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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.
24          Much higher concentrations of 8-epi-PGF2alpha (10-20 microM) alone induce weak, reversible a
25  in monolayer cultures and were treated with PGF2alpha, 11-deoxy-PGE1, or PhXA85 (the nonesterified a
26        Twenty-four-hour treatment with 20 nM PGF2alpha, 11-deoxy-PGE1, or PhXA85 reduced the amount o
27                    When the concentration of PGF2alpha, 11-deoxy-PGE1, or PhXA85 was increased to 200
28                           Prostaglandin (15R-PGF2alpha, 11B-dhk-PGF2alpha) and linoleic acid derivati
29 d 8-isoprostane-prostaglandin-F2alpha (8-iso-PGF2alpha), 2,3-dinor-5,6-dihydro-8-iso-PGF2alpha, 2,3-d
30  PBDEs were associated with increasing 8-iso-PGF2alpha, 2,3-dinor-8-iso-PGF2alpha, and PGF2alpha.
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
33                                              PGF2alpha also activates the extracellular signal-regula
34                                        8-Iso-PGF2alpha also had no effect on HMEC surface expression
35                                              PGF2alpha also induced eIF4E and 4E-BP1 phosphorylation,
36 the isoprostane 8-iso-prostaglandin F (8-iso-PGF2alpha), among other ligands examined, to activate G1
37              iPF2alpha-III (previously 8-iso-PGF2alpha), an isoprostane from Class III (previously kn
38           Microalbuminuria and urinary 8-iso-PGF2alpha, an index of in vivo oxidative stress, indepen
39                                    Recently, PGF2alpha analogs have been hypothesized to reduce intra
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
42                     In the dose ranges used, PGF2alpha and 17-phenyl trinor PGE2 decreased intraocula
43 ent administration of 12.5 microg of each of PGF2alpha and 17-phenyl trinor PGE2 did not produce an a
44 ed the intraocular pressure response to both PGF2alpha and 17-phenyl trinor PGE2.
45 dural values by 24 hours (122+/-18 for 8-epi-PGF2alpha and 457+/-102 for IPF2alpha-I).
46                                         Both PGF2alpha and 8,12-iso-iPF2alpha-III activate the p70S6
47                                   Thus, both PGF2alpha and 8,12-iso-iPF2alpha-III induce myocyte hype
48                                        Thus, PGF2alpha and 8,12-iso-iPF2alpha-III stimulate inositol
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
51                                   Therefore, PGF2alpha and Bimatoprost appear to interact with differ
52                                         Both PGF2alpha and Bimatoprost up-regulated Cyr61 mRNA expres
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
56                                        8-epi PGF2alpha and IPF2alpha-I are F2-isoprostanes produced i
57 (r=.68, P<.0001; n=33) between urinary 8-epi-PGF2alpha and IPF2alpha-I levels in patients receiving t
58              Our results indicate that 8-epi PGF2alpha and IPF2alpha-I, two distinct F2-isoprostanes
59 structurally distinct F2 isoprostanes, 8-epi-PGF2alpha and IPF2alpha-I.
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
62    The potency of the natural prostaglandins PGF2alpha and PGD2 was not enhanced by the mutations.
63 triggers the synthesis of the prostaglandins PGF2alpha and PGE2, but not PGD2, in rat cerebral cortic
64                                Urinary 8-iso-PGF2alpha and serum soluble NOX2-derived peptide levels
65 igate any possible correlation between 8-iso-PGF2alpha and the consumption of the two drugs.
66                                              PGF2alpha and the PG mixture at 25 muM concentration sig
67                                    Levels of PGF2alpha and thromboxane B2 (TXB2 ) were quantified by
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
70        Prostaglandin (15R-PGF2alpha, 11B-dhk-PGF2alpha) and linoleic acid derivatives (12,13 EpOME) a
71 se using progesterone, prostaglandin F2alpha(PGF2alpha) and pregnant mare serum gonadotrophin (PMSG).
