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1                                              PGF accounted for 23.4% (n=364) of all deaths (n=1555) i
2                                              PGF is a secreted factor that supports hypertrophy and c
3                                              PGF is induced in the heart after pressure-overload stim
4                                              PGF promoted metastasis of BCCs and also facilitated hom
5                                              PGF transgenic mice showed a more adaptive type of cardi
6                                              PGF was studied from the perspective of "hard outcomes"
7                                              PGF(2alpha) and 17,20beta-P thereby seemed to act throug
8                                              PGF(2alpha) and latanoprost acid induce coordinated alte
9                                              PGF(2alpha) at 8% WT levels was sufficient to induce coo
10                                              PGF(2alpha) has been implicated in wound healing and car
11                                              PGF(2alpha) increased the secretion of MMP-2 in a dose-d
12                                              PGF(2alpha) induces phosphorylation of JunD bound to the
13                                              PGF(2alpha) was also found to induce the expression of E
14                                              PGF(2alpha)-induced ERK1/2 phosphorylation was prevented
15                                              PGF-CTERM occurs in 29 archaeal species, some of which h
16                                              PGF-CTERM proteins include the major cell surface protei
17               Our results revealed that: (1) PGF varied depending on the pollinator species, and was
18 eroxide reductase activity and 9alpha,11beta-PGF(2) (PGF(2)(alphabeta)) from PGD(2) by the PGD(2) 11-
19 d correlated against severity; 9alpha,11beta-PGF(2) and PGI(2) metabolites were measured for control
20 easured as PGD(2) reduction to 9alpha,11beta-PGF(2) by ELISA) were impaired by small interfering RNA
21 changes in leukotriene E(4) or 9alpha,11beta-PGF(2) levels after AD.
22 re diminished only weakly, and 9alpha,11beta-PGF(2) levels conversely increased.
23 sed urinary tetranor PGDM > 2,3-dinor-11beta-PGF(2alpha) > 11beta-PGF(2alpha) in mice.
24 increased tetranor PGDM and 2,3-dinor-11beta-PGF(2alpha) in humans coincident with facial flushing.
25  elevated tetranor PGDM and 2,3-dinor-11beta-PGF(2alpha) in volunteers, coincident with a pyrexial an
26 respondingly, both PGDM and 2,3-dinor-11beta-PGF(2alpha) were suppressed by inhibition of COX-1 and C
27 tes, 11beta-PGF(2alpha) and 2,3-dinor-11beta-PGF(2alpha), in human urine and was the only endogenous
28 PGDM > 2,3-dinor-11beta-PGF(2alpha) > 11beta-PGF(2alpha) in mice.
29 abundant than the PGD(2) metabolites, 11beta-PGF(2alpha) and 2,3-dinor-11beta-PGF(2alpha), in human u
30 estion of higher urinary excretion of 11beta-PGF(2alpha) and a lower excretion of a PGE(2) metabolite
31                     The same strong inter-15-PGF correlations were observed in plasma from healthy yo
32                                All plasma 15-PGF isomers increased over time with in vitro cigarette
33  acidified, and total (free + esterified) 15-PGFs and AA were extracted with organic solvents.
34 itation of several 15-series PGF isomers (15-PGFs) and AA by high-performance liquid chromatography-t
35 ng HPLC-tandem MS applied to plasma total 15-PGFs.
36 0.83%) and lowest with P. rapae (2.71%); (2) PGF with B. ignitus depended on the distance between GM
37 reductase activity and 9alpha,11beta-PGF(2) (PGF(2)(alphabeta)) from PGD(2) by the PGD(2) 11-ketoredu
38 in levels of prostaglandin (PG)E(2), PGD(2), PGF(2alpha), and thromboxane B(2), as well as the expres
39  perfusion with 5 micromol/L PGE(2), PGD(2), PGF(2alpha), or carboprostacyclin.
