Search results for "messenger"

showing 10 items of 1493 documents

Granulocyte-macrophage colony-stimulating factor induces cytokine secretion by human polymorphonuclear leukocytes.

1989

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is known as an inducer of proliferation and functional activation of myeloid cells. This study was carried out to characterize the effects of GM-CSF on polymorphonuclear leukocytes (PMN) more extensively. Using Northern blot analysis, we show that PMN are able to accumulate mRNAs for different cytokines, including tumor necrosis factor-alpha (TNF-alpha); G-CSF, and M-CSF, all of which are involved in inflammation and hematopoiesis. Biological assays and immunoassays demonstrate that PMN translate these mRNAs, except TNF-alpha, into secretory proteins. However, the expression of these cytokines is dependent on stimulation by exogenous…

Macrophage colony-stimulating factorNeutrophilsT cellInflammationBiologyBiological FactorsMiceColony-Stimulating FactorsGranulocyte Colony-Stimulating FactormedicineAnimalsHumansRNA MessengerGrowth SubstancesTumor Necrosis Factor-alphaMacrophage Colony-Stimulating FactorLymphokineGranulocyte-Macrophage Colony-Stimulating FactorGeneral MedicineColony-stimulating factorRecombinant ProteinsRetractionCell biologymedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorImmunologyCytokinesTumor necrosis factor alphaCytokine secretionmedicine.symptomResearch Articlemedicine.drugJournal of Clinical Investigation
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Production of macrophage-, granulocyte-, granulocyte-macrophage- and multi-colony-stimulating factor by peripheral blood cells

1989

The specific cell sources and signals for induction of various colony-stimulating factors (CSF) in peripheral blood mononuclear cells (PBMC), purified T lymphocyte and monocyte (Mo) populations have been investigated. In the absence of exogenous activating stimuli, human PBMC, T cells and Mo failed to produce stable cytoplasmic mRNA for CSF for macrophages (M-CSF or CSF-1), for granulocytes (G-CSF), for granulocytes and macrophages (GM-CSF) and for multilineage CSF [multi-CSF, interleukin (IL) 3] and thus failed to release CSF proteins. However, after stimulation with phorbol myristate acetate and phytohemagglutinin, M-, G-, GM- and multi-CSF mRNA became detectable in PBMC, resulting in the…

Macrophage colony-stimulating factorT-Lymphocytesmedicine.medical_treatmentImmunologyGranulocyteBiologyPeripheral blood mononuclear cellMonocytesColony-Stimulating FactorsGranulocyte Colony-Stimulating FactormedicineHumansImmunology and AllergyMacrophageRNA MessengerGrowth SubstancesMacrophage Colony-Stimulating FactorMonocyteGranulocyte-Macrophage Colony-Stimulating FactorT lymphocyteMolecular biologyGranulocyte macrophage colony-stimulating factorCytokinemedicine.anatomical_structureImmunologyInterleukin-3medicine.drugEuropean Journal of Immunology
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Tumor necrosis factor (TNF)-alpha but not TNF-beta induces secretion of colony stimulating factor for macrophages (CSF-1) by human monocytes

1987

Abstract Tumor necrosis factor (TNF)-alpha has been identified as a major inducer of colony stimulating factor (CSF)-secretion by human vascular endothelial cells and fibroblasts. In the present study we assessed the capacity of TNFs to induce release of CSF-1 from highly purified peripheral blood monocyte preparations. Whereas monocytes do not accumulate CSF-1 messenger (m)RNA constitutively and consequently do not produce CSF-1 protein, CSF-1 mRNA and protein secretion became detectable, when monocytes were cultured in the presence of TNF-alpha, that was synergistically enhanced by interferon-gamma (IFN-gamma). However, under identical experimental conditions TNF-beta failed to induce mon…

Macrophage colony-stimulating factormedicine.medical_specialtyT-LymphocytesImmunologyIn Vitro TechniquesBiologyBiochemistryMonocytesColony-Forming Units AssayColony-Stimulating FactorsInternal medicinemedicineHumansSecretionLeukapheresisMessenger RNATumor Necrosis Factor-alphaMonocyteCell BiologyHematologyMacrophage ActivationColony-stimulating factorMolecular biologyHaematopoiesisEndocrinologySecretory proteinmedicine.anatomical_structureTumor necrosis factor alphaBlood
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Arachidonate 5-lipoxygenase (ALOX5) gene polymorphism is associated with Alzheimer's disease and body mass index

