Search results for "Microscopy"

showing 10 items of 3390 documents

Silver nanoparticles stabilized by a polyaminocyclodextrin as catalysts for the reduction of nitroaromatic compounds

2015

Abstract Silver nanoparticles stabilized by means of poly -(6- N , N -dimethyl-propylenediamino)-(6-deoxy)-β-cyclodextrin were synthesized, characterized by different techniques (UV–vis spectroscopy, Dynamic Light Scattering, High Resolution Transmission Electron Microscopy, Fourier-transform IR Spectroscopy) and used as catalysts for the reduction of various nitrobenzene derivatives with sodium borohydride. The nanocomposites obtained appear to have an organized structure, with a metal core surrounded by a layer-structured coating shell. Kinetic data, rationalized in terms of a modified Langmuir–Hinshelwood model, evidenced a non-linear dependence of the reaction rate on the concentration …

Process Chemistry and TechnologyInduction periodInorganic chemistryInfrared spectroscopySettore CHIM/06 - Chimica OrganicaCatalysisSilver nanoparticleCatalysisReaction rateSodium borohydridechemistry.chemical_compoundDynamic light scatteringchemistryPolyaminocyclodextrin Nitroarene reduction Silver nanocompositePhysical and Theoretical ChemistryHigh-resolution transmission electron microscopyJournal of Molecular Catalysis A: Chemical
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Pro-inflammatory T helper 17 directly harms oligodendrocytes in neuroinflammation.

2021

Significance Multiple sclerosis (MS) is a neuroinflammatory, demyelinating disease that represents one of the most frequent causes of irreversible disability in young adults. Treatment options to halt disability are limited. We discovered that T helper (Th)17 cells in contact with oligodendrocytes produce higher levels of glutamate and induce significantly greater oligodendrocyte damage than their Th2 counterpart. Blockade of CD29, which is linked to glutamate release pathways and expressed in high levels on Th17 cells, preserved human oligodendrocyte processes from Th17-mediated injury. Our data thus provide evidence for the direct and deleterious attack of Th17 cells on the myelin compart…

Programmed cell deathEncephalomyelitis Autoimmune ExperimentalCentral nervous systemFreund's AdjuvantoligodendrocytesMice Transgenicglutamate03 medical and health sciencesMyelinMice0302 clinical medicineImmunology and Inflammationintravital microscopymedicineAnimalsNeuroinflammation030304 developmental biologyInflammationMice Knockout0303 health sciencesMultidisciplinaryChemistryMultiple sclerosisGlutamate receptorMembrane ProteinsCD29Biological SciencesCD29 blockademedicine.disease420Oligodendrocyte3. Good healthCell biologyDNA-Binding ProteinsMice Inbred C57BLOligodendrogliamedicine.anatomical_structurePertussis ToxinTh17 CellsMyelin-Oligodendrocyte Glycoprotein030217 neurology & neurosurgeryProceedings of the National Academy of Sciences of the United States of America
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Caspase-dependent apoptosis during infection with Cryptosporidium parvum

1999

The protozoan parasite Cryptosporidium parvum causes persistent diarrhea and malnutrition in children and the diarrhea-wasting syndrome in AIDS. No therapy exists for eliminating the parasite in the absence of a healthy immune response. Although it had been reported that infection of intestinal cell lines with C. parvum leads to host cell death, the mechanisms of cytolysis have not been characterized. We show here that infection with C. parvum leads to typical apoptotic nuclear condensation and DNA fragmentation in host cells. Both nuclear condensation and DNA fragmentation are inhibited by a caspase inhibitor, showing that caspases are involved in this type of apoptosis. Finally, blocking …

Programmed cell deathImmunologyCryptosporidiosisApoptosisDNA FragmentationCysteine Proteinase InhibitorsMicrobiologyCaspase-Dependent ApoptosisAmino Acid Chloromethyl KetonesCell LineImmune systemparasitic diseasesAnimalsHumansComputingMilieux_MISCELLANEOUSCaspaseCryptosporidium parvumbiologybiology.organism_classificationCaspase InhibitorsVirologyCytolysisPOUVOIR PATHOGENE[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyInfectious DiseasesCryptosporidium parvumMicroscopy FluorescenceApoptosisCaspasesbiology.proteinDNA fragmentationHeLa CellsMicrobes and Infection
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Cytotoxicity and induction of DNA double-strand breaks by components leached from dental composites in primary human gingival fibroblasts

2012

Abstract Introduction The public interest steadily increases in the biological adverse effects caused by components released from resin-based dental restorations. Objective In this study, the cytotoxicity and the genotoxicity were investigated of following released components from dental resin restorations in human gingival fibroblasts (HGF): tetraethyleneglycol dimethacrylate (TEEGDMA), neopentylglycol dimethacrylate (Neopen), diphenyliodoniumchloride (DPIC), triphenyl-stibane (TPSB) and triphenylphosphane (TPP). Methods XTT based cell viability assay was used for cytotoxicity screening of substances. γ-H2AX assay was used for genotoxicity screening. In the γ-H2AX assay, HGFs were exposed …

