Search results for "Blood Physiological Phenomena"

showing 7 items of 7 documents

Involvement of hydrogen and lipid peroxides in acute tobacco smoking-induced platelet hyperactivity

1995

Previous studies have established that cigarette smoking results in acute platelet hyperaggregability. We investigated whether changes in plasma oxidative properties could occur after smoking and whether such changes could be responsible for this enhanced platelet activity. In the present work, we report that platelets from nonsmokers become hyperactive after incubation with plasma prepared from blood of smokers obtained 10 min after smoking. This effect was not observed with presmoking plasma and could be inhibited in vitro by adding either catalase or reduced glutathione plus peroxidase to plasma or 2,6-di-tert-butyl-p-cresol (BHT) to platelets before incubation. Comparison of pre- and p…

AdultBlood PlateletsMaleLipid Peroxidesmedicine.medical_specialtyPlatelet AggregationPhysiologymedicine.medical_treatmentFatty Acids NonesterifiedAntioxidantschemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineHumansPlateletPlatelet activationIncubationchemistry.chemical_classificationbiologyVitamin ESmokingThrombinFatty acidHydrogen PeroxideGlutathioneButylated HydroxytolueneMiddle AgedBlood Physiological PhenomenaAdenosine DiphosphateEndocrinologychemistryBiochemistryCatalasebiology.proteinCardiology and Cardiovascular MedicinePeroxidaseAmerican Journal of Physiology-Heart and Circulatory Physiology
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Antagonistic effects of fluconazole and 5-fluorocytosine on candidacidal action of amphotericin B in human serum

1994

This study addressed the effects of fluconazole and 5-fluorocytosine on the candidacidal activity of amphotericin B in the presence of human serum. A Candida albicans isolate that was susceptible to all three agents according to standard testing procedures was employed. Fungicidal activity was estimated by using a flow cytometric procedure that exploited the fact that yeast cells killed by amphotericin B diminish in size and take up propidium iodide. The following findings were made. (i) Fluconazole and 5-fluorocytosine each failed to inhibit pseudohyphal formation and cell aggregation even when applied at 10 and 50 micrograms/ml, respectively, for up to 10 h. Hence, these agents were not f…

FlucytosinePharmacologyFlucytosineMicrobiologychemistry.chemical_compoundAmphotericin BAmphotericin BCandida albicansmedicineHumansPharmacology (medical)Propidium iodideCandida albicansFluconazolePharmacologybiologyDrug interactionBlood Physiological PhenomenaFlow Cytometrybiology.organism_classificationCell aggregationIn vitroInfectious DiseaseschemistryFluconazoleResearch Articlemedicine.drugAntimicrobial Agents and Chemotherapy
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The role of bestatin, an inhibitor of cell surface proteases, in the interaction of serum with untransformed cells in culture.

1981

Bestatin is an inhibitor of cell surface-associated aminopeptidase B and leucine aminopeptidase. This microbial product simulates the role of serum as an activator of uridine uptake in quiescent BHK cells. The compound significantly stimulates the incorporation of labelled thymidine into the acid-insoluble fraction of serum-starved Nil 8 cells in the presence of low concentration of serum. The possible mechanisms of these interactions are discussed.

ProteasesCellBiologyArginineAminopeptidaseAminopeptidaseschemistry.chemical_compoundAminopeptidase BLeucyl AminopeptidaseLeucineDrug DiscoverymedicineUridineCells CulturedPharmacologyActivator (genetics)Cell MembraneDNABlood Physiological PhenomenaMolecular biologyUridineStimulation Chemicalmedicine.anatomical_structurechemistryBiochemistryLeucineThymidineThymidineThe Journal of antibiotics
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Phytoestrogens increase the capacity of serum to stimulate prostacyclin release in human endothelial cells

2003

Both the estrogen receptor (ER) alpha and beta isoforms are expressed in the endothelium. The ER beta has been assigned a crucial role in normal vascular wall function. Prostacyclin has been ascribed a beneficial effect on vessel wall physiology. Isoflavones bind with higher affinity to ER beta. We investigated the hypothesis that their administration to postmenopausal women can promote endothelial prostacyclin production.Twenty-five healthy postmenopausal women with mild climacteric symptoms received capsules containing 55 mg/day isoflavones derived from soy and red clover for 6 months. Cultured human umbilical vein endothelial cells (HUVECs) were exposed for 24 h to serum collected before…

