Search results for "Dox"

showing 10 items of 1345 documents

Human leukocyte elastase counteracts matrix metalloproteinase-7 induced apoptosis resistance of tumor cells.

2008

Matrix metalloproteinase-7 (MMP-7/Matrilysin) is a component of the tumor microenvironment associated with malignant progression. Its expression in tumors protects tumor cells from CD95-mediated apoptosis and the cytotoxic activity of tumor specific CD8(+) T cells. In the present study, we show that human leukocyte elastase (HLE) secreted by polymorphonuclear leukocytes cleaves MMP-7 resulting in loss of enzymatic activity. The anti-apoptotic effect of MMP-7 is reduced in the presence of HLE for CD95-, doxorubicin- and CTL-mediated apoptosis. Our data indicates that HLE may be a natural inactivator of MMP-7 which can counteract MMP-7-induced apoptosis resistance.

Cancer ResearchTumor microenvironmentbiologyChemistryNeutrophilsApoptosisMatrix metalloproteinaseFas receptorCell biologyOncologyApoptosisDoxorubicinNeutrophil elastaseMatrix Metalloproteinase 7NeoplasmsCancer researchbiology.proteinCytotoxic T cellHumanssense organsMatrilysinLeukocyte ElastaseCD8Cells CulturedT-Lymphocytes CytotoxicCancer letters
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Lysosomal alterations in heart and liver of mice treated with doxorubicin.

1985

This study was carried out to evaluate the influence of long-term treatment with doxorubicin (DXR) (4mg/kg IV for 5 weeks) on heart and liver lysosomes of mice. We evaluated the variations in both total and "sedimentable" enzyme activity of cathepsin D, which is the major endopeptidase of myocites and probably involved in physiologic and pathologic degradation of actomyosin and mitochondria, and that of acid phosphatase, which is more prominent in interstitial cells. Our results show that marked changes occur in both total and sedimentable enzyme activity of cathepsin D in the heart of treated animals and to a lesser extent in the liver. In contrast, no modification of either total or sedim…

Cancer Researchmedicine.medical_specialtyAcid Phosphatasecardiotoxicity lisosomal enzymesCathepsin DMice Inbred StrainsToxicologyCathepsin DPathogenesisAdriamycinMiceLysosomeInternal medicinemedicineAnimalsPharmacology (medical)DoxorubicinPharmacologyCardiotoxicitybiologyMyocardiumAcid phosphataseHeartEnzyme assayEndocrinologymedicine.anatomical_structureOncologyLiverDoxorubicinToxicitybiology.proteinFemaleLysosomesmedicine.drugCancer chemotherapy and pharmacology
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Composition as identity and plural Cantor's theorem

2016

In this paper, I argue that the thesis of Composition as Identity blocks the plural version of Cantor’s Theorem, and that this in turn has implications for our use of Cantor’s theorem in metaphysics. As an example, I show how this result blocks a recent argument by Hawthorne and Uzquiano, and might be turned around to become an abductive argument for Composition as Identity

Cantor's theoremPure mathematicsmedia_common.quotation_subject05 social sciencesMetaphysics06 humanities and the arts0603 philosophy ethics and religion050105 experimental psychologyEpistemologyPhilosophysymbols.namesakeArgumentIdentity (philosophy)060302 philosophysymbols0501 psychology and cognitive sciencesCantor's paradoxCantor's diagonal argumentmedia_commonMathematicsMereologyPluralLogic and Logical Philosophy
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0131 : Impact of overweight on anthracycline and trastuzumab-induced cardiotoxicity: experimental study in mice

2015

Trastuzumab (TRZ), a humanized monoclonal antibody against Human Epidermal Growth Factor Receptor 2 (HER2) oncogene, is believed to potentiate doxorubicin (DOX) cardiotoxicity, resulting in left ventricular dysfunction. Few data indicate that overweight could influence DOX-induced cardiotoxicity, and no study has already evaluated the impact of moderate overweight on the cardiotoxic effect of DOX alone or in combination with TRZ. Immediately after birth, litters of C57BL/6 mice were either maintained at 10 (normal litter, NL), or reduced to 3 (small litter, SL) in order to induce programming of ~15% overweight through postnatal overfeeding. At 4 months, in order to evaluate the potentiation…

