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Готові списки джерел за темами / Inflammation Mediators / Статті в журналах

Щоб переглянути інші типи публікацій з цієї теми, перейдіть за посиланням: Inflammation Mediators.

Статті в журналах з теми "Inflammation Mediators"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 25 липня 2025

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1

Finsnes, Finn, Torstein Lyberg, Geir Christensen, and Ole H. Skjønsberg. "Effect of endothelin antagonism on the production of cytokines in eosinophilic airway inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 4 (2001): L659—L665. http://dx.doi.org/10.1152/ajplung.2001.280.4.l659.

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Endothelin (ET)-1 has been launched as an important mediator in bronchial asthma, which is an eosinophilic airway inflammation. However, the interplay between ET-1 and other proinflammatory mediators during the development of airway inflammation has not been elucidated. We wanted to study 1) whether the production of ET-1 precedes the production of other proinflammatory mediators and 2) whether ET-1 stimulates the production of these mediators within the airways. These hypotheses were studied during the development of an eosinophilic airway inflammation in rats. The increase in ET-1 mRNA level

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2

GREAVES, M. W. "Inflammation and mediators." British Journal of Dermatology 119, no. 4 (1988): 419–26. http://dx.doi.org/10.1111/j.1365-2133.1988.tb03245.x.

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3

Sacca, R. "Mediators of inflammation." Current Opinion in Immunology 9, no. 6 (1997): 851–57. http://dx.doi.org/10.1016/s0952-7915(97)80189-6.

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4

Moore, Terry L., and Terry D. Weiss. "Mediators of inflammation." Seminars in Arthritis and Rheumatism 14, no. 4 (1985): 247–62. http://dx.doi.org/10.1016/0049-0172(85)90044-7.

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5

Lazarus, Stephen C. "Inflammation, Inflammatory Mediators, and Mediator Antagonists in Asthma." Journal of Clinical Pharmacology 38, no. 7 (1998): 577–82. http://dx.doi.org/10.1002/j.1552-4604.1998.tb04463.x.

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6

Sudo, Maki, and Koichi Fujimoto. "Diffusive mediator feedbacks control the health-to-disease transition of skin inflammation." PLOS Computational Biology 20, no. 1 (2024): e1011693. http://dx.doi.org/10.1371/journal.pcbi.1011693.

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The spatiotemporal dynamics of inflammation provide vital insights into the understanding of skin inflammation. Skin inflammation primarily depends on the regulatory feedback between pro- and anti-inflammatory mediators. Healthy skin exhibits fading erythema. In contrast, diseased skin exhibits expanding erythema with diverse patterns, which are clinically classified into five types: circular, annular, arcuate, gyrate, and polycyclic. Inflammatory diseases with expanding erythema are speculated to result from the overproduction of pro-inflammatory mediators. However, the mechanism by which fee

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7

Alderton, Gemma. "Lipid mediators of inflammation." Science 371, no. 6526 (2021): 248.9–250. http://dx.doi.org/10.1126/science.371.6526.248-i.

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8

Robinson, Dwight R. "Lipid Mediators of Inflammation." Rheumatic Disease Clinics of North America 13, no. 2 (1987): 385–405. http://dx.doi.org/10.1016/s0889-857x(21)00854-1.

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9

Laurent, G. J. "Mediators of Pulmonary Inflammation." Thorax 47, no. 9 (1992): 764. http://dx.doi.org/10.1136/thx.47.9.764-a.

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10

Lasky, Laurence A. "Combinatorial mediators of inflammation?" Current Biology 3, no. 6 (1993): 366–68. http://dx.doi.org/10.1016/0960-9822(93)90203-z.

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11

du Bois, R. M. "Mediators of pulmonary inflammation." Immunology Today 13, no. 10 (1992): 424. http://dx.doi.org/10.1016/0167-5699(92)90100-l.

