Search results for "ATR"

showing 10 items of 21758 documents

Cardiac Glycoside Glucoevatromonoside Induces Cancer Type-Specific Cell Death.

2018

Cardiac glycosides (CGs) are natural compounds used traditionally to treat congestive heart diseases. Recent investigations repositioned CGs as potential anticancer agents. To discover novel cytotoxic CG scaffolds, we selected the cardenolide glucoevatromonoside (GEV) out of 46 CGs for its low nanomolar anti-lung cancer activity. GEV presented reduced toxicity toward non-cancerous cell types (lung MRC-5 and PBMC) and high-affinity binding to the Na+/K+-ATPase α subunit, assessed by computational docking. GEV-induced cell death was caspase-independent, as investigated by a multiparametric approach, and culminates in severe morphological alterations in A549 cells, monitored by transmission el…

0301 basic medicineCell typeProgrammed cell deathNecroptosis03 medical and health sciences0302 clinical medicineglucoevatromonosideCytotoxic T cellPharmacology (medical)non-canonical cell deathOriginal ResearchA549 cellPharmacologyU937 cellbiologyChemistrylcsh:RM1-950apoptosisCalpaincardiac glycoside3. Good healthlung cancer030104 developmental biologylcsh:Therapeutics. PharmacologyApoptosis030220 oncology & carcinogenesisCancer researchbiology.proteinFrontiers in pharmacology
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Resveratrol-Induced Temporal Variation in the Mechanical Properties of MCF-7 Breast Cancer Cells Investigated by Atomic Force Microscopy

2019

Atomic force microscopy (AFM) combined with fluorescence microscopy has been used to quantify cytomechanical modifications induced by resveratrol (at a fixed concentration of 50 &micro

0301 basic medicineCellMotilityBreast Neoplasmsforce spectroscopyResveratrolresveratrolMicroscopy Atomic Forcefluorescence microscopyCatalysisArticleInorganic Chemistrylcsh:Chemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicinebreast cancerCell MovementElastic ModulusmedicineFluorescence microscopeCell AdhesionHumansPhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5SpectroscopyMechanical Phenomenaatomic force microscopyChemistryOrganic ChemistryForce spectroscopytechnology industry and agricultureGeneral MedicineAdhesioncytomechanicsComputer Science Applications030104 developmental biologymedicine.anatomical_structureMCF-7lcsh:Biology (General)lcsh:QD1-999030220 oncology & carcinogenesisCancer cellBiophysicsMCF-7 CellsFemaleMCF-7International Journal of Molecular Sciences
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CRISPR-Cas9 screen reveals a MYCN-amplified neuroblastoma dependency on EZH2.

2018

Pharmacologically difficult targets, such as MYC transcription factors, represent a major challenge in cancer therapy. For the childhood cancer neuroblastoma, amplification of the oncogene MYCN is associated with high-risk disease and poor prognosis. Here, we deployed genome-scale CRISPR-Cas9 screening of MYCN-amplified neuroblastoma and found a preferential dependency on genes encoding the polycomb repressive complex 2 (PRC2) components EZH2, EED, and SUZ12. Genetic and pharmacological suppression of EZH2 inhibited neuroblastoma growth in vitro and in vivo. Moreover, compared with neuroblastomas without MYCN amplification, MYCN-amplified neuroblastomas expressed higher levels of EZH2. ChIP…

0301 basic medicineCellular differentiationMedical and Health SciencesNeuroblastomaSUZ12Oncogene MYCNCRISPR-Cas SystemCancerPediatricNeuronsN-Myc Proto-Oncogene ProteinTumorEZH2EpigeneticCell DifferentiationGeneral MedicineUp-RegulationGene Expression Regulation NeoplasticOncology5.1 PharmaceuticalsEpigeneticsDevelopment of treatments and therapeutic interventionsHumanResearch ArticlePediatric Research InitiativePediatric CancerImmunologymacromolecular substancesBiologyN-Myc Proto-Oncogene ProteinCell Line03 medical and health sciencesRare DiseasesNeuroblastomaCell Line TumormedicineGeneticsHumansEnhancer of Zeste Homolog 2 ProteinTranscription factorneoplasmsNeoplasticHuman GenomeNeurosciencesGene AmplificationNeuronmedicine.disease030104 developmental biologyGene Expression RegulationCancer researchHistone deacetylaseCRISPR-Cas SystemsThe Journal of clinical investigation
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Differentiation and characterization of rat adipose tissue mesenchymal stem cells into endothelial-like cells

2018

In this study, mesenchymal stem cells were isolated from rat adipose tissue (AD-MSCs) to characterize and differentiate them into endothelial-like cells. AD-MSCs were isolated by mechanical and enzymatic treatments, and their identity was verified by colony-forming units (CFU) test and by differentiation into cells of mesodermal lineages. The endothelial differentiation was induced by plating another aliquot of cells in EGM-2 medium, enriched with specific endothelial growth factors. Five subcultures were performed. The expression of stemness genes (OCT4, SOX2 and NANOG) was investigated. The presence of CD90 and the absence of the CD45 were evaluated by flow cytometry. The endothelial-like…

