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1 ogenesis of diabetic retinopathy, can induce retinal ischemia.
2 on, panretinal photocoagulation, or both for retinal ischemia.
3 9 consecutive patients with MVL secondary to retinal ischemia.
4 cranial nerves and subsequently cerebral and retinal ischemia.
5  retinal neovascularization due to extensive retinal ischemia.
6 ffusivity alone in murine optic nerves after retinal ischemia.
7  protein attenuated Wnt signaling induced by retinal ischemia.
8 , plays a role in neuronal cell death during retinal ischemia.
9  clinically in diseases such as glaucoma and retinal ischemia.
10 RGCs) in animal models of glaucoma and acute retinal ischemia.
11  the occurrence of large contiguous areas of retinal ischemia.
12 n to be involved in the adaptive response to retinal ischemia.
13 e were subjected to 30 minutes of unilateral retinal ischemia.
14 upregulated and may be neuroprotective after retinal ischemia.
15 wn to play a role in cell death in transient retinal ischemia.
16 inal blood flow regulation in patients after retinal ischemia.
17 A and mRNA expression profiles in context of retinal ischemia.
18  expressed and have distinct functions after retinal ischemia.
19                      Twenty-four hours after retinal ischemia, A and B waves of vehicle-treated anima
20 athways may prove useful in the treatment of retinal ischemia, a leading cause of vision loss and bli
21  expression with steroids, or alleviation of retinal ischemia, a major stimulus for VEGF expression,
22                       Rats were subjected to retinal ischemia after IPC, or retinas were rendered isc
23 romotes the fibrovascular reaction in murine retinal ischemia after laser injury.
24 rimonidine, in animal models of glaucoma and retinal ischemia and in glaucoma patients.
25 tion of retinal ganglion cell (RGC) axons in retinal ischemia and in inducible and hereditary preclin
26             In pathologic settings including retinal ischemia and malignant tumors, robust angiogenes
27 can contribute to capillary obliteration and retinal ischemia and may be a practical target for early
28 was used to evaluate the effects of pHBSP on retinal ischemia and neovascularization (1-30 mug/kg pHB
29 th a selective loss of retinal neurons after retinal ischemia and possibly in glaucoma.
30                                 The model of retinal ischemia and reperfusion will be a useful tool f
31 fusion and eventual obliteration can lead to retinal ischemia and sight-threatening neovascularizatio
32  index terms: "retinal artery occlusion" OR "retinal ischemia" AND "thrombolysis" OR "fibrinolysis" O
33 stlaminar optic nerve 4 days following acute retinal ischemia, and 3 weeks following the chronic elev
34           Inflammation-mediated leukostasis, retinal ischemia, and neovascularization and their contr
35                            The mechanisms of retinal ischemia are not fully understood, however.
36            In a subsequent experiment, total retinal ischemia, as measured by a cessation of electror
37 wth factor (VEGF) levels are correlated with retinal ischemia-associated intraocular neovascularizati
38 d a similar sensitivity to hyperoxia-induced retinal ischemia at P12.
39                       Rats were subjected to retinal ischemia by elevation of intraocular pressure.
40 1 were measured in response to RHP and after retinal ischemia by immunoblot analysis and immunohistoc
41                                              Retinal ischemia can cause vision-threatening pathologic
42   Rats were subjected to 30 or 45 minutes of retinal ischemia followed by reperfusion for up to 48 ho
43  male Lewis albino rats was raised to create retinal ischemia for 1 hour.
44                                              Retinal ischemia for 5 minutes constituted the precondit
45  (NV) is a sight-threatening complication of retinal ischemia in diabetes, retinal vein occlusion, an
46 sitivity and to correlate with midperipheral retinal ischemia in diabetic subjects.
47  increased intraocular pressure (IOP) and/or retinal ischemia in glaucoma and leads to impairment of
48 outcome of high intraocular pressure-induced retinal ischemia in rats.
49 in the angiogenic response to oxygen-induced retinal ischemia in transgenic mice overexpressing PKC b
50  and immunolocalization analyses showed that retinal ischemia increased expression of the NAD(P)H oxi
51 ion of retinal arterioles was examined after retinal ischemia induced by elevated intraocular pressur
52 dies of rhEPO in a model of transient global retinal ischemia induced by raising intraocular pressure
53 cts at the synaptic level in a model of mild retinal ischemia induced by temporary middle cerebral ar
54                                              Retinal ischemia-induced upregulation of vascular endoth
55                                      Because retinal ischemia is a common cause of vision loss, we so
56                                      Because retinal ischemia is known to increase intracellular aden
57 layed cell death that occurs after transient retinal ischemia is, in part, apoptotic.
58                                         Mild retinal ischemia led to a significantly higher percentag
59                                     Diabetic retinal ischemia may be caused, in part, by the adhesion
60 ce protein (gfp+) and subjected to our adult retinal ischemia model.
61 nfirmed in Matrigel plug, wound healing, and retinal ischemia models in vivo.
62 l artery obstruction (n = 2), and peripheral retinal ischemia (n = 2).
