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1 the anatomic and functional consequences of optic nerve injury.
2 ation and elongation of axon re-growth after optic nerve injury.
3 tic RGC survival and axon regeneration after optic nerve injury.
4 t3 signaling in retinal ganglion cells after optic nerve injury.
5 rative responses occurring in RGCs following optic nerve injury.
6 d protection of RGCs from degeneration after optic nerve injury.
7 eficiency delayed RGC death after mechanical optic nerve injury.
8 rodegeneration above that normally seen with optic nerve injury.
9 ce cell survival and axon regeneration after optic nerve injury.
10 NgR became upregulated in RGCs following optic nerve injury.
11 ntiation and promotes RGC survival following optic nerve injury.
12 ene expression changes associated with early optic nerve injury.
13 TF) was observed within the retina following optic nerve injury.
14 l but not regeneration in vivo 2 weeks after optic nerve injury.
15 eutic approach to enhance RGC survival after optic nerve injury.
16 GCs) promotes robust axon regeneration after optic nerve injury.
17 ation in the glaucomatous eye, and following optic nerve injury.
18 t and robust regenerative response following optic nerve injury.
19 ls (RGCs) regenerating their axons following optic nerve injury.
20 n regulating adult RGC axon plasticity after optic nerve injury.
21 to regenerate long axons beyond the site of optic nerve injury.
22 is no effective treatment for this ischemic optic nerve injury.
23 sed RGC axon re-extension or sprouting after optic nerve injury.
24 rrelate with either IOP level or severity of optic nerve injury.
25 n of ephrin-A expression in conjunction with optic nerve injury.
26 after metamorphosis, to be reexpressed after optic nerve injury.
27 neuroprotectant in primate-sized eyes after optic nerve injury.
28 opment of novel and effective treatments for optic nerve injury.
29 and reestablish functional connections after optic nerve injury.
30 ells (RGCs) promotes axon regeneration after optic nerve injury.
31 ic nerve reserve or on the outcome of second optic nerve injuries.
32 consistently observed in glaucoma and other optic nerve injuries.
33 ere, we investigated axonal plasticity after optic nerve injury and found that macrophages recruited
35 r after spinal cord trauma, ischemic stroke, optic nerve injury and models of multiple sclerosis.
36 etinas from one group of eyes with extensive optic nerve injury and on RGCL isolated by laser capture
38 omotes long-distance axon regeneration after optic nerve injury and uncover a novel and important KLF
39 the secondary degeneration of RGCs following optic nerve injury, and is associated with JNK signaling
40 death in RGCs, including in a mouse model of optic nerve injury, and show that the same pathway is ac
41 ina, their regulated response to retinal and optic nerve injury, and the effects of altered neurotrop
42 ) are unable to regenerate their axons after optic nerve injury, and they soon undergo apoptotic cell
43 accounts for visual function deficits after optic nerve injury, but how axonal insults lead to neuro
44 ows retinal ganglion cell death in models of optic nerve injury, but the mechanism of action remains
45 n-like pattern and are upregulated following optic nerve injury, but the presence of Nogo-A does not
46 icant impact on ganglion cell survival after optic nerve injury, combined treatment of the eye and br
47 icroscopy, including masked determination of optic nerve injury grade (ONIG; 1, normal; 5, severe, di
48 vided measurements that correlated well with optic nerve injury grade, only the Tono-Pen documented s
50 c mechanisms involved in the pathogenesis of optic nerve injury has contributed to the use of empiric
54 drinking water, was tested for its effect on optic nerve injury in rats with ocular hypertension.
58 scription factor Sox11 as a key player after optic nerve injury-in DLK signaling of RGC cell death, a
61 iment suggests that primary RGC death due to optic nerve injury is associated with secondary death of
65 between our data and reports of retinal and optic nerve injury models in mice, rats, and monkeys.
66 ons in our non-regenerating and regenerating optic nerve injury models, a finding that is inconsisten
69 uction of regeneration associated genes upon optic nerve injury nor the increased regenerative potent
74 n promoting ganglion cell survival following optic nerve injury results, in part, due to drug-induced
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