Search results for "Permeability"

showing 10 items of 596 documents

Evaluation of positron-emission-tomography for visualisation of migration processes in geomaterials

2008

Abstract Positron-emission-tomography (PET) was applied for direct visualisation of solute transport in order to overcome the limitations of conventional methods for measuring advection and diffusion properties. At intervals from minutes to days the 3D-spatial distribution of the PET-tracer is determined. This spatiotemporal evolution of the tracer concentration can be used as experimental basis for clarification of the relevant transport processes, derivation of transport parameters, and model calibration. Here, 18 F and 124 I in 0.01 M carrier solution of KF and KI, respectively, have been chosen out of the limited number of available PET-tracers, primarily on account of their decay time …

Pressure dropPermeability (earth sciences)GeophysicsGeochemistry and PetrologyAdvectionChemistryAnalytical chemistryFracture (geology)Fluid dynamicsMechanicsDiffusion (business)Matrix (geology)Volumetric flow ratePhysics and Chemistry of the Earth, Parts A/B/C
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Novel path to apoptosis: small transmembrane pores created by staphylococcal alpha-toxin in T lymphocytes evoke internucleosomal DNA degradation.

1994

Peripheral-blood human T lymphocytes were treated with Staphylococcus aureus alpha-toxin. Membrane permeabilization was assessed by measuring efflux of K+ and Rb+ and influx of Na+, Ca2+, and propidium iodide. Cellular ATP and [3H]thymidine incorporation following lectin stimulation were measured as parameters for cell viability. Internucleosomal cleavage characteristic of programmed cell death was assessed by agarose gel electrophoresis and by quantifying low-molecular-weight, [3H]thymidine-labeled DNA fragments. Nanomolar concentrations of alpha-toxin evoked protracted, irreversible ATP depletion in both activated and resting T lymphocytes. Toxin-damaged cells also lost their ability to i…

Programmed cell deathCell Membrane PermeabilityStaphylococcusT-LymphocytesImmunologyBacterial ToxinsApoptosisBiologyMicrobiologychemistry.chemical_compoundHemolysin ProteinsAdenosine TriphosphateHumansPropidium iodideViability assaySodiumT lymphocyteDNANucleosomesInfectious DiseaseschemistryBiochemistryApoptosisAgarose gel electrophoresisBiophysicsPotassiumParasitologyCalciumThymidineAdenosine triphosphateResearch Article
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Nuclear Translocation of Nuclear Transcription Factor-κB by α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid Receptors Leads to Transcription of …

2003

We describe a new molecular mechanism of cell death by excitotoxicity mediated through nuclear transcription factor κB (NFκB) in rat embryonic cultures of dopaminergic neurons. Treatment of mesencephalic cultures with α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) resulted in a number of changes that occurred selectively in dopaminergic neurons, including persistent elevation in intracellular Ca2+ monitored with Fura-2, and a significant increase in intramitochondrial oxidation of dihydrorhodamine 123, probably associated with transient increase of mitochondrial permeability, cytochrome c release, nuclear translocation of NFκB, and transcriptional activation of the oncogenep53.…

Programmed cell deathCell Membrane PermeabilityTime FactorsCIENCIAS MÉDICAS Y DE LA SALUDTranscription GeneticNeuriteActive Transport Cell NucleusInmunologíaExcitotoxicitymedicine.disease_causeCELL DEATHReceptors DopamineRats Sprague-DawleymedicineAnimalsReceptors AMPAalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidTranscription factorPARKINSON DISEASECaspaseNeuronsPharmacologyCell DeathNUCLEAR TRANSCRIPTIONbiologyDopaminergicNF-kappa BNFKB1Molecular biologyMitochondriaRatsCell biologyMedicina Básicabiology.proteinMolecular MedicineCalciumFemaleTumor Suppressor Protein p53Signal transductionMolecular Pharmacology
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Cytocidal effects of Escherichia coli hemolysin on human T lymphocytes.

1993

Escherichia coli hemolysin is the prototype of a large family of pore-forming toxins produced by gram-negative organisms. Besides its known cytotoxic activities against granulocytes, monocytes, endothelial cells, and renal epithelial cells, we now demonstrate that the toxin potently kills human T lymphocytes. Evidence based on different and independent approaches indicates that lymphocidal activity is due to formation of transmembrane pores. Additionally, cells prestimulated with phytohemagglutinin respond to low doses of E. coli hemolysin with DNA fragmentation similar to that observed in cells undergoing programmed cell death. Kinetic considerations lead us to conclude that DNA degradatio…

Programmed cell deathCell Membrane PermeabilityTime FactorsDNA damageT-LymphocytesImmunologyBiologyIn Vitro Techniquesmedicine.disease_causeHemolysin ProteinsLymphocyte ActivationMicrobiologyMicrobiologyHemolysin ProteinsAdenosine TriphosphatemedicineEscherichia coliCytotoxic T cellHumansEscherichia coliCell DeathDose-Response Relationship DrugHemolysinT lymphocyteDNAInfectious DiseasesDNA fragmentationParasitologyResearch ArticleDNA Damage
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GD3 ganglioside directly targets mitochondria in a bcl-2-controlled fashion.

