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1 were not mirrored by other eicosanoids (i.e. leukotriene B4).
2 sion molecule 1, P-selectin, L-selectin, and leukotriene B4.
3 ary membrane protein permeability, IL-8, and leukotriene B4.
4 IL-8, IL-6, tumor necrosis factor-alpha, and leukotriene B4.
5 tion during sepsis and increased circulating leukotriene B4.
6 ed [Ca2+]i, while it inhibited the action of leukotriene B4.
7 the amniotic cavity reveals up-regulation of leukotriene B4.
8 ntly reduced without affecting the levels of leukotriene B4.
9 idase without affecting the bioproduction of leukotriene B4.
10 llular signaling that leads to production of leukotriene B4.
12 cosatetraenoic acid, cysteinyl leukotrienes, leukotriene B4 , 11-dehydro-thromboxane B2 , and prostag
14 eductase (AO), an enzyme heretofore known as leukotriene B4 12-hydroxydehydrogenase, 15-oxoprostaglan
16 tors (LM) via metabololipidomics, CO reduced leukotriene B4 (21 +/- 11 versus 59 +/- 24 pg/mouse, 6 h
17 oid metabolites 5-oxo-eicosatetraenoic acid, leukotriene B4 5-hydroxyeicosatetraenoic acid (HETE), 12
18 aT, significantly inhibited the formation of leukotriene B4, a potent chemotactic agent synthesized b
20 that BLT2, a G protein-coupled receptor for leukotriene B4 and 12(S)-hydroxyheptadecatrienoic acid (
24 sor to the potent pro-inflammatory mediators leukotriene B4 and leukotriene C4 Studies with small mol
25 ntegrins, in concert with neutrophil-derived leukotriene B4 and other chemoattractants, promote local
26 spect to inflammatory lipid mediators (i.e., leukotriene B4 and PGs) in omental adipose tissue from O
27 ediators including prostaglandin F2alpha and leukotriene B4 and pro-resolving mediators, including re
28 ectious exudates gave higher proinflammatory leukotriene B4 and procoagulating thromboxane B2, as wel
29 e included inflammation initiating mediators leukotriene B4 and prostaglandin E2 and pro-resolving me
30 vels of the pro-inflammatory lipid mediators leukotriene B4 and prostaglandin E2 are elevated in the
31 l infiltration and prevented the increase in leukotriene B4 and prostaglandin E2 in response to ische
33 n expansion of inflammatory lipid mediators, Leukotriene B4 and Prostaglandin E2, and a concomitant d
35 ities of cell-associated AA mimicked that of leukotriene B4 and PtdCho/PtdIns, while the specific act
36 howing a decrease in BALF levels of IL-8 and leukotriene B4 and the associated reduction of BALF neut
37 onophore (A23187), and the concentrations of leukotrienes B4 and B5, thromboxane A2, prostaglandin E2
38 mbers correlated with the enhanced levels of leukotrienes B4 and C4 and prostaglandin E2 produced aft
39 pha; prostaglandins E1, D2, and F2 alpha and leukotrienes B4 and C4 were detected in lower amounts.
