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1 to have antipruritic activity by suppressing histamine release.
2 ication, which may account for their role in histamine release.
3 s used as a priming agent for human basophil histamine release.
4 TCTP, which corresponded to the magnitude of histamine release.
5 antihistamine blockade, and measured dermal histamine release.
6 nd basophil responses to BmAg as measured by histamine release.
7 E of greater than 500:1 to suppress basophil histamine release.
8 ion as measured by D. pteronyssinus-specific histamine release.
9 in Fc epsilon RI-induced Ca(2+) response and histamine release.
10 effect on CD63 and CD203c externalization or histamine release.
11 cortex synaptosomes for inhibition of [(3)H]histamine release.
12 had a significant effect on antigen-induced histamine release.
13 on by means of the suppression of endogenous histamine release.
14 iled to reconstitute Fc epsilon RI-initiated histamine release.
15 k for downstream signaling events leading to histamine release.
16 on basophils and a decrease in Ag-triggered histamine release.
17 ing did not enhance FcvarepsilonRI-dependent histamine release.
18 protein expression and FcepsilonRI-mediated histamine release.
19 es and downstream propagation of signals for histamine release.
20 while inhibiting LTC4 generation as well as histamine release.
21 Four treated patients had no symptoms of histamine release.
22 ise [Ca(2+)](i) in ECL cells, and stimulated histamine release.
23 TBC-1269, was associated with a reduction in histamine release.
24 lipase C-gamma and a dramatic enhancement of histamine release.
25 induced prolonged airway hyperreactivity and histamine release.
26 ion (IC50 = approximately 2 microM), but not histamine release.
27 with resting T cells resulted in significant histamine release.
28 on of PMA-induced, but not anti-IgE-induced, histamine release.
29 and mitogen-activated protein kinase, and no histamine release.
30 ed to determine whether they were capable of histamine release.
31 he only cytokine shown to induce substantial histamine release.
32 , an increase in intracellular free Ca2+ and histamine release.
33 trin-driven enterochromaffin-like (ECL) cell histamine release.
34 effects of zolpidem do not depend on reduced histamine release.
35 ases showed >/=10% allergen-specific maximum histamine release.
36 tion of TRPM7 in mast cell degranulation and histamine release.
37 e levels with ten persons showing negligible histamine release.
38 by temperature, mast cell degranulation and histamine release.
39 loss occurred despite the presence of little histamine release.
40 EC did not significantly reduce constitutive histamine release.
41 nd IgE-dependent human lung mast cell (HLMC) histamine release.
43 to significant degranulation as evidenced by histamine release (24.5 +/- 4.4%): and up-regulation of
44 Since MIP-1alpha has potent inflammatory and histamine-releasing activities, its production by basoph
46 ted the effects on mast cell binding and the histamine-releasing activity of l-alanine substitutions
48 overexpression of UCP2 in LAD2 cells reduced histamine release after both allergic and nonallergic tr
50 ne, and is associated with increased central histamine release and alterations in histamine H(3) rece
51 ed by their immunoglobulin E (IgE)-dependent histamine release and by their characteristic proliferat
52 cell that inhibits gastrin-induced ECL cell histamine release and Ca2+ entry by activation of a Gi o
55 Y and related peptides on gastrin-stimulated histamine release and calcium signaling was eliminated b
56 measurement of basophil CD63 expression and histamine release and casein-specific CD4(+) regulatory
57 blast-mast cell interaction for induction of histamine release and chemokine production and the speci
58 L-902,688, TCS251) agonists on IgE-dependent histamine release and cyclic-AMP generation in mast cell
60 ells were analyzed in short-term culture for histamine release and for changes in intracellular calci
61 tudy examined the possible role of increased histamine release and granulocyte activity in the vascul
62 tely 2 microM), with only a modest effect on histamine release and IL-4 production at higher concentr
63 actor (HrHRF) is known to directly stimulate histamine release and IL-4 secretion from basophils of s
65 lls, aggregation of Fc epsilon RI induced no histamine release and no detectable increase in total ce
67 ebrin(-/-) mice exhibit reduced IgE-mediated histamine release and passive systemic anaphylaxis, and
69 nduced by rHRF significantly correlated with histamine release and the amount of protein generated, a
72 tyrosine phosphorylation of Syk and minimal histamine release and weak phosphorylation of activation
73 skin induced by PAF are not associated with histamine release and, therefore, appear to be independe
74 ts are mediated predominantly by C5a-induced histamine release, and 3) that C3a does not contribute s
77 F-heparin and LMWH inhibited antigen-induced histamine release as measured in BALF by 81% and 75%, re
78 null mice have reduced allergen/IgE-induced histamine release, as well as early airway hyperresponsi
79 at comparing basophil activation test (BAT), histamine release assay (HR), and passive sensitization
80 elease assay (HR), and passive sensitization histamine release assay (passive HR) in the diagnosis of
81 25% of CU patients have a positive basophil histamine release assay and show autoreactivity (a posit
83 ld reduction in allergenicity when tested by histamine release assay with basophils of yellow jacket-
85 d FcepsilonRIalpha by basophil and mast cell histamine release assays and by basophil activation assa
86 umvent potential soluble inhibitors, such as histamine released at sites of inflammation, and allow t
89 stamine release, together caused significant histamine release but no apparent PKC translocation.
