ライフサイエンスコーパス: iloprost

1 ayed a distinct sensitivity to cicaprost and iloprost.

2 oprevention agent and prostacyclin analogue, iloprost.

3 ased sensitivity to the prostacyclin mimetic iloprost.

4 aspirin, MRS-2179 (a P2Y(1) inhibitor), and iloprost.

5 hosphodiesterase 5 inhibitors or intravenous iloprost.

6 nd without the prostacyclin receptor agonist iloprost.

7 , similar to the effect of the PGI(2) analog iloprost.

8 rial hypertension (PAH) treated with inhaled iloprost.

9 esence of 4.8 microM pentoxyfilline or 80 nM iloprost.

10 filline and a 10% increase when treated with iloprost.

11 sal levels of ERK phosphorylation induced by iloprost.

12 were blocked by the MEK inhibitor, U0126, or iloprost.

13 sed Fzd9 expression and prevents response to iloprost.

14 hile dose-dependent NO release was evoked by iloprost.

15 low-dose, continuous intravenous infusion of iloprost (0.075 microg/kg/min) or an equivalent volume o

16 randomized to receive a constant infusion of iloprost (0.18 microg/kg/min) or an equivalent amount of

17 Exposure of transfected cells to iloprost (1 microM) for increasing times induced a rapid

18 Iloprost (1 microM, 10 min) desensitized HAhIP- and S374

19 omized 1:1 to masked intravenous infusion of iloprost, 1 ng/kg/min (n = 142), or placebo (n = 137) fo

20 hock and severe endotheliopathy, infusion of iloprost, 1 ng/kg/min, for 72 hours did not reduce mean

21 in (mUW); mUW+adenosine (1.34 g/L), and mUW+ iloprost (10(-8)mol/L), a prostacyclin analogue.

22 nts (59%) received active therapy (101 [15%] iloprost, 118 [18%] sitaxsentan, 204 [31%] sildenafil, a

23 randomized to receive a constant infusion of iloprost (20 ng/kg per minute) or an equivalent amount o

24 tagged hIP (hIP1D4) wild-type control (K(i), iloprost = 3 +/- 2 versus 7 +/- 3 nM, respectively).

25 ed, multicenter, double-blind trial, inhaled iloprost (5 mug) or placebo was added to stable monother

26 Fifteen of these treated patients (8 iloprost, 7 placebo) failed to complete all of the follo

27 e in intracellular levels of cAMP induced by iloprost (a prostaglandin I2 analog).

28 capability as compared with control hMSCs or iloprost (a stable PGI2 analogue).

29 Iloprost (a stable prostaglandin I2 analog) -induced ris

30 ion of pial arteriolar responses to ET-1 and iloprost, a cAMP-dependent dilator, in vivo, plus the ef

31 Additionally, we identified Iloprost, a prostacyclin analog, which initiates downstr

32 Treatment of COX-2-deficient PASMCs with iloprost, a prostaglandin I(2) analog, and prostaglandin

33 Conversely, iloprost, a stable analog of PGI(2), augmented IL-17 pro

34 hypoxia or adenosine, but not that evoked by iloprost, a stable analogue of prostacyclin (PGI(2)), or

35 Both PGE2 and iloprost, a stable PGI2 analog, evoke human umbilical ve

36 erns in human platelets after treatment with iloprost, a stable prostacyclin analog, for 0, 10, 30, a

37 Iloprost administration blocked CTGF induction in treate

38 hat, although the stable prostacyclin analog iloprost alone had no effect on the intracellular calciu

39 Iloprost alone induced Id1 expression in human pulmonary

40 Iloprost also attenuated the sustained activation of ERK

41 hundred fifty seven were assigned to receive iloprost and 151 to receive placebo.

42 ic effects of prostacyclin analogues such as iloprost and carbaprostacyclin.

43 ostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.

44 Iloprost and cicaprost also suppressed LPS-induced expre

45 +/- 3.6 pmol/mg protein; n = 4) affinity for iloprost and coupled to both cAMP (EC50 = 0.1 +/- 0.03 n

46 agonists (ADP, convulxin, thrombin, U46619, iloprost and GSNO used at 0.1, 1, and 10xEC50; 154 condi

47 se with KT 5720 reversed the effects of both iloprost and milrinone.

