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1 eir endogenous ligand prostaglandin F2alpha (PGF2alpha).
2 classes of isomers of prostaglandin F2alpha (PGF2alpha).
3 produced, 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha).
4 -8-iso-PGF2alpha, and prostaglandin-F2alpha (PGF2alpha).
5 pid mediators such as prostaglandin F2alpha (PGF2alpha).
6 ct's baseline urinary concentration of 8-iso-PGF2alpha.
7 iated cell rounding following treatment with PGF2alpha.
8 9220 on the intraocular pressure response to PGF2alpha.
9 contained F-type prostane rings analogous to PGF2alpha.
10 n synthesis and bFGF-2 expression induced by PGF2alpha.
11 effect on the ocular hypotensive response to PGF2alpha.
12 nsignificant effect on the pupil response to PGF2alpha.
13 s mediate hypertrophic growth in response to PGF2alpha.
14 , in addition to the cyclooxygenase product, PGF2alpha.
15 tion, PGHS-2, and the production of PGE2 and PGF2alpha.
16 GF2alpha, in addition to its cognate ligand, PGF2alpha.
17 the plaque were markedly positive for 8-epi PGF2alpha.
18 ng infusion of 500 microg of unlabeled 8-iso-PGF2alpha.
19 tural specificity versus 8-epi PGF3alpha and PGF2alpha.
20 so-PGF2alpha, 2,3-dinor-8-iso-PGF2alpha, and PGF2alpha.
21 apamycin, implicating mTOR in the actions of PGF2alpha.
22 he expression of which is also stimulated by PGF2alpha.
23 quartile of baseline concentrations of 8-iso-PGF2alpha.
25 in monolayer cultures and were treated with PGF2alpha, 11-deoxy-PGE1, or PhXA85 (the nonesterified a
29 d 8-isoprostane-prostaglandin-F2alpha (8-iso-PGF2alpha), 2,3-dinor-5,6-dihydro-8-iso-PGF2alpha, 2,3-d
31 -iso-PGF2alpha), 2,3-dinor-5,6-dihydro-8-iso-PGF2alpha, 2,3-dinor-8-iso-PGF2alpha, and prostaglandin-
32 ma concentrations of F(2)-isoprostane (8-iso-PGF2alpha), 9-hydroxyoctadecadieneoic acid (9-HODE), and
36 the isoprostane 8-iso-prostaglandin F (8-iso-PGF2alpha), among other ligands examined, to activate G1
40 Consistent with these observations, only PGF2alpha and 12-iso-PGF2alpha caused rapid homologous d
41 ntraocular pressure, indicating that in cats PGF2alpha and 17-phenyl trinor PGE2 act on the same rece
43 ent administration of 12.5 microg of each of PGF2alpha and 17-phenyl trinor PGE2 did not produce an a
49 sted, including 8-iso-prostaglandin F (8-iso-PGF2alpha and a purported antagonist (pinane thromboxane
50 se relationship exists between the levels of PGF2alpha and a steroid-inducible anti-inflammatory prot
53 , induced mkp1 mRNA to a greater extent than PGF2alpha and fluprostenol, which activate PKC signaling
54 atosus had higher urinary excretion of 8-epi-PGF2alpha and IPF2alpha -I than controls; urinary excret
55 urinary excretion of two isoprostanes, 8-epi-PGF2alpha and IPF2alpha -I, free radical catalyzed oxida
57 (r=.68, P<.0001; n=33) between urinary 8-epi-PGF2alpha and IPF2alpha-I levels in patients receiving t
60 er and a strong association of urinary 8-iso-PGF2alpha and of serum soluble NOX2-derived peptide with
61 her (p < 0.001) mean values of urinary 8-iso-PGF2alpha and of serum soluble NOX2-derived peptide, ala
63 triggers the synthesis of the prostaglandins PGF2alpha and PGE2, but not PGD2, in rat cerebral cortic
68 ar sex differences in PVAT function in which PGF2alpha and TXA2 antagonists can inhibit the PVAT-indu
69 n (NPV) stimulated by prostaglandin F2alpha (PGF2alpha ) and by the drug LY83583, which causes contra
71 se using progesterone, prostaglandin F2alpha(PGF2alpha) and pregnant mare serum gonadotrophin (PMSG).
