Search results for "antagonists & inhibitors"

showing 10 items of 21 documents

Determinants of the Quality of Warfarin Control after Venous Thromboembolism and Validation of the SAMe-TT2-R2 Score: An Analysis of Hokusai-VTE.

2019

Background Time in therapeutic range (TTR) measures the quality of vitamin K antagonist (VKA) anticoagulation. In patients with atrial fibrillation, the dichotomized SAMe-TT2-R2 score (≥2 vs. < 2 points) can predict if adequate TTR is unlikely to be achieved. Aims We validated the SAMe-TT2-R2 score in patients with venous thromboembolism (VTE) randomized to the warfarin arm of the Hokusai-VTE trial. Patients and Methods A total of 3,874 patients were included in the primary analysis (day 31–180 from randomization). The efficacy and safety outcomes were symptomatic recurrent VTE and major or clinically relevant non-major bleeding. Results The rates of recurrent VTE and bleeding events we…

0301 basic medicineMalevitamin K antagonistEXTERNAL VALIDATIONTime FactorsVitamin KWarfarin/therapeutic use030204 cardiovascular system & hematologyTHERAPYSeverity of Illness Indexlaw.inventionchemistry.chemical_compound0302 clinical medicineRandomized controlled trialEdoxabanlawRecurrenceAtrial FibrillationVitamin K/antagonists & inhibitorsStrokeRISKAtrial fibrillationHematologyVenous ThromboembolismVitamin K antagonistMiddle Agedrisk assessment modelTIMEPREDICTSTreatment OutcomeAnticoagulants/therapeutic useResearch DesignANTICOAGULATION CONTROLFemaleLife Sciences & Biomedicinemedicine.drugHemorrhage/drug therapyAdultmedicine.medical_specialtyRandomizationmedicine.drug_classvenous thromboembolismHemorrhageRisk AssessmentSensitivity and SpecificityEDOXABAN03 medical and health sciencesDouble-Blind MethodVITAMIN-K ANTAGONISTSInternal medicinemedicineNONVALVULAR ATRIAL-FIBRILLATIONORAL ANTICOAGULANTHumansInternational Normalized RatioBlood CoagulationScience & Technologybusiness.industryquality of treatmentWarfarinAnticoagulantsmedicine.diseasewarfarinClinical trial030104 developmental biologyPeripheral Vascular DiseasechemistryBlood Coagulation/drug effectsAtrial Fibrillation/bloodCardiovascular System & CardiologyLinear ModelsWarfarinbusinessVenous Thromboembolism/drug therapyThrombosis and haemostasis
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PACAP38 and PAC1 receptor blockade: a new target for headache?

2018

Abstract Pituitary adenylate cyclase activating polypeptide-38 (PACAP38) is a widely distributed neuropeptide involved in neuroprotection, neurodevelopment, nociception and inflammation. Moreover, PACAP38 is a potent inducer of migraine-like attacks, but the mechanism behind this has not been fully elucidated. Migraine is a neurovascular disorder, recognized as the second most disabling disease. Nevertheless, the antibodies targeting calcitonin gene-related peptide (CGRP) or its receptor are the only prophylactic treatment developed specifically for migraine. These antibodies have displayed positive results in clinical trials, but are not effective for all patients; therefore, new pharmacol…

0301 basic medicineSide effectPAC1 receptorMigraine DisordersMigraine Disorders/drug therapylcsh:MedicinePituitary Adenylate Cyclase-Activating Polypeptide/antagonists & inhibitorsReview ArticleTriptansPharmacologyCalcitonin gene-related peptidePACAPNeuroprotectionmigraine; PAC1 receptor; PACAP; prophylactic treatment; animals; disease models animal; headache; humans; migraine disorders; pituitary adenylate cyclase-activating polypeptide; receptors pituitary adenylate cyclase-activating polypeptide type I; neurology (clinical); anesthesiology and pain medicine03 medical and health sciences0302 clinical medicineAnimalsHumansMedicineMigraine treatmentReceptorMigraineHeadache/drug therapybusiness.industrylcsh:RHeadacheGeneral Medicinemedicine.disease3. Good healthBlockadeDisease Models Animal030104 developmental biologyAnesthesiology and Pain MedicineMigrainePituitary Adenylate Cyclase-Activating PolypeptideNeurology (clinical)businessProphylactic treatment030217 neurology & neurosurgeryReceptors Pituitary Adenylate Cyclase-Activating Polypeptide Type IReceptors Pituitary Adenylate Cyclase-Activating Polypeptide Type I/antagonists & inhibitorsmedicine.drugJournal of Headache and Pain
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Treatment of acute venous thromboembolism with dabigatran or warfarin and pooled analysis

