Search results for " 4"

showing 10 items of 3131 documents

Ceftaroline modulates the innate immune and host defense responses of immunocompetent cells exposed to cigarette smoke.

2017

Abstract Background Cigarette smoke, the principal risk factor for chronic obstructive pulmonary disease (COPD), negatively influences the effectiveness of the immune system’s response to a pathogen. The antibiotic ceftaroline exerts immune-modulatory effects in bronchial epithelial cells exposed to cigarette smoke. Aims and methods The present study aims to assess the effects of ceftaroline on TLR2 and TLR4 expression, LPS binding and TNF-α and human beta defensin (HBD2) release in an undifferentiated and PMA-differentiated human monocyte cell line (THP-1) exposed or not to cigarette smoke extracts (CSE). TLR2, TLR4, and LPS binding were assessed by flow cytometry, TNF-α and HBD2 release w…

0301 basic medicineLipopolysaccharidesbeta-DefensinsCell SurvivalCephalosporinLipopolysaccharideToxicologyMonocytes03 medical and health sciencesImmunologic Factor0302 clinical medicineImmune systemCell Line TumorSmokeAnti-Bacterial AgentmedicineHumansImmunologic FactorsInnate immune systemImmunocompetent cellDose-Response Relationship Drugbusiness.industryTumor Necrosis Factor-alphaMonocyteMacrophagesSmokingAntibioticCigarette smokeGeneral MedicineImmunity InnateToll-Like Receptor 2Anti-Bacterial AgentsCephalosporinsHost-Pathogen InteractionToll-Like Receptor 4TLR2030104 developmental biologymedicine.anatomical_structureBeta defensinCell cultureImmunologyHost-Pathogen InteractionsTLR4lipids (amino acids peptides and proteins)Tumor necrosis factor alphabusinessImmunocompetence030215 immunologyToxicology letters
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Cannabinoid Control of Learning and Memory through HCN Channels

2016

The mechanisms underlying the effects of cannabinoids on cognitive processes are not understood. Here we show that cannabinoid type-1 receptors (CB1Rs) control hippocampal synaptic plasticity and spatial memory through the hyperpolarization-activated cyclic nucleotide-gated (HCN) channels that underlie the h-current (Ih), a key regulator of dendritic excitability. The CB1R-HCN pathway, involving c-Jun-N-terminal kinases (JNKs), nitric oxide synthase, and intracellular cGMP, exerts a tonic enhancement of Ih selectively in pyramidal cells located in the superficial portion of the CA1 pyramidal cell layer, whereas it is absent from deep-layer cells. Activation of the CB1R-HCN pathway impairs d…

0301 basic medicineMAP Kinase Kinase 4medicine.medical_treatmentMorpholinesNeuroscience(all)RegulatorMice TransgenicBiologyNaphthalenesHippocampusBiophysical PhenomenaArticleMembrane Potentials03 medical and health sciencesMice0302 clinical medicineReceptor Cannabinoid CB1medicineHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsAnimalsEnzyme InhibitorsReceptorCyclic GMPSpatial MemoryMembrane potentialNeuronsGeneral NeuroscienceLong-term potentiationDendritesSynaptic PotentialsCalcium Channel BlockersBenzoxazines030104 developmental biologyMutationExcitatory postsynaptic potentialCannabinoidSignal transductionNitric Oxide SynthaseNeuroscience030217 neurology & neurosurgeryIntracellularSignal TransductionNeuron
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Unusual roles of caspase-8 in triple-negative breast cancer cell line MDA-MB-231

2015

Triple-negative breast cancer (TNBC) is a clinically aggressive form of breast cancer that is unresponsive to endocrine agents or trastuzumab. TNBC accounts for ~10-20% of all breast cancer cases and represents the form with the poorest prognosis. Patients with TNBC are at higher risk of early recurrence, mainly in the lungs, brain and soft tissue, therefore, there is an urgent need for new therapies. The present study was carried out in MDA-MB-231 cells, where we assessed the role of caspase-8 (casp-8), a critical effector of death receptors, also involved in non‑apoptotic functions. Analysis of casp-8 mRNA and protein levels indicated that they were up-regulated with respect to the normal…

