Search results for "tumor necrosis factor alpha"

showing 10 items of 479 documents

mRNA Induction and Cytokine Release of Inflammatory Mediators During In Vitro Exposure of Human Nasal Respiratory Epithelia to Acetaldehyde

2006

Acetaldehyde has been shown to be cytotoxic and carcinogenic to the upper respiratory tract epithelium of rodents following long-term exposure. Most animal studies have concentrated on carcinogenicity and DNA-protein cross-link formation, while less is known about potential dose- and time-dependent induction of aldehyde-induced rhinitis in humans. In this in vitro study, 22 primary cell cultures established from inferior turbinate tissue of healthy individuals were exposed to acetaldehyde concentrations of 50 (German MAK value) or 500 ppm for 4 or 24 h. mRNA expression and protein levels of cytokines and other inflammatory mediators were quantified at the end of the 4- and 24-h exposures. C…

Health Toxicology and Mutagenesismedicine.medical_treatmentAcetaldehydeRespiratory MucosaNoseBiologyToxicologychemistry.chemical_compoundmedicineHumansRNA MessengerCells CulturedMonocyteAcetaldehydeInterleukinReal-time polymerase chain reactionmedicine.anatomical_structureCytokineGene Expression RegulationchemistryCell cultureImmunologyCytokinesTumor necrosis factor alphaInflammation MediatorsRespiratory tractInhalation Toxicology
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Letter: switching from one to another anti-tumour necrosis factor alpha agent, and the risks of an overlap of exposure

2016

Hepatologybiologybusiness.industryImmunoglobulin Fab FragmentsGastroenterologyInflammatory Bowel DiseasesToxicology03 medical and health sciences0302 clinical medicineAntibodies monoclonal030220 oncology & carcinogenesisMonoclonalbiology.proteinCancer researchMedicine030211 gastroenterology & hepatologyPharmacology (medical)Tumor necrosis factor alphaAnti-tumour necrosis factor alpha agentAntibodybusinessAlimentary Pharmacology & Therapeutics
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Effects of tumor necrosis factor-alpha on tumor blood flow and hyperthermic treatment.

1989

The impact of recombinant human tumor necrosis factor-alpha (rhTNF-alpha), given alone or in combination with local hyperthermia, on perfusion and growth of a moderately rhTNF-alpha-sensitive rat tumor (DS-carcinosarcoma) was investigated. DS-carcinosarcomas were implanted into the hind foot dorsum of Sprague-Dawley rats. Tumor blood flow (TBF) was measured with the krypton-85 clearance technique. Treatment with either tumor necrosis factor-alpha (0.1-1.0 mg/kg) or hyperthermia (43.3 and 44.3 degrees C, 40 min) can decrease the perfusion of malignant tumors. The TBF reduction was fully established 2 h after rhTNF-alpha injection and lasted for at least 4 h. The application of local hyperthe…

HyperthermiaCancer ResearchNecrosisSoft Tissue NeoplasmsPharmacologyCarcinosarcomaTumor perfusionmedicineAnimalsTumor growthTumor necrosis factor αbusiness.industryTumor Necrosis Factor-alphaRats Inbred StrainsHematologyBlood flowHyperthermia Inducedmedicine.diseaseCombined Modality TherapyRecombinant ProteinsRatsOncologyRegional Blood FlowImmunologyTumor necrosis factor alphamedicine.symptombusinessPerfusionCell DivisionNeoplasm TransplantationOnkologie
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In vivo targets of recombinant human tumour necrosis factor-α: blood flow, oxygen consumption and growth of isotransplanted rat tumours

1989

The impact of recombinant human tumour necrosis factor-alpha (1 microgram kg-1 to 1 mg kg-1; 6.6 x 10(6) U mg protein-1) on blood flow, oxygen consumption and growth of a moderately TNF-sensitive rat tumour (DS-carcinosarcoma) was studied. Tumour growth was stimulated at low TNF doses (1 and 10 micrograms kg-1) and significantly retarded at higher TNF dose levels (0.1 and 1 mg kg-1). Growth changes were concomitant with variations in oxygen consumption, lactate release and acidification of the metabolic micromilieu. Both single and repeated application of low TNF doses (1-10 micrograms kg-1 i.v.) increased tumour perfusion whereas single administration of high TNF dose levels (0.1-1 mg kg-1…

