Search results for "Methyl Ketone"

showing 10 items of 14 documents

Effects of caspase inhibitors (z-VAD-fmk, z-VDVAD-fmk) on Nile Red fluorescence pattern in 7-ketocholesterol-treated cells: Investigation by flow cyt…

2007

Background: The 7-ketocholesterol (7KC)-induced cell death has some characteristics of apoptosis and is associated with polar lipid accumulation. So, we investigated the effects of the broad-spectrum caspase inhibitor z-VAD-fmk and of the caspase-2 inhibitor z-VDVAD-fmk on lipid profile evaluated by staining with Nile Red (NR). Methods: The 7KC-treated human monocytic U937 cells were cultured in the absence or in the presence of the caspase inhibitors z-VAD-fmk or z-VDVAD-fmk. When staining with NR is performed, neutral and polar lipids have yellow and orange/red emission, respectively, and fluorescence was then analyzed by flow cytometry (FCM) and by confocal laser scanning microscopy (CLS…

HistologyConfocalCaspase 2FluorescencePathology and Forensic Medicinelaw.inventionFlow cytometryAmino Acid Chloromethyl Ketones03 medical and health scienceschemistry.chemical_compound0302 clinical medicineConfocal microscopylawOxazinesmedicineImage Processing Computer-AssistedHumans[ SDV.IB ] Life Sciences [q-bio]/BioengineeringEnzyme InhibitorsKetocholesterols030304 developmental biology[SDV.IB] Life Sciences [q-bio]/BioengineeringCell Nucleus0303 health sciencesMicroscopyMicroscopy Confocalbiologymedicine.diagnostic_testNile redLipid metabolismCell BiologyU937 CellsFlow CytometryLipid MetabolismFluorescenceMolecular biologyCaspase Inhibitors3. Good healthStainingchemistry030220 oncology & carcinogenesisbiology.protein[SDV.IB]Life Sciences [q-bio]/Bioengineeringbiological phenomena cell phenomena and immunityFactor Analysis Statistical
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Caspase-dependent cell death involved in brain damage after acute subdural hematoma in rats

2006

Abstract Traumatic brain injury is associated with acute subdural hematoma (ASDH) that worsens outcome. Although early removal of blood can reduce mortality, patients still die or remain disabled after surgery and additional treatments are needed. The blood mass and extravasated blood induce pathomechanisms such as high intracranial pressure (ICP), ischemia, apoptosis and inflammation which lead to acute as well as delayed cell death. Only little is known about the basis of delayed cell death in this type of injury. Thus, the purpose of the study was to investigate to which extent caspase-dependent intracellular processes are involved in the lesion development after ASDH in rats. A volume o…

Brain InfarctionMalePathologymedicine.medical_specialtyTraumatic brain injuryIschemiaApoptosisBrain damageNeuroprotectionAmino Acid Chloromethyl KetonesBrain IschemiaRats Sprague-DawleyLesionIn Situ Nick-End LabelingmedicineAnimalsHematoma Subdural AcuteEnzyme InhibitorsSubdural spaceMolecular BiologyIntracranial pressurebusiness.industryVascular diseaseGeneral Neurosciencemedicine.diseaseRatsDisease Models AnimalBloodNeuroprotective AgentsTreatment Outcomemedicine.anatomical_structureBrain InjuriesCaspasesAnesthesiaNeurology (clinical)Intracranial Hypertensionmedicine.symptombusinessSignal TransductionDevelopmental BiologyBrain Research
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Staurosporine-induced apoptosis in Chang liver cells is associated with down-regulation of Bcl-2 and Bcl-XL.

2004

A potent inhibitor of serine/threonine kinases, staurosporine exerts antiproliferative and apoptotic effects in many cancer cells, although the exact mechanism of its action is still unclear. This study examines the effects of staurosporine on Chang liver cells, an immortalized non-tumor cell line, in comparison with those caused in HuH-6 and HepG2 cells, two human hepatoma cell lines. Our results provide evidence that staurosporine promotes apoptosis in Chang liver cells as observed by flow cytometric analysis and acridine orange/ethidium bromide staining. The effect appeared already after 8 h of treatment and increased with treatment time and dose. After 48 h of exposure to 200 nM stauros…