2014

Background— Dabigatran and warfarin have been compared for the treatment of acute venous thromboembolism (VTE) in a previous trial. We undertook this study to extend those findings. Methods and Results— In a randomized, double-blind, double-dummy trial of 2589 patients with acute VTE treated with low-molecular-weight or unfractionated heparin for 5 to 11 days, we compared dabigatran 150 mg twice daily with warfarin. The primary outcome, recurrent symptomatic, objectively confirmed VTE and related deaths during 6 months of treatment occurred in 30 of the 1279 dabigatran patients (2.3%) compared with 28 of the 1289 warfarin patients (2.2%; hazard ratio, 1.08; 95% confidence interval [CI], 0.…

AdultMalemedicine.medical_specialtyRE-COVER IIrecurrenceAntagonists & inhibitorsAdolescentvenous thromboembolismAntithrombinsDabigatranYoung AdultDouble-Blind MethodRisk FactorsPhysiology (medical)Internal medicinemedicineHumansdabigatrancardiovascular diseasesantagonists & inhibitorAgedacute venous thromboembolismHeparinbusiness.industryWarfarinFollow up studiesAnticoagulantsantagonists & inhibitors; hemorrhage; recurrence; thrombin; venous thromboembolism; warfarinHeparinHeparin Low-Molecular-WeightMiddle AgedthrombinSettore MED/11 - Malattie Dell'Apparato CardiovascolarewarfarinHeparin.low molecular weightPooled analysisAnesthesiaAcute Diseasebeta-AlanineBenzimidazolesFemaledabigatran; warfarin; acute venous thromboembolism; RE-COVER IIhemorrhageCardiology and Cardiovascular MedicinebusinessVenous thromboembolismFollow-Up Studiesmedicine.drug
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Angiotensin Receptor Neprilysin Inhibition Compared With Enalapril on the Risk of Clinical Progression in Surviving Patients With Heart Failure

2015

Background— Clinical trials in heart failure have focused on the improvement in symptoms or decreases in the risk of death and other cardiovascular events. Little is known about the effect of drugs on the risk of clinical deterioration in surviving patients. Methods and Results— We compared the angiotensin-neprilysin inhibitor LCZ696 (400 mg daily) with the angiotensin-converting enzyme inhibitor enalapril (20 mg daily) in 8399 patients with heart failure and reduced ejection fraction in a double-blind trial. The analyses focused on prespecified measures of nonfatal clinical deterioration. In comparison with the enalapril group, fewer LCZ696-treated patients required intensification of med…

Angiotensin receptorVascular damage Radboud Institute for Health Sciences [Radboudumc 16]receptorsTetrazolesheart failureAngiotensin-Converting Enzyme InhibitorsKaplan-Meier EstimateSacubitrilAngiotensin; Heart failure; Neprilysin; Receptors; Aminobutyrates; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Biomarkers; Double-Blind Method; Enalapril; Heart Failure; Humans; Kaplan-Meier Estimate; Natriuretic Peptide Brain; Neprilysin; Peptide Fragments; Risk Factors; Stroke Volume; Survivors; Tetrazoles; Treatment Outcome; Troponin; Disease Progression; Medicine (all); Cardiology and Cardiovascular Medicine; Physiology (medical)AngiotensinEnalaprilRisk FactorsEnalapril/therapeutic useNatriuretic Peptide BrainHeart Failure/bloodSurvivorsReceptorNeprilysinAminobutyrates: Systèmes cardiovasculaire & respiratoire [D03] [Sciences de la santé humaine]Troponin/bloodTroponinAngiotensin Receptor Antagonists/therapeutic useDrug CombinationsAngiotensin-Converting Enzyme Inhibitors/therapeutic useTreatment OutcomeTetrazoles/therapeutic useCardiologyDisease ProgressionValsartanNeprilysinHeart Failure/blood/drug therapy/physiopathologyCardiology and Cardiovascular Medicinemedicine.drugReceptormedicine.medical_specialtyHeart failureneprilysinAngiotensin Receptor Antagonistsreceptors angiotensinDouble-Blind MethodPhysiology (medical)Internal medicineRenin–angiotensin systemmedicineHumansheart failure neprilysin receptors angiotensinEnalaprilbusiness.industryBiphenyl CompoundsStroke Volumemedicine.diseasePeptide FragmentsEndocrinologyAminobutyrates/therapeutic useStroke Volume/physiologyHeart failureNatriuretic Peptide Brain/blood: Cardiovascular & respiratory systems [D03] [Human health sciences]businessNeprilysin/antagonists & inhibitorsPeptide Fragments/bloodSacubitril ValsartanBiomarkersBiomarkers/blood
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Evaluation of whole antioxidant defenses of human mononuclear cells by a new in vitro biological test: lack of correlation between erythrocyte and mo…