HyperthermiaCancer Researchmedicine.medical_specialtyNecrosismedicine.medical_treatmentBiologyOxygen ConsumptionCarcinosarcomaIn vivoInternal medicinemedicineAnimalsChemotherapyTumor Necrosis Factor-alphaCell growthAscitesRats Inbred StrainsBlood flowmedicine.diseaseRecombinant ProteinsRatsEndocrinologyOncologyRegional Blood FlowTumor necrosis factor alphamedicine.symptomPerfusionNeoplasm TransplantationResearch ArticleBritish Journal of Cancer
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Do Changes in Tumor Blood Flow Necessarily Lead to Changes in Tissue Oxygenation and in Bioenergetic Status?

1994

An increasing number of investigations carried out in recent years provide evidence suggesting that “chronic” decreases in tumor blood flow and/or tissue oxygenation (e.g., during tumor growth) or acute declines in the tissue perfusion (e.g., following therapeutic measures) might be accompanied by significant reductions in the energy status. In several instances, positive correlations between energy status and tumor blood flow or oxygenation have been reported (Lilly et al., 1985; Evelhoch et al., 1986; Tozer et al., 1989; Vaupel et al., 1989a, 1989b; Steen and Graham, 1991), and these investigations have led to the conclusion that blood flow may be the limiting factor in determining the bi…

Hyperthermiamedicine.medical_specialtybusiness.industryVasodilationBlood flowOxygenationHydralazinemedicine.diseaseEndocrinologyLymphotoxinInternal medicinemedicineTumor necrosis factor alphabusinessPerfusionmedicine.drug
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A20 deficiency in B cells enhances B-cell proliferation and results in the development of autoantibodies.

2011

A20/TNFAIP3 is an ubiquitin-editing enzyme, important for the regulation of the NF-κB pathway. Mutations in the TNFAIP3 gene have been linked to different human autoimmune disorders. In human B-cell lymphomas, the inactivation of A20 results in constitutive NF-κB activation. Recent studies demonstrate that in mice the germline inactivation of A20 leads to early lethality, due to inflammation in multiple organs of the body. In this report, we describe a new mouse strain allowing for the tissue-specific deletion of A20. We show that B-cell-specific deletion of A20 results in a dramatic reduction in marginal zone B cells. Furthermore, A20-deficient B cells display a hyperactive phenotype repre…

ImmunologyB-Lymphocyte SubsetsInflammationBiologymedicine.disease_causeLymphocyte ActivationGermlineAutoimmunityMiceimmune system diseaseshemic and lymphatic diseasesmedicineImmunology and AllergyAnimalsHumansTumor Necrosis Factor alpha-Induced Protein 3AutoantibodiesCell ProliferationMice KnockoutB-LymphocytesCell growthAutoantibodyIntracellular Signaling Peptides and ProteinsNF-kappa BMarginal zoneGerminal CenterMolecular biologyPhenotypeCell biologyCysteine EndopeptidasesModels Animalbiology.proteinmedicine.symptomAntibodySignal TransductionEuropean journal of immunology
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Immunologic Effects of Interferon

1990

Interferons can be defined as a family of induced proteins sharing the capacity to exert pleiotropic effects on cell functions and to render cells resistant to virus infection. They are activating genes coding for a number of enzymes, most of which have not yet been characterized, and also by enhancing the synthesis of cell surface components. This enables interferons to modulate the immune response at different levels. This article will focus on the effects of interferon on antigen presentation, regulation of the immune response, activation of macrophage functions, and on its role in the pathogenesis of some diseases.

