Search results for "CASP"

showing 10 items of 470 documents

Activation of the Proapoptotic Unfolded Protein Response in Plaques of the Human Carotid Artery

2014

Objective To analyze expression of keystone markers of apoptosis and the proapoptotic signaling pathway “unfolded protein response” (UPR) in rupture-prone plaques of the human carotid artery. Methods Plaque specimens were obtained during endarterectomy for high-grade carotid stenosis, and were formalin-fixed. Ten specimens were identified that exhibited criteria of advanced rupture-prone atherosclerotic plaques, and histological and immunohistological analysis of markers of apoptosis (cleaved Caspase-3, TUNEL) and UPR (KDEL, ATF3, CHOP, CHAC-1) was performed. In addition, co-localization of apoptosis and UPR-activation was assessed by double-immunohistochemistry. Results The mean size of th…

MalePathologymedicine.medical_specialtyReceptors PeptideArteriosclerosisKDELmedicine.medical_treatmentApoptosisCHOPImmunoenzyme TechniquesRisk FactorsIn Situ Nick-End LabelingMedicineHumansCarotid StenosisEndarterectomyAgedAtherosclerotic plaqueAged 80 and overMedicine(all)Endarterectomy CarotidTUNEL assayActivating Transcription Factor 3business.industryCaspase 3MacrophagesFibrous capMiddle AgedImmunohistochemistrymedicine.anatomical_structureCarotid ArteriesApoptosisUnfolded protein responseUnfolded Protein ResponseImmunohistochemistrySurgeryFemalebusinessCardiology and Cardiovascular MedicineBiomarkersTranscription Factor CHOPSignal TransductionEuropean Journal of Vascular and Endovascular Surgery
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A case of Candida krusei peritonitis secondary to duodenal perforation due to Candida duodenitis.

2011

A case of a 62-year-old man with Candida krusei peritonitis secondary to duodenal perforation due to Candida duodenitis that was successfully treated with a 14-day course of caspofungin is reported. The potential role of Candida infection in the pathogenesis of peptic ulcers and duodenal perforation is considered. If this role is confirmed, antifungal treatment should be included in the therapeutic armamentarium of peptic disease.

MalePeptic Ulcermedicine.medical_specialtyAntifungal AgentsVeterinary (miscellaneous)PepticPeritonitisPeritonitisApplied Microbiology and BiotechnologyMicrobiologyGastroenterologyPathogenesisEchinocandinsLipopeptideschemistry.chemical_compoundMedical microbiologyDuodenitisCaspofunginInternal medicineCandida kruseimedicineHumansDuodenal DiseasesDuodenal PerforationPeptic diseaseCandidaDuodenal perforationDuodenitibiologyPeritonitibusiness.industrySmokingCandidiasisCandida Peritonitis Duodenal perforation Duodenitis Peptic disease Caspofungin SmokingMiddle Agedmedicine.diseasebiology.organism_classificationdigestive system diseasesTreatment OutcomechemistryIntestinal PerforationCaspofunginbusinessAgronomy and Crop Science
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Posaconazole against Candida glabrata Isolates with Various Susceptibilities to Fluconazole

2008

ABSTRACT We investigated the in vitro activities of posaconazole (POS), fluconazole (FLC), amphotericin B (AMB), and caspofungin (CAS) against four clinical isolates of Candida glabrata with various susceptibilities to FLC (FLC MICs ranging from 1.0 to >64 μg/ml). POS MICs ranged from ≤0.03 to 0.5 μg/ml; AMB MICs ranged from 0.25 to 2.0 μg/ml, while CAS MICs ranged from 0.03 to 0.25 μg/ml. When FLC MICs increased, so did POS MICs, although we did not observe any isolate with a POS MIC greater than 0.5 μg/ml. Time-kill experiments showed that POS, FLC, and CAS were fungistatic against all isolates, while AMB at eight times the MIC was fungicidal against three out of four isolates of C. gl…

