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1 ion of proliferating MGPCs in the absence of retinal damage.
2 ptors is implicated as a causative factor to retinal damage.
3 used to treat ophthalmic infections without retinal damage.
4 n activator (uPA)] in excitotoxicity-induced retinal damage.
5 -antiplasmin, failed to attenuate KA-induced retinal damage.
6 l-glutamate have been implicated in ischemic retinal damage.
7 nts were inaccurate in the presence of outer retinal damage.
8 offer protection against excitotoxin-induced retinal damage.
9 ived neurotrophic factor (BDNF) reduces this retinal damage.
10 the material in vitreous and variable local retinal damage.
11 in parallel with the increasing severity of retinal damage.
12 stantial, and there was little other obvious retinal damage.
13 damage or by CNTF or FGF2 in the absence of retinal damage.
14 s been reported to play an important role in retinal damage.
15 equired to prevent the voriconazole-mediated retinal damage.
16 diffuse to the posterior segment, triggering retinal damage.
17 ociated with Muller glia and MGPCs following retinal damage.
18 -consuming, and carry risks of infection and retinal damage.
19 uller glia to reenter the cell cycle without retinal damage.
20 trols, as well as to identify early signs of retinal damage.
21 ts and by histopathologic evidence of severe retinal damage.
22 um that was mainly responsible for secondary retinal damage.
23 1 predispose mice to age- and light-mediated retinal damage.
24 in increased susceptibility to light-induced retinal damage.
25 se to intrinsic signals remain despite inner retinal damage.
26 dies against retinal antigens and results in retinal damage.
27 eared to vary with the severity of the laser retinal damage.
28 an important factor in toxoplasmosis-induced retinal damage.
29 eurogenic potential capable of responding to retinal damage.
30 n of photoreceptors or ouabain-induced inner retinal damage.
31 defense mechanism against pressure-mediated retinal damage.
32 betic macular edema without visible signs of retinal damage.
33 issue and was protective from photooxidative retinal damage.
34 filtration, therefore contributing to reduce retinal damage.
35 se provides early evidence of stress-related retinal damage.
36 gy examination was also performed to confirm retinal damage.
37 mice display increased retinal apoptosis and retinal damage.
38 st common and may be due to neurotoxicity or retinal damage.
39 own to block diabetes- and endotoxin-induced retinal damage.
40 response and those that result in extraneous retinal damage.
41 tine, factors besides SAG1 are important for retinal damage.
42 is specifically induced in these cells after retinal damage.
43 part, plays a causative role in KCl-induced retinal damage.
44 to a significant attenuation of KCl-induced retinal damage.
45 eutralizing antibody significantly decreased retinal damage after IR, whereas treatment of retinas or
49 dence that Muller glia can proliferate after retinal damage and generate new rods; however, the evide
50 te the mechanism by which alkali burns cause retinal damage and may have importance in designing ther
52 g of pathogenic T cells or for effecting the retinal damage and photoreceptor loss typical of EAU.
53 insulin-deficient diabetes, or light-induced retinal damage and protects ganglion cells from apoptosi
55 istology and ERG analysis revealed increased retinal damage and significant loss of retinal function.
56 l studies, acute blue light exposure induces retinal damage and the use of blue-blocking IOLs lessens
57 cotherapies may well be able to mitigate the retinal damage and vision loss associated with geographi
58 serum RBP4 levels could be a risk factor for retinal damage and vision loss in nondiabetic as well as
60 he effects of metipranolol, known to prevent retinal damage, and of other antiglaucoma drugs were det
64 ll-deficient mice developed profound RPE and retinal damage at doses that caused minimal effects in w
65 can be specified to avoid not only the inner retinal damage, but also permanent disorganization and s
66 has been proposed to play a pivotal role in retinal damage, but the mechanisms that underlie retinal
69 BDNF) rescues photoreceptors from collateral retinal damage caused by photodynamic therapy (PDT).
70 ty of cone arrestin to prevent light-induced retinal damage caused by prolonged activation of the pho
72 caspase-independent apoptosis contribute to retinal damage during murine cytomegalovirus (MCMV) reti
73 sion strikingly increased with the extent of retinal damage, especially at the photoreceptors, in con
74 cient diet rats exhibited protection against retinal damage from either intermittent or hyperthermic
75 tamate have been suggested to play a role in retinal damage in a number of blinding diseases such as
77 on of plasminogen activators might attenuate retinal damage in blinding retinal diseases in which hyp
86 tion factor Ascl1 is upregulated in MG after retinal damage in zebrafish and is necessary for regener
89 retinal glial cells contribute critically to retinal damage induced by RD and provide a new avenue fo
91 tis (EAU), recent work has demonstrated that retinal damage involves oxidative stress early in uveiti
97 ensity (20 000 lux for 30 min) light-induced retinal damage (LIRD) as compared with WT, indicating im
98 ansient amplification of Wnt signaling after retinal damage may unlock the latent regenerative capaci
102 d in Muller glia in response to NMDA-induced retinal damage or by CNTF or FGF2 in the absence of reti
106 jection-induced retinal detachment can cause retinal damage, particularly when SR vector bleb include
107 m permissible exposure safety limit produces retinal damage preceded by a transient reduction in the
108 infiltration in the inner retina, leading to retinal damage primarily localized to the ganglion cells
109 of the retina showed no evidence of residual retinal damage resulting from the colchicine injections
110 nflammatory protein production, leukostasis, retinal damage, signs of anterior uveitis, and uncouplin
111 retinal pigment epithelium (RPE) may lead to retinal damage similar to that associated with the early
112 After either kainate- or colchicine-induced retinal damage, some of the newly generated cells expres
113 Although high levels of glutamate induce retinal damage, subtoxic levels of glutamate directly st
115 rovides an alternative rod-dominant model of retinal damage that shares a surprising number of featur
129 No clinically apparent warning of outer retinal damage was seen in the SD-OCT images of long-ter
131 he inflamed retina, CD4(+) T cells can cause retinal damage when they are not properly regulated.
132 that IL-8 is upregulated upon laser-induced retinal damage, which recapitulates enhanced vasculariza
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