation of human bone-marrow derived mesenchymal stem cells (hMSCs) were investigated in this study. The results showed that AgNP coated surfaces do not affect the initial adhesion, spreading and proliferation of hMSCs. Furthermore, the silver coated surface promoted adipogenic differentiation of hMSCs as demonstrated by more accumulation of lipid droplets and upregulation of adipogenesis-related genes such as peroxisome proliferator activated receptor gamma (PPAR gamma), adipocyte determination and differentiation factor (ADD1) and CCAAT/enhancer bindi…

0301 basic medicineMaterials scienceMaterials ScienceBiomedical Engineeringmechanism02 engineering and technologysurfacesSilver nanoparticle03 medical and health sciencesEnhancer bindingLipid dropletGeneral Materials Scienceadipocyte differentiationfunctional-groupsAntibacterial agentnadph oxidasesMaterials Science BiomaterialstherapypathwayMesenchymal stem cellosteoblaststoxicityGeneral ChemistryGeneral Medicine021001 nanoscience & nanotechnologyCell biology030104 developmental biologyBiochemistryexposureAdipogenesisAlkaline phosphataseStem cell0210 nano-technologyJournal of materials chemistry. B
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Redox regulation of cardiovascular inflammation – Immunomodulatory function of mitochondrial and Nox-derived reactive oxygen and nitrogen species

2017

Oxidative stress is a major hallmark of cardiovascular diseases although a causal link was so far not proven by large clinical trials. However, there is a close association between oxidative stress and inflammation and increasing evidence for a causal role of (low-grade) inflammation for the onset and progression of cardiovascular diseases, which may serve as the missing link between oxidative stress and cardiovascular morbidity and mortality. With the present review we would like to highlight the multiple redox regulated pathways in inflammation, discuss the sources of reactive oxygen and nitrogen species that are of interest for these processes and finally discuss the importance of angiot…

0301 basic medicineNeutrophilsInflammationmedicine.disease_causeCardiovascular SystemExtracellular TrapsBiochemistrystat03 medical and health scienceschemistry.chemical_compoundPhysiology (medical)medicineHumansEndothelial dysfunctionInflammationMitoQChemistryAngiotensin IIEndothelial CellsNADPH OxidasesNF-κBmedicine.diseaseReactive Nitrogen SpeciesAngiotensin IIMitochondriaOxidative Stress030104 developmental biologyGene Expression RegulationCardiovascular DiseasesTRIFImmunologymedicine.symptomReactive Oxygen SpeciesOxidation-ReductionOxidative stressSignal TransductionFree Radical Biology and Medicine
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Crosstalk of mitochondria with NADPH oxidase via reactive oxygen and nitrogen species signalling and its role for vascular function

2016

Cardiovascular diseases are associated with and/or caused by oxidative stress. This concept has been proven by using the approach of genetic deletion of reactive species producing (pro-oxidant) enzymes as well as by the overexpression of reactive species detoxifying (antioxidant) enzymes leading to a marked reduction of reactive oxygen and nitrogen species (RONS) and in parallel to an amelioration of the severity of diseases. Likewise, the development and progression of cardiovascular diseases is aggravated by overexpression of RONS producing enzymes as well as deletion of antioxidant RONS detoxifying enzymes. Thus, the consequences of the interaction (redox crosstalk) of superoxide/hydroge…

0301 basic medicinePharmacologychemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseAntioxidantbiologySuperoxidemedicine.medical_treatmentMitochondrionmedicine.disease_cause03 medical and health scienceschemistry.chemical_compoundCrosstalk (biology)030104 developmental biologychemistryBiochemistrybiology.proteinmedicineReactive nitrogen speciesOxidative stressBritish Journal of Pharmacology
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Taking up the cudgels for the traditional reactive oxygen and nitrogen species detection assays and their use in the cardiovascular system

2017

Reactive oxygen and nitrogen species (RONS such as H2O2, nitric oxide) confer redox regulation of essential cellular functions (e.g. differentiation, proliferation, migration, apoptosis), initiate and catalyze adaptive stress responses. In contrast, excessive formation of RONS caused by impaired break-down by cellular antioxidant systems and/or insufficient repair of the resulting oxidative damage of biomolecules may lead to appreciable impairment of cellular function and in the worst case to cell death, organ dysfunction and severe disease phenotypes of the entire organism. Therefore, the knowledge of the severity of oxidative stress and tissue specific localization is of great biological …

0301 basic medicineProgrammed cell deathRedox signalingClinical BiochemistrySevere diseaseReview ArticleBiologymedicine.disease_causeCardiovascular SystemBiochemistry03 medical and health sciencesPhysiology (medical)medicineDihydroethidium oxidative fluorescence microtopographyAnimalsHumanslcsh:QH301-705.5Organismchemistry.chemical_classificationlcsh:R5-920Reactive oxygen speciesFluorescence and chemiluminescence-based assaysOrganic ChemistrySpecies detectionNADPH OxidasesPhenotypeReactive Nitrogen SpeciesOxidative Stress030104 developmental biologylcsh:Biology (General)chemistryBiochemistryL-012-enhanced chemiluminescenceLuminescent MeasurementsLucigenin-enhanced chemiluminescencelcsh:Medicine (General)Reactive Oxygen SpeciesNeuroscienceOxidation-ReductionFunction (biology)Oxidative stressFree Radical Biology and Medicine
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Redox Regulation by HGF/c-Met in Liver Disease

