Search results for "Amides"

showing 10 items of 552 documents

Sustained complete hematologic remission after administration of the tyrosine kinase inhibitor imatinib mesylate in a patient with refractory, second…

2002

Abstract Imatinib mesylate, a tyrosine kinase inhibitor targeting bcr-abl, platelet-derived growth factor receptor (PDGF-R), and c-Kit, effectively induces hematologic and cytogenetic remissions in bcr-abl+ chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) with only mild to moderate side effects. Here, we describe the successful treatment of a 64-year-old man with c-Kit+ secondary acute myeloid leukemia (AML) refractory to standard chemotherapy. Upon 2 weeks of imatinib mesylate administration, the patient achieved a complete hematologic remission in peripheral blood. In addition, complete clearance of leukemic blasts in bone marrow and a significant cytogenetic response…

MaleMyeloidmedicine.drug_classmedicine.medical_treatmentImmunologyAntineoplastic AgentsBiochemistryTyrosine-kinase inhibitorPiperazinesBone MarrowRecurrencehemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsmedicineSecondary Acute Myeloid LeukemiaHumansReceptors Platelet-Derived Growth FactorEnzyme InhibitorsneoplasmsSalvage TherapyChemotherapyAnemia Refractory with Excess of Blastsbusiness.industryAnemia RefractoryDaunorubicinRemission InductionCytarabineMyeloid leukemiaCell BiologyHematologyExonsMiddle Agedmedicine.diseaseNeoplasm ProteinsLeukemiaLeukemia Myeloid AcuteProto-Oncogene Proteins c-kitmedicine.anatomical_structureImatinib mesylatePyrimidinesDrug Resistance NeoplasmImmunologyBenzamidesCancer researchDisease ProgressionImatinib MesylateNeoplastic Stem CellsBone marrowbusinessBlood
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Effects of SCH 23390, Raclopride, and Haloperidol on Morphine Withdrawal-Induced Aggression in Male Mice

1999

Abstract RODRIGUEZ-ARIAS, M., J. PINAZO, J. MINARRO AND L. STINUS. Effects of SCH 23390, raclopride, and haloperidol on morphine withdrawal-induced aggression in male mice. PHARMACOL BIOCHEM BEHAV 64(1) 123–130, 1999.—Dopamine seems to play a very important role in aggressive behavior observed in morphine withdrawal. The effect of SCH 23390 (0.5 mg/kg), raclopride (0.3 mg/kg), and haloperidol (0.1 mg/kg) on morphine withdrawal-induced aggression has been studied in this work. Mice were rendered dependent by a daily injection of morphine (2.5 mg/kg) for 14 days. Three different experiments were carried out with the objective to evaluate the antiaggressive effect of the dopamine antagonists o…

MaleNarcoticsmedicine.medical_specialtyNarcotic AntagonistsClinical BiochemistryPharmacologyToxicologyBiochemistryMiceBehavioral Neurosciencechemistry.chemical_compoundDopamineInternal medicineSalicylamidesmedicineHaloperidolAnimalsSocial BehaviorBiological PsychiatryPharmacologyRacloprideSCH-23390MorphineNaloxonebusiness.industryDopaminergicAntagonistDopamine antagonistBenzazepinesSubstance Withdrawal SyndromeAggressionEndocrinologychemistryRacloprideMorphineDopamine AntagonistsHaloperidolbusinessAntipsychotic Agentsmedicine.drugPharmacology Biochemistry and Behavior
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Antiatherosclerotic Effects of Small-Molecular-Weight Compounds Enhancing Endothelial Nitric-Oxide Synthase (eNOS) Expression and Preventing eNOS Unc…

