Search results for "ALPHA"

showing 10 items of 3228 documents

SWATH-MS based quantitative proteomics analysis reveals that curcumin alters the metabolic enzyme profile of CML cells by affecting the activity of m…

2018

Background Chronic myelogenous leukemia (CML) is a myeloproliferative disorder caused by expression of the chimeric BCR-ABL tyrosine kinase oncogene, resulting from the t(9;22) chromosomal translocation. Imatinib (gleevec, STI-571) is a selective inhibitor of BCR-ABL activity highly effective in the treatment of CML. However, even though almost all CML patients respond to treatment with imatinib or third generation inhibitors, these drugs are not curative and need to be taken indefinitely or until patients become resistant. Therefore, to get a definitive eradication of leukemic cells, it is necessary to find novel therapeutic combinations, for achieving greater efficacy and fewer side effec…

0301 basic medicineProteomicsCancer ResearchCurcuminCML cellsCellReceptors Cytoplasmic and NuclearKaryopherinsTransfectionlcsh:RC254-282Mass SpectrometrymiR-22/IPO7/HIF-1α axis03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemiR-22/IPO7/HIF-1α axiSettore BIO/13 - Biologia Applicatahemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansCML cells; Curcumin; miR-22/IPO7/HIF-1α axis; SWATH-MS; Oncology; Cancer ResearchOncogeneChemistryResearchCML cellImatinibTransfectionmedicine.diseaseHypoxia-Inducible Factor 1 alpha Subunitlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthMicroRNAs030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchCurcuminSWATH-MSK562 CellsTyrosine kinaseK562 cellsChronic myelogenous leukemiamedicine.drug
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The Small Heat Shock Protein α-Crystallin B Shows Neuroprotective Properties in a Glaucoma Animal Model

2017

Glaucoma is a neurodegenerative disease that leads to irreversible retinal ganglion cell (RGC) loss and is one of the main causes of blindness worldwide. The pathogenesis of glaucoma remains unclear, and novel approaches for neuroprotective treatments are urgently needed. Previous studies have revealed significant down-regulation of α-crystallin B as an initial reaction to elevated intraocular pressure (IOP), followed by a clear but delayed up-regulation, suggesting that this small heat-shock protein plays a pathophysiological role in the disease. This study analyzed the neuroprotective effect of α-crystallin B in an experimental animal model of glaucoma. Significant IOP elevation induced b…

0301 basic medicineProteomicsRetinal Ganglion Cellsgenetic structuresNerve fiber layerGlaucomaCell CountMass Spectrometrylcsh:ChemistryPathogenesischemistry.chemical_compound0302 clinical medicineexperimental glaucoma; α-crystallin B; neuroprotection; proteomicsProtein Interaction Mapslcsh:QH301-705.5Spectroscopyα-crystallin BGeneral MedicineComputer Science ApplicationsUp-Regulationmedicine.anatomical_structureNeuroprotective AgentsRetinal ganglion cellneuroprotectionRetinal Neuronsmedicine.medical_specialtyDown-RegulationBiologyNeuroprotectionCatalysisArticleInorganic Chemistry03 medical and health sciencesCrystallinOphthalmologyHeat shock proteinmedicineElectroretinographyAnimalsPhysical and Theoretical ChemistryMolecular BiologyIntraocular Pressureexperimental glaucomaOrganic Chemistryalpha-Crystallin B ChainRetinalGlaucomamedicine.diseaseeye diseasesDisease Models Animal030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistry030221 ophthalmology & optometrysense organsInternational Journal of Molecular Sciences; Volume 18; Issue 11; Pages: 2418
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Human CD8(+) T Cells Damage Noninfected Epithelial Cells during Influenza Virus Infection In Vitro

2017

During severe influenza A virus (IAV) infections, a large amount of damage to the pulmonary epithelium is the result of the antiviral immune response. Specifically, whilst CD8+ T cells are important for killing IAV-infected cells, during a severe IAV infection, they can damage uninfected epithelial cells. At present, the mechanisms by which this occurs are unclear. Here, we used a novel in vitro coculture model of human NCl-H441 cells and CD8+ T cells to provide a new insight into how CD8+ T cells may affect uninfected epithelial cells during severe IAV infections. Using this model, we show that human IAV-specific CD8+ T cells produce soluble factors that reduce the barrier integrity of non…