MalePosaconazoleAntifungal AgentsCandida glabrataMicrobial Sensitivity TestsDrug resistanceBiologyKidneyMicrobiologyMicechemistry.chemical_compoundDrug Resistance Fungalhemic and lymphatic diseasesAmphotericin BmedicineAnimalsHumansExperimental TherapeuticsPharmacology (medical)FluconazolePharmacologyCandida glabrataExperimental modelCandidiasisFungi imperfectiTriazolesbiology.organism_classificationTreatment OutcomeInfectious DiseaseschemistryCaspofunginFluconazolemedicine.drugAntimicrobial Agents and Chemotherapy
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Sodium metabisulfite as a cytotoxic food additive induces apoptosis in HFFF2 cells

2021

Sodium metabisulfite (SMB), an antioxidant agent, is extensively used as a preservative in food industry. The current study was aimed to clarify its potential toxic effects on human fetal foreskin fibroblasts (HFFF2) cells, in vitro. Subsequently, MTT results illustrated that exposure to SMB significantly (p  0.0001) decreased HFFF2 cell viability in a dose-dependent manner, and the concentration of 25 μM reduced cell survival rates to 50% as the half-maximal inhibitory concentration of SMB. It was further shown that SMB exerted this cytotoxic effect on HFFF2 cells through apoptosis induction. qRT-PCR and western blotting results showed that treatment of HFFF2 cells with this food additive …

MalePreservativeAntioxidantfood.ingredientCell Survivalmedicine.medical_treatmentForeskinApoptosisPharmacology01 natural sciencesAnalytical Chemistrychemistry.chemical_compound0404 agricultural biotechnologyfoodAutophagymedicineHumansSulfitesCytotoxic T cellCytotoxicityCells Culturedbcl-2-Associated X ProteinCaspase 8Dose-Response Relationship DrugCaspase 3Food additive010401 analytical chemistry04 agricultural and veterinary sciencesGeneral MedicineSodium metabisulfiteFibroblasts040401 food scienceCaspase 9In vitro0104 chemical sciencesGene Expression RegulationchemistryApoptosisFood AdditivesReactive Oxygen SpeciesFood ScienceFood Chemistry
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In toxic demyelination oligodendroglial cell death occurs early and is FAS independent

2010

Oligodendroglial cell death is a frequent phenomenon of many neurological diseases, e.g. in demyelinating diseases such as multiple sclerosis (MS). The underlying mechanisms are largely unknown. Here, we demonstrate that in the toxic demyelination cuprizone model, oligodendroglial cell death and downregulation of myelin genes start days after initiation of the cuprizone diet and weeks before demyelination is obvious. In early – but not in later – stages, dying oligodendrocytes express activated caspase 3, suggesting a switch from classical apoptotic pathways to caspase 3-independent mechanisms during the course of the cuprizone diet. The expression level of FAS in the corpus callosum, a cel…

MaleProgrammed cell deathDown-RegulationMice TransgenicCaspase 3ApoptosisNerve Fibers MyelinatedArticleCorpus Callosumlcsh:RC321-571Mice03 medical and health sciencesMyelinCuprizone0302 clinical medicineDownregulation and upregulationmedicineAnimalsRNA Messengerfas Receptorlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCaspase030304 developmental biology0303 health sciencesCell DeathbiologyCaspase 3CytotoxinsMultiple sclerosisExperimental autoimmune encephalomyelitisFASmedicine.disease3. Good healthMice Inbred C57BLDisease Models AnimalOligodendrogliamedicine.anatomical_structureGene Expression RegulationNeurologyApoptosisMyelinImmunologybiology.proteinFemaleMyelin Proteins030217 neurology & neurosurgeryDemyelinating DiseasesSignal TransductionNeurobiology of Disease
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Glutamine potentiates TNF-α-induced tumor cytotoxicity