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12

Reilly, Christopher, Nicole Regna, and Abigail Peairs. "EGCG Inhibits Inflammation Independently of AMPK (87.10)." Journal of Immunology 184, no. 1_Supplement (2010): 87.10. http://dx.doi.org/10.4049/jimmunol.184.supp.87.10.

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Abstract Epigallocatechin-3-gallate (EGCG), a bioactive component of green tea, has been reported to exert anti-inflammatory effects in immune cells. EGCG has been shown to activate the metabolic regulator, AMP-activated protein kinase (AMPK). Mesangial cells from MRL/lpr lupus-like mice are hyper-responsive to immune stimulation and overproduce nitric oxide (NO) and other inflammatory mediators when stimulated. In our current studies, we sought to determine if EGCG would inhibit inflammation in AMPK deficient mesangial cells. Cultured mesangial cells from MRL/lpr mice were treated with siRNA

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13

Lu, Yan, Song Hong, Katherine Gotlinger, and Charles Serhan. "Lipid Mediator Informatics and Proteomics in Inflammation-Resolution." Scientific World JOURNAL 6 (2006): 589–614. http://dx.doi.org/10.1100/tsw.2006.118.

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Анотація:

Lipid mediator informatics is an emerging area denoted to the identification of bioactive lipid mediators (LMs) and their biosynthetic profiles and pathways. LM informatics and proteomics applied to inflammation, systems tissues research provides a powerful means of uncovering key biomarkers for novel processes in health and disease. By incorporating them with system biology analysis, we review here our initial steps toward elucidating relationships among a range of bimolecular classes and provide an appreciation of their roles and activities in the pathophysiology of disease. LM informatics e

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14

Ramon, Sesquile, Charles Serhan, and Richard Phipps. "Actions of novel inflammation-resolving lipid mediators on human B cells (84.9)." Journal of Immunology 184, no. 1_Supplement (2010): 84.9. http://dx.doi.org/10.4049/jimmunol.184.supp.84.9.

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Abstract The resolution of inflammation is an active and dynamic process. Newly identified lipid mediators have been recognized as key players during the process of inflammation resolution. These lipid-derived molecules constitute three classes of compounds (lipoxins, resolvins and protectins), all derived from essential fatty acids. New data demonstrates that these lipid mediators regulate aspects of the immune response, including inhibition of neutrophil infiltration, reduction of T cell cytokine production and stimulation of macrophage phagocytic activity. However, their effects on B lympho

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15

Eerden, Menno M. Van Der. "Mediators Of Inflammation In COPD." Pulmonary Medicine and Respiratory Research 5, no. 2 (2019): 1–10. http://dx.doi.org/10.24966/pmrr-0177/100026.

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16

Cooper, P. R., J. L. McLachlan, S. Simon, L. W. Graham, and A. J. Smith. "Mediators of Inflammation and Regeneration." Advances in Dental Research 23, no. 3 (2011): 290–95. http://dx.doi.org/10.1177/0022034511405389.

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Characterization of the molecular response under caries lesions requires a robust and reliable transcript isolation system, and analysis of data indicated that collection of extracted teeth in either liquid nitrogen/RNA-stabilizing solution facilitated this. Subsequent transcriptional analysis indicated higher general activity in carious pulps, while characterization of inflammatory mediators, including cytokines and S100 proteins, highlighted increasing expression levels associated with both microbial front progression and elevated cellular immune response. Analysis of the pleiotropic hormone

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17

Rankin, James A. "Biological Mediators of Acute Inflammation." AACN Clinical Issues: Advanced Practice in Acute and Critical Care 15, no. 1 (2004): 3–17. http://dx.doi.org/10.1097/00044067-200401000-00002.

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18

LUGER, T. "Mediators of immunity and inflammation." Journal of the European Academy of Dermatology and Venereology 11 (September 1998): S25—S26. http://dx.doi.org/10.1016/s0926-9959(98)94625-6.

