Search results for "Pyrrole"

showing 10 items of 311 documents

A microarray analysis highlights the role of tetrapyrrole pathways in grapevine responses to “stolbur” phytoplasma, phloem virus infections and recov…

2016

Abstract After providing a picture of the global transcriptomic changes of grapevine responses to “stolbur” phytoplasma, the recovery status and molecular responses to the phytoplasma and virus co-presence were analyzed. NimbleGen ® Vitis vinifera genome arrays were used. Lower transcript abundance of the genes involved in photosynthesis, trehalose, phospholipids was observed in response to the presence of “stolbur” phytoplasma. The expression of the genes involved in tetrapyrrole increased. The recovered plants showed that the transcripts involved in ATP synthesis and amino acid metabolism, secondary metabolism and biotic stress-related pathways increased. Recovery was associated with tetr…

0106 biological sciences0301 basic medicineGeneticsMicroarray analysis techniquesGenes Phytoplasma Recovery “Stolbur” Viruses Vitisfood and beveragesPlant ScienceBiologybiology.organism_classification01 natural sciencesTetrapyrroleGenomeTranscriptome03 medical and health scienceschemistry.chemical_compound030104 developmental biologyBiochemistrychemistryPhytoplasmaSettore AGR/07 - Genetica AgrariaGeneticsPhloemSecondary metabolismGene010606 plant biology & botanyPhysiological and Molecular Plant Pathology
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Phase I Study of the Indoleamine 2,3-Dioxygenase 1 (IDO1) Inhibitor Navoximod (GDC-0919) Administered with PD-L1 Inhibitor (Atezolizumab) in Advanced…

2019

Abstract Purpose: IDO1 induces immune suppression in T cells through l-tryptophan (Trp) depletion and kynurenine (Kyn) accumulation in the local tumor microenvironment, suppressing effector T cells and hyperactivating regulatory T cells (Treg). Navoximod is an investigational small-molecule inhibitor of IDO1. This phase I study evaluated safety, tolerability, pharmacokinetics, and pharmacodynamics of navoximod in combination with atezolizumab, a PD-L1 inhibitor, in patients with advanced cancer. Patients and Methods: The study consisted of a 3+3 dose-escalation stage (n = 66) and a tumor-specific expansion stage (n = 92). Navoximod was given orally every 12 hours continuously for 21 consecu…

0301 basic medicineAdultCancer ResearchIndoles[SDV]Life Sciences [q-bio][SDV.BC]Life Sciences [q-bio]/Cellular BiologyPharmacologyAntibodies Monoclonal HumanizedArticleB7-H1 Antigen03 medical and health sciences0302 clinical medicinePharmacokineticsAtezolizumabRenal cell carcinomaNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsmedicineBiomarkers TumorHumansIndoleamine-Pyrrole 23-DioxygenaseNeoplasm MetastasisAgedNeoplasm StagingAged 80 and overBladder cancerbusiness.industryMelanomaImidazolesMiddle Agedmedicine.diseaseMagnetic Resonance Imaging3. Good health030104 developmental biologyTreatment OutcomeOncologyTolerability030220 oncology & carcinogenesisPharmacodynamicsPD-L1 inhibitorbusinessTomography X-Ray Computed
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Immunosuppressive profiles in liquid biopsy at diagnosis predict response to neoadjuvant chemotherapy in triple-negative breast cancer.

2020

Background: Triple-negative breast cancer (TNBC) is characterised by high pathological complete response to neoadjuvant chemotherapy (NAC). However, refractory and poor NAC responders still face very poor outcome, emphasising the urgent need for tools that facilitate identification of these patients, so that surgery or alternatives to NAC are considered early in the treatment protocol. Materials and methods: We combined metabolomics, exosome circulating miRNAs and flow cytometry experimental approaches in TNBC patients at diagnosis with immunohistochemistry in needle biopsy tumours to generate NAC-response predictive models. We also co-cultured and studied crosstalk between isolated patient…

0301 basic medicineAdultCancer Researchmedicine.medical_treatmentTriple Negative Breast NeoplasmsExosomesExosome03 medical and health sciences0302 clinical medicineImmune systemBreast cancerTriple-negative breast cancermicroRNABiomarkers TumorImmune ToleranceMedicineHumansIndoleamine-Pyrrole 23-DioxygenaseMetabolomicsProspective StudiesLiquid biopsyTriple-negative breast cancerCells CulturedAgedChemotherapybusiness.industryLiquid BiopsyTryptophanImmunosuppressionMiddle Agedmedicine.diseaseImmunohistochemistryCoculture TechniquesNeoadjuvant TherapyMicroRNAs030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchFemaleNAC responsebusinessImmunosuppressionEuropean journal of cancer (Oxford, England : 1990)
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Rescuing Over-activated Microglia Restores Cognitive Performance in Juvenile Animals of the Dp(16) Mouse Model of Down Syndrome.

