Search results for " apoptosis."

showing 10 items of 359 documents

Demyelination patterns in a mathematical model of multiple sclerosis.

2016

In this paper we derive a reaction-diffusion-chemotaxis model for the dynamics of multiple sclerosis. We focus on the early inflammatory phase of the disease characterized by activated local microglia, with the recruitment of a systemically activated immune response, and by oligodendrocyte apoptosis. The model consists of three equations describing the evolution of macrophages, cytokine and apoptotic oligodendrocytes. The main driving mechanism is the chemotactic motion of macrophages in response to a chemical gradient provided by the cytokines. Our model generalizes the system proposed by Calvez and Khonsari (Math Comput Model 47(7–8):726–742, 2008) and Khonsari and Calvez (PLos ONE 2(1):e…

Multiple Sclerosismedicine.medical_treatmentInflammationApoptosisBiology01 natural sciencesModels BiologicalConcentric ring03 medical and health sciences0302 clinical medicineTuring instabilitymedicineHumansMultiple sclerosi0101 mathematicsSettore MAT/07 - Fisica MatematicaInflammationMicrogliaOligodendrocyte apoptosisPatternMultiple sclerosisTuring instabilityApplied MathematicsChemotaxismedicine.diseaseAgricultural and Biological Sciences (miscellaneous)Magnetic Resonance Imaging010101 applied mathematicsChemotaxis PDE modelCytokinemedicine.anatomical_structureModeling and SimulationImmunologymedicine.symptomNeuroscience030217 neurology & neurosurgeryDemyelinating DiseasesJournal of mathematical biology
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Small molecule inhibitors of Apaf-1-related caspase- 3/-9 activation that control mitochondrial-dependent apoptosis

2006

10 pages, 5 figures.-- PMID: 16341125 [PubMed].-- Available online Dec 9, 2005.

Multiprotein complexCytochromeProtein-protein interactionsApoptosisCaspase 3MitochondrionLigandsCell LineChemical librarychemistry.chemical_compoundPeptide LibraryApoptosomesPeptoidHumansCombinatorial libraries inhibitorApoptosomeProtein PrecursorsMolecular BiologybiologyCaspase 3Intrinsic apoptosisCytochromes cCell BiologyCaspase InhibitorsCaspase 9Recombinant ProteinsMitochondriaCell biologyEnzyme ActivationCaspasa-9Apoptotic Protease-Activating Factor 1chemistryBiochemistryN-substituted GlycinesApoptosisCaspasa-3biology.proteinApoptosomeApaf-1Molecular recognitionSmall moleculeProtein BindingCell Death & Differentiation
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Antiproliferative Effects of St. John’s Wort, Its Derivatives, and Other Hypericum Species in Hematologic Malignancies

2021

Hypericumis a widely present plant, and extracts of its leaves, flowers, and aerial elements have been employed for many years as therapeutic cures for depression, skin wounds, and respiratory and inflammatory disorders. Hypericum also displays an ample variety of other biological actions, such as hypotensive, analgesic, anti-infective, anti-oxidant, and spasmolytic abilities. However, recent investigations highlighted that this species could be advantageous for the cure of other pathological situations, such as trigeminal neuralgia, as well as in the treatment of cancer. This review focuses on the in vitro and in vivo antitumor effects of St. John’s Wort (Hypericum perforatum), its derivat…

MyeloidAngiogenesisDrug Evaluation PreclinicalReviewPharmacologylcsh:Chemistrychemistry.chemical_compoundhyperforinDrug InteractionsMyeloid CellsLymphocyteslcsh:QH301-705.5SpectroscopybiologyapoptosisleukemiaHypericum perforatumGeneral MedicineComputer Science ApplicationsHypericinLeukemiamedicine.anatomical_structurephotodynamic therapyHematologic NeoplasmsHypericumHypericumSt. John’s wortlymphomaCatalysisInorganic ChemistryStructure-Activity Relationshipmultidrug resistanceIn vivoCell Line TumormedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyCell ProliferationPlant Extractsbusiness.industryOrganic Chemistry<i>Hypericum</i>biology.organism_classificationmedicine.diseaseAntineoplastic Agents PhytogenicApoptosis; Hyperforin; Hypericin; Hypericum; Leukemia; Lymphoma; Mul-tidrug resistance; Photodynamic therapy; St. John’s wort; Animals; Antineoplastic Agents Phytogenic; Apoptosis; Cell Line Tumor; Cell Proliferation; Drug Evaluation Preclinical; Drug Interactions; Drug Resistance Neoplasm; Hematologic Neoplasms; Humans; Hypericum; Lymphocytes; Myeloid Cells; Plant Extracts; Structure-Activity RelationshipHyperforinchemistrylcsh:Biology (General)lcsh:QD1-999Drug Resistance NeoplasmhypericinbusinessInternational Journal of Molecular Sciences
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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The Role of Erythropoietin in Neuroprotection: Therapeutic Perspectives

