Search results for "Pyrazole"

showing 10 items of 315 documents

Combined heterologies for monoclonal antibody-based immunoanalysis of fluxapyroxad

2018

Nowadays, instrumental methodologies and rapid bioanalytical techniques complement each other for the analysis of toxic chemical compounds. Fluxapyroxad was commercialized a few years ago as a fungicide and today it is being used worldwide to control a variety of pests. In the present study, the development of monoclonal antibody-based immunochemical methods for the analysis of this chemical in food samples was evaluated for the first time. Novel haptens were synthesized and protein bioconjugates were prepared. High-affinity and specific monoclonal antibodies to fluxapyroxad were generated from two haptens with alternative linker tethering sites. Haptens with linker site heterology and a st…

Bioanalysismedicine.drug_classEnzyme-Linked Immunosorbent AssayFood ContaminationFluxapyroxadMonoclonal antibody01 natural sciencesBiochemistryAnalytical ChemistryMice0404 agricultural biotechnologyLimit of DetectionElectrochemistrymedicineIc50 valuesAnimalsEnvironmental ChemistryMoietySpectroscopyChromatographymedicine.diagnostic_testChemistry010401 analytical chemistryAntibodies Monoclonal04 agricultural and veterinary sciencesAmides040401 food scienceFungicides Industrial0104 chemical sciencesFruitImmunoassayPyrazolesHaptensHaptenLinkerThe Analyst
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Heme oxygenase-1 induction by nitric oxide in RAW 264.7 macrophages is upregulated by a cyclo-oxygenase-2 inhibitor.

2001

Unstimulated RAW 264.7 macrophages express negligible heme oxygenase-1 (HO-1) protein but incubation with the nitric oxide (NO) donor spermine nonoate (SPNO) induced HO-1 and weakly cyclo-oxygenase-2 (COX-2) protein. This effect was potentiated by coincubation with the COX-2 selective inhibitor, SC58125. Cells incubated with SPNO showed a strong increase in HO-1 mRNA levels after 4 h with a significant potentiation in the presence of SC58125, which did not modify HO-1 mRNA stability. The induction of HO-1 by NO and its potentiation by anti-inflammatory agents may play a role in inflammatory and immune responses.

BiophysicsSpermineNitric OxideBiochemistryNitric oxideCell Linechemistry.chemical_compoundMiceDownregulation and upregulationMacrophageAnimalsCyclooxygenase InhibitorsRNA MessengerMolecular BiologyHemeCyclooxygenase 2 InhibitorsMacrophagesMembrane ProteinsLong-term potentiationDrug SynergismMolecular biologyUp-RegulationHeme oxygenaseIsoenzymeschemistryBiochemistryCell cultureCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesHeme Oxygenase (Decyclizing)PyrazolesNitrogen OxidesSpermineHeme Oxygenase-1Biochimica et biophysica acta
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Acute activation of cannabinoid receptors by anandamide reduces gastrointestinal motility and improves postprandial glycemia in mice.

2015

International audience; The endocannabinoid system (ECS) is associated with an alteration of glucose homeostasis dependent on cannabinoid receptor-1 (CB1R) activation. However, very little information is available concerning the consequences of ECS activation on intestinal glucose absorption. Mice were injected intraperitoneally with anandamide, an endocannabinoid binding both CB1R and CB2R. We measured plasma glucose and xylose appearance after oral loading, gastrointestinal motility, and glucose transepithelial transport using the everted sac method. Anandamide improved hyperglycemia after oral glucose charge whereas glucose clearance and insulin sensitivity were impaired, pointing out so…

