Relevant bibliographies by topics / Lipid Mediators of Inflammation (LMI)

Academic literature on the topic 'Lipid Mediators of Inflammation (LMI)'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Lipid Mediators of Inflammation (LMI).'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Lipid Mediators of Inflammation (LMI)"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Raizman, Michael B. "New Trends in Lipid Mediators Research, vol 5, Lipid Mediators in Eye Inflammation." Archives of Ophthalmology 109, no. 10 (October 1, 1991): 1361. http://dx.doi.org/10.1001/archopht.1991.01080100041026.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

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

Full text
Abstract:
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, antagonists, and dietary manipulation in the treatment of gastric ulcer. Potential directions for future research in this field are suggested as are some of the pitfalls to be avoided in such studies.
APA, Harvard, Vancouver, ISO, and other styles
5

Serhan, Charles N., Nan Chiang, Jesmond Dalli, and Bruce D. Levy. "Lipid Mediators in the Resolution of Inflammation." Cold Spring Harbor Perspectives in Biology 7, no. 2 (October 30, 2014): a016311. http://dx.doi.org/10.1101/cshperspect.a016311.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Rocha, Paulo N., Troy J. Plumb, and Thomas M. Coffman. "Eicosanoids: lipid mediators of inflammation in transplantation." Springer Seminars in Immunopathology 25, no. 2 (September 1, 2003): 215–27. http://dx.doi.org/10.1007/s00281-003-0132-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

González-Périz, Ana, and Joan Clària. "Resolution of Adipose Tissue Inflammation." Scientific World JOURNAL 10 (2010): 832–56. http://dx.doi.org/10.1100/tsw.2010.77.

Full text
Abstract:
The presence of the so-called “low-grade” inflammatory state is recognized as a critical event in adipose tissue dysfunction in obesity. This chronic “low-grade” inflammation in white adipose tissue is powerfully augmented through the infiltration of macrophages, which, together with adipocytes, perpetuate a vicious cycle of macrophage recruitment and secretion of free fatty acids and deleterious adipokines that predispose the development of obesity-related comorbidities, such as insulin resistance and nonalcoholic fatty liver disease. In the last decade, many factors have been identified that contribute to mounting uncontrolled inflammation in obese adipose tissue. Among them, bioactive lipid mediators derived from the cyclooxygenase and 5-lipoxygenase pathways, which convert the ω-6-polyunsaturated fatty acid (PUFA) arachidonic acid into potent proinflammatory eicosanoids (i.e., prostaglandins [PGs] and leukotrienes), have emerged. Interestingly, the same lipid mediators that initially trigger the inflammatory response also signal the termination of inflammation by stimulating the biosynthesis of anti-inflammatory and proresolving lipid autacoids. This review discusses the current status, characteristics, and progress in this class of “stop signals”, including the lipoxins, which were the first identified ω-6 PUFA–derived lipid mediators with potent anti-inflammatory properties; the recently described ω-3 PUFA–derived lipid mediators resolvins and protectins; and the cyclopentenone PGs of the D series. Special emphasis is given to the participation of these bioactive lipid autacoids in the resolution of adipose tissue inflammation and in preventing the development of obesity-related complications.
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Full text
Abstract:
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 a functional lipidomic approach employing LC-MS-MS–based informatics, recent studies, reviewed herein, uncovered new families of local-acting chemical mediators actively biosynthesized during the resolution phase from the essential fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). These new families of local chemical mediators are generated endogenously in exudates collected during the resolution phase, and were coined resolvins and protectins because specific members of these novel chemical families control both the duration and magnitude of inflammation in animal models of complex diseases. Recent advances on the biosynthesis, receptors, and actions of these novel anti-inflammatory and proresolving lipid mediators are reviewed with the aim to bring to attention the important role of specific lipid mediators as endogenous agonists in inflammation resolution.
APA, Harvard, Vancouver, ISO, and other styles
9

Ramon, Sesquile, Charles Serhan, and Richard Phipps. "Actions of novel inflammation-resolving lipid mediators on human B cells (112.12)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 112.12. http://dx.doi.org/10.4049/jimmunol.186.supp.112.12.