40 at vasodilatory prostaglandins (PGs) PGE(2), PGF(2alpha), and PGE(3) accompany the erythema in the fi
41  and COX-2 as well as their products PGE(2), PGF(2alpha), and thromboxane B(2) and their receptors fo
42                              PGD(2), PGE(2), PGF(2alpha), carbaprostacyclin (cPGI(2); a stable prosta
43 IV-1, while 9,10-dihydro-15d-PGJ(2), PGE(2), PGF(2alpha), or PGD(2) that lack the reactive alpha,beta
44 nfluent OCCM cells were treated with PGE(2), PGF(2alpha), specific activators/inhibitors of the EP pr
45  both isoforms with prostaglandin F(2alpha) (PGF(2alpha)) activates the small G-protein Rho, leading
46 ormonal pheromones, prostaglandin F(2alpha) (PGF(2alpha)) and 17alpha,20beta-dihydroxy-4-pregnen-3-on
47 and regioisomers of prostaglandin F(2alpha) (PGF(2alpha)) and are used as biomarkers for lipid peroxi
48 mechanisms by which prostaglandin F(2alpha) (PGF(2alpha)) increases intracellular Ca2+ concentration
49 y demonstrated that prostaglandin F(2alpha) (PGF(2alpha)) induces a rapid and transient expression of
50                     Prostaglandin F(2alpha) (PGF(2alpha)) is a potent antiadipogenic factor in cultur
51 e of the major PGs, prostaglandin F(2alpha) (PGF(2alpha)) is present in human urine in significant co
52  of prostaglandins E(2) (PGE(2)), F(2alpha) (PGF(2alpha)), lipoxin A(4) (LXA(4)) and its receptor FPR
53 ogical activator is prostaglandin-F(2alpha) (PGF(2alpha)).
54 re stereoisomers of prostaglandin F(2alpha) (PGF(2alpha)).
55 hly effective ocular hypotensive agent, is a PGF(2)(alpha) analogue that inhibits both the PGD(2) 11-
56                             Travoprost acid, PGF(2alpha,) unoprostone, and S-1033 were tested in addi
57  approximately 30% enhancement by activating PGF(2alpha) receptor or thromboxane receptor, or approxi
58 ured in expression of PAPPA, FLT1, ENG, AFP, PGF, and LGALS14, but not LGALS13 or the lineage marker
59 how the regulation of EGR-1 expression after PGF(2alpha) activation of FP receptors and suggests that
60  luteolytic mediator prostaglandin F2-alpha (PGF) significantly increased TNF in the ovaries when com
61                                     Although PGF transgenic mice did not have a baseline phenotype or
62                        Furthermore, although PGF(2alpha) increases intracellular cyclic AMP via Galph
63 t cryptococcal production of both PGE(2) and PGF(2 alpha) can be chemically inhibited by caffeic acid
64 red colonic motility index, lower TxA(2) and PGF(2) and higher PGE(2) levels than controls.
65 on of 9 alpha,11 beta-PGF(2) from PGD(2) and PGF(2)(alpha) from PGH(2) in the presence of NADPH.
66 31 and increased the synthesis of PGE(2) and PGF(2)alpha.
67 f PGE(2) and PGF(2alpha) and that PGE(2) and PGF(2alpha) act as paracrine factors that stimulate mela
68                                   PGE(2) and PGF(2alpha) alter cell function by binding and activatin
69 ocyte PAR-2 stimulates release of PGE(2) and PGF(2alpha) and that PGE(2) and PGF(2alpha) act as parac
70             The prostaglandins (PG) E(2) and PGF(2alpha) are important cytokines in periodontal physi
71    In this study, we examined the PGE(2) and PGF(2alpha) effects on the immortalized cementoblastic O
72                  We conclude that PGE(2) and PGF(2alpha) exert an anabolic effect on OCCM mineralizat
73 endricity observed in response to PGE(2) and PGF(2alpha) is cAMP-independent.
74                                   PGE(2) and PGF(2alpha) significantly increased mineralization of OC
75 nocytes, as well as by release of PGE(2) and PGF(2alpha) that stimulate melanocyte dendricity through
76 dins involved in inflammation are PGE(2) and PGF(2alpha).