Cardiac function curveCardiotoxicitymedicine.medical_specialtyEjection fractionOncogeneAnthracyclinebusiness.industrymedicine.medical_treatmentIntraperitoneal injectionEndocrinologyTrastuzumabInternal medicinepolycyclic compoundsMedicineDoxorubicinCardiology and Cardiovascular Medicinebusinessmedicine.drugArchives of Cardiovascular Diseases Supplements
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Dystrophin-deficiency increases the susceptibility to doxorubicin-induced cardiotoxicity

2007

Background and aim: The clinical use of doxorubicin (DOX) and other anthracyclines is limited by a dosage-dependent cardiotoxicity, which can lead to cardiomyopathy. The role of the individual genetic makeup in this disorder is poorly understood. Alterations in genes encoding cardiac cytoskeleton or sarcolemma proteins may increase the susceptibility to doxorubicin-related cardiotoxicity. Methods: Female dystrophin-deficient mice (MDX) and age-matched wild-type mice underwent chronic treatment with doxorubicin. Cardiac function and tissue damage were assessed by echocardiography and histopathology, respectively. Gene expression changes were investigated using microarrays. Results: DOX treat…

Cardiac function curveProgrammed cell deathPathologymedicine.medical_specialtyHeart DiseasesCytoskeleton organizationCardiomyopathyGene Expression030204 cardiovascular system & hematologyDystrophinMice03 medical and health sciences0302 clinical medicineRisk FactorsmedicineAnimalsDoxorubicinUltrasonography030304 developmental biology0303 health sciencesCardiotoxicityAntibiotics AntineoplasticSarcolemmabiologybusiness.industryGenetic VariationMicroarray Analysismedicine.disease3. Good healthDoxorubicinDisease Progressionbiology.proteinCancer researchFemaleDisease SusceptibilityCardiology and Cardiovascular MedicineDystrophinbusinessmedicine.drugEuropean Journal of Heart Failure
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Doxorubicin induces wide-spread transcriptional changes in the myocardium of hearts distinguishing between mice with preserved and impaired cardiac f…

2021

Abstract Aims Doxorubicin (DOX) is an important drug for the treatment of various tumor entities. However, the occurrence of heart failure limits its application. This study investigated differential gene expression profiles in the left and right ventricles of DOX treated mice with either preserved or impaired myocardial function. We provide new mechanistic insights into the pathophysiology of DOX-induced heart failure and have discovered pathways that counteract DOX-induced cardiotoxicity. Main methods We used in total 48 male mice and applied a chronic low dose DOX administration (5 mg/kg per injection, in total 20 mg/kg over 4 weeks) to induce heart failure. Echocardiographic parameters …

Cardiac function curveTranscription GeneticPharmacologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyElectrocardiographypolycyclic compoundsmedicineAnimalsCluster AnalysisDoxorubicinGeneral Pharmacology Toxicology and Pharmaceuticschemistry.chemical_classificationReactive oxygen speciesCardiotoxicitybusiness.industryGene Expression ProfilingMyocardiumGeneral Medicinemedicine.diseasePathophysiologyMice Inbred C57BLGene expression profilingOxidative StresschemistryDoxorubicinHeart failureHeart Function TestsbusinessOxidative stressmedicine.drugLife Sciences
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Iron overload does not potentiate doxorubicin induced cardiotoxicity in vivo in mice and in vitro in cardiomyocytes cell cultures