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19

Rand, Royden. "Mediators of immunity and inflammation." Clinical Biochemistry 22, no. 3 (1989): 241–43. http://dx.doi.org/10.1016/s0009-9120(89)80083-9.

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20

Schlag, G., and H. Redl. "Mediators of Injury and Inflammation." World Journal of Surgery 20, no. 4 (1996): 406–10. http://dx.doi.org/10.1007/s002689900064.

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21

Agrawal, Anshu. "Vision for Mediators of Inflammation." Mediators of Inflammation 2020 (March 4, 2020): 1. http://dx.doi.org/10.1155/2020/9202849.

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22

Lai, Kar Neng, Sydney C. W. Tang, and Joseph C. K. Leung. "Mediators of Inflammation and Fibrosis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 27, no. 2_suppl (2007): 65–71. http://dx.doi.org/10.1177/089686080702702s12.

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During peritoneal dialysis, peritoneal cells are repeatedly exposed to a non-physiologic hypertonic environment with high glucose content and low pH. Current sterile dialysis solutions cause inflammation in the submesothelial compact zone, leading to fibrosis, angiogenesis, and, eventually, ultrafiltration failure. Although the normal interstitium separates the peritoneal microvasculature from the dialysis fluid and makes transperitoneal transport less efficient, changes in the submesothelial compact zone can result in progressive increases in solute transfer and ultrafiltration diminution. Th

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23

Abboud, Hanna E. "Cytokine mediators of renal inflammation." Current Opinion in Nephrology and Hypertension 3, no. 3 (1994): 329–33. http://dx.doi.org/10.1097/00041552-199405000-00015.

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24

Schirripa, Maria Laura, Maria Pia Scarpelli, and Cristian Palmiere. "Mediators of Inflammation in Asthma." American Journal of Forensic Medicine and Pathology 38, no. 2 (2017): 153–58. http://dx.doi.org/10.1097/paf.0000000000000306.

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25

Steinhubl, Steven R. "Platelets as Mediators of Inflammation." Hematology/Oncology Clinics of North America 21, no. 1 (2007): 115–21. http://dx.doi.org/10.1016/j.hoc.2006.11.015.

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26

Hoch, Matti, Jannik Rauthe, Konstantin Cesnulevicius, et al. "Cell-Type-Specific Gene Regulatory Networks of Pro-Inflammatory and Pro-Resolving Lipid Mediator Biosynthesis in the Immune System." International Journal of Molecular Sciences 24, no. 5 (2023): 4342. http://dx.doi.org/10.3390/ijms24054342.

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Lipid mediators are important regulators in inflammatory responses, and their biosynthetic pathways are targeted by commonly used anti-inflammatory drugs. Switching from pro-inflammatory lipid mediators (PIMs) to specialized pro-resolving (SPMs) is a critical step toward acute inflammation resolution and preventing chronic inflammation. Although the biosynthetic pathways and enzymes for PIMs and SPMs have now been largely identified, the actual transcriptional profiles underlying the immune cell type-specific transcriptional profiles of these mediators are still unknown. Using the Atlas of Inf

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27

Ishihara, Tomoaki, Mio Yoshida, and Makoto Arita. "Omega-3 fatty acid-derived mediators that control inflammation and tissue homeostasis." International Immunology 31, no. 9 (2019): 559–67. http://dx.doi.org/10.1093/intimm/dxz001.

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AbstractOmega-3 polyunsaturated fatty acids (PUFAs), including eicosapentaenoic acid, docosapentaenoic acid and docosahexaenoic acid, display a wide range of beneficial effects in humans and animals. Many of the biological functions of PUFAs are mediated via bioactive metabolites produced by fatty acid oxygenases such as cyclooxygenases, lipoxygenases and cytochrome P450 monooxygenases. Liquid chromatography–tandem mass spectrometry-based mediator lipidomics revealed a series of novel bioactive lipid mediators derived from omega-3 PUFAs. Here, we describe recent advances on omega-3 PUFA-derive

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28

Harold Adrian, Liemena, Budi Satrijo, Djanggan Sargowo, and Indra Prasetya. "The Role of Colchicine in Acute Coronary Syndrome." Heart Science Journal 1, no. 4 (2020): 4–8. http://dx.doi.org/10.21776/ub.hsj.2020.001.04.02.