2016

IF 2.126; International audience; Dementias of old age, in particular Alzheimer's disease (AD), pose a growing threat to the longevity and quality of life of individuals as well as whole societies world-wide. The risk factors are both genetic and environmental (lifestyle) and there is an overlap with similar factors predisposing to cardiovascular diseases (CVD). Using a case control genetic approach, we have identified a SNP (rs10507391) in ALOX5 gene, previously associated with an increased risk of stroke, as a novel genetic risk factor for AD. ALOX5 gene encodes a 5'-lipoxygenase (5'-LO) activating protein (FLAP), a crucial component of the arachidonic acid/leukotriene inflammatory cascad…

Male0301 basic medicineDiseaseBioinformaticsBody Mass Index0302 clinical medicinePutative roleSurveys and QuestionnairesGenotypeMedicineCzech RepublicAged 80 and over2. Zero hungerGeneticsbiologyAlzheimer's disease3. Good healthRisk-factorsArachidonic acidNeurologyArachidonate 5-lipoxygenaseActivating proteinFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Neuronal 5-LipoxygenaseLeukotrienesCurcuminGenotypeDna methylationFLAPPolymorphism Single NucleotideMouse modelAssociation03 medical and health sciencesMessenger-RnaAlzheimer DiseaseGeneticsHumansSNPPolymorphismSingle-Nucleotide polymorphisms5-lipoxygenase-activating proteinLife StyleGenetic Association StudiesAgedAmyloidotic phenotypeInflammationCaffeic acidArachidonate 5-Lipoxygenasebusiness.industryBody WeightOdds ratio030104 developmental biology[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Relative riskbiology.proteinNeurology (clinical)businessBody mass index030217 neurology & neurosurgeryJournal of the Neurological Sciences
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Long-Term Calorie Restriction Enhances Cellular Quality-Control Processes in Human Skeletal Muscle

2015

Calorie restriction (CR) retards aging, acts as a hormetic intervention, and increases serum corticosterone and HSP70 expression in rodents. However, less is known regarding the effects of CR on these factors in humans. Serum cortisol and molecular chaperones and autophagic proteins were measured in the skeletal muscle of subjects on CR diets for 3-15 years and in control volunteers. Serum cortisol was higher in the CR group than in age-matched sedentary and endurance athlete groups (15.6 ± 4.6 ng/dl versus 12.3 ± 3.9 ng/dl and 11.2 ± 2.7 ng/dl, respectively; p ≤ 0.001). HSP70, Grp78, beclin-1, and LC3 mRNA and/or protein levels were higher in the skeletal muscle of the CR group compared to…

Male0301 basic medicineGenetics and Molecular Biology (all)Time FactorsHydrocortisoneBiochemistryCortisolBody Mass IndexCluster Analysislcsh:QH301-705.5Endoplasmic Reticulum Chaperone BiPAldosteroneHeat-Shock ProteinsHSP70Serum cortisolMiddle Agedmedicine.anatomical_structureBeclin-1Femalemedicine.symptomMicrotubule-Associated Proteinsmedicine.drugAdultmedicine.medical_specialtyCalorie restrictionInflammationBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesEndurance trainingInternal medicineHeat shock proteinmedicineAutophagyHumansHSP70 Heat-Shock ProteinsRNA MessengerMuscle SkeletalExerciseCalorie restrictionCaloric RestrictionHydrocortisoneHSP70; aldosterone; autophagy; calorie restriction; cortisol; adult; apoptosis regulatory proteins; beclin-1; body mass index; cluster analysis; exercise; female; gene expression regulation; hsp70 heat-shock proteins; heat-shock proteins; humans; hydrocortisone; male; membrane proteins; microtubule-associated proteins; middle aged; muscle skeletal; RNA messenger; time factors; transcription factors; caloric restrictionCalorie restriction (CR)AutophagyMembrane ProteinsSkeletal muscleHsp70030104 developmental biologyEndocrinologylcsh:Biology (General)Gene Expression RegulationAldosterone; Autophagy; Calorie restriction; Cortisol; HSP70; Biochemistry Genetics and Molecular Biology (all)Apoptosis Regulatory ProteinsTranscription Factors
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Obesogen effects after perinatal exposure of 4,4′-sulfonyldiphenol (Bisphenol S) in C57BL/6 mice

