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1 PGF2alpha also activates the extracellular signal-regula
2 PGF2alpha also induced eIF4E and 4E-BP1 phosphorylation,
3 PGF2alpha induced the activities of extracellular signal
4 PGF2alpha-induced phosphorylation of eIF4E and 4E-BP1 wa
5 PGF2alpha-induced up-regulation of Cyr61 appeared to exc
6 ertrophic agonists in culture, endothelin-1, PGF2alpha, and phorbol 12-myristate 13-acetate, also ind
7 cosanoids analyzed, tetranor-PGEM and 11beta-PGF2alpha as well as 11-dehydro-TXB2 showed a significan
8 in PGF2alpha-induced activation of ERK2; 2) PGF2alpha-induced eIF4E and 4E-BP1 phosphorylation appea
11 d decreased myometrial NF-kappaB activation, PGF2alpha, and expression of contraction-associated gene
12 ted amniotic fluid IL-1beta, IL-6, IL-8, and PGF2alpha, resulting in PTB and marked neonatal mortalit
13 ane B2 (TXB2 ) were quantified by ELISA, and PGF2alpha (FP) and thromboxane A2 (TP) receptor expressi
14 novel functions for parasite-derived LBs and PGF2alpha in the cellular metabolism of Leishmania and i
16 rations of TXB2 (stable TXA2 metabolite) and PGF2alpha , soluble cell adhesion molecules and blood pr
17 ther cycloxygenase products, PGE2, PGD2, and PGF2alpha, failed to activate p38 kinase in aspirin-trea
20 sanoids, such as prostaglandin E2 (PGE2) and PGF2alpha, precedes the onset of labor as a result of in
21 taglandin profile: TxB2>6-keto PGF1alpha and PGF2alpha>PGE2, despite the comparable release of total
23 Recombinant trout Tnfalpha (rTnfalpha) and PGF2alpha recapitulate the stimulatory in vitro effects
24 the cyclooxygenase products thromboxane and PGF2alpha are released from coronary artery PVAT from pi
25 of inositol phosphates to the same extent as PGF2alpha in cells expressing either the FPA or FPB isof
26 of FPB-expressing cells with PGE2-attenuated PGF2alpha-stimulated Tcf/beta-catenin signaling in a dos
33 n of intraocular pressure in cats induced by PGF2alpha is mediated by FP or other prostaglandin recep
37 ntraocular pressure, indicating that in cats PGF2alpha and 17-phenyl trinor PGE2 act on the same rece
41 the four Gq/Gi-coupled receptors [EP1, EP3, PGF2alpha (FP), thromboxane A2 (TP)] suggests that prost
46 e blockade by thromboxane antagonists, 8-epi PGF2alpha does not activate either of the thromboxane re
49 receptor by systemic concentrations of 8-epi PGF2alpha is unlikely to occur, even in syndromes of exc
54 ute MI (105+/-17.8 versus 230+/-66 for 8-epi-PGF2alpha [P=.009] and 466+/-91 versus 833+/-153 for IPF
56 atosus had higher urinary excretion of 8-epi-PGF2alpha and IPF2alpha -I than controls; urinary excret
57 urinary excretion of two isoprostanes, 8-epi-PGF2alpha and IPF2alpha -I, free radical catalyzed oxida
58 (r=.68, P<.0001; n=33) between urinary 8-epi-PGF2alpha and IPF2alpha-I levels in patients receiving t
61 on, human monocytes may form bioactive 8-epi-PGF2alpha either via free radical- or enzyme-catalyzed p
64 There was a slight increase in urinary 8-epi-PGF2alpha levels (64.7+/-9.5 versus 84.9+/-10.6; P=.02)
68 (previously called 8-iso-PGF2alpha or 8-epi-PGF2alpha), which demonstrated the utility of monitoring
70 ith L 745,337, suppressed formation of 8-epi-PGF2alpha, thiobarbituric acid-reactive substances, and
71 a (TNFalpha) and prostaglandin (PG) F2alpha (PGF2alpha) are involved in the control of ovulation but
72 n (NPV) stimulated by prostaglandin F2alpha (PGF2alpha ) and by the drug LY83583, which causes contra
73 boxane A2 (TXA2 ) and prostaglandin F2alpha (PGF2alpha ), on skin microcirculatory blood flow, as wel
75 We demonstrate that prostaglandin F2alpha (PGF2alpha) as well as two analogues augment muscle cell
77 type I (AT1R) and the prostaglandin F2alpha (PGF2alpha) F prostanoid (FP) receptors are both potent r
81 rogesterone (DHP) and prostaglandin F2alpha (PGF2alpha) levels rise in teleost fish around the time o
82 COX) enzyme product, prostaglandin F2alpha (PGF2alpha), has exhibited promise as an index of oxidant
84 endent relaxations in prostaglandin F2alpha (PGF2alpha)-contracted strips of porcine coronary artery.