73 sed the ability of 8-isoPGF2alpha, 5iPF2 VI, PGF2alpha, and a mixture containing these PGs in a 0.5/0
74 d decreased myometrial NF-kappaB activation, PGF2alpha, and expression of contraction-associated gene
77 ertrophic agonists in culture, endothelin-1, PGF2alpha, and phorbol 12-myristate 13-acetate, also ind
80 because unreactive lipids, e.g. PGB1, PGE2, PGF2alpha, and TxB2, did not inhibit LKB1 activity (p >
82 ontraction in arteries from females, whereas PGF2alpha appears to mediate the contraction in arteries
85 the cyclooxygenase products thromboxane and PGF2alpha are released from coronary artery PVAT from pi
86 a (TNFalpha) and prostaglandin (PG) F2alpha (PGF2alpha) are involved in the control of ovulation but
87 intraocular pressure and pupil responses to PGF2alpha, are mediated by EP1 and FP receptors, respect
88 present study shows the potential for 8-iso-PGF2alpha as a wastewater biomarker for the assessment o
89 c-fos and identify the diffusable messenger PGF2alpha as obligatory for NMDA receptor-mediated trans
90 cosanoids analyzed, tetranor-PGEM and 11beta-PGF2alpha as well as 11-dehydro-TXB2 showed a significan
91 , urinary 8-iso prostaglandin F2alpha (8-iso PGF2alpha) as a marker of oxidative stress, and gastric
92 We demonstrate that prostaglandin F2alpha (PGF2alpha) as well as two analogues augment muscle cell
93 identified as 8-isoPGF2alpha, 5iPF2 VI, and PGF2alpha based on their retention times and MS/MS spect
94 roxylamine (HA, 100 mum), altered the NPV to PGF2alpha (BCA increased, HA inhibited) and/or LY83583 (
100 ro-15-F2t-IsoP (2,3-dinor-5, 6-dihydro-8-iso-PGF2alpha), by gas chromotography/negative ion chemical
103 hese observations, only PGF2alpha and 12-iso-PGF2alpha caused rapid homologous desensitization of FP
108 indings are consistent with a model in which PGF2alpha communicates fertility status via Ptgfr to cir
109 as associated with a 4.50% decrease in 8-iso-PGF2alpha concentrations (95% CI: -6.32%, -2.65%) and a
111 endent relaxations in prostaglandin F2alpha (PGF2alpha)-contracted strips of porcine coronary artery.
114 c ring contraction experiments revealed that PGF2alpha-dependent activation of FP potentiated angiote
117 e blockade by thromboxane antagonists, 8-epi PGF2alpha does not activate either of the thromboxane re
119 ne chip technology, we first identified that PGF2alpha dramatically up-regulated Cyr61 and CTGF mRNA