G2 PhaseProgrammed cell deathTime FactorsCell SurvivalLiver cytologyBlotting Westernbcl-X ProteinDown-RegulationMitosisApoptosisBcl-xLAmino Acid Chloromethyl KetonesCell LineMembrane PotentialsEthidiumSettore BIO/10 - BiochimicaGeneticsmedicineHumansStaurosporineEnzyme InhibitorsBcl-2 family factors.CaspaseApoptosis staurosporineDose-Response Relationship DrugbiologyCaspase 3Cell CycleGeneral MedicineFlow CytometryStaurosporineMolecular biologyAcridine OrangeMitochondriaEnzyme ActivationLiverProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureCaspasesCancer cellbiology.proteinCell Divisionmedicine.drug
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Organocatalytic Enantioselective Vinylogous Henry Reaction of 3,5-Dimethyl-4-nitroisoxazole with Trifluoromethyl Ketones

2017

The enantioselective vinylogous Henry reaction of 3,5-dimethyl-4-nitroisoxazole with trifluoromethyl ketones employing a bifunctional squaramide organocatalyst has been developed. A series of isoxazole bearing trifluoromethyl-substituted tertiary alcohols, 2-substituted (R)-1,1,1-trifluoro-3-(3-methyl-4-nitroisoxazol-5-yl)propan-2-ols, were obtained under these mild reaction conditions in good yields and moderate to good enantioselectivities

trifluoromethyl ketoneReaction conditionsNitroaldol reactionTrifluoromethyl010405 organic chemistryasymmetric synthesisisoxazoleOrganic ChemistryEnantioselective synthesisSquaramide010402 general chemistry01 natural sciencesCatalysis0104 chemical scienceschemistry.chemical_compoundchemistrysquaramide organocatalystvinylogous Henry reactionOrganic chemistryIsoxazoleBifunctionalTertiary alcoholsSynthesis
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Conditions for the Enhancing Effect of Protease Inhibitors on the Concanavalin A Induced Thymidine Response of Murine Lymphocytes

1983

Incorporation of [<sup>3</sup>H]-thymidine – [<sup>3</sup>H]-TdR – into concanavalin A (Con A) stimulated murine splenocytes and thymocytes was found to be enhanced by addition of certain concentrations of phenyl-methyl-sulfonylfluoride (PMSF), di-isopropylfluorophosphate (DFP), N-α-tosyl-<i>L</i>-lysyl-<i>L</i>-chloromethylketone (TLCK), and soybean trypsin inhibitor (SBTI). No enhancement could be observed when mononuclear cells of the peripheral blood were used, and a medium enhancement when thymocytes were applied. Furthermore, no enhancing effect of the protease inhibitors (PI) on the Con A response of murine splenocytes could be observed…

MaleIsoflurophateTime Factorsmedicine.medical_treatmentImmunologyBiologyLymphocyte ActivationTosyllysine Chloromethyl KetoneMicechemistry.chemical_compoundPhagocytosisConcanavalin AmedicineAnimalsImmunology and AllergyProtease InhibitorsMice Inbred BALB CProteaseDose-Response Relationship DrugMurine splenocytesDrug SynergismGeneral MedicineMolecular biologyKineticschemistryBiochemistryConcanavalin AImmunologybiology.proteinThymidineSpleenThymidineInternational Archives of Allergy and Immunology
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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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Implication of three isoforms of PLA2in human T-cell proliferation

2002

We observed that human (Jurkat) T-cells constitutively expressed the mRNA, encoding for the four isoforms of phospholipase A(2) (PLA(2)), i.e. two secretory (type IB and type V), and two cytosolic (type IV, Ca(2+)-dependent and type VI, Ca(2+)-independent). In order to assess whether these PLA(2) isoforms are active, we labeled Jurkat T-cells with [(3)H]arachidonic acid ([(3)H]AA) and determined its release into the extracellular medium in the presence of phorbol 12-myristate 13-acetate (PMA) and ionomycin. The three PLA(2) isoforms seem functional as aristolochic acid and bromoenol lactone (BEL), the respective inhibitors of type IB/type V and type VI PLA(2)s, significantly inhibited the r…

BiophysicsAristolochic acidArachidonic AcidsPhospholipaseTritiumBiochemistryJurkat cellsGene Expression Regulation EnzymologicPhospholipases AJurkat Cellschemistry.chemical_compoundPhospholipase A2Structural BiologyGeneticsHumansPhospholipaseRNA MessengerEnzyme InhibitorsMolecular BiologyArachidonyl trifluoromethyl ketoneArachidonic AcidbiologyIonomycinCell BiologyJurkat T-cellIsoenzymesGene Expression RegulationchemistryBiochemistryIonomycinPhorbolbiology.proteinInterleukin-2Tetradecanoylphorbol AcetateCalciumlipids (amino acids peptides and proteins)Arachidonic acidCell DivisionFEBS Letters
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Parthenolide induces caspase-independent and AIF-mediated cell death in human osteosarcoma and melanoma cells