2017

Reactive oxygen species (ROS) have gained considerable attention in recent years because of their direct involvement in the regulation of multiple physiological and pathological processes. Under normal conditions, ROS have an important role in cell signaling and function as essential mediators of cell homeostasis. However, imbalance between ROS and antioxidant systems induces oxidative stress, which leads to cell and tissue damage. The cellular redox modulation by hepatocyte growth factor (HGF) and its receptor c-Met in the liver has been studied extensively in the past. The generation of liver-specific c-Met–knockout mice has allowed to demonstrate the fundamental importance of HGF/c-Met i…

0301 basic medicinechemistry.chemical_classificationReactive oxygen speciesC-MetNADPH oxidaseCellBiologymedicine.disease_causeCell biology03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicinemedicine.anatomical_structurechemistrymedicinebiology.proteinHepatocyte growth factorReceptor030217 neurology & neurosurgeryOxidative stressHomeostasismedicine.drug
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2016

AbstractAlcoholic cardiomyopathy (ACM) resulting from excess alcohol consumption is an important cause of heart failure (HF). Although it is assumed that the cardiotoxicity of the ethanol (EtOH)-metabolite acetaldehyde (ACA) is central for its development and progression, the exact mechanisms remain obscure. Murine cardiomyocytes (CMs) exposed to ACA or EtOH showed increased superoxide (O2•−) levels and decreased mitochondrial polarization, both being normalized by NADPH oxidase (NOX) inhibition. C57BL/6 mice and mice deficient for the ACA-degrading enzyme mitochondrial aldehyde dehydrogenase (ALDH-2−/−) were fed a 2% EtOH diet for 5 weeks creating an ACA-overload. 2% EtOH-fed ALDH-2−/− mic…

0301 basic medicinechemistry.chemical_classificationmedicine.medical_specialtyReactive oxygen speciesMultidisciplinaryNADPH oxidasebiologyChemistrySuperoxideCardiomyopathy030204 cardiovascular system & hematologyAlcoholic cardiomyopathyMitochondrionmedicine.diseaseMalondialdehydeLipid peroxidation03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicineEndocrinologyInternal medicinecardiovascular systembiology.proteinmedicineScientific Reports
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Takotsubo Syndrome: Impact of endothelial dysfunction and oxidative stress

2021

Takotsubo Syndrome (TTS) is characterized by a transient left ventricular dysfunction recovering spontaneously within days or weeks. Although the pathophysiology of TTS remains obscure, there is growing evidence suggesting TTS to be associated with increased production of reactive oxygen species (ROS), which may be involved in causing transient coronary and peripheral endothelial dysfunction leading to a transient impairment of myocardial contraction due to stunning (apical ballooning). Endothelial dysfunction is mainly caused by decreased vascular and myocardial nitric oxide bioavailability in response to increased ROS production. Accordingly, studies in humans and animal models demonstrat…

0301 basic medicinemedicine.medical_specialty1303 Biochemistry610 Medicine & healthSodium hydrosulfidemedicine.disease_causeBiochemistryNitric oxide03 medical and health scienceschemistry.chemical_compound2737 Physiology (medical)0302 clinical medicineSuperoxidesTakotsubo CardiomyopathyPhysiology (medical)Internal medicinemedicineAnimalsHumansEndothelial dysfunctionchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologySuperoxideNADPH OxidasesHydrogen PeroxideMalondialdehydemedicine.diseaseOxidative Stress030104 developmental biologyEndocrinologychemistry10209 Clinic for Cardiologybiology.proteinReactive Oxygen Species030217 neurology & neurosurgeryOxidative stressFree Radical Biology and Medicine
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Crucial role for Nox2 and sleep deprivation in aircraft noise-induced vascular and cerebral oxidative stress, inflammation, and gene regulation

2018

Abstract Aims Aircraft noise causes endothelial dysfunction, oxidative stress, and inflammation. Transportation noise increases the incidence of coronary artery disease, hypertension, and stroke. The underlying mechanisms are not well understood. Herein, we investigated effects of phagocyte-type NADPH oxidase (Nox2) knockout and different noise protocols (around-the-clock, sleep/awake phase noise) on vascular and cerebral complications in mice. Methods and results C57BL/6j and Nox2 −/− (gp91phox −/−) mice were exposed to aircraft noise (maximum sound level of 85 dB(A), average sound pressure level of 72 dB(A)) around-the-clock or during sleep/awake phases for 1, 2, and 4 days. Adverse effec…

0301 basic medicinemedicine.medical_specialtyEndotheliumAircraft10208 Institute of NeuropathologyInflammation610 Medicine & health030204 cardiovascular system & hematologySystemic inflammationmedicine.disease_cause2705 Cardiology and Cardiovascular Medicine03 medical and health sciences0302 clinical medicineBasic ScienceVascular BiologyInternal medicineeNOS uncouplingmedicineHumansEndothelial dysfunctionEndothelial dysfunctionInflammationSystemic inflammationbusiness.industryEnvironmental stressorCerebral redox balancemedicine.diseaseEnvironmental stressorSleep deprivationNoiseSleep deprivationOxidative Stress030104 developmental biologymedicine.anatomical_structureEndocrinologyNADPH oxidase-derived oxidative stress570 Life sciences; biologymedicine.symptombusinessNoiseCardiology and Cardiovascular MedicineOxidative stressNoise exposure
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