Search results for "DAMAGE"

showing 10 items of 1289 documents

Host–pathogen interactions in Vibrio vulnificus: responses of monocytes and vascular endothelial cells to live bacteria

2015

ABSTRACT  Aim: To demonstrate that Vibrio vulnificus, a sepsis-related aquatic pathogen, can provoke a strong pro-inflammatory reaction in blood-associated target cells. Materials & methods: We selected two strains of the two main phylogenetic lineages, two human cell lines, monocytes and vascular endothelial cells and designed an in vitro infection model simulating early septicemia. Results: Both strains caused a strong cell-specific pro-inflammatory response and produced a high degree of cell damage that ended with death by lysis (endothelial cells) or apoptosis/lysis (monocytes). The interaction with endothelial cells was stronger than expected and significantly different for both l…

InflammationMicrobiology (medical)LysisbiologyGene Expression ProfilingEndothelial CellsVibrio vulnificusbiology.organism_classificationmedicine.diseaseMicrobiologyVirologyMonocytesIn vitroMicrobiologySepsisStress PhysiologicalApoptosisHost-Pathogen InteractionsmedicineHumansVibrio vulnificusPathogenCell damageCells CulturedBacteriaFuture Microbiology
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Pathophysiology of traumatic brain injury.

2007

The knowledge of the pathophysiology after traumatic head injury is necessary for adequate and patient-oriented treatment. As the primary insult, which represents the direct mechanical damage, cannot be therapeutically influenced, target of the treatment is the limitation of the secondary damage (delayed non-mechanical damage). It is influenced by changes in cerebral blood flow (hypo- and hyperperfusion), impairment of cerebrovascular autoregulation, cerebral metabolic dysfunction and inadequate cerebral oxygenation. Furthermore, excitotoxic cell damage and inflammation may lead to apoptotic and necrotic cell death. Understanding the multidimensional cascade of secondary brain injury offers…

InflammationNecrosisTraumatic brain injurybusiness.industryInflammationVasospasmBrain Edemamedicine.disease_causemedicine.diseaseBioinformaticsPathophysiologyOxidative StressAnesthesiology and Pain MedicineOxygen ConsumptionCerebral blood flowAnesthesiaBrain InjuriesCerebrovascular CirculationmedicineHumansmedicine.symptombusinessCell damageOxidative stressBritish journal of anaesthesia
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An Interface Mechanical Model with a Cohesive to Frictional Transition

2009

A thermodynamically consistent mechanical interface model is presented. The model is based on the interface damage mechanic theory applied in a special fashion such that the interface damage variable is also used as a parameter which drives the continuous and smooth transition from the sound initial cohesive state to the final fully fractured frictional state. Interface damage activation and fictional sliding are promoted by a damage activation function and a Coulomb frictional yielding function. The main features of the model are discussed in details and some numerical results for the material response are shown in monotonic and cyclic loading regimes.

Interface damage cohesive fracture process zone frictional cyclic loading finite elementsSettore ICAR/08 - Scienza Delle Costruzioni
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Study of the cytolethal distending toxin (CDT)-activated cell cycle checkpoint. Involvement of the CHK2 kinase.

2001

AbstractThe bacterial cytolethal distending toxin (CDT) triggers a G2/M cell cycle arrest in eukaryotic cells by inhibiting the CDC25C phosphatase-dependent CDK1 dephosphorylation and activation. We report that upon CDT treatment CDC25C is fully sequestered in the cytoplasmic compartment, an effect that is reminiscent of DNA damage-dependent checkpoint activation. We show that the checkpoint kinase CHK2, an upstream regulator of CDC25C, is phosphorylated and activated after CDT treatment. In contrast to what is observed with other DNA damaging agents, we demonstrate that the activation of CHK2 can only take place during S-phase. Use of wortmannin and caffeine suggests that this effect is no…