72 1alpha (PGF1alpha), prostaglandin F(2alpha) (PGF2alpha), and prostaglandin D2 (PGD2).
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
75  However, the TP receptor agonists U-46,619, PGF2alpha, and PGD2 were more potent than PGE2.
76  increasing 8-iso-PGF2alpha, 2,3-dinor-8-iso-PGF2alpha, and PGF2alpha.
77 ertrophic agonists in culture, endothelin-1, PGF2alpha, and phorbol 12-myristate 13-acetate, also ind
78 5,6-dihydro-8-iso-PGF2alpha, 2,3-dinor-8-iso-PGF2alpha, and prostaglandin-F2alpha (PGF2alpha).
79            We show that NFAT is activated by PGF2alpha, and the isoform NFATC2 is required for PGF2al
80  because unreactive lipids, e.g. PGB1, PGE2, PGF2alpha, and TxB2, did not inhibit LKB1 activity (p >
81 catalyzed the transport of PGE1, PGE2, PGD2, PGF2alpha, and, to a lesser degree, TXB2.
82 ontraction in arteries from females, whereas PGF2alpha appears to mediate the contraction in arteries
83         The rank order substrate profile was PGF2alpha approximately PGE2 > TXB2 >> 6 keto-PGF1alpha.
84                    The biological effects of PGF2alpha are mediated via the G protein-coupled recepto
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 (
95 iently quantified by this method, with 8-iso-PGF2alpha being identified as a major isomer.
96                       It is established that PGF2alpha binds to a G-proteincoupled receptor (GPCR) to
97 ocytes resulted in marked formation of 8-epi-PGF2alpha, but not of PGE2 or TxB2.
98                  We further demonstrate that PGF2alpha, but not PGE2 or PGD2, is necessary but not su
99 istent with the enzymatic formation of 8-epi PGF2alpha by cyclooxygenases.
100 ro-15-F2t-IsoP (2,3-dinor-5, 6-dihydro-8-iso-PGF2alpha), by gas chromotography/negative ion chemical
101                     The data show that 8-iso-PGF2alpha can suppress the attachment of monocytes to HM
102                              Although 12-iso-PGF2alpha caused a dose-dependent activation of the FP,
103 hese observations, only PGF2alpha and 12-iso-PGF2alpha caused rapid homologous desensitization of FP
104                                    Moreover, PGF2alpha causes a robust activation ( approximately 50-
105                                   Similarly, PGF2alpha causes translocation of cytosolic phospholipas
106          For example, prostaglandin F2alpha (PGF2alpha) causes hypertrophy of neonatal rat ventricula
107 idly metabolized to inactive products, 8-epi PGF2alpha circulates in plasma.
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
110                The run-in diet reduced 8-iso-PGF2alpha concentrations by 33% (P < 0.0001).
111 endent relaxations in prostaglandin F2alpha (PGF2alpha)-contracted strips of porcine coronary artery.
112 induced endothelium-dependent relaxations in PGF2alpha-contracted porcine coronary arteries.
113                       It was also found that PGF2alpha-could activate T-cell factor (Tcf)/beta-cateni
114 c ring contraction experiments revealed that PGF2alpha-dependent activation of FP potentiated angiote
115                               Treatment with PGF2alpha did not increase AKT phosphorylation but incre
116                       Urinary CC16 and 8-iso-PGF2alpha did not increase.
117 e blockade by thromboxane antagonists, 8-epi PGF2alpha does not activate either of the thromboxane re
118                                  Thus, 8-epi-PGF2alpha does not compete for binding at the stably exp
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
123 tor of activated T cells (NFAT) in mediating PGF2alpha-enhanced cell growth was examined.
