Search results for "GENI"

showing 10 items of 6843 documents

Anti-angiogenic agents in the age of resistance to immune checkpoint inhibitors: Do they have a role in non-oncogene-addicted non-small cell lung can…

2020

The introduction of licensed front-line immunotherapies has heralded a new era for the treatment of non-oncogene-addicted, advanced non-small cell lung cancer (NSCLC). Yet as with all evolutions in clinical management, changes in practice can outpace the availability of the clinical evidence needed to inform subsequent therapeutic decision making. At the time of writing, there is limited available evidence on the optimum therapeutic options after progression on immunotherapy. Further research is needed to define mechanisms of immunotherapy resistance in patients with advanced NSCLC, and to understand the implications for subsequent treatment response. Pending the availability of robust clin…

0301 basic medicinePulmonary and Respiratory MedicineOncologyCancer Researchmedicine.medical_specialtyLung Neoplasmsmedicine.medical_treatmentNintedanibContext (language use)Angiogenesis InhibitorsAnti-angiogenic drugNon-oncogene-addicted non-small cell lung cancer (NSCLC)03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineCarcinoma Non-Small-Cell LungmedicineTumor MicroenvironmentHumansTumor microenvironment (TME)Lung cancerImmune Checkpoint InhibitorsTumor microenvironmentAnti-angiogenic drug; Immunotherapy resistance; Nintedanib; Non-oncogene-addicted non-small cell lung cancer (NSCLC); Tumor microenvironment (TME); Vascular endothelial growth factor (VEGF)Oncogenebusiness.industryVascular endothelial growth factor (VEGF)ImmunosuppressionImmunotherapymedicine.diseaseImmunotherapy resistance030104 developmental biologyOncologychemistry030220 oncology & carcinogenesisNintedanibNon small cellImmunotherapybusiness
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Noncoding RNAs in Critical Limb Ischemia

2020

Peripheral artery disease, caused by chronic arterial occlusion of the lower extremities, affects over 200 million people worldwide. Peripheral artery disease can progress into critical limb ischemia (CLI), its more severe manifestation, which is associated with higher risk of limb amputation and cardiovascular death. Aiming to improve tissue perfusion, therapeutic angiogenesis held promise to improve ischemic limbs using delivery of growth factors but has not successfully translated into benefits for patients. Moreover, accumulating studies suggest that impaired downstream signaling of these growth factors (or angiogenic resistance) may significantly contribute to CLI, particularly under h…

0301 basic medicineRNA UntranslatedAngiogenesisCritical IllnessNeovascularization PhysiologicDisease030204 cardiovascular system & hematologyBioinformaticsArticlePeripheral Arterial Disease03 medical and health sciences0302 clinical medicineIschemiaRisk FactorsmicroRNADiabetes MellitusAnimalsHumansMedicineTherapeutic angiogenesisProgenitor cellHypoxiaInflammationbusiness.industryStem CellsHemodynamicsCritical limb ischemiaHypoxia (medical)Prognosisbody regions030104 developmental biologyGene Expression RegulationRegional Blood FlowArteriogenesismedicine.symptomCardiology and Cardiovascular MedicinebusinessSignal TransductionArteriosclerosis, Thrombosis, and Vascular Biology
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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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Nucleocytoplasmic transport of the RNA-binding protein CELF2 regulates neural stem cell fates.

2020

The development of the cerebral cortex requires balanced expansion and differentiation of neural stem/progenitor cells (NPCs), which rely on precise regulation of gene expression. Because NPCs often exhibit transcriptional priming of cell-fate-determination genes, the ultimate output of these genes for fate decisions must be carefully controlled in a timely fashion at the post-transcriptional level, but how that is achieved is poorly understood. Here, we report that de novo missense variants in an RNA-binding protein CELF2 cause human cortical malformations and perturb NPC fate decisions in mice by disrupting CELF2 nucleocytoplasmic transport. In self-renewing NPCs, CELF2 resides in the cyt…

0301 basic medicineRegulation of gene expressionNeurogenesisRNA-Binding ProteinsTranslation (biology)RNA-binding proteinCell DifferentiationNerve Tissue ProteinsBiologyCell fate determinationGeneral Biochemistry Genetics and Molecular BiologyNeural stem cellCell biology03 medical and health sciences030104 developmental biology0302 clinical medicineNeural Stem CellsNucleocytoplasmic TransportCELF ProteinsHumansProgenitor cell030217 neurology & neurosurgeryCell reports
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Generation of an inducible RPE-specific Cre transgenic-mouse line.