Intracellular FluidCell cycle checkpointCytolethal distending toxinCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiochemistryS PhaseWortmanninchemistry.chemical_compoundStructural BiologyPhosphorylation0303 health sciences030302 biochemistry & molecular biologyCell CycleCell cycleProtein-Tyrosine Kinases3. Good healthCell biologyDNA-Binding Proteinsbiological phenomena cell phenomena and immunityWortmanninG2 PhaseCytolethal distending toxinBacterial ToxinsProto-Oncogene Proteins pp60(c-src)Biophysics[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesCell Line03 medical and health sciencesCaffeineGeneticsHumanscdc25 PhosphatasesCHEK1Molecular Biology[SDV.BC] Life Sciences [q-bio]/Cellular Biology030304 developmental biologyCheckpoint 2 kinaseCyclin-dependent kinase 1Cell growthTumor Suppressor ProteinsCell BiologyG2-M DNA damage checkpointCDC25CAndrostadienesGenes cdcchemistryCancer researchHeLa CellsFEBS letters
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Large diurnal variation of intraocular pressure in open angle glaucoma in subjects with type A behaviour pattern

2014

Aim : To evaluate the possible causes of the greater perimetric damage found in OAG subjects with type A behaviour and the possible role of psycho-physiological stress. Materials and methods : 80 patients with OAG, 44 women and 36 men, 40 with type A behaviour and 40 with type B studied with the Type A/B Personality Questionnaire (A modified version of the Jenkins Activity Survey), underwent a complete ophthalmologic examination consisting of bio-microscopy, tonometry and daily tonometric curve, examination of the visual field by means of Octopus 1-2-3 computerised perimeter and its assessment with the Glaucoma Staging System 2 (GSS2), morphological monitoring of the Retinal Nerve Fibre Lay…

Intraocular pressuremedicine.medical_specialtyOpen angle glaucomabusiness.industrySettore MED/30 - Malattie Apparato VisivoeducationDiurnal temperature variationType A behaviour patternhumanitiesStress (mechanics)Blood pressureOphthalmologyType a behaviour pattern open angle glaucoma intraocular pressure perimetric damage arterial pressureOptometryMedicinebusiness
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Concentration-Dependent Protection by Ethanol Extract ofPropolis against &#947

2011

[EN] Radioprotection with natural products may be relevant to the mitigation of ionizing radiation-induced damage in mammalian systems; in this sense, propolis extracts have shown effects such as antioxidant, antitumoral, anti-inflammatory, and immunostimulant. We report for the first time a cytogenetic study to evaluate the radioprotective effect, in vitro, of propolis against radiation-induced chromosomal damage. Lymphocytes were cultured with increasing concentrations of ethanol extract of propolis (EEP), including 20, 40, 120, 250, 500, 750, 1000, and 2000 ¿g mL-1 and then exposed to 2 Gy ¿-rays. A significant and concentration-dependent decrease is observed in the frequency of chromoso…

Ionizing radiationRadiation protectionIn vitro studyDicentric chromosomeINGENIERIA NUCLEARPropolisArticleCell protectionCytogeneticsAntioxidant activityHuman cellFree radicalGamma radiationChromosome damageConcentration (parameters)LymphocyteChromosome aberrationRadiation injuryAlcoholLymphocyte cultureHumanPriority journal
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The elemental role of iron in DNA synthesis and repair

2017

Iron is an essential redox element that functions as a cofactor in many metabolic pathways. Critical enzymes in DNA metabolism, including multiple DNA repair enzymes (helicases, nucleases, glycosylases, demethylases) and ribonucleotide reductase, use iron as an indispensable cofactor to function. Recent striking results have revealed that the catalytic subunit of DNA polymerases also contains conserved cysteine-rich motifs that bind iron–sulfur (Fe/S) clusters that are essential for the formation of stable and active complexes. In line with this, mitochondrial and cytoplasmic defects in Fe/S cluster biogenesis and insertion into the nuclear iron-requiring enzymes involved in DNA synthesis a…

