ライフサイエンスコーパス: retinal ischemia

1 s model did not prevent capillary closure or retinal ischemia.

2 retinal neovascularization due to extensive retinal ischemia.

3 ogenesis of diabetic retinopathy, can induce retinal ischemia.

4 the occurrence of large contiguous areas of retinal ischemia.

5 ulator, was shown to be a promising drug for retinal ischemia.

6 Ls) are OCT findings associated with chronic retinal ischemia.

7 erfusion could be restored without permanent retinal ischemia.

8 A and mRNA expression profiles in context of retinal ischemia.

9 on, panretinal photocoagulation, or both for retinal ischemia.

10 orescein angiography demonstrated peripheral retinal ischemia.

11 useful to understand the pathophysiology of retinal ischemia.

12 9 consecutive patients with MVL secondary to retinal ischemia.

13 cranial nerves and subsequently cerebral and retinal ischemia.

14 ffusivity alone in murine optic nerves after retinal ischemia.

15 protein attenuated Wnt signaling induced by retinal ischemia.

16 , plays a role in neuronal cell death during retinal ischemia.

17 clinically in diseases such as glaucoma and retinal ischemia.

18 RGCs) in animal models of glaucoma and acute retinal ischemia.

19 n to be involved in the adaptive response to retinal ischemia.

20 e were subjected to 30 minutes of unilateral retinal ischemia.

21 upregulated and may be neuroprotective after retinal ischemia.

22 wn to play a role in cell death in transient retinal ischemia.

23 inal blood flow regulation in patients after retinal ischemia.

24 expressed and have distinct functions after retinal ischemia.

25 Twenty-four hours after retinal ischemia, A and B waves of vehicle-treated anima

26 athways may prove useful in the treatment of retinal ischemia, a leading cause of vision loss and bli

27 expression with steroids, or alleviation of retinal ischemia, a major stimulus for VEGF expression,

28 Rats were subjected to retinal ischemia after IPC, or retinas were rendered isc

29 romotes the fibrovascular reaction in murine retinal ischemia after laser injury.

30 rom blood, which plays a significant role in retinal ischemia and angiogenesis in diabetic retinopath

31 rimonidine, in animal models of glaucoma and retinal ischemia and in glaucoma patients.

32 tion of retinal ganglion cell (RGC) axons in retinal ischemia and in inducible and hereditary preclin

33 In pathologic settings including retinal ischemia and malignant tumors, robust angiogenes

34 can contribute to capillary obliteration and retinal ischemia and may be a practical target for early

35 was used to evaluate the effects of pHBSP on retinal ischemia and neovascularization (1-30 mug/kg pHB

36 In the eye, these processes initiate retinal ischemia and neovascularization resulting in sic

37 th a selective loss of retinal neurons after retinal ischemia and possibly in glaucoma.

38 The model of retinal ischemia and reperfusion will be a useful tool f

39 fusion and eventual obliteration can lead to retinal ischemia and sight-threatening neovascularizatio

40 al surgery for PDR, potentially triggered by retinal ischemia and surgical inflammation.

41 index terms: "retinal artery occlusion" OR "retinal ischemia" AND "thrombolysis" OR "fibrinolysis" O

42 stlaminar optic nerve 4 days following acute retinal ischemia, and 3 weeks following the chronic elev

43 Inflammation-mediated leukostasis, retinal ischemia, and neovascularization and their contr

44 The mechanisms of retinal ischemia are not fully understood, however.

45 In a subsequent experiment, total retinal ischemia, as measured by a cessation of electror

46 wth factor (VEGF) levels are correlated with retinal ischemia-associated intraocular neovascularizati

47 d a similar sensitivity to hyperoxia-induced retinal ischemia at P12.

48 Rats were subjected to retinal ischemia by elevation of intraocular pressure.

49 1 were measured in response to RHP and after retinal ischemia by immunoblot analysis and immunohistoc

50 We present a case report showing retinal ischemia can be linked with aHUS.

51 Retinal ischemia can cause vision-threatening pathologic

52 EC apoptosis cause capillary regression and retinal ischemia followed by neovascularization.

53 Rats were subjected to 30 or 45 minutes of retinal ischemia followed by reperfusion for up to 48 ho

54 male Lewis albino rats was raised to create retinal ischemia for 1 hour.