Full text
Abstract:
Abstract The resolution of inflammation is an active and dynamic process. Newly identified lipid mediators are now recognized as key players during the process of inflammation resolution. These lipid-derived molecules constitute four families of endogenous mediators (lipoxins, resolvins, protectins and maresins) derived from essential fatty acids. New findings also demonstrated 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. Their actions on B lymphocytes are not known. Our results indicate that the lipoxin B4 and 17-HDHA, used at 100nM, increase the ability of normal human B cells to produce IgM and IgG when activated with CpG plus anti-IgM. The two lipid mediators also enhance B cell differentiation towards antibody secreting cells. In addition, resolvin D1 and aspirin-triggered resolvin increase antibody production in CpG-stimulated B cells. None of these inflammation resolution lipid mediators affect proliferation and are non-toxic to B cells. Increase of plasma cell differentiation and antibody production coincides with the known involvement of pro-resolving mediators during the late stages of inflammation and pathogen clearance.
APA, Harvard, Vancouver, ISO, and other styles
10

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 (April 21, 2021): 4356. http://dx.doi.org/10.3390/ijms22094356.

Full text
Abstract:
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 inflammation. On the other side, eosinophils have also been recognized as crucial mediators with regulatory and homeostatic roles in local immunity and repair. Thus, targeting the complex network of lipid mediators offer a unique opportunity to target the over-activation and ‘pro-inflammatory’ phenotype of eosinophils without compromising the survival and functions of tissue-resident and homeostatic eosinophils. Here we provide a comprehensive overview of the critical role of phospholipase-derived lipid mediators in modulating eosinophil activity in health and disease. We focus on lysophospholipids, polyunsaturated fatty acids, and eicosanoids with exciting new perspectives for future drug development.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Lipid Mediators of Inflammation (LMI)"

1

Blaho, Victoria Alison. "Lipid mediators in the development and resolution of experimental lyme arthritis." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/4819.

Full text
Abstract:
Thesis (Ph. D.)--University of Missouri-Columbia, 2007.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. "May 2007" Includes bibliographical references.
APA, Harvard, Vancouver, ISO, and other styles
2

McDaniel, J., Karen A. Massey, and Anna Nicolaou. "Fish oil supplementation alters levels of lipid mediators of inflammation in microenvironment of acute human wounds." Wiley, 2010. http://hdl.handle.net/10454/4577.

Full text
Abstract:
no
Chronic wounds often result from prolonged inflammation involving excessive polymorphonuclear leukocyte activity. Studies show that the omega-3 polyunsaturated fatty acids eicosapentaenoic and docosahexaenoic acids found in fish oils generate bioactive lipid mediators that reduce inflammation and polymorphonuclear leukocyte recruitment in numerous inflammatory disease models. The purpose of this study was to test the hypotheses that boosting plasma levels of eicosapentaenoic and docosahexaenoic acids with oral supplementation would alter lipid mediator levels in acute wound microenvironments and reduce polymorphonuclear leukocyte levels. Eighteen individuals were randomized to 28 days of either eicosapentaenoic + docosahexaenoic acid supplementation (Active Group) or placebo. After 28 days the Active Group had significantly higher plasma levels of eicosapentaenoic (p<0.001) and docosahexaenoic acid (p<0.001) than the Placebo Group and significantly lower wound fluid levels of two 15-lipoxygenase products of omega-6 polyunsaturated fatty acids, [9- hydroxyoctadecadienoic (HODE) acid (p = 0.033) and15-hydroxyeicosatrienoic acid (HETrE) (p = 0.006)], at 24 hours post wounding. The Active Group also had lower mean levels of myeloperoxidase, a leukocyte marker, at 12 hours and significantly more re-epithelialization on Day 5 post wounding. We suggest that lipid mediator profiles can be manipulated by altering polyunsaturated fatty acid intake to create a wound microenvironment more conducive to healing.
APA, Harvard, Vancouver, ISO, and other styles
3

Moore, Andrea Rossi. "COX-2 inhibition impaired resolution of chronic inflammation in a murine model of autoimmune arthritis." Diss., Temple University Libraries, 2010. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/81890.

