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1 educes antigen-induced secretion of PGD2 and cysteinyl-leukotriene.
2 ial killing, and production of TNF-alpha and cysteinyl leukotrienes.
3 , whereas mRECs produced both LTB(4) and the cysteinyl leukotrienes.
4 nflux through CRAC channels and responded to cysteinyl leukotrienes.
5 -5, interleukin-13, eotaxin, prostanoids and cysteinyl leukotrienes.
6 ed in the generation of both prostanoids and cysteinyl leukotrienes.
7 intracellular parent of the proinflammatory cysteinyl leukotrienes.
8 s such as histamine, prostaglandin D(2), and cysteinyl leukotrienes.
9 ntrast, M1 macrophages gave higher levels of cysteinyl leukotrienes.
10 piratory tissues and excessive production of cysteinyl leukotrienes.
11 cterise the responsiveness of human P2Y12 to cysteinyl leukotrienes.
12 classes of molecules: uracil-nucleotides and cysteinyl-leukotrienes.
13 lasses of human G protein-coupled receptors, cysteinyl leukotriene 1 (CysLT(1)) and CysLT(2) receptor
14 in a strain with targeted disruption of the cysteinyl leukotriene 1 (CysLT(1)) receptor suggested th
15 rienes (CysLTs) are mediated by 2 receptors: cysteinyl leukotriene 1 receptor (CysLT1R) and cysteinyl
17 study, we determined whether montelukast, a cysteinyl leukotriene 1 receptor antagonist, could preve
19 rienes, which are competitive antagonists of cysteinyl-leukotriene-1 receptors, are the first new cla
20 ulted in the generation of 23.9 +/- 6.0 pmol cysteinyl leukotrienes/10(6) eosinophil-lineage cells (m
21 hore-induced production of 94.6 +/- 9.0 pmol cysteinyl leukotrienes/10(6) eosinophil-lineage cells (n
23 he mast cell mediators histamine (9.0-fold), cysteinyl leukotrienes (4.5-fold), and prostaglandin (PG
24 decreased eicosanoid biosynthesis, including cysteinyl leukotrienes (80% mean decrease) that mediated
26 Pharmacological studies have determined that cysteinyl leukotrienes activate at least two receptors,
28 cellular calcium mobilization in response to cysteinyl leukotriene administration was detected in hum
29 nvolved in the extrusion of reduced folates, cysteinyl leukotrienes and bile acids, and the molecular
30 and mast cells to promote avoidance requires cysteinyl leukotrienes and growth and differentiation fa
31 kast and loratadine inhibited the release of cysteinyl leukotrienes and histamine into the airways, b
32 reatments being developed beyond blockade of cysteinyl leukotrienes and IgE and improvements in inhal
34 HLMC with a strong and specific increase in cysteinyl leukotrienes and PGD(2) but also the bronchoco
35 ophagoides farinae through the generation of cysteinyl leukotrienes and proinflammatory cytokines, re
36 , eicosanoids implicated in allergy (such as cysteinyl leukotrienes and prostaglandin D(2)) and the n
37 and suggest downstream provocative roles for cysteinyl leukotrienes and protective roles for SOCS3 in
38 to leukotriene D(4), the most potent of the cysteinyl leukotrienes and the immediate precursor of le
39 require 5-lipoxygenase-mediated synthesis of cysteinyl leukotrienes and their efflux from the cell.
40 abelled LTD4 binding to this receptor by the cysteinyl leukotrienes and three structurally distinct c
41 nsible for the scavenging of proinflammatory cysteinyl leukotrienes and thromboxanes at the feeding s
42 AM phagocytosis, killing, and production of cysteinyl leukotrienes and TNF-alpha are restored in the
46 ncreases in metabolites of prostaglandin D2, cysteinyl leukotrienes, and isoprostanes following the c
47 proinflammatory mediators, including IL-13, cysteinyl leukotrienes, and PGD(2), and airway hyperresp
48 andomized, double-blind crossover study, the cysteinyl leukotriene antagonist montelukast and antihis
50 tors occurs during EIB and how histamine and cysteinyl leukotriene antagonists alter the airway event
61 trong scientific rationale for their use, as cysteinyl-leukotrienes are increased in asthma and can m
62 The paracrine signal was identified as a cysteinyl leukotriene because 1) RNAi knockdown or pharm
64 lso demonstrate direct binding of U46619 and cysteinyl leukotrienes C(4), D(4) and E(4) to the P. pap
66 The antioxidant GSH and the pro-inflammatory cysteinyl leukotriene C4 have been identified as key phy
69 ry and immunomodulatory mediators, including cysteinyl leukotrienes, chemokines, and cytokines, which
