Relevant bibliographies by topics / Inflammation Mediators

Academic literature on the topic 'Inflammation Mediators'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Journal articles on the topic "Inflammation Mediators":

1

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

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

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

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

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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 (April 1, 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 in lung tissue preceded the increase in mRNA levels of tumor necrosis factor-α, interleukin (IL)-1β, and IL-8. Treatment of the animals with the ET receptor antagonist bosentan resulted in a substantial decrease in the concentrations of tumor necrosis factor-α, IL-4, IL-1β, interferon-γ, and ET-1 in bronchoalveolar lavage fluid. In conclusion, the synthesis of ET-1 as measured by increased mRNA level precedes the synthesis of other proinflammatory cytokines of importance for the development of an eosinophilic airway inflammation, and ET antagonism inhibits the production of these mediators within the airways. Whether treatment with ET antagonists will prove beneficial for patients with eosinophilic airway inflammations like bronchial asthma is not yet known.
6

Alderton, Gemma. "Lipid mediators of inflammation." Science 371, no. 6526 (January 14, 2021): 248.9–250. http://dx.doi.org/10.1126/science.371.6526.248-i.

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

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Laurent, G. J. "Mediators of Pulmonary Inflammation." Thorax 47, no. 9 (September 1, 1992): 764. http://dx.doi.org/10.1136/thx.47.9.764-a.

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

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

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Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Inflammation Mediators":

1

Farrell, Adrian J. "Mediators of synovial inflammation." Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284326.

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Woollard, Kevin J. "Mediators of monocyte activity in inflammation." Thesis, Aston University, 2003. http://publications.aston.ac.uk/11001/.

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The effects of incubation of CRP with human primary and monocytic cell lines were examined using monocytic cytokine expression, adhesion molecule expression and adhesion to endothelial cells and intracellular peroxide formation, as end points. Monocytic intracellular signalling events were investigated after interaction of CRP with specific CRP receptors on monocytes. These initial signalling events were examined for their role in modulating monocyric adhesipn molecule and cytokine expression. Monocyte recruitment and retention in the vasculature is also influenced by oxidative stress. Therefore the effect of 6 weeks of antioxidant intervention in vivo was examined on monocytic adhesion molecule expression, adhesion to endothelial cells ex vivo and on serum CRP concentrations, pre- and post- supplementation with the antioxidants vitamin C and vitamin E. In summary, CRP is able to bind Fc?RIIa. CRP binding Fc?R initiates an intracellular signalling cascade that phosphorylates the non-receptor ryrosine kinase, Syk, associated with intracellular ryrosine activating motifs on the cytoplasmic tail of Fey receptors. CRP incubations increased phosphatidyl inositol turnover and Syk phosphorylation ultimately led to Ca2+ mobilisation in monocytes. CRP mediated Syk phosphorylation in monocytes leads to an increase in CD1 lb and IL-6 expression. CRP engagement with monocytes also leads to an increase in peroxide production, which can be inhibited in vitro using the antioxidants a-tocopherol and ascorbic acid. CRP mediated CDllb expression is not redox regulated by CRP mediated changes in cytosolic peroxides. The Fc?RIIa polymorphism at codon 131 effects the phenotypic driven changes described in monocytes by CRP, where R/R allotypes have a greater increase in CD1 lb, in response to CRP, which may be involved in promoting the monocytic inflammatory response. CRP leads to an increase in the expression of pro-inflammatory cytokines, which alters the immune phenotype of circulating monocytes. Vitamin C supplementation reduced monocytic adhesion to endothelial cells, but had no effect on serum levels of CRP.
3

Robinson, Emily. "Mediators of inflammation in acute neurotoxicity." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/mediators-of-inflammation-in-acute-neurotoxicity(a657668f-f6de-4fb6-878d-65846fc18e66).html.