Full text
Abstract:
Microbiology and Immunology
Ph.D.
Rheumatoid arthritis (RA) is a chronic disease characterized by cycles of inflammation and resolution. Previously, it was believed that the resolution of inflammation is simply dissipation of pro-inflammatory signals, although current research indicates that resolution is an active process. Acute inflammation follows defined phases of induction, inflammation and resolution, and resolution occurs by an active process that requires COX-2 activity. This study aims to address whether this paradigm extends to a recognized model of chronic inflammation. We demonstrated in murine collageninduced arthritis that chronic inflammation follows the same sequential course. While there is the normal production of pro-inflammatory cytokines during inflammation and anti-inflammatory mediators such as 15-deoxyΔ12,14PGJ2 (15d-PGJ2) during resolution, interestingly there is sustained production of both COX-2 and the presumably proinflammatory PGE2 during both phases. Blocking COX-2 activity and therefore production of PGE2 during the resolution phase perpetuated instead of attenuated inflammation. Repletion with PGE2 analogs restored homeostasis, and this function is mediated by the pro-resolving lipoxygenase metabolite, lipoxin A4 (LXA4), which is a potent stop signal. Thus, the study provided in vivo evidence for a natural, endogenous link between the cyclooxygenase-lipoxygenase pathways and showed that PGE2 serves as a feedback inhibitor essential for limiting chronic inflammation in autoimmune arthritis. These findings may explain the enigma regarding why COX-2 inhibitors are palliative rather than curative in humans because blocking resolution may mitigate the benefit of preventing induction.
Temple University--Theses
APA, Harvard, Vancouver, ISO, and other styles
4

Bena, Stefania. "Expression and function of the formyl peptide receptor 2 in experimental myocardial infarct." Thesis, Queen Mary, University of London, 2014. http://qmro.qmul.ac.uk/xmlui/handle/123456789/7905.

Full text
Abstract:
In Acute Myocardial Infarction (AMI), inflammation is a prerequisite for healing but it can paradoxically extend tissue injury; hence it needs to be modulated. Here, we investigated the role of the pro resolving GPCR FPR2/ALX and its agonist Annexin A1 (AnxA1) in AMI using mice lacking of the Fpr2/3 genes and with an in-frame GFP gene ‘knocked-in’. We developed protocols aimed to determine GFP expression as an indication of Fpr2 gene activity. Also, the Left Anterior Descending Coronary Artery of male Fpr2/3 KO and littermate controls (WT) was occluded for 30min and re-opened for 90min. At the end tissue injury and inflammatory response were studied. A significant proportion of Fpr2/3 KO perished during the procedure. The rest survived up to 90 min and exhibited a larger infarct size, with higher troponin I and inflammation markers (KC, TNFα) than WT animals. At the end of reperfusion, Fpr2/3 KO displayed an unbalanced production of pro and anti-inflammatory lipids (higher PGE2, PGI2, LTB4 and attenuated PGA1, RvD2, LXA4) and a deregulated activation of the cardioprotective IL-6/JAK/STAT3 signalling. Administration of AnxA1 afforded cardioprotection (reduction of infarct size; Troponin I, Caspase3 activity and TNFα) in WT but not in Fpr2/3 KO. A parallel in vitro investigation on the functional FPR2/ALX domains required by AnxA1 and other agonists was also conducted. HEK-293 cells transfected with FPR1, FPR2/ALX and FPR1/FPR2 chimeric receptor were used and calcium flux, 4 pERK and gene modulation analysed. AnxA1 required the N-terminus and the II and III extracellular loops of FPR2/ALX to evoke canonical responses. SAA interacted/activated the I and the II extracellular loops of FPR2/ALX, whereas the compound 43 suffices the I extracellular loop. In summary, the FPR2/AnxA1 pathway exerts a protective role in AMI. AnxA1 mimetic that activated selective FPR2/ALX domains can be synthetize to prevent tissue damage caused by AMI.
APA, Harvard, Vancouver, ISO, and other styles
5

Bresolin, Adriana Chassot. "Análise do efeito de tratamentos periodontais na evolução da periodontite em crianças portadoras de cardiopatia congênita e crianças com coração estruturalmente normal." Universidade Estadual do Oeste do Parana, 2013. http://tede.unioeste.br:8080/tede/handle/tede/631.