InflammationInterleukin 2Immunity CellularMacrophagesCellAntigen presentationCell BiologyDermatologyBiologyBiochemistryInterferon-gammamedicine.anatomical_structureImmune systemInterferonImmune SystemImmunologymedicineAnimalsHumansMacrophageTumor necrosis factor alphaInterferonsMolecular Biologymedicine.drugInterferon regulatory factorsJournal of Investigative Dermatology
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Methylprednisolone neutralizes the beneficial effects of erythropoietin in experimental spinal cord injury

2005

Inflammation plays a major pathological role in spinal cord injury (SCI). Although antiinflammatory treatment using the glucocorticoid methyprednisolone sodium succinate (MPSS) improved outcomes in several multicenter clinical trials, additional clinical experience suggests that MPSS is only modestly beneficial in SCI and poses a risk for serious complications. Recent work has shown that erythropoietin (EPO) moderates CNS tissue injury, in part by reducing inflammation, limiting neuronal apoptosis, and restoring vascular autoregulation. We determined whether EPO and MPSS act synergistically in SCI. Using a rat model of contusive SCI, we compared the effects of EPO [500-5,000 units/kg of bod…

InflammationPharmacologyProinflammatory cytokineRats Sprague-DawleymedicineAnimalsDrug InteractionsMethylprednisolone HemisuccinateInterleukin 6ErythropoietinSpinal cord injurySpinal Cord InjuriesMultidisciplinarybiologyInterleukin-6Tumor Necrosis Factor-alphabusiness.industryBiological Sciencesmedicine.diseaseRecombinant ProteinsRatscytokines glucocorticoids inflammation neuroprotection traumaMethylprednisoloneErythropoietinImmunologybiology.proteinTumor necrosis factor alphamedicine.symptombusinessGlucocorticoidmedicine.drugProceedings of the National Academy of Sciences
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Cross-talk between oxidative stress and pro-inflammatory cytokines in acute pancreatitis: a key role for protein phosphatases.

2009

Acute pancreatitis is an acute inflammatory process localized in the pancreatic gland that frequently involves peripancreatic tissues. It is still under investigation why an episode of acute pancreatitis remains mild affecting only the pancreas or progresses to a severe form leading to multiple organ failure and death. Proinflammatory cytokines and oxidative stress play a pivotal role in the early pathophysiological events of the disease. Cytokines such as interleukin 1beta and tumor necrosis factor alpha initiate and propagate almost all consequences of the systemic inflammatory response syndrome. On the other hand, depletion of pancreatic glutathione is an early hallmark of acute pancreat…

Inflammationmedicine.disease_causeProinflammatory cytokineDrug DiscoveryPhosphoprotein PhosphatasesMedicineAnimalsHumansPharmacologyInflammationbiologybusiness.industrymedicine.diseaseSystemic inflammatory response syndromeOxidative StressPancreatitisMitogen-activated protein kinaseImmunologyAcute Diseasebiology.proteinAcute pancreatitisPancreatitisCytokinesTumor necrosis factor alphamedicine.symptomMitogen-Activated Protein KinasesbusinessOxidation-ReductionOxidative stressSignal TransductionCurrent pharmaceutical design
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Human GITR Ligand Is Expressed on Tumor Cells and Reduces Cytokine Production and Cellular Cytotoxicity of NK Cells Identified to Express GITR.

2005

Abstract Members of the tumor necrosis factor (TNF) superfamily mediate multiple cellular functions including cellular proliferation, differentiation, and cell death. Human Glucocorticoid-induced TNF Receptor (GITR) has been shown to be expressed on T cells, is upregulated following activation and mediates costimulatory signals. The human GITR ligand (GITRL) has been reported to be expressed on antigen presenting cells and various healthy nonlymphoid tissues including small intestine, ovary, testis, kidney and endothelial cells. We analyzed multiple tumor cell lines of hematopoietic and epithelial origin as well as of germ cell lineage and various gliomas by RT-PCR and FACS analysis. Both G…

Innate immune systemmedicine.medical_treatmentImmunologyCell BiologyHematologyBiologyAcquired immune systemBiochemistryCell biologyInterleukin 21CytokineInterleukin 15medicineInterleukin 12Tumor necrosis factor alphaAntigen-presenting cellBlood
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