2020

Microglia are brain-resident immune cells and regulate mechanisms essential for cognitive functions. Down syndrome (DS), the most frequent cause of genetic intellectual disability, is caused by a supernumerary chromosome 21, containing also genes related to the immune system. In the hippocampus of the Dp(16) mouse model of DS and DS individuals, we found activated microglia, as assessed by their morphology; activation markers; and, for DS mice, electrophysiological profile. Accordingly, we found increased pro-inflammatory cytokine levels and altered interferon signaling in Dp(16) hippocampi. DS mice also showed decreased spine density and activity of hippocampal neurons and hippocampus-depe…

0301 basic medicineAdultMaleDown syndromeDendritic spinemedicine.medical_treatmentAminopyridinesMice TransgenicHippocampal formationHippocampus03 medical and health sciencesMice0302 clinical medicineImmune systemCognitionMedicineHippocampus (mythology)AnimalsHumansPyrrolesNeuroinflammationMicrogliabusiness.industryGeneral NeuroscienceAnti-Inflammatory Agents Non-SteroidalAge Factorsmedicine.disease3. Good healthMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structureCytokinenervous systemFemaleMicrogliaDown SyndromebusinessNeuroscience030217 neurology & neurosurgeryNeuron
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Kinase Inhibitors in Multitargeted Cancer Therapy

2017

The old-fashioned anticancer approaches, aiming in arresting cancer cell proliferation interfering with non-specific targets (e.g. DNA), have been replaced, in the last decades, by more specific target oriented ones. Nonetheless, single-target approaches have not always led to optimal outcomes because, for its complexity, cancer needs to be tackled at various levels by modulation of several targets. Although at present, combinations of individual single-target drugs represent the most clinically practiced therapeutic approaches, the modulation of multiple proteins by a single drug, in accordance with the polypharmacological strategy, has become more and more appealing. In the perspective of…

0301 basic medicineDrugNiacinamideIndolesPyridinesmedia_common.quotation_subjectPharmacologyBioinformaticsBiochemistryReceptor tyrosine kinase03 medical and health sciencesCrizotinibPiperidinesMultitargeted drugs anticancer agents polypharmacology tyrosine kinase receptors oncogene addiction tumor microenvironment FDA-approved drugsNeoplasmsDrug DiscoverymedicineSunitinibHumansAnilidesPyrrolesProtein Kinase Inhibitorsmedia_commonPharmacologyTumor microenvironmentbiologybusiness.industryPhenylurea CompoundsOrganic ChemistryImidazolesCancerReceptor Protein-Tyrosine KinasesSorafenibmedicine.diseaseOncogene AddictionSettore CHIM/08 - Chimica FarmaceuticaClinical trialPyridazines030104 developmental biologyMechanism of actionbiology.proteinImatinib MesylateQuinazolinesMolecular MedicinePyrazolesmedicine.symptombusinessTyrosine kinase
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TGF-β inhibitor Smad7 regulates dendritic cell-induced autoimmunity

2017

TGF-β is an anti-inflammatory cytokine whose signaling is negatively controlled by Smad7. Previously, we established a role for Smad7 in the generation of autoreactive T cells; however, the function of Smad7 in dendritic cells (DCs) remains elusive. Here, we demonstrate that DC-specific Smad7 deficiency resulted in elevated expression of the transcription factors Batf3 and IRF8, leading to increased frequencies of CD8(+)CD103(+) DCs in the spleen. Furthermore, Smad7-deficient DCs expressed higher levels of indoleamine 2,3-dioxygenase (IDO), an enzyme associated with tolerance induction. Mice devoid of Smad7 specifically in DCs are resistant to the development of experimental autoimmune ence…