124    This increased myotube size is not due to PGF2alpha-enhancing cell fusion that initially forms myo
125                                Urinary 8-iso PGF2alpha excretion was associated with the risk of gast
126                         Median urinary 8-iso PGF2alpha excretion was higher in cases (0.014; IQR: 0.0
127           Furthermore, the response to 8-epi PGF2alpha exhibits structural specificity versus 8-epi P
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
130                    Exposure of HMEC to 8-iso-PGF2alpha for 1-2 h was sufficient to reduce monocyte ad
131 GE2 has much lower efficacy as compared with PGF2alpha for the activation of Tcf/beta-catenin signali
132                         Although serum 8-iso-PGF2alpha formation is substantially depressed by COX in
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
135                 Thus, prostaglandin F2alpha (PGF2alpha) (FP receptor agonist), Butaprost (EP2 recepto
136 in the following order of activity: PGE2-G > PGF2alpha-G > PGD2-G; LYPLA2 hydrolyzed 1- but not 2-ara
137                                      PGD2-G, PGF2alpha-G and PGD2-EA, but not PGE2-EA or PGF2alpha-EA
138       The primary outcomes 2,3-dinor-11-beta-PGF2alpha, GETE score, and standard clinical biomarkers
139           In monocyte adhesion assays, 8-iso-PGF2alpha (&gt;10(-8) M) suppressed both basal and TNF-alph
140 taglandin profile: TxB2>6-keto PGF1alpha and PGF2alpha&gt;PGE2, despite the comparable release of total
141                                        8-Iso-PGF2alpha had no effect on the viability (Trypan Blue ex
142       Thus, the ratio of endogenous PGE2 and PGF2alpha has the potential to selectively regulate one
143          One F-ring IsoP, 15-F2t-IsoP (8-iso-PGF2alpha) has been shown to be formed in abundance in v
144 Bs in biosynthesis of prostaglandin F2alpha (PGF2alpha) has not been investigated.
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
147                     Following the removal of PGF2alpha, however, FPA-expressing cells return to their
148 poral trends observed in the levels of 8-iso-PGF2alpha, however, spatial differences were found at th
149                                        8-epi PGF2alpha immunoreactivity was also detected in cells po
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
154                    Given this novel role for PGF2alpha in skeletal muscle cell growth, these studies
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
157  potential anti-inflammatory effect of 8-iso-PGF2alpha in the microvasculature.
158 om female animals and greater sensitivity to PGF2alpha in the porcine coronary artery from males.
159                      Concentrations of 8-epi-PGF2alpha in the range 1 nM to 1 microM induce a dose-de
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
162                           In cardiomyocytes, PGF2alpha increases the hydrolysis of inositol phosphate
163                                              PGF2alpha induced the activities of extracellular signal
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
172                                              PGF2alpha-induced phosphorylation of eIF4E and 4E-BP1 wa
173 mplicated p38 and JNK, but not ERK, in 8-iso-PGF2alpha-induced suppression of monocyte adhesion.
174                                              PGF2alpha-induced up-regulation of Cyr61 appeared to exc
175 (CM) transfer experiments suggest that 8-iso-PGF2alpha induces a secondary mediator, which also suppr
176                We show that, within minutes, PGF2alpha injection activates a naturalistic pattern of
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
179       Four additional F2 isoprostanes, 8-iso-PGF2alpha, IPF2alpha-I, IPF2alpha-III, and 9beta,11beta-
180                                        8-Epi-PGF2alpha is a more abundant product of monocyte PG G/H
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
184                       Prostaglandin F2alpha (PGF2alpha) is a product of cyclooxygenase-catalyzed meta
185                       Prostaglandin F2alpha (PGF2alpha) is an important mediator of corpus luteum (CL
186 compounds, 8-epiprostaglandin F2alpha (8-epi-PGF2alpha), is a mitogen and vasoconstrictor.
187           However, IPF2alpha-I, unlike 8-iso-PGF2alpha, is not formed in a COX-dependent manner by pl
188 There was a slight increase in urinary 8-epi-PGF2alpha levels (64.7+/-9.5 versus 84.9+/-10.6; P=.02)
189          Although there was no difference in PGF2alpha levels in PVAT between females and males, PGF2
190 d PORH and increased TXA2 but did not change PGF2alpha levels.
