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1 educes antigen-induced secretion of PGD2 and cysteinyl-leukotriene.
2 , whereas mRECs produced both LTB(4) and the cysteinyl leukotrienes.
3 nflux through CRAC channels and responded to cysteinyl leukotrienes.
4 -5, interleukin-13, eotaxin, prostanoids and cysteinyl leukotrienes.
5 ed in the generation of both prostanoids and cysteinyl leukotrienes.
6 ntrast, M1 macrophages gave higher levels of cysteinyl leukotrienes.
7 intracellular parent of the proinflammatory cysteinyl leukotrienes.
8 piratory tissues and excessive production of cysteinyl leukotrienes.
9 cterise the responsiveness of human P2Y12 to cysteinyl leukotrienes.
10 ial killing, and production of TNF-alpha and cysteinyl leukotrienes.
11 classes of molecules: uracil-nucleotides and cysteinyl-leukotrienes.
12 lasses of human G protein-coupled receptors, cysteinyl leukotriene 1 (CysLT(1)) and CysLT(2) receptor
13 in a strain with targeted disruption of the cysteinyl leukotriene 1 (CysLT(1)) receptor suggested th
14 rienes (CysLTs) are mediated by 2 receptors: cysteinyl leukotriene 1 receptor (CysLT1R) and cysteinyl
15 study, we determined whether montelukast, a cysteinyl leukotriene 1 receptor antagonist, could preve
17 rienes, which are competitive antagonists of cysteinyl-leukotriene-1 receptors, are the first new cla
18 ulted in the generation of 23.9 +/- 6.0 pmol cysteinyl leukotrienes/10(6) eosinophil-lineage cells (m
19 hore-induced production of 94.6 +/- 9.0 pmol cysteinyl leukotrienes/10(6) eosinophil-lineage cells (n
21 decreased eicosanoid biosynthesis, including cysteinyl leukotrienes (80% mean decrease) that mediated
23 Pharmacological studies have determined that cysteinyl leukotrienes activate at least two receptors,
25 cellular calcium mobilization in response to cysteinyl leukotriene administration was detected in hum
26 nvolved in the extrusion of reduced folates, cysteinyl leukotrienes and bile acids, and the molecular
27 kast and loratadine inhibited the release of cysteinyl leukotrienes and histamine into the airways, b
28 reatments being developed beyond blockade of cysteinyl leukotrienes and IgE and improvements in inhal
30 ophagoides farinae through the generation of cysteinyl leukotrienes and proinflammatory cytokines, re
31 and suggest downstream provocative roles for cysteinyl leukotrienes and protective roles for SOCS3 in
32 to leukotriene D(4), the most potent of the cysteinyl leukotrienes and the immediate precursor of le
33 require 5-lipoxygenase-mediated synthesis of cysteinyl leukotrienes and their efflux from the cell.
34 abelled LTD4 binding to this receptor by the cysteinyl leukotrienes and three structurally distinct c
35 AM phagocytosis, killing, and production of cysteinyl leukotrienes and TNF-alpha are restored in the
37 ncreases in metabolites of prostaglandin D2, cysteinyl leukotrienes, and isoprostanes following the c
38 proinflammatory mediators, including IL-13, cysteinyl leukotrienes, and PGD(2), and airway hyperresp
39 andomized, double-blind crossover study, the cysteinyl leukotriene antagonist montelukast and antihis
41 tors occurs during EIB and how histamine and cysteinyl leukotriene antagonists alter the airway event
51 trong scientific rationale for their use, as cysteinyl-leukotrienes are increased in asthma and can m
52 The paracrine signal was identified as a cysteinyl leukotriene because 1) RNAi knockdown or pharm
53 The antioxidant GSH and the pro-inflammatory cysteinyl leukotriene C4 have been identified as key phy