77 rachidonate metabolites (PGD(2), PGE(2), and PGF(2)) by the action of three groups of enzymes.
78 rachidonate metabolites (PGD(2), PGE(2), and PGF(2)) by the action of three groups of enzymes.
79 ers and ethanolamides of PGE(2), PGD(2), and PGF(2alpha) were major products of the endocannabinoid-d
80 GH(2) mimetic (U-51605), PGD(2,) PGJ(2), and PGF(2alpha).
81 lpha,11beta-prostaglandin (PG) F(2alpha) and PGF(2alpha) prostanoids that sustain the growth of myelo
82  cortex expression of VEGFB, FLT4, FLT1, and PGF was associated with worse cognitive trajectories (p
83 g on PGHS-1 pathways involving PGD, PGE, and PGF.
84 t levels of PGE(2), PGD(2), thromboxane, and PGF(2alpha), but not PGI(2).
85 d catalyzes the formation of 9 alpha,11 beta-PGF(2) from PGD(2) and PGF(2)(alpha) from PGH(2) in the
86 dogenic-associated gene (VEGF, VEGFR2, BFGF, PGF, HGF, Ang-1, VWF, PECAM-1 and ENOS) expression analy
87                                        Bound PGF(2alpha) isomers are derivatized by 1-pyrenyldiazomet
88 ong the 414 heart transplants complicated by PGF, 354 (85.5%) recipients died and 60 (14.5%) were ret
89       Thus, induction of EGR-1 expression by PGF(2alpha) was blocked using dominant-negative construc
90 blocked the induction of EGR-1 expression by PGF(2alpha).
91  PGE(2) treatment or, to a lesser extent, by PGF(2alpha), but not by other prostaglandins, such as PG
92 ased uveoscleral outflow of aqueous humor by PGF(2alpha).
93 bit contractions and inflammation induced by PGF(2alpha).
94 vation of ERK1/2 mediates nur77 induction by PGF(2alpha).
95 t-negative JunD abolished nur77 induction by PGF(2alpha).
96  that activation of the human FP receptor by PGF(2alpha) could induce the expression of EGR-1 and fou
97 ents contraction of rat uterus stimulated by PGF(2alpha) and induces relaxation of aorta previously c
98  sites, but its binding is not stimulated by PGF(2alpha).
99                   FP receptor stimulation by PGF(2alpha) induced the phosphorylation of C-Raf, MEK1/2
100 iadipogenic properties possibly supported by PGF(2alpha) synthase activity.
101                                Cloprostenol (PGF(2alpha) agonist) administration to Akr1b7(-/-) mice
102 ure, two model structures of PGFS containing PGF(2)(alpha) and PGH(2) were built.
103                                 In contrast, PGF(2alpha) levels remained unchanged and were three-fol
104 e Trp53 induces preterm birth through a COX2/PGF synthase/PGF(2alpha) pathway.
105                  CRP significantly decreased PGF-1alpha release from HAECs under basal (48% decrease,
106    Akr1b7 loss was associated with decreased PGF(2alpha) WAT contents.
107  An important difference between COX-derived PGF(2alpha) and the IsoPs is that the former is an optic
108 le resolution in the separation of different PGF(2alpha) isomers and can be used not only for sample
109 PKC inhibitor bisindolylmaleimide I enhanced PGF(2alpha)-stimulated IP accumulation in transfected ce
110 pects to PGF(2alpha) and its enantiomer, ent-PGF(2alpha), are formed in equal amounts esterified in t
111 pared by centrifugation and esterified 8-epi PGF(2alpha) measured at the start and finish of each tre
112  resulted in a significant decrease in 8-epi PGF(2alpha) production, from 38.8 (95% CI 24.9 to 52.7)
113 tion on 8-epi prostaglandin F(2alpha) (8-epi PGF(2alpha)) content and the effect of concurrent oral a
114  in an increase in platelet-esterified 8-epi PGF(2alpha), a free radical and cyclooxygenase-dependent
115 ficant increase in platelet-esterified 8-epi PGF(2alpha), from 32.9 (95% confidence interval [CI] 11.
