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1  for ECP, tryptase, PGE2 , PGD2 , LTD4 , and LTE4 .
2 ed concentrations of urinary leukotriene E4 (LTE4).
3  of leukotriene D4 (LTD4) to leukotriene E4 (LTE4).
4 ia and the highest concentrations of urinary LTE4.
5 complexes with another receptor to recognize LTE4.
6 vel receptor that preferentially responds to LTE4.
7       Smokers with asthma had higher urinary LTE4 ; 83 (59, 130) vs 59 (40, 90) pg/mg creatinine, P =
8                                     PGD2 and LTE4 activate TH2 cells through different pathways but a
9 e, we demonstrate that LTC4, but not LTD4 or LTE4, activates mouse platelets exclusively through CysL
10  which is converted into LTD4 and finally to LTE4 after extracellular transport.
11                                     PGD2 and LTE4 altered the transcription of a wide range of genes
12                Following ASA administration, LTE4 and 9alpha,11beta-PGF2 levels were increased in bot
13           Interestingly, addition of IL-2 to LTE4 and epithelial cytokines significantly amplified IL
14 tory actions of the stable abundant mediator LTE4 and is a novel potential therapeutic target for ast
15  EpC function and suggest that inhibition of LTE4 and of GPR99 may have therapeutic benefits in asthm
16 s demonstrate that the conversion of LTD4 to LTE4 and the degradation of cys-bis-gly are catalyzed by
17 fer between the groups, but levels of LTD4 , LTE4 , and PGD2 were significantly higher in AERD group.
18 nes (cys-LTs; leukotriene [LT] C4, LTD4, and LTE4), and prostaglandin (PG) E2 are generated at the si
19 to comprehensively define the roles of PGD2, LTE4, and their combination in activating human TH2 cell
20                         The effects of PGD2, LTE4, and their combination on human TH2 cell gene expre
21 In animal models, these drugs inhibit LTD4-, LTE4-, and antigen-induced bronchoconstriction, reduce i
22 s (cysLTs), leukotriene C4 (LTC4), LTD4, and LTE4 are proinflammatory lipid mediators with pathobiolo
23    Leukotrienes (LTA4, LTB4, LTC4, LTD4, and LTE4) are inflammatory lipid mediators.
24 C4), leukotriene D4(LTD4) and leukotriene E4(LTE4)-are important mediators of human bronchial asthma.
25                         CysLTs, particularly LTE4, are important contributors to the triggering of hu
26 traenoic acid, and its metabolites, LTD4 and LTE4, are lipid mediators of smooth muscle constriction
27 s), including leukotriene (LT) C4, LTD4, and LTE4, are metabolites of arachidonic acid and mediate in
28 of LTC4 or LTD4 and an augmented response to LTE4 as compared with WT mice.
29                      These results show that LTE4 as well as other cysLTs do not activate intracellul
30  intracellular calcium signalling induced by LTE4 but did not restore full agonist responses at the g
31 ition between radiolabeled ADP and unlabeled LTE4 but not for direct binding of LTE4, suggesting that
32 ved in AERD (at 60 min for PGD2 , LTD4 , and LTE4 ) but not in MNSAID-UA or control subjects (P < 0.0
33 topy traits, blood eosinophilia, and urinary LTE4 concentrations were evaluated.
34 r leukotriene D4 (LTD4 ) and leukotriene E4 (LTE4 ) concentrations.
35                                              LTE4 enhanced the effect of PGD2, IL-25, IL-33, and TSLP
36 nd cysLTs (notably cysteinyl leukotriene E4 [LTE4]) enhances TH2 cytokine production.
37 or LTD4, revealing a preference of GPR99 for LTE4 even when CysLT1R is present.
38 d transmission using Bluetooth Low Energy 4 (LTE4) for wireless communication with cell phone.
39 ling elicited by Alternaria or by intranasal LTE4 GPR99 expression is detected on lung and nasal EpCs
40  similar lesser potency for CysLT2R, whereas LTE4 has little potency for either receptor.