85 and the mechanisms of prostaglandin F2alpha (PGF2alpha)-induced protein synthesis in vascular smooth
89 se using progesterone, prostaglandin F2alpha(PGF2alpha) and pregnant mare serum gonadotrophin (PMSG).
91 ated intracellular pathways are required for PGF2alpha to induce morphological and genetic features c
92 lpha, and the isoform NFATC2 is required for PGF2alpha-induced muscle cell growth and nuclear accreti
94 al hydrophobic cavity, thereby preventing FP-PGF2alpha interaction and suppressing the production of
96 in the following order of activity: PGE2-G > PGF2alpha-G > PGD2-G; LYPLA2 hydrolyzed 1- but not 2-ara
98 ence that the Tnfalpha-dependent increase in PGF2alpha production is necessary for the pro-ovulatory
100 ependent mechanisms appear to be involved in PGF2alpha-induced activation of ERK2; 2) PGF2alpha-induc
106 , urinary 8-iso prostaglandin F2alpha (8-iso PGF2alpha) as a marker of oxidative stress, and gastric
107 the plasma marker of oxidative stress, 8-iso PGF2alpha, was increased in PHF animals (P < 0.01).
109 hese observations, only PGF2alpha and 12-iso-PGF2alpha caused rapid homologous desensitization of FP
111 o be activated by the F2 isoprostane, 12-iso-PGF2alpha, in addition to its cognate ligand, PGF2alpha.
112 ree radical-catalyzed F2 isoprostane, 12-iso-PGF2alpha, in addition to the cyclooxygenase product, PG
116 sted, including 8-iso-prostaglandin F (8-iso-PGF2alpha and a purported antagonist (pinane thromboxane
117 er and a strong association of urinary 8-iso-PGF2alpha and of serum soluble NOX2-derived peptide with
118 her (p < 0.001) mean values of urinary 8-iso-PGF2alpha and of serum soluble NOX2-derived peptide, ala
121 present study shows the potential for 8-iso-PGF2alpha as a wastewater biomarker for the assessment o
124 as associated with a 4.50% decrease in 8-iso-PGF2alpha concentrations (95% CI: -6.32%, -2.65%) and a
130 Elevated serum and urine levels of 8-iso-PGF2alpha have been reported in a variety of diseases, m
131 we investigated the potential role of 8-iso-PGF2alpha in inflammation, focusing on its effects on ad
132 he estimated per capita daily loads of 8-iso-PGF2alpha in the 11 cities ranged between 2.5 and 9.9 mg
134 (CM) transfer experiments suggest that 8-iso-PGF2alpha induces a secondary mediator, which also suppr
135 pha-I, (IPF2alpha-I) a class I isomer (8-iso-PGF2alpha is class IV), using gas chromatography/mass sp
138 2-iP, iPF2alpha-III (previously called 8-iso-PGF2alpha or 8-epi-PGF2alpha), which demonstrated the ut
140 re patient on hemodialysis and urinary 8-iso-PGF2alpha was 7.1-fold higher in a cigarette smoker than
141 nificant reduction in the excretion of 8-iso-PGF2alpha was induced by the run-in diet and the high-VF
144 iet, whereas urinary concentrations of 8-iso-PGF2alpha were further reduced (P < 0.01) by the high-VF
145 In addition, the levels of urinary 8-iso-PGF2alpha were independent predictors of non-alcoholic f
149 Cell 16 (CC16) and 15-isoprostane F2t (8-iso-PGF2alpha) levels were used to assess lung injury and ov
150 his work, 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha) was analysed in raw 24 h-composite wastewater
151 ry excretion of 8-isoprostane F2alpha (8-iso-PGF2alpha) was used as an index of whole-body lipid pero
152 ma concentrations of F(2)-isoprostane (8-iso-PGF2alpha), 9-hydroxyoctadecadieneoic acid (9-HODE), and
153 the isoprostane 8-iso-prostaglandin F (8-iso-PGF2alpha), among other ligands examined, to activate G1
155 ro-15-F2t-IsoP (2,3-dinor-5, 6-dihydro-8-iso-PGF2alpha), by gas chromotography/negative ion chemical
158 poral trends observed in the levels of 8-iso-PGF2alpha, however, spatial differences were found at th
161 assessed by measuring the isoprostane 8-iso-PGF2alpha, was decreased in the lungs of GM-/- mice.
162 eralfold as abundant in human urine as 8-iso-PGF2alpha, with mean values of 737 +/- 20.6 pg/mg creati
163 mplicated p38 and JNK, but not ERK, in 8-iso-PGF2alpha-induced suppression of monocyte adhesion.