54 ry and immunomodulatory mediators, including cysteinyl leukotrienes, chemokines, and cytokines, which
57 feedback cascade involving CRAC channels and cysteinyl leukotrienes constitute a novel mechanism for
61 Dermatophagoides farinae (Df) that mediates cysteinyl leukotriene (cys-LT) generation from pulmonary
62 il infiltration, and increased levels of the cysteinyl leukotriene (cys-LT) leukotriene C(4) (LTC(4))
64 s, and induces a calcium flux in response to cysteinyl leukotrienes (cys-LTs) and uridine diphosphate
79 stimulated a rapid and robust production of cysteinyl leukotrienes (cys-LTs), proinflammatory lipid
81 ported in coculture generated low amounts of cysteinyl-leukotrienes (cys-LT) after FcepsilonRI-depend
83 -IgE or SCF and the generation of histamine, cysteinyl-leukotrienes (cys-LTs) and prostaglandin D(2)
87 flammatory cells, LTA4 is converted into the cysteinyl leukotriene (cysLT) LTC4, which is converted i
91 rolled clinical trials have established that cysteinyl leukotriene (cysLT) receptor antagonists and 5
93 model is reversible by administration of the cysteinyl leukotriene (CysLT)1 receptor antagonist monte
94 patients with asthma and may participate in cysteinyl leukotriene (CysLT; C(4), D(4), and E(4)) synt
96 ion was evaluated as Ca2+ flux, secretion of cysteinyl leukotrienes (CysLT), and eosinophil-derived n
97 tion of partner receptors (nucleotide P2Y12, cysteinyl-leukotriene CysLT1) to reconstitute the elusiv
98 et release of histamine (29.8 +/- 10.8%) and cysteinyl leukotrienes (cysLTs) (31.4 +/- 8.7 ng/10(6) b
104 The proinflammatory and vascular actions of cysteinyl leukotrienes (CysLTs) are mediated by 2 recept
107 Leukotriene E4 (LTE4) the most stable of the cysteinyl leukotrienes (cysLTs) binds poorly to classica
112 nstrictive and proinflammatory properties of cysteinyl leukotrienes (cysLTs) in allergic asthma media
114 ctures show that the N-terminal domain binds cysteinyl leukotrienes (cysLTs) with high affinities (50
116 r of the airways, involves overproduction of cysteinyl leukotrienes (cysLTs), activation of airway ma
117 thma, tissue eosinophilia, overproduction of cysteinyl leukotrienes (cysLTs), and respiratory reactio
118 eukotriene E4 (LTE4), the most stable of the cysteinyl leukotrienes (cysLTs), binds poorly to classic
124 contractile and inflammatory actions of the cysteinyl leukotrienes (CysLTs), LTC(4), LTD(4), and LTE
125 is unclear whether lipid mediators, such as cysteinyl leukotrienes (CysLTs), which are present in as
128 capable of both producing and responding to cysteinyl leukotrienes (CystLTs), allowing for the killi
130 Herein we report that uracil nucleotides and cysteinyl leukotrienes do not activate human, mouse, or
131 Measurement of the release of histamine and cysteinyl leukotrienes documented that this bronchoprote
132 The combination of PGD2 and cysLTs (notably cysteinyl leukotriene E4 [LTE4]) enhances TH2 cytokine p
133 ils, when activated, become major sources of cysteinyl leukotrienes, eicosanoid mediators pertinent t
134 st cell precursors and selectively increased cysteinyl leukotriene formation by mast cells in a manne
136 ar lavage fluid cells, prostaglandin D2, and cysteinyl leukotrienes from hyperventilated airways pret
138 that is responsible for the biosynthesis of cysteinyl leukotrienes, has been deleted by targeted gen
140 form LTC4, the parent of the receptor active cysteinyl leukotrienes implicated in the pathobiology of
141 to produce LTC4, the parent compound of the cysteinyl leukotrienes, important mediators of asthma.
