Search results for "tumor necrosis factor-alpha"

showing 10 items of 504 documents

Intraperitoneal injection of tetracyclines protects mice from lethal endotoxemia downregulating inducible nitric oxide synthase in various organs and…

1997

We have tested whether tetracyclines (TETs) are able to protect mice from lipopolysaccharide (LPS)-induced shock, a cytokine-mediated inflammatory reaction. Mice, injected with a single dose of tetracycline base (TETb; 1.5, 10 and 20 mg/kg of body weight) or doxycycline (DOXY; 1.5 mg/kg), were significantly protected from a lethal intraperitoneal injection of LPS (500 micrograms per mouse). TETs acted in early events triggered in response to LSP; in fact, they were no longer significantly protective if injected more than 1 h after the injection of endotoxin. LPS-treated mice protected by TETs showed a significant inhibition of tumor necrosis factor alpha (TNF-alpha), interleukin-1 alpha (IL…

medicine.medical_specialtyLipopolysaccharidemedicine.medical_treatmentIntraperitoneal injectionDown-RegulationAlpha (ethology)SpleenBiologyMicechemistry.chemical_compoundInternal medicinemedicineAnimalsPharmacology (medical)LungAntibacterial agentPharmacologyMice Inbred BALB CNitratesTumor Necrosis Factor-alphaTetracyclineShock SepticEndotoxemiaAnti-Bacterial AgentsNitric oxide synthaseInfectious DiseasesEndocrinologyCytokinemedicine.anatomical_structurechemistryDoxycyclineEnzyme InductionMacrophages Peritonealbiology.proteinCytokinesFemaleTumor necrosis factor alphaNitric Oxide SynthaseInjections IntraperitonealSpleenInterleukin-1Research ArticleAntimicrobial Agents and Chemotherapy
researchProduct

Heart failure and anti tumor necrosis factor-alpha in systemic chronic inflammatory diseases.

2013

Tumor necrosis factor alpha (TNF-alpha) antagonists have emerged as an effective therapy for patients with diseases as Crohn's disease, rheumatoid arthritis, and other chronic systemic inflammatory diseases. In the last years, there has been a growing interest in the role that inflammatory cytokines, which sustain the pathogenesis of these diseases, plays in regulating cardiac structure and function, particularly in the progression of chronic heart failure. In fact there is an increase of anti-TNF alpha levels in advanced heart failure but the treatment with anti-TNF alpha has been shown to worsen the prognosis of heart failure in randomized controlled trials. Patients with rheumatoid arthr…

medicine.medical_specialtyPathologySettore MED/09 - Medicina InternaAlpha (ethology)DiseaseGastroenterologyProinflammatory cytokinePathogenesisRisk FactorsInternal medicineInternal MedicinemedicineHumansHeart FailureInflammationCrohn's diseaseTumor Necrosis Factor-alphabusiness.industrymedicine.diseaseHeart failureRheumatoid arthritishearth failure.biologicsChronic DiseaseTumor necrosis factor alphabusiness
researchProduct

Is there a role for recombinant tumor necrosis factor alpha in the intravesical treatment of superficial bladder tumors?--a phase II study

1995

Clinical use of recombinant tumor necrosis factor-alpha is strongly limited by its severe toxicity, mainly cardiovascular, when systemically administered. Recent studies suggest that topical (intrapleural, intraperitoneal, intratumoral) administration is free of significant toxicity. Human recombinant tumor necrosis factor-alpha was administered intravesically, at a dose of 500 mg dissolved in 30 ml of phosphate buffer (pH7.6-7.8) plus 0.25% human albumin, weekly for two months to 18 patients with papillary transitional cell carcinoma of the bladder. Of the 15 evaluable patients, four (26%) achieved a complete response. Systemic and local tolerability were excellent. Int J Urol 1995;2:100-1…

medicine.medical_specialtyPathologyUrologyUrologyPhases of clinical researchlaw.inventionlawRecurrencemedicineHumansPapillary transitional cell carcinomaCarcinoma Transitional Cellbusiness.industryTumor Necrosis Factor-alphaRecombinant ProteinRecombinant ProteinsRecombinant Tumor Necrosis Factor-AlphaIntravesical treatmentAdministration IntravesicalTolerabilityUrinary Bladder NeoplasmsToxicityRecombinant DNATumor necrosis factor alphabusinessHuman
researchProduct

Exercise restores decreased physical activity levels and increases markers of autophagy and oxidative capacity in myostatin/activin blocked mdx mice