Full text
Abstract:
Made available in DSpace on 2017-07-10T14:17:02Z (GMT). No. of bitstreams: 1 adriana.pdf: 2337170 bytes, checksum: e5390349b6b7e1277dc2720b1b76d735 (MD5) Previous issue date: 2013-07-01
The effects of periodontal disease in the oral cavity are well known, however, they can also produce systemic side effects, including the association with the acquired cardiovascular disease. It may be possible to accept as mechanisms of this interrelation, the changes in the lipid metabolism, the inflammatory markers action, which are common to both diseases, and also the direct action of oral bacteria in the atherosclerosis process. Thus, due to the biological associations between diseases and the fact of the atherosclerosis to begin in the childhood period, a behavior based on oral health care and metabolic control, from an early age, is essential for patients with cardiovascular disease. The aim of this research was to evaluate the effectiveness of two periodontal treatment methods, such as the conventional scaling and root planing (SRP) and the full-mouth scaling and root planing (FMSRP), applied to children suffering from periodontal disease with congenital heart disease and structurally normal heart. In this study, the treatments were related to the clinical periodontal parameters [plaque index (PI), gingival index (GI), probing depth (PD), clinical attachment level (CAL) and bleeding on probing (BOP)] as well as the blood parameters, such as lipid profile [total cholesterol (TC) and fractions, triglycerides (TRG)] and inflammatory markers [fibrinogen (FGN), C-reactive protein (CRP ULTRA), interleukin 6 (IL6), and tumor necrosis factor alpha (TNF)]. The patients were divided into 4 groups: group 1 (17) - Congenital Heart Disease and SRP, group 2 (14) - Normal Heart and SRP, group 3 (16) Congenital Heart Disease and FMSRP and group 4 (15) - Normal Heart and FMSRP. The results showed a significant improvement in clinical periodontal parameters (p <0.05) in the studied groups. Considering the lipid parameters, there was a greater evidence in the TC, TRG and VLDL parameters results, with a significant improvement (p <0.05). There was also an improvement in PCR ULTRA with the congenital heart disease and also normal children treated with SRP (p <0,05). The FGN and IL6 parameters (p <0.05) were really improved in all groups. Thus, within these results, we conclude that both periodontal treatments were effective in these children groups
Os efeitos da doença periodontal sobre a cavidade oral são bem conhecidos, contudo, os mesmos também podem produzir efeitos sistêmicos, incluindo a associação com a doença cardiovascular adquirida. Aceitam-se como possíveis mecanismos desta inter-relação as alterações do metabolismo lipídico, a ação de marcadores inflamatórios, que são comuns a ambas as doenças, e até mesmo a ação direta de bactérias orais no processo da aterosclerose. Sendo assim, devido às associações biológicas entre as doenças e o fato da doença aterosclerótica iniciar-se na infância, um comportamento voltado aos cuidados com a saúde oral e controle metabólico, desde a mais tenra idade, é essencial para pacientes portadores de doenças cardiovasculares. O objetivo desta pesquisa foi avaliar a efetividade de duas modalidades de tratamento, a saber, a Raspagem e Alisamento Radicular Convencional (RAR) e a Desinfecção Total de Boca em Estágio Único (DBEU), aplicados a crianças portadoras de doença periodontal com cardiopatia congênita e com coração estruturalmente normal. Neste estudo relacionou-se os tratamentos tanto com parâmetros clínicos periodontais [índice de placa (IP), índice gengival (IG), profundidade de sondagem (PS), nível de inserção clínica (NI) e sangramento à sondagem (SS)], quanto com parâmetros sanguíneos de perfil lipídico [colesterol total (CT) e frações, triglicerídeos (TRG)] e marcadores inflamatórios [fibrinogênio (FGN), proteína C reativa ultrassensível (PCR ULTRA), interleucina 6 (IL6), fator de necrose tumoral alfa (TNF)]. Os pacientes foram distribuídos em 4 grupos, grupo 1 (17) Cardiopatia Congênita e RAR, grupo 2 (14) Coração Normal e RAR, grupo 3 (16) Cardiopatia Congênita e DBEU e grupo 4 (15) Coração Normal e DBEU. Os resultados demonstraram uma significante melhora nos parâmetros clínicos periodontais (p<0.05) nos grupos estudados. Quanto aos parâmetros lipídicos, houve destaque maior, com melhora significativa (p<0.05) nos parâmetros de CT, TRG e VLDL. Houve também melhora do PCR ULTRA nos grupos de pacientes com cardiopatia congênita e crianças normais tratados com RAR (p<0.05). Destaques ocorreram nos parâmetros de FGN e IL6 (p<0.05) com a melhora em todos os grupos. Assim, dentro desses resultados, podemos concluir que ambos os tratamentos periodontais foram efetivos nesses grupos de crianças
APA, Harvard, Vancouver, ISO, and other styles
6

