A computer model simulates the effect of different types of coals on blast furnace operations. In this study, two kinds of programs, CHEMIX and ESTIMA as parts of a thermochemistry package known as THER-MOCHEMISTRY were used for checking the adiabatic flame temperature. Results showed that the adiabatic temperature decreased considerably as the pulverized coal injection (PCI) rate increased, with the rate of decrease largely dependent on the chemical properties of the coal-mainly the carbon content and calorific value. The coal with the least carbon content has the least effect on the flame temperature. However, the coal/coke replacement ratio is very low. PCI increases the rate of generation of the reducing gases, namely CO(g) and H2(g), which depend largely on the chemical properties of coal. The results suggest that a simple calculation using computing programs may be useful for determining the suitability of a coal for injection in blast furnaces.
Background:Ankylosing Spondylitis (AS) is a chronic inflammatory rheumatic disease, which is characterized by the enthesitis, peripheral arthritis, and chronic inflammation of the spine, leading to bony ankylosis. Signal transducer and activator of transcription (STAT) family proteins are latent cytoplasmic transcription factors that convey signals to the nucleus. It is activated by IL-6, IL-23, and IL-22 through JAK-mediated phosphorylation. Moreover, genetic studies implicate interleukin-23 (IL-23) receptor signal, including STAT3 in the development of AS. IL-17A has recently emerged as a potential target that regulates the extensive inflammation and abnormal bone formation observed in AS. It was reported that STAT3 is a regulatory factor that induces Th17 cell development from naive CD4 T cells.Objectives:The aim of this study is to investigate whether the STAT3 phosphorylation (stat3-p) inhibitor has a therapeutic effect on inflammation and new bone formation in AS.Methods:Eight weeks after curdlan injection, SKG mice were treated with stat3-p inhibitor or mock as a control. Clinical and histologic scores for arthritis and enthesitis were evaluated. Synovial fluid mononuclear cells (SFMC) samples were obtained from AS patients. Inflammatory cytokine producing cells were analyzed using flow cytometry. Bone tissue samples were obtained from the facet joints of patients with AS at surgery. Primary bone-derived cells (BdCs) were isolated and cultured. The osteogenic differentiation was assessed in vitro for 3 weeks using ALP activity, Alizarin red S (ARS), Type I collagen, von kossa,and hydroxyapatitestains. Statistical analysis was performed using Prism 5.0 Software. A p < 0.05 was considered statistically significant.Results:The stat3-p inhibitor significantly suppressed peripheral arthritis and enthesitis in SKG mice (figure 1). Inflammatory infiltration around the tendon–bone insertion site and along the tendon, as well as bony involvement were all reduced in stat3-p inhibitor-treated mice compared to control mice. We found that the levels of IFN-±, IL-17, TNF-± were higher in AS Synovial fluid. A significantly decreased frequencies of IFN-±, IL-17, TNF-± producing cells in AS SFMC were shown after stat3-p inhibitor treatment (P < 0.01).In vitro experiment of bone formation, the stat3-p inhibitor suppressed ALP activity. In addition, there were significant decrease in Alizarin red S (ARS), Type I collagen, von kossa staining scores due to stat3-p inhibitor at a concentration of 5 μM.Light intensity of hydroxyapatitestaining was also decreased by stat3-p inhibitor in a dose dependent manner (figure 2). Intriguingly, the stat3-p inhibitor suppressed osteogenesis in both early phase and late phase in AS-BdCs, down-regulating osteoblast-involved genes.Conclusion:The stat3-p inhibitor had beneficial effects on reducing inflammation and new bone formation in AS animal model. In addition, stat3-p inhibitor suppressed bone formation in vitro experiment. These findings suggest that the stat3-p inhibitor could be a potential therapeutic agent for AS.References:[1]Arthritis Res Ther 2018;20:115.[2]Nat Med 2012;18:1069-76.[3]Rheumatology (Oxford) 2017;56:488-493.[4]Nat Rev Immunol. 2011;11:239–50.[5]J Exp Med 2005;201:949–60.Acknowledgments:NoneDisclosure of Interests:None declared