116 the levels of the isoprostane product, 8-epi-PGF(2alpha).
117 e, and 2 microg PGF(2alpha)-isopropyl ester (PGF(2alpha)-IE) was applied to the other eye of cynomolg
118 andin E2 (PGE(2)) and prostaglandin F2alpha (PGF(2alpha)), are enzymatically degraded by 15-hydroxypr
119  and MSCs expressed placental growth factor (PGF) and its cognate receptor VEGFR1, respectively, in a
120  VEGF family member placental growth factor (PGF) as an aldosterone-regulated vascular MR target gene
121 , VEGFD (FIGF), and placental growth factor (PGF); VEGF receptors VEGFR1 (FLT1), VEGFR2 (KDR), and VE
122                       Primary graft failure (PGF) is the most common cause of short-term mortality af
123 sculopathy (CAV), and primary graft failure (PGF).
124 iments to measure pollen-mediated gene flow (PGF) in the absence and presence of pollinators (Bombus
125 a a transporter, which has high affinity for PGF(2alpha) and PGE(2), but not prostacyclin (PGI(2)).
126 the g-HCM cells than in the n-HCM cells (for PGF(2alpha), 60% vs. 151%).
127 at the necessary and sufficient elements for PGF(2alpha) induction of Nur77 promoter activity are loc
128  as the likely protein-processing enzyme for PGF-CTERM.
129 pathway indicates that a single pathway from PGF(2alpha) receptor to CREB is responsible for inducing
130    In recipients with prompt graft function (PGF), the mean cold storage time was 22+/-9 hr versus 29
131          All four PG-Gs (PGE(2)-G, PGD(2)-G, PGF(2alpha)-G, and 6-keto-PGF(1alpha)-G) and the prostag
132 on were in the following order: CCh > ET-1 > PGF(2alpha).
133 7 nM) > bimatoprost acid (EC(50) = 112 nM) > PGF(2alpha) (EC(50) = 120 nM) >> unoprostone (UF-021; EC
134               In summary, we have identified PGF as what we believe to be a novel downstream target o
135       There was no significant difference in PGF at 90 days or recipient mortality after up to 5 year
136                  Secondary outcomes included PGF and other postoperative events, such as renal failur
137 the anti-substituted isoprostanes, including PGF(2)(alpha), were, however, observed in the product mi
138 mulated Pgf gene transcription and increased PGF protein expression and secretion in the mouse vascul
139 nerated cardiac-specific and adult inducible PGF-overexpressing transgenic mice and analyzed Pgf(-/-)
140 otic human vessels, MR antagonists inhibited PGF expression.
141 th OTR-As, atosiban and nolasiban, inhibited PGF(2alpha)-induced contractions in a dose-dependent man
142                            Urinary F(2)-iPs, PGF(2alpha) isomers derived from arachidonic acid (AA) a
143 -1); P < 0.05) at day 14 and the renal 8-iso PGF(2alpha) excretion (3.53 +/- 0.71 pg. d(-1); P < 0.05
144                     Renal excretion of 8-iso PGF(2alpha) was increased in AngII400 group at day 12 (2
145 (PG) E(1) and 8-iso-PGE(2), but not by 8-iso-PGF(1alpha), 8-iso-PGF(2alpha), and 8-iso-PGF(3)alpha.
146  of cells with TP antagonists, whereas 8-iso-PGF(2 alpha) was without effect.
147 rostane using an antibody specific for 8-Iso-PGF(2) (15-F(2t)-IsoP).
148 GE(2) , 8-iso-PGE(2) , tetranor-PGE-M, 8-iso-PGF(2) alpha, and leukotriene C(4) , D(4) , and E(4) , w
149                               However, 8-iso-PGF(2alpha) also originates from enzymatic sources linke
150 flammation or oxidative stress derived 8-iso-PGF(2alpha) and estimate their associations with phthala
151            For example, a 22.4% higher 8-iso-PGF(2alpha) concentration (95% confidence interval = 14.
152 e, associations between phthalates and 8-iso-PGF(2alpha) could have been misinterpreted.