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Neuroinflammation is a major feature of most neurodegenerative conditions, and can leadto the exacerbation of neuronal injury. Inflammatory challenges in the central nervoussystem (CNS) have been shown to activate peripheral immune cells, which subsequentlyinfiltrate into the brain. Concurrently, resident inflammatory cells in the CNS, such asmicroglia, become activated and release inflammatory mediators, including cytokines.The pro-inflammatory cytokine interleukin-1 (IL-1) is a key mediator of neuronal injury.Although two IL-1 agonists exist, IL-1α and IL-1β, the majority of research has focussedon the contribution of IL-1β to neuronal injury. Excitotoxic cell death in the rat brain,induced by striatal injection of the glutamate agonist AMPA, is exacerbated by coadministrationof recombinant IL-1β. To identify possible mediators which facilitate theexacerbation of neuronal injury by IL-1 this study investigated the early peripheral andcentral mediators of inflammation in response to AMPA + IL-1β.Neutrophil infiltration and increased neuronal activity were found to be present at 4h post-AMPA + IL-1β injection, which lead to the induction of microglial IL-1α in the ipsilateralcortex, in the absence of any IL-1β expression. To target the peripheral neutrophil responsean intervention study was performed to inhibit peripheral TNFα, which is thought tomobilise neutrophils. No significant effect of pre-treatment with etanercept, a TNFαinhibitor, was observed on neuronal injury produced in response to AMPA + IL-1β, thougha slight trend for protection was seen. To target the central IL-1α response after AMPA +IL-1β treatment an anti-IL-1α antibody was injected directly into the cerebral cortex, butthis had no effect on AMPA + IL-1β induced cell death. Therefore, using a reductionist invitro approach in organotypic slice cultures haemin, an inducer of endogenous IL-1α, wasused to investigate IL-1α mediated cell death. Haemin induced cell death was shown to beIL-1 dependent and preliminary studies using IL-1αKO mice indicated that IL-1α maypartially mediate this effect. This suggests that in the AMPA + IL-1β paradigm IL-1α is thedominant IL-1 isoform early after AMPA + IL-1β treatment, which can trigger subsequentneuronal cell death, as a result of the additive effects of neutrophil infiltration and highneuronal activity in the cortex. This study highlights the potential therapeutic value ofinhibiting IL-1α expression early following acute neuronal injury.
4

Wesseldijk, Feikje. ""Inflammatory Soup" mediators of inflammation in CRPS." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/13553.

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McKay, Anne. "The role of immune mediators in airway inflammation." Thesis, University of Glasgow, 2004. http://theses.gla.ac.uk/4828/.