2007

Nervous system diseases are very complex conditions comprising a large variety of local and systemic responses. Several therapeutic agents interfering with all or in part the biochemical steps that ultimately cause neuronal death have been demonstrated to be neuroprotective in preclinical models. However, all the agents so far investigated have inexorably failed in the phase III trials carried out. A large body of evidence suggests that the hormone erythropoietin (EPO), besides its well-known hematopoietic action, exerts beneficial effects in the central nervous system. EPO's effect has been assessed in several experimental models of brain and spinal cord injury thus becoming a serious cand…

Nervous systemEXPERIMENTAL SUBARACHNOID HEMORRHAGECentral nervous systemSIGNAL-TRANSDUCTIONPharmacologyModels BiologicalNeuroprotectionErythropoietin in neuroprotectionNEURONAL APOPTOSISCEREBROSPINAL-FLUIDAnimalsHumansMedicineIN-VIVO EVIDENCEErythropoietinSpinal cord injuryPharmacologyCEREBRAL-ISCHEMIACOMMON BETA-SUBUNITbusiness.industryRECOMBINANT-HUMAN-ERYTHROPOIETIN; GLYCOGEN-SYNTHASE KINASE-3-BETA; EXPERIMENTAL SUBARACHNOID HEMORRHAGE; COMMON BETA-SUBUNIT; IN-VIVO EVIDENCE; CEREBRAL-ISCHEMIA; SIGNAL-TRANSDUCTION; CEREBROSPINAL-FLUID; NEURONAL APOPTOSIS; CYTOKINE RECEPTORSRECOMBINANT-HUMAN-ERYTHROPOIETINmedicine.diseaseRecombinant ProteinsEnzyme ActivationStrokeClinical trialNeuroprotective AgentsTreatment Outcomemedicine.anatomical_structureErythropoietinGLYCOGEN-SYNTHASE KINASE-3-BETACYTOKINE RECEPTORSBone marrowMitogen-Activated Protein Kinasesbusinessmedicine.drugDrug News &amp; Perspectives
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The columnar gene vnd is required for tritocerebral neuromere formation during embryonic brain development of Drosophila.

2006

International audience; In Drosophila, evolutionarily conserved transcription factors are required for the specification of neural lineages along the anteroposterior and dorsoventral axes, such as Hox genes for anteroposterior and columnar genes for dorsoventral patterning. In this report, we analyse the role of the columnar patterning gene ventral nervous system defective (vnd) in embryonic brain development. Expression of vnd is observed in specific subsets of cells in all brain neuromeres. Loss-of-function analysis focussed on the tritocerebrum shows that inactivation of vnd results in regionalized axonal patterning defects, which are comparable with the brain phenotype caused by mutatio…

Nervous systemMutantApoptosis0302 clinical medicineMESH: Gene Expression Regulation DevelopmentalDrosophila ProteinsMESH: AnimalsAxonHox geneMESH: MelatoninGenetics0303 health sciencesMESH: Pineal GlandBrainGene Expression Regulation DevelopmentalMESH: Transcription FactorsNeuromerePhenotypeBiological EvolutionCell biologymedicine.anatomical_structureDrosophila melanogasterPhenotypeMESH: Photic StimulationMESH: Body PatterningMESH: MutationMESH: Drosophila ProteinsBiologyMESH: PhenotypeMESH: Drosophila melanogaster03 medical and health sciencesMESH: BrainNeuroblastMESH: EvolutionMESH: Homeodomain ProteinsmedicineAnimalsMESH: Circadian RhythmMolecular Biology030304 developmental biologyBody PatterningHomeodomain ProteinsMESH: HumansMESH: ApoptosisEmbryogenesis[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMESH: LightMutationMESH: SerotoninMESH: Seasons030217 neurology & neurosurgeryDevelopmental BiologyTranscription Factors
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Overexpression of Nicotinamide n-Methyl- transferase in HSC-2 OSCC cell line: effect on apoptosis and cell proliferation

2016

Nicotinamide n-Methyl- transferaseHSC-2 OSCC cell line apoptosis cell proliferation
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Expression of cell cycle markers and human papillomavirus infection in oral squamous cell carcinoma: use of fuzzy neural networks.

