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1 alling and are mutated in familial exudative vitreoretinopathy.
2 proliferative diseases such as proliferative vitreoretinopathy.
3 cations in the pathogenesis of proliferative vitreoretinopathy.
4 ated in Norrie disease or familial exudative vitreoretinopathy.
5 otic diseases, in RPE cells in proliferative vitreoretinopathy.
6 could be useful in preventing proliferative vitreoretinopathy.
7 RPE dedifferentiation such as proliferative vitreoretinopathy.
8 and a female infant with familial exudative vitreoretinopathy.
9 ch as diabetic retinopathy and proliferative vitreoretinopathy.
10 proliferative diseases such as proliferative vitreoretinopathy.
11 ogression in a rabbit model of proliferative vitreoretinopathy.
12 related human diseases such as proliferative vitreoretinopathy.
13 lmitis, retinal detachment and proliferative vitreoretinopathy.
14 nal detachment associated with proliferative vitreoretinopathy.
15 al hemangioblastomas, and familial exudative vitreoretinopathy.
16 ch as diabetic retinopathy and proliferative vitreoretinopathy.
17 ascular retinopathies, such as proliferative vitreoretinopathy.
18 the current approach to treatment of various vitreoretinopathies.
20 surgery is the development of proliferative vitreoretinopathy, accounting for the failure of 7% to 1
23 s of such retinal disorders as proliferative vitreoretinopathy and age-related macular degeneration.
24 s reparative processes such as proliferative vitreoretinopathy and as a laboratory tool for RPE behav
25 inal membranes associated with proliferative vitreoretinopathy and idiopathic epiretinal membranes.
26 opathy autosomal dominant familial exudative vitreoretinopathy and suggest that it also may be a susc
27 be a useful strategy to treat proliferative vitreoretinopathy and uveitis, ocular diseases initiated
28 ailure to reattach the retina, proliferative vitreoretinopathy, and delayed reabsorption of subretina
29 tinal redetachment by limiting proliferative vitreoretinopathy, and protect against photoreceptor cel
30 imetabolites for modulation of proliferative vitreoretinopathy, antimicrobial agents for endophthalmi
33 crostructural features of familial exudative vitreoretinopathy (FEVR) have not been well described.
34 d with autosomal dominant familial exudative vitreoretinopathy (FEVR) in families linking to the EVR1
42 typically associated with familial exudative vitreoretinopathy (FEVR), can result from mutations in K
43 pants with a diagnosis of familial exudative vitreoretinopathy (FEVR), Norrie disease, Coats' disease
47 oxocariasis (n = 22; 4%), familial exudative vitreoretinopathy (FEVR; n = 18; 3%), rhegmatogenous ret
48 ent retinal detachments due to proliferative vitreoretinopathy, focusing on the most recent reports i
50 rent retinal detachment due to proliferative vitreoretinopathy has grown concomitantly with more expe
53 he later contractile stages of proliferative vitreoretinopathy, interleukin-1 beta (IL-1 beta) and tr
55 inal detachment complicated by proliferative vitreoretinopathy is now most frequently treated by pars
56 Complications consisted of proliferative vitreoretinopathy (n = 13), recurrent neovascularization
57 l vasculitis (n = 4, 6%), familial exudative vitreoretinopathy (n = 3, 4%), and others (n = 12, 18%).
58 amponading agent, preoperative proliferative vitreoretinopathy (PVR) and axial length (AL) of the eye
59 inal membranes associated with proliferative vitreoretinopathy (PVR) and idiopathic epiretinal membra
60 raction) that are intrinsic to proliferative vitreoretinopathy (PVR) and induce the disease itself.
61 n vivo models for experimental proliferative vitreoretinopathy (PVR) and provide a detailed protocol
63 th factor (PDGF) contribute to proliferative vitreoretinopathy (PVR) in experimental models of the di
76 F-alpha is widely expressed in proliferative vitreoretinopathy (PVR) membranes and is present in the
79 ts with retinal detachment and proliferative vitreoretinopathy (PVR) plus vitreous from eyes obtained
81 ctive review of three cases of proliferative vitreoretinopathy (PVR) that developed after successful
83 ailure rates when grade 0 or B proliferative vitreoretinopathy (PVR) was present and higher level 2 f
84 vent or inhibit development of proliferative vitreoretinopathy (PVR) was tested in a dispase-induced
85 ) isoforms are associated with proliferative vitreoretinopathy (PVR), a sight-threatening complicatio
86 PE-19 is an in vitro model for proliferative vitreoretinopathy (PVR), an aberrant wound healing respo
87 e of NF-kappaB in experimental proliferative vitreoretinopathy (PVR), and may offer a novel approach
89 t that drives RPE responses in proliferative vitreoretinopathy (PVR), suggesting that the IGF system
90 ith (n = 7) or without (n = 9) proliferative vitreoretinopathy (PVR), vitreous hemorrhage (n = 10), v
91 cular hole (n = 33), recurrent proliferative vitreoretinopathy (PVR)-related retinal detachment (n =
107 nvestigation were: (1) grade B proliferative vitreoretinopathy (PVR; n = 917), (2) grade C-1 PVR (n =
108 CNV recurrence (OR, 2.6), and proliferative vitreoretinopathy (PVR; OR, 17.6) were statistically sig
109 intraocular fibrosis, known as proliferative vitreoretinopathy, results in a blinding tractional reti
110 retinal detachment (3.65) and proliferative vitreoretinopathy stages A, B, and C (2.06) were elevate
112 typical of human hypovascularization-related vitreoretinopathies, such as familial exudative vitreore
114 ice for management of a variety of pediatric vitreoretinopathies were offered participation in an oph
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