153 (P<0.01) and diastolic BP (P<0.01) and 8-iso-PGF(2alpha) decreased (P<0.05), whereas urinary NO(X) in
154 atterns, chromatographic separation of 8-iso-PGF(2alpha) from its isomers is necessary for its quanti
155 was optimized for rapid measurement of 8-iso-PGF(2alpha) in urine, and it is ideally suited for clini
156 menadione and alphaEE showed increased 8-iso-PGF(2alpha) levels compared with untreated controls, whe
157 assay had a linear range of 1-40 pg of 8-iso-PGF(2alpha) on column and can quantify as little as 40 p
158 eated controls, whereas no increase in 8-iso-PGF(2alpha) was detected in kidneys of alphaEE-treated g
159 urinary 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)) as the oxidative stress biomarker.
160 jor urinary metabolite of 15-F2t-IsoP (8-iso-PGF(2alpha)) is 2,3-dinor-5,6-dihydro-15-F2t-IsoP (15-F2
161 ease in 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)) levels compared with untreated controls.
162 urinary 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)), a biomarker of lipid peroxidation.
163 insulin, 8-isoprostaglandin F(2alpha) (8-iso-PGF(2alpha)), and glucose measurements.
164 -PGE(2), but not by 8-iso-PGF(1alpha), 8-iso-PGF(2alpha), and 8-iso-PGF(3)alpha.
165  of prostaglandin F(2alpha), including 8-iso-PGF(2alpha), following derivatization with 1-pyrenyldiaz
166 r prostaglandins (e.g. PGE(1), PGE(2), 8-iso-PGF(2alpha), prostacyclin), leukotrienes (e.g. LTB(4), L
167 ) were associated with both sources of 8-iso-PGF(2alpha).
168 ociated with a significant increase in 8-iso-PGF(2alpha).
169 sociated with oxidative stress derived 8-iso-PGF(2alpha).
170 d solely with oxidative stress derived 8-iso-PGF(2alpha).
171  biomarkers than the commonly measured 8-iso-PGF(2alpha).
172                   To clarify this, the 8-iso-PGF(2alpha)/prostaglandin F(2alpha) ratio approach was u
173 so-PGF(1alpha), 8-iso-PGF(2alpha), and 8-iso-PGF(3)alpha.
174 ostane E(2) (8-iso-PGE) and F(2alpha) (8-iso-PGF) sensitize nociceptors and capsaicin-sensitive DRG n
175                                8-Isoprostane PGF(2alpha) and malonyldialdehyde were measured in group
176  and 6-keto prostaglandin F(1alpha) (6-kepto PGF(1alpha)).
177 fold) and the prostacyclin metabolite 6-keto PGF(1alpha) (5.7-fold).
178 inor TxB2 (Tx-M), and PGI2, 2,3-dinor 6-keto PGF(1alpha) (PGI-M), only PGI-M was depressed by the COX
179 g/ml for control and 10(-6) M NOC/oFQ 6-Keto PGF(1alpha) and TXB(2), respectively).
180 y increased cerebrospinal fluid (CSF) 6-Keto PGF(1alpha) and TXB(2), the stable breakdown products of
181  ex vivo, depressed urinary 2,3 dinor 6-keto PGF(1alpha) by approximately 60% but had no effect on th
182  depressed, whereas urinary 2,3-dinor 6-keto PGF(1alpha), but not 2,3-dinor-TxB(2), was increased in
183 immunoassay of its stable metabolite, 6-keto PGF(1alpha), that was abolished by diclofenac.
184 rothromboxane B2 (Tx-M) and 2'3-donor-6-keto-PGF(1alpha) (PGI-M).
185  significantly increased secretion of 6-keto-PGF(1alpha) and PGE(2).