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Asthma is a chronic inflammatory condition of the airways characterised by reversible airflow obstruction, airway hyper-responsiveness and inflammatory infiltrates in the airway walls containing eosinophils, T lymphocytes and mast cells. T helper (Th) lymphocyte subsets, defined by the cytokines they secrete, are thought to play a key role in the in the initiation and perpetuation of chronic airway inflammation. Th2 cells, producing interleukin (IL)-4, IL-5, IL-9 and IL-13, are thought to be of particular importance. In contrast, Thl cells producing interferon (IFN)-y may counteract the development of Th2 responses and so down-regulate the asthmatic response. The prevalence of asthma is increasing but the reasons for this are not fully understood. In addition, some patients do not respond adequately to treatment with corticosteroids, currently the most effective anti-inflammatory agents used routinely in human asthma. There is therefore continual interest in developing new therapeutic agents for asthma. A greater understanding of the regulation of inflammatory responses in asthma will assist in the identification of potential targets for therapeutic intervention. The aims of this thesis were (i) to assess the role of the cytokine IL-18 in allergic airway inflammation by determining IL-18 levels in induced sputum in asthmatic subjects in comparison to normal subjects, and by studies in a murine model of allergic asthma using IL-18 gene deficient mice and (ii) to assess the potential antiinflammatory actions of simvastatin and thymosin beta 4 sulfoxide in the murine asthma model. IL-18 is a pro-inflammatory cytokine which can promote IFN-y secretion and, in association with IL-12, enhance the development of Thl responses. However, in some circumstances it may also stimulate Th2 responses. IL-18 therefore has the potential to suppress or exacerbate allergic airway inflammation. The role of IL-18 in both clinical and experimental asthma remains unclear. Statins are inhibitors of the rate-limiting enzyme, 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, in cholesterol biosynthesis. As such they have been widely used as cholesterol lowering agents in clinical practice. They have previously been shown to have anti-inflammatory properties independent of their cholesterol-lowering ability in clinical studies of atherosclerotic disease and in animal models of Thlmediated inflammation. Thymosin beta 4 sulfoxide (T~4S0) is a 5 kDa peptide. Intracellularly its principal activity is to regulate actin polymerization. Corticosteroid treatment of monocytes in vitro induces the release of T~4S0 extracellularly, where it can inhibit neutrophil chemotaxis. Exogenous administration of T~4S0 has been shown to reduce neutrophilic inflammation in animal models. In this study it is shown that IL-18 is detectable in induced sputum fluid and IL-18 mRNA is expressed in induced sputum cells from asthmatic and nOlmal subjects. IL- 18 protein levels in induced sputum, and IL-18 mRNA expression in induced sputum cells were not significantly different between these groups. IL-18 production was localised to sputum macrophages. However, cigarette smoking significantly reduced IL-18 levels in induced sputum fluid in both asthmatic and normal subjects. In asthmatics, but not normal subjects, the reduction in IL-18 levels in sputum fluid was associated with reduced IL-18 mRNA expression in induced sputum cells. A murine model of allergic asthma, using BALB/C mice sensitised and challenged with ovalbumin (OVA), was used to examine the role of IL-18 in allergic responses in vivo. IL-18 gene knockout (ko) had significantly reduced bronchoalveolar lavage (BAL) total cell count and eosinophilia compared to wild-type (WT) mice. IL-18 ko mice had reduced IL-4 expression in thoracic lymph nodes, as assessed by quantitative peR, and significantly reduced OVA-specific IL-4 secretion from thoracic lymph node cultures assessed by ELISA. Serum OVA-specific IgG 1, IgG2a and IgE and total IgE levels were not significantly different between IL-18 ko and WT mice. The murine model of allergic asthma was also used to examine the anti-inflammatory activities of simvastatin and T~4S0 in a Th2-mediated, eosinophilic condition. Simvastatin treatment, either orally or intraperitoneally, and T~4S0 intraperitoneally reduced the total inflammatory cell infiltrate and eosinophilia in BAL fluid in response to inhaled OV A challenge. At higher doses of simvastatin intraperitoneally, a histological reduction in inflammatory infiltrates in the lungs was observed. Treatment with simvastatin intraperitoneally, but not orally, and T~4S0 were also associated with a reduction in IL-4 and IL-5 levels in BAL fluid. OVA-induced IL-4 and IL-5 secretion was reduced in thoracic lymph node cultures from both simvastatin-treated and T~4S0-treated mice. Neither simvastatin nor T~4S0 treatment altered serum total IgE or OVA-specific IgG 1 and IgG2a levels. The results described show that IL-18 can be detected in the induced sputum fluid of asthmatic and normal subjects and that cigarette smoking significantly reduces its levels. Studies in a murine model of allergic asthma suggest that IL-18 has a proinflammatory role in allergic airway inflammation, at least in part through its ability to induce IL-4 secretion. Both simvastatin and thymosin beta 4 sulfoxide had convincing anti-inflammatory properties in the murine model of asthma used, and these agents, or related compounds, may have therapeutic potential in human asthma.
6

Wilson, Susan Jane. "Mucosal inflammation in allergic rhinitis." Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295233.

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李蕙琛 and Wai-sum Rachel Li. "Control of adenosine in human umbilical vein endothelial cells during inflammation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557479.