0301 basic medicineMDA-MB-231 cellCancer ResearchDown-RegulationTriple Negative Breast NeoplasmsTransfectionResting Phase Cell Cycle03 medical and health sciencesKruppel-Like Factor 40302 clinical medicineHMGA2Breast cancerCell Line TumormedicineHumansRNA Small InterferingCaspase-8 unusual roleTriple-negative breast cancerCaspase 8Triple-negative breast cancer cellbiologyOncogeneCaspase-8 knockdownCell CycleG1 PhaseCancerCell cyclemedicine.diseaseMolecular medicineKLF4Invasivity and metastasi030104 developmental biologyOncologyKLF4030220 oncology & carcinogenesisbiology.proteinCancer researchFemaleCell cycle regulator
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Shared DNA methylation signatures in childhood allergy: The MeDALL study

2021

Contains fulltext : 232514.pdf (Publisher’s version ) (Open Access) BACKGROUND: Differential DNA methylation associated with allergy might provide novel insights into the shared or unique etiology of asthma, rhinitis, and eczema. OBJECTIVE: We sought to identify DNA methylation profiles associated with childhood allergy. METHODS: Within the European Mechanisms of the Development of Allergy (MeDALL) consortium, we performed an epigenome-wide association study of whole blood DNA methylation by using a cross-sectional design. Allergy was defined as having symptoms from at least 1 allergic disease (asthma, rhinitis, or eczema) and positive serum-specific IgE to common aeroallergens. The discove…

0301 basic medicineMaleAllergyMESH: Asthmalnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]EczemaImmunoglobulin EEpigenesis GeneticCohort Studies0302 clinical medicineMESH: DNA MethylationMESH: ChildImmunology and AllergyMedicineMESH: Epigenesis GeneticChildMESH: CpG IslandsMESH: Cohort StudiesDNA methylationbiologyMESH: Immunoglobulin EEpigeneticMethylation3. Good healthCpG site030220 oncology & carcinogenesisChild PreschoolDNA methylationMESH: Rhinitis AllergicFemaleEpigeneticsIgEAdolescentMESH: HypersensitivityImmunologyeducationSingle-nucleotide polymorphismArticle03 medical and health sciencesMESH: Cross-Sectional StudieschildrenHypersensitivityHumansEpigeneticsAsthmaMESH: AdolescentMESH: Humansbusiness.industryMESH: TranscriptomeMESH: Child PreschoolImmunoglobulin Emedicine.diseaseallergyRhinitis AllergicAsthmaMESH: Male030104 developmental biologyCross-Sectional StudiesMESH: Eczema3121 General medicine internal medicine and other clinical medicineImmunologybiology.proteinCpG IslandsbusinessTranscriptomeMESH: Female[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
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Meta-analysis identifies novel risk loci and yields systematic insights into the biology of male-pattern baldness

2017

Male-pattern baldness (MPB) is a common and highly heritable trait characterized by androgen-dependent, progressive hair loss from the scalp. Here, we carry out the largest GWAS meta-analysis of MPB to date, comprising 10,846 early-onset cases and 11,672 controls from eight independent cohorts. We identify 63 MPB-associated loci (P<5 × 10−8, METAL) of which 23 have not been reported previously. The 63 loci explain ∼39% of the phenotypic variance in MPB and highlight several plausible candidate genes (FGF5, IRF4, DKK2) and pathways (melatonin signalling, adipogenesis) that are likely to be implicated in the key-pathophysiological features of MPB and may represent promising targets for the de…