2001

L-glutamine (Gln) sensitizes tumor cells to tumor necrosis factor (TNF)-alpha-induced cytotoxicity. The type and mechanism of cell death induced by TNF-alpha was studied in Ehrlich ascites tumor (EAT)-bearing mice fed a Gln-enriched diet (GED; where 30% of the total dietary nitrogen was from Gln). A high rate of Gln oxidation promotes a selective depletion of mitochondrial glutathione (mtGSH) content to approximately 58% of the level found in tumor mitochondria of mice fed a nutritionally complete elemental diet (standard diet, SD). The mechanism of mtGSH depletion involves a glutamate-induced inhibition of GSH transport from the cytosol into mitochondria. The increase in reactive oxygen in…

MaleProgrammed cell deathFree RadicalsCell SurvivalGlutamineApoptosisCytochrome c GroupMitochondrionBiologyBiochemistryMembrane PotentialsMiceNecrosischemistry.chemical_compoundAdenosine TriphosphateSuperoxidesPhysiology (medical)Tumor Cells CulturedAnimalsButhionine sulfoximineCaspase 3Tumor Necrosis Factor-alphaDrug SynergismHydrogen PeroxideGlutathioneGlutathioneMolecular biologyDietMitochondriaCell biologyOxygenGlutamineOxidative StressCytosolProto-Oncogene Proteins c-bcl-2chemistryApoptosisCaspasesReactive Oxygen SpeciesOxidation-ReductionCell DivisionIntracellularFree Radical Biology and Medicine
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Intrinsically determined cell death of developing cortical interneurons.

2009

The cell death of inhibitory neurons, which originate far from the cortical areas to which they migrate during embryonic development, is determined autonomously rather than by competition for trophic signals from other cell types. It has long been known that apoptosis, a form of programmed cell death, eliminates young cells from developing tissues. In the field of neurobiology, it is widely believed that developmental neuronal-cell death results from cellular competition for environmentally derived survival signals that selects for an optimally sized and properly wired population of neurons. This study of developmental cell death in the mouse cortex in vivo, in vitro and after transplantati…

MaleProgrammed cell deathInterneurongenetic structuresCell SurvivalPopulationApoptosisCell CountNeocortexBiologyArticle03 medical and health sciencesMice0302 clinical medicineNeural Stem CellsInterneuronsmedicineAnimalseducationCellular Senescence030304 developmental biologybcl-2-Associated X Protein0303 health scienceseducation.field_of_studyMultidisciplinaryNeocortexMembrane GlycoproteinsCaspase 3musculoskeletal neural and ocular physiologyPyramidal CellsfungiProtein-Tyrosine KinasesCell biologyTransplantationMice Inbred C57BLmedicine.anatomical_structurenervous systemAnimals NewbornInhibitory Postsynaptic PotentialsCerebral cortexbiology.proteinFemaleCell aging030217 neurology & neurosurgeryNeurotrophinNature
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Regulation of X-Chromosome-Linked Inhibitor of Apoptosis Protein in Kainic Acid-Induced Neuronal Death in the Rat Hippocampus

2001

XIAP (X-chromosome-linked inhibitor of apoptosis protein) is an antiapoptotic protein which inhibits the activity of caspases and suppresses cell death. However, little is known about the presence and function of XIAP in the nervous system. Here we report that XIAP mRNA is expressed in developing and adult rat brain. Using a specific antibody, we observed XIAP-immunoreactive cells in different brain regions, among others, in the hippocampus and cerebral cortex. Kainic acid, which induces delayed cell death of specific neurons, increased the levels of XIAP in the CA3 region of hippocampus. XIAP was, however, largely absent in cells undergoing cell death, as shown by TUNEL labeling and staini…