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Background: Despite the advances of current optimal treatment of atherosclerotic disease, the incidence of events after acute coronary syndrome (ACS) remains high. Colchicine, with its well-established pleiotropic anti-inflam- matory effects, may inhibit NLRP3 inflammasome, a key mediator in atherosclerosis-associated inflammation (AAI) thus reducing systemic inflammation. NRLP3 inflammasome activation inside leukocytes (mainly monocytes and neutrophils) is precipitated by cholesterol crystals that are present in all atherosclerosis stages. 􏰟􏰋􏰡􏰈􏰇􏱎􏰋􏰇􏰆􏰂 􏰍􏰀􏰂􏰅􏰩􏰍􏰂􏰅􏰃􏰆 􏰃􏰜 􏰢􏰎􏰃􏰐􏰅􏰆􏰜􏰏􏰍􏰝􏰝􏰍􏰂􏰃􏰎􏰁 􏰀􏰁􏰂􏰃􏰄􏰅􏰆􏰇􏰈 􏰈

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29

Bannenberg, Gerhard, Makoto Arita, and Charles N. Serhan. "Endogenous Receptor Agonists: Resolving Inflammation." Scientific World JOURNAL 7 (2007): 1440–62. http://dx.doi.org/10.1100/tsw.2007.188.

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Controlled resolution or the physiologic resolution of a well-orchestrated inflammatory response at the tissue level is essential to return to homeostasis. A comprehensive understanding of the cellular and molecular events that control the termination of acute inflammation is needed in molecular terms given the widely held view that aberrant inflammation underlies many common diseases. This review focuses on recent advances in the understanding of the role of arachidonic acid and ω-3 polyunsaturated fatty acids (PUFA)–derived lipid mediators in regulating the resolution of inflammation. Using

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30

Lam, Derek, Devon Harris, and Zhenyu Qin. "Inflammatory Mediator Profiling Reveals Immune Properties of Chemotactic Gradients and Macrophage Mediator Production Inhibition during Thioglycollate Elicited Peritoneal Inflammation." Mediators of Inflammation 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/931562.

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Understanding of spatiotemporal profiling of inflammatory mediators and their associations with MΦ accumulation is crucial to elucidate the complex immune properties. Here, we used murine thioglycollate elicited peritonitis to determine concentrations of 23 inflammatory mediators in peritoneal exudates and plasma before (day 0) and after (days 1 and 3) thioglycollate administration to peritoneal cavities; these mediators included TNF-α, FGF-9, IFN-γ, IP-10, RANTES, IL-1α, IL-6, IL-7, IL-10, IL-11, IL-12p70, IL-17A, lymphotactin, OSM, KC/GRO, SCF, MIP-1β, MIP-2, TIMP-1, VEGF-A, MCP-1, MCP-3, an

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31

Shavazi, Nurali Mamedovich Tagayeva Aziza Odiljonovna. "SARS IN NEONATOLOGY." Yosh olimlar 1, no. 8 (2023): 91–93. https://doi.org/10.5281/zenodo.8050697.

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SARS is the most common pathology in both children and adults, especially in the winter period of diseases. Inflammation of the mucosa of the upper and lower respiratory tract is accompanied by hypersecretion of viscous mucus, edema of the mucous membrane of the respiratory tract, impaired mucociliary transport and bronchial obstruction. Inflammation of the mucous membrane occurs with the participation of humoral and cellular mediators of inflammation, the main role in this case belongs to the cellular mediator - eicosanoids.