Blood GlucoseMaleIndolesCannabinoid receptorMESH : Piperidines[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionEndocrinology Diabetes and Metabolismmedicine.medical_treatmentMESH: EndocannabinoidsMESH : PyrazolesMESH : Receptors CannabinoidMicechemistry.chemical_compoundPiperidinesMESH : IndolesMESH: Receptors CannabinoidMESH: Reverse Transcriptase Polymerase Chain ReactionMESH : Arachidonic AcidsGlucose homeostasisMESH: Gastrointestinal TransitMESH: AnimalsReceptors CannabinoidMESH: IndolesReverse Transcriptase Polymerase Chain ReactionMESH : RatsMESH : Reverse Transcriptase Polymerase Chain ReactionAnandamidePostprandial PeriodEndocannabinoid systemMESH : Gastrointestinal MotilityPostprandialMESH: PiperidinesMESH: Postprandial PeriodMESH: Gastrointestinal MotilityRimonabantMESH : EndocannabinoidsMESH : Gastrointestinal Transitmedicine.medical_specialtyMESH: RatsPolyunsaturated AlkamidesMESH : MaleArachidonic AcidsMESH : Mice Inbred C57BLMESH : Rats WistarMESH: Mice Inbred C57BLInternal medicineMESH : MiceInternal MedicinemedicineAnimalsMESH: Arachidonic AcidsMESH : Polyunsaturated AlkamidesRats WistarGastrointestinal TransitMESH: MiceGastric emptyingMESH: Polyunsaturated AlkamidesGlucose transporterMESH: Rats WistarMESH : Blood GlucoseMESH: MaleRatsMice Inbred C57BL[SDV.AEN] Life Sciences [q-bio]/Food and NutritionEndocrinologychemistryHyperglycemiaMESH : HyperglycemiaMESH: Blood GlucosePyrazolesMESH : AnimalsCannabinoidMESH : Postprandial PeriodGastrointestinal MotilityMESH: Hyperglycemia[SDV.AEN]Life Sciences [q-bio]/Food and NutritionMESH: PyrazolesEndocannabinoids
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Eltrombopag in chronic hepatitis C

2014

Chronic hepatitis C is a public health problem worldwide. Unfortunately, not all patients may benefit from antiviral therapy due to thrombocytopenia. Its causes are represented by portal hypertension and platelet sequestration in the spleen, decreased serum levels or activity of thrombopoietin, the bone marrow suppression induced by hepatitis C virus and a possible adverse effect of interferon. Thrombopoietin receptor analogs may contribute to increase platelet counts in these patients. Eltrombopag binds to another region of the thrombopoietin receptor compared to endogenous thrombopoietin and stimulates the proliferation and maturation of megakaryocytes and the platelet production in a dos…

Blood PlateletsCirrhosisHepatitis C virusEltrombopagmedicine.disease_causeAntiviral AgentsBenzoatesThrombopoiesischemistry.chemical_compoundRisk FactorsHematologic AgentsmedicineHumansThrombopoiesisThrombopoietinThrombopoietin receptorbusiness.industryGastroenterologyBone marrow failureMinireviewsGeneral MedicineHepatitis C Chronicmedicine.diseaseThrombocytopeniaHydrazinesTreatment OutcomeBone marrow suppressionchemistryImmunologyPyrazolesbusinessReceptors ThrombopoietinSignal TransductionWorld Journal of Gastroenterology
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Evidence for a modulatory role of cannabinoids on the excitatory NANC neurotransmission in mouse colon

2007

Abstract It is well accepted that endogenous cannabinoids and CB1 receptors are involved in the regulation of smooth muscle contractility and intestinal motility, through a mechanism mainly related to reduction of acetylcholine release from cholinergic nerve endings. Because, few data exist on a possible modulatory action of the cannabinoid agents on the non-adrenergic non-cholinergic (NANC) excitatory and inhibitory neurotransmission, the aim of the present study was to investigate the effects of cannabinoid drugs on the NANC responses elicited by electrical field stimulation (EFS) in the circular muscle of mouse proximal colon. Colonic contractions were monitored as changes in endoluminal…

CB1 receptorIndolesCannabinoid receptormedicine.medical_treatmentSynaptic TransmissionSettore BIO/09 - FisiologiaEnteric Nervous SystemReceptor Cannabinoid CB2Micechemistry.chemical_compoundPiperidinesReceptor Cannabinoid CB1Fatty acid amide hydrolaseCannabinoid receptor type 2musculoskeletal neural and ocular physiologyAnandamideSmooth muscle contractionRimonabantAgonistmedicine.medical_specialtyColonPolyunsaturated Alkamidesmedicine.drug_classMorpholinesNeuromuscular JunctionArachidonic AcidsIn Vitro TechniquesNaphthalenesTachykininsInternal medicineCannabinoid Receptor ModulatorsIntestinal motilitymedicineAnimalsCannabinoidReceptors TachykininPharmacologyDose-Response Relationship DrugCannabinoidsExcitatory Postsynaptic PotentialsNANC relaxationURB597Electric StimulationBenzoxazinesMice Inbred C57BLEndocrinologyInhibitory Postsynaptic PotentialschemistryPyrazolesNANC contractionCannabinoidGastrointestinal MotilityEndocannabinoidsPharmacological Research
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The novel NF-κB inhibitor DHMEQ synergizes with celecoxib to exert antitumor effects on human liver cancer cells by a ROS-dependent mechanism

