Search results for "T1"

showing 10 items of 587 documents

Comparison of the Effects of Glibenclamide on Metabolic Parameters, GLUT1 Expression, and Liver Injury in Rats With Severe and Mild Streptozotocin-In…

2012

Background and Objective. Glucose transport via GLUT1 protein could be one of additional mechanisms of the antidiabetic action of sulfonylureas. Here, the GLUT1 gene and the protein expression was studied in rats in the course of severe and mild streptozotocin-induced diabetes mellitus and under glibenclamide treatment. Material and Methods. Severe and mild diabetes mellitus was induced using different streptozotocin doses and standard or high fat chow. Rats were treated with glibenclamide (2 mg/kg daily, per os for 6 weeks). The therapeutic effect of glibenclamide was monitored by measuring several metabolic parameters. The GLUT1 mRNA and the protein expression in the kidneys, heart, and l…

Blood GlucoseMalemedicine.medical_specialtymedicine.medical_treatmentGene ExpressionDiabetes Mellitus ExperimentalGlibenclamideInternal medicineDiabetes mellitusGlyburideInsulin SecretionmedicineAnimalsHypoglycemic AgentsInsulinRats WistarLiver injuryGlucose Transporter Type 1Kidneybiologybusiness.industryInsulinGlucose transporternutritional and metabolic diseasesGeneral Medicinemedicine.diseaseStreptozotocinRatsSulfonylurea Compoundsmedicine.anatomical_structureEndocrinologyLiverProtein Biosynthesisglibenclamide; GLUT1; kidney; streptozotocin; expressionbiology.proteinGLUT1businessmedicine.drugMedicina; Volume 48; Issue 10; Pages: 78
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Correction of glycaemia and GLUT1 level by mildronate in rat streptozotocin diabetes mellitus model

2011

Anti-ischaemic drug mildronate suppresses fatty acid metabolism and increases glucose utilization in myocardium. It was proposed that it could produce a favourable effect on metabolic parameters and glucose transport in diabetic animals. Rats with streptozotocin diabetes mellitus were treated with mildronate (100 mg/kg daily, per os, 6 weeks). Therapeutic effect of mildronate was monitored by measuring animal weight, concentrations of blood glucose, insulin, blood triglycerides, free fatty acids, blood ketone bodies and cholesterol, glycated haemoglobin per cent (HbA1c%) and glucose tolerance. GLUT1 mRNA and protein expression in kidneys, heart, liver and muscles were studied by means of re…

Blood Glucosemedicine.medical_specialtyendocrine system diseasesmedicine.medical_treatmentClinical BiochemistryBiochemistryStreptozocinDiabetes Mellitus Experimentalchemistry.chemical_compoundInternal medicineDiabetes mellitusDiabetes MellitusmedicineAnimalsBody SizeHypoglycemic AgentsInsulinRNA MessengerRats WistarTriglyceridesGlycated HemoglobinGlucose Transporter Type 1Glucose tolerance testmedicine.diagnostic_testFatty acid metabolismbiologyCholesterolbusiness.industryInsulinFatty AcidsGlucose transporternutritional and metabolic diseasesCell BiologyGeneral MedicineGlucose Tolerance Testmedicine.diseaseRatsEndocrinologychemistrybiology.proteinKetone bodiesGLUT1businessMethylhydrazinesCell Biochemistry and Function
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Carbocysteine counteracts the effects of cigarette smoke on cell growth and on the SIRT1/FoxO3 axis in bronchial epithelial cells

2016

Abstract Background Cigarette smoke may accelerate cellular senescence by increasing oxidative stress. Altered proliferation and altered expression of anti-aging factors, including SIRT1 and FoxO3, characterise cellular senescence. The effects of carbocysteine on the SIRT1/FoxO3 axis and on downstream molecular mechanisms in human bronchial epithelial cells exposed to cigarette smoke are largely unknown. Aims Aim of this study was to explore whether carbocysteine modulated SIRT1/FoxO3 axis, and downstream molecular mechanisms associated to cellular senescence, in a bronchial epithelial cell line (16-HBE) exposed to cigarette smoke. Methods 16HBE cells were stimulated with/without cigarette …