120 PGF2alpha-G and PGD2-EA, but not PGE2-EA or PGF2alpha-EA, also increased the frequency of mIPSCs.
121 alpha was less potent (EC50 = 5 microM) than PGF2alpha (EC50 = 10 nM) in generating inositol phosphat
122 on, human monocytes may form bioactive 8-epi-PGF2alpha either via free radical- or enzyme-catalyzed p
124 This increased myotube size is not due to PGF2alpha-enhancing cell fusion that initially forms myo
128 type I (AT1R) and the prostaglandin F2alpha (PGF2alpha) F prostanoid (FP) receptors are both potent r
129 ther cycloxygenase products, PGE2, PGD2, and PGF2alpha, failed to activate p38 kinase in aspirin-trea
131 GE2 has much lower efficacy as compared with PGF2alpha for the activation of Tcf/beta-catenin signali
133 ane B2 (TXB2 ) were quantified by ELISA, and PGF2alpha (FP) and thromboxane A2 (TP) receptor expressi
134 the four Gq/Gi-coupled receptors [EP1, EP3, PGF2alpha (FP), thromboxane A2 (TP)] suggests that prost
136 in the following order of activity: PGE2-G > PGF2alpha-G > PGD2-G; LYPLA2 hydrolyzed 1- but not 2-ara
140 taglandin profile: TxB2>6-keto PGF1alpha and PGF2alpha>PGE2, despite the comparable release of total
145 COX) enzyme product, prostaglandin F2alpha (PGF2alpha), has exhibited promise as an index of oxidant
146 Elevated serum and urine levels of 8-iso-PGF2alpha have been reported in a variety of diseases, m
148 poral trends observed in the levels of 8-iso-PGF2alpha, however, spatial differences were found at th
150 oportion of the ocular hypotensive action of PGF2alpha in cats is mediated by EP1 but not by FP recep
151 of inositol phosphates to the same extent as PGF2alpha in cells expressing either the FPA or FPB isof
152 y isoprostanes may complement the actions of PGF2alpha in clinical syndromes where oxidant stress and
153 we investigated the potential role of 8-iso-PGF2alpha in inflammation, focusing on its effects on ad
155 he estimated per capita daily loads of 8-iso-PGF2alpha in the 11 cities ranged between 2.5 and 9.9 mg
156 novel functions for parasite-derived LBs and PGF2alpha in the cellular metabolism of Leishmania and i
158 om female animals and greater sensitivity to PGF2alpha in the porcine coronary artery from males.
160 o be activated by the F2 isoprostane, 12-iso-PGF2alpha, in addition to its cognate ligand, PGF2alpha.
161 ree radical-catalyzed F2 isoprostane, 12-iso-PGF2alpha, in addition to the cyclooxygenase product, PG
164 and the mechanisms of prostaglandin F2alpha (PGF2alpha)-induced protein synthesis in vascular smooth
165 ependent mechanisms appear to be involved in PGF2alpha-induced activation of ERK2; 2) PGF2alpha-induc
166 in PGF2alpha-induced activation of ERK2; 2) PGF2alpha-induced eIF4E and 4E-BP1 phosphorylation appea
167 ty by PD 098059 led to a significant loss of PGF2alpha-induced eIF4E and 4E-BP1 phosphorylation, glob
168 nhibitor of p70(S6k), also failed to prevent PGF2alpha-induced global protein synthesis and bFGF-2 ex
169 ependent p70(S6k) activation correlates with PGF2alpha-induced global protein synthesis and bFGF-2 ex
170 lpha, and the isoform NFATC2 is required for PGF2alpha-induced muscle cell growth and nuclear accreti
171 minant-interfering proteins demonstrate that PGF2alpha-induced myocyte hypertrophy occurs independent
173 mplicated p38 and JNK, but not ERK, in 8-iso-PGF2alpha-induced suppression of monocyte adhesion.
175 (CM) transfer experiments suggest that 8-iso-PGF2alpha induces a secondary mediator, which also suppr
177 al hydrophobic cavity, thereby preventing FP-PGF2alpha interaction and suppressing the production of
178 n by binding and most likely by sequestering PGF2alpha into its central hydrophobic cavity, thereby p
181 pha-I, (IPF2alpha-I) a class I isomer (8-iso-PGF2alpha is class IV), using gas chromatography/mass sp
182 n of intraocular pressure in cats induced by PGF2alpha is mediated by FP or other prostaglandin recep
183 receptor by systemic concentrations of 8-epi PGF2alpha is unlikely to occur, even in syndromes of exc
188 There was a slight increase in urinary 8-epi-PGF2alpha levels (64.7+/-9.5 versus 84.9+/-10.6; P=.02)
191 rogesterone (DHP) and prostaglandin F2alpha (PGF2alpha) levels rise in teleost fish around the time o