48 date biomarkers for precision application of iloprost and monitoring of treatment progress.

49 lls responded only to high concentrations of iloprost and N(7),N(78)-Q(7),Q(78) were unresponsive.

50 In addition, iloprost and treprostinil enhanced BMP-induced phosphory

51 tion and time of exposure to the PGI2 analog iloprost and was blocked by both RO3244794 and PKA knock

52 on and time of exposure to the PGI(2) analog iloprost and was blocked by both RO3244794 and PKA knock

53 re the inhaled prostanoids (prostacyclin and iloprost), and there is growing interest in novel therap

54 subcutaneously infused treprostinil, inhaled iloprost, and oral beraprost.

55 es, including the stable prostacyclin analog iloprost, and suppressed cytokine-induced inflammation.

56 S328A and S328A/S374A showed a markedly less iloprost- and no PMA-induced phosphorylation.

57 HAhIP and S374A underwent iloprost- and PMA-induced phosphorylation (1 and 5 micro

58 prove blood flow in vivo (pentoxyfilline and iloprost) are shown to increase both the release of RBC-

59 either a continuous intravenous infusion of iloprost at 0.075 microg/kg/min (n = 6) or an equal volu

60 Oral iloprost at a dosage of 50 microg twice daily is no bett

61 PGI2 or iloprost at the IP receptor inhibited basal ERK phosphor

62 lammation suggest that PGI2 and its analogue iloprost, both Food and Drug Administration-approved dru

63 The effects of iloprost, carbaprostacyclin, and treprostinil on the reg

64 Inhaled iloprost caused sustained functional improvement in some

65 We report that PGI(2) analogs (iloprost, cicaprost, treprostinil) differentially modula

66 To investigate the relationship between iloprost, cigarette smoke, and Fzd9 expression, we used

67 ilator responses, elicited by acetylcholine, iloprost, cromakalim, and elevated [K+], were greatly di

68 ) increases expression of miR-520a-5p, while iloprost decreases expression.

69 Iloprost delayed the time to clinical worsening (p = 0.0

70 On the basis of the observation that iloprost did not alter thapsigargin stimulation of Ca(2+

71 Postburn administration of iloprost did not improve the hepatic arterial hemodynami

72 h septic shock and persistent hypoperfusion, iloprost did not reduce the severity of organ failure.

73 The concept that iloprost does not directly modulate calcium entry was fu

74 ving long-term iloprost therapy, 36% stopped iloprost, due to lower airway reactivity, clinical deter

75 Pretreatment with intravenous iloprost effectively increased intestinal blood flow in

76 r of FZD9 activity and a mediator of CSC and iloprost effects in the lung.

77 Iloprost failed to reverse PPARdelta siRNA-induced impai

78 Iloprost failed to suppress AM functions to the same deg

79 Several studies show efficacy of intravenous iloprost for severe Raynaud's and skin ulcers, and of bo

80 e baseline levels in animals pretreated with iloprost (from 363 +/- 85 to 485 +/- 81 mL/min).

81 One hundred forty-three patients in the iloprost group (91.1%) and 144 in the placebo group (95.

82 anges in SOFA score were -4 (-7 to 7) in the iloprost group and -5 (-8 to 5) in the placebo group (me

83 e daily frequency of attacks was 1.02 in the iloprost group and 0.83 in the placebo group (P = 0.459)

84 ty of RP attacks, was reduced by 1.32 in the iloprost group and 1.00 in the placebo group (P = 0.323)

85 daily SOFA score was 10.6 (6.4-14.8) in the iloprost group and 10.5 (5.9-15.5) in the placebo group

86 9 [58-77] years; 171 (62%) male), 142 in the iloprost group and 136 in the placebo group.

87 events occurred in 10 patients (6.4%) in the iloprost group and 3 (2.0%) in the placebo group (P = 0.