0301 basic medicineEncephalomyelitis Autoimmune Experimentalmedicine.medical_treatmentCellular differentiationAutoimmunitychemical and pharmacologic phenomenaCD8-Positive T-LymphocytesBiologyT-Lymphocytes RegulatorySmad7 ProteinImmune toleranceMice03 medical and health sciences0302 clinical medicineTransforming Growth Factor betaImmune TolerancemedicineAnimalsIndoleamine-Pyrrole 23-DioxygenaseMultidisciplinaryintegumentary systemExperimental autoimmune encephalomyelitisCell Differentiationhemic and immune systemsDendritic CellsDendritic cellTransforming growth factor betamedicine.diseaseCell biologyMice Inbred C57BLTolerance inductionBasic-Leucine Zipper Transcription Factors030104 developmental biologyCytokinePNAS PlusInterferon Regulatory FactorsImmunologybiology.proteinCytokinesSpleenCD8Signal Transduction030215 immunology
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Sunitinib in patients with pre-treated pancreatic neuroendocrine tumors: A real-world study.

2018

Abstract Introduction Besides data reported in a Phase-III trial, data on sunitinib in pancreatic Neuroendocrine Tumors (panNETs) are scanty. Aim To evaluate sunitinib efficacy and tolerability in panNETs patients treated in a real-world setting. Patients and methods Retrospective analysis of progressive panNETs treated with sunitinib. Efficacy was assessed by evaluating progression-free survival, overall survival, and disease control (DC) rate (stable disease (SD) + partial response + complete response). Data are reported as median (25th–75th IQR). Results Eighty patients were included. Overall, 71.1% had NET G2, 26.3% had NET G1, and 2.6% had NET G3 neoplasms. A total of 53 patients (66.3…

0301 basic medicineIndolesEndocrinology Diabetes and MetabolismNeuroendocrine tumorsPyrroleGastroenterologyTarget therapyEfficacyAntineoplastic Agent0302 clinical medicineEndocrinologyRetrospective StudieSunitinibPancreadiabetes and metabolismSunitinibGastroenterologyPancreatic NeoplasmMiddle AgedDiabetes and MetabolismNeuroendocrine TumorsTreatment OutcomeTolerabilityNeuroendocrine tumors; Pancreas; Progressive disease; Sunitinib; Target therapy; Endocrinology Diabetes and Metabolism; Hepatology; EndocrinologyItaly030220 oncology & carcinogenesisNeuroendocrine tumorsmedicine.drugHumanAdultmedicine.medical_specialtyAntineoplastic AgentsNeutropenia03 medical and health sciencesNeuroendocrine tumorInternal medicinemedicineHumansPyrrolesProgression-free survivalPancreasCancer stagingAgedRetrospective StudiesHepatologybusiness.industryProgressive diseasemedicine.diseasePancreatic Neoplasms030104 developmental biologyNeuroendocrine tumors; pancreas; progressive disease; Sunitinib; target therapy; endocrinology; diabetes and metabolism; hepatology; endocrinologyIndolebusinessProgressive diseasePancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
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Regulation of kynurenine biosynthesis during influenza virus infection.

2017

Influenza A viruses (IAVs) remain serious threats to public health because of the shortage of effective means of control. Developing more effective virus control modalities requires better understanding of virus–host interactions. It has previously been shown that IAV induces the production of kynurenine, which suppresses T-cell responses, enhances pain hypersensitivity and disturbs behaviour in infected animals. However, the regulation of kynurenine biosynthesis during IAV infection remains elusive. Here we showed that IAV infection induced expression of interferons (IFNs), which upregulated production of indoleamine-2,3-dioxygenase (IDO1), which catalysed the kynurenine biosynthesis. Furt…

0301 basic medicineIndoleshost-pathogen interactionViral Nonstructural Proteinsmedicine.disease_causeVirus ReplicationBiochemistryinfluenza viruschemistry.chemical_compoundMiceInfluenza A Virus H1N1 SubtypeInterferonOximesinnate immunityLungOxazolesKynurenineRegulation of gene expressionMice Inbred BALB CSulfonamidesTryptophaninterferon3. Good healthHost-Pathogen InteractionsFemaleMetabolic Networks and Pathwaysmedicine.drugHost–pathogen interaction030106 microbiologyPrimary Cell CultureBiologyta3111Antiviral AgentsVirus03 medical and health sciences3-dioxygenase (IDO1)Orthomyxoviridae InfectionsmedicineAnimalsHumansImmunologic FactorsIndoleamine-Pyrrole 23-DioxygenasePyrrolesMolecular BiologyInnate immune systemta1184Macrophagesta1183ta1182Cell BiologyVirologyindoleamine-pyrrole 2Thiazoles030104 developmental biologyHerpes simplex virusViral replicationchemistryGene Expression RegulationInterferonsTranscriptomeKynurenineThe FEBS journal
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Pyrrolo[3',2':6,7]cyclohepta[1,2-b]pyridines with potent photo-antiproliferative activity.