2013

Background: Doxorubicin (DOX), an anticancer anthracycline, is known to induce serious cardiotoxicity, which is believed to be mediated by oxidative stress and complex interactions with iron. However, the relations between iron metabolism and DOX-induced cardiotoxicity remain a matter of controversy. Methods: Firstly, we used an in vivo murine model of iron overloading (IO) where male C57BL/6 mice received during 3 weeks (D0-D20) a daily dextran-iron injection (15 mg/kg/day.) and then (D21) a single dose of 6 mg/kg DOX. We evaluated cardiac function with echocardiography, myocardial gene's expression, nitro-oxidative stress levels and iron status. Secondly, the anti-proliferative activity o…

Cardiac function curvemedicine.medical_specialtyCardiotoxicityAnthracyclinebusiness.industrymedicine.disease_causeEndocrinologyAtrial natriuretic peptideIn vivoInternal medicinepolycyclic compoundsmedicineDoxorubicinViability assayCardiology and Cardiovascular MedicinebusinessOxidative stressmedicine.drugEuropean Heart Journal
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Inorganic Nitrate Therapy Improves Doxorubicin-Induced Cardiomyopathy

2011

The anthracycline doxorubicin (DOX) is a potent and effective antineoplastic antibiotic agent widely used in the treatment of a broad range of forms of cancer. The clinical use of DOX is limited by cardiotoxicity, which increases dose dependently and may lead to dilated cardiomyopathy and clinical

Cardioprotectionmedicine.medical_specialtyCardiotoxicityAnthracyclinebusiness.industryAntineoplastic AntibioticCancerDilated cardiomyopathyPharmacologymedicine.diseasecarbohydrates (lipids)Internal medicineHeart failurepolycyclic compoundsmedicineCardiologyDoxorubicinbusinessCardiology and Cardiovascular Medicinemedicine.drugJournal of the American College of Cardiology
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C022 Experimental approaches of oxidative stress and cardiotoxicity associated with anthracyclines administration

2009

The chronic cardiotoxicity of anthracyclines anticancer drugs is one of the main factors which limits their prolonged use. Clinically, this cardiotoxicity results in a cardiomyopathy with irreversible congestive heart failure with high mortality. The molecular mechanisms, which could explain this cardiac toxicity, are complex but seem distinct from the anticancer mechanism. Several hypotheses were advanced, but it appears that the production of reactive oxygen and nitrogen species (RONS) constitutes the common denominator.In a first study, we evaluated the acute effect of epirubicin administration on the evolution of cardiac functional parameters and production of RONS. Isolated perfused ra…

CardiotoxicityChemotherapybusiness.industrymedicine.medical_treatmentCardiomyopathyGeneral MedicinePharmacologymedicine.diseasemedicine.disease_causeHeart failureAnesthesiamedicineDoxorubicinCardioprotective AgentCardiology and Cardiovascular MedicinebusinessOxidative stressmedicine.drugEpirubicinArchives of Cardiovascular Diseases
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Nanoparticle Assembly of Surface-Modified Proteins

2016

Nature's biomaterials such as peptides and proteins represent a valuable source of highly defined macromolecules. Herein we developed a nanoparticle drug delivery system based on the assembly of surface-modified proteins that can be transferred into organic solvents and represent the structural material of the carrier system. The particles are prepared by an oil-in-water nanoemulsion technique without the need of additional denaturation or cross-linking steps for stabilization. We achieve the necessary lipophilic solubility switch of the protein material by high surface PEGylation under conservation of the native three-dimensional protein structure. This study focuses on lysozyme as model e…

Carrier systemCell SurvivalSurface PropertiesNanoparticleNanotechnology02 engineering and technology010402 general chemistry01 natural sciencesBiochemistryCatalysisStructure-Activity RelationshipColloid and Surface ChemistryProtein structureHumansDenaturation (biochemistry)Particle SizeSolubilityDrug CarriersDose-Response Relationship DrugChemistryGeneral Chemistry021001 nanoscience & nanotechnology0104 chemical sciencesDoxorubicinDrug deliveryBiophysicsPEGylationNanoparticlesMuramidase0210 nano-technologyHeLa CellsMacromoleculeJournal of the American Chemical Society
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