72 feedback cascade involving CRAC channels and cysteinyl leukotrienes constitute a novel mechanism for
76 Dermatophagoides farinae (Df) that mediates cysteinyl leukotriene (cys-LT) generation from pulmonary
77 il infiltration, and increased levels of the cysteinyl leukotriene (cys-LT) leukotriene C(4) (LTC(4))
79 s, and induces a calcium flux in response to cysteinyl leukotrienes (cys-LTs) and uridine diphosphate
95 stimulated a rapid and robust production of cysteinyl leukotrienes (cys-LTs), proinflammatory lipid
97 ported in coculture generated low amounts of cysteinyl-leukotrienes (cys-LT) after FcepsilonRI-depend
99 -IgE or SCF and the generation of histamine, cysteinyl-leukotrienes (cys-LTs) and prostaglandin D(2)
104 flammatory cells, LTA4 is converted into the cysteinyl leukotriene (cysLT) LTC4, which is converted i
108 rolled clinical trials have established that cysteinyl leukotriene (cysLT) receptor antagonists and 5
111 model is reversible by administration of the cysteinyl leukotriene (CysLT)1 receptor antagonist monte
112 patients with asthma and may participate in cysteinyl leukotriene (CysLT; C(4), D(4), and E(4)) synt
114 ion was evaluated as Ca2+ flux, secretion of cysteinyl leukotrienes (CysLT), and eosinophil-derived n
116 tion of partner receptors (nucleotide P2Y12, cysteinyl-leukotriene CysLT1) to reconstitute the elusiv
117 et release of histamine (29.8 +/- 10.8%) and cysteinyl leukotrienes (cysLTs) (31.4 +/- 8.7 ng/10(6) b
125 The proinflammatory and vascular actions of cysteinyl leukotrienes (CysLTs) are mediated by 2 recept
129 Leukotriene E4 (LTE4) the most stable of the cysteinyl leukotrienes (cysLTs) binds poorly to classica
135 nstrictive and proinflammatory properties of cysteinyl leukotrienes (cysLTs) in allergic asthma media
138 ctures show that the N-terminal domain binds cysteinyl leukotrienes (cysLTs) with high affinities (50
140 r of the airways, involves overproduction of cysteinyl leukotrienes (cysLTs), activation of airway ma
141 Urinary metabolites of prostaglandins (PGs), cysteinyl leukotrienes (CysLTs), and isoprostanes were q
142 thma, tissue eosinophilia, overproduction of cysteinyl leukotrienes (cysLTs), and respiratory reactio
143 eukotriene E4 (LTE4), the most stable of the cysteinyl leukotrienes (cysLTs), binds poorly to classic
146 iated with overproduction of proinflammatory cysteinyl leukotrienes (CysLTs), defective generation of
152 contractile and inflammatory actions of the cysteinyl leukotrienes (CysLTs), LTC(4), LTD(4), and LTE
153 is unclear whether lipid mediators, such as cysteinyl leukotrienes (CysLTs), which are present in as
157 capable of both producing and responding to cysteinyl leukotrienes (CystLTs), allowing for the killi
159 Herein we report that uracil nucleotides and cysteinyl leukotrienes do not activate human, mouse, or
160 Measurement of the release of histamine and cysteinyl leukotrienes documented that this bronchoprote
161 The combination of PGD2 and cysLTs (notably cysteinyl leukotriene E4 [LTE4]) enhances TH2 cytokine p
162 ils, when activated, become major sources of cysteinyl leukotrienes, eicosanoid mediators pertinent t
163 st cell precursors and selectively increased cysteinyl leukotriene formation by mast cells in a manne
165 ar lavage fluid cells, prostaglandin D2, and cysteinyl leukotrienes from hyperventilated airways pret
167 braking" of mast cell activation and further cysteinyl leukotriene generation induced by cyclooxygena
169 that is responsible for the biosynthesis of cysteinyl leukotrienes, has been deleted by targeted gen
171 form LTC4, the parent of the receptor active cysteinyl leukotrienes implicated in the pathobiology of
172 to produce LTC4, the parent compound of the cysteinyl leukotrienes, important mediators of asthma.
175 bute to the excessive baseline production of cysteinyl leukotrienes in patients with AERD compared wi
176 entify previously unrecognized roles for the cysteinyl leukotrienes in regulating the pulmonary traff
179 These data suggest an important role for cysteinyl leukotrienes in the pathogenesis of chronic al
180 combination of antagonists of histamine and cysteinyl leukotrienes in the presence of indomethacin.
183 r findings suggest a novel critical role for cysteinyl-leukotrienes in HIV-associated brain injury.