192 Cell 16 (CC16) and 15-isoprostane F2t (8-iso-PGF2alpha) levels were used to assess lung injury and ov
193 urition initiation via COX1 and COX2 derived PGF2alpha leveraging epithelial specific Shp2 knockout m
197 r second-trimester levels of 2,3-dinor-8-iso-PGF2alpha (mean change per quartile increase = 0.25, 95%
200 boxane A2 (TXA2 ) and prostaglandin F2alpha (PGF2alpha ), on skin microcirculatory blood flow, as wel
201 2-iP, iPF2alpha-III (previously called 8-iso-PGF2alpha or 8-epi-PGF2alpha), which demonstrated the ut
203 ute MI (105+/-17.8 versus 230+/-66 for 8-epi-PGF2alpha [P=.009] and 466+/-91 versus 833+/-153 for IPF
204 28767, and misoprostol but not with 10(-6) M PGF2alpha, PGD2, PGI2, or butaprost, suggesting a princi
205 sanoids, such as prostaglandin E2 (PGE2) and PGF2alpha, precedes the onset of labor as a result of in
206 anges in c-Jun-dependent gene transcription, PGF2alpha preferentially activates the MEK-Erk2- cytosol
207 ha levels in PVAT between females and males, PGF2alpha produced a larger contraction in arteries from
208 We conclude that the 22-carbon analogue of PGF2alpha, produced from docosahexaenoic acid by a cyclo
209 ence that the Tnfalpha-dependent increase in PGF2alpha production is necessary for the pro-ovulatory
215 Recombinant trout Tnfalpha (rTnfalpha) and PGF2alpha recapitulate the stimulatory in vitro effects
221 that initially forms myotubes, but rather to PGF2alpha recruiting the fusion of cells with preexistin
222 d also exhibited cross-desensitization, with PGF2alpha resulting in a maximum of approximately 60% de
223 ted amniotic fluid IL-1beta, IL-6, IL-8, and PGF2alpha, resulting in PTB and marked neonatal mortalit
224 rations of TXB2 (stable TXA2 metabolite) and PGF2alpha , soluble cell adhesion molecules and blood pr
226 e-dependent manner while having no effect on PGF2alpha-stimulated inositol phosphates formation.
227 of FPB-expressing cells with PGE2-attenuated PGF2alpha-stimulated Tcf/beta-catenin signaling in a dos
229 eriments were performed to determine whether PGF2alpha stimulates the mammalian target of rapamycin (
230 suggest that GPCR activation in response to PGF2alpha stimulates the mTOR pathway which increases th
234 (TxS), and the receptors for TxA2 (the TP), PGF2alpha (the FP), and PGI2 (the IP) were upregulated a
235 ith L 745,337, suppressed formation of 8-epi-PGF2alpha, thiobarbituric acid-reactive substances, and
236 ated intracellular pathways are required for PGF2alpha to induce morphological and genetic features c
239 deposition (MMP9), and prostanoids (PGE(2), PGF2alpha, TXA2) were all more effectively reduced by na
241 trictor responses to norepinephrine, U46619, PGF2alpha, vasopressin, BAY K8644; biphasic responses to
242 ction of intraocular pressure by 50.0 microg PGF2alpha was 5.0+/-1.4 mm Hg, whereas that by 50 microg
243 re patient on hemodialysis and urinary 8-iso-PGF2alpha was 7.1-fold higher in a cigarette smoker than
245 nificant reduction in the excretion of 8-iso-PGF2alpha was induced by the run-in diet and the high-VF
251 his work, 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha) was analysed in raw 24 h-composite wastewater
252 ry excretion of 8-isoprostane F2alpha (8-iso-PGF2alpha) was used as an index of whole-body lipid pero
253 assessed by measuring the isoprostane 8-iso-PGF2alpha, was decreased in the lungs of GM-/- mice.
254 the plasma marker of oxidative stress, 8-iso PGF2alpha, was increased in PHF animals (P < 0.01).
256 iet, whereas urinary concentrations of 8-iso-PGF2alpha were further reduced (P < 0.01) by the high-VF
257 In addition, the levels of urinary 8-iso-PGF2alpha were independent predictors of non-alcoholic f
261 er PGT nor PG15DH, exogenously added PGE2 or PGF2alpha were rapidly oxidized to the 13, 14-dihydro, 1
262 (previously called 8-iso-PGF2alpha or 8-epi-PGF2alpha), which demonstrated the utility of monitoring
265 synthesis of the most complex prostaglandin, PGF2alpha, with high levels of control of relative and a
266 eralfold as abundant in human urine as 8-iso-PGF2alpha, with mean values of 737 +/- 20.6 pg/mg creati