Search results for "programme"

showing 10 items of 874 documents

A novel form of ataxia oculomotor apraxia characterized by oxidative stress and apoptosis resistance

2007

Several different autosomal recessive genetic disorders characterized by ataxia with oculomotor apraxia (AOA) have been identified with the unifying feature of defective DNA damage recognition and/or repair. We describe here the characterization of a novel form of AOA showing increased sensitivity to agents that cause single-strand breaks (SSBs) in DNA but having no gross defect in the repair of these breaks. Evidence for the presence of residual SSBs in DNA was provided by dramatically increased levels of poly (ADP-ribose)polymerase (PARP-1) auto-poly (ADP-ribosyl)ation, the detection of increased levels of reactive oxygen/nitrogen species (ROS/RNS) and oxidative damage to DNA in the patie…

MaleMethylnitronitrosoguanidineProgrammed cell deathAtaxiaDNA RepairApraxiasDNA damageMitomycinBlotting WesternPoly (ADP-Ribose) Polymerase-1Apoptosismedicine.disease_causeAntioxidantschemistry.chemical_compoundRadiation IonizingmedicineHumansDNA Breaks Single-StrandedOculomotor apraxiaMolecular BiologyCells CulturedEtoposideMembrane Potential MitochondrialbiologyCytochrome cHydrogen PeroxideCell BiologyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicReactive Nitrogen SpeciesMolecular biologyOxidative StresschemistryApoptosisbiology.proteinAtaxiaCamptothecinFemalePoly(ADP-ribose) Polymerasesmedicine.symptomDNAOxidative stressDNA DamageCell Death & Differentiation
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Preconditioning by Mitochondrial Reactive Oxygen Species Improves the Proangiogenic Potential of Adipose-Derived Cells-Based Therapy

2009

Objective— Transplantation of adipose-derived stroma cells (ADSCs) stimulates neovascularization after experimental ischemic injury. ADSC proangiogenic potential is likely mediated by their ability to differentiate into endothelial cells and produce a wide array of angiogenic and antiapoptotic factors. Mitochondrial reactive oxygen species (ROS) have been shown to control ADSC differentiation. We therefore hypothesized that mitochondrial ROS production may change the ADSC proangiogenic properties. Methods and Results— The use of pharmacological strategies (mitochondrial inhibitors, antimycin, and rotenone, with or without antioxidants) allowed us to specifically and precisely modulate mito…

MaleMitochondrial ROSProgrammed cell deathStromal Cells/cytology/metabolismAngiogenesisCellsReactive Oxygen Species/*metabolismNeovascularization PhysiologicBiologyMitochondrionmedicine.disease_causeMice03 medical and health sciences0302 clinical medicineAdipocytesmedicineAnimalsEndothelial Cells/*cytology/*physiologyCells CulturedNeovascularization030304 developmental biologyMitochondria/*metabolismchemistry.chemical_classificationReperfusion Injury/physiopathology0303 health sciencesReactive oxygen speciesCulturedEndothelial CellsCell DifferentiationMitochondriaCell biologyCell Differentiation/*physiologyTransplantationPhysiologic/*physiologychemistryReperfusion Injury030220 oncology & carcinogenesisImmunologyStromal CellsStem cellReactive Oxygen SpeciesCardiology and Cardiovascular MedicineOxidative stressArteriosclerosis, Thrombosis, and Vascular Biology
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A possible biomarker for methadone related deaths

2017

Abstract Methadone (MTH) concentrations in those dying of MTH toxicity totally overlap concentrations where the presence of MTH is only an incidental finding, making it very difficult to make distinctions in actual cases. A biomarker, be it anatomical or biochemical for MTH toxicity is badly needed, particularly if that markers were known to disrupt effective ventilation. Because the brainstem houses the regulatory centers for cardiorespiratory-control enters, it would seem to be the most likely anatomical site to seek abnormalities in cardiorespiratory control. Objective To locate and describe the cells of nucleus of the solitary tract (TS)(NTS) in human brainstem and determine if neuronal…

MalePathologyNecrosisApoptosisAutopsyCohort Studies0302 clinical medicineRetrospective StudieMedicineForensic PathologyNeuronsPoisoningSolitary tractGeneral MedicineRostral ventrolateral medullaNecrosiImmunohistochemistryCaspase 9Narcotic030220 oncology & carcinogenesisToxicityFemaleBrainstemmedicine.symptomBrainstemCaspase-9HumanNarcoticsAdultProgrammed cell deathmedicine.medical_specialty2734Pathology and Forensic MedicineNecrosisForensic ToxicologyYoung Adult03 medical and health sciencesSettore MED/43 - Medicina LegaleSolitary NucleuSolitary NucleusNeurotoxicityHumansRetrospective Studiesbusiness.industryfungiApoptosiBiomarkerNeuronApoptosisApoptosis; Biomarker; Brainstem; Caspase-9; Methadone; Neurotoxicity; Adult; Apoptosis; Brain Stem; Caspase 9; Cohort Studies; Female; Forensic Pathology; Forensic Toxicology; Humans; Immunohistochemistry; Male; Methadone; Narcotics; Necrosis; Neurons; Poisoning; Retrospective Studies; Solitary Nucleus; Young Adult; 2734; LawCohort StudiebusinessLawMethadone030217 neurology & neurosurgeryBrain Stem
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On the threshold of effective well infant nursery hearing screening in Western Sicily.

