PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11284446-3 2001 There were no significant changes in the plasma levels of NO2-/NO3-levels over time following treatment with TNF-alpha, but there was a significant increase (approximately twofold) in the activity of the iNOS in the lungs of animals treated with TNF-alpha. Nitrogen Dioxide 58-61 tumor necrosis factor Rattus norvegicus 246-255 16398938-2 2006 Exposure of rats to NO2 has recently been shown to induce a shift in the activation type of AM that is characterized by reduced TNF-alpha and increased IL-10 production. Nitrogen Dioxide 20-23 tumor necrosis factor Rattus norvegicus 128-137 8760140-2 1996 Stimulation of rat pleural mesothelial cells with combinations of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), and LPS induced the synthesis of nitric oxide as measured by the oxidation products nitrite (NO2-) and nitrate (NO3-). Nitrogen Dioxide 262-265 tumor necrosis factor Rattus norvegicus 98-125 1919006-11 1991 In addition, increased levels of NO2- were observed in medium of A23187, TNF-alpha, or WEHI-164-stimulated PMC. Nitrogen Dioxide 33-36 tumor necrosis factor Rattus norvegicus 73-82 7536858-3 1995 LPS, tumor necrosis factor-alpha (TNF-alpha) and the combination of both were able to induce NO synthesis in a dose-dependent manner as measured with the determination of NO2- levels. Nitrogen Dioxide 171-174 tumor necrosis factor Rattus norvegicus 5-32 7536858-3 1995 LPS, tumor necrosis factor-alpha (TNF-alpha) and the combination of both were able to induce NO synthesis in a dose-dependent manner as measured with the determination of NO2- levels. Nitrogen Dioxide 171-174 tumor necrosis factor Rattus norvegicus 34-43 1729374-10 1992 Macrophages incubated with rTNF-alpha in combination with a nonactivating concentration of rIFN-gamma released substantial amounts of NO2-, but rTNF-alpha and rIL-1 alpha alone, and the combination of rIL-1 alpha and a nonactivating concentration of rIFN-gamma induced only little NO2(-)-release by macrophages. Nitrogen Dioxide 134-137 tumor necrosis factor Rattus norvegicus 27-37 1729374-10 1992 Macrophages incubated with rTNF-alpha in combination with a nonactivating concentration of rIFN-gamma released substantial amounts of NO2-, but rTNF-alpha and rIL-1 alpha alone, and the combination of rIL-1 alpha and a nonactivating concentration of rIFN-gamma induced only little NO2(-)-release by macrophages. Nitrogen Dioxide 281-284 tumor necrosis factor Rattus norvegicus 27-37 8760140-4 1996 Stimulation with IL-1 beta and TNF-alpha plus H2O2 or IL-1 beta and LPS plus H2O2 increased the synthesis of NO2- and NO3- by 3.8- and 3.5-fold, respectively. Nitrogen Dioxide 109-112 tumor necrosis factor Rattus norvegicus 31-40 7539274-9 1995 Finally, in the immune complex model of alveolitis, the appearance of iNOS in macrophages as well as macrophage production in vitro of NO2-/NO3- was dependent on the in vivo availability of tumor necrosis factor alpha, IL-1, and IFN-gamma. Nitrogen Dioxide 135-138 tumor necrosis factor Rattus norvegicus 190-217 8102159-4 1993 Stimuli such as PMA, LPS, and/or IFN-gamma induce micromolar concentrations of NO2- within 24 h. TNF-alpha increases IFN gamma but not LPS-induced NO2- production. Nitrogen Dioxide 79-82 tumor necrosis factor Rattus norvegicus 97-106 8102159-4 1993 Stimuli such as PMA, LPS, and/or IFN-gamma induce micromolar concentrations of NO2- within 24 h. TNF-alpha increases IFN gamma but not LPS-induced NO2- production. Nitrogen Dioxide 147-150 tumor necrosis factor Rattus norvegicus 97-106 8102159-6 1993 NO2- production is inhibited by NO synthase antagonists, transforming growth factor-beta, and anti TNF-alpha. Nitrogen Dioxide 0-3 tumor necrosis factor Rattus norvegicus 99-108 8473748-6 1993 Neutralizing concentrations of anti-TNF mAb completely abrogated IFN-gamma- and IFN-gamma plus rTNF-alpha-induced NO2- production in ANA-1 macrophages, but only decreased by approximately 50% the synergistic interaction between IFN-gamma and picolinic acid. Nitrogen Dioxide 114-117 tumor necrosis factor Rattus norvegicus 95-105 7681038-4 1993 Like M phi, these clones were found to release high levels of NO2- in response to recombinant interferon-gamma (rIFN-gamma) as a priming signal together with either bacterial lipopolysaccharide (LPS) or exogenous recombinant tumor necrosis factor-alpha (rTNF-alpha). Nitrogen Dioxide 62-65 tumor necrosis factor Rattus norvegicus 254-264 1915557-4 1991 As shown here, the capacity of phagocytosis to elicit NO2- production by IFN-gamma-treated M phi was inhibited by antibody to murine recombinant tumor necrosis factor-alpha (rTNF-alpha), suggesting that phagocytosis enabled IFN-gamma to activate M phi via the induction of TNF-alpha as an autocrine second signal. Nitrogen Dioxide 54-57 tumor necrosis factor Rattus norvegicus 174-184 1915557-6 1991 However, addition of either Leishmania promastigotes or latex beads to M phi cultures simultaneously exposed to both IFN-gamma and exogenous murine or human rTNF-alpha further potentiated activation as measured by NO2- release. Nitrogen Dioxide 214-217 tumor necrosis factor Rattus norvegicus 157-167 25912222-8 2015 Recombinant TNFalpha (rTNFalpha) enhanced NO2(-) synthesis and C666-1 NPC cell proliferation. Nitrogen Dioxide 42-45 tumor necrosis factor Rattus norvegicus 22-31 25912222-9 2015 NOS2 selective inhibition (1400W) and TNFalpha antagonization with an anti-TNFalpha mAb potently inhibited rTNFalpha induced C666-1 proliferation and NO2(-) production. Nitrogen Dioxide 150-153 tumor necrosis factor Rattus norvegicus 107-116 3142779-2 1988 Recombinant interferon-gamma (rIFN-gamma) and recombinant tumor necrosis factor (rTNF) synergize to induce nitrite (NO2-) and nitrate (NO3-) synthesis from L-arginine as well as to cause inhibition of the iron-dependent enzyme aconitase in macrophages. Nitrogen Dioxide 116-119 tumor necrosis factor Rattus norvegicus 81-85