2000

Lipid and glycolipid diffusible mediators are involved in the intracellular progression and amplification of apoptotic signals. GD3 ganglioside is rapidly synthesized from accumulated ceramide after the clustering of death-inducing receptors and triggers apoptosis. Here we show that GD3 induces dissipation of DeltaPsim and swelling of isolated mitochondria, which results in the mitochondrial release of cytochrome c, apoptosis inducing factor, and caspase 9. Soluble factors released from GD3-treated mitochondria are sufficient to trigger DNA fragmentation in isolated nuclei. All these effects can be blocked by cyclosporin A, suggesting that GD3 is acting at the level of the permeability tran…

Programmed cell deathCeramideApoptosisMitochondria LiverMitochondrionliverBiochemistryMembrane Potentialschemistry.chemical_compoundGangliosidesGeneticsAnimalsMolecular BiologySettore MED/04 - Patologia GeneralebiologyCytochrome cCaspase 9SialyltransferasesCell biologyRatsmitochondriaEnzyme ActivationchemistryMitochondrial permeability transition poreProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinCyclosporinecaspases; cyclosporine; proto-oncogene proteins c-bcl-2; sialyltransferases; caspase 9; rats; animals; enzyme activation; apoptosis; membrane potentials; gangliosides; mitochondria liver; subcellular fractionsApoptosis-inducing factorlipids (amino acids peptides and proteins)ApoptosomeBiotechnologySubcellular FractionsFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Characterization of cells with different mitochondrial membrane potential during apoptosis.

2005

Background Until now, the simultaneous analysis of several parameters during apoptosis, including DNA content and mitochondrial membrane potential (ΔΨ), has not been possible because of the spectral characteristics of the commonly used dyes. Using polychromatic flow cytometry based upon multiple laser and UV lamp excitation, we have characterized cells with different ΔΨ during apoptosis. Methods U937 cells were treated with the flavonoid quercetin (Qu) and stained with JC-1 to detect ΔΨ, propidium iodide (PI) for cell viability, Hoechst 33342 for DNA content, Annexin V conjugated with Alexa Fluor-647 for detection of phosphatidilserine (PS) exposure, marker of early apoptosis, or Mitotracke…

Programmed cell deathHistologyCell Membrane PermeabilityCell Survivalpolychromatic flow cytometry • mitochondrial membrane potential • apoptosis • JC-1 • propidium iodide • Hoechst • Annexin-VPopulationApoptosisHL-60 CellsDNA FragmentationPhosphatidylserinesBiologyPathology and Forensic MedicineFlow cytometryMembrane Potentialschemistry.chemical_compoundAnnexinCell Line TumormedicineHumansViability assayPropidium iodideeducationFluorescent Dyeseducation.field_of_studymedicine.diagnostic_testDaunorubicinCell BiologyDNAIntracellular MembranesU937 CellsCarbocyaninesFlow CytometryMolecular biologyMitochondriachemistryApoptosisCell cultureDoxorubicinLeukocytes MononuclearBenzimidazolesQuercetinCytometry. Part A : the journal of the International Society for Analytical Cytology
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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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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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Interferons increase cell resistance to Staphylococcal alpha-toxin.

2007

ABSTRACTMany bacterial pathogens, includingStaphylococcus aureus, use a variety of pore-forming toxins as important virulence factors. Staphylococcal alpha-toxin, a prototype β-barrel pore-forming toxin, triggers the release of proinflammatory mediators and induces primarily necrotic death in susceptible cells. However, whether host factors released in response to staphylococcal infections may increase cell resistance to alpha-toxin is not known. Here we show that prior exposure to interferons (IFNs) prevents alpha-toxin-induced membrane permeabilization, the depletion of ATP, and cell death. Moreover, pretreatment with IFN-α decreases alpha-toxin-induced secretion of interleukin 1β (IL-1β)…

Programmed cell deathStaphylococcus aureusCell Membrane Permeabilitymedicine.medical_treatmentImmunologyBacterial ToxinsInterleukin-1betaBiologyStaphylococcal infectionsMicrobiologyProinflammatory cytokineMicrobiologyCell LineHemolysin ProteinsAdenosine TriphosphateInterferonmedicineHumansSecretionCell DeathKinaseEpithelial CellsBacterial Infectionsmedicine.diseaseInfectious DiseasesCytokineProtein BiosynthesisParasitologyTumor necrosis factor alphaInterferonsFatty Acid Synthasesmedicine.drugInfection and immunity
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Highlighting Curcumin-Induced Crosstalk between Autophagy and Apoptosis as Supported by Its Specific Subcellular Localization

2020

Curcumin, a major active component of turmeric (Curcuma longa, L.), is known to have various effects on both healthy and cancerous tissues. In vitro studies suggest that curcumin inhibits cancer cell growth by activating apoptosis, but the mechanism underlying the anticancer effect of curcumin is still unclear. Since there is a recent consensus about endoplasmic reticulum (ER) stress being involved in the cytotoxicity of natural compounds, we have investigated using Image flow cytometry the mechanistic aspects of curcumin&rsquo

Programmed cell deathautophagyCell Membrane PermeabilityCurcumin[SDV]Life Sciences [q-bio][SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Article03 medical and health scienceschemistry.chemical_compound0302 clinical medicineLysosomeCell Line TumorxCELLigencemedicine[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Humanscancerlcsh:QH301-705.5030304 developmental biologyreal-time cellular impedanceCell Nucleus0303 health sciencescalciumEndoplasmic reticulumAutophagyapoptosisROSGeneral Medicine3. Good healthCell biologyMitochondriaendoplasmic reticulummedicine.anatomical_structurecell deathchemistrylcsh:Biology (General)Apoptosis030220 oncology & carcinogenesisCancer cellCurcuminUnfolded protein responseUnfolded Protein ResponselysosomeLysosomes[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologySubcellular Fractions
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