0301 basic medicinePulmonary and Respiratory MedicineEpithelial sodium channelCD8(+) T cellsClinical BiochemistryCell BiologyLung injuryBiologyVirologyinfluenza virusepithelial cellsbystander damage03 medical and health sciencesInterleukin 21030104 developmental biology0302 clinical medicineImmune systemBystander effectCytotoxic T cellTumor necrosis factor alphaMolecular BiologyCD8030215 immunologyAmerican Journal of Respiratory Cell and Molecular Biology
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Accelerated telomere attrition in children and teenagers with α1-antitrypsin deficiency.

2016

Numerous studies have shown that oxidative stress accelerates telomere shortening in several lung pathologies. Since oxidative stress is involved in the pathophysiology of α1-antitrypsin deficiency (AATD), we hypothesised that telomere shortening would be accelerated in AATD patients. This study aimed to assess telomere length in AATD patients and to study its association with α1-antitrypsin phenotypes.Telomere length, telomerase activity, telomerase reverse transcriptase (hTERT) expression and biomarkers of oxidative stress were measured in 62 children and teenagers (aged 2–18 years) diagnosed with AATD and 18 controls (aged 3–16 years).Our results show that intermediate-risk (MZ; SZ) and …

0301 basic medicinePulmonary and Respiratory MedicineOncologyMalemedicine.medical_specialtyTelomeraseAdolescentmedicine.disease_causeBody Mass Index03 medical and health sciencesInternal medicinealpha 1-Antitrypsin DeficiencymedicineHumansTelomerase reverse transcriptaseChildLungTelomeraseTelomere ShorteningAlpha 1-antitrypsin deficiencybusiness.industryCase-control studyTelomeremedicine.diseaseMolecular biologyPathophysiologyTelomereOxidative Stress030104 developmental biologyPhenotypeSpirometryCase-Control StudiesChild PreschoolBiomarker (medicine)FemalebusinessOxidative stress
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Mechanical ventilation alters the development of staphylococcus aureus pneumonia in rabbit

2016

Ventilator-associated pneumonia (VAP) is common during mechanical ventilation (MV). Beside obvious deleterious effects on muco-ciliary clearance, MV could adversely shift the host immune response towards a pro-inflammatory pattern through toll-like receptor (TLRs) up-regulation. We tested this hypothesis in a rabbit model of Staphylococcus aureus VAP. Pneumonia was caused by airway challenge with S. aureus, in either spontaneously breathing (SB) or MV rabbits (n = 13 and 17, respectively). Pneumonia assessment regarding pulmonary and systemic bacterial burden, as well as inflammatory response was done 8 and 24 hours after S. aureus challenge. In addition, ex vivo stimulations of whole blood…

0301 basic medicinePulmonologyPhysiologyStaphylococcusmedicine.medical_treatment[SDV]Life Sciences [q-bio]lcsh:MedicinePharmacologyPathology and Laboratory Medicinemedicine.disease_causeStaphylococcal/immunology/pathologyImmune ReceptorsBiochemistry0302 clinical medicineImmune PhysiologyPneumonia StaphylococcalMedicine and Health SciencesMedicineStaphylococcus Aureuslcsh:ScienceImmune ResponseToll-like ReceptorsMammalsddc:616Innate Immune SystemImmune System ProteinsMultidisciplinaryddc:617RespirationPneumonia Ventilator-AssociatedInterleukinAnimal ModelsHematologyBacterial PathogensBody Fluids3. Good healthBloodmedicine.anatomical_structureMedical MicrobiologyStaphylococcus aureusVertebratesArtificialCytokinesRabbitsPathogensAnatomymedicine.symptomStaphylococcus aureus/immunologyResearch ArticleSignal TransductionToll-Like Receptor 2/immunologyImmunologyInflammationLung injuryResearch and Analysis MethodsMicrobiology03 medical and health sciencesModel OrganismsSigns and SymptomsDiagnostic MedicineAnimalsMicrobial PathogensInflammationMechanical ventilationInterleukin-8/immunologyLung[ SDV ] Life Sciences [q-bio]BacteriaTumor Necrosis Factor-alphabusiness.industrylcsh:RInterleukin-8OrganismsBiology and Life SciencesProteins030208 emergency & critical care medicineCell BiologyPneumoniaMolecular Developmentmedicine.diseaseTumor Necrosis Factor-alpha/immunologyRespiration ArtificialToll-Like Receptor 2Pneumonia030104 developmental biologyVentilator-Associated/immunology/microbiology/pathologyImmune SystemAmniotesImmunologylcsh:QbusinessSpleenEx vivoDevelopmental Biology
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A genome-wide association study of corneal astigmatism: The CREAM Consortium

