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3 -dinor thromboxane B(2) and 2,3-dinor-6-keto prostaglandin F(1 alpha), metabolites of thromboxane and
4 ary excretion of thromboxane B(2) and 6-keto-prostaglandin F(1)(alpha) and the ratio of the 2 compoun
5 te and nitrite (+36% versus +2%), and 6-keto-prostaglandin F(1alpha) (+71% versus +1%), whereas it de
6 ogen (BUN); thromboxane B2 (TXB2) and 6-keto prostaglandin F(1alpha) (6 kPGF(2alpha)) levels; creatin
8 elial cells synthesized twice as much 6-keto-prostaglandin F(1alpha) (P<0.01) and 16% less leukotrien
11 Plasma levels of nitrate and nitrite, 6-keto-prostaglandin F(1alpha), endothelin-1, asymmetrical dime
12 oxane B(2) (TXB(2)) and prostacyclin (6-keto prostaglandin F(1alpha); 6-keto PGF(1alpha)) metabolite
15 concentrations of an F(2)-isoprostane, 8-epi-prostaglandin F(2)(alpha) (8-epi-PGF(2)(alpha)), a bioma
18 tent organic nitrate administration on 8-epi prostaglandin F(2alpha) (8-epi PGF(2alpha)) content and
20 ing kidneys showed >2-fold increase in 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)) levels compa
21 veloped for the measurement of urinary 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)), a biomarker
22 mean changes (and 95% CIs) in urinary 8-iso-prostaglandin F(2alpha) (pg/mg creatinine) were 9.0 (-12
23 shown that stimulation of both isoforms with prostaglandin F(2alpha) (PGF(2alpha)) activates the smal
25 erential effects of two hormonal pheromones, prostaglandin F(2alpha) (PGF(2alpha)) and 17alpha,20beta
26 isoprostanes are stereo- and regioisomers of prostaglandin F(2alpha) (PGF(2alpha)) and are used as bi
33 P) are G protein-coupled receptors that bind prostaglandin F(2alpha) (PGF(2alpha)), resulting in the
35 2)>6-keto prostaglandin F1alpha (PGF1alpha), prostaglandin F(2alpha) (PGF2alpha), and prostaglandin D
36 s G(q) in preference to G(13), whereas 8-iso-prostaglandin F(2alpha) activates G(13) in preference to
38 ally, rings from remodeled LCs contracted to prostaglandin F(2alpha) and relaxed to acetylcholine in
39 actions of other neurohormones (endothelin, prostaglandin F(2alpha) angiotensin II) that also act on
40 onatal uterus was responsive to carbachol or prostaglandin F(2alpha) application; it showed a marked
42 ntrations nor the percentage change in 8-iso-prostaglandin F(2alpha) differed significantly among tre
44 crog/mL of either latanoprost (free acid) or prostaglandin F(2alpha) ethanolamide and compared with c
47 exes is identified here as FPRP, the 133-kDa prostaglandin F(2alpha) receptor regulatory protein.
49 ither the FP(A) or the FP(B) receptor cDNAs, prostaglandin F(2alpha) stimulates inositol phosphate ac
51 xposed to Ad.CMVeNOS, maximum contraction to prostaglandin F(2alpha) was reduced compared with viral
52 1401 U/L), blood urea (53 mg/dl), and 8-iso-prostaglandin F(2alpha), a marker of oxidative stress (3
53 ng blood glucose, and the excretion of 8-iso-prostaglandin F(2alpha), a measure of oxidative stress,
54 LC-MS/MS) method to quantify 2,3-dinor-8-iso prostaglandin F(2alpha), a urinary metabolite of 8-iso-p
55 n and quantification of different isomers of prostaglandin F(2alpha), including 8-iso-PGF(2alpha), fo
56 alpha(1)-adrenergic agonists, endothelin-1, prostaglandin F(2alpha), interleukin 1beta, and phorbol
58 were changes from baseline in urinary 8-iso-prostaglandin F(2alpha), urinary malondialdehyde + 4-hyd
59 d urinary excretion of the isoprostane 8-iso-prostaglandin F(2alpha), which is an indicator of oxidat
65 din F(2alpha), a urinary metabolite of 8-iso-prostaglandin F(2alpha.) Urine was purified by solid-pha
67 (protein carbonyls, oxidized LDLs, and 8-iso-prostaglandin-F(2alpha)) were measured at baseline and 6
68 fect in reducing protein carbonyls and 8-iso-prostaglandin-F(2alpha); the reductions were 6-8% and 4-
69 ncentrations of tumor necrosis factor (TNF), prostaglandin F(6-keto-PGF1 alpha), and interleukin (IL)
70 alpha that no ligand tested, including 8-iso-prostaglandin F (8-iso-PGF2alpha and a purported antagon
71 ly in the potential of the isoprostane 8-iso-prostaglandin F (8-iso-PGF2alpha), among other ligands e
72 l C(1) alkylphosphinic acid analogues of the prostaglandin-F family have been evaluated at the eight
73 Omidenpag isopropyl (OMDI) in comparison to prostaglandin F(FP) agonists used in glaucoma management
74 P (1.55-fold), Isoprostane-8 (1.34-fold) and prostaglandin F metabolites (1.97-fold) were lower in CO
77 ivity was not limited to TP receptor because prostaglandin F receptor activated with U46619 and prost
78 type-4 chemokine receptors, but not for the prostaglandin F receptor that cannot interact with beta-
79 le 2, potassium inwardly-rectifying channel, prostaglandin F receptor, and RXR-beta cis-11-retinoic a
80 rm of which is a dual agonist targeting both prostaglandin F receptors and prostaglandin E receptor 3
81 We found that agonist-mediated activation of prostaglandin F receptors and prostaglandin E(2) recepto
84 We infer from the phylogenetic analysis that prostaglandin F synthase may represent a recent recruit
85 ebrate hydroxysteroid dehydrogenase enzymes, prostaglandin F synthase, and rho-crystallin of Xenopus
86 rostaglandin F synthases, such as prostamide/prostaglandin F synthase, to prostaglandin F2alpha ethan
87 ndamide may be converted by PTGS2 (COX2) and prostaglandin F synthases, such as prostamide/prostaglan