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
194                                    The 8-iso-PGF2alpha mass load was found to be strongly associated
195                                        8-Epi PGF2alpha may amplify the response to platelet agonists
196                               Although 8-iso-PGF2alpha may be formed as a minor product of COX, this
197 r second-trimester levels of 2,3-dinor-8-iso-PGF2alpha (mean change per quartile increase = 0.25, 95%
198 vely, whereas neither compound abrogates the PGF2alpha-mediated response.
199                                   Similarly, PGF2alpha-mediated vasoconstriction was symmetrically re
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
202 had little or no effect on the NPV caused by PGF2alpha or LY83583.
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
210 med that COX-1 accounted for the majority of PGF2alpha production.
211 lowing luteolysis in the absence of elevated PGF2alpha production.
212 tes mRNA levels of the putative receptor for PGF2alpha (Ptgfr).
213  and is highly correlated with urinary 8-iso-PGF2alpha (r = 0.9; P < 0.001).
214                                        8-epi PGF2alpha ranged from 1.310-3.450 pmol/micromol phosphol
215   Recombinant trout Tnfalpha (rTnfalpha) and PGF2alpha recapitulate the stimulatory in vitro effects
216          This growth is mediated through the PGF2alpha receptor (FP receptor).
217        To investigate the molecular basis of PGF2alpha receptor (FP) activation in the eye, we cloned
218                                  We detected PGF2alpha receptor (FP) on the Leishmania PV surface.
219 f neonatal rat ventricular myocytes, via the PGF2alpha receptor (FP).
220 lon to the myocyte membrane, consistent with PGF2alpha receptor coupling to Gq.
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
225                           In contrast, 8-iso-PGF2alpha stimulated monocyte adhesion to human umbilica
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
228          Additional studies demonstrate that PGF2alpha stimulates protein tyrosine phosphorylation an
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
231 t metacyclic stage, as did the expression of PGF2alpha synthase (PGFS).
232                 Here we show that Lh induces PGF2alpha synthesis through its stimulation of Tnfalpha
233 w strategies for therapeutic intervention in PGF2alpha-target tissues.
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
237                          We demonstrate that PGF2alpha treatment results in a timeand concentration-d
238       The stimulation of S6K1 in response to PGF2alpha treatment was abolished by the mTOR inhibitor
239  deposition (MMP9), and prostanoids (PGE(2), PGF2alpha, TXA2) were all more effectively reduced by na
240                                         Only PGF2alpha up-regulated CTGF mRNA expression in the cat i
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
244                                Urinary 8-epi-PGF2alpha was highly correlated with both aCL titer (Rho
245 nificant reduction in the excretion of 8-iso-PGF2alpha was induced by the run-in diet and the high-VF
246                20 microCi of tritiated 8-iso-PGF2alpha was infused over 1 h into a male volunteer.
247                                       12-iso-PGF2alpha was less potent (EC50 = 5 microM) than PGF2alp
248                                  Urine 8-iso PGF2alpha was measured primarily by ELISA, and by gas ch
249                          The effect of 8-iso-PGF2alpha was mimicked by a thromboxane receptor (TP) ag
250                       No difference of 8-epi-PGF2alpha was observed between patients with and without
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).
255 respectively) on the intraocular response to PGF2alpha were also examined.
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
258                               The effects of PGF2alpha were mimicked by the PKC activator PMA and inh
259               The amount of parasite LBs and PGF2alpha were modulated by exogenous arachidonic acid.
260             The greatest reductions in 8-iso-PGF2alpha were observed in subjects in the highest quart
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
263                       Prostaglandin F2alpha (PGF2alpha), which is released from cells of the myocardi
264                       The excretion of 8-iso-PGF2alpha with the low-VF diet remained the same as that
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

 
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