63 tration of rhEPO before or immediately after retinal ischemia not only reduced histopathological dama
64   Varying degrees of cardiac involvement and retinal ischemia occurred, with TMA evident on kidney bi
65                        At 3 and 7 days after retinal ischemia, optic nerves were removed for CAP meas
66 ed 24 hours earlier with either 5 minutes of retinal ischemia or by exposing conscious animals to hyp
67                                              Retinal ischemia or IPC was produced in anesthetized Spr
68 de disruption was correlated with peripheral retinal ischemia (P = .025).
69  with chronic vascular arrest and peripheral retinal ischemia persisting beyond standard screening ti
70                   Vascular insufficiency and retinal ischemia precede many proliferative retinopathie
71 ut had no measurable effect on the extent of retinal ischemia, preretinal neovascularization, or neur
72 In proliferative diabetic retinopathy (PDR), retinal ischemia promotes neovascularization (NV), which
73 ression plays a neuroprotective role against retinal ischemia reperfusion injury due to decreasing of
74                                      Using a retinal ischemia reperfusion injury model in mice, we ob
75                                              Retinal ischemia-reperfusion (IR) injury causes irrevers
76                                              Retinal ischemia-reperfusion after transient elevated IO
77 he expression of EDG receptors in a model of retinal ischemia-reperfusion injury and also tested LXR-
78 lpha and its receptor in an in vivo model of retinal ischemia-reperfusion injury by investigating its
79 lear layer (INL) was noted in a rat model of retinal ischemia-reperfusion injury by transient elevate
80 ns, and retinal ganglion cells (RGCs) in rat retinal ischemia-reperfusion injury in vivo.
81                              The etiology of retinal ischemia-reperfusion injury is orchestrated by c
82 study was conducted to examine the effect of retinal ischemia-reperfusion injury on protein tyrosine
83                                              Retinal ischemia-reperfusion injury was performed on p55
84 e function was evaluated in a mouse model of retinal ischemia-reperfusion injury.
85 play an important role in neuroprotection in retinal ischemia-reperfusion injury.
86          Streptozotocin-induced diabetes and retinal ischemia-reperfusion models were used in in vivo
87 ystemically or directly into the vitreous of retinal ischemia-reperfusion-injured adult nonobese diab
88 d two models of Bmal1(fx/fx);Tek-Cre mice, a retinal ischemia/reperfusion model and a neointimal hype
89 etabolism has an influence on the outcome of retinal ischemia/reperfusion.
90                                              Retinal ischemia resulted in significant, duration-depen
91                          The pathogenesis of retinal ischemia results from a series of events involvi
92  radial diffusivity was seen at 3 days after retinal ischemia, suggesting axonal injury without myeli
93               A brief period of noninjurious retinal ischemia, termed preconditioning, has been docum
94                   In response to the ensuing retinal ischemia, there was consistent preretinal neovas
95 pillaries, lesions that produce irreversible retinal ischemia through their inability to support bloo
96 lts were then applied to an in vivo model of retinal ischemia to determine whether CoCl(2) upregulate
97 aded MnCl(2) was also conducted in eyes with retinal ischemia, to evaluate whether the enhancements r
98 nction of mouse optic nerves after transient retinal ischemia using in vitro electrophysiologic recor
99                                   Unilateral retinal ischemia was created in Long-Evans and Sprague-D
100                                              Retinal ischemia was induced 24 hours after either IPC o
101 -1 (50 mg/kg) or vehicle, and then transient retinal ischemia was induced by acute IOP elevation.
102                                              Retinal ischemia was induced by raising the intraocular
103                                              Retinal ischemia was induced by transiently raising the
104                                              Retinal ischemia was induced for 0, 5, 30, 60, 75, or 90
105                                              Retinal ischemia was induced in 7- to 8-week-old female
106                                              Retinal ischemia was induced in rats by acutely increasi
107 multilineage reconstitution was established, retinal ischemia was induced to promote neovascularizati
108 e hematopoietic engraftment was established, retinal ischemia was induced to promote neovascularizati
109                                    Transient retinal ischemia was induced using a high intraocular pr
110                                              Retinal ischemia was produced for 60 minutes in anesthet
111                                              Retinal ischemia was produced for 60 minutes in ketamine
112                                              Retinal ischemia was produced in Lewis rats by increasin
113 tinal neovascularization in animal models of retinal ischemia, we tested whether IGF-I could act as a
114 escein transit time, and the presence of any retinal ischemia were associated with a higher incidence
115         Up-regulation of NOS2 and COX2 after retinal ischemia were blunted in CD40(-/-) mice.
116 egulation of proinflammatory molecules after retinal ischemia were dependent on CD40 expression in th
117                 Similar amounts of posterior retinal ischemia were observed in all mice at both PND-1
118  this period of long-term tolerance (LTT) to retinal ischemia were sustained increases in retinal lev
119 nisotropy (RA) progressively decreased after retinal ischemia when compared with that of the controls
120 ed nerves also progressively decreased after retinal ischemia, which correlated with the reduced RA (
121 raphy allowed determination of the extent of retinal ischemia, which was treated with laser photocoag
122 ctive strategy for preventing oxygen-induced retinal ischemia without provoking retinal neovasculariz

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