Search results for "TNF"

showing 10 items of 161 documents

Regulation of the effects of CYP2E1-induced oxidative stress by JNK signaling

2014

The generation of excessive amounts of reactive oxygen species (ROS) leads to cellular oxidative stress that underlies a variety of forms of hepatocyte injury and death including that from alcohol. Although ROS can induce cell damage through direct effects on cellular macromolecules, the injurious effects of ROS are mediated largely through changes in signal transduction pathways such as the mitogen-activated protein kinase c-Jun N-terminal kinase (JNK). In response to alcohol, hepatocytes have increased levels of the enzyme cytochrome P450 2E1 (CYP2E1) which generates an oxidant stress that promotes the development of alcoholic steatosis and liver injury. These effects are mediated in larg…

Alcoholic liver diseaseClinical BiochemistryReview ArticleMitogen-activated protein kinase kinasemedicine.disease_causeBiochemistryCytochrome P450 2E10302 clinical medicineMolecular Targeted TherapyMitogen-activated protein kinaseslcsh:QH301-705.5c-Jun N-terminal kinasechemistry.chemical_classificationTNF tumor necrosis factorlcsh:R5-9200303 health sciencesCell DeathCYP2E1 cytochrome P450 2E1Cytochrome P-450 CYP2E13. Good healthCell biologyPKD protein kinase DLiverJNK c-Jun N-terminal kinaseSab SH3 homology associated BTK binding protein030211 gastroenterology & hepatologySignal transductionlcsh:Medicine (General)MAP Kinase Signaling SystemAPAP acetaminophenMKK MAPK kinaseBiology03 medical and health sciencesROS reactive oxygen speciesPKC protein kinase CmedicineAnimalsHumansMAPKKK MAPK kinase kinaseProtein kinase ACell damage030304 developmental biologyReactive oxygen speciesMAP kinase kinase kinaseOrganic ChemistryJNK Mitogen-Activated Protein KinasesAlcoholic liver diseasemedicine.diseaseERK1/2 extracellular signal-regulated kinase 1/2Fatty Liverlcsh:Biology (General)chemistryOxidative stressNAFLD nonalcoholic fatty liver diseaseReactive Oxygen SpeciesMAPK mitogen-activated protein kinaseOxidative stressRedox Biology
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Sinergy of action between rehabilitation protocol and anti-TNF alpha versus biological therapy

2012

AS is a chronic and progressive pathology that notably cripples the patient's psyco-physical status, with a remarkable compromising of the relational life. Practising regularly the therapeutic exercise along with the anti-TNF alpha, allowed a quick pain reduction, a long maintenance of the rachis functional elasticity and a correct posture, giving a better social and professional life quality.

Ankylosing Spondylitis anti-TNF alpha biological therapy rehabilitationSettore MED/34 - Medicina Fisica E Riabilitativa
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Le infezioni in corso di terapia anti- TNF alfa

2012

Anti TNF-alfa infezioni leishmaniosi cutanea
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Induction of annexin-1 during TRAIL-induced apoptosis in thyroid carcinoma cells

2005

We investigated the expression of annexin-1 (ANXA1) in thyroid carcinoma cell lines and in thyroid cancers with a different degree of differentiation. The highest level of ANXA1 expression examined by Western blotting was detected in the papillary carcinoma cells (NPA) and in the follicular cells (WRO). On the other hand, the most undifferentiated thyroid carcinoma cells (ARO and FRO) presented the lowest level of ANXA1 expression. In surgical tissue specimens from 32 patients with thyroid cancers, we found high immunoreactivity for ANXA1 in papillary (PTC) and follicular (FTC) thyroid cancers while in undifferentiated thyroid cancers (UTC) the expression of the protein was barely detectabl…

ApoptosisTNF-Related Apoptosis-Inducing LigandApoptosis Regulatory ProteinsthyroidThyroid carcinomaTNF-Related Apoptosis-Inducing LigandText miningAnnexinMedicineHumansThyroid NeoplasmsMolecular BiologyThyroid NeoplasmAnnexin A1Apoptosis Regulatory ProteinMembrane Glycoproteinsbusiness.industryTumor Necrosis Factor-alphaApoptosiCell BiologyApoptosisCancer researchMembrane GlycoproteinbusinessApoptosis Regulatory ProteinsHuman
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Involvement of PAR-4 in Cannabinoid-Dependent Sensitization of Osteosarcoma Cells to TRAIL-Induced Apoptosis