2012

In a previous work of ours dehydroxymethyl-epoxyquinomicin (DHMEQ), an inhibitor of NF-κB, was shown to induce apoptosis through Reactive Oxygen Species (ROS) production in hepatoma cells. The present study demonstrated that DHMEQ cooperates with Celecoxib (CLX) to decrease NF-κB DNA binding and to inhibit cell growth and proliferation more effectively than treatment with these single agents alone in the hepatoma cell lines HA22T/VGH and Huh-6. ROS production induced by the DHMEQ-CLX combination in turn generated the expression of genes involved in endoplasmic reticulum (ER) stress and silencing TRB3 mRNA significantly decreased DHMEQ-CLX-induced cell growth inhibition. Moreover, the DHMEQ-…

Cancer ResearchCarcinoma HepatocellularAntineoplastic AgentsApoptosisCell Cycle ProteinsProtein Serine-Threonine KinasesBiologyDHMEQ Celecoxib NF-jB CD95/CD95L Liver cancer cellsCell Line TumorSurvivinHumansGene silencingfas ReceptorProtein kinase BCell ProliferationSulfonamidesGene knockdownCyclooxygenase 2 InhibitorsCyclohexanonesCell growthEndoplasmic reticulumLiver NeoplasmsNF-kappa BDrug SynergismEndoplasmic Reticulum StressMolecular biologyAcetylcysteineRepressor ProteinsOncologyCelecoxibCell cultureApoptosisBenzamidesCancer researchPyrazolesPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesCancer Letters
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Cyclooxygenase-2 inhibition induces apoptosis signaling via death receptors and mitochondria in hepatocellular carcinoma.

2006

AbstractInhibition of cyclooxygenase (COX)-2 elicits chemopreventive and therapeutic effects in solid tumors that are coupled with the induction of apoptosis in tumor cells. We investigated the mechanisms by which COX-2 inhibition induces apoptosis in hepatocellular carcinoma (HCC) cells. COX-2 inhibition triggered expression of the CD95, tumor necrosis factor (TNF)-R, and TNF-related apoptosis-inducing ligand (TRAIL)-R1 and TRAIL-R2 death receptors. Addition of the respective specific ligands further increased apoptosis, indicating that COX-2 inhibition induced the expression of functional death receptors. Overexpression of a dominant-negative Fas-associated death domain mutant reduced COX…

Cancer Researchmedicine.medical_specialtyProgrammed cell deathCarcinoma HepatocellularApoptosisMitochondria LiverBiologyTransfectionReceptors Tumor Necrosis FactorInternal medicineCell Line TumormedicineHumansfas ReceptorDeath domainInhibitor of apoptosis domainSulfonamidesCyclooxygenase 2 InhibitorsIntrinsic apoptosisLiver NeoplasmsFas receptorReceptors TNF-Related Apoptosis-Inducing LigandEndocrinologyOncologyUVB-induced apoptosisApoptosisCelecoxibCyclooxygenase 2Cancer researchPyrazolesSignal transductionSignal TransductionCancer research
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Adherence to ruxolitinib, an oral JAK1/2 inhibitor, in patients with myelofibrosis: interim analysis from an Italian, prospective cohort study (ROMEI…

2021

ROMEI, a prospective, observational study in patients with myelofibrosis receiving the oral JAK1/2 inhibitor ruxolitinib in real-world practice, assesses treatment adherence based on the 8-item Morisky Medication Adherence Scale (MMAS-8). Here, we present MMAS-8 results at week 24. Overall, 101 of 188 evaluable patients completed the questionnaire at every visit (full completers). Mean (±standard deviation) total MMAS-8 scores remained stable from week 4 to week 24 in the overall population (7.54 ± 0.77 and 7.67 ± 0.70, respectively) and full completers (7.53 ± 0.79 and 7.67 ± 0.73, respectively). Rates of low (MMAS-8 ˂6) or medium (MMAS-8 ≥ 6 to ˂8) adherence were 25–40% and 26–36%, respec…