2016

International audience; Bisphenol A were removed from consumer products and replaced by chemical substitutes such as Bisphenol S (BPS). Based on their structural similarity, BPS may be obesogen like Bisphenol A in mice. Our objective was to determine the impact of BPS on lipid homeostasis in C57B1/6 mice after perinatal and chronic exposure. Pregnant mice were exposed to BPS via the drinking water (0.2; 1.5; 50 mu g/kg bw/d). Treatment began at gestational day 0 and continued in offspring up to 23-weeks old. Then, offspring mice were fed with a standard or high fat diet. The body weight, food consumption, fat mass and energy expenditure were measured. A lipid load test was performed to chec…

Male0301 basic medicineLeptinBisphenol S[ SDV.TOX ] Life Sciences [q-bio]/ToxicologyAdipose tissue010501 environmental sciencesToxicologyurologic and male genital diseases01 natural sciencesPolyethylene GlycolsMicechemistry.chemical_compoundPregnancyInduced ObesityHyperinsulinemiapériode perinataleObesogenSulfones2. Zero hungerLeptinHigh-Fat Dietsanté humaineLipidsEnergy-Balance3. Good healthSafe AlternativesobésitéAdipose TissuePrenatal Exposure Delayed Effects[SDV.TOX]Life Sciences [q-bio]/Toxicologybisphénol sFemalehormones hormone substitutes and hormone antagonistsmedicine.medical_specialtyOffspringDiet High-Fat03 medical and health sciencesInsulin resistancePhenolsInternal medicinemedicineAnimalshoméostasie lipidiqueObesityRNA MessengerTriglycerides0105 earth and related environmental sciencesDose-Response Relationship DrugAdiponectinTriglycerideInsulin-ResistanceBody WeightOverweightmedicine.diseasebisphenol S;food contaminant;perinatal exposure;low dose;obesogenPerinatal exposureMice Inbred C57BLFood contaminant030104 developmental biologyEndocrinologycontaminant chimiqueLow doseGlucoseMetabolismGene Expression RegulationchemistryIn-VitroObesogenAnalogs
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Molecular mechanisms mediating the neuroprotective role of the selective estrogen receptor modulator, bazedoxifene, in acute ischemic stroke: A compa…

2017

As the knowledge on the estrogenic system in the brain grows, the possibilities to modulate it in order to afford further neuroprotection in brain damaging disorders so do it. We have previously demonstrated the ability of the selective estrogen receptor modulator, bazedoxifene (BZA), to reduce experimental ischemic brain damage. The present study has been designed to gain insight into the molecular mechanisms involved in such a neuroprotective action by investigating: 1) stroke-induced apoptotic cell death; 2) expression of estrogen receptors (ER) ERα, ERβ and the G-protein coupled estrogen receptor (GPER); and 3) modulation of MAPK/ ERK1/2 and PI3K/Akt signaling pathways. For comparison, …

Male0301 basic medicineMAPK/ERK pathwayIndolesSignaling pathwaysEndocrinology Diabetes and MetabolismClinical BiochemistryEstrogen receptorApoptosisEstrogen receptorsSecond Messenger SystemsBiochemistryBrain IschemiaReceptors G-Protein-Coupled0302 clinical medicineEndocrinologyPhosphatidylinositol PhosphatesCerebral CortexNeuronsEstradiolNeuroprotectionStrokeNeuroprotective AgentsSelective estrogen receptor modulatorReperfusion InjuryMolecular MedicineSelective estrogen receptor modulatorsGPERmedicine.medical_specialtyMAP Kinase Signaling Systemmedicine.drug_classAcute ischemic strokeNerve Tissue ProteinsBazedoxifeneBiologyNeuroprotection03 medical and health sciencesInternal medicinemedicineAnimalsEstrogen Receptor betaRats WistarMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayEstrogen Receptor alphaEstrogensCell BiologyEstrogen030104 developmental biologyEndocrinologyEstrogen030217 neurology & neurosurgeryThe Journal of Steroid Biochemistry and Molecular Biology
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Clinical Implications of Discordant Early Molecular Responses in CML Patients Treated with Imatinib

