Search results for " INDUCTION"

showing 10 items of 526 documents

Valproate and Short-Chain Fatty Acids Activate Transcription of the Human Vitamin D Receptor Gene through a Proximal GC-Rich DNA Region Containing Tw…

2022

The vitamin D receptor (VDR) mediates 1,25-dihydroxyvitamin D3 pleiotropic biological actions through transcription regulation of target genes. The expression levels of this ligand-activated nuclear receptor are regulated by multiple mechanisms both at transcriptional and post-transcriptional levels. Vitamin D3 is the natural VDR activator, but other molecules and signaling pathways have also been reported to regulate VDR expression and activity. In this study, we identify valproic acid (VPA) and natural short-chain fatty acids (SCFAs) as novel transcriptional activators of the human VDR (hVDR) gene. We further report a comprehensive characterization of VPA/SCFA-responsive elements in the 5…

BioquímicaBiologiaVDR induction; human VDR promoter; valproic acid; SCFA; Sp1.Binding SitesNutrition and DieteticsSp1 Transcription FactorValproic AcidDNAHumansReceptors Calcitriollipids (amino acids peptides and proteins)ChildPromoter Regions GeneticFood Science
researchProduct

Hormonal and metabolic adaptation to fasting: effects on the hypothalamic-pituitary-ovarianaxis and reproductive performance of rabbit does

2006

To assess the impact of acute caloric shortage on reproduction, rabbit does were either fed ad libitum (control, AL), or fasted for 24 (STF) or 48 h (LTF) before induction of ovulation with GnRH injection. Blood samples were collected during the last 3 h of fasting, and the following 4 h after GnRH injection, when feed was provided again, to measure plasma concentrations of LH, estradiol-17β, leptin, insulin, T3, corticosterone, glucose, and NEFA. Before re-feeding, plasma leptin, insulin, and T3 concentrations were lower (P ≤ 0.01) in both fasted groups than in controls, but then gradually increased following realimentation to match those of controls. During fasting, corticoster…

Blood GlucoseLHHypothalamo-Hypophyseal Systemmedicine.medical_specialtymedia_common.quotation_subjectmedicine.medical_treatmentPituitary-Adrenal SystemHypothalamic–pituitary–gonadal axisGonadotropin-releasing hormoneBiologyGonadotropin-Releasing HormoneRandom Allocationchemistry.chemical_compoundLEPTINEndocrinologyNEFAOvulation InductionFood AnimalsPregnancyRABBITCorticosteroneInternal medicineFASTINGmedicineAnimalsOvulationmedia_commonEstradiolReproductionLeptinInsulinOvaryEstradiol-17Luteinizing HormoneT3INSULINHormonesEndocrinologychemistryTriiodothyronineFemaleAnimal Science and ZoologyRabbitsCorticosteroneLuteinizing hormone
researchProduct

Heme oxygenase-1 induction and regulation in unstimulated mouse peritoneal macrophages

2003

Heme oxygenase-1 (HO-1) is a stress protein induced by a variety of stimuli in inflammatory cells. This study was set up to investigate the induction of this protein in unstimulated macrophages. Resident mouse peritoneal macrophages purified by adhesion and cultured in basal conditions strongly induced HO-1 in a time-dependent manner, with a peak at 20 hr. At the same time, low levels of nitrite accumulated in the culture medium and expression of nitric oxide synthase-2 (NOS-2) and NOS-3 protein was detected. Inhibition of NO production and/or NOS expression by incubating macrophages with different drugs inhibiting NOS activity or modulating the redox state of the cell, such as N-acetylcyst…

Blotting WesternInflammationNitric Oxidemedicine.disease_causeBiochemistryNitric oxideMicechemistry.chemical_compoundmedicineAnimalsMacrophageHemeCells CulturedPharmacologybiologyChemistryMembrane ProteinsEndogenous mediatorImmunohistochemistryCell biologyNitric oxide synthaseHeme oxygenaseBiochemistryEnzyme InductionHeme Oxygenase (Decyclizing)Macrophages Peritonealbiology.proteinNitric Oxide Synthasemedicine.symptomOxidation-ReductionHeme Oxygenase-1Oxidative stressBiochemical Pharmacology
researchProduct

MitoKATP-channel opener protects against neuronal death in rat venous ischemia.