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Airila-Månsson, Stella. "Progression of periodontitis and influence of periodontal bacteria on release of inflammatory markers in Swedish adults /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-622-0/.

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Khan, Sarah Basir. "Mediators of inflammation and fibrosis in experimental crescentic glomerulonephritis." Thesis, Imperial College London, 2005. http://hdl.handle.net/10044/1/11303.

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Porter, John Robert Stephen. "Microvesicles as mediators of inflammation in severe burn injury." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/43963.

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The host response to a severe burn injury is characterised by exaggerated systemic inflammation. Early clinical manifestations include shock, respiratory failure, renal failure and immunosuppression. The signalling pathways that propagate the inflammatory response are unclear but have traditionally been thought to involve overspill of proinflammatory cytokines. The importance of microvesicles, sub-cellular membrane-bound particles, is increasingly being recognised in the context of intercellular communication. Although circulating microvesicles are elevated in proinflammatory states such as sepsis, their relevance to the post-burn inflammatory response has not previously been evaluated. We hypothesised that circulating microvesicles play a crucial role in propagating the post-burn inflammatory response. Our overall aims were to 1) optimise protocols for the processing and analysis of plasma samples for microvesicle content; 2) characterise the circulating microvesicle profile associated with severe burn injury; 3) develop in vitro techniques to assess microvesicle production and function. The major findings of this work were that microvesicles derived from leukocytes, neutrophils, monocytes and endothelial cells were significantly elevated within 24 hours of burn injury. Microvesicle levels fell rapidly and were significantly decreased by day two post-injury. Total leukocyte- and neutrophil-derived microvesicles were significantly higher in non-survivors of burn injury as compared to survivors. In vitro studies demonstrated that neutrophil microvesicle release could be elicited by incubation with opsonised heat-killed cells. Pilot analysis of burn patient samples, using an endothelial co-culture assay, suggested that microvesicles may regulate the innate immune response to burn injury. These findings indicated that circulating microvesicles are an important component of the post-burn inflammatory response. Their precise activity is likely to be subtype-specific but the association of neutrophil-derived microvesicles with patient outcome alludes to a key role in burn pathophysiology.
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Books on the topic "Inflammation Mediators":

1

A, Willoughby D., ed. Inflammation: Mediators and mechanisms. Edinburgh: Churchill Livingstone for the British Council, 1987.

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R, Ruffolo Robert, and Hollinger Mannfred A, eds. Inflammation--mediators and pathways. Boca Raton: CRC Press, 1995.

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M, Henson P., and Murphy Robert C, eds. Mediators of the inflammatory process. Amsterdam: Elsevier, 1989.

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1951-, Morgan Douglas W., Forssmann Ulf 1967-, and Nakada Marian T. 1961-, eds. Cancer and inflammation. Basel: Birkhauser, 2004.

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Sharma, Jagdish N. Topics in mediator pharmacology. Hauppauge, N.Y: Nova Science Publishers, 2011.

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1986), Bodensee Symposium on Microcirculation (6th. Microcirculation and inflammation: Vessel wall inflammatory cells - mediator interaction. Basel: Karger, 1987.

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Symposium on Phospholipase A₂: Pathophysiological Role of Soluble and Membrane-Bound Enzymes (1989 New York, N.Y.). Phospholipase A₂: Role and function in inflammation. New York: Plenum Press, 1990.

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1953-, Eden Willem van, ed. Heat shock proteins and inflammation. Basel: Birkhäuser Verlag, 2003.

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Gesellschaft für Biologische Chemie. (42nd 1991 Mosbach, Baden-Württemberg, Germany). Molecular aspects of inflammation. Berlin: Springer-Verlag, 1991.

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Zoppo, Gregory J. Del. Innate inflammation and stroke. Edited by New York Academy of Sciences. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2010.