2013

The importance of adequate levels of muscle size and function and physical activity is widely recognized. Myostatin/activin blocking increases skeletal muscle mass but may decrease muscle oxidative capacity and can thus be hypothesized to affect voluntary physical activity. Soluble activin receptor IIB (sActRIIB-Fc) was produced to block myostatin/activins. Modestly dystrophic mdx mice were injected with sActRIIB-Fc or PBS with or without voluntary wheel running exercise for 7 wk. Healthy mice served as controls. Running for 7 wk attenuated the sActRIIB-Fc-induced increase in body mass by decreasing fat mass. Running also enhanced/restored the markers of muscle oxidative capacity and autoph…

medicine.medical_specialtyPhysiologyActivin Receptors Type IIEndocrinology Diabetes and MetabolismBlotting WesternCitrate (si)-SynthaseMyostatinMotor ActivityHematocritMuscle hypertrophyEatingHemoglobinsMice03 medical and health sciences0302 clinical medicinePhysical Conditioning AnimalPhysiology (medical)Internal medicineAutophagymedicineAnimalsMuscle Skeletalta315Creatine KinaseAdiposity030304 developmental biology0303 health sciencesbiologymedicine.diagnostic_testTumor Necrosis Factor-alphaBody WeightAutophagySkeletal muscleDNAActivin receptorMyostatinActivinsMice Inbred C57BLmedicine.anatomical_structureEndocrinologyHematocritMice Inbred mdxbiology.proteinCreatine kinaseTumor necrosis factor alphaOxidation-Reduction030217 neurology & neurosurgeryAmerican Journal of Physiology-Endocrinology and Metabolism
researchProduct

Anti-Tumour Necrosis Factor-?? Therapy for Rheumatoid and Other Inflammatory Arthropathies

2006

Anti-tumour necrosis factor (TNF)-alpha represents a major advance in the treatment of rheumatoid arthritis (RA), ankylosing spondylitis and psoriatic arthritis. It is usually well tolerated, but a potential increase in the incidence of some infections in patients taking anti-TNFalpha agents has been reported. Compared with younger people, elderly patients have more co-morbidities and are likely to be taking more medications. Moreover, the aging process induces an increase in the rate of infections. Nevertheless, in recent studies analysing the databases of etanercept trials, the normalised incidence of adverse events, serious adverse events, medically important infections and deaths was no…

medicine.medical_specialtyPopulationArthritisSubgroup analysisEtanerceptArthritis RheumatoidPsoriatic arthritisInternal medicinemedicineHumansPharmacology (medical)Adverse effecteducationAgedRandomized Controlled Trials as TopicAged 80 and overeducation.field_of_studyAnkylosing spondylitisTumor Necrosis Factor-alphabusiness.industryArthritismedicine.diseaseAntirheumatic AgentsRheumatoid arthritisImmunologyGeriatrics and Gerontologybusinessmedicine.drugDrugs & Aging
researchProduct

Protein oxidation in metabolic syndrome

2013

Purpose: Oxidative stress plays a pivotal role in the pathogenesis of the metabolic syndrome and in the progression of its complications. Carbonylated proteins are a stable marker of severe oxidative stress because damage to the protein structure is irreversible and may cause an inhibition of their enzymatic activity or an increased susceptibility to proteolysis. There are few data regarding protein oxidation in metabolic syndrome, although elevated levels of carbonyl groups are often detected in subjects with obesity, diabetes mellitus, hypertension or dyslipidemia, well-known components of the metaboic syndrome. In particular, obesity, insulin resistance and diabetes mellitus are frequent…

medicine.medical_specialtySettore MED/09 - Medicina InternaProtein CarbonylationBiologyProtein oxidationmedicine.disease_causeProtein CarbonylationInsulin resistanceDiabetes mellitusInternal medicinemedicineAnimalsHumansMetabolic SyndromeInterleukin-6Tumor Necrosis Factor-alphaGeneral Medicinemedicine.diseaseOxidative Stressprotein oxidation metabolic syndromeEndocrinologyResistinMetabolic syndromeInsulin ResistanceDyslipidemiaOxidative stress
researchProduct

Differential regulation of interleukin-6 expression in human fibroblasts by tumor necrosis factor-alpha and lymphotoxin.

1990

The treatment of human diploid fibroblasts with tumor necrosis factor (TNF)-alpha and with lymphotoxin (LT) is associated with induction of interleukin-6 (IL-6) transcripts with TNF-alpha being 10-fold more potent than LT. Here we report on the TNF-alpha/LT-induced signaling mechanisms responsible for the regulation of IL-6 gene expression in these cells. Run-on assays demonstrated that both TNF-alpha and LT increase IL-6 mRNA levels by transcriptional activation of this gene. Stability studies of IL-6 transcripts in fibroblasts showed that TNF-alpha delayed IL-6 mRNA decay but not LT. The induction of IL-6 transcripts by TNF-alpha and LT was not inhibited by the isoquinoline sulfonamide de…

medicine.medical_specialtyTime FactorsTranscription Geneticmedicine.medical_treatmentCellular differentiationBiophysicsCycloheximideBiologyBiochemistrychemistry.chemical_compoundStructural BiologyInternal medicineGene expressionGeneticsmedicineHumansRNA MessengerMolecular BiologyLymphotoxin-alphaProtein kinase CCells CulturedProtein Kinase CInterleukin-6Tumor Necrosis Factor-alphaCell BiologyFibroblastsMolecular biologyKineticsCytokineLymphotoxinEndocrinologychemistryGene Expression RegulationProtein BiosynthesisTumor necrosis factor alphaSignal transductionFEBS letters
researchProduct

Update on the principles and novel local and systemic therapies for the treatment of non-infectious uveitis.