186 e cardiac prostaglandin (PG) E(2) and 6-keto-PGF(1alpha) levels were significantly decreased in heart
187                             Levels of 6-keto-PGF(1alpha), a stable metabolite of prostacyclin, were r
188 sgenics exhibited only an increase in 6-keto-PGF(1alpha), not a decrease in PGE(2).
189 GE(2)-G, PGD(2)-G, PGF(2alpha)-G, and 6-keto-PGF(1alpha)-G) and the prostaglandins (PGs) that are for
190 crease in tissue levels of PGE(2) and 6-keto-PGF(1alpha).
191   In this report we show, using mice lacking PGF(2)alpha receptor and pregnant rats, that PGF(2)alpha
192 o commands for the vector graphics languages PGF/TikZ that can be compiled into scalable vector graph
193  [9,11-dideoxy-9 alpha,11 alpha-methanoepoxy PGF(2 alpha) (U46619)] in CHO cells transfected with the
194 s topically applied to one eye, and 2 microg PGF(2alpha)-isopropyl ester (PGF(2alpha)-IE) was applied
195 crease in the Fura PE-3 signal to 0.1 microM PGF(2alpha) was abolished, whereas 10 microM PGF(2alpha)
196 au rise in [Ca2+]i in response to 0.1 microM PGF(2alpha) was insensitive to diltiazem, and was abolis
197           The [Ca2+]i response to 0.1 microM PGF(2alpha) was mimicked by the FP receptor agonist flup
198 han that seen for the response to 0.1 microM PGF(2alpha), and were also much less sensitive to U-7312
199  Both responses became maximal at 0.1 microM PGF(2alpha).
200 he rises in [Ca2+]i in response to 10 microM PGF(2alpha) and 0.01 microM U-46619 were partially inhib
201 PGF(2alpha) was abolished, whereas 10 microM PGF(2alpha) and 0.05 microM U-46619 still caused substan
202 fluprostenol, whilst the effect of 10 microM PGF(2alpha) was mimicked by the TP receptor agonist U-46
203                    U-46619 and 10-100 microM PGF(2alpha) cause a TP receptor-mediated Ca2+ influx inv
204 ls: PGE2 (3.7+/-0.7 versus 1.1+/-0.2 pg/mL), PGF(1alpha) (16.2+/-2.8 versus 7.2+/-1.2 pg/mL), and bra
205 ng that links a specific pheromone molecule (PGF(2alpha)) to neurogenesis in a vertebrate animal.
206 upport targeting the vascular aldosterone/MR/PGF/Flt1 pathway as a therapeutic strategy for ischemic
207                        The addition of 1 muM PGF(2alpha) also increased MMP-2 secretion in a time-dep
208 the expression of EGR-1 and found that 1 muM PGF(2alpha) produced a time-dependent induction of both
209                                      Neither PGF(2alpha) or PGE(2) elevated cAMP in human melanocytes
210 s showed that 24 hours of exposure to 100 nM PGF(2alpha) significantly increased mRNA for MMP-1 and -
211 cleral tissues were exposed to 100 to 500 nM PGF(2alpha), 17-phenyltrinor PGF(2alpha), or PhXA85 (the
212                      The secretory action of PGF(2alpha) was inhibited by pretreatment with a protein
213                              The addition of PGF(2alpha) and latanoprost acid increased ERK1/2 activi
214                   Interestingly, addition of PGF(2alpha), which was not known to affect lymphocytes,
215 (2alpha)-G but is observed after addition of PGF(2alpha).
216 donate independent of COX and is composed of PGF(2alpha) and its enantiomer, although the latter comp
217 e results suggest that low concentrations of PGF(2alpha) act via FP receptors to cause IP3-dependent
218                  At higher concentrations of PGF(2alpha), a further slower rise in [Ca2+]i was superi
219 e mixture (10:1), fluorescent derivatives of PGF(2alpha) remain bound to cellulose while a significan
220 1- or 5-year mortality or the development of PGF (odds ratio, 1.11; 95% CI, 0.88-1.39; P = .37).
221 .14; P =.18) mortality or the development of PGF (odds ratio, 1.11; 95% CI, 0.88-1.39; P =.37).