168 28767, and misoprostol but not with 10(-6) M PGF2alpha, PGD2, PGI2, or butaprost, suggesting a princi
169 ha levels in PVAT between females and males, PGF2alpha produced a larger contraction in arteries from
171 c-fos and identify the diffusable messenger PGF2alpha as obligatory for NMDA receptor-mediated trans
172 ction of intraocular pressure by 50.0 microg PGF2alpha was 5.0+/-1.4 mm Hg, whereas that by 50 microg
176 oportion of the ocular hypotensive action of PGF2alpha in cats is mediated by EP1 but not by FP recep
177 y isoprostanes may complement the actions of PGF2alpha in clinical syndromes where oxidant stress and
179 We conclude that the 22-carbon analogue of PGF2alpha, produced from docosahexaenoic acid by a cyclo
182 ent administration of 12.5 microg of each of PGF2alpha and 17-phenyl trinor PGE2 did not produce an a
186 se relationship exists between the levels of PGF2alpha and a steroid-inducible anti-inflammatory prot
188 ty by PD 098059 led to a significant loss of PGF2alpha-induced eIF4E and 4E-BP1 phosphorylation, glob
191 e-dependent manner while having no effect on PGF2alpha-stimulated inositol phosphates formation.
193 Consistent with these observations, only PGF2alpha and 12-iso-PGF2alpha caused rapid homologous d
194 PGF2alpha-G and PGD2-EA, but not PGE2-EA or PGF2alpha-EA, also increased the frequency of mIPSCs.
195 er PGT nor PG15DH, exogenously added PGE2 or PGF2alpha were rapidly oxidized to the 13, 14-dihydro, 1
197 because unreactive lipids, e.g. PGB1, PGE2, PGF2alpha, and TxB2, did not inhibit LKB1 activity (p >
198 nhibitor of p70(S6k), also failed to prevent PGF2alpha-induced global protein synthesis and bFGF-2 ex
200 synthesis of the most complex prostaglandin, PGF2alpha, with high levels of control of relative and a
202 triggers the synthesis of the prostaglandins PGF2alpha and PGE2, but not PGD2, in rat cerebral cortic
204 n by binding and most likely by sequestering PGF2alpha into its central hydrophobic cavity, thereby p
207 , induced mkp1 mRNA to a greater extent than PGF2alpha and fluprostenol, which activate PKC signaling
208 alpha was less potent (EC50 = 5 microM) than PGF2alpha (EC50 = 10 nM) in generating inositol phosphat
212 minant-interfering proteins demonstrate that PGF2alpha-induced myocyte hypertrophy occurs independent
215 ne chip technology, we first identified that PGF2alpha dramatically up-regulated Cyr61 and CTGF mRNA
216 c ring contraction experiments revealed that PGF2alpha-dependent activation of FP potentiated angiote
223 This increased myotube size is not due to PGF2alpha-enhancing cell fusion that initially forms myo
224 roxylamine (HA, 100 mum), altered the NPV to PGF2alpha (BCA increased, HA inhibited) and/or LY83583 (
225 that initially forms myotubes, but rather to PGF2alpha recruiting the fusion of cells with preexistin
226 suggest that GPCR activation in response to PGF2alpha stimulates the mTOR pathway which increases th
233 intraocular pressure and pupil responses to PGF2alpha, are mediated by EP1 and FP receptors, respect
234 om female animals and greater sensitivity to PGF2alpha in the porcine coronary artery from males.
235 (TxS), and the receptors for TxA2 (the TP), PGF2alpha (the FP), and PGI2 (the IP) were upregulated a
236 anges in c-Jun-dependent gene transcription, PGF2alpha preferentially activates the MEK-Erk2- cytosol
237 trictor responses to norepinephrine, U46619, PGF2alpha, vasopressin, BAY K8644; biphasic responses to
240 ontraction in arteries from females, whereas PGF2alpha appears to mediate the contraction in arteries
241 eriments were performed to determine whether PGF2alpha stimulates the mammalian target of rapamycin (
242 ar sex differences in PVAT function in which PGF2alpha and TXA2 antagonists can inhibit the PVAT-indu
243 indings are consistent with a model in which PGF2alpha communicates fertility status via Ptgfr to cir
244 GE2 has much lower efficacy as compared with PGF2alpha for the activation of Tcf/beta-catenin signali
246 ependent p70(S6k) activation correlates with PGF2alpha-induced global protein synthesis and bFGF-2 ex
247 d also exhibited cross-desensitization, with PGF2alpha resulting in a maximum of approximately 60% de
248 in monolayer cultures and were treated with PGF2alpha, 11-deoxy-PGE1, or PhXA85 (the nonesterified a
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