0301 basic medicineMaleCandidate genegenetics [Trans-Activators]SRD5A2 protein humanMedizinGeneral Physics and Astronomygenetics [3-Oxo-5-alpha-Steroid 4-Dehydrogenase]Genome-wide association studyBioinformatics0302 clinical medicinegenetics [Interferon Regulatory Factors]GenotypeMelatoninGeneticsMultidisciplinaryAdipogenesisEBF1 protein humanintegumentary systemgenetics [Intercellular Signaling Peptides and Proteins]QPhenotypeFGF5 protein humangenetics [Membrane Proteins]Phenotype030220 oncology & carcinogenesisMeta-analysisUrological cancers Radboud Institute for Health Sciences [Radboudumc 15]Interferon Regulatory FactorsIntercellular Signaling Peptides and ProteinsMale-pattern baldnessddc:500Signal TransductionDKK2 protein humanGenotypeFibroblast Growth Factor 53-Oxo-5-alpha-Steroid 4-Dehydrogenase/genetics; Adipogenesis/genetics; Alopecia/genetics; Case-Control Studies; Fibroblast Growth Factor 5/genetics; Genetic Association Studies; Genome-Wide Association Study; Genotype; Humans; Intercellular Signaling Peptides and Proteins/genetics; Interferon Regulatory Factors/genetics; Male; Melatonin; Membrane Proteins/genetics; Phenotype; Signal Transduction/genetics; Trans-Activators/geneticsScienceGenomicsBiologygenetics [Signal Transduction]General Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesinterferon regulatory factor-43-Oxo-5-alpha-Steroid 4-DehydrogenasemedicineHumansgenetics [Adipogenesis]Genetic Association Studiesgenetics [Alopecia]Case-control studyMembrane ProteinsAlopeciaGeneral Chemistrymedicine.diseasegenetics [Fibroblast Growth Factor 5]030104 developmental biologyCase-Control StudiesTrans-ActivatorsGenome-Wide Association Study
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Silencing of hepatic fate-conversion factors induce tumorigenesis in reprogrammed hepatic progenitor-like cells

2016

Abstract Background Several studies have reported the direct conversion of mouse fibroblasts to hepatocyte-like cells with different degrees of maturation by expression of hepatic fate-conversion factors. Methods We have used a combination of lentiviral vectors expressing hepatic fate-conversion factors with Oct4, Sox2, Klf4, and Myc to convert mouse embryonic fibroblasts into hepatic cells. Results We have generated hepatic cells with progenitor-like features (iHepL cells). iHepL cells displayed basic hepatocyte functions but failed to perform functions characteristic of mature hepatocytes such as significant Cyp450 or urea cycle activities. iHepL cells expressed multiple hepatic-specific …

0301 basic medicineMaleCarcinogenesisCellular differentiationMedicine (miscellaneous)Gene ExpressionReceptors G-Protein-CoupledMiceMice Inbred NODHepatocyteTransgenesStem CellsTeratomaCell DifferentiationForkhead Transcription FactorsCellular ReprogrammingCell biologyKLF4Molecular MedicineStem cellReprogrammingDirect reprogrammingGenetic VectorsKruppel-Like Transcription FactorsBiologyBiochemistry Genetics and Molecular Biology (miscellaneous)Proto-Oncogene Proteins c-myc03 medical and health sciencesKruppel-Like Factor 4SOX2AnimalsHepatectomyGene SilencingProgenitor cellResearchXenograftSOXB1 Transcription FactorsLentivirusCD24 AntigenCell BiologyFibroblastsEmbryo MammalianEmbryonic stem cell030104 developmental biologyTumorigenesisHepatic stellate cellHepatocytesOctamer Transcription Factor-3BiomarkersProgenitorStem Cell Research & Therapy
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CD16+ Macrophages Mediate Fibrosis in Inflammatory Bowel Disease.

2017

Background and Aims Fibrosis is a common complication of Crohn's disease [CD], and is related to dysregulated tissular repair following inflammation, in which macrophages play a central role. We have previously observed that STAT6-/- mice present delayed mucosal recovery after 2,4,6-trinitrobenzenesulfonic acid [TNBS]-induced colitis due to a deficiency in reparatory interleukin-4 [IL4]/STAT6-dependent M2 macrophages, which can be reverted by the exogenous transfer of this cell type. In the present study, we analyse the role of STAT6-dependent macrophages in intestinal fibrosis. Methods Colitis was induced by weekly intra-rectal administration of TNBS [6 weeks] to STAT6-/- mice and wild-typ…