Programmed cell deathMaterials scienceNecrosisCell SurvivalCell Culture TechniquesGingivaTetrazolium SaltsApoptosismedicine.disease_causeComposite ResinsCell LinePolyethylene GlycolsHistonesDental MaterialsNecrosisOnium CompoundsOrganophosphorus CompoundsPolymethacrylic AcidsMaterials TestingStilbenesmedicineHumansDNA Breaks Double-StrandedGeneral Materials ScienceViability assayCytotoxicityGeneral DentistryDose-Response Relationship DrugBiphenyl CompoundsFibroblastsMolecular biologyBiphenyl compoundMicroscopy FluorescenceMechanics of MaterialsApoptosisToxicityMethacrylatesIndicators and Reagentsmedicine.symptomGenotoxicityMutagensDental Materials
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Induction of oxiapoptophagy, a mixed mode of cell death associated with oxidative stress, apoptosis and autophagy, on 7-ketocholesterol-treated 158N …

2013

7-Ketocholesterol (7KC) has been suggested to induce a complex mode of cell death on monocytic cells: oxiapoptophagy (OXIdation, APOPTOsis, and autoPHAGY) (Monier et al. (2003) [12]). The aim of the present study, realized on 158N murine oligodendrocytes, was to bring new evidence on this mixed form of cell death. On 158N cells, 7KC induces an overproduction of reactive oxygen species (ROS) revealed by dihydroethidium staining, a loss of transmembrane mitochondrial potential measured with DiOC6(3), caspase-3 activation, and condensation and/or fragmentation of the nuclei which are typical criteria of oxidative stress and apoptosis. Moreover, 7KC enhances cytoplamic membrane permeability to …

Programmed cell deathMembrane permeabilityalpha-TocopherolBiophysicsApoptosisBiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundMicemedicineAutophagyAnimalsMicroscopy Phase-ContrastPropidium iodideFragmentation (cell biology)Molecular BiologyKetocholesterolsCells Culturedchemistry.chemical_classificationReactive oxygen speciesCell DeathDose-Response Relationship DrugAutophagyCell BiologyCell biologyOligodendrogliaOxidative StresschemistryApoptosisMicrotubule-Associated ProteinsOxidative stressBiochemical and biophysical research communications
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In vivo real-time imaging of the liver with confocal endomicroscopy permits visualization of the temporospatial patterns of hepatocyte apoptosis.

2011

Apoptosis is a dynamic process of programmed cell death and is involved in multiple diseases. However, its mechanisms and sequence of events are still incompletely understood, partly because of the inability to visualize single cells continuously in vivo. The aim of the present study was to monitor hepatocyte apoptosis with confocal endomicroscopy in living rodents. In 73 anaesthetized mice, apoptotic liver injury was induced by injection of the CD95-agonistic antibody Jo2. Individual hepatocytes were followed for up to 240 min with a handheld confocal probe (FIVE1; Optiscan) providing 0.7 μm resolution (1,000-fold magnification). Different fluorescence staining protocols were used for cell…

Programmed cell deathMicroscopy ConfocalHepatologyPhysiologyConfocalGastroenterologyReal time imagingApoptosisEndoscopyBiologyCell biologylaw.inventionMiceLiverIn vivoApoptosisConfocal microscopylawPhysiology (medical)EndomicroscopyHepatocytesAnimalsHepatocyte apoptosisAmerican journal of physiology. Gastrointestinal and liver physiology
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Phospholipidosis and down-regulation of the PI3-K/PDK-1/Akt signalling pathway are vitamin E inhibitable events associated with 7-ketocholesterol-ind…

2007

International audience; Among the oxysterols accumulating in atherosclerotic plaque, 7-ketocholesterol (7KC) is a potent apoptotic inducer, which favours myelin figure formation and polar lipid accumulation. This investigation performed on U937 cells consisted in characterizing the myelin figure formation process; determining the effects of 7KC on the PI3-K/PDK-1/Akt signalling pathway; evaluating the activities of vitamin E (Vit-E) (α-tocopherol) on the formation of myelin figures and the PI3-K/PDK-1/Akt signalling pathway and assessing the effects of PI3-K inhibitors (LY-294002, 3-methyladenine) on the activity of Vit-E on cell death and polar lipid accumulation. The ultrastructural and b…

