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1 ceptor subunit NR1 promoted axon survival in experimental glaucoma.
2 t both substrates were cleaved by calpain in experimental glaucoma.
3 o elevate intraocular pressure as a model of experimental glaucoma.
4 nes of evidence that calpain is activated in experimental glaucoma.
5 lated-Stat3 levels were increased in RGCs in experimental glaucoma.
6 authors used a well-established rat model of experimental glaucoma.
7 ocation and character of early ONH change in experimental glaucoma.
8 m that CNTF can exert a protective effect in experimental glaucoma.
9 for normal eyes were applied to monkeys with experimental glaucoma.
10 at the onset of ONH surface change in early experimental glaucoma.
11 to the increase in Hsp27 and pHsp27 seen in experimental glaucoma.
12 change in young adult monkey eyes with early experimental glaucoma.
13 effective to reduce changes associated with experimental glaucoma.
14 he onset of detectable ONH surface change in experimental glaucoma.
15 h significant visual field defects caused by experimental glaucoma.
16 reduction of functional loss associated with experimental glaucoma.
17 tissues occurs early in the monkey model of experimental glaucoma.
18 resent in young adult monkey eyes with early experimental glaucoma.
19 trophic factor (BDNF) could be protective in experimental glaucoma.
20 asured in the untreated eyes of monkeys with experimental glaucoma.
21 yes with anatomic and functional damage from experimental glaucoma.
22 afferent input to the blobs were affected by experimental glaucoma.
23 affected by the duration and severity of the experimental glaucoma.
26 onfirm previous reports of elevated Hsp27 in experimental glaucoma and extend them to the DBA/2J mous
29 RG, and the actual PERG all were affected by experimental glaucoma and TTX, indicating that they cont
30 titatively identify proteomic alterations in experimental glaucoma, and highlight many immune mediato
32 orded from macaques with advanced unilateral experimental glaucoma, and were simulated by averaging O
33 uniform field and PERG responses produced by experimental glaucoma are related and are largely a cons
34 eactive astrocytes in optic nerve heads with experimental glaucoma but not in the optic nerve head of
36 objective measurements in monkeys with early experimental glaucoma correlated highly, with a mean +/-
38 total of 41 rhesus macaques with unilateral experimental glaucoma (EG) each had three or more weekly
39 lative axon loss was -14% on average for all experimental glaucoma (EG) eyes within 6% (measurement n
59 rease of albumin in the retinas of eyes with experimental glaucoma may serve to protect the retina ag
60 and its phosphorylation were evaluated in an experimental glaucoma model in Brown Norway rats and in
61 IOP should be maintained below this level in experimental glaucoma models if selective ganglion cell
63 .3-3.8 mM, n = 3) or laser-induced monocular experimental glaucoma (n = 6), and from six normal human
72 ained from 10 rhesus monkeys with unilateral experimental glaucoma that was induced by argon laser tr
73 igate the neural and sensitivity losses from experimental glaucoma to establish the framework for a q
74 uthors studied RGC neurotrophin transport in experimental glaucoma using acute intraocular pressure (
87 Rs that could be eliminated by TTX or severe experimental glaucoma were present in responses to brief
88 epends on spiking activity and is reduced in experimental glaucoma when visual sensitivity losses are
89 labeling were not significantly affected by experimental glaucoma, with a mean decrease of 15% compa
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