40 secrete the inflammatory eicosanoid products leukotrienes B4 and C4, the cytokines IL-6 and TNF, and
41 on between rs174537 and the ratio of ARA/LA, leukotriene B4, and 5-HETE but no effect on levels of cy
42 ils exposed to chemoattractants (IL-8, FMLP, leukotriene B4, and C5a) failed to show increases in int
44 ositol hexakisphosphate, lipopolysaccharide, leukotriene B4, and granulocyte-macrophage colony-stimul
45 h the chemoattractants N-formyl-Met-Leu-Phe, leukotriene B4, and interleukin-8 exhibits threshold beh
47 f synthesis of the potent chemotactic factor leukotriene B4, and that process was reversed by rottler
49 phonuclear leukocyte infiltration induced by leukotriene B4 (approximately 78% inhibition) or phorbol
51 To determine the opsonin dependence of the leukotriene B4 augmentation of phagocytosis, we assessed
54 -lipoxygenase-deficient mice, the absence of leukotriene B4 biosynthesis did not detectably alter m-B
55 oup V phospholipase A2 (hVPLA2) could elicit leukotriene B4 biosynthesis in human neutrophils through
56 nd of the thiazole series, by inhibiting the leukotriene B4 biosynthesis in the RPAR assay (3 h pretr
57 show that PGE2-G, but not PGE2-EA, inhibits leukotriene B4 biosynthesis, superoxide production, migr
59 B4/mg protein, p < .001) generation of ileal leukotriene B4, but did not alter the cyclooxygenase pro
60 N-formyl-methionyl-leucyl-phenylalanine and leukotriene B4, by approximately 65%, but had no effect
61 ctive on the same responses when elicited by leukotriene B4, C5a, FMLP, platelet-activating factor, I
65 plication of this method to the synthesis of leukotriene B4 demonstrates its utility and extraordinar
66 s, i.e. platelet activating factor (PAF) and leukotriene B4, did not inhibit the responses of peptide
69 the release of high mobility group box 1 and leukotriene B4 from the epithelial cells and this releas
70 ociated with significant reductions in ileal leukotriene B4 generation and neutrophilic infiltrate.
71 Two major G-protein-coupled receptors for leukotriene B4 have been identified: the high-affinity r
72 oncentration in exhaled breath condensate of leukotriene B4, hydrogen peroxide and hydrogen ions rose
73 .05), but there was no significant change in leukotriene B4, hydrogen peroxide, or hydrogen ion conce
75 ive prostaglandin E2 (iPGE2), immunoreactive leukotriene B4 (iLTB4), and pain after periodontal surge
76 d in decreased levels of prostaglandin E2 or leukotriene B4 in intestinal polyps or apparently normal
77 ic acid, 5-hydroxyeicosatetraenoic acid, and leukotriene B4 in particular could serve as potential bi
78 clusion, we have identified a novel role for leukotriene B4 in the augmentation of neutrophil phagocy
81 study, we explored the effect of the C5 and leukotriene B4 inhibitor Ornithodoros moubata complement
82 dimethyl fumarate, phosphodiesterase 4, and leukotriene B4 inhibitors in pemphigoid disorders, and c
83 -Leu-Phe (fMLP), platelet-activating factor, leukotriene B4, interleukin-8, or the chemokine RANTES e
87 ly increase bronchoalveolar lavage levels of leukotriene B4, leukotriene C4/D4, and thromboxane B2 ab
88 ronchoalveolar lavage fluid was analyzed for leukotriene B4, leukotriene C4/D4, thromboxane B2, prost
91 e (fMLP)), platelet activating factor (PAF), leukotriene B4 (LTB(4)), C5a anaphylotoxin (C5a), and in
92 -) eosinophils and neutrophils had decreased leukotriene B4 (LTB(4))-dependent chemotactic responses
93 ly hypertensive rat (SHR) support a role for leukotriene B4 (LTB4 ), a potent chemoattractant involve
94 ly hypertensive rat (SHR) support a role for leukotriene B4 (LTB4 ), a potent chemoattractant involve
95 lbumin (65.6 versus 53.0 micrograms/ml), and leukotriene B4 (LTB4) (243 versus 0 pg/ml) in BAL fluid