2017

Abstract Pyrrolo[3′,2′:6,7]cyclohepta[1,2-b]pyridines were synthesized as a new class of tricyclic system in which the pyridine ring is annelated to a cycloheptapyrrole scaffold, with the aim of obtaining new photosensitizing agents with improved antiproliferative activity and lower undesired toxic effects. A versatile synthetic pathway was approached, which allowed the isolation of derivatives of the title ring system with a good substitution pattern on the pyrrole moiety. Photobiological studies revealed that the majority of the new compounds showed a potent cytotoxic effect upon photoactivation with light of the proper wavelength, especially when decorated with a 2-ethoxycabonyl group an…

0301 basic medicineLightPyridines01 natural sciencesAntioxidantschemistry.chemical_compound7]cyclohepta[1NeoplasmsDrug DiscoveryTumor Cells CulturedMoietyPyrrolechemistry.chemical_classificationPhotosensitizing AgentsGeneral MedicinePhotosensitizing AgentPyrrolo[3′2′:67]cyclohepta[12-b]pyridine-9(1H)-oneReactive oxygen speciemedicine.symptomPhototoxicity2-b]pyridine-9(1H)-onesStereochemistryBlotting WesternPhoto-antiproliferative activityAntineoplastic AgentsRing (chemistry)Phototoxicity03 medical and health sciencesStructure-Activity RelationshipPyridinemedicineHumansPyrrolo[3′PyrrolesCell ProliferationPharmacologyPhotosensitizing agent010405 organic chemistry2′:6Drug Discovery3003 Pharmaceutical ScienceOrganic ChemistryPhoto-antiproliferative activity; Photosensitizing agents; Phototoxicity; Pyrrolo[3′2′:67]cyclohepta[12-b]pyridine-9(1H)-ones; Reactive oxygen species; Pharmacology; Drug Discovery3003 Pharmaceutical Science; Organic ChemistryCombinatorial chemistry0104 chemical sciences030104 developmental biologychemistryMechanism of actionPhoto-antiproliferative activity; Photosensitizing agents; Phototoxicity; Pyrrolo[3′; 2′:6; 7]cyclohepta[1; 2-b]pyridine-9(1H)-ones; Reactive oxygen species; Pharmacology; Drug Discovery3003 Pharmaceutical Science; Organic ChemistryDrug Screening Assays AntitumorReactive Oxygen SpeciesTricyclicEuropean journal of medicinal chemistry
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AMPK phosphorylation modulates pain by activation of NLRP3 inflammasome

2016

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0301 basic medicineMESH : Carrier Proteins/geneticsMaleMESH: Fibromyalgia/geneticsFibromyalgiaIndolesPhysiologyInflammasomesClinical BiochemistryInterleukin-1betaInjuryAMP-Activated Protein KinasesNeuropathic painBiochemistryPyrin domainMice0302 clinical medicineAMP-activated protein kinaseRestrictionSunitinibDiseasePhosphorylationGeneral Environmental Sciencebiologyintegumentary systemChemistryInterleukin-18InflammasomePain Perception[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismMiddle AgedMetforminCell biologyOriginal Research CommunicationsMESH : Fibromyalgia/geneticsHyperalgesiaPhosphorylationFemalemedicine.symptommedicine.drugMESH : Inflammasomes/metabolismAdultmedicine.medical_specialtyPain03 medical and health sciencesMESH: Carrier Proteins/geneticsInternal medicineNLR Family Pyrin Domain-Containing 3 ProteinmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPyrrolesProtein kinase AMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Inflammasomes/metabolismFibromialgia patientsAMPK ; fibromyalgia ; NLRP3 InflammasomeDangerAMPKCell BiologyAdenosineMESH: AMP-Activated Protein Kinases/genetics030104 developmental biologyEndocrinologyMetabolismProtein-Kinase AMPKbiology.proteinGeneral Earth and Planetary SciencesMESH : AMP-Activated Protein Kinases/geneticsAnalgesiaCarrier Proteins030217 neurology & neurosurgery
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