2014

The synthetic cannabinoid WIN 55,212-2 is a potent cannabinoid receptor agonist with anticancer potential. Experiments were performed to determine the effects of WIN on proliferation, cell cycle distribution, and programmed cell death in human osteosarcoma MG63 and Saos-2 cells. Results show that WIN induced G2/M cell cycle arrest, which was associated with the induction of the main markers of ER stress (GRP78, CHOP and TRB3). In treated cells we also observed the conversion of the cytosolic form of the autophagosome marker LC3-I into LC3-II (the lipidated form located on the autophagosome membrane) and the enhanced incorporation of monodansylcadaverine and acridine orange, two markers of t…

AutophagosomeautophagyProgrammed cell deathCannabinoids ER stress autophagy TRAIL osteosarcoma cells GRP78/PAR-4 complex.Cannabinoid receptorMorpholinesCellApoptosisTRAILNaphthalenesBiologyGRP78/PAR-4 complex.Applied Microbiology and BiotechnologyTNF-Related Apoptosis-Inducing LigandCadaverineCell Line TumorSettore BIO/10 - BiochimicamedicineHumansRNA Small InterferingEndoplasmic Reticulum Chaperone BiPMolecular BiologyHeat-Shock ProteinsEcology Evolution Behavior and SystematicsCell ProliferationCannabinoid Receptor AgonistsOsteosarcomaCannabinoidsAutophagyCell Cycle Checkpointsosteosarcoma cellsCell BiologyCell cycleEndoplasmic Reticulum StressAcridine OrangeBenzoxazinesCell biologymedicine.anatomical_structureApoptosisAutophagosome membraneApoptosis Regulatory ProteinsER stressMicrotubule-Associated ProteinsResearch PaperDevelopmental Biology
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Obesity and Outcomes in COVID-19: When an Epidemic and Pandemic Collide.

2020

Obesity has reached epidemic proportions in the United States and in much of the westernized world, contributing to considerable morbidity. Several of these obesity-related morbidities are associated with greater risk for death with coronavirus disease 2019 (COVID-19). Severe acute respiratory syndrome coronavirus 2 penetrates human cells through direct binding with angiotensin-converting enzyme 2 receptors on the cell surface. Angiotensin-converting enzyme 2 expression in adipose tissue is higher than that in lung tissue, which means that adipose tissue may be vulnerable to COVID-19 infection. Obese patients also have worse outcomes with COVID-19 infection, including respiratory failure, n…

BMI body mass indexmedicine.medical_treatmentAdipose tissue030204 cardiovascular system & hematologyCHD coronary heart diseaseHF heart failureUS United States0302 clinical medicineRAAS renin-angiotensin-aldosterone systemPandemicMedicine030212 general & internal medicineCDC Centers for Disease Control and PreventionCOVID-19 coronavirus disease 2019TNF tumor necrosis factorHFpEF HF with preserved ejection fractionCV cardiovascularGeneral MedicinePrognosisICU intensive care unitPA physical activityMetS metabolic syndromePAH pulmonary arterial hypertensionCoronavirus Infectionsmedicine.medical_specialtyAF atrial fibrillationACE angiotensin-converting enzymePneumonia ViralCVD cardiovascular diseaseSARS-CoV-2 severe acute respiratory syndrome coronavirus 2ArticleSeverity03 medical and health sciencesBetacoronavirusInternal medicineIPF idiopathic pulmonary fibrosisHumansObesityMortalityHTN hypertension or hypertensivePandemicsMechanical ventilationAng II angiotensin IIbusiness.industrySARS-CoV-2CKD chronic kidney diseaseCOVID-19T2DM type 2 diabetes mellitusmedicine.diseaseAngiotensin IIObesityIL interleukinPneumoniaRespiratory failureMetabolic syndromebusinessSNS sympathetic nervousMayo Clinic proceedings
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A Key Regulatory Role of the Transcription Factor NFATc2 in Bronchial Adenocarcinoma via CD8+ T Lymphocytes

2009

AbstractThe Ca2+-regulated calcineurin/nuclear factor of activated T cells (NFAT) cascade controls alternative pathways of T-cell activation and peripheral tolerance. Here, we describe reduction of NFATc2 mRNA expression in the lungs of patients with bronchial adenocarcinoma. In a murine model of bronchoalveolar adenocarcinoma, mice lacking NFATc2 developed more and larger solid tumors than wild-type littermates. The extent of central tumor necrosis was decreased in the tumors in NFATc2(−/−) mice, and this finding was associated with reduced tumor necrosis factor-α and interleukin-2 (IL-2) production by CD8+ T cells. Adoptive transfer of CD8+ T cells of NFATc2(−/−) mice induced transforming…