0301 basic medicineCellular differentiationSettore VET/09 - Clinica Chirurgica VeterinariaSettore BIO/13 - Biologia Applicataimmunophenotypical analysiCell DifferentiationNanog Homeobox ProteinGeneral MedicineCadherinsFlow CytometryUp-RegulationPlatelet Endothelial Cell Adhesion Molecule-1Endothelial stem cellDrug CombinationsAdipose Tissueembryonic structuresVeterinary (all)ProteoglycansCollagenStem cellHomeobox protein NANOGadipose-derived mesenchymal stem cellDown-RegulationCD146 AntigenBiology03 medical and health sciencesMatrigel assaySOX2Antigens CDAdipose-derived mesenchymal stem cellsAnimalsEndothelial cells differentiationRats WistarImmunophenotypical analysisMatrigelGeneral VeterinaryGene Expression ProfilingSOXB1 Transcription FactorsMesenchymal stem cellEndothelial CellsMesenchymal Stem Cells3T3-L1Molecular biologyAdipose-derived mesenchymal stem cells; Endothelial cells differentiation; Gene expression; Immunophenotypical analysis; Matrigel assay; Rat; Veterinary (all)Culture MediaRats030104 developmental biologyadipose-derived mesenchymal stem cells; endothelial cells differentiation; gene expression; immunophenotypical analysis; matrigel assay; ratLeukocyte Common AntigensThy-1 AntigensRatLamininGene expressionOctamer Transcription Factor-3
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Fungal Infections of the Central Nervous System in Children.

2017

Although uncommon in children, fungal infections of the central nervous system can be devastating and difficult to treat. A better understanding of basic mycologic, immunologic, and pharmacologic processes has led to important advances in the diagnosis and management of these diseases, but their mortality rates remain unacceptably high. In this focused review, we examine the epidemiology and clinical features of the most common fungal pathogens of the central nervous system in children and explore recent advances in diagnosis and antifungal therapy.

0301 basic medicineCentral Nervous Systemmedicine.medical_specialtyAntifungal Agents030106 microbiologyCentral nervous systemAspergillosisHistoplasmosisBlastomycosis03 medical and health sciencesCentral Nervous System Fungal InfectionsEpidemiologymedicineAspergillosisHumansMucormycosisIntensive care medicineChildHistoplasmosisCoccidioidomycosisbusiness.industryMortality rateMucormycosisCandidiasisFungiGeneral MedicineCryptococcosismedicine.diseaseInfectious Diseasesmedicine.anatomical_structurePediatrics Perinatology and Child HealthCryptococcosisbusinessBlastomycosisJournal of the Pediatric Infectious Diseases Society
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Molecular Mechanism Involved in the Pathogenesis of Early-Onset Epileptic Encephalopathy

2019

Recent studies have shown that neurologic inflammation may both precipitate and sustain seizures, suggesting that inflammation may be involved not only in epileptogenesis but also in determining the drug-resistant profile. Extensive literature data during these last years have identified a number of inflammatory markers involved in these processes of “neuroimmunoinflammation” in epilepsy, with key roles for pro-inflammatory cytokines such as: IL-6, IL-17 and IL-17 Receptor (IL-17R) axis, Tumor-Necrosis-Factor Alpha (TNF-α) and Transforming-Growth-Factor Beta (TGF-β), all responsible for the induction of processes of blood-brain barrier (BBB) disruption and inflammation of the Central Nervou…

0301 basic medicineCentral nervous systemInflammationContext (language use)ReviewEpileptogenesisNOlcsh:RC321-571pathogenic mechanismsPathogenesis03 medical and health sciencesCellular and Molecular NeuroscienceEpilepsy0302 clinical medicineImmune systemMedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyPathologicalchildhoodbusiness.industrybiological markermedicine.diseaseepileptic encephalopathy030104 developmental biologymedicine.anatomical_structureinflammationmedicine.symptombusinessNeurosciencebiological markers030217 neurology & neurosurgeryNeurosciencebiological markers epileptic encephalopathy inflammation pathogenic mechanisms childhoodFrontiers in Molecular Neuroscience
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Overview of General and Discriminating Markers of Differential Microglia Phenotypes.