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Book chapters on the topic "Inflammation Mediators":

1

Saria, A., and J. M. Lundberg. "Neurogenic Inflammation." In Inflammatory Mediators, 73–85. London: Palgrave Macmillan UK, 1985. http://dx.doi.org/10.1007/978-1-349-07834-9_8.

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Galvão, Izabela, Michelle A. Sugimoto, Juliana P. Vago, Marina G. Machado, and Lirlândia P. Sousa. "Mediators of Inflammation." In Immunopharmacology and Inflammation, 3–32. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77658-3_1.

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Gonçalves, William Antonio, Alesandra Côrte Reis Melão, Mauro Martins Teixeira, Barbara Maximino Rezende, and Vanessa Pinho. "Pro-resolving Mediators." In Immunopharmacology and Inflammation, 133–75. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77658-3_6.

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Saldeen, T. "The Fibrinolytic System in Inflammation." In Inflammatory Mediators, 87–97. London: Palgrave Macmillan UK, 1985. http://dx.doi.org/10.1007/978-1-349-07834-9_9.

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Foreman, J. C. "The Role of Histamine in Inflammation." In Inflammatory Mediators, 7–18. London: Palgrave Macmillan UK, 1985. http://dx.doi.org/10.1007/978-1-349-07834-9_2.

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Glaser, K. B., and M. S. Barnette. "Lipid Mediators: Mechanisms." In Inflammation: Mechanisms and Therapeutics, 185–88. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7343-7_21.

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Ait-Oufella, Hafid, Ziad Mallat, and Alain Tedgui. "Mediators of Vascular Inflammation." In Inflammation and Atherosclerosis, 197–217. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0338-8_10.

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Hedqvist, Per, and Lennart Lindbom. "Lipid Mediators of Inflammation." In Physiology of Inflammation, 111–30. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4614-7512-5_7.

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Parker, C. W. "Lipid Mediators and Inflammation." In New Trends in Allergy II, 78–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71316-3_8.

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Krane, Stephen M. "Peptide Mediators of Inflammation." In Cellular and Molecular Aspects of Inflammation, 67–73. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5487-1_5.

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Conference papers on the topic "Inflammation Mediators":

1

Dalli, Jesmond, Ana Rodriguez, Bernd Spur, and Charles Serhan. "Structure elucidation and biological evaluations of sulfido-conjugated specialized pro-resolving mediators." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/mqgv6628.

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Inflammatory diseases are characterized by unabated inflammation that leads tissue destruction resulting in malaise. Whilst much is known on the mechanism that perpetuate inflammation, less is known about the molecules and pathways that coordinate the termination of inflammation and facilitate the repair and regeneration of damaged tissues. To evaluate the potential contribution of essential fatty acid-derived mediators in coordinating this life saving response we interrogated inflammatory exudates obtained following self-limited inflammatory challenge. Using radio-isotope tracking we found that the omega-3 fatty acid docosahexaenoic acid is utilized to produce novel bioactive molecules in these exudates. The structures of these molecules were elucidated using a range of physical techniques, demonstrating that these molecules were peptide lipid conjugated mediators and the stereochemistry of the functional groups was established using total organic synthesis. Investigations into their biosynthetic pathways demonstrated that the formation of their formation was initiated via the 14-lipoxygenation of DHA, that was then converted into an intermediate allylic epoxide and then conjugated to glutathione to yield the first mediator in the family which was coined as maresin conjugated in tissue regeneration (MCTR)1. This was then further converted to to 13-cysteinylglycinyl,14-hydroxy-docosahexaenoic acid (MCTR2) and 13-glycinyl,14-hydroxy-docosahexaenoic acid (MCTR3). Evaluation of the biological activities of these molecules demonstrated that they limited the recruitment of inflammatory cells to the sites of both sterile and infectious challenge. They reprogrammed biology towards a tissue protective phenotype and promoted the repair and regeneration of damaged tissues. Evaluation of the levels of these mediators in human peripheral blood demonstrated that the production of MCTR3 is significantly reduced in patients with rheumatoid arthritis that display signs of erosive joint disease. Together, these findings identify previously undescribed chemical signals that enhance host responses to limit inflammation, stimulate resolution of inflammation, and promote the restoration of function.
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Jones, Caleb W. "Reactive Aldehydes As Mediators Of Pulmonary Inflammation." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2732.

