ライフサイエンスコーパス: PGE1

1 PGE1 administration after OLT resulted in improved renal

2 PGE1 infusion was, however, associated with improved ear

3 hich specifically blocked the binding of [3H]PGE1 to the high-affinity PGI2 receptors of normal plate

4 hain of IgG that inhibits the binding of [3H]PGE1 to the high-affinity platelet PGI2 receptor, demons

5 by Scatchard analysis of the binding of [3H]PGE1.

6 Misoprostol, a PGE1 analog, was developed as an antiulcer agent because

7 s exposed to hypoxia, we hypothesized that a PGE1-mediated increase in cAMP levels within the preserv

8 In contrast, the EP4 agonist (PGE1-OH) stimulated macrophage MMP-9 expression, which w

9 Although PGE1 is thought to act as a pulmonary vasodilator during

10 , iloprost (stable prostacyclin analog), and PGE1 (EP2/IP ligand) was determined using a cAMP-depende

11 of 60) and 6.9% (4 of 58) in the control and PGE1 groups, respectively.

12 Moreover, both PGA1 and PGE1 reduced the formation of sorbitol in an ex-vivo mod

13 unstimulated), beta-adrenergic receptor- and PGE1-stimulated adenylyl cyclase activities were observe

14 ed for some time that prostaglandins such as PGE1 increase cAMP production and activate PKA, but they

15 with cAMP levels significantly increased by PGE1 supplementation (approximately 2-fold by 6 hours, P

16 n of glucose-stimulated insulin secretion by PGE1 is substantially blunted by small interfering RNA-m

17 mulating the cAMP second messenger system by PGE1 supplementation resulted in marked hemodynamic bene

18 The EP4 receptor-specific agonist, 11-deoxy-PGE1, induced a time-dependent phosphorylation of protei

19 ltures and treated with PGF2 alpha, 11-deoxy-PGE1, or PhXA85 (the nonesterified analogue of PhXA41) f

20 es and were treated with PGF2alpha, 11-deoxy-PGE1, or PhXA85 (the nonesterified analogue of PhXA41) f

21 Treatment with 200 nM PGF2 alpha, 11-deoxy-PGE1, or PhXA85 for 72 hours increased the combined dens

22 n addition, exposure to PGF2 alpha, 11-deoxy-PGE1, or PhXA85 increases production of all four MMPs.

23 our treatment with 20 nM PGF2alpha, 11-deoxy-PGE1, or PhXA85 reduced the amount of collagen type I in

24 hen the concentration of PGF2alpha, 11-deoxy-PGE1, or PhXA85 was increased to 200 nM, the amount of c

25 ulated insulin secretion by prostaglandin E (PGE1) is pertussis-toxin insensitive, indicating that ot

26 (PGE2) (P<0.01), 400% more prostaglandin E1 (PGE1) (P<0.01), and 250% more cAMP (P<0.05) than Adnull-

27 ctivity map, we identified prostaglandin E1 (PGE1) as a small molecule that partly elicited the gene

28 Prostaglandin E1 (PGE1) has been used after orthotopic liver transplantati

29 Prostaglandin E1 (PGE1) is often added to the donor pulmonary flush soluti

30 Prostaglandin E1 (PGE1) prevents 4N1K-dependent aggregation on immobilized

31 c fatty acid derivative of prostaglandin E1 (PGE1) used for chronic constipation.

32 Prostaglandin E1 (PGE1)-mediated inhibition of thrombin-stimulated shape c

33 nse to isoproterenol), and prostaglandin E1 (PGE1)-stimulated lymphocyte adenylyl cyclase activities

34 n patients were randomized to receive either PGE1 or crystalloid placebo intravenously after allograf

35 ited the enzyme, including non-electrophilic PGE1 and PGE2, currently used in clinical practice.

36 However, PGE1 undergoes extensive metabolic inactivation by the l

37 Seven patients receiving intravenous PGE1 for hepatic dysfunction (0.11-1.30 microg/kg/hr) ha

38 Mechanistically, PGE1 acted on the EP4 receptor and repressed Fosb and Fo

39 Moreover, PGE1 augments MP in improving graft function.

40 The combination of MP+PGE1 may be important in optimizing the ability to use e

41 tudy, we confirm that isoproterenol, but not PGE1, is able to produce cAMP-dependent stimulation of t

42 The addition of PGE1 to perfusate improved MP characteristics, reduced t

43 protocols for intravenous administration of PGE1 are not likely to affect perihepatic hemodynamics.

