INT4810
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Histamine was released in 8/10 subjects (control: 7.06 +/- 4.19 nM/L, codeine phosphate: 18.2 +/- 15.7 nM/L, P < .018), PGD2 was released in 8/10 subjects (control: 0 codeine phosphate: 273.3 +/- 408.9 ng/L). | |||||||||||||||
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Disodium cromoglycate blocked the release of histamine and PGD2. | |||||||||||||||
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In contrast, both compounds inhibit PGD2-mediated arrestin translocation via a G protein-independent mechanism. | |||||||||||||||
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Next, we used immunohistohemistry to analyze the localization and the expression level of L-PGDS and H-PGDS proteins in healthy and OA cartilage. | |||||||||||||||
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Histamine and immunoreactive LTC4 and PGD2 release was monitored in all experiments. | |||||||||||||||
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The effects of increasing concentrations of three opioids (morphine, buprenorphine, and fentanyl) were studied on the release of preformed (histamine and tryptase) and de novo synthesized (prostaglandin D2 [PGD2] and peptide-leukotriene C4 [LTC4]) chemical mediators from human peripheral blood basophils and mast cells isolated from skin tissues or lung parenchyma. | |||||||||||||||
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The effects of increasing concentrations of three opioids (morphine, buprenorphine, and fentanyl) were studied on the release of preformed (histamine and tryptase) and de novo synthesized (prostaglandin D2 [PGD2] and peptide-leukotriene C4 [LTC4]) chemical mediators from human peripheral blood basophils and mast cells isolated from skin tissues or lung parenchyma. | |||||||||||||||
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The recent development of in vitro techniques to study the release of preformed (histamine and tryptase) and de novo synthesized mediators (PGD2, LTC4, and PAF) from purified basophils and mast cells has made it possible to quantify the mediator-releasing activity of anesthetics such as muscle relaxants, general anesthetics, opioids, and benzodiazepines and RCM on human basophils and mast cells isolated from lung, skin and heart tissues. | |||||||||||||||
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When niacin is administered orally in amounts of 500 mg or topically via a 6-inch patch of 10-1 M aqueous methylnicotinate on the forearm, PGD2 is markedly released in the skin and its metabolite appears in high amounts in the plasma [22,23]. | |||||||||||||||
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Maximal stimulation of HHMC with anti-IgE led to the release of LTC4 (17.5 +/- 5.1 ng/10(6) mast cells) and PGD2 (17.8 +/- 5.0 ng/10(6) mast cells, whereas HSMC synthesized more PGD2 (65.0 +/- 6.8 ng/10(6) mast cells) and much less LTC4 (< 5 ng/10(6) cells). | |||||||||||||||
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Cross-linking of the high-affinity receptor for IgE (Fc epsilon RI) by a polyclonal anti-Fc epsilon antibody caused the release of preformed (histamine and tryptase) and de novo synthesized mediators [peptide leukotriene C4 (LTC4) and prostaglandin D2 (PGD2)]. | |||||||||||||||
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Cross-linking of the high-affinity receptor for IgE (Fc epsilon RI) by a polyclonal anti-Fc epsilon antibody caused the release of preformed (histamine and tryptase) and de novo synthesized mediators [peptide leukotriene C4 (LTC4) and prostaglandin D2 (PGD2)]. | |||||||||||||||
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Approximately 180 kb toward the telomere from LCN6, is the gene encoding the complement C8 gamma subunit (C8G), and the prostaglandin D2 synthase (PTGDS) gene [48] is located another 30 kb beyond C8G. | |||||||||||||||
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Approximately 180 kb toward the telomere from LCN6, is the gene encoding the complement C8 gamma subunit (C8G), and the prostaglandin D2 synthase (PTGDS) gene [48] is located another 30 kb beyond C8G. | |||||||||||||||
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, PGD2, prostacyclin (PGI2), and thromboxane(TX) A2 that are immediately released outside the cell after intracellular biosynthesis and modulate a wide variety of physiologic and pathologic processes via the interaction with specific receptors expressed mostly on the surface of target cells (Narumiya et al 1999; Breyer et al 2001). | |||||||||||||||
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Effects of palmitoylethanolamide on immunologically induced histamine, PGD2 and TNFalpha release from canine skin mast cells. | |||||||||||||||
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Hence, collectively, both NO-donors and the vasodilatory prostanoids prostacyclin and PGD2 readily desensitize TP-mediated Rho activation and cytoskeletal signaling in 1° h.AoSMCs, findings entirely predicted from and in keeping with outcomes from other systems [6,8,35,36]. | |||||||||||||||
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The effects of increasing concentrations of three opioids (morphine, buprenorphine, and fentanyl) were studied on the release of preformed (histamine and tryptase) and de novo synthesized (prostaglandin D2 [PGD2] and peptide-leukotriene C4 [LTC4]) chemical mediators from human peripheral blood basophils and mast cells isolated from skin tissues or lung parenchyma. | |||||||||||||||
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The effects of increasing concentrations of three opioids (morphine, buprenorphine, and fentanyl) were studied on the release of preformed (histamine and tryptase) and de novo synthesized (prostaglandin D2 [PGD2] and peptide-leukotriene C4 [LTC4]) chemical mediators from human peripheral blood basophils and mast cells isolated from skin tissues or lung parenchyma. | |||||||||||||||
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The recent development of in vitro techniques to study the release of preformed (histamine and tryptase) and de novo synthesized mediators (PGD2, LTC4, and PAF) from purified basophils and mast cells has made it possible to quantify the mediator-releasing activity of anesthetics such as muscle relaxants, general anesthetics, opioids, and benzodiazepines and RCM on human basophils and mast cells isolated from lung, skin and heart tissues. | |||||||||||||||
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