2008

Many cardiovascular diseases are associated with reduced levels of bioactive nitric oxide (NO) and an uncoupling of oxygen reduction from NO synthesis in endothelial NO synthase (eNOS uncoupling). In human endothelial EA.hy 926 cells, two small-molecular-weight compounds with related structures, 4-fluoro-N-indan-2-yl-benzamide (CAS no. 291756-32-6; empirical formula C16H14FNO; AVE9488) and 2,2-difluoro-benzo[1,3]dioxole-5-carboxylic acid indan-2-ylamide (CAS no. 450348-85-3; empirical formula C17H13F2NO3; AVE3085), enhanced eNOS promoter activity in a concentration-dependent manner; with the responsible cis-element localized within the proximal 263 base pairs of the promoter region. RNA int…

MaleNeointimamedicine.medical_specialtyNitric Oxide Synthase Type IIINitric Oxide Synthase Type IINitric OxideProtective AgentsUmbilical veinCell LineNitric oxideMicechemistry.chemical_compoundApolipoproteins EEnosInternal medicinemedicineAnimalsHumansBenzodioxolesRNA MessengerAortaMice KnockoutPharmacologychemistry.chemical_classificationSp1 transcription factorReactive oxygen speciesGene knockdownbiologyEndothelial CellsAtherosclerosisbiology.organism_classificationVasoprotectiveMice Inbred C57BLMolecular WeightEndocrinologychemistryBenzamidesIndansMolecular MedicineJournal of Pharmacology and Experimental Therapeutics
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Inhibitors of poly (ADP-ribose) synthetase reduce renal ischemia-reperfusion injury in the anesthetized rat in vivo.

2000

The activation of poly (ADP-ribose) synthetase (PARS) subsequent to DNA damage caused by reactive oxygen or nitrogen species has been implicated in several pathophysiological conditions, including ischemia-reperfusion injury and shock. The aim of this study was to investigate whether PARS inhibitors could provide protection against renal ischemia-reperfusion injury in the rat in vivo. Male Wistar rats were subjected to 45 min bilateral clamping of the renal pedicles, followed by 6 h reperfusion (control animals). Animals were administered the PARS inhibitors 3-aminobenzamide, 1, 5-dihydroxyisoquinoline, or nicotinamide during the reperfusion period. Ischemia, followed by reperfusion, produc…

MaleNiacinamideIschemiaRenal functionNatriuresisKidney; Poly (ADP-ribose) synthetase inhibitors; Proximal tubule; Reactive oxygen species; Reperfusion injuryPharmacologyPoly(ADP-ribose) Polymerase InhibitorsKidneyBiochemistryExcretionchemistry.chemical_compoundIn vivoGeneticsmedicineAnimalsUreaAnesthesiaEnzyme InhibitorsRats WistarMolecular BiologyKidneyCreatinineNicotinamidemedicine.diseaseIsoquinolinesRatsOxidative Stressmedicine.anatomical_structurechemistryCreatinineReperfusion InjuryBenzamidesReactive Oxygen SpeciesReperfusion injuryBiotechnologyGlomerular Filtration RateFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Five-Year Follow-up of Patients Receiving Imatinib for Chronic Myeloid Leukemia

2006

The cause of chronic myeloid leukemia (CML) is a constitutively active BCR-ABL tyrosine kinase. Imatinib inhibits this kinase, and in a short-term study was superior to interferon alfa plus cytarabine for newly diagnosed CML in the chronic phase. For 5 years, we followed patients with CML who received imatinib as initial therapy.We randomly assigned 553 patients to receive imatinib and 553 to receive interferon alfa plus cytarabine and then evaluated them for overall and event-free survival; progression to accelerated-phase CML or blast crisis; hematologic, cytogenetic, and molecular responses; and adverse events.The median follow-up was 60 months. Kaplan-Meier estimates of cumulative best …