2005

OBJECTIVE: Mitochondrial adenosine triphosphate-dependent potassium (mitoK ATP ) channels are present in the brain, and several reports have shown their neuroprotective, preconditioning effect against an ischemic insult. The role of mitoK ATP channels in the penumbra area has not been studied thoroughly. In a model of venous ischemia, widespread penumbra-like low flow areas are created, which are susceptible to cortical spreading depression. Thus, we studied effects of mitoK ATP channels on infarct size in this model. METHODS: Male Wistar rats were subjected to two-vein occlusion by photochemical thrombosis of two adjacent cortical veins combined with KCI-induced cortical spreading depressi…

Brain InfarctionMalemedicine.medical_specialtyPotassium ChannelsPhotochemistryIschemiaBrain EdemaPotassium ChlorideIschemiaInternal medicinemedicineDiazoxideLaser-Doppler FlowmetryAnimalsChannel blockerDrug InteractionsRats WistarNeuronsAnalysis of VarianceCell Deathbusiness.industryPenumbraCortical Spreading DepressionDiazoxidemedicine.diseaseCerebral VeinsPotassium channelRatsTolerance inductionDisease Models AnimalNeuroprotective AgentsCerebral blood flowRegional Blood FlowAnesthesiaCortical spreading depressionCardiologySurgeryNeurology (clinical)businessHydroxy AcidsAnti-Arrhythmia AgentsDecanoic Acidsmedicine.drugNeurosurgery
researchProduct

Medical management of Crohn's disease

2011

The medical approach to Crohn's disease has been modified in recent years thanks to the introduction of new therapies, like biologics. Also, well-designed studies and systematic reviews have allowed better evaluation of the role of old drugs like steroids and immunosuppressors. This review aims to evaluate the recent evidence on the medical approach to Crohn's disease in the different settings of the disease.Randomized controlled trials and meta-analyses were included in the review. The research on all the studies discussed was based on the Cochrane Library, Medline and Embase, using the following medical subject headings: Crohn's disease, clinical trial, therapy, 5-aminosalicylic acid, ste…

Budesonidemedicine.medical_specialtyPathologyAnti-Inflammatory AgentsMEDLINEDiseaseCochrane LibraryManagement of Crohn's diseaselaw.inventionCrohn DiseaseRandomized controlled trialAdrenal Cortex HormoneslawmedicineHumansPharmacology (medical)BudesonideIntensive care medicineBone Marrow TransplantationPharmacologyBiological ProductsTumor Necrosis Factor-alphabusiness.industryRemission InductionGeneral Medicinemedicine.diseaseAnti-Bacterial AgentsIntestinesClinical trialAminosalicylic AcidsMethotrexateTreatment OutcomeSystematic reviewPurinesbusinessImmunosuppressive Agentsmedicine.drugExpert Opinion on Pharmacotherapy
researchProduct

A miRNA181a/NFAT5 axis links impaired T cell tolerance induction with autoimmune type 1 diabetes.

2018

Molecular checkpoints that trigger the onset of islet autoimmunity or progression to human type 1 diabetes (T1D) are incompletely understood. Using T cells from children at an early stage of islet autoimmunity without clinical T1D, we find that a microRNA181a (miRNA181a)-mediated increase in signal strength of stimulation and costimulation links nuclear factor of activated T cells 5 (NFAT5) with impaired tolerance induction and autoimmune activation. We show that enhancing miRNA181a activity increases NFAT5 expression while inhibiting FOXP3+ regulatory T cell (Treg) induction in vitro. Accordingly, Treg induction is improved using T cells from NFAT5 knockout (NFAT5ko) animals, whereas alter…

CD4-Positive T-Lymphocytes0301 basic medicineRegulatory T cellBiologymedicine.disease_causeAutoimmunityMice03 medical and health sciencesNFAT5microRNAImmunogeneticsmedicineAnimalsHumansPI3K/AKT/mTOR pathwaygeographygeography.geographical_feature_categoryNFATC Transcription FactorsAntagomirsFOXP3Forkhead Transcription FactorsGeneral MedicineIsletMice Mutant StrainsMicroRNAsTolerance inductionDiabetes Mellitus Type 1030104 developmental biologymedicine.anatomical_structureCancer researchFemale
researchProduct

Low zone tolerance induced by systemic application of allergens inhibits TC1-mediated skin inflammation

2005

Background The induction of tolerance may be a promising target of strategies aimed at preventing harmful allergic diseases. Low zone tolerance (LZT), induced by epicutaneous application of low doses of contact allergens, inhibits the development of T C 1-mediated contact hypersensitivity (CHS). Objective We evaluated the effect of systemic (oral, intravenous) administration of low amounts of haptens on specific immune reactions and tolerance induction. Methods By using the mouse model of LZT, we analyzed immune reactions in vivo (skin inflammation) and T-cell responses in vitro after oral, intravenous, or epicutaneous application of low amounts of the contact allergen 2,4,6-trinitro-1-chlo…

CD4-Positive T-LymphocytesAdoptive cell transferAllergymedicine.medical_treatmentImmunologyDose-Response Relationship ImmunologicAdministration OralInflammationPicryl ChlorideAdministration CutaneousDermatitis ContactT-Lymphocytes RegulatoryImmune toleranceMiceImmune systemImmune TolerancemedicineAnimalsImmunology and AllergyMice KnockoutChemistryCell DifferentiationImmunotherapyAllergensmedicine.diseaseMice Inbred C57BLTolerance inductionTrinitrobenzenesulfonic AcidOrgan SpecificityInjections IntravenousImmunologymedicine.symptomCD8T-Lymphocytes CytotoxicJournal of Allergy and Clinical Immunology
researchProduct