184 te the selective role of LTB4, as opposed to cysteinyl-leukotrienes, in murine models of inflammation
186 d urinary leukotriene E(4) levels indicating cysteinyl leukotriene inflammation can differentiate LAB
187 , ATLa treatment led to marked reductions in cysteinyl leukotrienes, interleukin-4 (IL-4), and IL-10,
189 cts: 5-,12-,15-hydroxyeicosatetraenoic acid, cysteinyl leukotrienes, leukotriene B4 , 11-dehydro-thro
196 tes 20-hydroxy-LTB4 and 20-carboxy-LTB4, the cysteinyl leukotriene LTC4, the 15-lipoxygenase product
197 d lipoxygenase products of arachidonic acid, cysteinyl leukotrienes (LTs), contribute to E. coli K1 i
199 lipid inflammatory mediators comprising the cysteinyl leukotrienes (LTs; LTC4, LTD4, and LTE4), only
200 triad of preclinical areas of investigation-cysteinyl leukotrienes, mast cells, and complement-with
202 and increasing alveolar fluid reabsorption, cysteinyl leukotrienes may, in part, have a beneficial r
203 es, and (3) IgE-stimulated mast cell-derived cysteinyl-leukotriene mediated avoidance of toxins.
207 ccompanied by a surge in bronchoconstrictory cysteinyl leukotrienes produced at the expense of LTB4 i
208 polymorphism was associated with changes in cysteinyl leukotriene production, lung function, airway
209 nied by high levels of mast cell activation, cysteinyl leukotriene production, platelet activation, a
211 s in s/s mice were associated with increased cysteinyl-leukotriene production in vivo and in AMs in v
212 have been described; the mechanisms by which cysteinyl leukotrienes promote the development of inflam
214 abolites of vasoactive molecules showed that cysteinyl leukotrienes, prostacyclin metabolites, and PG
215 ase (AERD) is associated with high levels of cysteinyl leukotrienes, prostaglandin D(2), and low leve
218 oth murine and human fibrocytes express both cysteinyl leukotriene receptor (CysLT) 1 and CysLT2.
220 da G-protein-coupled receptor 5 [TGR5]), and cysteinyl leukotriene receptor (CYSLTR) 1 are G-protein-
221 eries of compounds with dual activity toward cysteinyl leukotriene receptor 1 (CysLT(1)R) and G-prote
222 ndent increase in cell-surface expression of cysteinyl leukotriene receptor 1 (CysLT1) as determined
225 "proatopic" neutrophil subset that expressed cysteinyl leukotriene receptor 1 (CysLTR1) and produced
229 s and found a recurrent mutation in CYSLTR2 (cysteinyl leukotriene receptor 2) encoding a p.Leu129Gln
232 zed by some as a dualistic uracil nucleotide/cysteinyl leukotriene receptor and by others as inactive
233 stigated the effectiveness of montelukast, a cysteinyl leukotriene receptor antagonist, in the treatm
238 ing montelukast (an antagonist of the type 1 cysteinyl leukotriene receptor) also inhibited E. coli i
240 e cloning and characterization of the second cysteinyl leukotriene receptor, CysLT(2), a 346-amino ac
241 TC4S) and, pharmacological inhibition of the cysteinyl-leukotriene receptor 1 (CYSLTR1) protects cere
243 mine H1 receptor antagonist, cetirizine, and cysteinyl-leukotriene receptor antagonist, montelukast,
247 e inflammatory cells and their expression of cysteinyl leukotriene receptors 1 and 2 (CysLT(1) and Cy
248 antiangiogenic small molecule antagonist of cysteinyl leukotriene receptors 1 and 2 (CysLT1 and CysL
249 rectly target VEGF receptors but antagonizes cysteinyl leukotriene receptors 1 and 2 (CysLT1-2) at mi
253 made in three areas: genetic control of the cysteinyl leukotriene response, in which alterations in
254 exercise challenge, histamine, tryptase, and cysteinyl leukotrienes significantly increased and prost
257 1/2, cytosolic phospholipase A(2) alpha, and cysteinyl-leukotriene synthesis confers resistance to s/
258 bstance of anaphylaxis was composed of three cysteinyl leukotrienes that act in the inflammatory resp
259 (4)S) is responsible for the biosynthesis of cysteinyl leukotrienes that participate in allergic and
261 al protists, stimulate tuft cells to release cysteinyl leukotrienes to amplify anti-helminth immunity
262 ut the contributions of mediators other than cysteinyl leukotrienes to aspirin reactions and to the t
264 diating the leukotriene responses in asthma, cysteinyl leukotriene type 1 receptor (CysLT1R), have no
265 inic and H1 histamine receptor and expressed cysteinyl leukotriene type 1 receptor in human embryonic
267 t cytoplasmic Ca(2+) oscillations induced by cysteinyl leukotriene type I receptor activation run dow
268 ations can be evoked by modest activation of cysteinyl leukotriene type I receptors by the physiologi
270 Here, we show that following stimulation of cysteinyl leukotriene type I receptors in rat basophilic
274 GE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways
275 sharp contrast, mean levels of prophlogistic cysteinyl leukotrienes were increased in samples from se
276 n and the accompanying in vivo generation of cysteinyl leukotrienes were markedly attenuated in group
277 FLAP), but lacked LTC4S and did not generate cysteinyl leukotrienes when stimulated with 20 mumol/L c
279 ablysin-15 was found to bind proinflammatory cysteinyl leukotrienes with submicromolar affinities.