44 targets CML LSCs and that the combination of PGE1/misoprostol with conventional tyrosine-kinase inhib

45 ptor-mediated responses, compartmentation of PGE1 responses was not due to concurrent activation of a

46 ivation by the lung and the concentration of PGE1 reaching the liver during intravenous administratio

47 Systemic arterial concentrations of PGE1 were </= 62 pg/ml.

48 multicenter trial to evaluate the effect of PGE1 on early hepatic and renal function in patients und

49 in of RGSZ1, blocks the inhibitory effect of PGE1 on glucose-stimulated insulin secretion.

50 , it lacked other nonvasodilating effects of PGE1 and resulted in poor preservation.

51 e also determined the hemodynamic effects of PGE1 infusion in swine.

52 These beneficial effects of PGE1 were abrogated by simultaneous administration of th

53 of PGE1 of 0.54 +/- 0.23, and (3) levels of PGE1 in the systemic circulation of </= 78 pg/ml, even a

54 ng treated with PGE1 and in a swine model of PGE1 infusion.

55 aft function was improved in the presence of PGE1+MP, compared with function in the presence of other

56 lood flow via the vasodilating properties of PGE1.

57 - 0.12, (2) a splanchnic extraction ratio of PGE1 of 0.54 +/- 0.23, and (3) levels of PGE1 in the sys

58 trating: (1) a pulmonary extraction ratio of PGE1 of 0.78 +/- 0.12, (2) a splanchnic extraction ratio

59 full-length clone catalyzed the transport of PGE1, PGE2, PGD2, PGF2alpha, and, to a lesser degree, TX

60 ct and a preventive and corrective effect on PGE1 in chronically diabetic nerve associated with impro

61 MP characteristics when added to perfusate: PGE1, trifluoperazine, verapamil, and papaverine.

62 ly increase in the production of PGI2, PGE2, PGE1 (known to cause vasodilation), and cAMP.

63 Thus, we measured plasma PGE1 concentrations in patients with hepatic dysfunction

64 T) based on limited clinical data suggesting PGE1 infusion improves immediate hepatic allograft funct

65 icient to enhance lung preservation and that PGE1 enhances lung preservation by stimulating the cAMP-

66 mpact on normal hematopoiesis, we found that PGE1 treatment impaired the persistence and activity of

67 on of the molecular mechanisms revealed that PGE1 induced the phosphorylation of RhoA on serine(188)

68 epatic hemodynamics were not affected by the PGE1 infusions in healthy swine.

69 group (0.7 +/- 2.0 per patient) than in the PGE1 group (0.2 +/- 1.0 per patient; P = 0.10).

70 tly in the placebo group (26.7%) than in the PGE1 group (13.8%; P = 0.65).

71 Instead, compartmentation of the PGE1 response in cardiac myocytes appears to be due to t

72 ese findings suggest that activation of this PGE1-EP4 pathway specifically targets CML LSCs and that

73 wever, addition of ketorolac tromethamine to PGE1 and heparin decreased the incidence of thrombosis (

74 , the precise mechanism(s) of action whereby PGE1 enhances lung preservation is unknown.

75 mpartments of intact cardiac myocytes, while PGE1 only stimulates cAMP production in the cytosolic co

76 vein, and hepatic vein in swine infused with PGE1 (range, 0.67-4.9 microg/kg/hr) demonstrating: (1) a

77 Treatment of platelets with PGE1 prevented thrombin-induced phospho-MYPT1-thr(853) i

78 it stay was shorter in patients treated with PGE1 (4.0 +/- 3.6 days) compared with controls (10.5 +/-

79 with hepatic dysfunction being treated with PGE1 and in a swine model of PGE1 infusion.

80 1.0 and 2.0 +/- 1.0 in patients treated with PGE1 and placebo, respectively; P < 0.001).