2018

Contains fulltext : 191261.pdf (Publisher’s version ) (Open Access) Purpose: To identify genes and genetic markers associated with corneal astigmatism. Methods: A meta-analysis of genome-wide association studies (GWASs) of corneal astigmatism undertaken for 14 European ancestry (n=22,250) and 8 Asian ancestry (n=9,120) cohorts was performed by the Consortium for Refractive Error and Myopia. Cases were defined as having >0.75 diopters of corneal astigmatism. Subsequent gene-based and gene-set analyses of the meta-analyzed results of European ancestry cohorts were performed using VEGAS2 and MAGMA software. Additionally, estimates of single nucleotide polymorphism (SNP)-based heritability for …

0301 basic medicineReceptor Platelet-Derived Growth Factor alphaAcid PhosphataseGene Expression610 Medicine & healthbiomarkkeritPolymorphism Single NucleotideWhite PeopleSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Corneal DiseasesCohort StudiesCornea03 medical and health sciences0302 clinical medicineAsian PeopleOdds RatioHumansGenetic Predisposition to Disease610 Medicine & healthsarveiskalvogeenitIntracellular Signaling Peptides and ProteinsAstigmatism030104 developmental biologysilmätauditClaudinsgenetic markers030221 ophthalmology & optometrycorneal astigmatismSoftwaresilmätResearch ArticleGenome-Wide Association Study
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Recovery from Toxic-Induced Demyelination Does Not Require the NG2 Proteoglycan

2016

NG2 cells are defined as CNS cells expressing chondroitin sulfate proteoglycan nerve/glia antigen. The vast majority of NG2-positive cells also express platelet-derived growth factor receptor alpha (PDGFRα) and are oligodendroglial progenitors (OPC). In addition a subpopulation of pericytes expresses NG2, but is positive for PDGF receptor beta (PDGFRβ) [1]. NG2-positive OPC comprise approximately 5% of the cells in the CNS where they are evenly distributed in grey and white matter [2, 3]. NG2-positive OPC form synapses with neurons [4–6] and react to brain injury with proliferation, as has been shown in several animal models as well as in human demyelinating and degenerative diseases [7–9].…

0301 basic medicineReceptor Platelet-Derived Growth Factor alphaCellular differentiationlcsh:MedicineGene ExpressionMice TransgenicOLIG203 medical and health scienceschemistry.chemical_compoundCuprizone0302 clinical medicineCell MovementExtracellularmedicineAnimalsRemyelinationAntigenslcsh:ScienceCells CulturedCell ProliferationMice KnockoutMultidisciplinarybiologyMicrogliaReverse Transcriptase Polymerase Chain ReactionStem Cellslcsh:RBrainCorrectionCell DifferentiationImmunohistochemistryCell biologyMicroscopy ElectronOligodendroglia030104 developmental biologymedicine.anatomical_structurenervous systemchemistryChondroitin sulfate proteoglycanCell cultureImmunologybiology.proteinlcsh:QProteoglycans030217 neurology & neurosurgeryPlatelet-derived growth factor receptorDemyelinating DiseasesPloS one
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The actin remodeling protein cofilin is crucial for thymic αβ but not γδ T-cell development

2018

Cofilin is an essential actin remodeling protein promoting depolymerization and severing of actin filaments. To address the relevance of cofilin for the development and function of T cells in vivo, we generated knock-in mice in which T-cell–specific nonfunctional (nf) cofilin was expressed instead of wild-type (WT) cofilin. Nf cofilin mice lacked peripheral αβ T cells and showed a severe thymus atrophy. This was caused by an early developmental arrest of thymocytes at the double negative (DN) stage. Importantly, even though DN thymocytes expressed the TCRβ chain intracellularly, they completely lacked TCRβ surface expression. In contrast, nf cofilin mice possessed normal numbers of γδ T cel…