98 ease in the abundance of the proinflammatory leukotriene B4 (LTB4) and a corresponding decrease in th
99 r the conversion of leukotriene A4 (LTA4) to leukotriene B4 (LTB4) and also possesses an aminopeptida
103 on and secretion of interleukin 8 (IL-8) and leukotriene B4 (LTB4) and was prevented by mitochondrial
104 ediators such as prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) are implicated in the development
105 mediated) biosynthesis of the lipid mediator leukotriene B4 (LTB4) are pivotal components of host def
106 Important roles for tyrosine kinase Syk and leukotriene B4 (LTB4) are recognized in FcgammaR-mediate
108 x was largely dependent on the generation of leukotriene B4 (LTB4) by neutrophils and their expressio
112 23 activates the synthesis and production of leukotriene B4 (LTB4) in myeloid cells, which modulate i
113 ion has demonstrated the mechanistic role of leukotriene B4 (LTB4) in the molecular pathogenesis of l
120 of airway hyperresponsiveness (AHR) and that leukotriene B4 (LTB4) is involved in the chemotaxis of e
124 ith palmitate, enhanced arginase 1 and lower leukotriene B4 (LTB4) levels were detected in macrophage
125 udy was designed to test the hypothesis that leukotriene B4 (LTB4) may have a role in graft rejection
127 (approximately 80% reduction) in response to leukotriene B4 (LTB4) plus prostaglandin E2 (PGE2) as we
128 5-lipoxygenase (5-LO) activity and increased leukotriene B4 (LTB4) production have been implicated in
129 rease exudate volume, cell infiltration, and leukotriene B4 (LTB4) production in response to zymosan
132 ctivity study based around the high-affinity leukotriene B4 (LTB4) receptor antagonist SB 201146 (1)
135 rrow-derived DCs (BM-DCs) express functional leukotriene B4 (LTB4) receptors as observed in dose-depe
137 e lymphotoxin-stimulated neovasculature with leukotriene B4 (LTB4) resulted in stable cell adhesion f
138 Mucosal synthesis of the chemoattractant leukotriene B4 (LTB4) significantly increased after I-R
142 e demonstrate that the lipid chemoattractant leukotriene B4 (LTB4) was efficacious at causing loss of
146 )-mediated C5 activation and also sequesters leukotriene B4 (LTB4) within an internal binding pocket.
147 g by autocoids with opposing actions on PMN: leukotriene B4 (LTB4), a potent chemoattractant, and lip
152 B4(LXB4) blocked PMN migration stimulated by leukotriene B4 (LTB4), a well established agonist for PM
153 glandin E2 (PGE2) and 5-LO-derived products, leukotriene B4 (LTB4), and the biosynthesis interaction
154 s known that 5-lipoxygenase and its product, leukotriene B4 (LTB4), are highly expressed in several h
155 ), and the ratio of SPMs to pro-inflammatory leukotriene B4 (LTB4), are significantly decreased in th
156 on of leukotrienes, and more specifically on leukotriene B4 (LTB4), for disease induction as well as
157 ), LXA4, and its counterregulatory compound, leukotriene B4 (LTB4), in patients with childhood asthma
158 (TxB2), prostaglandin 6-keto-F1alpha (PGI), leukotriene B4 (LTB4), leukotriene C4D4E4 (LTC4D4E4), in
160 than C5a, platelet-activating factor (PAF), leukotriene B4 (LTB4), or FMLP in stimulating Eo chemota
161 onditions and after administration of either leukotriene B4 (LTB4), platelet-activating factor (PAF),
162 15-epi-lipoxin A4 (15-epi-LXA4), lipoxin A4, leukotriene B4 (LTB4), prostaglandin E2 (PGE2), and inte
163 X favors the biosynthesis of proinflammatory leukotriene B4 (LTB4), whereas, in theory, cytoplasmic 5
164 ion of inflammatory mediators, TNF-alpha and leukotriene B4 (LTB4), which are involved in parasite ki
165 eukotoxin (LKT) stimulates the production of leukotriene B4 (LTB4), which is believed to be an import
178 s, synthetic N-acetyl-PGP, positive control (leukotriene B4 [LTB4]), or negative control (Hanks' bala