2019

A reduction in BCR-ABL1/ABL1IS transcript levels to &lt

Male0301 basic medicineOncologyTreatment outcomeFusion Proteins bcr-ablAntineoplastic Agentlcsh:ChemistryBcr abl10302 clinical medicinehemic and lymphatic diseasesimatinib mesylateBCR-ABL1; European Leukemia Net; chronic myeloid leukemia; early molecular response; imatinib mesylatelcsh:QH301-705.5<i>BCR-ABL1</i>SpectroscopyAged 80 and overGeneral MedicineMiddle AgedComputer Science ApplicationsTreatment Outcome030220 oncology & carcinogenesisFemaleHumanmedicine.drugAdultmedicine.medical_specialtyProtein Kinase InhibitorAntineoplastic AgentsArticleCatalysisEuropean Leukemia NetInorganic Chemistry03 medical and health scienceschronic myeloid leukemiaLeukemia Myelogenous Chronic BCR-ABL PositiveInternal medicineBiomarkers TumormedicineHumansIn patientRNA MessengerPhysical and Theoretical ChemistryProtein Kinase InhibitorsMolecular BiologyAgedbusiness.industryOrganic ChemistryImatinibBCR-ABL1030104 developmental biologyImatinib mesylatelcsh:Biology (General)lcsh:QD1-999early molecular responsebusiness
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H-ferritin and CD68+/H-ferritin+ monocytes/macrophages are increased in the skin of adult-onset Still's disease patients and correlate with the multi…

2016

Summary Adult-onset Still's disease (AOSD) patients may show an evanescent salmon-pink erythema appearing during febrile attacks and reducing without fever. Some patients may experience this eruption for many weeks. During AOSD, exceptionally high serum levels of ferritin may be observed; it is an iron storage protein composed of 24 subunits, heavy (H) subunits and light (L) subunits. The ferritin enriched in L subunits (L-ferritin) and the ferritin enriched in H subunits (H-ferritin) may be observed in different tissues. In this work, we aimed to investigate the skin expression of both H-and L-ferritin and the number of macrophages expressing these molecules from AOSD patients with persist…

Male0301 basic medicinePathologymedicine.medical_specialtyAdult-onset Still's diseaseDermal immune systemErythemaMacrophageBiopsyImmunologyAntigens Differentiation MyelomonocyticGene ExpressionDiseaseAdult-onset Still's diseaseMonocytesH-Ferritin03 medical and health sciences0302 clinical medicineAntigens CDadult-onset Still's disease; dermal immune system; ferritin; hyperferritinaemic syndrome; macrophagemedicineHumansImmunology and AllergyMonocytes macrophagesMacrophageRNA MessengerSkin030203 arthritis & rheumatologyFerritinbiologyCD68MacrophagesOriginal ArticlesFerritinSettore MED/16 - Reumatologia030104 developmental biologyApoferritinsImmunologyLeukocytes Mononuclearbiology.proteinCytokinesFemaleInflammation Mediatorsmedicine.symptomHyperferritinaemic syndromeStill's Disease Adult-OnsetBiomarkersClinical and Experimental Immunology
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Both cholestatic and steatotic drugs trigger extensive alterations in the mRNA level of biliary transporters in rat hepatocytes: Application to devel…

2016

Disruption of the vectorial bile acid transport in the liver is a key feature of cholestatic drugs, although many causal and mechanistic aspects are still unknown. The aim of the present study was to explore if cholestatic drugs can repress or induce the expression of hepatic transporters. To this end, sandwich-cultured rat hepatocytes were treated with cholestatic and non-cholestatic (steatotic, non-hepatotoxic, etc.) drugs and the mRNA expression of 10 uptake and efflux biliary transporters was measured. Results evidenced that all cholestatic drugs cause extensive alterations in the mRNA expression of most biliary transporters. Surprisingly, nearly all steatotic drugs also affected the ex…

Male0301 basic medicinePathologymedicine.medical_specialtyDrug-Related Side Effects and Adverse ReactionsDrug Evaluation PreclinicalOrganic Anion Transporters Sodium-IndependentPharmacologyBiologyToxicology030226 pharmacology & pharmacyRats Sprague-Dawley03 medical and health sciences0302 clinical medicineCholestasisPredictive Value of TestsIn vivomedicineAnimalsBileRNA MessengerCells CulturedCholestasisMultidrug resistance-associated protein 2Fatty liverTransporterGeneral Medicinemedicine.diseaseRatsFatty Liver030104 developmental biologyTetracyclinesHepatocytesBiomarker (medicine)EffluxSteatosisCarrier ProteinsBiomarkersToxicology Letters
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