MaleOncologymedicine.medical_specialtyFusion Proteins bcr-ablAntineoplastic AgentsKaplan-Meier EstimateChronic phase chronic myelogenous leukemiaDisease-Free SurvivalPiperazineschemistry.chemical_compoundLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesInternal medicineAntineoplastic Combined Chemotherapy ProtocolsOmacetaxine mepesuccinatemedicineHumansneoplasmsbusiness.industryPonatinibCytarabineInterferon-alphaMyeloid leukemiaImatinibGeneral MedicineProtein-Tyrosine KinasesSurvival AnalysisSurvival RateDasatinibPyrimidinesTreatment OutcomeImatinib mesylatechemistryNilotinibBenzamidesImmunologyImatinib MesylateFemalebusinessFollow-Up Studiesmedicine.drugNew England Journal of Medicine
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Ceramide inhibits Kv currents and contributes to TP-receptor-induced vasoconstriction in rat and human pulmonary arteries

2011

et al.

MalePatch-Clamp TechniquesPhysiologyReceptors ThromboxaneSpider Venoms030204 cardiovascular system & hematologyMuscle Smooth VascularMembrane Potentialschemistry.chemical_compound0302 clinical medicineHypoxic pulmonary vasoconstrictionVasoconstrictor AgentsProtein Kinase C0303 health sciencesAniline Compounds3. Good healthSphingomyelin Phosphodiesterasemedicine.anatomical_structurePotassium Channels Voltage-GatedCirculatory systemmedicine.symptomSphingomyelinSignal TransductionBlood vesselmedicine.medical_specialtyCeramidePhosphinesMyocytes Smooth MusclePulmonary ArteryBiologyCeramidesBenzylidene Compounds03 medical and health sciencesInternal medicinemedicineAnimalsHumansRats Wistar030304 developmental biologyCell BiologySphingolipidRatsHEK293 CellsEndocrinologychemistryVasoconstriction15-Hydroxy-11 alpha9 alpha-(epoxymethano)prosta-513-dienoic AcidVascular resistanceVascular ResistancePeptidesVasoconstrictionAmerican Journal of Physiology-Cell Physiology
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Enzyme replacement therapy with agalsidase alfa in children with Fabry disease.

2006

Aim: To assess the effects of enzyme replacement therapy (ERT) in children with Fabry disease. Methods: Safety and efficacy of ERT with agalsidase alfa, 0.2 mg/kg infused over 40 minutes every 2 weeks for 23 weeks, were studied in a multicentre open-label trial in nine boys and four girls. Median age at the start of the study was 11.0 years (range 3.5–18 years). Results: Fifty-four adverse events were reported in 11 patients. No serious adverse events related to ERT were reported. Twelve of the 54 adverse events were considered possibly or probably related to ERT. Infusion reactions (8 mild, 3 moderate) occurred in four boys, in seven infusions. One boy developed IgG antibodies, although he…

MalePediatricsmedicine.medical_specialtyAdolescentGlobotriaosylceramideSweatingchemistry.chemical_compoundQuality of lifemedicineHumansBrief Pain InventoryAdverse effectChildPain Measurementbusiness.industryTrihexosylceramidesGeneral MedicineEnzyme replacement therapymedicine.diseaseFabry diseaseRecombinant ProteinsSurgeryClinical trialIsoenzymesTreatment OutcomeEl NiñochemistryChild Preschoolalpha-GalactosidasePediatrics Perinatology and Child HealthFabry DiseaseFemalebusinessActa paediatrica (Oslo, Norway : 1992)
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Clinical and neuroradiological findings in classic infantile and late-onset globoid-cell leukodystrophy (Krabbe disease)

1996

In the present study the clinical course and imaging of early and late-onset forms of Krabbe disease are analyzed. We report on 11 patients with a biochemical diagnosis of galactosyl ceramide β-galactoside deficiency. Two presented as the classic infantile form and died within the second year of life. In 9 children the first clinical signs, such as gait difficulties and visual failure, started after age 2 years. All these patients developed slow regression of motor and mental capacities, and most of them died within their first decade. In patients of both groups computed tomography (CT) and magnetic resonance imaging (MRI) were performed. In the late-onset form, hypodensities of the central…