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32

Avenatti, R. C. "The intersection of inflammation, insulin resistance and ageing: implications for the study of molecular signalling pathways in horses." Comparative Exercise Physiology 8, no. 3-4 (2012): 153–71. http://dx.doi.org/10.3920/cep12018.

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Inflammation-associated insulin resistance contributes to chronic disease in humans and other long-lived species, such as horses. Insulin resistance arises due to an imbalance among molecular signalling mediators in response to pro-inflammatory cytokines in the aged and obese. The mammalian heat shock protein response has received much attention as an avenue for attenuating inflammatory mediator signalling and for contributing to preservation and restoration of insulin signalling in metabolically important tissues. Data on heat shock proteins and inflammatory signalling mediators in untrained

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33

Kharbanda, Rajat, and Tarun Bansal. "Adipokines: mediators of immunity and inflammation." International Journal of Research in Medical Sciences 8, no. 7 (2020): 2746. http://dx.doi.org/10.18203/2320-6012.ijrms20202929.

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White adipose tissue has emerged as a highly dynamic organ that releases a plethora of immune and inflammatory mediators that are involved in obesity, metabolic syndrome and immune mediated diseases. Adipokines have complex role in various physiological and pathological processes by exerting potent modulatory actions on target tissues In this Review, In this review, we explore the effects of different adipokines, focusing primarily on leptin, adiponectin, visfatin and resistin in causing immune-mediated and/or inflammatory diseases.

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34

Herkel, Johannes, and Dirk Schmidt-Arras. "Mediators of liver inflammation and carcinogenesis." Seminars in Immunopathology 43, no. 4 (2021): 477–79. http://dx.doi.org/10.1007/s00281-021-00880-x.

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35

Flower, R. J. "Inflammation: The mediators of steroid action." Nature 320, no. 6057 (1986): 20. http://dx.doi.org/10.1038/320020a0.

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36

Jose, P. J. "Complement-derived peptide mediators of inflammation." British Medical Bulletin 43, no. 2 (1987): 336–49. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072186.

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37

Lerner, Ulf H., and Goran Sundquist. "Mediators of inflammation-induced bone resorption." Dental Traumatology 7, no. 4 (1991): 186. http://dx.doi.org/10.1111/j.1600-9657.1991.tb00206.x.

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38

Wallace, John L., Angela Ianaro, Kyle L. Flannigan, and Giuseppe Cirino. "Gaseous mediators in resolution of inflammation." Seminars in Immunology 27, no. 3 (2015): 227–33. http://dx.doi.org/10.1016/j.smim.2015.05.004.

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39

LUGER, T. "C057 Mediators of immunity and inflammation." Journal of the European Academy of Dermatology and Venereology 9 (September 1997): S70—S71. http://dx.doi.org/10.1016/s0926-9959(97)89132-5.

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40

Leid, R. Wes, and Kathleen A. Potter. "Inflammation and Mediators of Lung Injury." Veterinary Clinics of North America: Food Animal Practice 1, no. 2 (1985): 377–400. http://dx.doi.org/10.1016/s0749-0720(15)31332-3.

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41

FORD-HUTCHINSON, A. W., and ANITA RACKMAN. "Leukotrienes as mediators of skin inflammation." British Journal of Dermatology 109 (July 29, 2006): 26–29. http://dx.doi.org/10.1111/j.1365-2133.1983.tb06814.x.

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42

BATSFORD, STEPHEN R. "Cationic antigens as mediators of inflammation." APMIS 99, no. 1-6 (1991): 1–9. http://dx.doi.org/10.1111/j.1699-0463.1991.tb05110.x.

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43

Spiropoulos, Kostas, Nikolaos Siafakas, Marc Miravitlles, Francesco Blasi, and Kiriakos Karkoulias. "Mediators of Inflammation in Pulmonary Diseases." Mediators of Inflammation 2015 (2015): 1–2. http://dx.doi.org/10.1155/2015/739219.