2012

Ocular inflammatory disorders constitute a sight-threatening group of diseases that might be managed according to their severity. Their treatment guidelines experience constant changes with new agents that improve the results obtained with former drugs. Nowadays we can make use of a five step protocol in which topical, periocular and systemic corticosteroids remain as the main therapy for non-infectious uveitis. In addition, immunosuppresive drugs can be added in order to enhance the anti-inflammatory effects and to play the role of corticosteroid-sparing agents. These can be organized in four other steps: cyclosporine and methotrexate in a second one; azathioprine, mycophenolate and tacrol…

medicine.medical_specialtyTreatment protocolCyclophosphamideAdministration TopicalImmunologyAnti-Inflammatory AgentsAzathioprineUveitisInfectious uveitisAdrenal Cortex HormonesmedicineImmunology and AllergyAnimalsHumansIntensive care medicinePharmacologyChlorambucilbusiness.industryTumor Necrosis Factor-alphaGeneral Medicinemedicine.diseaseTacrolimusSurgeryInjections IntravenousPractice Guidelines as TopicMethotrexateImmunotherapybusinessUveitisAlgorithmsImmunosuppressive Agentsmedicine.drugInflammationallergy drug targets
researchProduct

Mitochondrial complex I impairment in leukocytes from polycystic ovary syndrome patients with insulin resistance.

2009

Insulin resistance is a feature of polycystic ovary syndrome (PCOS) and is related to mitochondrial function.Our objective was to assess mitochondrial function by evaluating mitochondrial oxygen (O(2)) consumption, reactive oxygen species (ROS) production, levels of glutathione (GSH), the oxidized glutathione/GSH ratio, TNFalpha levels, and membrane potential. Additionally, we have evaluated mitochondrial complex I as a target of the oxidative stress responsible for PCOS in polymorphonuclear cells.This was a prospective controlled study conducted in an academic medical center.The study population consisted of 20 lean reproductive-age women with PCOS and 20 body composition-matched controls.…

medicine.medical_specialtyendocrine system diseasesEndocrinology Diabetes and Metabolismmedicine.medical_treatmentClinical BiochemistryContext (language use)BiologyMitochondrionmedicine.disease_causeBiochemistrychemistry.chemical_compoundEndocrinologyInsulin resistanceOxygen ConsumptionInternal medicinemedicineLeukocytesHumanschemistry.chemical_classificationMembrane Potential MitochondrialReactive oxygen speciesElectron Transport Complex ITumor Necrosis Factor-alphaInsulinBiochemistry (medical)nutritional and metabolic diseasesGlutathionemedicine.diseasePolycystic ovaryGlutathionefemale genital diseases and pregnancy complicationsEndocrinologychemistryFemaleInsulin ResistanceReactive Oxygen SpeciesOxidative stressPolycystic Ovary Syndrome
researchProduct

Human antiphospholipid antibodies induce TNFα in monocytes via Toll-like receptor 8

2009

The antiphospholipid syndrome (APS) is characterized by recurrent arterial and/or venous thromboses, pregnancy loss and the presence of antiphospholipid antibodies (aPL). One of the discussed mechanisms of this thrombotic activity in APS patients is attributed to TNFalpha secretion in monocytes after aPL stimulation. To investigate this mechanism in detail, we employed a monoclonal aPL and IgG fractions of APS patients for stimulation of human peripheral monocytes. Stimulation with this monoclonal aPL resulted in an increased expression and secretion of TNFalpha, caused by specific upregulation of TLR8 mRNA and protein expression levels. To confirm the specificity of this finding we could d…

medicine.medical_specialtymedicine.drug_classBlotting WesternImmunologyEnzyme-Linked Immunosorbent AssayStimulationCell SeparationBiologyMonoclonal antibodyPeripheral blood mononuclear cellMonocytesProinflammatory cytokineDownregulation and upregulationimmune system diseasesAntiphospholipid syndromeInternal medicinemedicineHumansImmunology and AllergyReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaAntibodies MonoclonalHematologyAntiphospholipid SyndromeFlow Cytometrymedicine.diseaseEndocrinologyToll-Like Receptor 8MonoclonalImmunologyAntibodies AntiphospholipidElectrophoresis Polyacrylamide GelTumor necrosis factor alphaImmunobiology
researchProduct