Programmed cell deathOxysterolEndocrinology Diabetes and MetabolismClinical BiochemistryDown-RegulationApoptosisPyrimidinones[SDV.BC]Life Sciences [q-bio]/Cellular BiologyProtein Serine-Threonine KinasesBiochemistryDephosphorylationPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineMicroscopy Electron TransmissionOxazinesHumansVitamin EKetocholesterolsMolecular BiologyProtein kinase BPhospholipids030304 developmental biologyPhospholipidosis0303 health sciencesNutrition and DieteticsPhosphoinositide 3-kinasebiologyChemistryPyruvate Dehydrogenase Acetyl-Transferring KinaseU937 CellsProtein phosphatase 2Cell biology030220 oncology & carcinogenesisbiology.proteinBenzimidazolesSignal transductionProto-Oncogene Proteins c-aktSignal TransductionThe Journal of Nutritional Biochemistry
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Studies on the subcellular pathophysiology of acute lethal cell injury.

1974

Summary In this paper we have summarized the effects of acute lethal injury on the cell. Such injuries are defined as injuries that result in cell death within a relatively short period of time usually minutes or hours. Following death; the cell undergoes necrosis. Ultrastructural and biochemical methods are needed to study pathophysiology. The cell passes through a series of stages numbered 1 through 7. Stages 1 through 4 are reversible while 5 through 7 are irreversible. Injuries resulting in acute cell death and necrosis include direct damage to the cell membrane, for example by antibody and complement or non-penetrating mercurials or interference with mitochondrial energy supply as in i…

Programmed cell deathPathologymedicine.medical_specialtyNecrosisTime FactorsCell SurvivalCellsCellIschemiaMitochondrionBiologyPermeabilityPathology and Forensic MedicineCell Physiological PhenomenaCell membraneKidney Tubules Proximal03 medical and health sciencesNecrosis0302 clinical medicineIschemiamedicineAnimalsHypoxia030304 developmental biology0303 health sciencesCell MembraneGeneral MedicineHypoxia (medical)medicine.diseasePathophysiology3. Good healthMitochondriaRatsMicroscopy Electronmedicine.anatomical_structuremedicine.symptomMitochondrial Swelling030217 neurology & neurosurgeryBeitrage zur Pathologie
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µ-Calpain conversion of antiapoptotic Bfl-1 (BCL2A1) into a prodeath factor reveals two distinct alpha-helices inducing mitochondria-mediated apoptos…

2011

Anti-apoptotic Bfl-1 and pro-apoptotic Bax, two members of the Bcl-2 family sharing a similar structural fold, are classically viewed as antagonist regulators of apoptosis. However, both proteins were reported to be death inducers following cleavage by the cysteine protease µ-calpain. Here we demonstrate that calpain-mediated cleavage of full-length Bfl-1 induces the release of C-terminal membrane active α-helices that are responsible for its conversion into a pro-apoptotic factor. A careful comparison of the different membrane-active regions present in the Bfl-1 truncated fragments with homologous domains of Bax show that helix α5, but not α6, of Bfl-1 induces cell death and cytochrome c r…

Programmed cell deathProtein StructureCancer Treatmentlcsh:MedicineApoptosisMitochondrionCleavage (embryo)BiochemistryProtein Structure SecondaryMinor Histocompatibility AntigensMiceCell Line TumorMolecular Cell BiologyAnimalsHumanslcsh:ScienceProtein InteractionsBiologyMultidisciplinaryMicroscopy ConfocalbiologyCell DeathCalpainCytochrome clcsh:RCytochromes cProteinsCalpainCysteine proteaseCell biologyMitochondriaProto-Oncogene Proteins c-bcl-2OncologyApoptosisbiology.proteinMedicinelcsh:QElectrophoresis Polyacrylamide GelGlobular ProteinsBCL2-related protein A1Research ArticlePloS one
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A new technique for real-time analysis of caspase-3 dependent neuronal cell death

2007

Several markers are available to identify cells undergoing programmed cell death, but so far they are only applicable on fixed material. Therefore, no information on the kinetics of apoptosis can be obtained, although apoptosis is a dynamic cell process. Here, we describe a new technique that allows the real-time observation of the onset of apoptosis in primary neurons. Neurons are transfected with a plasmid that codes for a fluorescent protein localized in the soma. Upon activation of caspase-3, which represents the point-of-no-return in the apoptosis process, the fusion protein is cleaved and as a consequence translocates into the nucleus. The onset of apoptosis is thus visualized by tran…

Programmed cell deathRecombinant Fusion ProteinsCellApoptosisCaspase 3BiologyMiceComputer SystemsmedicineAnimalsCells CulturedNeuronsMice Inbred BALB CTUNEL assayStaining and LabelingCaspase 3General NeuroscienceImage EnhancementFusion proteinCell biologymedicine.anatomical_structureAnimals NewbornMicroscopy FluorescenceApoptosisSomaNucleusJournal of Neuroscience Methods
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