2012

Abstract Objective To determine the feasibility and effectiveness of well-infant nursery hearing screening programme for the early identification of hearing impairment, based on transient evoked otoacoustic emission (TEOAE) with a high “screen sensitivity” reducing the number of more expensive secondary level exams. Methods The newborns were screened by non-specialist health workers in well babies nursery at the twentieth day of life for 6 years consecutive. Based on PASS/FAIL criteria and presence/absence of audiological risk factors the newborns were divided into four groups each one with its personal step programme: G1 – PASS without risk factor, free to go home; G2 – PASS with risk fact…

MalePediatricsmedicine.medical_specialtyReferralHearing lossOtoacoustic Emissions SpontaneousOtoacoustic emissionAudiologyHearing screeningScreening programmeCohort StudiesNeonatal ScreeningClinical ProtocolsPredictive Value of TestsRisk FactorsWell-infant nurseryMedicineHumansRisk factorHearing LossSicilybusiness.industryIncidence (epidemiology)Infant NewbornInfantGeneral Medicinemedicine.diseaseSettore MED/32 - AudiologiaAudiometry Evoked ResponseNeonatal screening; Well-infant nursery; Sensorineural hearing loss; Otoacoustic emission;Settore MED/31 - OtorinolaringoiatriaOtorhinolaryngologySensorineural hearing loPediatrics Perinatology and Child HealthFeasibility StudiesOtoacoustic emissionSensorineural hearing lossFemalemedicine.symptombusinessInternational journal of pediatric otorhinolaryngology
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Neuroprotection of lipoic acid treatment promotes angiogenesis and reduces the glial scar formation after brain injury

2012

After trauma brain injury, a large number of cells die, releasing neurotoxic chemicals into the extracellular medium, decreasing cellular glutathione levels and increasing reactive oxygen species that affect cell survival and provoke an enlargement of the initial lesion. Alpha-lipoic acid is a potent antioxidant commonly used as a treatment of many degenerative diseases such as multiple sclerosis or diabetic neuropathy. Herein, the antioxidant effects of lipoic acid treatment after brain cryo-injury in rat have been studied, as well as cell survival, proliferation in the injured area, gliogenesis and angiogenesis. Thus, it is shown that newborn cells, mostly corresponded with blood vessels …

MaleProgrammed cell deathAngiogenesisBlotting WesternNeovascularization PhysiologicPharmacologyBiologyNeuroprotectionAntioxidantsGlial scarNeovascularizationLesionCicatrixchemistry.chemical_compoundMicroscopy Electron TransmissionIn Situ Nick-End LabelingmedicineAnimalsRats WistarChromatography High Pressure LiquidGliogenesisThioctic AcidGeneral NeuroscienceImmunohistochemistryRatsLipoic acidNeuroprotective AgentschemistryBrain Injuriesmedicine.symptomNeurogliaNeuroscienceNeuroscience
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Cytotoxic activity of the novel small molecule AKT inhibitor SC66 in hepatocellular carcinoma cells

2014

Hepatocellular carcinoma (HCC) is characterized by limited response to current drug therapies. Here, we report that SC66, a novel AKT inhibitor, reduced cell viability in a dose- and time-dependent manner, inhibited colony formation and induced apoptosis in HCC cells. SC66 treatment led to a reduction in total and phospho-AKT levels. This was associated with alterations in cytoskeleton organization, a reduction in expression levels of E-cadherin, β-catenin and phospho-FAK, together with up-regulation of Snail protein levels. All these alterations were coupled with anoikis cell death induction. In addition, SC66 induced the production of reactive oxygen species (ROS) and DNA damage. Pre-trea…

MaleProgrammed cell deathCarcinoma HepatocellularCytoskeleton organizationPyridinesMice NudeApoptosisBiologyMice03 medical and health sciences0302 clinical medicineanoikisCell Line TumorAnimalsHumansAnoikisViability assayHCCProtein Kinase InhibitorsProtein kinase BPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biologySC660303 health sciencesCyclohexanonesCell growthAKTLiver NeoplasmsXenograft Model Antitumor AssaysMolecular biology3. Good healthOncologyApoptosis030220 oncology & carcinogenesismTORCancer researchHCC AKT mTOR SC66 anoikisProto-Oncogene Proteins c-aktResearch Paper
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Cocaine hepatotoxicity: two different toxicity mechanisms for phenobarbital-induced and non-induced rat hepatocytes.