Iron-Sulfur Proteins0301 basic medicineDNA RepairDNA polymeraseDNA damageDNA repairIronBiophysicsDNA repairEukaryotic DNA replicationSaccharomyces cerevisiaeBiochemistryDNA GlycosylasesBiomaterials03 medical and health sciencesRibonucleotide ReductasesHumansProtein–DNA interactionRibonucleotide reductaseReplication protein Achemistry.chemical_classificationDNA ligaseDeoxyribonucleasesDNA synthesis030102 biochemistry & molecular biologybiologyIron deficiencyDNA HelicasesMetals and AlloysHelicaseDNAYeast030104 developmental biologyIron cofactorBiochemistrychemistryChemistry (miscellaneous)biology.proteinIron-sulfur clusterMetallomics
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The Friedreich's Ataxia protein frataxin modulates DNA base excision repair in prokaryotes and mammals

2010

DNA-repair mechanisms enable cells to maintain their genetic information by protecting it from mutations that may cause malignant growth. Recent evidence suggests that specific DNA-repair enzymes contain ISCs (iron–sulfur clusters). The nuclearencoded protein frataxin is essential for the mitochondrial biosynthesis of ISCs. Frataxin deficiency causes a neurodegenerative disorder named Friedreich's ataxia in humans. Various types of cancer occurring at young age are associated with this disease, and hence with frataxin deficiency. Mice carrying a hepatocyte-specific disruption of the frataxin gene develop multiple liver tumours for unresolved reasons. In the present study, we show that frata…

Iron-Sulfur ProteinsDNA Repairmedicine.disease_causeBiochemistryDNA Glycosylases8-oxoG 78-dihydro-8-oxoguanineMice0302 clinical medicineIron-Binding Proteinsoxidative stressBER base excision repairCells CulturedMammalsMice Knockout0303 health sciencesfrataxinDMEM Dulbecco's modified Eagle's mediumbiologyLiver NeoplasmsSalmonella entericairon–sulfur clusterLife SciencesIron-binding proteinsTransfection3. Good healthLB Luria–BertaniOGG1 8-oxoguanine DNA glycosylase 1ISC iron–sulfur clusterFpg formamido-pyrimidine DNA glycosylaseHPRT hypoxanthine phosphoribosyltransferaseResearch ArticleDNA damageDNA repairSSB DNA single-strand breakTransfectionCell Line03 medical and health sciencesFRDA Friedreich's ataxiaROS reactive oxygen speciesmedicineAnimalsHumansMUTYH human mutY homologue (Escherichia coli)Molecular BiologyGene030304 developmental biologyFriedreich's ataxiaCell BiologyFibroblastsMolecular biologytumorigenesisProkaryotic CellsFriedreich AtaxiaDNA base excision repairDNA glycosylaseMutationHepatocytesFrataxinbiology.proteinInstitut für ErnährungswissenschaftCarcinogenesisMAPK mitogen-activated protein kinase030217 neurology & neurosurgeryDNA Damage
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High dose infusion of activated protein C (rhAPC) fails to improve neuronal damage and cognitive deficit after global cerebral ischemia in rats

2013

Abstract Purpose : Recent studies demonstrated anticoagulatory, antiinflammatory, antiapoptotic, and neuroprotective properties of activated protein C (APC) in rodent models of acute neurodegenerative diseases, suggesting APC as promising broad acting therapeutic agent. Unfortunately, continuous infusion of recombinant human APC (rhAPC) failed to improve brain damage following cardiac arrest in rats. The present study was designed to investigate the neuroprotective effect after global cerebral ischemia (GI) with an optimized infusion protocol. Methods : Rats were subjected to bilateral clip occlusion of the common carotid arteries (BCAO) and controlled hemorrhagic hypotension to 40 mmHg for…

IschemiaInflammationBrain damagePharmacologyNeuroprotectionBrain IschemiaRats Sprague-DawleyBrain ischemiamedicineAnimalsHumansCerebral perfusion pressureInfusions IntravenousCell Deathbusiness.industryGeneral NeuroscienceDrotrecogin alfaBrainmedicine.diseaseRecombinant ProteinsRatsAnesthesiamedicine.symptombusinessProtein CProtein Cmedicine.drugNeuroscience Letters
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Strain localization and fracture in isotropic damaging materials: a novel augmented-finite element strategy

2022

Isotropic Damage ModelCrack tracking algorithmStrain localizationSettore ICAR/08 - Scienza Delle CostruzioniAugmented-Finite Element Method
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