2009

1873-2933 (Electronic) Journal Article; OBJECTIVES: This work aims to evaluate the resistance of mononuclear cells to oxidative stress using a "KRL" test, formerly utilized to evaluate the resistance of erythrocyte to free radicals. METHODS: The "KRL" test evaluates the resistance to lysis of cells treated by free radicals generated under standardized conditions. RESULTS: We defined new analytical parameters (level of radical production, time course, number of cells) to obtain an accurate assay determining the resistance to oxidative stress of mononuclear cells, in comparison to that of erythrocytes. This test allows the evaluation of change in the redox state of mononuclear cells (improved…

AntioxidantLysisErythrocytesmedicine.medical_treatmentRadicalClinical BiochemistryStatistics as TopicCell Culture TechniquesAntimycin AInflammationImmunologic Testsmedicine.disease_causePeripheral blood mononuclear cellAntioxidantsAnti-Bacterial Agents/pharmacologyImmunologic Tests/*methodsElectron Transport Complex IIIReactive Oxygen Species/metabolismAntioxidants/*metabolism/pharmacologymedicineErythrocytes/*metabolismLeukocytesHumansDiagnosticOxidative Stress/*drug effectschemistry.chemical_classificationReactive oxygen speciesAntimycin A/pharmacologyElectron Transport Complex III/antagonists & inhibitorsChemistryMononuclear/drug effects/*metabolismReproducibility of ResultsGeneral MedicineIn vitroAnti-Bacterial AgentsOxidative StressBiochemistryLeukocytes MononuclearReagent KitsReagent Kits Diagnosticmedicine.symptomReactive Oxygen SpeciesOxidation-ReductionOxidative stress
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MS4A12 is a colon-selective store-operated calcium channel promoting malignant cell processes.

2008

AbstractUsing a data mining approach for the discovery of new targets for antibody therapy of colon cancer, we identified MS4A12, a sequence homologue of CD20. We show that MS4A12 is a cell surface protein. Expression analysis and immunohistochemistry revealed MS4A12 to be a colonic epithelial cell lineage gene confined to the apical membrane of colonocytes with strict transcriptional repression in all other normal tissue types. Expression is maintained upon malignant transformation in 63% of colon cancers. Ca2+ flux analyses disclosed that MS4A12 is a novel component of store-operated Ca2+ entry in intestinal cells. Using RNAi-mediated gene silencing, we show that loss of MS4A12 in LoVo co…

Calcium Channel Blockers/pharmacologyCancer ResearchColorectal cancerColonCalcium Channels/geneticsCell Differentiation/geneticsEpidermal Growth Factor/pharmacologyBiologyRNA Small Interfering/pharmacologyModels BiologicalMalignant transformationEpidermal growth factorCell Line TumormedicineMembrane Proteins/antagonists & inhibitorsHumansGrowth factor receptor inhibitorNeoplasm InvasivenessRNA Small InterferingEpidermal Growth FactorGene Expression ProfilingMembrane ProteinsColonic Neoplasms/geneticsCell DifferentiationApical membranemedicine.diseaseCalcium Channel BlockersColon/metabolismCell biologyChemokines/metabolismProtein Structure TertiaryGene Expression Regulation NeoplasticOncologyCell cultureOrgan SpecificityCancer cellColonic NeoplasmsDisease ProgressionCalcium ChannelsChemokinesA431 cellsCancer research
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Tumour-derived and host-derived nitric oxide differentially regulate breast carcinoma metastasis to the lungs.