Poloso, N. J., Paula Urquhart, Anna Nicolaou, J. Wang, and D. F. Woodward. "PGE2 differentially regulates monocyte-derived dendritic cell cytokine responses depending on receptor usage (EP2/EP4)." 2012. http://hdl.handle.net/10454/7252.

Full text
Abstract:
no
Dendritic cells (DCs) are central players in coordinating immune responses, both innate and adaptive. While the role of lipid mediators in the immune response has been the subject of many investigations, the precise role of prostaglandins has often been plagued by contradictory studies. In this study, we examined the role of PGE2 on human DC function. Although studies have suggested that PGE2 specifically plays a role in DC motility and cytokine release profile, the precise receptor usage and signaling pathways involved remain unclear. In this report we found that irrespective of the human donor, monocyte-derived dendritic cells (MoDCs) express three of the four PGE2 receptor subtypes (EP2–4), although only EP2 and EP4 were active with respect to cytokine production. Using selective EP receptor antagonists and agonists, we demonstrate that PGE2 coordinates control of IL-23 release (a promoter of Th17, an autoimmune associated T cell subset) in a dose-dependent manner by differential use of EP2 and EP4 receptors in LPS-activated MoDCs. This is in contrast to IL-12, which is dose dependently inhibited by PGE2 through both receptor subtypes. Low concentrations (∼1–10 nM) of PGE2 promoted IL-23 production via EP4 receptors, while at higher (>50 nM), but still physiologically relevant concentrations, IL-23 is suppressed by an EP2 dependent mechanism. These results can be explained by differential regulation of the common subunit, IL-12p40, and IL-23p19, by EP2 and EP4. By these means, PGE2 can act as a regulatory switch of immune responses depending on its concentration in the microenvironment. In addition, we believe these results may also explain why seemingly conflicting biological functions assigned to PGE2 have been reported in the literature, as the concentration of ligand (PGE2) fundamentally alters the nature of the response. This finding also highlights the potential of designing therapeutics which differentially target these receptors.
APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Lipid Mediators of Inflammation (LMI)"

1

G, Bazán Nicholás, ed. Lipid mediators in ischemic brain damage and experimental epilepsy. Basel: Karger, 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

International Conference on Advances in Prostaglandin, Leukotriene, and Other Bioactive Lipid Research (12th 2002 Istanbul, Turkey). Advances in prostaglandin, leukotriene, and other bioactive lipid research: Basic science and clinical applications. New York: Kluwer Academic/Plenum Publishers, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

