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1 rts leukotriene C4 (LTC4) to leukotriene D4 (LTD4).
2 e MBD-3 cleaves cystinyl-bis-glycine but not LTD4.
3  ring segments were unresponsive to LTC4 and LTD4.
4 al coronary arteries in response to LTC4 and LTD4.
5 mes greater than that of the natural ligand, LTD4.
6 fect signaling by methacholine, thrombin, or LTD4.
7              Finally, compared with control, LTD4 (1 x 10(-11) M) increased alveolar fluid clearance
8                                              LTD4 (1 x 10(-7) M) increased Na,K-ATPase activity at 1
9                  Intracellular dialysis with LTD4 (1.5 microM) elevated intracellular Ca2+ from 143+/
10                                              LTD4 (10-1000 nM) enhanced proliferation of human MCs in
11                 In conclusion, intracellular LTD4 activates a chloride conductance in hepatocytes iso
12 s, leukotriene C4 (LTC4) and leukotriene D4 (LTD4) also provoked PMN-endothelial cell adhesion, but v
13 -lipoxygenase products in this regard, since LTD4 and 5-hydroxyeicosatetraenoic acid (HETE) were unab
14 lar leak to intradermal injection of LTC4 or LTD4 and an augmented response to LTE4 as compared with
15 ized the effects of exogenously administered LTD4 and cysLTs released endogenously in response to phy
16 triene (cysLT) LTC4, which is converted into LTD4 and finally to LTE4 after extracellular transport.
17 n (calcium mobilization) of this receptor by LTD4 and LTC4, and competition for radiolabelled LTD4 bi
18                     Following the challenge, LTD4 and LTE4 increased, while PGE2 and LTB4 decreased i
19  eicosatetraenoic acid, and its metabolites, LTD4 and LTE4, are lipid mediators of smooth muscle cons
20 C4 (LTC4) and its extracellular metabolites, LTD4 and LTE4, mediate airway inflammation.
21 lia correlated with a higher leukotriene D4 (LTD4 ) and leukotriene E4 (LTE4 ) concentrations.
22  were observed in AERD (at 60 min for PGD2 , LTD4 , and LTE4 ) but not in MNSAID-UA or control subjec
23 re analyzed for ECP, tryptase, PGE2 , PGD2 , LTD4 , and LTE4 .
24              Significant increases in PGD2 , LTD4 , and LTE4 were observed in AERD (at 60 min for PGD
25 9), which is known to cleave leukotriene D4 (LTD4) and cystinyl-bis-glycine.
26 trienes-leukotriene C4(LTC4), leukotriene D4(LTD4) and leukotriene E4(LTE4)-are important mediators o
27 of leukotriene C4 (LTC4) and leukotriene D4 (LTD4) and their binding activity in both atherosclerotic
28 eukotrienes (cysLTs), leukotriene C4 (LTC4), LTD4, and LTE4 are proinflammatory lipid mediators with
29              Leukotrienes (LTA4, LTB4, LTC4, LTD4, and LTE4) are inflammatory lipid mediators.
30 of peptidoleukotrienes (leukotriene [LT] C4, LTD4, and LTE4) was measured in esophageal circular musc
31  leukotrienes (cys-LTs; leukotriene [LT] C4, LTD4, and LTE4), and prostaglandin (PG) E2 are generated
32 ising the cysteinyl leukotrienes (LTs; LTC4, LTD4, and LTE4), only LTE4 is stable and abundant in viv
33 nes (cysLTs), including leukotriene (LT) C4, LTD4, and LTE4, are metabolites of arachidonic acid and
34 ed PI production and calcium mobilization by LTD4, and significantly attenuated the effects of PKC in
35                           These agents block LTD4- and LTE4-induced contractions of isolated guinea p
36 inhibitor nordihydro-guaiaretic acid and the LTD4 antagonist ICI 198,615 inhibited ACh-induced contra
37 the drug-glutathione S-conjugate DNP-SG, the LTD4 antagonist MK571 and arsenate were also competitive
38 l-glutathione, oxidized glutathione, and the LTD4 antagonist MK571 were competitive inhibitors of dau
39  conjugate APA-SG, oxidized glutathione, the LTD4 antagonist MK571, arsenate, and genistein were comp
40 enyl)glutathione (DNP-SG), arsenate, and the LTD4 antagonist MK571.
41                   Specific [3H]-LTC4 but not LTD4 binding to atherosclerotic coronary artery was evid
42  and LTC4, and competition for radiolabelled LTD4 binding to this receptor by the cysteinyl leukotrie
43                MBD-2 cleaves leukotriene D4 (LTD4) but not cystinyl-bis-glycine, while MBD-3 cleaves
44                               Interestingly, LTD4, but not IL-33, induced high levels of IL-4 by ILC2
45 ted at selected times from 4 h to 4 wk after LTD4 challenge.