55 Retinal ischemia for 5 minutes constituted the precondit

56 (NV) is a sight-threatening complication of retinal ischemia in diabetes, retinal vein occlusion, an

57 sitivity and to correlate with midperipheral retinal ischemia in diabetic subjects.

58 increased intraocular pressure (IOP) and/or retinal ischemia in glaucoma and leads to impairment of

59 enables reliable non-invasive assessment of retinal ischemia in mild to moderate cases.

60 outcome of high intraocular pressure-induced retinal ischemia in rats.

61 f Black and Hispanic/Latino individuals with retinal ischemia in the IRIS Registry had higher likelih

62 in the angiogenic response to oxygen-induced retinal ischemia in transgenic mice overexpressing PKC b

63 and immunolocalization analyses showed that retinal ischemia increased expression of the NAD(P)H oxi

64 ion of retinal arterioles was examined after retinal ischemia induced by elevated intraocular pressur

65 dies of rhEPO in a model of transient global retinal ischemia induced by raising intraocular pressure

66 cts at the synaptic level in a model of mild retinal ischemia induced by temporary middle cerebral ar

67 Retinal ischemia-induced upregulation of vascular endoth

68 Because retinal ischemia is a common cause of vision loss, we so

69 Because retinal ischemia is known to increase intracellular aden

70 layed cell death that occurs after transient retinal ischemia is, in part, apoptotic.

71 Mild retinal ischemia led to a significantly higher percentag

72 Diabetic retinal ischemia may be caused, in part, by the adhesion

73 ce protein (gfp+) and subjected to our adult retinal ischemia model.

74 nfirmed in Matrigel plug, wound healing, and retinal ischemia models in vivo.

75 protective in cardiac, cerebral, renal, and retinal ischemia models, but the mechanism is unknown.

76 l artery obstruction (n = 2), and peripheral retinal ischemia (n = 2).

77 emonstrating the abnormalities-such as acute retinal ischemia (n = 5 [3.1%]); optic disc edema (n = 1

78 because of severe ophthalmic (ptosis, n = 2; retinal ischemia, n = 2) or systemic (hypotension, n = 1

79 tration of rhEPO before or immediately after retinal ischemia not only reduced histopathological dama

80 Varying degrees of cardiac involvement and retinal ischemia occurred, with TMA evident on kidney bi

81 vascular arcade, but there was no associated retinal ischemia on fluorescein angiography.

82 At 3 and 7 days after retinal ischemia, optic nerves were removed for CAP meas

83 ed 24 hours earlier with either 5 minutes of retinal ischemia or by exposing conscious animals to hyp

84 Retinal ischemia or IPC was produced in anesthetized Spr

85 loss, typically due to macular involvement, retinal ischemia, or neovascular complications.

86 de disruption was correlated with peripheral retinal ischemia (P = .025).

87 In case of retinal ischemia, panretinal photocoagulation should be

88 with chronic vascular arrest and peripheral retinal ischemia persisting beyond standard screening ti

89 Vascular insufficiency and retinal ischemia precede many proliferative retinopathie

90 ut had no measurable effect on the extent of retinal ischemia, preretinal neovascularization, or neur

91 In proliferative diabetic retinopathy (PDR), retinal ischemia promotes neovascularization (NV), which

92 ression plays a neuroprotective role against retinal ischemia reperfusion injury due to decreasing of

93 Using a retinal ischemia reperfusion injury model in mice, we ob

94 We used a glaucoma model of retinal ischemia-reperfusion (I/R) injury in rats and fo

95 Retinal ischemia-reperfusion (I/R) injury is a common ca

96 Retinal ischemia-reperfusion (IR) injury causes irrevers

97 Retinal ischemia-reperfusion after transient elevated IO

98 he expression of EDG receptors in a model of retinal ischemia-reperfusion injury and also tested LXR-

99 lpha and its receptor in an in vivo model of retinal ischemia-reperfusion injury by investigating its

100 lear layer (INL) was noted in a rat model of retinal ischemia-reperfusion injury by transient elevate

101 ns, and retinal ganglion cells (RGCs) in rat retinal ischemia-reperfusion injury in vivo.