2013

The mechanism of the cytotoxic effect exerted by parthenolide on tumor cells is not clearly defined today. This article shows that parthenolide stimulates in human osteosarcoma MG63 and melanoma SK-MEL-28 cells a mechanism of cell death, which is not prevented by z-VAD-fmk and other caspase inhibitors. In particular treatment with parthenolide rapidly stimulated (1-2 h) reactive oxygen species (ROS) generation by inducing activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) and NADPH oxidase. This event caused depletion of thiol groups and glutathione, NF-κB inhibition, c-Jun N-terminal kinase (JNK) activation, cell detachment from the matrix, and cellular shrinkage. The increa…

Programmed cell deathMAP Kinase Signaling SystemPhysiologyClinical BiochemistryAmino Acid Chloromethyl Ketoneschemistry.chemical_compoundCell Line TumorSettore BIO/10 - BiochimicaHumansParthenolidePropidium iodideFragmentation (cell biology)MelanomaCaspaseOsteosarcomaCell DeathbiologyNF-kappa BApoptosis Inducing FactorNADPH OxidasesCell BiologyCaspase InhibitorsCell biologyGene Expression Regulation NeoplasticchemistryApoptosisCell cultureCaspasesbiology.proteinApoptosis-inducing factorReactive Oxygen SpeciesSesquiterpenesParthenolide caspase-independent cell death ROS AIFJournal of Cellular Physiology
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Effects of thermal processing and storage on available lysine and furfural compounds contents of infant formulas.

2000

The Maillard reaction-related effects that thermal treatments during the manufacturing process and storage (at 20 and 37 degrees C) have on powdered adapted and follow-up milk-based infant formulas were estimated by measuring the available lysine and furfural compounds contents of raw cow milk used in manufacturing, intermediate products and formulas. A fluorimetric method was used to measure the available lysine contents, and free and total furfural compounds were determined by HPLC. Statistically significant losses in available lysine (about 20%) in the infant formulas with respect to raw milk were found. The storage period did not affect the available lysine contents of adapted formulas …

ChromatographyFood HandlingLysineLysineGeneral ChemistryRaw milkFurfuralHigh-performance liquid chromatographyCow milkchemistry.chemical_compoundMaillard reactionsymbols.namesakechemistryMethyl KetonesymbolsFuraldehydeInfant FoodFood scienceGeneral Agricultural and Biological SciencesHydroxymethylfurfuralJournal of agricultural and food chemistry
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Hsp72 controls bortezomib-induced HepG2 cell death via interaction with pro-apoptotic factors.

2007

The proteasome inhibitor bortezomib is an efficacious inducer of apoptosis in the hepatoma HepG2 cell line. This study shows that bortezomib increased in these cells the level of the survival factor Hsp72 in a time- and dose-dependent manner. In a first phase of treatment, Hsp72 rapidly increased so that at 24 h of incubation with 50 nM bortezomib its level was approximately five-fold higher than the control. In this phase Hsp72 seemed to play a role in preventing HepG2 cell death, since it interacted with and sequestered the pro-apoptotic factors p53, AIF, Bax and Apaf-1. During a second day of treatment, although the nuclear levels of Hsp72, p53 and AIF increased, the interaction of Hsp72…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularTime FactorsCellBlotting WesternApoptosisHSP72 Heat-Shock ProteinsAmino Acid Chloromethyl KetonesBortezomibCell Line TumormedicineHumansImmunoprecipitationProtease Inhibitorscardiovascular diseasesCaspasebcl-2-Associated X ProteinOncogenebiologyBortezomibReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsApoptosis Inducing Factorproteasome inhibitor hepatocarcinoma apoptosisGeneral MedicineCell cycleBoronic Acidsmedicine.anatomical_structureApoptotic Protease-Activating Factor 1OncologyApoptosisPyrazinesProteasome inhibitorCancer researchbiology.proteinTumor Suppressor Protein p53Apoptosis Regulatory Proteinsmedicine.drugProtein Binding
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