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1 spectrometry as 2,3-dinor-5, 6-dihydro-8-iso-prostaglandin F2alpha.
2                                              Prostaglandin F2alpha (0.01 micromol/L; n=6), which redu
3  to 10(-6) mol/L), KCl (5 to 50 mmol/L), and prostaglandin F2alpha (10(-9) to 10(-6) mol/L) was compa
4 retory phospholipase A2 (sPLA2 ), and 11beta prostaglandin F2alpha (11betaPGF2alpha ), and, in a subg
5 nary metabolite of 15-F2t-isoprostane (8-iso-prostaglandin-F2alpha), 2,3-dinor-5,6-dihydro-F2t-IsoP,
6 ntake of dietary antioxidants, urinary 8-iso prostaglandin F2alpha (8-iso PGF2alpha) as a marker of o
7                          In this work, 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha) was analysed in
8 ore abundant F2-isoprostanes produced, 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha).
9 ell as products of lipid peroxidation (8-iso-prostaglandin F2alpha (8-isoPF2alpha) and 4-hydroxy-2-no
10 third trimesters) and included 8-isoprostane-prostaglandin-F2alpha (8-iso-PGF2alpha), 2,3-dinor-5,6-d
11                   Urinary excretion of 8-iso-prostaglandin F2alpha, an isomer of the PGG/H synthase (
12                                              Prostaglandin F2alpha analog plus BAB or ROCKI showed an
13           The medications evaluated included prostaglandin F2alpha analogs (PGFAs), nitric oxide-dona
14                               Latanoprost, a prostaglandin F2alpha analogue, reduces IOP and is used
15  inflammation-initiating mediators including prostaglandin F2alpha and leukotriene B4 and pro-resolvi
16 dative stress was assessed by urinary 8-iso- prostaglandin F2alpha and serum soluble NOX2-derived pep
17 ssess the relationship between urinary 8-iso-prostaglandin F2alpha and serum soluble NOX2-derived pep
18 inflammation-initiating mediators (including prostaglandin F2alpha) and select proresolving pathways
19 NEAC); 2) markers of systemic (urinary 8-iso-prostaglandin-F2alpha) and muscle (carbonylated protein
20  D2 (DP)1, DP2, prostaglandin E2 (EP)1, EP4, prostaglandin F2alpha, and thromboxane A2 receptors but
21 The identification of 2, 3-dinor-5,6-dihydro-prostaglandin F2alpha as the major urinary metabolite of
22   Selective inhibition of PGF2alphaEA versus prostaglandin F2alpha biosynthesis accelerates adipogene
23 h as prostamide/prostaglandin F synthase, to prostaglandin F2alpha ethanolamide (PGF2alphaEA), of whi
24 e eye of each cat was treated topically with prostaglandin F2alpha, fluprostenol (FP receptor agonist
25 ntiated constriction of isolated arteries to prostaglandin F2alpha in proportion to the amount of PVA
26                                  Addition of prostaglandin F2alpha, known to limit PPARgamma activity
27 lhistamine (P < .01) and 2,3-dinor-11beta-prostaglandin F2alpha (P < .05).
28 tion of labor, prostaglandin E2 (PGE(2)) and prostaglandin F2alpha (PGF(2alpha)), are enzymatically d
29 lmonary vasoconstriction (NPV) stimulated by prostaglandin F2alpha (PGF2alpha ) and by the drug LY835
30 r prostaglandins, thromboxane A2 (TXA2 ) and prostaglandin F2alpha (PGF2alpha ), on skin microcircula
31                                        Thus, prostaglandin F2alpha (PGF2alpha) (FP receptor agonist),
32                          We demonstrate that prostaglandin F2alpha (PGF2alpha) as well as two analogu
33                                 For example, prostaglandin F2alpha (PGF2alpha) causes hypertrophy of
34     The angiotensin II type I (AT1R) and the prostaglandin F2alpha (PGF2alpha) F prostanoid (FP) rece
35  the role of parasite LBs in biosynthesis of prostaglandin F2alpha (PGF2alpha) has not been investiga
36                                              Prostaglandin F2alpha (PGF2alpha) is a product of cycloo
37                                              Prostaglandin F2alpha (PGF2alpha) is an important mediat
38 alpha,20beta-dihydroxyprogesterone (DHP) and prostaglandin F2alpha (PGF2alpha) levels rise in teleost
39 hase (cyclooxygenase or COX) enzyme product, prostaglandin F2alpha (PGF2alpha), has exhibited promise
40                                              Prostaglandin F2alpha (PGF2alpha), which is released fro
41 licited endothelium-dependent relaxations in prostaglandin F2alpha (PGF2alpha)-contracted strips of p
42              To understand the mechanisms of prostaglandin F2alpha (PGF2alpha)-induced protein synthe
43 tion of inflammatory lipid mediators such as prostaglandin F2alpha (PGF2alpha).
44 ignaling pathways by their endogenous ligand prostaglandin F2alpha (PGF2alpha).
45 -iPs, consists of four classes of isomers of prostaglandin F2alpha (PGF2alpha).
46 so-PGF2alpha, 2,3-dinor-8-iso-PGF2alpha, and prostaglandin-F2alpha (PGF2alpha).
47  to the follicular phase using progesterone, prostaglandin F2alpha(PGF2alpha) and pregnant mare serum
48  five primary prostanoids: prostaglandin E2, prostaglandin F2alpha, prostaglandin I2, thromboxane A2,
49 pha as the major urinary metabolite of 8-iso-prostaglandin F2alpha provides the basis for the develop
50 -2'-deoxyguanosine (r = 0.53, P < 0.001) and prostaglandin F2alpha (r = 0.26, P < 0.001), and the gre
51  E2 receptors (EPs) EP1 (266) and EP4 (117), prostaglandin F2alpha receptor (FP) (61), and thromboxan
52 s, angiotensin II type I receptor (AT1R) and prostaglandin F2alpha receptor (FP), bioluminescence res
53 used to develop allosteric modulators of the prostaglandin F2alpha receptor.
54 ivo administration of the luteolytic hormone prostaglandin F2alpha resulted in an upregulation of PLI
55 s secreted inflammatory mediators, including prostaglandin F2alpha, the cytokines TNF-alpha and IL-6,
56  the oxidant stress marker isoprostane 8-epi-prostaglandin F2alpha) were identical in incubations wit