Umbilical Veinsmedicine.medical_specialtyTime FactorsEndotheliumAdministration OralAlpha (ethology)Estrogen receptorPhytoestrogensProstacyclinDrug Administration ScheduleUmbilical veinchemistry.chemical_compoundInternal medicinemedicineHumansEstrogens Non-SteroidalEstrogen receptor betaPlant Extractsbusiness.industryObstetrics and GynecologyGeneral MedicineMiddle AgedIsoflavonesBlood Physiological PhenomenaEpoprostenolIsoflavonesPostmenopauseEndocrinologymedicine.anatomical_structurechemistryFemaleTrifoliumPhytoestrogensEndothelium VascularPlant PreparationsSoybeansbusinessPlatelet Aggregation Inhibitorsmedicine.drugActa Obstetricia et Gynecologica Scandinavica
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Candida albicans-epithelial interactions: dissecting the roles of active penetration, induced endocytosis and host factors on the infection process

2012

International audience; Candida albicans frequently causes superficial infections by invading and damaging epithelial cells, but may also cause systemic infections by penetrating through epithelial barriers. C. albicans is a remarkable pathogen because it can invade epithelial cells via two distinct mechanisms: induced endocytosis, analogous to facultative intracellular enteropathogenic bacteria, and active penetration, similar to plant pathogenic fungi. Here we investigated the contributions of the two invasion routes of C. albicans to epithelial invasion. Using selective cellular inhibition approaches and differential fluorescence microscopy, we demonstrate that induced endocytosis contri…

[SDV]Life Sciences [q-bio]lcsh:MedicineYeast and Fungal ModelsPathogenesisCandidiasis OralMolecular Cell BiologyCandida albicanslcsh:ScienceCandida albicansPathogencandida albicans;epithelial interaction;endocytosis;infection0303 health sciencesFungal proteinMultidisciplinaryFungal DiseasesBlood Physiological PhenomenaCadherinsEndocytosisCorpus albicansepithelial interactionCell biologyHost-Pathogen InteractionInfectious Diseases[SDE]Environmental SciencesHost-Pathogen InteractionsMedicineCellular TypesSuperficial MycosesCandidalysinResearch ArticleMycologyBiologyEndocytosisMicrobiologyCell LineMicrobiologyFungal Proteins03 medical and health sciencesModel OrganismsMicroscopy Electron TransmissionCell Adhesion[SDV.BV]Life Sciences [q-bio]/Vegetal BiologyHumansCell adhesionBiology030304 developmental biology030306 microbiologyIntracellular parasitelcsh:RFungiMouth MucosaEpithelial Cellsbiology.organism_classificationinfectionYeastlcsh:Q
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Absence of binding of human salivary glycoprotein to human gingival fibroblast-like cells in vitro.

1996

The aim of this study was to determine whether human high molecular weight salivary glycoprotein binds in vitro to human gingival fibroblast-like cells. Primary monolayer cultures of 2 human gingival fibroblast-like cell lines were incubated with a high molecular weight fraction of salivary glycoprotein which expressed blood group A activity and glycoprotein-cell binding probed using an FITC-conjugated mouse monoclonal antibody to human blood group A antigen. Surface fluorescence of protein-treated cells was found to be no greater than that of untreated or serum-treated control cultures. As significant binding of salivary glycoprotein to gingival fibroblast-like cells does not occur in vitr…

chemistry.chemical_classificationChemistryGingivaMucinsPlasma protein bindingFibroblastsBlood Physiological PhenomenaGroup AMolecular biologyIn vitroCell Linemedicine.anatomical_structureAntigenCell culturemedicineCell AdhesionHumansGingival fibroblastSalivary Proteins and PeptidesGlycoproteinFibroblastSalivaGeneral DentistryProtein BindingEuropean journal of oral sciences
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Translocation of the nuclear autoantigen La to the cell surface of herpes simplex virus type 1 infected cells.

1992

Recently we developed a procedure to translocalize one of the extractable nuclear antigens (ENAs), the La protein, to the cell surface of CV-1 cells. Here we report that herpes simplex virus type 1 infection can also induce a translocation of the autoantigen to the cell surface. On the cell surface we detected La protein assembled with large protrusions. Within these protrusions La protein colocalized with virus particles. These protrusions are known to be released from the cell after virus infections. Such complexes consisting of self and virus could provide helper determinants for an anti-self response, and therefore be important in generation of autoimmunity.

virusesImmunologyCellmedicine.disease_causeAutoantigensVirusHerpesviridaeSingle-stranded binding proteinAntigenAlphaherpesvirinaeCricetinaemedicineImmunology and AllergyAnimalsNuclear proteinCells CulturedCell NucleusbiologyAntibodies MonoclonalBiological TransportHerpes Simplexbiology.organism_classificationBlood Physiological PhenomenaVirologymedicine.anatomical_structureHerpes simplex virusRibonucleoproteinsbiology.proteinAutoimmunity
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