2018

The retinal pigment epithelium (RPE) is an epithelial monolayer in the back of the vertebrate eye. RPE dysfunction is associated with retinal degeneration and blindness. In order to fully understand how dysregulation affects visual function, RPE-specific gene knockouts are indispensable. Since the currently available RPE-specific Cre recombinases show lack of specificity or poor recombination, we sought to generate an alternative. We generated a tamoxifen-inducible RPE-specific Cre transgenic mouse line under transcriptional control of an RPE-specific Tyrosinase enhancer. We characterized the Cre-mediated recombinant expression by crossing our RPE-Tyrosinase-CreErT2 mouse line with the tdTo…

0301 basic medicineRetinal degenerationMaleEmbryologylcsh:MedicineGene ExpressionRetinal Pigment EpitheliumBiochemistry0302 clinical medicineRecombinaseMedicine and Health Scienceslcsh:ScienceStainingMultidisciplinaryMonophenol MonooxygenaseAnimal ModelsSpecimen preparation and treatmentCell biologyEnzymesmedicine.anatomical_structureExperimental Organism SystemsModels AnimalFemaleAnatomyResearch ArticleGenetically modified mouseImaging TechniquesTransgeneOcular AnatomyMice TransgenicMouse ModelsBiologyResearch and Analysis MethodsRetinaRecombinases03 medical and health sciencesModel OrganismsOcular SystemFluorescence ImagingmedicineGeneticsAnimalsEnhancerGene knockoutRetinaRetinal pigment epitheliumIntegraseslcsh:REmbryosDAPI stainingBiology and Life SciencesProteinsmedicine.diseaseeye diseasesMice Inbred C57BLLuminescent Proteins030104 developmental biologyNuclear stainingEnzymologyAnimal StudiesEyeslcsh:Qsense organsHead030217 neurology & neurosurgeryDevelopmental BiologyPloS one
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Root Canal Morphology of 116 Maxillary Second Premolars by Micro–Computed Tomography in a Mixed Swiss-German Population with Systematic Review

2020

Abstract Introduction The aim of this investigation was to examine the root canal system morphology of maxillary second premolars (Mx2Ps) of a Swiss-German population by means of micro–computed tomography and provide systematic review of the root canal configuration (RCC) literature of Mx2Ps. Methods The RCC, main foramina as well as accessory canals and foramina frequency of 116 Mx2Ps, were investigated by means of micro–computed tomography and 3-dimensional software imaging. The RCC from the coronal to apical thirds of the root as well as the main foramina number were described by using a four-digit system code. The literature review follows the PRISMA guideline analyzing randomized contr…

0301 basic medicineRoot canalPopulationurologic and male genital diseases03 medical and health sciences0302 clinical medicineMaxillaForamenHumansMedicineBicuspidTooth RooteducationGeneral DentistryOrthodonticseducation.field_of_studySystem codebusiness.industryMicro computed tomographyX-Ray Microtomography030206 dentistryRoot canal morphologyCross-Sectional Studies030104 developmental biologymedicine.anatomical_structureCoronal planeDental Pulp CavitybusinessMaxillary second premolarSwitzerlandJournal of Endodontics
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Brain size and limits to adult neurogenesis

2015

The walls of the cerebral ventricles in the developing embryo harbor the primary neural stem cells from which most neurons and glia derive. In many vertebrates, neurogenesis continues postnatally and into adulthood in this region. Adult neurogenesis at the ventricle has been most extensively studied in organisms with small brains, such as reptiles, birds, and rodents. In reptiles and birds, these progenitor cells give rise to young neurons that migrate into many regions of the forebrain. Neurogenesis in adult rodents is also relatively widespread along the lateral ventricles, but migration is largely restricted to the rostral migratory stream into the olfactory bulb. Recent work indicates t…