144 entify previously unrecognized roles for the cysteinyl leukotrienes in regulating the pulmonary traff
147 These data suggest an important role for cysteinyl leukotrienes in the pathogenesis of chronic al
150 te the selective role of LTB4, as opposed to cysteinyl-leukotrienes, in murine models of inflammation
152 d urinary leukotriene E(4) levels indicating cysteinyl leukotriene inflammation can differentiate LAB
153 , ATLa treatment led to marked reductions in cysteinyl leukotrienes, interleukin-4 (IL-4), and IL-10,
154 cts: 5-,12-,15-hydroxyeicosatetraenoic acid, cysteinyl leukotrienes, leukotriene B4 , 11-dehydro-thro
160 tes 20-hydroxy-LTB4 and 20-carboxy-LTB4, the cysteinyl leukotriene LTC4, the 15-lipoxygenase product
161 d lipoxygenase products of arachidonic acid, cysteinyl leukotrienes (LTs), contribute to E. coli K1 i
163 lipid inflammatory mediators comprising the cysteinyl leukotrienes (LTs; LTC4, LTD4, and LTE4), only
164 triad of preclinical areas of investigation-cysteinyl leukotrienes, mast cells, and complement-with
166 and increasing alveolar fluid reabsorption, cysteinyl leukotrienes may, in part, have a beneficial r
170 ccompanied by a surge in bronchoconstrictory cysteinyl leukotrienes produced at the expense of LTB4 i
171 polymorphism was associated with changes in cysteinyl leukotriene production, lung function, airway
173 s in s/s mice were associated with increased cysteinyl-leukotriene production in vivo and in AMs in v
174 have been described; the mechanisms by which cysteinyl leukotrienes promote the development of inflam
176 abolites of vasoactive molecules showed that cysteinyl leukotrienes, prostacyclin metabolites, and PG
179 oth murine and human fibrocytes express both cysteinyl leukotriene receptor (CysLT) 1 and CysLT2.
180 ndent increase in cell-surface expression of cysteinyl leukotriene receptor 1 (CysLT1) as determined
183 "proatopic" neutrophil subset that expressed cysteinyl leukotriene receptor 1 (CysLTR1) and produced
187 s and found a recurrent mutation in CYSLTR2 (cysteinyl leukotriene receptor 2) encoding a p.Leu129Gln
189 zed by some as a dualistic uracil nucleotide/cysteinyl leukotriene receptor and by others as inactive
190 stigated the effectiveness of montelukast, a cysteinyl leukotriene receptor antagonist, in the treatm
195 ing montelukast (an antagonist of the type 1 cysteinyl leukotriene receptor) also inhibited E. coli i
197 e cloning and characterization of the second cysteinyl leukotriene receptor, CysLT(2), a 346-amino ac
201 e inflammatory cells and their expression of cysteinyl leukotriene receptors 1 and 2 (CysLT(1) and Cy
202 antiangiogenic small molecule antagonist of cysteinyl leukotriene receptors 1 and 2 (CysLT1 and CysL
203 rectly target VEGF receptors but antagonizes cysteinyl leukotriene receptors 1 and 2 (CysLT1-2) at mi
207 made in three areas: genetic control of the cysteinyl leukotriene response, in which alterations in
208 exercise challenge, histamine, tryptase, and cysteinyl leukotrienes significantly increased and prost
210 1/2, cytosolic phospholipase A(2) alpha, and cysteinyl-leukotriene synthesis confers resistance to s/
211 bstance of anaphylaxis was composed of three cysteinyl leukotrienes that act in the inflammatory resp
212 (4)S) is responsible for the biosynthesis of cysteinyl leukotrienes that participate in allergic and
214 ut the contributions of mediators other than cysteinyl leukotrienes to aspirin reactions and to the t
216 diating the leukotriene responses in asthma, cysteinyl leukotriene type 1 receptor (CysLT1R), have no
217 inic and H1 histamine receptor and expressed cysteinyl leukotriene type 1 receptor in human embryonic
219 t cytoplasmic Ca(2+) oscillations induced by cysteinyl leukotriene type I receptor activation run dow
220 ations can be evoked by modest activation of cysteinyl leukotriene type I receptors by the physiologi
222 Here, we show that following stimulation of cysteinyl leukotriene type I receptors in rat basophilic
226 GE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways
227 sharp contrast, mean levels of prophlogistic cysteinyl leukotrienes were increased in samples from se
228 n and the accompanying in vivo generation of cysteinyl leukotrienes were markedly attenuated in group
229 FLAP), but lacked LTC4S and did not generate cysteinyl leukotrienes when stimulated with 20 mumol/L c
231 ablysin-15 was found to bind proinflammatory cysteinyl leukotrienes with submicromolar affinities.
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