MaleProgrammed cell deathKainic acidX ChromosomeGenetic LinkageHippocampusApoptosisX-Linked Inhibitor of Apoptosis ProteinCaspase 3Hippocampal formationInhibitor of apoptosisHippocampusCellular and Molecular Neurosciencechemistry.chemical_compoundExcitatory Amino Acid AgonistsIn Situ Nick-End LabelingAnimalsRNA MessengerMolecular BiologyCells CulturedCaspaseNeuronsKainic AcidCell DeathbiologyCaspase 3Gene Expression Regulation DevelopmentalProteinsCell BiologyMolecular biologyRatsXIAPnervous systemchemistryCaspasesNerve Degenerationbiology.proteinBiomarkersMolecular and Cellular Neuroscience
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Occurrence of Retinal Ganglion Cell Loss via Autophagy and Apoptotic Pathways in an Autoimmune Glaucoma Model

2020

In glaucoma, an apoptotic death of retinal ganglion cells (RGCs) has been shown. However, little is known about other cell death mechanisms, like autophagy or necrosis. Therefore, we investigated these mechanisms in addition to antibody deposits in an experimental autoimmune glaucoma model.Rats were immunized with a retinal ganglion cell-layer homogenate (RGA), while controls received sodium chloride. Untreated rats served as natїve group. After seven weeks, retinal cross-sections were stained with antibodies against RGCs (Brn-3a), apoptosis (cleaved caspase 2, cleaved caspase 3 as well as caspase 3, 8, and 9), autophagy (LC3BII and LAMP1), and necrosis (RIPK3) followed by cell counts. Auto…

MaleRetinal Ganglion CellsProgrammed cell deathNecrosisgenetic structuresGlaucomaApoptosisAutoantigensRetinal ganglionAutoimmune Diseases03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineMicroscopy Electron TransmissionAutophagymedicineAnimalsAutoantibodiesCaspase 8biologyCaspase 3business.industryAutophagyLysosome-Associated Membrane GlycoproteinsGlaucomamedicine.diseaseCaspase 9eye diseasesSensory SystemsRatsDisease Models AnimalOphthalmologymedicine.anatomical_structureMicroscopy FluorescenceRetinal ganglion cellRats Inbred LewApoptosisImmunoglobulin G030221 ophthalmology & optometryCancer researchbiology.proteinsense organsAntibodymedicine.symptombusinessMicrotubule-Associated Proteins030217 neurology & neurosurgeryCurrent Eye Research
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Retinal oxidation, apoptosis and age- and sex-differences in the mnd mutant mouse, a model of neuronal ceroid lipofuscinosis

2004

Retinal degeneration is an early and progressive event in many forms of neuronal ceroid lipofuscinoses (NCLs), a heterogeneous group of neurodegenerative disorders with unknown pathogenesis. We here used the mutant motor neuron degeneration (mnd) mouse, a late-infantile NCL variant, to investigate the retinal oxidative state and apoptotic cell death as a function of age and sex. Total superoxide dismutase (SOD) activities and thiobarbituric acid-reactive substance (TBARS) levels revealed progressive increases in retinal oxyradicals and lipid peroxides of mnd mice of both sexes. Female mnd retinas showed a higher oxidation rate and consistently exhibited the 4-hydroxy-2-nonenal (4-HNE)-adduc…

MaleRetinal degenerationPathologymedicine.medical_specialtyApoptosisBiologymedicine.disease_causeThiobarbituric Acid Reactive SubstancesRetinaMiceMice Neurologic Mutantschemistry.chemical_compoundSex FactorsNeuronal Ceroid-LipofuscinosesIn Situ Nick-End LabelingmedicineAnimalsOuter nuclear layerMolecular BiologyAldehydesRetinaTUNEL assayLipid peroxideCaspase 3Superoxide DismutaseGeneral NeuroscienceRetinal DegenerationRetinalmedicine.diseaseImmunohistochemistryEnzyme ActivationMice Inbred C57BLDisease Models AnimalOxidative Stressmedicine.anatomical_structureBiochemistrychemistryCaspasesFemaleNeuronal ceroid lipofuscinosisNeurology (clinical)Oxidation-ReductionOxidative stressDevelopmental BiologyBrain Research
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