Bronchial epithelial cell0301 basic medicineSenescenceAgingPathologymedicine.medical_specialtyApoptosisSettore MED/10 - Malattie Dell'Apparato RespiratorioBiologyBiochemistryCell LineFlow cytometry03 medical and health sciencesSIRT10302 clinical medicineEndocrinologyGeneticSirtuin 1Western blotSmokeTobaccoSurvivinGeneticsmedicineHumansClonogenic assayMolecular BiologyCellular SenescenceCell ProliferationRegulation of gene expressionmedicine.diagnostic_testCell growthCarbocysteineForkhead Box Protein O3Cigarette smokeEpithelial CellsCarbocysteineCell BiologyCell biologyOxidative Stress030104 developmental biology030220 oncology & carcinogenesisFoxO3Experimental Gerontology
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Efectos del desarrollo sostenible percibido por el consumidor. Una propuesta de modelo de hipermercados en Ecuador

2020

Resumen El objetivo de este trabajo fue analizar la incidencia del desarrollo sostenible sobre la cadena de efectos: valor percibido - capital de marca - lealtad. Para ello, se propone un modelo teórico de relaciones que se contrasta a partir de una muestra de 317 clientes de hiper mercados en Ecuador. Los resultados, aplicando una metodología exploratoria y confirmatoria, combinada con regresión por mínimos cuadrados parciales, mostraron que tanto las acciones de desarrollo sostenible como el valor percibido son pilares maestros sobre los que se puede apoyar la estrategia minorista. Ambas se muestran como variables clave por su naturaleza, en cuanto son multidimensio nales, y por su alcanc…

Business managementKnowledge management//vocabularies.unesco.org/thesaurus/concept7775 [http]Strategy and ManagementConsumidoresEmpresasManagement of Technology and InnovationBusinessInnovación tecnológica//id.loc.gov/authorities/subjects/sh92005743 [http]desarrollo sostenibleperceived valueMarketingQ16 Agricultural technologysustainable developmentBusiness enterprisesAgriculturavalor percebidoAgroindustria//id.loc.gov/authorities/subjects/sh85031491 [http]AgricultureInnovaciones tecnológicasCapitalpercepção do consumidorcapital de marcaO33 Technological changedesenvolvimento sustentável//id.loc.gov/authorities/subjects/sh94002204 [http]Economics and Econometricslealdade//vocabularies.unesco.org/thesaurus/concept10614 [http]lcsh:BusinessAgroindustry//vocabularies.unesco.org/thesaurus/concept598 [http]Business and International Managementlealtadpercepción del consumidor//vocabularies.unesco.org/thesaurus/concept4616 [http]//id.loc.gov/authorities/subjects/sh85133143 [http]O35 Social InnovationAdministración de empresas//vocabularies.unesco.org/thesaurus/concept1749 [http]consumer perceptionEmpresas familiaresbrand equityEstrategia de desarrolloloyaltyvalor percibido//vocabularies.unesco.org/thesaurus/concept1351 [http]//id.loc.gov/authorities/subjects/sh85018285 [http]Gestión del conocimientoMarcas de empresasConsumersTechnological innovationsHouse brandslcsh:HF5001-6182//id.loc.gov/authorities/subjects/sh85002415 [http]Finance//id.loc.gov/authorities/subjects/sh97007353 [http]Estudios Gerenciales
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IL-27 improves migrational and antiviral potential of CB dendritic cells.

2013

Abstract Interleukin (IL)-27 is known to be increased considerably in cord blood (CB) dendritic cells (DCs) after TLR ligation. Previously, we demonstrated that also basal IL-27 levels are higher in CB DCs. Here, we examined effects of IL-27 on monocyte derived dendritic cells (moDCs) to approach its particular role in the specialized immune system of the human neonate. Exogenous IL-27 promotes IL-27 transcription in CB and adult blood (AB) moDCs. IL-27 acts on CB moDCs primarily by significantly augmenting IL-27 protein, secondarily by increasing transcription of CXCL10 among other chemokines, chemokine receptor CCR1, interferon stimulated genes, transcription factor IRF8 and genes involve…

CCR1AdultChemokineTranscription GeneticImmunologyAntigen presentationReceptors CCR1MonocytesChemokine receptorInterferonCell MovementmedicineImmunology and AllergyCXCL10HumansCells CulturedbiologyTumor Necrosis Factor-alphaInterleukinsInterleukin-8Infant NewbornInterleukinCell DifferentiationGeneral MedicineDendritic CellsFetal BloodChemokine CXCL10STAT1 Transcription FactorGene Expression RegulationInterferon Regulatory Factorsbiology.proteinCancer researchIRF8medicine.drugSignal TransductionHuman immunology
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Activation pattern of signal transducers and activators of transcription (STAT) factors in inflammatory bowel diseases.