0301 basic medicineRostral migratory streamGeneral NeuroscienceNeurogenesisBiologyNeural stem cellOlfactory bulb03 medical and health sciencesLateral ventricles030104 developmental biology0302 clinical medicinenervous systemBrain sizeForebrainProgenitor cellNeuroscience030217 neurology & neurosurgeryJournal of Comparative Neurology
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Nuclear inclusions of pathogenic ataxin-1 induce oxidative stress and perturb the protein synthesis machinery

2020

Spinocerebellar ataxia type-1 (SCA1) is caused by an abnormally expanded polyglutamine (polyQ) tract in ataxin-1. These expansions are responsible for protein misfolding and self-assembly into intranuclear inclusion bodies (IIBs) that are somehow linked to neuronal death. However, owing to lack of a suitable cellular model, the downstream consequences of IIB formation are yet to be resolved. Here, we describe a nuclear protein aggregation model of pathogenic human ataxin-1 and characterize IIB effects. Using an inducible Sleeping Beauty transposon system, we overexpressed the ATXN1(Q82) gene in human mesenchymal stem cells that are resistant to the early cytotoxic effects caused by the expr…

0301 basic medicineSCA1 Spinocerebellar ataxia type-1Intranuclear Inclusion BodiesClinical BiochemistryMSC mesenchymal stem cellProtein aggregationBiochemistry0302 clinical medicineMutant proteinProtein biosynthesisDE differentially expressed genesNuclear proteinlcsh:QH301-705.5FTIR Fourier-transform infrared spectroscopyAtaxin-1lcsh:R5-920biologyChemistryNuclear ProteinspolyQ polyglutamineRibosomeCell biologySB Sleeping BeautyRibosome ; Polyglutamine ; Ataxin-1 ; Oxidative stress ; Transposon ; Sleeping beauty transposon ; Protein networkSpinocerebellar ataxiaProtein foldingCellular modelFunction and Dysfunction of the Nervous Systemlcsh:Medicine (General)Research PaperiPSC induced pluripotent stem cellAtaxin 1Nerve Tissue ProteinsPPI protein-protein interaction03 medical and health sciencesROS reactive oxygen speciesProtein networkSleeping beauty transposonGSEA Gene Set Enrichment AnalysismedicineHumansNPC neural progenitor cellOrganic Chemistrymedicine.diseaseAFM atomic force microscopyOxidative Stress030104 developmental biologylcsh:Biology (General)IIBs intranuclear inclusion bodiesMS mass spectrometryCardiovascular and Metabolic Diseasesbiology.proteinPolyglutamine030217 neurology & neurosurgery
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Programming of Intestinal Epithelial Differentiation by IL-33 Derived from Pericryptal Fibroblasts in Response to Systemic Infection.

2016

SummaryThe intestinal epithelium constitutes an efficient barrier against the microbial flora. Here, we demonstrate an unexpected function of IL-33 as a regulator of epithelial barrier functions. Mice lacking IL-33 showed decreased Paneth cell numbers and lethal systemic infection in response to Salmonella typhimurium. IL-33 was produced upon microbial challenge by a distinct population of pericryptal fibroblasts neighboring the intestinal stem cell niche. IL-33 programmed the differentiation of epithelial progenitors toward secretory IEC including Paneth and goblet cells. Finally, IL-33 suppressed Notch signaling in epithelial cells and induced expression of transcription factors governing…

0301 basic medicineSalmonella typhimuriumCellular differentiationPopulationNotch signaling pathwayMice TransgenicBiologydigestive systemGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineIntestine SmallmedicineAnimalsHumansCell LineageProgenitor cellIntestinal Mucosaeducationlcsh:QH301-705.5Cell Proliferationeducation.field_of_studySalmonella Infections AnimalReceptors NotchCell growthCell DifferentiationEpithelial CellsFibroblastsInterleukin-33Intestinal epitheliumInterleukin-1 Receptor-Like 1 ProteinCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)Organ SpecificityImmunologyPaneth cellSignal transduction030215 immunologySignal TransductionCell reports
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