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1 ayed a distinct sensitivity to cicaprost and iloprost.
2 aspirin, MRS-2179 (a P2Y(1) inhibitor), and iloprost.
3 nd without the prostacyclin receptor agonist iloprost.
4 , similar to the effect of the PGI(2) analog iloprost.
5 rial hypertension (PAH) treated with inhaled iloprost.
6 esence of 4.8 microM pentoxyfilline or 80 nM iloprost.
7 filline and a 10% increase when treated with iloprost.
8 sed Fzd9 expression and prevents response to iloprost.
9 sal levels of ERK phosphorylation induced by iloprost.
10 were blocked by the MEK inhibitor, U0126, or iloprost.
11 hile dose-dependent NO release was evoked by iloprost.
12 low-dose, continuous intravenous infusion of iloprost (0.075 microg/kg/min) or an equivalent volume o
13 randomized to receive a constant infusion of iloprost (0.18 microg/kg/min) or an equivalent amount of
17 nts (59%) received active therapy (101 [15%] iloprost, 118 [18%] sitaxsentan, 204 [31%] sildenafil, a
18 randomized to receive a constant infusion of iloprost (20 ng/kg per minute) or an equivalent amount o
19 tagged hIP (hIP1D4) wild-type control (K(i), iloprost = 3 +/- 2 versus 7 +/- 3 nM, respectively).
20 ed, multicenter, double-blind trial, inhaled iloprost (5 mug) or placebo was added to stable monother
25 ion of pial arteriolar responses to ET-1 and iloprost, a cAMP-dependent dilator, in vivo, plus the ef
27 Treatment of COX-2-deficient PASMCs with iloprost, a prostaglandin I(2) analog, and prostaglandin
29 hypoxia or adenosine, but not that evoked by iloprost, a stable analogue of prostacyclin (PGI(2)), or
31 erns in human platelets after treatment with iloprost, a stable prostacyclin analog, for 0, 10, 30, a
33 hat, although the stable prostacyclin analog iloprost alone had no effect on the intracellular calciu
40 +/- 3.6 pmol/mg protein; n = 4) affinity for iloprost and coupled to both cAMP (EC50 = 0.1 +/- 0.03 n
41 agonists (ADP, convulxin, thrombin, U46619, iloprost and GSNO used at 0.1, 1, and 10xEC50; 154 condi
44 lls responded only to high concentrations of iloprost and N(7),N(78)-Q(7),Q(78) were unresponsive.
46 tion and time of exposure to the PGI2 analog iloprost and was blocked by both RO3244794 and PKA knock
47 on and time of exposure to the PGI(2) analog iloprost and was blocked by both RO3244794 and PKA knock
48 re the inhaled prostanoids (prostacyclin and iloprost), and there is growing interest in novel therap
52 prove blood flow in vivo (pentoxyfilline and iloprost) are shown to increase both the release of RBC-
53 either a continuous intravenous infusion of iloprost at 0.075 microg/kg/min (n = 6) or an equal volu
56 lammation suggest that PGI2 and its analogue iloprost, both Food and Drug Administration-approved dru
61 ilator responses, elicited by acetylcholine, iloprost, cromakalim, and elevated [K+], were greatly di
66 ving long-term iloprost therapy, 36% stopped iloprost, due to lower airway reactivity, clinical deter
70 Several studies show efficacy of intravenous iloprost for severe Raynaud's and skin ulcers, and of bo
73 e daily frequency of attacks was 1.02 in the iloprost group and 0.83 in the placebo group (P = 0.459)
74 ty of RP attacks, was reduced by 1.32 in the iloprost group and 1.00 in the placebo group (P = 0.323)
75 events occurred in 10 patients (6.4%) in the iloprost group and 3 (2.0%) in the placebo group (P = 0.
76 aseline to week 5-6 was 24.32 minutes in the iloprost group and 34.34 minutes in the placebo group (P
77 fter the tamponade (422 +/- 87 mL/min in the iloprost group vs. 232 +/- 111 mL/min in the control gro
81 Only during the postburn endotoxic phase, iloprost improved hDO2 and hVO2 (140% and 79%, respectiv
82 udy demonstrate that the addition of inhaled iloprost in patients with PAH with reduced exercise capa
83 enous bradykinin, inhaled NO, or intravenous iloprost in reducing right ventricular systolic pressure
84 ase in RBC-derived ATP was also measured for iloprost-incubated RBCs in flow (362 +/- 45 nM ATP).
87 nduced a rapid desensitization of subsequent iloprost-induced (1 microM) HAhIP and S374A adenylyl cyc
88 Thus, cerebral hematoma appears to attenuate iloprost-induced dilation and reduce basal cAMP level 4
97 ndard lung function testing before and after iloprost inhalation, 6-min walk test, World Health Organ
100 duced MCP-1 production and demonstrated that iloprost inhibited STAT1 activation by several actions a
101 activation by several actions as follows: 1) iloprost inhibited the phosphorylation of STAT1-S727 in
104 tes IFN-gamma-signaling, was not involved in iloprost-mediated inhibition of STAT1, indicating diverg
105 e therapies using either Wnt7a or its mimic, Iloprost, might represent a new class of therapeutic tre
107 d attenuation of pial arteriolar dilation to iloprost on day 4 (14%, 21% and 29% at 10(-12) M, 10(-10
108 We evaluated the acute effects of inhaled iloprost on hemodynamic status and lung function and the
109 lar inflammation, we examined the effects of iloprost on IFN-gamma- and IL-6-stimulated cytokine prod
114 Pericardial fluid was then removed, and iloprost or normal saline infusion was continued for ano
115 ericardial tamponade was induced, during the iloprost or normal saline infusion with pericardial tamp
118 of COX-1 were rescued by the treatment with iloprost or the selective peroxisome proliferator-activa
119 elaxation responses to sodium nitroprusside, iloprost, or the K(+) channel activators (NS1619 and bim
120 omly assigned to receive either 50 microg of iloprost orally twice daily or an identical gelatin-coat
122 a 2-hr storage, beta-NTP regeneration in mUW+iloprost produced +57.7% (P<0.01) more beta-NTP, at a fa
123 PKA by injection of the prostacyclin analog iloprost reduced PAK activation and inflammatory gene ex
125 rmer smokers using the prostacyclin analogue iloprost reduces endobronchial dysplasia, a premalignant
131 tylase and coactivator CBP/p300 to STAT1; 2) iloprost selectively inhibited activation of JAK2 but no
132 f the mutant receptors by PGE2 (EP2 ligand), iloprost (stable prostacyclin analog), and PGE1 (EP2/IP
133 inhibitor milrinone mirrored the actions of iloprost, suggesting that the prostacyclin analog exerte
134 demonstrate an inverse regulation by ADP and Iloprost, suggesting that these are central modulators o
135 7 nm) was evident at those concentrations of iloprost that induce PKC-dependent desensitization.
137 nt of patients continued receiving long-term iloprost therapy, 36% stopped iloprost, due to lower air
138 y provides new information on the ability of iloprost to primarily attenuate inositol-1,4,5-triphosph
141 e cardiac output returned to baseline in the iloprost-treated group but remained decreased in the con
148 inally, a known inhibitor of CTGF synthesis, Iloprost, was administered to 2-AAF/PHx treated rats to
150 otein phosphorylation in response to ADP and Iloprost, which inversely overlap and represent major ac
151 resulted in a selective gain of function for iloprost, which is consistent with the proposed phylogen
153 ependently dilated to topical application of iloprost with increases in diameter of 10%, 16% and 21%
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