2005

Cytokine signaling pathways involving transcription factors of the signal transducers and activators of transcription (STAT) family play a key role in the pathogenesis of inflammatory bowel diseases (IBD). STAT proteins are latent cytoplasmic transcription factors that induce transcription upon phosphorylation, dimerization, and nuclear translocation. However, their activation pattern in IBD is poorly understood. The aim of our study was to characterize STAT-expression in IBD.Mononuclear cells were isolated from 36 colonic specimens of Crohn's disease, ulcerative colitis, or from control patients. Cells were stimulated overnight with antibodies against human CD2 and CD28 and mononuclear cel…

CD4-Positive T-LymphocytesSTAT3 Transcription FactorColonActivation patternstatTranscription (biology)MedicineHumansSTAT4Transcription factorHepatologybusiness.industryActivator (genetics)digestive oral and skin physiologyGastroenterologySTAT2 Transcription FactorSTAT3 Transcription FactorSTAT4 Transcription FactorInflammatory Bowel Diseasesdigestive system diseasesDNA-Binding ProteinsSTAT1 Transcription FactorCase-Control StudiesImmunologyCancer researchTrans-ActivatorsSignal transductionbusinessSTAT6 Transcription FactorThe American journal of gastroenterology
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IL-28A Is a Key Regulator of T-Cell–Mediated Liver Injury via the T-Box Transcription Factor T-Bet

2006

Background & Aims: T-cell–mediated fulminant hepatitis is a potentially life-threatening event for which the underlying pathogenic mechanisms are not fully understood. Here, we demonstrate a key regulatory role of IL-28A in T-cell–mediated hepatitis. Methods: We cloned the murine IL-28A gene by reverse-transcription polymerase chain reaction, assessed the effects of recombinant IL-28A, and generated IL-28A–transgenic mice. Results: IL-28A induced TH1 cytokine production by CD4+ T lymphocytes in a T-bet–dependent manner and was up-regulated in a murine model of T-cell–mediated hepatitis upon Con A administration. In vivo, CD4+ T cells from newly created IL-28A–transgenic animals revealed an …

CD4-Positive T-Lymphocytesmedicine.medical_treatmentT cellCodon InitiatorMice TransgenicBiologyAntibodiesProinflammatory cytokineInterferon-gammaMiceT-Lymphocyte SubsetsInterferonConcanavalin AmedicineAnimalsCloning MolecularReceptors CytokineFulminant hepatitisLiver injuryHepatitisHepatologyInterleukinsGastroenterologyLiver Failure AcuteOligonucleotides Antisensemedicine.diseaseMolecular biologyMice Inbred C57BLSTAT1 Transcription FactorReal-time polymerase chain reactionCytokinemedicine.anatomical_structureInterleukin-2Interleukin-4MitogensT-Box Domain ProteinsCell DivisionSignal Transductionmedicine.drugGastroenterology
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Novel insulin receptor substrate 1 and 2 variants in breast and colorectal cancer

2013

The insulin/insulin-like growth factor pathway is involved in breast and colorectal cancer (CRC) development. In the present study, we analyzed the coding region and short intron-exon borders of the insulin receptor substrate 1 and 2 (IRS‑1 and IRS‑2) genes in 12 cell lines derived from breast cancer (BC), 14 cell lines derived from CRC and 33 primary CRCs. The nucleotide variants identified in BC were 3 in IRS‑1, 1 of which (p.Arg267Cys) was novel and with a pathogenic potential as predicted by in silico analysis and 6 in IRS‑2. Twenty‑one variants in IRS‑1 and 18 in IRS‑2 were identified in the CRC samples. These included 11 novel IRS‑1 variants detected exclusively in CRCs, which include…

Cancer ResearchInsulin Receptor Substrate ProteinsSettore MED/06 - Oncologia MedicaIn silicoMutation MissenseBreast NeoplasmsColorectal NeoplasmBiologymedicine.disease_causeFrameshift mutationBreast cancerBreast cancerMCF-7 CellCell Line TumormedicineHumansMissense mutationFrameshift MutationInsulin Receptor Substrate ProteinSequence DeletionGeneticsMutationCaco-2 CellPolymorphism GeneticCancerGenetic VariationInsulin receptor substrate 1ArticlesGeneral MedicineInsulin receptor substrate 2HCT116 Cellsmedicine.diseaseColorectal cancerIRS1Mutagenesis InsertionalCell Transformation NeoplasticHT29 CellOncologyHCT116 CellBreast cancer; Colorectal cancer; Insulin receptor substrate 1; Insulin receptor substrate 2; Breast Neoplasms; Caco-2 Cells; Cell Line Tumor; Cell Transformation Neoplastic; Colorectal Neoplasms; Female; Frameshift Mutation; Genetic Variation; HCT116 Cells; HT29 Cells; Humans; Insulin Receptor Substrate Proteins; MCF-7 Cells; Mutagenesis Insertional; Mutation Missense; Polymorphism Genetic; Sequence Deletion; Signal Transduction; Cancer Research; OncologyInsulin Receptor Substrate ProteinsMCF-7 CellsFemaleCaco-2 CellsColorectal NeoplasmsHT29 CellsBreast NeoplasmHumanSignal Transduction
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Multivalent DR5 peptides activate the TRAIL death pathway and exert tumoricidal activity.