102 The etiology of retinal ischemia-reperfusion injury is orchestrated by c

103 study was conducted to examine the effect of retinal ischemia-reperfusion injury on protein tyrosine

104 Retinal ischemia-reperfusion injury was performed on p55

105 e function was evaluated in a mouse model of retinal ischemia-reperfusion injury.

106 play an important role in neuroprotection in retinal ischemia-reperfusion injury.

107 In the rat retinal ischemia-reperfusion model, runcaciguat treatmen

108 Streptozotocin-induced diabetes and retinal ischemia-reperfusion models were used in in vivo

109 ystemically or directly into the vitreous of retinal ischemia-reperfusion-injured adult nonobese diab

110 d two models of Bmal1(fx/fx);Tek-Cre mice, a retinal ischemia/reperfusion model and a neointimal hype

111 etabolism has an influence on the outcome of retinal ischemia/reperfusion.

112 Two months later, as the disc swelling and retinal ischemia resolved, we found that the occluded ar

113 Retinal ischemia resulted in significant, duration-depen

114 The pathogenesis of retinal ischemia results from a series of events involvi

115 radial diffusivity was seen at 3 days after retinal ischemia, suggesting axonal injury without myeli

116 perior nerve fiber area, and well-demarcated retinal ischemia superior to the fovea in the right eye.

117 A brief period of noninjurious retinal ischemia, termed preconditioning, has been docum

118 In eyes with retinal ischemia, the outcome was NVG.

119 In response to the ensuing retinal ischemia, there was consistent preretinal neovas

120 Of 312 106 eyes with retinal ischemia, there were 5885 (1.9%) with NVG.

121 sponse, particularly in patients with severe retinal ischemia, though findings were not statistically

122 pillaries, lesions that produce irreversible retinal ischemia through their inability to support bloo

123 lts were then applied to an in vivo model of retinal ischemia to determine whether CoCl(2) upregulate

124 aded MnCl(2) was also conducted in eyes with retinal ischemia, to evaluate whether the enhancements r

125 nction of mouse optic nerves after transient retinal ischemia using in vitro electrophysiologic recor

126 Unilateral retinal ischemia was created in Long-Evans and Sprague-D

127 Retinal ischemia was induced 24 hours after either IPC o

128 -1 (50 mg/kg) or vehicle, and then transient retinal ischemia was induced by acute IOP elevation.

129 Retinal ischemia was induced by raising the intraocular

130 Retinal ischemia was induced by transiently raising the

131 Retinal ischemia was induced for 0, 5, 30, 60, 75, or 90

132 Retinal ischemia was induced in 7- to 8-week-old female

133 Retinal ischemia was induced in rats by acutely increasi

134 e hematopoietic engraftment was established, retinal ischemia was induced to promote neovascularizati

135 multilineage reconstitution was established, retinal ischemia was induced to promote neovascularizati

136 Transient retinal ischemia was induced using a high intraocular pr

137 Retinal ischemia was produced for 60 minutes in anesthet

138 Retinal ischemia was produced for 60 minutes in ketamine

139 Retinal ischemia was produced in Lewis rats by increasin

140 tinal neovascularization in animal models of retinal ischemia, we tested whether IGF-I could act as a

141 escein transit time, and the presence of any retinal ischemia were associated with a higher incidence

142 Up-regulation of NOS2 and COX2 after retinal ischemia were blunted in CD40(-/-) mice.

143 egulation of proinflammatory molecules after retinal ischemia were dependent on CD40 expression in th

144 Similar amounts of posterior retinal ischemia were observed in all mice at both PND-1

145 this period of long-term tolerance (LTT) to retinal ischemia were sustained increases in retinal lev

146 nisotropy (RA) progressively decreased after retinal ischemia when compared with that of the controls

147 ed nerves also progressively decreased after retinal ischemia, which correlated with the reduced RA (

148 raphy allowed determination of the extent of retinal ischemia, which was treated with laser photocoag

149 yes with NVG, outcomes included treatment of retinal ischemia with pan-retinal photocoagulation (PRP)

150 ctive strategy for preventing oxygen-induced retinal ischemia without provoking retinal neovasculariz