41  both a functional and a binding response to LTE4 in these transfectants.
42            Following the challenge, LTD4 and LTE4 increased, while PGE2 and LTB4 decreased in AERD su
43                         CysLTs, particularly LTE4, induced migration, reduced apoptosis, and promoted
44            P2Y12 receptor expression permits LTE4-induced activation of extracellular signal-regulate
45                 These agents block LTD4- and LTE4-induced contractions of isolated guinea pig trachea
46  CysLT1 as a receptor responsible for potent LTE4-induced response in LAD2 but not in LUVA cells, an
47 ukotrienes (LTs; LTC4, LTD4, and LTE4), only LTE4 is stable and abundant in vivo.
48                                           As LTE4 is the predominant cys-LT species in inflamed tissu
49 ant alleles had significantly higher urinary LTE4 levels (38 vs. 30 nmol/mol creatinine, P = 0.0134),
50 ased cysLT exposure as determined by urinary LTE4 levels, reduced lung function and potentially worse
51 om control, exhaled nitric oxide and urinary LTE4 levels.
52  and its extracellular metabolites, LTD4 and LTE4, mediate airway inflammation.
53 he purinergic receptor P2Y12 is required for LTE4 mediated pulmonary inflammation in a mouse model of
54  purinergic (P2Y12) receptor is required for LTE4-mediated pulmonary inflammation.
55 ed kinase (Erk) activation, are required for LTE4-mediated regulation of gene expression in human cel
56 99(-/-) mice showed a dose-dependent loss of LTE4-mediated vascular permeability, but not to LTC4 or
57                               The effects of LTE4 on P2Y12 in the airway were abrogated by platelet d
58  nasal EpCs, which release mucin to doses of LTE4 one log lower than that required to elicit submucos
59 cysteinyl leukotrienes (LTs; LTC4, LTD4, and LTE4), only LTE4 is stable and abundant in vivo.
60         Combined inhibition of both PGD2 and LTE4 pathways might provide an effective therapeutic str
61 otriene (LT)E4 , induced sputum fluid LTB4 , LTE4 , PGD2 , and PGE2 , plasma secretory phospholipase
62 ificantly negatively correlated with urinary LTE4 (r = -0.192, P = 0.009).
63 ce retain partial ability to convert LTD4 to LTE4, ranging from 80-90% of the wild-type values in sma
64 tor or receptor heterodimers but no specific LTE4 responses were observed.
65                                           As LTE4 retains a cysteine residue and might provide recogn
66                                     Although LTE4 shows negligible activity at the type 1 and 2 recep
67 cting through P2Y12 and suggest that another LTE4 specific receptor has yet to be identified.
68 unlabeled LTE4 but not for direct binding of LTE4, suggesting that P2Y12 complexes with another recep
69 pplication of LTB4 with LTA4, LTC4, LTD4, or LTE4 suppressed LTB4-induced activation.
70 tified GPR99 as a high-affinity receptor for LTE4 that mediates cutaneous vascular permeability.
71                              Leukotriene E4 (LTE4) the most stable of the cysteinyl leukotrienes (cys
72                              Leukotriene E4 (LTE4), the most stable of the cysteinyl leukotrienes (cy
73                                              LTE4, the stable cysLT, is a weak agonist for the type 1
74                            Administration of LTE4 to the airways of sensitized mice potentiates eosin
75                                The effect of LTE4 was inhibited by montelukast, a CysLT1 antagonist.
76                         Blockade of PGD2 and LTE4 was tested by using TM30089, an antagonist of chemo
77 leukotrienes (leukotriene [LT] C4, LTD4, and LTE4) was measured in esophageal circular muscle tissue.
78   Significant increases in PGD2 , LTD4 , and LTE4 were observed in AERD (at 60 min for PGD2 , LTD4 ,
79 re selected that differentially responded to LTE4 when analysed by intracellular signalling and gene
80 s critically important for responsiveness to LTE4 within a human cell system.