BackgroundAnkylosing spondylitis (AS) is a rheumatic disease characterized by chronic inflammation. Several lines of evidence implicate interleukin (IL)-17A-secreting T helper (Th)17 cells in AS pathogenesis. One of the receptors of Th17 cell, C-C motif chemokine ligand 20 (CCL20) is known to attract C-C chemokine receptor 6 (CCR6) expressing cells to the site of inflammation. However, the role and mechanisms of CCL20 in AS are not well understood.ObjectivesTherefore, this study aimed to evaluate the function of CCL20 in patients with AS.MethodsPeripheral blood mononuclear cells (PBMCs) and synovial fluid mononuclear cells (SFMCs) were obtained from AS patients. Inflammatory cytokine-producing cells were analyzed using flow cytometry and enzyme-linked immunosorbent assay (ELISA). To determine the direct effect of cell migration in the presence of CCL20, a transwell migration assay was performed. In in vivo experiments, SKG mice were treated with either CCL20 blocking antibody or isotype control antibody. Clinical signs of mice were monitored twice a week and scored by two independent observers. At the experimental endpoint, specimens of the ankle was obtained from mice. Two blinded readers then performed pathological scoring for arthritis using immunohistochemistry.ResultsIL-17A producing cells were significantly higher expressed in SFMCs of AS patients than in PBMCs of AS or healthy controls. CCL20-positive cells showed significantly increased IL-17A production than CCL20-negative cells. To confirm the relationship between CCL20 and IL-17A production, IL-17A expression was observed with either CCL20 agonist or antagonist. Treatment with CCL20 agonist showed an increase in IL-17A in PBMCs from AS patients. Meanwhile decreasing IL-17A level was observed in SFMCs from AS patients when treated with CCL20 inhibitors. In cell migration assay experiments, cell migration increased when CCL20 was added to the CD4-positive cells. In an vivo model, CCL20 inhibitors significantly suppressed arthritis symptoms (Figure 1). In addition, histologic evaluation showed that mice treated with CCL20 inhibitor had lower arthritis scores than isotype-treated control mice.ConclusionThis study demonstrates CCL20 blockade improved joint inflammation in AS. Therefore, CCL20-target therapy could be a promising treatment for AS.Figure 1.CCL20 Inhibition ameliorates peripheral arthritis in SKG miceReferences[1]Taurog, J.D., A. Chhabra, and R.A. Colbert,Ankylosing Spondylitis and Axial Spondyloarthritis.N Engl J Med, 2016.375(13): p. 1303.[2]Watad, A., et al.,The Early Phases of Ankylosing Spondylitis: Emerging Insights From Clinical and Basic Science.Front Immunol, 2018.9: p. 2668.[3]Lee, Y., et al.,Induction and molecular signature of pathogenic TH17 cells.Nat Immunol, 2012.13(10): p. 991-9.[4]Yasuda, K., Y. Takeuchi, and K. Hirota,The pathogenicity of Th17 cells in autoimmune diseases.Semin Immunopathol, 2019.41(3): p. 283-297.[5]Hu, J., et al.,C-C motif chemokine ligand 20 regulates neuroinflammation following spinal cord injury via Th17 cell recruitment.J Neuroinflammation, 2016.13(1): p. 162.Acknowledgements:NIL.Disclosure of InterestsNone Declared.
BackgroundAnkylosing spondylitis (AS) is a sort of inflammatory arthritis that affects axial skeleton, peripheral joints, and certain extra-articular organs, including the eyes, skin, and gut. Recently, many attempts have been made to use parasite administration (e.g., ingestion of eggs of the nematode Trichuris suis) as a new modality for treating inflammatory disorders. Our group published that Clonorchis sinensis protein attenuated inflammation in AS.ObjectivesThus, this study aimed to assess the therapeutic potential of Clonorchis sinensis-Excretory/Secretory protein (Cs-ESP) for AS.MethodsCytotoxicity of Cs-ESP at different doses was assessed by MTS and flow cytometry before performing experiments. Peripheral blood mononuclear cells (PBMCs) and synovial fluid mononuclear cells (SFMCs) were obtained from AS patients. Inflammatory cytokine-producing cells were analyzed using flow cytometry. The levels of INF-g, IL-17A, TNF-a, and IL-6 were measured by enzyme-linked immunosorbent assay (ELISA). SKG mice were treated with Cs-ESP or vehicles. Inflammation was evaluated using immunohistochemistry.ResultsTreatment with Cs-ESP resulted in no reduced cell viability of PBMCs or SFMCs. In experiments culturing PBMCs and SFMCs, the frequencies of IFN-g and IL-17A producing cells were significantly reduced after Cs-ESP treatment. In the SKG mouse model, Cs-ESP treatment significantly suppressed arthritis and enthesitis.ConclusionWe provide the evidence demonstrating that Cs-ESP can ameliorate clinical signs and cytokine derangements in AS.Figure 1.Clonorchis sinensis-Excretory/Secretory protein (Cs-ESP) ameliorates clinical symptoms in SKG miceReferences[1]Kim TJ, Kim TH. Clinical spectrum of ankylosing spondylitis in Korea. Joint Bone Spine (2010) 77(3):235–40.[2]Martinez FD. The coming-of-age of the hygiene hypothesis. Respir Res (2001) 2(3):129–32.[3]Summers RW, Elliott DE, Urban JF Jr., Thompson RA, Weinstock JV. Trichuris suis therapy for active ulcerative colitis: a randomized controlled trial. Gastroenterology (2005) 128(4):825–32.[4]Osada Y, Shimizu S, Kumagai T, Yamada S, Kanazawa T. Schistosoma mansoni infection reduces severity of collagen-induced arthritis via downregulation of pro-inflammatory mediators. Int J Parasitol (2009) 39(4):457– 64.[5]Song X, Shen J, Wen H, Zhong Z, Luo Q, Chu D, et al. Impact of Schistosoma japonicum infection on collagen-induced arthritis in DBA/1 mice: a murine model of human rheumatoid arthritis. PloS One (2011) 6(8):e23453.Acknowledgements:NIL.Disclosure of InterestsNone Declared.
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