2020

Inflammatory processes and microglia activation accompany most of the pathophysiological diseases in the central nervous system. It is proven that glial pathology precedes and even drives the development of multiple neurodegenerative conditions. A growing number of studies point out the importance of microglia in brain development as well as in physiological functioning. These resident brain immune cells are divergent from the peripherally infiltrated macrophages, but their precise in situ discrimination is surprisingly difficult. Microglial heterogeneity in the brain is especially visible in their morphology and cell density in particular brain structures but also in the expression of cell…

0301 basic medicineCentral nervous systemInflammationReviewBiologylcsh:RC321-571M1/M2 phenotype03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineImmune systemneurotoxicitymedicineCytotoxic T celllcsh:Neurosciences. Biological psychiatry. NeuropsychiatrypolarizationMicrogliaRegeneration (biology)Neurotoxicityinfiltrating macrophagesmedicine.diseasePhenotype030104 developmental biologymedicine.anatomical_structureinflammationCellular Neuroscienceregenerationmicroglial heterogeneitymedicine.symptomNeuroscience030217 neurology & neurosurgeryFrontiers in cellular neuroscience
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NG2/CSPG4 and progranulin in the posttraumatic glial scar.

2018

Traumatic injury of the central nervous system is one of the leading causes of death and disability in young adults. Failure of regeneration is caused by autonomous neuronal obstacles and by formation of the glial scar, which is essential to seal the injury but also constitutes a barrier for regrowing axons. The scar center is highly inflammatory and populated by NG2+ glia, whereas astrocytes form the sealing border and trap regrowing axons, suggesting that the non-permissive environment of activated astrocytes and extracellular matrix components is one of the reasons for the regenerative failure. Particularly, secreted chondroitin-sulfate proteoglycans, CSPGs, of the lectican family hinder…

0301 basic medicineCentral nervous systemPerlecanCell CommunicationBiologyGlial scarExtracellular matrix03 medical and health scienceschemistry.chemical_compoundCicatrix0302 clinical medicineProgranulinsmedicineLecticanAnimalsHumansMolecular BiologyMicrogliaReceptors NotchMembrane ProteinsCell biology030104 developmental biologymedicine.anatomical_structurenervous systemchemistryChondroitin Sulfate ProteoglycansChondroitin sulfate proteoglycanBrain InjuriesImmunologybiology.proteinSynaptic signalingNeuroglia030217 neurology & neurosurgeryHeparan Sulfate ProteoglycansSignal TransductionMatrix biology : journal of the International Society for Matrix Biology
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Brain Distribution and Modulation of Neuronal Excitability by Indicaxanthin From Opuntia Ficus Indica Administered at Nutritionally-Relevant Amounts

2018

Several studies have recently investigated the role of nutraceuticals in complex pathophysiological processes such as oxidative damages, inflammatory conditions and excitotoxicity. In this regard, the effects of nutraceuticals on basic functions of neuronal cells, such as excitability, are still poorly investigated. For this reason, the possible modulation of neuronal excitability by phytochemicals (PhC) could represent an interesting field of research given that excitotoxicity phenomena are involved in neurodegenerative alterations leading, for example, to Alzheimer's disease. The present study was focused on indicaxanthin from Opuntia ficus indica, a bioactive betalain pigment, with a pro…

0301 basic medicineCerebellumAgingCognitive NeuroscienceExcitotoxicityHippocampusindicaxanthinBiologyHippocampal formationmedicine.disease_causeNeuroprotectionmicroiontophoresisbrain localizationlcsh:RC321-57103 medical and health scienceschemistry.chemical_compound0302 clinical medicineexcitabilitymedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal ResearchnutraceuticalselectrophysiologyCortex (botany)brain localization; electrophysiology; excitability; indicaxanthin; microiontophoresis; neuroprotection; nutraceuticals030104 developmental biologymedicine.anatomical_structurechemistrynervous systemmicroiontophoresineuroprotectionNeuronIndicaxanthinNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Aging Neuroscience
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The Role of Iron in Friedreich's Ataxia: Insights From Studies in Human Tissues and Cellular and Animal Models.

2019

Friedreich’s ataxia (FRDA) is a rare early-onset degenerative disease that affects both the central and peripheral nervous systems, and other extraneural tissues, mainly the heart and endocrine pancreas. This disorder progresses as a mixed sensory and cerebellar ataxia, primarily disturbing the proprioceptive pathways in the spinal cord, peripheral nerves and nuclei of the cerebellum. FRDA is an inherited disease with an autosomal recessive pattern caused by an insufficient amount of the nuclear-encoded mitochondrial protein frataxin, which is an essential and highly evolutionary conserved protein whose deficit results in iron metabolism dysregulation and mitochondrial dysfunction. The firs…

0301 basic medicineCerebellumAtaxiaFriedreich’s ataxiaReviewMitochondrionmedicine.disease_causelcsh:RC321-57103 medical and health sciencesiron0302 clinical medicineDegenerative diseasemedicineoxidative stresslcsh:Neurosciences. Biological psychiatry. Neuropsychiatrychemistry.chemical_classificationReactive oxygen speciesfrataxinbiologyCerebellar ataxialipid deregulationGeneral Neurosciencemedicine.diseaseanimal modelsCell biology030104 developmental biologymedicine.anatomical_structurechemistryFrataxinbiology.proteiniron chelatorsmedicine.symptom030217 neurology & neurosurgeryOxidative stressNeuroscienceFrontiers in neuroscience
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