MalePediatricsmedicine.medical_specialtyGalactosylceramidesDiseaseWhite matterCentral nervous system diseasemedicineHumansAge of OnsetGenetics (clinical)Pyramidal tractsmedicine.diagnostic_testbusiness.industryBrainInfantMagnetic resonance imagingmedicine.diseaseMagnetic Resonance ImagingLeukodystrophy Globoid Cellmedicine.anatomical_structureEl NiñoSpinal CordChild PreschoolKrabbe diseaseFemaleAge of onsetbusinessTomography X-Ray Computed
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Downregulation of nNOS and synthesis of PGs associated with endotoxin-induced delay in gastric emptying

2002

A single intraperitoneal injection of endotoxin (40 μg/kg) significantly delayed gastric emptying of a solid nutrient meal. Blockade of nitric oxide synthase (NOS) with 30 mg/kg ip N G-nitro-l-arginine methyl ester or 20 mg/kg ip 7-nitroindazole [neuronal NOS (nNOS) inhibitor] significantly delayed gastric emptying in control animals but failed to modify gastric emptying in endotoxin-treated rats. Administration of 2.5, 5, and 10 mg/kg ip N 6-iminoethyl-l-lysine [inducible NOS (iNOS) inhibitor] had no effect in either experimental group. Indomethacin (5 mg/kg sc), NS-398 (cyclooxygenase-2 inhibitor; 10 mg/kg ip), and dexamethasone (10 mg/kg sc) but not quinacrine (20 mg/kg ip) significantl…

MalePhysiologymedicine.medical_treatmentIndomethacinNitric Oxide Synthase Type IINitric Oxide Synthase Type IprostaglandinsRats Sprague-Dawleychemistry.chemical_compoundPyloric AntrumEnzyme InhibitorsAntrumSulfonamidesArachidonic AcidbiologyReverse Transcriptase Polymerase Chain ReactionStomachdigestive oral and skin physiologyGastroenterologyNitric oxide synthasemedicine.anatomical_structureNG-Nitroarginine Methyl EsterQuinacrinenutrient mealsantrum. pylorusmedicine.medical_specialtyIndazolesIntraperitoneal injectionNitric OxidePhospholipases ANitric oxidenitric oxidePhysiology (medical)Internal medicinemedicineAnimalsCyclooxygenase InhibitorsRNA MessengerNitrobenzenesHepatologyGastric emptyingPylorusdigestive system diseasesRatsEndotoxinsEndocrinologyPyloric AntrumchemistryGastric EmptyingFoodbiology.proteinProstaglandinsNitric Oxide Synthase
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Comparison of Active and Passive Targeting of Docetaxel for Prostate Cancer Therapy by HPMA Copolymer–RGDfK Conjugates

2011

N-(2-Hydroxypropyl)methacrylamide (HPMA) copolymer-docetaxel-RGDfK conjugate was synthesized, characterized, and evaluated in vitro and in vivo in comparison with untargeted low and high molecular weight HPMA copolymer-docetaxel conjugates. The targeted conjugate was designed to have a hydrodynamic diameter below renal threshold to allow elimination post treatment. All conjugates demonstrated the ability to inhibit the growth of DU145 and PC3 human prostate cancer cells and the HUVEC at low nanomolar concentrations. The targeted conjugate showed active binding to α(v)β(3) integrins in both HUVEC and DU145 cells, whereas the untargeted conjugate demonstrated no evidence of specific binding. …

MalePolymersMice NudePharmaceutical ScienceAntineoplastic AgentsDocetaxelPharmacologyurologic and male genital diseasesArticleMicechemistry.chemical_compoundProstate cancerstomatognathic systemIn vivoCell Line TumorDrug DiscoveryCopolymermedicineAnimalsMethacrylamideCell ProliferationAcrylamidesChemistryProstatic Neoplasmsmedicine.diseaseIn vitroDocetaxelTargeted drug deliveryMolecular MedicineTaxoidsmedicine.drugConjugateMolecular Pharmaceutics
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