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Bevilacqua, M. A., and M. A. Gimbrone. "LEUKOCYTE-ENDOTHELIAL INTERACTIONS: IMPLICATIONS FOR INFLAMMATION AND COAGULATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642948.

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A rapidly increasing body of data indicates that the vascular endothelium plays an active role in the development of inflammatory and thrombotic processes. Our laboratory has focused on the modulation of certain endothelial cell functions by inflammatory/immune mediators. Initially, we demonstrated that human monocyte derived interleukin-1 (hmIL-1) can act directly on cultured human endothelial cells (HEC) to increase the expression of tissue factor procoagulant activity in a time- and protein-synthesis dependent fashion (J. Exp. Med. 160:618, 1984). Increased expression of HEC tissue factor was also elicited with recombinant IL-1α (rlL-lα), rIL-1 β, and recombinant human tumor necrosis factor (rTNF), as well as with bacterial endotoxin (1 ipopolysaccharide, LPS) (Am. J. Pathol. 121:393, 1985; Proc. Natl. Acad. Sci. USA 83:4533, 1986). The kinetics of the HEC tissue factor responses to these stimuli were similar, demonstrating a rapid use rise to peak activity at ~ 4 hr, and a decline toward basal levels by 24 hr. This characteristic decline in tissue factor PCA after prolonged incubation with IL-1 or TNF was accompanied by selective endothelial hyporesponsiveness to the initially stimulating monokine. Interestingly, the effects of IL-1 and TNF were found to be additive even at apparent maximal doses of the individual monokines. We have also examined the effects of IL-1 and other mediators on HEC production of fibrinolytic components (J. Clin. Invest. 78:587, 1986). HEC monolayers which had been treated for 24 hr with IL-1 or TNF exhibited decreased tissue type plasminogen activator (tPA) and increased plasminogen activator inhibitor (PAI) as assessed in functional and immunological assays. Thus, certain inflammatory mediators such as IL-1 and TNF can act on vascular endothelial cells to induce the expression of tissue factor in a rapid and transient fashion, and to decrease the expression of fibrinolytic activity in a more prolonged fashion. In a parallel series of studies, we have demonstrated that IL-1, TNF and LPS also act on HEC to increase the adhesion of polymorphonuclear leukocytes (PMN), monocytes and the related cell lines HL-60 and U937 (J. Clin. Invest. 76:2003, 1985; Fed. Proc. 46:405A, 1987). The kinetics of this modulation of HEC adhesiveness parallel that of the change in tissue factor PCA. Recently, we have developed two monoclonal antibodies (mAb), H4/18 and H18/7, which identify a surface antigen expressed on monokine- and LPS-stimulated HEC but not on unstimulated HEC. The mediator specificity, kinetics, and protein synthesis-dependence of the expression of this antigen correlate with increased HEC adhesiveness for leukocytes. Neither mAb binds to unstimulated or stimulated PMN, HL-60 cells or dermal fibroblasts. H18/7 inhibits the adhesion of PMN (>50%) and HL-60 cells (>60%) to stimulated HEC by comparison to isotype matched control mAb; H4/18 also inhibits HL-60 adhesion but to a lesser extent. H4/18 and H18/7 immunoprecipitate the same polypeptides from biosynthetically-1abeled monokine-stimulated HEC, but not unstimulated HEC. We have designated this inducible endothelial cell surface protein, endothelial-leukocyte adhesion molecule-1 (E-LAM 1). Thus, vascular endothelium can be activated by inflammatory/immune mediators to express both prothrombotic and pro-inflammatory functions. In vivo, these endothelial responses may contribute to a variety of pathophysiologic processes.
4

Lim, Henry W. "Role mediators of inflammation and cells in porphyrin-induced phototoxicity." In OE/LASE '89, edited by Thomas J. Dougherty. SPIE, 1989. http://dx.doi.org/10.1117/12.978000.