2004

To study the role of nitric oxide (NO) in lung metastasis of breast carcinoma, we isolated two cell clones (H and J) from the parental EMT-6 murine breast carcinoma cell line, based on their differential NO production. In vitro, EMT-6 J cells, but not EMT-6H cells, constitutively expressed inducible NO synthase (NOS II) and secreted high levels of NO. IL-1beta increased NO production in both clones, and TNF-alpha had a synergistic effect on IL-1beta-induced NO production, but NO production by EMT-6 J cells was always higher than by EMT-6H cells. Proliferation, survival and adhesion to lung-derived endothelial cells of both clones were similar and were not affected by NO. In vivo, both clone…

Cancer ResearchPathologymedicine.medical_specialtyLung NeoplasmsCell SurvivalCellNitric Oxide Synthase Type IINitric OxideGuanidinesNitric oxideMetastasischemistry.chemical_compoundMiceCarcinomamedicineCell AdhesionTumor Cells CulturedAnimalsEnzyme InhibitorsCell adhesionMice KnockoutMice Inbred BALB CbiologyIndium RadioisotopesEndothelial CellsMammary Neoplasms ExperimentalGeneral Medicinemedicine.diseaseIn vitroNitric oxide synthaseMice Inbred C57BLSurvival Ratemedicine.anatomical_structurechemistryCell cultureembryonic structuresCancer researchbiology.proteinFemaleNitric Oxide SynthaseCell DivisionAnimals/Cell Adhesion/Cell Division/Cell Survival/Endothelial Cells/metabolism/Pathology/Enzyme Inhibitors/pharmacology/Female/Guanidines/Indium Radioisotopes/Interleukin-1/Lung Neoplasms/enzymology/secondary/Mammary NeoplasmsExperimental/Mice/MiceInbred BALB C/MiceInbred C57BL/MiceKnockout/Nitric Oxide/physiology/Nitric Oxide Synthase/antagonists & inhibitors/Nitric Oxide Synthase Type II/Survival Rate/Tumor CellsCulturedInterleukin-1Carcinogenesis
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Dynamics of Ca2+ and guanosine 5'-[gamma-thio]triphosphate action on insulin secretion from alpha-toxin-permeabilized HIT-T15 cells.

1994

The time course of Ca2+ and GTP-analogue effects on insulin secretion was investigated in HIT-T15 cells permeabilized with Staphylococcus alpha-toxin. These cells responded to Ca2+ in the range 0.1-10 microM and could be used in a dynamic perifusion system because of the minimal run-down of the secretory response. High Ca2+ (10 microM) elicited a monophasic ATP-dependent stimulation of insulin secretion that reached a peak within 5 min (approximately 20-fold increase) and rapidly decreased during the subsequent 15 min to a plateau remaining above basal rates (0.1 microM Ca2+). The decrease in Ca(2+)-induced insulin secretion with time could not be attributed to decreased capacity to respond…

Cell Membrane PermeabilityGTP'medicine.medical_treatmentStimulationCalcium-Calmodulin-Dependent Protein Kinases - antagonists & inhibitorsBiochemistryPiperazinesAdenosine TriphosphateDesensitization (telecommunications)1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineInsulin SecretionGuanosine 5'-O-(3-Thiotriphosphate) - pharmacologyStaphylococcus aureus alpha-toxinInsulinGuanosine Triphosphate - pharmacologyGuanylyl ImidodiphosphateKinasePiperazines - pharmacologyInsulin secretionAdenosine Triphosphate - pharmacologyPermeabilized cellsGuanosine TriphosphateResearch Articlemedicine.medical_specialtyStaphylococcus aureuschemistry.chemical_elementBiologyCalciumGuanylyl Imidodiphosphate - pharmacologyExocytosisCell LineInsulin - secretionInternal medicinemedicine1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivativesSecretionMolecular BiologyInsulinCell BiologyIsoquinolinesATPKineticsEndocrinologyCalcium - pharmacologychemistryIsoquinolines - pharmacologyGuanosine 5'-O-(3-Thiotriphosphate)Type C PhospholipasesCalcium-Calmodulin-Dependent Protein KinasesCalciumType C Phospholipases - pharmacologyGTP
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Impact of a Three Amino Acid Deletion in the CH2 Domain of Murine IgG1 on Fc-Associated Effector Functions

2008

Abstract Four murine IgG subclasses display markedly different Fc-associated effector functions because of their differential binding to three activating IgG Fc receptors (FcγRI, FcγRIII, and FcγRIV) and C1q. Previous analysis of IgG subclass switch variants of 34-3C anti-RBC monoclonal autoantibodies revealed that the IgG1 subclass, which binds only to FcγRIII and fails to activate complement, displayed the poorest pathogenic potential. This could be related to the presence of a three amino acid deletion at positions 233–235 in the CH2 domain uniquely found in this subclass. To address this question, IgG1 insertion and IgG2b deletion mutants at positions 233–235 of 34-3C anti-RBC Abs were …