PD-1 signalling in CD4+T cells restrains their clonal expansion to an immunogenic stimulus, but is not critically required for peptide-induced tolera…

2010

Summary The ultimate outcome of T-cell recognition of peptide–major histocompatibility complex (MHC) complexes is determined by the molecular context in which antigen presentation is provided. The paradigm is that, after exposure to peptides presented by steady-state dendritic cells (DCs), inhibitory signals dominate, leading to the deletion and/or functional inactivation of antigen-reactive T cells. This has been utilized in a variety of models providing peptide antigen in soluble form in the absence of adjuvant. A co-inhibitory molecule of considerable current interest is PD-1. Here we show that there is the opportunity for the PD-1/PD-L1 interaction to function in inhibiting the T-cell r…

CD4-Positive T-LymphocytesOvalbuminTransgeneProgrammed Cell Death 1 ReceptorImmunologyAntigen presentationMice TransgenicCell SeparationCD8-Positive T-LymphocytesBiologyLymphocyte ActivationMajor histocompatibility complexMiceImmune systemBlocking antibodyImmune ToleranceAnimalsImmunology and AllergyT-cell receptorOriginal ArticlesFlow CytometryAntigens DifferentiationPeptide FragmentsCell biologyMice Inbred C57BLTolerance inductionPhenotypeImmunologybiology.proteinCD8Signal TransductionImmunology
researchProduct

Induction of the alkyltransferase (MGMT) gene by DNA damaging agents and the glucocorticoid dexamethasone and comparison with the response of base ex…

1996

Repair of alkylated bases in DNA is performed by O6-methylguanine-DNA methyltransferase (MGMT) and a set of enzymes of the base excision repair pathway involving N-methylpurine-DNA glycosylase (MPG), apurinic endonuclease (APE), DNA polymerase beta (Pol beta) and DNA ligase. The level of expression of these enzymes may exert a profound effect on resistance of cells towards alkylating drugs. We have comparatively analyzed the expression of MGMT and the different base excision repair genes in rat hepatoma cells (line H4IIE) after exposure to alkylating agents, X-rays and the glucocorticoid hormone dexamethasone. Furthermore, the effect of these agents on the activity of the cloned human MGMT …

Cancer ResearchAlkylationDNA RepairDNA damageDNA polymerase betaBiologyDexamethasoneGene Expression Regulation Enzymologicchemistry.chemical_compoundO(6)-Methylguanine-DNA MethyltransferaseLiver Neoplasms ExperimentalAnimalsRNA MessengerPromoter Regions GeneticneoplasmsAntineoplastic Agents AlkylatingGlucocorticoidschemistry.chemical_classificationDNA ligaseO-6-methylguanine-DNA methyltransferaseGeneral MedicineBase excision repairDNA NeoplasmMethyltransferasesMolecular biologyDNA-(apurinic or apyrimidinic site) lyasedigestive system diseasesRatsUp-RegulationGene Expression Regulation NeoplasticKineticschemistryDNA glycosylaseEnzyme InductionAlkyltransferaseDNA DamageCarcinogenesis
researchProduct

Overexpression of Ogg1 in mammalian cells: effects on induced and spontaneous oxidative DNA damage and mutagenesis

1999

Chinese hamster ovary cell lines (AA8 and AS52) were stably transfected to overexpress hOgg1 protein, the human DNA repair glycosylase for 7,8-dihydro-8-oxoguanine (8-oxoG). In the transfectants, the repair rate of 8-oxoG residues induced by either potassium bromate or the photosensitizer [R]-1-[(10-chloro-4-oxo-3-phenyl-4H-benzo[a]quinolizin-1-yl)-carbo nyl ]-2-pyrrolidinemethanolplus light was up to 3-fold more rapid than in the parental cells. However, the improved repair had little effect on the mutagenicity of potassium bromate in the guanine phosphoribosyl transferase (gpt) locus of the OGG1-transfected AS52 cells. The steady-state (background) levels of DNA base modifications sensiti…

Cancer ResearchPyrrolidinesDNA RepairPhotochemistryDNA repairDNA damageBiologyTransfectionPolymerase Chain ReactionCell LineDNA-formamidopyrimidine glycosylasechemistry.chemical_compoundCricetulusGenes ReporterCricetinaeAnimalsheterocyclic compoundsN-Glycosyl HydrolasesPhotosensitizing AgentsBromatesChinese hamster ovary cellOvaryGeneral MedicineTransfectionDNA repair protein XRCC4OxidantsMolecular biologyOxidative StressDNA-Formamidopyrimidine GlycosylasechemistryGenes BacterialMutagenesisDNA glycosylaseEnzyme InductionFemaleQuinolizinesDNADNA DamageCarcinogenesis
researchProduct