Cancer Researchmedicine.medical_specialtyRuxolitinib8-item Morisky Medication Adherence ScalePsychometricsTreatment adherenceruxolitiniboral therapiesMedication AdherenceCohort StudiesTreatment complianceInternal medicineSurveys and QuestionnairesNitrilesmedicineHumansIn patientProspective StudiesProspective cohort studyMyelofibrosistreatment compliance8-item Morisky Medication Adherence Scale oral therapies ruxolitinib treatment compliance Adherencebusiness.industryHematologyJanus Kinase 1Janus Kinase 2Interim analysismedicine.disease8-item Morisky Medication Adherence Scale; Adherence; oral therapies; ruxolitinib; treatment compliancePyrimidinesOncologyAdherencePrimary MyelofibrosisPyrazolesObservational studybusinessmedicine.drugLeukemialymphoma
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The endocannabinoid N-arachidonoyldopamine (NADA) exerts neuroprotective effects after excitotoxic neuronal damage via cannabinoid receptor 1 (CB(1)).

2012

Endocannabinoids exert numerous effects in the CNS under physiological and pathological conditions. The aim of the present study was to examine whether the endocannabinoid N-arachidonoyldopamine (NADA) may protect neurons in excitotoxically lesioned organotypic hippocampal slice cultures (OHSC). OHSC were excitotoxically lesioned by application of N-methyl-d-aspartate (NMDA, 50 μM) for 4 h and subsequently treated with different NADA concentrations (0.1 pM-50 μM) alone or in combination with cannabinoid receptor antagonists. NADA protected dentate gyrus granule cells and caused a slight reduction in the number of microglial cells. The number of degenerated neurons significantly decreased be…

Cannabinoid receptorDopamineTRPV1Arachidonic AcidsPharmacologyNeuroprotectionHippocampusCellular and Molecular NeuroscienceMicePiperidinesReceptor Cannabinoid CB1Neuronal damageAnimalsRats WistarCells CulturedPharmacologyNeuronsChemistryDentate gyrusExcitatory Postsynaptic PotentialsEndocannabinoid systemRatsNeuroprotective Agentsnervous systemNerve DegenerationCannabinoid receptor antagonistNMDA receptorPyrazolesNeuropharmacology
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Cannabinoid receptor 1 modulates the autophagic flux independent of mTOR- and BECLIN1-complex

2013

Cannabinoid Receptor 1 (CB1) has been initially described as the receptor for Delta-9-Tetrahydrocannabinol in the central nervous system (CNS), mediating retrograde synaptic signaling of the endocannabinoid system. Beside its expression in various CNS regions, CB1 is ubiquituous in peripheral tissues, where it mediates, among other activities, the cell's energy homeostasis. We sought to examine the role of CB1 in the context of the evolutionarily conserved autophagic machinery, a main constituent of the regulation of the intracellular energy status. Manipulating CB1 by siRNA knockdown in mammalian cells caused an elevated autophagic flux, while the expression of autophagy-related genes rema…

Cannabinoid receptorMorpholinesGreen Fluorescent ProteinsDown-RegulationmTORC1NaphthalenesBiochemistryMiceCellular and Molecular NeurosciencePiperidinesReceptor Cannabinoid CB1RimonabantAutophagymedicineAnimalsHumansEnzyme InhibitorsCannabinoid Receptor AntagonistsCells CulturedPI3K/AKT/mTOR pathwayAdenine NucleotidesChemistryTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCalcium Channel BlockersEmbryo MammalianEndocannabinoid systemBenzoxazinesCell biologyMice Inbred C57BLnervous systemAstrocytesPyrazolesBeclin-1lipids (amino acids peptides and proteins)MacrolidesSynaptic signalingRimonabantApoptosis Regulatory ProteinsFlux (metabolism)medicine.drugJournal of Neurochemistry
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