222 sted predictive model for the development of PGF was formulated in a similar fashion.
223 ion has been well studied, but the effect of PGF(2alpha) on mucin production remains poorly understoo
224  This resorption is preceded by elevation of PGF(2~) but is not preceded by a decrease in circulating
225                The 1-pyrenylmethyl esters of PGF(2alpha) can be quantitatively extracted from cellulo
226  quantification of 1-pyrenylmethyl esters of PGF(2alpha) isomers at picogram level are complicated by
227       The purified 1-pyrenylmethyl esters of PGF(2alpha) were quantitatively analyzed by reverse-phas
228 clerosis, aldosterone enhanced expression of PGF and its receptor, FMS-like tyrosine kinase 1 (Flt1).
229  has dual catalytic activities: formation of PGF(2)(alpha) from PGH(2) by the PGH(2) 9,11-endoperoxid
230                                 Formation of PGF(2)(alpha) from PGH(2) most likely involves a direct
231 idate the effect and underlying mechanism of PGF(2alpha) on MUC5AC production, we investigated the si
232        Low concentrations (0.01-1 microM) of PGF(2alpha) caused a transient followed by a plateau ris
233 roxyprostaglandin dehydrogenase oxidation of PGF(2 alpha)-G was observed.
234                        The low prevalence of PGF has limited efforts at identifying risk factors for
235 of follow-up, nor any difference in rates of PGF at 90 days and CAV at 5 years between recipients of
236 own to coordinate the specific regulation of PGF in human trophoblast cell lines.
237                            The regulation of PGF(2alpha)-induced MUC5AC expression by CREB was furthe
238                               The release of PGF-1alpha, a stable product of PGI2, was also assayed i
239                     Following the removal of PGF(2alpha), however, FP(A)-expressing cells show rapid
240 edure of derivatization includes sorption of PGF(2alpha) isomers from solution in a hexane:ethyl acet
241 hibitory effects involved the suppression of PGF(2alpha)-mediated increase in intracellular calcium l
242 , we investigated the signal transduction of PGF(2alpha) associated with this effect using normal hum
243 d CXCL10 expression by MSCs was dependent on PGF expression by BCCs.
244 tors independently have a positive effect on PGF gene expression, when combined, DLX3 acts as an anta
245 ned the effects of atosiban and nolasiban on PGF(2alpha)-induced contractions and pro-inflammatory re
246 simultaneous effect of multiple variables on PGF.
247 cinoma cell line, with HGF, IL-6, PGE(2), or PGF(2)alpha resulted in significantly increased cell gro
248 hout increasing recipient mortality, CAV, or PGF.
249 erved after addition of PGE(2), PGD(2)-G, or PGF(2alpha)-G but is observed after addition of PGF(2alp
250 erefore, controlling tissue levels of HRG or PGF might be a promising strategy in chronic inflammator
251  PGE(2) release were in the following order: PGF(2alpha) > CCh > ET-1; and their effects on inositol
252 and g-HCM cells were in the following order: PGF(2alpha) > ET-1 > CCh; their effects on PGE(2) releas
253 O2, VO2, HCO3, K+, phosphate, lactate, PGE2, PGF(1alpha), and bradykinin) potentially involved in erg
254 receptor agonists fluprostenol and 17-phenyl PGF(2alpha).
255 o 100 to 500 nM PGF(2alpha), 17-phenyltrinor PGF(2alpha), or PhXA85 (the active form of latanoprost)
256 n), exposure to PGF(2alpha), 17-phenyltrinor PGF(2alpha), or PhXA85 each increased scleral permeabili
257 h exposure to PGF(2alpha) or 17-phenyltrinor-PGF(2alpha).
258 n matrix adhesion, we demonstrate a profound PGF(2alpha)-induced alteration in cytoskeletal remodelli
259  spectrometry, the vast majority of putative PGF(2alpha) in human urine is derived from the free radi
260 determined, however, that levels of putative PGF(2alpha) in urine cannot be suppressed by nonsteroida
261 of their functional antagonism in regulating PGF promoter activity.