0301 basic medicineReceptors Antigen T-Cell alpha-betaT-LymphocytesJurkat cellsenvironment and public healthImmune ReceptorsBiochemistryWhite Blood CellsJurkat CellsMice0302 clinical medicineContractile ProteinsSpectrum Analysis TechniquesShort ReportsAnimal CellsCell MovementT-Lymphocyte SubsetsMedicine and Health SciencesGene Knock-In TechniquesBiology (General)Post-Translational ModificationPhosphorylationThymocytesImmune System ProteinsT CellsGeneral NeuroscienceStem CellsReceptors Antigen T-Cell gamma-deltaTransfectionAnimal ModelsCofilinFlow CytometryCell biologyThymusmedicine.anatomical_structureExperimental Organism SystemsActin Depolymerizing FactorsSpectrophotometry030220 oncology & carcinogenesisPhosphorylationCytophotometryCellular TypesGeneral Agricultural and Biological SciencesSignal TransductionHematopoietic Progenitor CellsProlineQH301-705.5T cellImmune CellsImmunologyDouble negativeMouse Modelsmacromolecular substancesThymus GlandBiologyResearch and Analysis MethodsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesModel OrganismsmedicineAnimalsHumansActinBlood CellsGeneral Immunology and MicrobiologyActin remodelingBiology and Life SciencesProteinsCell BiologyActinsT Cell ReceptorsCytoskeletal Proteins030104 developmental biologyImmune SystemMutationPLoS Biology
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Reply to Comment on Huang, X., et al. “Sourdough Fermentation Degrades Wheat Alpha-Amylase/Trypsin Inhibitor (ATI) and Reduces Pro-Inflammatory Activ…

2020

We thank Dr [...]

0301 basic medicineReplyHealth (social science)INTESTINAL INFLAMMATIONTrypsin inhibitoreducationPlant Sciencelcsh:Chemical technologyHealth Professions (miscellaneous)MicrobiologyACTIVATION03 medical and health sciences0302 clinical medicineIntestinal inflammationlcsh:TP1-1185Food science2. Zero hungerbiologyChemistrySourdough fermentationn/a030104 developmental biology416 Food Sciencebiology.protein030211 gastroenterology & hepatologyAlpha-amylaseFood ScienceFoods
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The Absence of HIF-1α Increases Susceptibility to Leishmania donovani Infection via Activation of BNIP3/mTOR/SREBP-1c Axis

2020

Summary: Hypoxia-inducible factor-1 alpha (HIF-1α) is considered a global regulator of cellular metabolism and innate immune cell functions. Intracellular pathogens such as Leishmania have been reported to manipulate host cell metabolism. Herein, we demonstrate that myeloid cells from myeloid-restricted HIF-1α-deficient mice and individuals with loss-of-function HIF1A gene polymorphisms are more susceptible to L. donovani infection through increased lipogenesis. Absence of HIF-1α leads to a defect in BNIP3 expression, resulting in the activation of mTOR and nuclear translocation of SREBP-1c. We observed the induction of lipogenic gene transcripts, such as FASN, and lipid accumulation in inf…

0301 basic medicineSREBP-1cHIF1A Gene[SDV]Life Sciences [q-bio]Leishmania donovaniHIF-1αGeneral Biochemistry Genetics and Molecular BiologyMitochondrial Proteins03 medical and health sciences0302 clinical medicinevisceral leishmaniasisAnimalsHumansMyeloid Cellslcsh:QH301-705.5GenelipogenesisPI3K/AKT/mTOR pathwayDisease ResistanceMice Inbred BALB CInnate immune systembiologyIntracellular parasiteLipogenesisMacrophagesTOR Serine-Threonine KinasesGenetic VariationMembrane Proteinsbiology.organism_classificationLeishmaniaHypoxia-Inducible Factor 1 alpha SubunitFASNLipidsmacrophages3. Good healthCell biologyUp-RegulationMice Inbred C57BL030104 developmental biologylcsh:Biology (General)myeloid cellsLipogenesisLeishmaniasis VisceralDisease SusceptibilityacetateSterol Regulatory Element Binding Protein 1030217 neurology & neurosurgeryLeishmania donovaniSignal Transduction
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