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Pidaparti, Ramana M., and Kevin R. Ward. "Airway Inflammation Induced by Mechanical Ventilation Through Multiscale Modeling." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80174.

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Abstract:
Inflammation has been recognized as a major integral component for most of the acute and chronic diseases. Inflammation can be initiated within the body as an innate process or by external factors such as infections and trauma. Inflammation is a complex and dynamic process, and involves nonlinearity and stochasticity. Without the inflammation, the harmful stimuli cannot be removed and the healing process cannot occur. However, an over-expression or under-expression of inflammatory responses can lead to severe consequences, such as Multiple Organ Dysfunction Syndrome (MODS), which is characterized by sequential organ failure. Acute lung injury (ALI) is typically one of the first manifestation of MODS. It can be triggered by external stimuli such as pathogens or from inflammatory mediators produced from various other processes ranging from other damaged organs or to blood transfusions to even the biomechanical forces of mechanical ventilation itself.
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Baraldo, Simonetta, Simone Agostini, Graziella Turato, Erica Bazzan, Francesca Lunardi, Deborah Snijders, Kim Lokar-Oliani, et al. "Non-eosinophilic Asthma In Children: Mediators Of Airway Remodeling And Inflammation." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2507.

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De Paula Vieira, R., R. Moraes-Ferreira, M. A. R. Brandao-Rangel, A. Silva-Reis, V. H. S. Palmeira, H. C. Aquino-Santos, and C. R. Frison. "Aerobic Training Reduces Chronic Airway Inflammation and Mediators of Remodelingin Asthma." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.74.

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Branković, Jovica, Vesna Milovanović, and Vladimir P. Petrović. "CYCLOOXYGENASE-2 AS „IN SILICO“ TARGET OF PHENOLIC HYDRAZONE- TYPE DERIVATIVES." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.324b.

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In the present work, a series of phenolic hydrazone analogs were investigated in silico for their potential inhibitory activity toward COX-2. These examinations were based on the capability of hydrazone-based compounds to interact with numerous enzymes, as well as on their versatile biological features and therapeutical applications. COX-2 was selected due to its involvement in the inflammation and carcinogenesis processes. Regarding this, COX-2 represents a valid target for the development of compounds that could block the formation of harmful inflammation mediators.
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Al-amodi, O., H. Jodeleit, F. Beigel, E. Wolf, M. Siebeck, and R. Gropp. "CD1a expressing monocytes as sensors and mediators of inflammation in ulcerative colitis." In 46. Jahrestagung der Gesellschaft für Gastroenterologie in Bayern e.V. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1648568.

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Serhan, Charles. "Resolvins and Pro-resolving Mediators from n-3 Pufas in Infectious Inflammation." In Virtual 2021 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2021. http://dx.doi.org/10.21748/am21.127.

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Reports on the topic "Inflammation Mediators":

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DeMar, James C., Miya I. Hill, Robert B. Gharavi, Joseph R. Andrist, Andrea A. Edwards, Stephen A. VanAlbert, and Joseph B. Long. Evaluation of Novel Polyunsaturated Fatty Acid Derived Lipid Mediators of Inflammation to Ameliorate the Deleterious Effects of Blast Overpressure on Eye and Brain Visual Processing Centers in Rats. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada606425.

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DeMar, James. Evaluation of Novel Polyunsaturated Fatty Acid Derived Lipid Mediators of Inflammation to Ameliorate the Deleterious Effects of Blast Over Pressure on Eye and Brain Visual Processing Centers in Rats. Fort Belvoir, VA: Defense Technical Information Center, August 2015. http://dx.doi.org/10.21236/ada621266.

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To the bibliography