1993

Abstract Hepatocytes isolated from both phenobarbital-induced and control rats were short-term cultured and exposed to cocaine (8–2000 μM) for varying times. Intracellular lactate dehydrogenase activity, free calcium levels ([Ca 2+ ] i ), reduced glutathione (GSH) and lipid peroxidation were investigated to evaluate the toxic effect of cocaine on hepatocytes. Cytochrome P450 induction by phenobarbital potentiated the in vitro cytotoxicity of cocaine by a factor of 13 (IC 50 = 84 μ M induced cells vs 1100 μM in non-induced cells). This difference in the susceptibility of the two types of hepatocytes to cocaine correlated well with the activity of cytochrome P450 2 B 1 2 . Rapid depletion of …

MaleProgrammed cell deathCell SurvivalPharmacologyBiochemistryLipid peroxidationRats Sprague-Dawleychemistry.chemical_compoundCocaineCytochrome P-450 Enzyme SystemLactate dehydrogenasemedicineAnimalsCells CulturedPharmacologybiologyDose-Response Relationship DrugCytochrome P450GlutathioneGlutathioneRatschemistryLiverPhenobarbitalToxicityCytochrome P-450 CYP2B1biology.proteinPhenobarbitalCalciumLipid PeroxidationOxidoreductasesIntracellularmedicine.drugBiochemical pharmacology
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Nitric Oxide Mediates Natural Polyphenol-induced Bcl-2 Down-regulation and Activation of Cell Death in Metastatic B16 Melanoma

2007

Intravenous administration to mice of trans-pterostilbene (t-PTER; 3,5-dimethoxy-4'-hydroxystilbene) and quercetin (QUER; 3,3',4',5,6-pentahydroxyflavone), two structurally related and naturally occurring small polyphenols, inhibits metastatic growth of highly malignant B16 melanoma F10 (B16M-F10) cells. t-PTER and QUER inhibit bcl-2 expression in metastatic cells, which sensitizes them to vascular endothelium-induced cytotoxicity. However, the molecular mechanism(s) linking polyphenol signaling and bcl-2 expression are unknown. NO is a potential bioregulator of apoptosis with controversial effects on Bcl-2 regulation. Polyphenols may affect NO generation. Short-term exposure (60 min/day) t…

MaleProgrammed cell deathCeramideEndotheliumDown-RegulationBiologyNitric OxideBiochemistryMicechemistry.chemical_compoundPhenolsCell Line TumorCell AdhesionmedicineAnimalsRNA MessengerNeoplasm MetastasisCytotoxicityMelanomaMolecular BiologyNitritesFlavonoidsNitratesCell DeathReverse Transcriptase Polymerase Chain ReactionPolyphenolsHydrogen PeroxideCell BiologyGenes bcl-2Cell biologyMice Inbred C57BLEndothelial stem cellmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2Mitochondrial permeability transition porechemistryCell cultureApoptosisMitochondrial MembranesCancer researchEndothelium VascularJournal of Biological Chemistry
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Chemotactic response of human alveolar macrophages and blood monocytes elicited by exposure to sulfur dioxide.

1996

An experimental study was undertaken to investigate the in vitro effect of sulfur dioxide on the chemotactic activity of alveolar macrophages (AM) and blood monocytes (BM). The cells were placed on a polycarbonate membrane and exposed to SO2 0.5, 1.5 and 2.5 ppm for 15 min. Control experiments were performed with exposure of the cells to synthetic air with 5% CO2. After gas exposure the cells were incubated with the chemotactic active agent C5a in 5% carbon dioxide (CO2) at 37 degrees C for 60 min. The numbers of AM and BM passing actively through the membrane were quantified using light microscopy. Our results show a dose-dependent reduction in the migration rate of cells under SO2 exposur…

MaleProgrammed cell deathComplement C5aIn Vitro Techniquescomplex mixturesMonocyteschemistry.chemical_compoundMacrophages AlveolarCytotoxic T cellHumansSulfur DioxideSulfur dioxideAgedAir PollutantsChemistryChemotaxisChemotaxisGeneral MedicineMiddle AgedMolecular biologyIn vitrorespiratory tract diseasesChemotaxis LeukocyteMembraneActive agentBiochemistryCarbon dioxideFemaleResearch in experimental medicine. Zeitschrift fur die gesamte experimentelle Medizin einschliesslich experimenteller Chirurgie
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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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