90 t from IL-3, which also primes basophils for histamine release, but does show phosphorylation of thes
93 lanin inhibited basal and gastrin-stimulated histamine release by approximately 60% with a median eff
94 f mast cell degranulation potently inhibited histamine release by mast cells and inhibited adipocyte
96 on of dura with estradiol slightly augmented histamine release by SP, an effect possibly mediated thr
97 Until recently, it was mainly attributed to histamine released by mast cells activated by allergen c
99 us and allergen-induced basophil reactivity (histamine release, CD63 expression, and IL-4 production)
100 la(17) (6), and Ala(21) (7) showed a loss of histamine release compared to the parent MCD peptide 1.
102 CM-specific IgE and IgG(4) levels, basophil histamine release, constitutive CD63 expression, CD203c
103 mechanism by which mast cell activation and histamine release contribute to skin barrier defects in
104 ng mast cell-fibroblast coculture, increased histamine release could be attenuated either by separati
105 oclonal antibody significantly inhibited net histamine release, cysLT production, and IL-4 generation
106 GE2 1) significantly inhibited IgE-mediated histamine release, cytokine production, and Ca(2+) mobil
109 findings suggest that the diurnal rhythm of histamine release entrains striatal function which, duri
110 ive correlation between histamine release to histamine releasing factor/translationally controlled tu
111 I, Ando et al. provide a causal link between histamine-releasing factor (HRF) interactions with IgE a
112 protein (TCTP) is a homolog of the mammalian histamine-releasing factor (HRF), which causes histamine
119 that HrHRF, in addition to functioning as a histamine-releasing factor, can differentially modulate
122 analogues showed a 5- to 6-fold decrease in histamine release for analogues 6, 7, and 4 and a 10-fol
123 is a calcium-binding protein that can cause histamine release from basophil/mast cells and induce eo
124 ombinant malarial TCTP, like HRF, stimulated histamine release from basophils and IL-8 secretion from
125 ckers were found to inhibit anti-IgE-induced histamine release from basophils in nonallergic subjects
127 ent inhibition of Fel d1-driven IgE-mediated histamine release from cat-allergic donors' basophils an
132 In vivo, gastric acid secretion and in vitro histamine release from enterochromaffin-like (ECL) cells
134 c rhinitis proceeded in two distinct stages: histamine release from FcepsilonRI-activated mast cells,
135 nt inhibition of antigen-driven IgE-mediated histamine release from fresh human basophils sensitized
136 5a-induced thromboxane (TXB2) generation and histamine release from HMC-1 cells and whole-blood basop
137 stamine-releasing factor (HRF), which causes histamine release from human basophils and IL-8 secretio
138 preparations was also tested in an assay of histamine release from human basophils in whole blood.
142 f peripheral blood eosinophils and to induce histamine release from IL-3-primed peripheral blood baso
143 study was to determine whether PYY inhibits histamine release from isolated enterochromaffin-like (E
144 in vitro method to analyze the properties of histamine release from LAD2 cells and characterize the s
145 loped a sensitive and rapid method to detect histamine release from LAD2 cells using liquid chromatog
146 f the gadolinium-based MRI contrast media on histamine release from mast cells and to compare the act
149 vated by PMA or immobilized anti-CD3 mAb, on histamine release from murine bone marrow-derived cultur
150 or histamine antagonism in vitro (Ki for [3H]histamine release from rat cerebral cortex synaptosomes)
152 part by inhibition of calcium signaling and histamine release from the ECL cells due to activation o
153 of the untreated BP patients were tested for histamine release from their basophils in response to NC
162 Constitutive and FcepsilonRI-dependent HLMC histamine release, HASMC contraction, and beta2-AR phosp
164 within three months prior to OFC to measure histamine release (HR) and specific IgE antibody titers.
165 in a paradoxical increase in their basophil histamine release (HR) response ex vivo to cross-linking
166 specific, and HDM-allergen-specific basophil histamine release (HR), plus helminth- and HDM-specific
167 g D1 and D2 and lipoxin A(4) attenuated HLMC histamine release in a dose-dependent fashion but were n
168 lone was able to drive substantial levels of histamine release in about a third of all preparations s
169 in biological fluids and inhibited cellular histamine release in an in vitro bioassay of IgE activit
170 ion of A(3) receptors could induce mast cell histamine release in association with increases in intra
171 and CNX-774) on IgE-dependent activation and histamine release in blood basophils obtained from aller
172 heparin [ULMWH]) on antigen-induced AHR and histamine release in bronchoalveolar lavage fluid (BALF)
174 whether galanin inhibits Ca2+ signaling and histamine release in enterochromaffin-like (ECL) cells.