Deletion mutantImmunologyAntibody AffinityDown-Regulationddc:616.07BiologySubclassProtein Structure Tertiary/geneticsMiceAnimalsImmunology and AllergyAmino AcidsEffector functionsSequence DeletionMice Knockoutchemistry.chemical_classificationMice Inbred BALB CMice Inbred NZBAnemia Hemolytic Autoimmune/genetics/immunologyReceptors IgGAutoantibodyAmino Acids/chemistry/genetics/metabolismIgg subclassesReceptors IgG/antagonists & inhibitors/genetics/metabolismPathogenicityProtein Structure TertiaryImmunoglobulin G/genetics/metabolismImmunoglobulin Switch RegionCell biologyAmino acidImmunoglobulin Heavy Chains/biosynthesis/genetics/metabolismAntibody Affinity/geneticsBiochemistrychemistryImmunoglobulin GMonoclonalMutagenesis Site-DirectedAnemia Hemolytic AutoimmuneDown-Regulation/genetics/immunologyImmunoglobulin Heavy ChainsThe Journal of Immunology
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Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2.

2006

International audience; Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. TRAIL-induced apoptosis is mediated by the transmembrane receptors death receptor 4 (DR4) (also known as TRAIL-R1) and DR5 (TRAIL-R2). TRAIL can also bind decoy receptor 1 (DcR1) (TRAIL-R3) and DcR2 (TRAIL-R4) that fail to induce apoptosis since they lack and have a truncated cytoplasmic death domain, respectively. In addition, DcR1 and DcR2 inhibit DR4- and DR5-mediated, TRAIL-induced apoptosis and we demonstrate here that this occurs through distinct mechanisms. While DcR1 prevents the assembly of the…

MESH : Hela CellsMESH: Membrane GlycoproteinsMESH: Membrane MicrodomainsDecoy Receptor 1ApoptosisMESH : Membrane GlycoproteinsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandJurkat Cells0302 clinical medicineMESH : Tumor Necrosis Factor Decoy ReceptorsMESH: Jurkat CellsDecoy receptorsReceptorCells CulturedMESH : Jurkat CellsMESH : Tumor Necrosis Factor-alpha0303 health sciencesMembrane GlycoproteinsMESH : Protein BindingArticlesMESH : Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsTumor Necrosis Factor Receptor-Associated Peptides and ProteinsCell biology030220 oncology & carcinogenesisCaspasesDeath-inducing signaling complexApoptosis/drug effects; Apoptosis Regulatory Proteins/antagonists & inhibitors; Apoptosis Regulatory Proteins/pharmacology; Caspases/metabolism; Cells Cultured; Death Domain Receptor Signaling Adaptor Proteins; Enzyme Activation/drug effects; GPI-Linked Proteins; HeLa Cells; Humans; Jurkat Cells; Membrane Glycoproteins/antagonists & inhibitors; Membrane Glycoproteins/pharmacology; Membrane Microdomains/drug effects; Protein Binding/drug effects; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor/metabolism; TNF-Related Apoptosis-Inducing Ligand; Tumor Necrosis Factor Decoy Receptors; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins/metabolism; Tumor Necrosis Factor-alpha/antagonists & inhibitors; Tumor Necrosis Factor-alpha/pharmacologyMESH : Apoptosis Regulatory ProteinsMESH: TNF-Related Apoptosis-Inducing LigandProtein BindingMESH: Cells CulturedDeath Domain Receptor Signaling Adaptor ProteinsMESH: Enzyme ActivationBiologyMESH: Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsGPI-Linked Proteins03 medical and health sciencesMembrane MicrodomainsCell surface receptorMESH : Cells Cultured[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyReceptors Tumor Necrosis Factor Member 10cHumansMESH: Protein Binding[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing LigandMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyDeath domainMESH: CaspasesMESH: HumansTumor Necrosis Factor-alphaMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell BiologyMESH: Receptors Tumor Necrosis FactorMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : Receptors Tumor Necrosis FactorEnzyme ActivationMESH: Hela CellsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsApoptosisMESH: Tumor Necrosis Factor-alphaMESH : Membrane MicrodomainsMESH : CaspasesApoptosis Regulatory ProteinsMESH : Enzyme ActivationMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy ReceptorsHeLa CellsMESH: Death Domain Receptor Signaling Adaptor Proteins
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