2005

Our aim was to evaluate in oral squamous cell carcinoma (OSCC) the relationship between some cell cycle markers and HPV infection, conditionally to age, gender and certain habits of patients, and to assess the ability of fuzzy neural networks (FNNs) in building up an adequate predictive model based on logic inference rules. Eighteen cases of OSCC were examined by immunohistochemistry for MIB-1, PCNA and survivin expression; presence of HPV DNA was investigated in exfoliated oral mucosa cells by nested PCR (nPCR, MY09-MY11/GP5-GP6), and HPV genotype was determined by direct DNA sequencing. Data were analyzed by traditional statistics (TS) and FNNs. HPV DNA was found in 9/18 OSCCs (50.0 %) wi…

OncologyMaleCancer ResearchSurvivinmedicine.disease_causeInhibitor of Apoptosis ProteinsRisk FactorsOral mucosaPapillomaviridaeAged 80 and overCell CycleSmokingHPV infectionAge FactorsAnatomical pathologyCell cycleMiddle AgedImmunohistochemistryNeoplasm Proteinsoral squamous cell carcinomamedicine.anatomical_structureCell Transformation NeoplasticOncologyCarcinoma Squamous CellImmunohistochemistryFemaleMouth NeoplasmscarcinogenesisMicrotubule-Associated ProteinsAdultmedicine.medical_specialtyBiologySex FactorsFuzzy LogicInternal medicineSurvivinmedicineHumanshuman papillomaviruAgedfuzzy neural networkGene Expression ProfilingPapillomavirus Infectionsmedicine.diseaseProliferating cell nuclear antigenstomatognathic diseasesImmunologyDNA Viralbiology.proteinNeural Networks ComputerCarcinogenesisInternational journal of cancer
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Bcl-xL and Myeloid cell leukaemia-1 contribute to apoptosis resistance of colorectal cancer cells

2008

AIM: To explore the role of Bcl-x(L) and Myeloid cell leukaemia (Mcl)-1 for the apoptosis resistance of colorectal carcinoma (CRC) cells towards current treatment modalities. METHODS: Bcl-x(L) and Mcl-1 mRNA and protein expression were analyzed in CRC cell lines as well as human CRC tissue by Western blot, quantitative PCR and immunohistochemistry. Bcl-x(L) and Mcl-1 protein expression was knocked down or increased in CRC cell lines by applying specific siRNAs or expression plasmids, respectively. After modulation of protein expression, CRC cells were treated with chemotherapeutic agents, an antagonistic epidermal growth factor receptor (EGFR1) antibody, an EGFR1 tyrosine kinase inhibitor, …

Organoplatinum CompoundsCell SurvivalCellbcl-X ProteinAntineoplastic AgentsApoptosisBcl-xLAdenocarcinomaBiologyIrinotecanTNF-Related Apoptosis-Inducing LigandDownregulation and upregulationhemic and lymphatic diseasesCell Line TumormedicineHumansRNA Messengerfas ReceptorViability assayneoplasmsColorectal CancerGastroenterologyGeneral MedicineTransfectionFas receptorMolecular biologydigestive system diseasesErbB ReceptorsOxaliplatinmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureCancer researchbiology.proteinMyeloid Cell Leukemia Sequence 1 ProteinCamptothecinFluorouracilColorectal NeoplasmsWorld Journal of Gastroenterology
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Survivin is regulated by interleukin-4 in colon cancer stem cells

2010

Colorectal cancer has provided an important model to test the stem cell hypothesis of cancer origin, which implies that cancer arises as a result of genetic aberrations in stem cells leading to deregulation of the proliferation/differentiation balance. We and others have demonstrated that, similarly to other solid tumors, colon carcinogenesis and progression are dictated by highly apoptosis-resistant stem-like cells. Our data have suggested that protection from apoptosis is achieved by autocrine production of interleukin-4 (IL-4) through up-regulation of anti-apoptotic mediators. In this study, we extend our analysis to another apoptosis inhibitor widely expressed in tumors, namely survivin…

Organoplatinum CompoundsPhysiologyColorectal cancerSurvivinmedicine.medical_treatmentClinical BiochemistryFluorescent Antibody TechniqueAntineoplastic AgentsApoptosisBiologyInhibitor of Apoptosis ProteinsSurvivin inetrleukin-4Cancer stem cellSurvivinIn Situ Nick-End LabelingmedicineHumansPhosphorylationAutocrine signallingInterleukin 4Staining and LabelingCancerIsoxazolesCell Biologymedicine.diseaseGene Expression Regulation NeoplasticOxaliplatinProtein TransportCytokineImmunologyNeoplastic Stem CellsCancer researchInterleukin-4Stem cellColorectal NeoplasmsSTAT6 Transcription FactorMicrotubule-Associated ProteinsLeflunomideJournal of Cellular Physiology
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