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44

Bacon, Kevin B., and Thomas J. Schall. "Chemokines as Mediators of Allergic Inflammation." International Archives of Allergy and Immunology 109, no. 2 (1996): 97–109. http://dx.doi.org/10.1159/000237207.

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45

Scott, Dugald T., Francis Y. Lam, and William R. Ferrell. "Acute joint inflammation—Mechanisms and mediators." General Pharmacology: The Vascular System 25, no. 7 (1994): 1285–96. http://dx.doi.org/10.1016/0306-3623(94)90151-1.

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46

Lowry, Stephen F. "Cytokine Mediators of Immunity and Inflammation." Archives of Surgery 128, no. 11 (1993): 1235. http://dx.doi.org/10.1001/archsurg.1993.01420230063010.

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47

Shi, Xuan-Zheng, John H. Winston, and Sushil K. Sarna. "Differential immune and genetic responses in rat models of Crohn's colitis and ulcerative colitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 300, no. 1 (2011): G41—G51. http://dx.doi.org/10.1152/ajpgi.00358.2010.

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Анотація:

Crohn's disease and ulcerative colitis are clinically, immunologically, and morphologically distinct forms of inflammatory bowel disease (IBD). However, smooth muscle function is impaired similarly in both diseases, resulting in diarrhea. We tested the hypothesis that differential cellular, genetic, and immunological mechanisms mediate smooth muscle dysfunction in two animal models believed to represent the two diseases. We used the rat models of trinitrobenzene sulfonic acid (TNBS)- and dextran sodium sulfate (DSS)-induced colonic inflammations, which closely mimic the clinical and morphologi

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48

Wallace, J. L. "Lipid mediators of inflammation in gastric ulcer." American Journal of Physiology-Gastrointestinal and Liver Physiology 258, no. 1 (1990): G1—G11. http://dx.doi.org/10.1152/ajpgi.1990.258.1.g1.

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The interest in lipid mediators of inflammation as potential contributors to the pathogenesis of gastric ulcer has increased markedly over the past 20 yr. Although a great deal is known about the actions of mediators such as leukotrienes, thromboxane, and platelet-activating factor in experimental models of ulceration, evidence supporting a role for these mediators in human gastric ulcer is sorely lacking. This review attempts to answer a number of questions regarding the contribution of these mediators to the pathogenesis of gastric ulceration and the possible use of specific inhibitors, anta

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49

Gushchin, Igor S. "Interactions of mast cells and eosinophils in allergic response." Russian Journal of Allergy 17, no. 2 (2020): 5–17. http://dx.doi.org/10.36691/rja1363.

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Mast cells (MCs) and eosinophils (EOs) appeared hundreds of millions of years ago during the evolutionary process and continue to be retained by all vertebrate species. There is no convincing evidence of the absence of these cells in vertebrates under normal conditions. These cells are involved in the reactions of innate and adaptive immunity, in the control of tissue growth and tissue remodeling, activation of adipose tissue, affect reproductive functions and have a wide range of mediators involved in homeostasis. It is known that the interaction of these cells is involved in the initiation a

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Knuplez, Eva, Eva Maria Sturm, and Gunther Marsche. "Emerging Role of Phospholipase-Derived Cleavage Products in Regulating Eosinophil Activity: Focus on Lysophospholipids, Polyunsaturated Fatty Acids and Eicosanoids." International Journal of Molecular Sciences 22, no. 9 (2021): 4356. http://dx.doi.org/10.3390/ijms22094356.

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Анотація:

Eosinophils are important effector cells involved in allergic inflammation. When stimulated, eosinophils release a variety of mediators initiating, propagating, and maintaining local inflammation. Both, the activity and concentration of secreted and cytosolic phospholipases (PLAs) are increased in allergic inflammation, promoting the cleavage of phospholipids and thus the production of reactive lipid mediators. Eosinophils express high levels of secreted phospholipase A2 compared to other leukocytes, indicating their direct involvement in the production of lipid mediators during allergic infla

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