2010

Abstract Ongoing clinical trials are exploring anticancer approaches based on signaling by TRAIL, a ligand for the cell death receptors DR4 and DR5. In this study, we report on the selective apoptotic effects of multivalent DR5 binding peptides (TRAILmim/DR5) on cancer cells in vitro and in vivo. Surface plasmon resonance revealed up to several thousand-fold increased affinities of TRAILmim/DR5-receptor complexes on generation of divalent and trivalent molecules, the latter of which was achieved with a conformationally restricted adamantane core. Notably, only multivalent molecules triggered a substantial DR5-dependent apoptotic response in vitro. In tumor models derived from human embryoni…

Cancer ResearchMembrane transport and intracellular motility [NCMLS 5]Apoptosis[CHIM.THER]Chemical Sciences/Medicinal Chemistry[ SDV.CAN ] Life Sciences [q-bio]/CancerTNF-Related Apoptosis-Inducing LigandMice0302 clinical medicineStilbenesReceptorCells Cultured0303 health sciencesDrug Synergism[ CHIM.THER ] Chemical Sciences/Medicinal ChemistryLigand (biochemistry)Tumor Burden3. Good healthMitochondrial medicine [IGMD 8]Oncology030220 oncology & carcinogenesisColonic NeoplasmsFemaleOligopeptidesSignal Transductionmedicine.medical_specialtyProgrammed cell deathBlotting WesternMolecular Sequence DataMice Nude[SDV.CAN]Life Sciences [q-bio]/CancerCell Line03 medical and health sciencesIn vivoInternal medicinemedicineAnimalsHumansAmino Acid Sequence030304 developmental biologybusiness.industrySurface Plasmon ResonanceHCT116 CellsAntineoplastic Agents PhytogenicXenograft Model Antitumor AssaysIn vitroReceptors TNF-Related Apoptosis-Inducing LigandEndocrinologyResveratrolCell cultureApoptosisCancer cellCancer researchbusiness
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MLL-Rearranged Leukemia Is Dependent on Aberrant H3K79 Methylation by DOT1L

2011

SummaryThe histone 3 lysine 79 (H3K79) methyltransferase Dot1l has been implicated in the development of leukemias bearing translocations of the Mixed Lineage Leukemia (MLL) gene. We identified the MLL-fusion targets in an MLL-AF9 leukemia model, and conducted epigenetic profiling for H3K79me2, H3K4me3, H3K27me3, and H3K36me3 in hematopoietic progenitor and leukemia stem cells (LSCs). We found abnormal profiles only for H3K79me2 on MLL-AF9 fusion target loci in LSCs. Inactivation of Dot1l led to downregulation of direct MLL-AF9 targets and an MLL translocation-associated gene expression signature, whereas global gene expression remained largely unaffected. Suppression of MLL translocation-a…

Cancer ResearchOncogene Proteins FusionCellular differentiationApoptosisBiologyMethylationArticleHistonesMice03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesmedicineAnimalsHumansEpigeneticsMyeloid Ecotropic Viral Integration Site 1 ProteinneoplasmsMyeloid Progenitor Cells030304 developmental biologyGene RearrangementHomeodomain Proteins0303 health sciencesLysineMyelodysplastic syndromesCell CycleCell DifferentiationCell BiologyHistone-Lysine N-MethyltransferaseMethyltransferasesMethylationDOT1Lmedicine.diseaseMolecular biologyHematopoiesisNeoplasm Proteins3. Good healthLeukemiaCell Transformation NeoplasticOncologyGenetic Loci030220 oncology & carcinogenesisHistone methyltransferaseCancer researchH3K4me3Protein Processing Post-TranslationalMyeloid-Lymphoid Leukemia ProteinCancer Cell
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