CD4-Positive T-LymphocytesCancer ResearchAdoptive cell transferTranscription GeneticTransplantation HeterologousMice TransgenicReceptors Nerve Growth FactorAdenocarcinomaCD8-Positive T-LymphocytesBiologyReceptors Tumor Necrosis FactorTransforming Growth Factor beta1Interferon-gammaMiceGlucocorticoid-Induced TNFR-Related ProteinAnimalsHumansIL-2 receptorInterleukin-7 receptorMice Inbred BALB CReceptors Interleukin-7NFATC Transcription FactorsTumor Necrosis Factor-alphaBronchial NeoplasmsInterleukin-2 Receptor alpha SubunitPeripheral toleranceForkhead Transcription FactorsNFATCalcineurinDisease Models AnimalOncologyCancer researchInterleukin-2Tumor necrosis factor alphaCD8Cancer Research
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Regulatory activity of human CD4 CD25 T cells depends on allergen concentration, type of allergen and atopy status of the donor.

2005

Regulatory CD4+ CD25+ FoxP3-positive T cells (Treg) are functional in most atopic patients with allergic rhinitis and are able to inhibit T helper type 1 (Th1) and Th2 cytokine production of CD4+ CD25- T cells. This study was designed to analyse the following additional aspects: influence of allergen concentration, influence of the type of allergen, and influence of the atopy status of the donor on the strength of the regulatory activity. CD4+ CD25- T cells from healthy non-atopic controls or from grass-pollen-allergic or wasp-venom-allergic donors were stimulated alone or in the presence of Treg with autologous mature monocyte-derived dendritic cells which were pulsed with different concen…

CD4-Positive T-LymphocytesHypersensitivity ImmediateAllergymedicine.medical_treatmentImmunologyDose-Response Relationship Immunologicchemical and pharmacologic phenomenaWasp VenomsReceptors Nerve Growth FactorBiologymedicine.disease_causePoaceaeReceptors Tumor Necrosis FactorAtopyInterleukin 21AllergenTh2 CellsAntigenT-Lymphocyte SubsetsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyHumansIL-2 receptorReceptorCells CulturedCell Proliferationhemic and immune systemsForkhead Transcription FactorsReceptors Interleukin-2Original ArticlesAllergensTh1 Cellsmedicine.diseaseCoculture TechniquesCytokineImmunologyCytokinesPollenImmunology
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NFATc2 and NFATc3 transcription factors play a crucial role in suppression of CD4+ T lymphocytes by CD4+ CD25+ regulatory T cells

2005

The phenotype of NFATc2(-/-) c3(-/-) (double knockout [DKO]) mice implies a disturbed regulation of T cell responses, evidenced by massive lymphadenopathy, splenomegaly, and autoaggressive phenomena. The population of CD4(+) CD25(+) T cells from DKO mice lacks regulatory capacity, except a small subpopulation that highly expresses glucocorticoid-induced tumor necrosis factor receptor family-related gene (GITR) and CD25. However, neither wild-type nor DKO CD4(+) CD25(+) regulatory T cells (T reg cells) are able to suppress proliferation of DKO CD4(+) CD25(-) T helper cells. Therefore, combined NFATc2/c3 deficiency is compatible with the development of CD4(+) CD25(+) T reg cells but renders c…

CD4-Positive T-LymphocytesT cellImmunologyPopulationchemical and pharmacologic phenomenaReceptors Nerve Growth FactorBiologyLymphocyte ActivationReceptors Tumor Necrosis FactorInterleukin 21MiceT-Lymphocyte SubsetsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorReceptoreducationTranscription factorMice Knockouteducation.field_of_studyNFATC Transcription FactorsZAP70Brief Definitive ReportNuclear Proteinshemic and immune systemsReceptors Interleukin-2Molecular biologyCoculture TechniquesDNA-Binding Proteinsmedicine.anatomical_structureTranscription FactorsThe Journal of Experimental Medicine
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Increased percentages of tumor necrosis factor-alpha+/interferon-gamma+ T lymphocytes and calprotectin+/tumor necrosis factor-alpha+ monocytes in pat…

2012

CalprotectinSettore MED/38 - Pediatria Generale E SpecialisticaKawasaki Disease; Calprotectin; TNF alfaKawasaki DiseaseTNF alfa
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