International, Conference on Advances in Prostaglandin Leukotriene and Other Bioactive Lipid Research (12th 2002 Istanbul Turkey). Advances in prostaglandin, leukotriene, and other bioactive lipid research: Basic science and clinical applications. New York: Kluwer Academic/Plenum Publishers, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Zeliha, Yazıcı, ed. Advances in prostaglandin, leukotriene, and other bioactive lipid research: Basic science and clinical applications. New York: Kluwer Academic/Plenum Publishers, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

V, Honn Kenneth, and International Conference on Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury (4th : 1995 : Hong Kong), eds. Eicosanoids and other bioactive lipids in cancer, inflammation, and radiation injury 3. New York: Plenum Press, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

K, Nigam S., ed. Eicosanoids and other bioactive lipids in cancer, inflammation, and radiation injury: Proceedings of the 2nd international conference, September 17-21, 1991, Berlin, FRG. Boston: Kluwer Academic Publishers, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

G, Bazán Nicolás, ed. Lipid mediators in eye inflammation. Basel: Karger, 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

De Sanctis, Juan Bautista, Martin Giera, and Danuta Radzioch, eds. Quo Vadis Lipid Mediators – Lipid Mediators Implication in Inflammation and Chronic Inflammatory Diseases. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88966-989-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

1958-, Robinson Clive, ed. Lipid mediators in allergic diseases of the respiratory tract. Boca Raton, Fla: CRC Press, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Ray, Abhijit, and Punit Kumar Srivastava. Obstructive Airway Diseases: Role of Lipid Mediators. Taylor & Francis Group, 2016.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Lipid Mediators of Inflammation (LMI)"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Narumiya, Shuh, Takehiko Yokomizo, and Junken Aoki. "Lipid Mediators in Inflammation." In Inflammation - From Molecular and Cellular Mechanisms to the Clinic, 651–94. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2017. http://dx.doi.org/10.1002/9783527692156.ch26.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Bennett, Melanie, and Derek W. Gilroy. "Lipid Mediators in Inflammation." In Myeloid Cells in Health and Disease, 343–66. Washington, DC, USA: ASM Press, 2017. http://dx.doi.org/10.1128/9781555819194.ch19.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Isobe, Yosuke, and Makoto Arita. "Omega-3 Fatty Acid Metabolism and Regulation of Inflammation." In Bioactive Lipid Mediators, 155–62. Tokyo: Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-55669-5_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

DeVries, G. W., and R. S. Jacobs. "Poster Discussion Lipid Mediators — New Agents." In Inflammation: Mechanisms and Therapeutics, 203–5. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7343-7_25.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Camussi, Giovanni, and Jan R. Brentjens. "The Role of Platelet-Activating Factor in Inflammation." In Platelet-Activating Factor and Related Lipid Mediators, 299–322. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5284-6_14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Borgeat, Pierre, Serge Picard, Nancy Dallaire, Marc Pouliot, and Marc E. Surette. "Quantitative Studies of the Lipid Mediators of Inflammation Using Liquid Chromatography-Electrospray Mass Spectrometry." In Molecular and Cellular Basis of Inflammation, 275–88. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-253-1_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Spite, Matthew, and Charles N. Serhan. "Roles of Specialized Proresolving Lipid Mediators in Inflammation Resolution and Tissue Repair." In Inflammation - From Molecular and Cellular Mechanisms to the Clinic, 1447–66. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2017. http://dx.doi.org/10.1002/9783527692156.ch57.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Lipid Mediators of Inflammation (LMI)"

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
2

Singh, K. P., G. Lawyer, T. Muthumalage, N. A. Khan, S. R. McDonough, D. Ye, K. P. Maremanda, S. McIntosh, and I. Rahman. "Biomarkers of Inflammation, Oxidative Stress, Pro-Resolving Lipid Mediators, Triglycerides, Growth Factors and Tissue Injury in Electronic Cigarette Users: Implications for Non-Invasive Assessment of Vaping Associated Lung Injuries." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1225.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Lipid Mediators of Inflammation (LMI)"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Lipid Mediators of Inflammation (LMI)' for particular source types:
Journal articles Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography