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Relevant bibliographies by topics / Leukotrienes

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Academic literature on the topic 'Leukotrienes'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 August 2024

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Journal articles on the topic "Leukotrienes"

1

Uotila, P., K. Punnonen, R. Tammivaara, and CT Jansén. "Detection of leukotrienes in the serum of asthmatic and psoriatic patients." Acta Dermato-Venereologica 66, no. 5 (September 1, 1986): 381–85. http://dx.doi.org/10.2340/0001555566381385.

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Purified serum samples from asthmatic and psoriatic patients and healthy controls were analysed by high-pressure liquid chromatography (HPLC) and the amounts of leukotrienes were measured from the corresponding HPLC fractions by specific radioimmunoassays. In the serum of healthy controls the amounts of leukotrienes B4, C4 and D4 were very small or negligible. Rather great amount of leukotriene B4 was, however, detected in the serum of many asthmatic and psoriatic patients. The amount of leukotriene B4 was in the serum of asthmatic patients 120 +/- 20 pmol/ml (n = 11, mean +/- SEM) and in that of psoriatic patients 100 +/- 10 pmol/ml (n = 10). The amounts of leukotrienes C4 and D4 were rather small in the serum of most patients. The amount of leukotriene C4 was, however, very high (250 pmol/ml) in the serum of a psoriatic patient. Significant amount of leukotriene D4 was also detected in the serum of this patient. The present study indicated that leukotrienes are formed during blood clotting in the leukocytes of asthmatic and psoriatic patients and that the rate of formation is so high that leukotrienes may have a role in these diseases.

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Paterson, N. A. "Influence of hypoxia on histamine and leukotriene release from dispersed porcine lung cells." Journal of Applied Physiology 61, no. 5 (November 1, 1986): 1790–95. http://dx.doi.org/10.1152/jappl.1986.61.5.1790.

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The ability of hypoxia (PO2 57 Torr) and anoxia (PO2 0 Torr) to induce the release of histamine or sulfidopeptide leukotrienes from dispersed porcine parenchymal lung cells was examined. Spontaneous release of histamine (9.2 +/- 1.3%) was not significantly increased during hypoxia or anoxia, and spontaneous leukotriene release was not detected under any conditions. The release of leukotriene induced by A23187 (78 +/- 11 pmol leukotriene D4 equivalent/10(7) parenchymal lung cells) was unchanged during hypoxia and was significantly reduced (55.4 +/- 7.7% control leukotriene release) during anoxia, whereas A23187-induced histamine release (63.2 +/- 4.2% total cell histamine) was unaffected by reduced oxygenation. Reduction of final buffer pH from 7.4 to 7.0 did not affect mediator release. High-pressure liquid chromatographic analysis of the released leukotrienes revealed a mixture of leukotrienes C4 and D4, with a symmetrical reduction in product during anoxia. Although leukotriene release in response to hypoxia was not demonstrated, the findings do not preclude limited local release of leukotrienes, perhaps in association with increased smooth muscle responsiveness.

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3

Petersen, Bodil, K. Frank Austen, Kenneth D. Bloch, Yukako Hotta, Fumito Ichinose, Yoshihide Kanaoka, and Warren M. Zapol. "Cysteinyl Leukotrienes Impair Hypoxic Pulmonary Vasoconstriction in Endotoxemic Mice." Anesthesiology 115, no. 4 (October 1, 2011): 804–11. http://dx.doi.org/10.1097/aln.0b013e31822e94bd.

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Background Sepsis impairs hypoxic pulmonary vasoconstriction (HPV) in patients and animal models, contributing to systemic hypoxemia. Concentrations of cysteinyl leukotrienes are increased in the bronchoalveolar lavage fluid of patients with sepsis, but the contribution of cysteinyl leukotrienes to the impairment of HPV is unknown. Methods Wild-type mice, mice deficient in leukotriene C(4) synthase, the enzyme responsible for cysteinyl leukotriene synthesis, and mice deficient in cysteinyl leukotriene receptor 1 were studied 18 h after challenge with either saline or endotoxin. HPV was measured by the increase in left pulmonary vascular resistance induced by left mainstem bronchus occlusion. Concentrations of cysteinyl leukotrienes were determined in the bronchoalveolar lavage fluid. Results In the bronchoalveolar lavage fluid of all three strains, cysteinyl leukotrienes were not detectable after saline challenge; whereas endotoxin challenge increased cysteinyl leukotriene concentrations in wild-type mice and mice deficient in cysteinyl leukotriene receptor 1, but not in mice deficient in leukotriene C(4) synthase. HPV did not differ among the three mouse strains after saline challenge (120 ± 26, 114 ± 16, and 115 ± 24%, respectively; mean ± SD). Endotoxin challenge markedly impaired HPV in wild-type mice (41 ± 20%) but only marginally in mice deficient in leukotriene C(4) synthase (96 ± 16%, P < 0.05 vs. wild-type mice), thereby preserving systemic oxygenation. Although endotoxin modestly decreased HPV in mice deficient in cysteinyl leukotriene receptor 1 (80 ± 29%, P < 0.05 vs. saline challenge), the magnitude of impairment was markedly less than in endotoxin-challenged wild-type mice. Conclusion Cysteinyl leukotrienes importantly contribute to endotoxin-induced impairment of HPV in part via a cysteinyl leukotriene receptor 1-dependent mechanism.

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4

Jackson, W. F. "Regional differences in mechanism of action of oxygen on hamster arterioles." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 2 (August 1, 1993): H599—H603. http://dx.doi.org/10.1152/ajpheart.1993.265.2.h599.

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Leukotrienes have been implicated in the arteriolar constriction induced by elevated PO2 in the hamster cheek pouch. The role of leukotrienes in arteriolar O2 reactivity in other tissues has not been studied. To test the hypothesis that leukotrienes mediate O2 reactivity in all tissues, the effects of a leukotriene receptor antagonist, SKF-102922 (10 microM), a 5-lipoxygenase inhibitor, SC-43251 (30 microM), and a 5-lipoxygenase-activating protein antagonist, MK-886 (10 microM), on arteriolar O2 reactivity in hamster cheek pouch were compared with their effects on cremasteric arteriolar O2 reactivity. All three agents significantly decreased O2-induced arteriolar constriction in the cheek pouch, as reported previously. However, none of the antagonists inhibited O2-induced constriction of cremasteric arterioles. The efficacy of the leukotriene receptor antagonist, SKF-102922, was verified in the cremaster muscle: 10 microM SKF-102922 completely abolished constriction induced by topical application of leukotriene D4. These data support the hypothesis that leukotrienes mediate O2 reactivity in the cheek pouch. However, leukotrienes do not appear to mediate O2 reactivity in the cremaster muscle. These data suggest that there are significant regional differences in the mechanism of action of O2 on arterioles.

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5

Denzlinger, C., A. Kapp, M. Grimberg, HH Gerhartz, and W. Wilmanns. "Enhanced endogenous leukotriene biosynthesis in patients treated with granulocyte-macrophage colony-stimulating factor." Blood 76, no. 9 (November 1, 1990): 1765–70. http://dx.doi.org/10.1182/blood.v76.9.1765.1765.

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Abstract The hematopoietic cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) is being used in clinical trials for its potential in the treatment of hematopoietic insufficiency due to various causes. Involvement of leukotrienes in the effects of GM-CSF is suggested by analytical and pharmacologic evidence obtained in vitro. However, until now no data in support of a role of leukotrienes in GM-CSF action in vivo have been presented. In the present investigation this question was approached by measurement of endogenous cysteinyl leukotriene formation in patients treated with the cytokine for cytopenia induced by cytostatic drugs or for refractory anemia with excess of blasts (RAEB). Endogenous cysteinyl leukotriene formation was assessed by determination of urinary leukotriene metabolites using combined high- performance liquid chromatography and radioimmunoassay analysis. After GM-CSF administration a distinct increase in urinary cysteinyl leukotrienes was found in the cytopenic and the RAEB patients that ranged from 2.3- to 57-fold and 2.4- to 333-fold, respectively. In the cytopenic patients the increase in leukotriene production was correlated to an expansion of peripheral blood leukocytes; RAEB patients responded to GM-CSF with enhanced leukotriene biosynthesis even if the peripheral leukocytes decreased, possibly due to an abnormal number and/or irritability of leukotriene-producing cells. The increase in endogenous leukotriene production during therapy with GM- CSF may indicate that leukotrienes play a role in GM-CSF action in vivo.

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Denzlinger, C., A. Kapp, M. Grimberg, HH Gerhartz, and W. Wilmanns. "Enhanced endogenous leukotriene biosynthesis in patients treated with granulocyte-macrophage colony-stimulating factor." Blood 76, no. 9 (November 1, 1990): 1765–70. http://dx.doi.org/10.1182/blood.v76.9.1765.bloodjournal7691765.

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The hematopoietic cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) is being used in clinical trials for its potential in the treatment of hematopoietic insufficiency due to various causes. Involvement of leukotrienes in the effects of GM-CSF is suggested by analytical and pharmacologic evidence obtained in vitro. However, until now no data in support of a role of leukotrienes in GM-CSF action in vivo have been presented. In the present investigation this question was approached by measurement of endogenous cysteinyl leukotriene formation in patients treated with the cytokine for cytopenia induced by cytostatic drugs or for refractory anemia with excess of blasts (RAEB). Endogenous cysteinyl leukotriene formation was assessed by determination of urinary leukotriene metabolites using combined high- performance liquid chromatography and radioimmunoassay analysis. After GM-CSF administration a distinct increase in urinary cysteinyl leukotrienes was found in the cytopenic and the RAEB patients that ranged from 2.3- to 57-fold and 2.4- to 333-fold, respectively. In the cytopenic patients the increase in leukotriene production was correlated to an expansion of peripheral blood leukocytes; RAEB patients responded to GM-CSF with enhanced leukotriene biosynthesis even if the peripheral leukocytes decreased, possibly due to an abnormal number and/or irritability of leukotriene-producing cells. The increase in endogenous leukotriene production during therapy with GM- CSF may indicate that leukotrienes play a role in GM-CSF action in vivo.

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7

Jones, T. R., Y. Guindon, R. Young, E. Champion, L. Charette, D. Denis, D. Ethier, et al. "L-648,051, sodium 4-[3-(4-acetyl-3-hydroxy-2-propylphenoxy)-propylsulfonyl]-γ-oxo-benzenebutanoate: a leukotriene D4 receptor antagonist." Canadian Journal of Physiology and Pharmacology 64, no. 12 (December 1, 1986): 1535–42. http://dx.doi.org/10.1139/y86-258.

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L-648,051, sodium 4-[3-(4-acetyl-3-hydroxy-2-propylphenoxy)propylsulfonyl]-γ-oxo-benzenebutanoate is a selective and competitive inhibitor of [3H]leukotriene D4 (KB value of 4.0 μM) and to a lesser extent [3H]leukotriene C4 (Ki value of 36.7 μM) binding in guinea pig lung homogenates. Functionally, it selectively antagonized contractions of guinea pig trachea induced by leukotrienes C4, D4, E4, and F4 in concentrations that did not antagonize contractions induced by acetylcholine, histamine, serotonin, prostaglandin F2α, or U-44069 (endoperoxide analogue). Schild plot analysis indicated that L-648,051 competitively antagonized contractions of guinea pig ileum induced by leukotriene D4 (pA2 7.7) and contractions of trachea induced by leukotrienes D4, E4, and F4 (pA2 7.3, 7.4, and 7.5, respectively). Contractions of guinea pig trachea induced by leukotriene C4 were inhibited in a noncompetitive fashion (Schild plot slope, 0.45). Developed contractions of trachea induced by the leukotrienes were rapidly reversed by L-648,051 > FPL-55712 > L-649,923. Intravenous L-648,051 selectively blocked bronchoconstriction induced in anaesthetized guinea pigs by intravenous leukotrienes C4, D4, and E4 but not that induced by arachidonic acid, serotonin, U-44069, or acetylcholine. The compound displayed poor activity following intraduodenal administration. The profile of activity for L-648,051 indicates that it may be a useful topical agent for studying the role of leukotrienes in diseases such as bronchial asthma.

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Mancuso, Peter, Theodore J. Standiford, Teresa Marshall, and Marc Peters-Golden. "5-Lipoxygenase Reaction Products Modulate Alveolar Macrophage Phagocytosis of Klebsiella pneumoniae." Infection and Immunity 66, no. 11 (November 1, 1998): 5140–46. http://dx.doi.org/10.1128/iai.66.11.5140-5146.1998.

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ABSTRACT The leukotrienes are potent lipid mediators of inflammation formed by the 5-lipoxygenase-catalyzed oxidation of arachidonic acid. Although the effects of leukotrienes on neutrophil chemotaxis and activation have been established, their role in modulating innate host defense mechanisms is poorly understood. In a previous study (M. Bailie, T. Standiford, L. Laichalk, M. Coffey, R. Strieter, and M. Peters-Golden, J. Immunol. 157:5221–5224, 1996), we used 5-lipoxygenase knockout mice to establish a critical role for endogenous leukotrienes in pulmonary clearance and alveolar macrophage phagocytosis ofKlebsiella pneumoniae. In the present study, we investigated the role of specific endogenous leukotrienes in phagocytosis of K. pneumoniae and explored the possibility that exogenous leukotrienes could restore phagocytosis in alveolar macrophages with endogenous leukotriene synthesis inhibition and enhance this process in leukotriene-competent cells. Rat alveolar macrophages produced leukotriene B4 (LTB4), LTC4, and 5-hydoxyeicosatetraenoic acid (5-HETE) during the process of phagocytosis, and the inhibition of endogenous leukotriene synthesis with zileuton and MK-886 dramatically attenuated phagocytosis. We also observed a reduction in phagocytosis when we treated alveolar macrophages with antagonists to the plasma membrane receptors for either LTB4, cysteinyl-leukotrienes, or both. In leukotriene-competent cells, LTC4 augmented phagocytosis to the greatest extent, followed by 5-HETE and LTB4. These 5-lipoxygenase reaction products demonstrated similar relative abilities to reconstitute phagocytosis in zileuton-treated rat alveolar macrophages and in alveolar macrophages from 5-lipoxygenase knockout mice. We conclude that endogenous synthesis of all major 5-lipoxygenase reaction products plays an essential role in phagocytosis. The restorative and pharmacologic effects of LTC4, LTB4, and 5-HETE may provide a basis for their exogenous administration as an adjunctive treatment for patients with gram-negative bacterial pneumonia.

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9

Meshram, Deepak, Khushbo Bhardwaj, Charulata Rathod, Gail B. Mahady, and Kapil K. Soni. "The Role of Leukotrienes Inhibitors in the Management of Chronic Inflammatory Diseases." Recent Patents on Inflammation & Allergy Drug Discovery 14, no. 1 (March 30, 2020): 15–31. http://dx.doi.org/10.2174/1872213x14666200130095040.

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Background: Leukotrienes are powerful mediators of inflammation and interact with specific receptors in target cell membrane to initiate an inflammatory response. Thus, Leukotrienes (LTs) are considered to be potent mediators of inflammatory diseases including allergic rhinitis, inflammatory bowel disease and asthma. Leukotriene B4 and the series of cysteinyl leukotrienes (C4, D4, and E4) are metabolites of arachidonic acid metabolism that cause inflammation. The cysteinyl LTs are known to increase vascular permeability, bronco-constriction and mucus secretion. Objectives: To review the published data for leukotriene inhibitors of plant origin and the recent patents for leukotriene inhibitors, as well as their role in the management of inflammatory diseases. Methods: Published data for leukotrienes antagonists of plant origin were searched from 1938 to 2019, without language restrictions using relevant keywords in both free text and Medical Subject Headings (MeSH terms) format. Literature and patent searches in the field of leukotriene inhibitors were carried out by using numerous scientific databases including Science Direct, PubMed, MEDLINE, Google Patents, US Patents, US Patent Applications, Abstract of Japan, German Patents, European Patents, WIPO and NAPRALERT. Finally, data from these information resources were analyzed and reported in the present study. Results: Currently, numerous anti-histaminic medicines are available including chloropheneremine, brompheniramine, cetirizine, and clementine. Furthermore, specific leukotriene antagonists from allopathic medicines are also available including zileuton, montelukast, pranlukast and zafirlukast and are considered effective and safe medicines as compared to the first generation medicines. The present study reports leukotrienes antagonistic agents of natural products and certain recent patents that could be an alternative medicine in the management of inflammation in respiratory diseases. Conclusion: The present study highlights recent updates on the pharmacology and patents on leukotriene antagonists in the management of inflammation respiratory diseases.

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Steinhilber, D. "5-Lipoxygenase: A Target for Antiinflammatory Drugs Revisited." Current Medicinal Chemistry 6, no. 1 (January 1999): 71–85. http://dx.doi.org/10.2174/0929867306666220207211259.

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Abstract: Arachidonate 5-lipoxygenase is the key enzyme in leukotriene biosynthesis and catalyzes the initial steps in the conversion of arachidonic acid to biologically active leukotrienes. Leukotrienes are considered as potent potent mediators of inflammatory and allergic reactions which are locally released by leukocytes and other 5-LO expressing cells and exert their effects via binding to specific membrane receptors and, as suggested recently, the nuclear receptor PPARa. Because of the proinflammatory profile of leukotrienes it was assumed that leukotriene biosynthesis inhibitors and leukotriene receptor antagonists have a therapeutical potential in a variety of inflammatory diseases. Clinical studies confirmed the therapeutic value of the antileukotriene therapy in asthma but the results with leukotriene biosynthesis inhibitors in psoriasis, arthritis and inflammatory bowel disease were more or less disappointing. This review summarizes the biochemistry of the 5-lipoxygenase pathway, the pharmacology of FLAP and 5-lipoxygenase inhibitors and discusses possible criteria for the development of these drugs.

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Dissertations / Theses on the topic "Leukotrienes"

1

Qiu, Hong. "Leukotrienes and leukotriene receptors : potential roles in cardiovascular diseases /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-056-5/.

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Crawley, John Edward. "Leukotrienes." Thesis, University of Nottingham, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334790.

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Gyllfors, Pär. "Clinical studies of asthma phenotypes focusing on the role of the leukotrienes /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7357-001-X/.

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Bäck, Magnus. "Studies of receptors and modulatory mechanisms in functional responses to cysteinyl-leukotrienes in smooth muscle /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4846-1/.

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Manro, A. "Synthesis of compounds related to leukotrienes." Thesis, University of Salford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381849.

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McColl, Shaun Reuss. "Factors affecting the regulation of leukotriene production by neutrophils." Title page, contents and summary only, 1987. http://web4.library.adelaide.edu.au/theses/09PH/09phm1288.pdf.

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Caroppo, V. "EFFECTS OF CYSTEINYL LEUKOTRIENES ON PLATELET ACTIVATION." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/363389.

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Platelet are key players in haemostasis and represent a pivotal link between inflammation, immunity and atherogenesis. Cysteinyl leukotrienes (CysLTs) such as LTC4, LTD4, and LTE4 are potent lipid inflammatory mediators which interact with G protein-coupled receptors, CysLT1R, CysLT2R . However, LTE4, the most stable cystenyl leukotriene, is not putative substrate for these two receptor. Recently have been hypothesized that a third cystenyl leukotreine receptor exists, and a computer modeling suggests P2Y12, receptor for ADP present on platelet surface, as the putative receptor. But GPR99 is also hypothesized as LTE4 putative receptor. It is known that LTE4 needs P2Y12 on platelet to mediate inflammation in sensitized mice, and LTC4 can induce release of P-selectin in sensitized mice. In human platelet LTE4 cannot increase level of cAMP, or of p-selectin. Aim of this study was to test whether cystenyl leukotrienes elicit platelet functional responses, by interacting with the platelet P2Y12, receptor for ADP. We measure the platelet aggregation induced by CysLTs alone or in combination with epinephrine or ADP; the cAMP level in presence of PGE1, ADP and CysLTs, and finally the p-selectin expression on platelet surface after stimulation with ADP and CysLTs and in presence/absence of cangrelor. Ours results shows that CysLTs cannot affect platelet aggregation alone or in combination with other agonist, independently of presence of physiological level of calcium. CysLTs failed to show an effect also on cAMP level. Also when platelet activation was tested by measuring the expression of p-selectin on the platelet membrane induced by ADP, CysLTs failed to show any effect. The negative results of our studies are not due to alterations of the CysLTs that we used, as they were identified correctly at mass spectrometry and induced normal cellular response of HUVEC, as previously shown. The inflammatory effects of CysLTs mediated by the platelet P2Y12 receptor, which have been demonstrated in vivo experiments, were most likely indirect, rather than induced by a direct interaction of CysLTs with platelets.

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Butler, Paul Ian. "The synthesis and evaluation of potential inhibitors of 5-lipoxygenase." Thesis, University of Reading, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357783.

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9

Sousa, Paula T. de. "The synthesis of novel thiophene analogues of leukotrienes." Thesis, University of East Anglia, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317613.

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Galton, S. A. "Production of leukotrienes by the porcine pulmonary artery." Thesis, University College London (University of London), 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376096.

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Books on the topic "Leukotrienes"

1

Roberto, Levi, Krell Robert D, New York Academy of Sciences., and Conference on the Biology of the Leukotrienes (1987 : Philadelphia, Pa.), eds. Biology of the leukotrienes. New York, N.Y: New York Academy of Sciences, 1988.

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2

Rodger, Ian, Jack Botting, and Sven-Erik Dahlén, eds. Leukotrienes. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-4880-1.

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3

E, Pike John, and Morton Douglas R, eds. Chemistry of the prostaglandins and leukotrienes. New York: Raven Press, 1985.

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Uriel, Zor, Naor Zvi, Kohen Fortüne, and International Conference on: Leukotrienes and Prostanoids in Health and Disease (1985 : Tel Aviv, Israel and Rehovot, Israel), eds. Leukotrienes and prostanoids in health and disease. New York: Raven Press, 1986.

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5

Martyn, Bailey J., and International Spring Symposium on Health Sciences (4th : 1984 : Washington, D.C.), eds. Prostaglandins, leukotrienes, and lipoxins: Biochemistry, mechanism of action, and clinical applications. New York: Plenum Press, 1985.

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Bailey, J. Martyn, ed. Prostaglandins, Leukotrienes, and Lipoxins. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4946-4.

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Folco, Giancarlo, Bengt Samuelsson, and Robert C. Murphy, eds. Novel Inhibitors of Leukotrienes. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8703-8.

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Giancarlo, Folco, Murphy Robert C, and Samuelsson Bengt, eds. Novel inhibitors of leukotrienes. Basel: Birkhäuser Verlag, 1999.

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Giancarlo, Folco, Samuelsson Bengt, and Murphy Robert C, eds. Novel inhibitors of leukotrienes. Basel: Birkhäuser Verlag, 1999.

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Bailey, J. Martyn, ed. Prostaglandins, Leukotrienes, Lipoxins, and PAF. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4899-0727-1.

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Book chapters on the topic "Leukotrienes"

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Mayatepek, Ertan. "Leukotrienes." In Physician's Guide to the Diagnosis, Treatment, and Follow-Up of Inherited Metabolic Diseases, 617–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-40337-8_38.

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Hay, Douglas W. P., and David Raeburn. "Leukotrienes." In Airways Smooth Muscle: Neurotransmitters, Amines, Lipid Mediators and Signal Transduction, 199–225. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7504-2_6.

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Okunishi, Katsuhide, and Marc Peters-Golden. "Leukotrienes." In Inflammation and Allergy Drug Design, 285–95. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444346688.ch23.

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Sjölander, Anita. "Leukotrienes." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_3334-2.

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Bäck, Magnus. "Leukotrienes." In Compendium of Inflammatory Diseases, 849–57. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_105.

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Bach, Michael K. "Leukotrienes." In The Reticuloendothelial System, 267–320. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5158-0_11.

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Sjölander, Anita. "Leukotrienes." In Encyclopedia of Cancer, 2481–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_3334.

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Sjölander, Anita. "Leukotrienes." In Encyclopedia of Cancer, 2028–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3334.

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Gooch, Jan W. "Leukotrienes." In Encyclopedic Dictionary of Polymers, 904. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14113.

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Nakamura, Motonao, and Takehiko Yokomizo. "Leukotrienes." In Encyclopedia of Molecular Pharmacology, 1–10. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-21573-6_87-1.

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Conference papers on the topic "Leukotrienes"

1

Eap, R., E. Jacques, S. Plante, and J. Chakir. "Cysteinyl Leukotrienes Increase Collagen Production in Bronchial Fibroblasts of Asthmatic Subjects Via Cysteinyl Leukotriene Receptor 2." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5060.

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Jaksch-Bogensperger, H., A. Koller, Th Fischer, L. Aigner, C. Fazelnia, D. Gharehbaghi, A. Zurl, and KM Hillerer. "The role of Cysteinyl-Leukotrienes in preeclamptic patients." In Kongressabstracts zur Gemeinsamen Jahrestagung der Österreichischen Gesellschaft für Gynäkologie und Geburtshilfe (OEGGG) und der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde e.V. (BGGF). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1730483.

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Ptaszynski, S., V. Arsenault, A. Al-Rabea, and C. Bergeron. "Leukotrienes and Airway Epithelial-Mesenchymal Transition – Implications in Bronchiolitis Obliterans." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5634.

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Kaditis, A., K. Chaidas, E. Alexopoulos, G. Ntamagka, A. Karathanasi, E. Boultadakis, T. Kiropoulos, I. Tsilioni, and K. Gourgoulianis. "Urine Concentrations of Cysteinyl Leukotrienes in Children with Obstructive Sleep-Disordered Breathing." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6342.

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Matsuyama, T., K. Machida, H. Matsuyama, Y. Dotake, K. Takagi, and H. Inoue. "The Effect of Long-acting Muscarinic Antagonist on Airway Inflammation Through Leukotrienes." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1300.

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Parker, D., D. A. Flores, J. K. Bentley, and M. B. Hershenson. "Cysteinyl Leukotrienes Are Required for Rhinovirus-induced Mucous Metaplasia in Immature Mice." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a1383.

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Crimi, C., S. Sichili, A. Salamone, P. Pistorio, E. Gili, C. Mastruzzo, C. Vancheri, and N. Crimi. "Exhaled Breath Condensate (EBC) Cysteinyl Leukotrienes (cys-LTs) in Gastroesophageal Reflux Disease-Related Asthma." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5703.

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Krohne, Sheryl G. "Use of the KOWA FC-1000 to Measure Aqueous Humor Protein and Cells in the Dog." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1991. http://dx.doi.org/10.1364/navs.1991.md3.

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Abstract:

Breakdown of the blood-aqueous barrier (BAB) resulting in protein and cells in the aqueous humor of humans and many animals has been documented.1 This breakdown occurs during uveitis, and following surgery and paracentesis. BAB breakdown occurs following these initiating insults because endothelial cells contract in the ciliary body, causing protein leakage from the vascular system which results Jn dysjunction of the epithelial layers, further vascular damage and protein leakage.2,3 These changes are mediated by prostaglandins, leukotrienes, free radicals, neurostimulators (such as in the anti-dromic reflex) and mechanical disruption.3,4,5,6 Sequelae to the BAB breakdown can be severe and include hypopyon, cataract, synechia, vitreal opacities, glaucoma, blindness and occasionally phthisis bulbi.

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Altraja, S., J. Jaama, and A. Altraja. "Cysteinyl Leukotrienes Cause Down-Regulation of Glucocorticoid Receptor in Human Bronchial Epithelial Cells Via CysLT1Receptor." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1403.

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Bikov, András, Orsolya Gall, Zoltan Sutto, Aniko Bohacs, Eszter Csiszer, Gyorgy Losonczy, and Veronika Muller. "Bronchoalveolar lavage fluid leukotrienes in the pathomechanism of acute inflammatory events in lung transplant recipients." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa4148.

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Reports on the topic "Leukotrienes"

1

Muza, S. R., D. Kaminsky, C. S. Fulco, L. E. Banderet, and A. Cymerman. Cysteinyl Leukotriene Blockade Does Not Prevent Acute Mountain Sickness. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada423394.

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Goldman, Gideon, Richard Welbourn, C. R. aleri, David Shepro, and Herbert B. Hechtman. Leukotriene B4 and Thromboxane A2 are Essential Cofactors in CD 18 Dependent Neutrophil Diapedesis. Fort Belvoir, VA: Defense Technical Information Center, July 1990. http://dx.doi.org/10.21236/ada360180.

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