46                            Secreted PLA2 and LTD4 contracted normal ESO more than esophagitis ESO.
47 TD4 raises the possibility that clearance of LTD4 during asthma and in related inflammatory condition
48                  These results indicate that LTD4 elicits airway eosinophil influx in guinea pigs whi
49                                Both LTC4 and LTD4 enhanced endothelial adhesiveness for PMN, in part,
50      Our data demonstrate that both LTB4 and LTD4 facilitate eosinophil migration from lamina propria
51 e exposed to aerosols of 0.3 to 30 microg/ml LTD4 for 1 min, during which specific airway conductance
52      In vitro, these agents compete with [3H]LTD4 for binding to cysLT, receptors present on guinea p
53 pe 1 cys-LT receptor (CysLT1R), and LTC4 and LTD4 have similar lesser potency for CysLT2R, whereas LT
54                        In contrast, LTC4 and LTD4 induced concentration-dependent contractions in ath
55                   In IL-4-primed LAD2 cells, LTD4 induced the generation of MIP-1beta, a response blo
56 istologic characteristics of leukotriene D4 (LTD4)-induced eosinophil influx into the airways of cons
57  first evidence that IL-5 may have a role in LTD4-induced airways inflammation.
58                                              LTD4-induced alpha1 Na,K-ATPase membrane translocation w
59                      Zafirlukast antagonized LTD4-induced bronchoconstriction, with effects still evi
60 mma (1,000 U/ml for 24 h) markedly increased LTD4-induced changes in cell stiffness, from 4.6 +/- 1 [
61 neally), produced dose-related inhibition of LTD4-induced eosinophilia, measured in 24 h or 3 wk BAL,
62 t, a CysLT1 antagonist, completely inhibited LTD4-induced increases in cell stiffness.
63                                              LTD4-induced phosphorylation of ERK required transactiva
64 swell chamber experiments and also augmented LTD4-induced production of monocyte chemotactic protein
65                                              LTD4 is the most potent ligand for the type 1 cys-LT rec
66 1 +/- 0.2 nM) and by 6-trans-12-epi-LTB4 and LTD4 (Ki > 1 microM).
67 not differ between the groups, but levels of LTD4 , LTE4 , and PGD2 were significantly higher in AERD
68        In animal models, these drugs inhibit LTD4-, LTE4-, and antigen-induced bronchoconstriction, r
69 eviously reported proinflammatory effects of LTD4 may contribute significantly to its overall influen
70                   Surprisingly, both UDP and LTD4-mediated ERK activation and cytoprotection were abs
71 ed rats, this concentration of intracellular LTD4 neither raised intracellular Ca2+ nor activated the
72                     Neither IL-8, FMLP, C5a, LTD4, nor platelet-activating factor act topically to pr
73  we determined the effect of leukotriene D4 (LTD4) on the function of Na,K-ATPase in alveolar epithel
74 s article, we demonstrate that LTC4, but not LTD4 or LTE4, activates mouse platelets exclusively thro
75      Co-application of LTB4 with LTA4, LTC4, LTD4, or LTE4 suppressed LTB4-induced activation.
76           We sought to determine the role of LTD4-PGE2 crosstalk in inducing vascular inflammation in
77                 Our results unravel a unique LTD4-PGE2 interaction affecting mast cells through CysLT
78                                              LTD4 plus PGE2 potentiated vascular permeability and ede
79                                 Furthermore, LTD4 plus PGE2, through cysteinyl leukotriene receptor 1
80                                              LTD4 plus PGE2-potentiated effects are partially sensiti
81                                              LTD4 produced maximal decreases in sGaw (70 to 90% reduc
82  with granulocytes before it is converted to LTD4, promoting mediator generation and the formation of
83 ation of a second enzyme capable of cleaving LTD4 raises the possibility that clearance of LTD4 durin
84                        Pretreatment with the LTD4 receptor antagonist, pranlukast (ONO-1078, SB 20531
85 uaiaretic acid, the specific leukotriene D4 (LTD4) receptor antagonist MK-571, and the 5-lipoxygenase
86 e results were obtained with zafirlukast, an LTD4-receptor antagonist.
87                                          The LTD4 response could be induced in normal hepatocytes by
88  these data suggest that IFN-gamma increases LTD4 responses in HASM cells by increasing cell-surface
89 ed vascular permeability, but not to LTC4 or LTD4, revealing a preference of GPR99 for LTE4 even when
90 d with both [3H]LXA4 and [3H]leukotriene D4 (LTD4)-specific binding in vitro to neutrophils and endot
91 or human monocytes, PKC inhibition augmented LTD4-stimulated calcium flux and cell migration assessed
92 ion of endogenous CysLT1Rs augments multiple LTD4-stimulated cellular functions, with associated incr
93 ontraction ex vivo, PKC inhibition augmented LTD4-stimulated contraction, and increased phosphoinosit
94                           Rapid and profound LTD4-stimulated internalization was observed for the wil
95 ervations demonstrate that the conversion of LTD4 to LTE4 and the degradation of cys-bis-gly are cata
96 utant mice retain partial ability to convert LTD4 to LTE4, ranging from 80-90% of the wild-type value
97 nsible for the conversion of leukotriene D4 (LTD4) to leukotriene E4 (LTE4).
98 ression in HASM, cell stiffness responses to LTD4 were measured with magnetic twisting cytometry.
99 ction and calcium mobilization stimulated by LTD4 yet had almost no effect on H1 histamine receptor i

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