0301 basic medicineMaleCell CountInflammatory bowel diseaseMiceCrohn DiseaseFibrosisMacrophageIntestinal MucosaCells CulturedMice Knockouteducation.field_of_studyMice Inbred BALB Cintegumentary systemGastroenterologyGeneral MedicineColitisColonic NeoplasmsFemalemedicine.symptomMannose ReceptorAdultAdolescentColonPopulationInflammationReceptors Cell SurfaceCD1603 medical and health sciencesYoung AdultProto-Oncogene Proteinsparasitic diseasesmedicineAnimalsHumansLectins C-TypeColitiseducationInterleukin 4business.industryMacrophagesReceptors IgGmedicine.diseaseFibrosisWnt Proteins030104 developmental biologyMannose-Binding LectinsTrinitrobenzenesulfonic AcidImmunologyInterleukin-4businessSTAT6 Transcription FactorJournal of Crohn'scolitis
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Gut Microbiota Restricts NETosis in Acute Mesenteric Ischemia-Reperfusion Injury.

2020

Objective: Recruitment of neutrophils and formation of neutrophil extracellular traps (NETs) contribute to lethality in acute mesenteric infarction. To study the impact of the gut microbiota in acute mesenteric infarction, we used gnotobiotic mouse models to investigate whether gut commensals prime the reactivity of neutrophils towards formation of neutrophil extracellular traps (NETosis). Approach and Results: We applied a mesenteric ischemia-reperfusion (I/R) injury model to germ-free (GF) and colonized C57BL/6J mice. By intravital imaging, we quantified leukocyte adherence and NET formation in I/R-injured mesenteric venules. Colonization with gut microbiota or monocolonization with Esch…

0301 basic medicineMaleExtracellular TrapsMesenteric infarctionLipopolysaccharideNeutrophilsGut floraExtracellular Traps03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAcute mesenteric ischemiaVenulesmedicineCell AdhesionEscherichia coliLeukocytesAnimalsGerm-Free LifeLeukocyte RollingMesenteryCells CulturedMice Knockoutbiologybusiness.industryNeutrophil extracellular trapsbiology.organism_classificationmedicine.diseaseGastrointestinal MicrobiomeMice Inbred C57BLToll-Like Receptor 4Disease Models Animal030104 developmental biologychemistryNeutrophil Infiltration030220 oncology & carcinogenesisMesenteric IschemiaReperfusion InjuryImmunologyHost-Pathogen InteractionsFemaleCardiology and Cardiovascular MedicinebusinessReperfusion injuryBacillus subtilisSignal TransductionArteriosclerosis, thrombosis, and vascular biology
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Generation of a disease-specific iPS cell line derived from a patient with Charcot-Marie-Tooth type 2K lacking functional GDAP1 gene

2016

Human CMT2-FiPS4F1 cell line was generated from fibroblasts of a patient with Charcot-Marie-Tooth disease harbouring the following mutations in the GDAP1 gene in heterozygosis: p.Q163X/p.T288NfsX3. This patient did not present mutations in the PM22, MPZ or GJB genes. Human reprogramming factors OCT3/4, KLF4, SOX2 and C-MYC were delivered using a non-integrative methodology that involves the use of Sendai virus.

0301 basic medicineMaleHeterozygoteCellular differentiationCèl·lulesDNA Mutational AnalysisGenetic VectorsInduced Pluripotent Stem CellsKaryotypeNerve Tissue ProteinsBiologyPolymorphism Single NucleotideSendai virusCell Line03 medical and health sciencesKruppel-Like Factor 4stomatognathic systemCharcot-Marie-Tooth DiseaseHumansInduced pluripotent stem cellGeneTranscription factorMedicine(all)GeneticsBase SequenceHeterozygote advantageCell DifferentiationCell BiologyGeneral MedicineFibroblastsbiology.organism_classificationCellular ReprogrammingSendai virus030104 developmental biologyMicroscopy FluorescenceKLF4embryonic structuresSistema nerviós MalaltiesReprogrammingDevelopmental BiologyTranscription Factors
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