88 aseline to week 5-6 was 24.32 minutes in the iloprost group and 34.34 minutes in the placebo group (P

89 t 28 days, 48 patients (42%) had died in the iloprost group and 47 (39%) had died in the placebo grou

90 se events occurred in 15% of patients in the iloprost group and 7% of patients in the placebo group (

91 occurred in 26 of 142 patients (18%) for the iloprost group vs 20 of 136 patients (15%) for the place

92 fter the tamponade (422 +/- 87 mL/min in the iloprost group vs. 232 +/- 111 mL/min in the control gro

93 Mortality at 90 days in the iloprost group was 57% (81 of 142) vs 51% (70 of 136) in

94 verage SOFA score was 11.2 (7.4-15.9) in the iloprost group, compared with 10.5 (6.8-16.5) in the pla

95 At Week 12, patients receiving iloprost had a mean increase in 6-MWD of 30 m (p = 0.001

96 Since low-dose iloprost had no effect on mean arterial pressure, it may

97 Inhaled iloprost has been approved for the treatment of adults w

98 Only during the postburn endotoxic phase, iloprost improved hDO2 and hVO2 (140% and 79%, respectiv

99 udy demonstrate that the addition of inhaled iloprost in patients with PAH with reduced exercise capa

100 enous bradykinin, inhaled NO, or intravenous iloprost in reducing right ventricular systolic pressure

101 ase in RBC-derived ATP was also measured for iloprost-incubated RBCs in flow (362 +/- 45 nM ATP).

102 Stimulation of transfected cells with iloprost induced a rapid time- and concentration-depende

103 Iloprost induced a time- and concentration-dependent los

104 nduced a rapid desensitization of subsequent iloprost-induced (1 microM) HAhIP and S374A adenylyl cyc

105 Thus, cerebral hematoma appears to attenuate iloprost-induced dilation and reduce basal cAMP level 4

106 Iloprost-induced dilation was attenuated by hematoma to

107 sal phosphorylation and dramatically reduced iloprost-induced HAhIP phosphorylation.

108 Deletion of the C terminus prevented iloprost-induced internalization, demonstrating the crit

109 Iloprost-induced sequestration of HAhIP-GFP, followed in

110 These data suggest that iloprost induces apoptosis via a cAMP-mediated suppressi

111 Iloprost infusion increased SMA blood flow by 60% in thi

112 The effect of iloprost infusion was more prominent after the tamponade

113 Acute iloprost inhalation reduced forced expiratory volume in

114 ndard lung function testing before and after iloprost inhalation, 6-min walk test, World Health Organ

115 ++Cicaprost and iloprost inhibit DNA synthesis and proliferation to a gr

116 We found that iloprost inhibited IFN-gamma- and IL-6-induced MCP-1, IL

117 duced MCP-1 production and demonstrated that iloprost inhibited STAT1 activation by several actions a

118 activation by several actions as follows: 1) iloprost inhibited the phosphorylation of STAT1-S727 in

119 In this study, the mechanisms by which iloprost interacts with calcium signaling pathways stimu

120 Acute administration of inhaled iloprost lowered mean pulmonary artery pressure equivale

121 ng FZD9 expression and improving response to iloprost lung cancer chemoprevention.

122 omodulin is a marker of endotheliopathy, and iloprost may improve endothelial function.

123 l and preliminary clinical data suggest that iloprost may improve tissue perfusion in septic shock.

124 tes IFN-gamma-signaling, was not involved in iloprost-mediated inhibition of STAT1, indicating diverg

125 e therapies using either Wnt7a or its mimic, Iloprost, might represent a new class of therapeutic tre

126 in some children with PAH, although inhaled iloprost occasionally induced bronchoconstriction.

127 d attenuation of pial arteriolar dilation to iloprost on day 4 (14%, 21% and 29% at 10(-12) M, 10(-10

128 We evaluated the acute effects of inhaled iloprost on hemodynamic status and lung function and the

129 lar inflammation, we examined the effects of iloprost on IFN-gamma- and IL-6-stimulated cytokine prod

130 Hx treated rats to investigate the effect of Iloprost on oval cell response.

131 The infusion with iloprost or carrier solution was continued for the durat

132 lone on day 1 did not affect the dilation to iloprost or constriction to ET-1, 4 days later.

133 When iloprost or milrinone was introduced after the initial m

134 Pericardial fluid was then removed, and iloprost or normal saline infusion was continued for ano

135 ericardial tamponade was induced, during the iloprost or normal saline infusion with pericardial tamp

136 imals were randomized to receive intravenous iloprost or normal saline.