175 onfirmed by demonstrating that IgE-dependent histamine release in ex vivo blood basophils is largely
177 riction in sheep, inhibits anti-IgE mediated histamine release in isolated mast cells, and prevents t
178 an essential role in Fc epsilon RI-mediated histamine release in mast cells by regulating the phosph
180 wed a >/=10% concentration-dependent maximum histamine release in response to the anti-human IgE stim
181 hibitor with an expected IC(50), and induced histamine release in strict proportion to release induce
184 occurrence of satiety onset while increasing histamine release in the CNS with an H3 receptor antagon
186 i in the scotopic range during the day, when histamine release in the retina is expected to be at its
187 lices to examine the effects of photo-evoked histamine release in the ventrolateral TMN and VLPO.
194 nstriction, allergic cutaneous reaction, and histamine release into bronchoalveolar lavage fluid (BAL
195 t changes in airway resistance and attenuate histamine release into the bronchoalveolar lavage, sugge
196 factor determining quantal size of 5-HT and histamine release, intragranular association with the he
197 nic responses in the surrounding tissue, and histamine release is known to promote rapid diapedesis o
199 analyzed by video imaging of [Ca(2+)](i) and histamine release; its effects on gastric glands were ex
200 it prostaglandin E2-stimulated secretion via histamine release, likely from mast cells, and actions o
201 multaneous phenotyping and quantification of histamine release might add to our knowledge about the b
202 nhibited neurons, resulting in excitation of histamine-releasing neurons in the TMN through disinhibi
203 degranulation of mast cells, accompanied by histamine release, occurs adjacent to short-term i.p. im
204 r mast cell proteases-1, -4, -5, and -6, and histamine release on ligation of surface IgE or stimulat
207 generation by phosphorylating cPLA2, but not histamine release or IL-4 production, in human basophils
208 o detectable effect on Fc epsilon RI-induced histamine release or on the phosphorylation of total cel
209 The lipopeptide had no effect on basophil histamine release or on the proliferation of B cells and
210 oduction by the primed hMCs occurred without histamine release or PGD(2) generation and was inhibited
215 the clinical significance of the spontaneous histamine release ratio (SHR/T) and low responders in th
218 io, cell-surface FcepsilonRI expression, and histamine release responses to anti-IgE antibody or pean
220 3)- and Panx1 HC-dependent MC dye uptake and histamine release, responses that were only Cx43 HC depe
221 ng/mL IL-3, the concentration-dependence of histamine release shifted to 100-fold lower concentratio
222 In inflammatory skin diseases with enhanced histamine release, such as psoriasis and atopic dermatit
224 ific IgE (Immunocap(R) ; Phadia AB, Sweden), histamine release test (HR) (RefLab ApS, Denmark), skin
225 ter of specific IgE antibody and/or basophil histamine release test against Glupearl 19S(R) revealed
226 ly identified a negative correlation between histamine release to histamine releasing factor/translat
227 alone caused no PKC translocation and little histamine release, together caused significant histamine
228 tion of TRPM7 on mast cell degranulation and histamine release using wild-type (TRPM7(+/+) ), TRPM7(+
229 ups, whereas CM-specific IgE and spontaneous histamine release values decreased in only the OIT group
231 pyridone 16 by dose-dependent inhibition of histamine release was demonstrated in a rodent pharmacod
234 combined with SCF, a synergistic increase in histamine release was induced in upper airway, but not b
239 activation, the marked shift in the EC50 for histamine release was not accompanied by similar shifts
240 On the other hand, concentration-dependent histamine release was not seen in the"NON"responders, su
246 ress the hypothesis that mycoplasma provokes histamine release, we exposed mice to Mycoplasma pulmoni
247 eactions are triggered by mast cell-mediated histamine release, we investigated the function of TRPM7
249 inhibitory activity for IgE-FAB and basophil histamine release were also significantly greater in all
250 Both constitutive and IgE-dependent HLMC histamine release were attenuated by BEAS-2B, primary AE
252 Allergen-induced basophil responsiveness and histamine release were inhibited in the presence of rfhS
254 Furthermore, those donors who have direct histamine release when exposed to HRF/TCTP (HRF/TCTP res
255 onists did not affect the PGE2 inhibition of histamine release, whereas EP2 -selective antagonists ca
256 BMMCs from Ucp2(-/-) mice exhibited greater histamine release, whereas overexpression of UCP2 in LAD
257 ) stimulation revealed strong suppression of histamine release, whereas removal of extracellular Mg(2
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