262 method for quantitation of several 15-series PGF isomers (15-PGFs) and AA by high-performance liquid
263 ddition, the OTR-As significantly suppressed PGF(2alpha)-induced activation of pro-inflammatory pathw
264 es preterm birth through a COX2/PGF synthase/PGF(2alpha) pathway.
265 shed, using luteinized granulosa cells, that PGF(2alpha) stimulates in vitro nur77 expression in a ti
266                  Our research confirmed that PGF depended on pollinator species, distance between pla
267                Our results demonstrated that PGF(2alpha) induces MUC5AC overproduction via a signalin
268 PGF(2)alpha receptor and pregnant rats, that PGF(2)alpha is responsible for the rapid and massive exp
269                Mechanistically, we show that PGF does not have a direct effect on cardiomyocytes but
270                                          The PGF(2alpha)- and latanoprost-acid-induced ERK1/2 activat
271 ty was less intense in the sections from the PGF(2alpha)-IE-treated eyes compared with the vehicle-tr
272        Pressure reductions of 5 mm Hg in the PGF(2alpha)-IE-treated eyes were confirmed.
273 , a TNF-neutralizing antibody, inhibited the PGF-induced decrease in P4 and delayed luteal regression
274  role in ovarian physiology by mediating the PGF(2alpha) induction of 20alpha-HSD, a steroidogenic en
275                 Proteomics suggests that the PGF-CTERM region is removed.
276 era to prostaglandin (PG)F(2alpha) or to the PGF(2alpha) analogue latanoprost acid alters mRNA for ma
277 treatment with PGF and were resistant to the PGF-induced decrease in P4.
278                                   Therefore, PGF(2alpha) seemed to modulate male brain plasticity tha
279                 Moreover, we show that these PGF(2alpha)-induced alterations in adhesion and morpholo
280 osure to PhXA85 and similar with exposure to PGF(2alpha) or 17-phenyltrinor-PGF(2alpha).
281 (-6) cm/sec for 70 kDa dextran), exposure to PGF(2alpha), 17-phenyltrinor PGF(2alpha), or PhXA85 each
282 ts of compounds identical in all respects to PGF(2alpha) and its enantiomer, ent-PGF(2alpha), are for
283               Moreover, IOP-lowering topical PGF(2alpha)-IE treatment decreases the amount of TIGR pr
284 nce between GM and non-GM cottons; (3) total PGF to Shiyuan321 (8.61%) was higher than to Hai7124 (4.
285 ator of WAT development through at least two PGF(2alpha)-dependent mechanisms: inhibition of adipogen
286 d in understanding the mechanisms underlying PGF and in matching recipients with donors in efforts to
287 the nonsupplemented group; P<0.001); urinary PGF(2-alpha) excretion was also highest in the JO group
288 the renal-cell membrane and elevated urinary PGF(2-alpha) excretion, and the precipitous fall in inul
289              Thus, quantification of urinary PGF(2alpha) actually reflects oxidative stress status as
290                 The elucidation that urinary PGF(2alpha) in humans is derived from the IsoP pathway h
291                       Exposure to waterborne PGF(2alpha) induced a multitude of changes in male goldf
292 was to evaluate risk factors associated with PGF after heart transplantation.
293 s of pretransplant variables associated with PGF included: ischemic time, donor gender, donor age, mu
294 nd donor characteristics are associated with PGF.
295 ute treatment of FP(B)-expressing cells with PGF(2alpha) leads to a subcellular reorganization of bet
296 ansporter (hPGT), stimulation of the FP with PGF(2alpha) (1 nM-1 microM), or the less potent FP agoni
297 were significantly better in recipients with PGF (90% and 74%) versus DGF (79% and 54%) (P<0.002).
298 d for 24 hours with medium supplemented with PGF(2a), latanoprost acid, or vehicle.
299                               Treatment with PGF also reduced serum progesterone (P4) concentrations
300  luteal regression 24 h after treatment with PGF and were resistant to the PGF-induced decrease in P4

 
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