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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.
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,
25 tion of retinal ganglion cell (RGC) axons in retinal ischemia and in inducible and hereditary preclin
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
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
37 wth factor (VEGF) levels are correlated with retinal ischemia-associated intraocular neovascularizati
40 1 were measured in response to RHP and after retinal ischemia by immunoblot analysis and immunohistoc
42 Rats were subjected to 30 or 45 minutes of retinal ischemia followed by reperfusion for up to 48 ho
45 (NV) is a sight-threatening complication of retinal ischemia in diabetes, retinal vein occlusion, an
47 increased intraocular pressure (IOP) and/or retinal ischemia in glaucoma and leads to impairment of
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
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
66 ed 24 hours earlier with either 5 minutes of retinal ischemia or by exposing conscious animals to hyp
69 with chronic vascular arrest and peripheral retinal ischemia persisting beyond standard screening ti
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
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
82 study was conducted to examine the effect of retinal ischemia-reperfusion injury on protein tyrosine
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
92 radial diffusivity was seen at 3 days after retinal ischemia, suggesting axonal injury without myeli
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
101 -1 (50 mg/kg) or vehicle, and then transient retinal ischemia was induced by acute IOP elevation.
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
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
116 egulation of proinflammatory molecules after retinal ischemia were dependent on CD40 expression in th
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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