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1 served upon stimulation of HEK293 cells with prostaglandin E1.
2 onophosphate (cAMP)-dependent secretagogues, prostaglandin E1 (1 mumol/L), forskolin (1 mumol/L), and
4 not significantly different in the liposomal prostaglandin E1 (40%) or placebo-treated (37%) groups.
5 ing stimulated platelets with the inhibitory prostaglandin E1, a cyclic RGD peptide, the monoclonal a
6 patients with ARDS, treatment with liposomal prostaglandin E1 accelerated improvement in indexes of o
8 lation, 16.9 in patients receiving liposomal prostaglandin E1 and 19.6 in those administered placebo;
9 ntially inhibited by the platelet inhibitors prostaglandin E1 and theophylline, these inhibitors had
12 d in 69% of the patients receiving liposomal prostaglandin E1 compared with 33% of the placebo group,
13 data indicate that AS-013, a new prodrug of prostaglandin E1, could provide an effective and accepta
14 ndin E2 (PGE2), TxB2, and 6-keto PGF1 alpha; prostaglandins E1, D2, and F2 alpha and leukotrienes B4
16 ratio >300 mm Hg: 9.8 days in the liposomal prostaglandin E1 group and 13.7 days in patients receivi
17 uation of ventilation, 10.3 in the liposomal prostaglandin E1 group and 16.3 days in patients receivi
18 mortality, 57 of 176 (32%) in the liposomal prostaglandin E1 group and 50 of 170 (29%) in patients r
19 continuation of ventilation in the liposomal prostaglandin E1 group compared with the placebo group (
21 clinical trial of AS-0:3, a novel prodrug of prostaglandin E1 incorporated into lipid microspheres th
22 timulated phosphoprotein phosphorylation and prostaglandin E1-induced increase in cyclic adenosine mo
23 We evaluated a system by which alprostadil (prostaglandin E1) is delivered transurethrally to treat
24 tify risk factors; 4) routine use of BAS and prostaglandin E1 may not be indicated in all cases; 5) e
25 l dose (i.e., > 45.9 microg/kg) of liposomal prostaglandin E1 (median number of days to discontinuati
26 was similar among patients in the liposomal prostaglandin E1 (n = 177) and the placebo (n = 171) tre
29 monophosphorothioate, Sp-isomer (Sp-cAMPS), prostaglandin E1, or the adenosine A2A receptor is suffi
30 prostaglandin E2 (PGE2) (P<0.01), 400% more prostaglandin E1 (PGE1) (P<0.01), and 250% more cAMP (P<
35 synthetic bicyclic fatty acid derivative of prostaglandin E1 (PGE1) used for chronic constipation.
37 imulated (in response to isoproterenol), and prostaglandin E1 (PGE1)-stimulated lymphocyte adenylyl c
39 30 min resulted in a significant increase in prostaglandin E1-stimulated cAMP accumulation in cells e
41 icant attenuation of isoproterenol-, but not prostaglandin E1-, stimulated adenylylcyclase activity.
42 linolenic acid diet released 35% or 24% more prostaglandin E1 than macrophages from rats given either
43 surgical timing, balloon atrial septostomy, prostaglandin E1 therapy, intraoperative techniques, ima
44 a (occurring in 52% and 24% of the liposomal prostaglandin E1-treated patients, respectively, and 17%
45 Scatchard analysis of the binding of [3H]prostaglandin E1, used as a prostacyclin receptor probe,
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