179 ided exogenously) inhibited the formation of leukotriene B4, (LTB4) and 20-hydroxy-leukotriene B4 (20
181 ulated (16.0 +/- 4.9 vs. 80.0 +/- 15.5 pg of leukotriene B4/mg protein, p < .001) generation of ileal
182 th basal (8.0 +/- 1.9 vs. 33.0 +/- 8.1 pg of leukotriene B4/mg protein, p < .05) and ionophore-stimul
187 after stimulation of either neutrophils (by leukotriene B4) or coronary endothelium (by thrombin) in
191 duced 5-[3H]oxoETE binding, whereas 15-HETE, leukotriene B4, platelet-activating factor, IL-8, C5a, a
192 s may involve local intestinal inhibition of leukotriene B4 production and subsequent neutrophilic in
193 of neutrophilic infiltrate, an inhibition of leukotriene B4 production, and a facilitation of mucosal
194 cant decrease in IgE-mediated degranulation, leukotriene B4 production, cytokine secretion, and survi
199 B4) activates the G-protein-coupled receptor leukotriene B4 receptor 1 (BLT1) to mediate a diverse ar
200 that signals via its cell surface receptor, leukotriene B4 receptor 1 (BLT1), to attract and activat
203 nstrate a unique, non-redundant role for the leukotriene B4 receptor BLT1 in mediating neutrophil rec
204 strategy was applied to a typical GPCR, the leukotriene B4 receptor BLT2, reconstituted in a lipid b
205 erved in human neutrophils pretreated with a leukotriene B4 receptor but not a cysteinyl-leukotriene
206 this study, we investigated the roles of the leukotriene B4 receptor, BLT1, and CXCR3, the receptor f
207 splicing were further investigated with the leukotriene B4 receptor, known for its aberrant responsi
208 e lung tumour burden and genetic deletion of leukotriene B4 receptor-1 (BLT1(-/-)) attenuates this in
211 mmunohistochemical analysis showed that both leukotriene B4 receptors were expressed in peripheral se
213 osatetraenoic acid produced by platelets and leukotriene B4 released from calcium ionophore-activated
215 of this defect, as it leads to activation of leukotriene B4 signaling and induction of the alpha4beta
216 covers a previously undefined role of innate leukotriene B4 signaling as a gatekeeper of the hematopo
218 hors show that changing miRNA biogenesis and leukotriene B4 signaling in mice modulates this switch i
221 cosanoids--e.g., 12(R)-HETE, 12(S)-HETE, and leukotriene B4--stimulated the activation of NF-kappaB r
222 LF levels of total protein, neutrophils, and leukotriene B4 tended to decrease in EPA+GLA patients ov
223 L)-8, IL-6, tumor necrosis factor-alpha, and leukotriene B4 that are responsible, in part, for pulmon
224 ammatory arachidonic acid-derived mediators, leukotriene B4, thromboxane B2, and prostaglandin E2 fro
225 ctions in the generation of pro-inflammatory leukotriene B4, thus LTA4H exhibits opposing pro- and an
226 olites of the 5-lipoxygenase pathway such as leukotriene B4 to activate the peroxisome proliferator-a
227 of phagocytosis, we assessed the ability of leukotriene B4 to modulate neutrophil phagocytosis and t
228 ediated phagocytosis, increased adherence to leukotriene B4-treated neutrophils was limited to comple
229 ic acid, 5-hydroxyeicosatetraenoic acid, and leukotriene B4), TRPV4 (5,6-epoxyeicosatrienoic acid [EE
230 spectively) but generated greater amounts of leukotriene B4 upon maximal stimulation (26.6 versus 7.6
231 enylalanine, platelet activating factor, and leukotriene B4 was phosphoinositide-3 kinase-dependent,
232 potent neutrophil activator/chemoattractant leukotriene B4 were measured by mass spectrometry in ski
233 The eicosanoid mediators, thromboxane and leukotriene B4, were also highest in the severe asthma g
234 ntrations of leukotrienes C4, D4, and E4 and leukotriene B4, whereas prostacyclin infusion suppressed
235 elay among neutrophils mediated by the lipid leukotriene B4, which acutely amplifies local cell death
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