137 to receive a 48-hour intravenous infusion of iloprost or placebo.

138 Infusion of iloprost or saline was continued after pericardial tampo

139 of COX-1 were rescued by the treatment with iloprost or the selective peroxisome proliferator-activa

140 elaxation responses to sodium nitroprusside, iloprost, or the K(+) channel activators (NS1619 and bim

141 omly assigned to receive either 50 microg of iloprost orally twice daily or an identical gelatin-coat

142 in the seventh transmembrane domain enhanced iloprost potency approximately 100-fold.

143 a 2-hr storage, beta-NTP regeneration in mUW+iloprost produced +57.7% (P<0.01) more beta-NTP, at a fa

144 Objectives: To investigate whether iloprost provides organ protection in septic shock with

145 PKA by injection of the prostacyclin analog iloprost reduced PAK activation and inflammatory gene ex

146 Under basal conditions, U0126 or iloprost reduced the number of viable cells and increase

147 rmer smokers using the prostacyclin analogue iloprost reduces endobronchial dysplasia, a premalignant

148 Iloprost requires the presence of the WNT receptor Frizz

149 Furthermore, iloprost rescued the deficit in Smad1/5 phosphorylation

150 % for RBCs incubated with pentoxyfilline and iloprost, respectively.

151 In a randomized and controlled trial, iloprost resulted in improvement in a combined end point

152 lial-derived prostacyclin, we determined how Iloprost reverses ADP-mediated signaling events.

153 tylase and coactivator CBP/p300 to STAT1; 2) iloprost selectively inhibited activation of JAK2 but no

154 andin E(2) receptor subtype 3 activated with iloprost showed a similar reaction to depolarization as

155 owever, prostacyclin receptor activated with iloprost showed no detectable voltage dependence.

156 f the mutant receptors by PGE2 (EP2 ligand), iloprost (stable prostacyclin analog), and PGE1 (EP2/IP

157 inhibitor milrinone mirrored the actions of iloprost, suggesting that the prostacyclin analog exerte

158 demonstrate an inverse regulation by ADP and Iloprost, suggesting that these are central modulators o

159 7 nm) was evident at those concentrations of iloprost that induce PKC-dependent desensitization.

160 Inhaled iloprost therapy may provide selectivity of the hemodyna

161 nt of patients continued receiving long-term iloprost therapy, 36% stopped iloprost, due to lower air

162 ZD9 is required in lung epithelial cells for iloprost to activate peroxisome proliferator activated r

163 y provides new information on the ability of iloprost to primarily attenuate inositol-1,4,5-triphosph

164 In contrast, iloprost-treated animals did not show hepatic arterial v

165 Portal hypertension did not occur in iloprost-treated animals, as portal venous pressure rema

166 e cardiac output returned to baseline in the iloprost-treated group but remained decreased in the con

167 44 +/- .23) in the control group than in the iloprost-treated group.

168 Postburn iloprost treatment yielded a significant improvement in

169 cts of a miR-520a-5p mimic were rescued with iloprost treatment, and effects of cigarette smoke were

170 channels by BAY-K 8644 was unchanged during iloprost treatment.

171 the context of cigarette smoke exposure and iloprost treatment.

172 l pressure was not affected by the dosage of iloprost used in this experiment.

173 NYHA status improved by one class in 34% of iloprost versus 6% of placebo patients (p = 0.002).

174 The inhibition of CTGF induction by Iloprost was associated with a significant decrease in o

175 inally, a known inhibitor of CTGF synthesis, Iloprost, was administered to 2-AAF/PHx treated rats to

176 oned from intravenous prostanoids to inhaled iloprost, which continued during follow-up.

177 otein phosphorylation in response to ADP and Iloprost, which inversely overlap and represent major ac

178 resulted in a selective gain of function for iloprost, which is consistent with the proposed phylogen

179 In a clinical context, administration of iloprost will be unlikely to improve outcome in these pa

180 Coadministration of iloprost with AngII attenuated both the immediate peak (

181 ependently dilated to topical application of iloprost with increases in diameter of 10%, 16% and 21%