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1 o induce endothelial cell chemotaxis and rat corneal neovascularization.
2 he VEGF receptor Flt-1 effectively prevented corneal neovascularization.
3  neutralizing antibodies potently suppressed corneal neovascularization.
4 sed to determine the requirement for VEGF in corneal neovascularization.
5 y endothelial cells and cytokine-induced rat corneal neovascularization.
6 10 from IPF-PF CM resulted in an increase in corneal neovascularization.
7  capillary endothelial cell migration and of corneal neovascularization.
8 an objective method for analyzing changes in corneal neovascularization.
9  keratitis lesion severity and the extent of corneal neovascularization.
10 l angle, reduced anterior chamber volume and corneal neovascularization.
11 80% of ADAMTS9+/- mice developed spontaneous corneal neovascularization.
12  assessed 7 days after chemical burn-induced corneal neovascularization.
13 normal histology, lack of K12 expression and corneal neovascularization.
14 l keratitis lesions as well as the extent of corneal neovascularization.
15 ncreased TSP-1 and endostatin, and inhibited corneal neovascularization.
16  are effective in suppressing injury-induced corneal neovascularization.
17  bone marrow suppression but did not inhibit corneal neovascularization.
18 st that ephrinB1 plays a synergistic role in corneal neovascularization.
19  BM-derived hematopoietic precursor cells in corneal neovascularization.
20 ulation of VEGF, leukocyte infiltration, and corneal neovascularization.
21 ne essential component in the development of corneal neovascularization.
22 t FasL is an important factor in controlling corneal neovascularization.
23 rected visual acuity loss (41%), and central corneal neovascularization (14%).
24               Group 1 developed more central corneal neovascularization (22 eyes; 73.3%) compared to
25  symptoms/signs of dry eye disease including corneal neovascularization (29%), best-corrected visual
26 mon abnormalities were conjunctivitis (51%), corneal neovascularization (44%), dry eye (38%), corneal
27 of VEGF bioactivity potently suppressed both corneal neovascularization (8.3% +/- 8.1% vs. 41.1% +/-
28                                              Corneal neovascularization, a frequent complication of c
29 val CsA implants do not significantly affect corneal neovascularization after high-risk penetrating k
30 f corneal limbal stem cells often results in corneal neovascularization and an optically inferior epi
31 ssion were measured by immunohistochemistry, corneal neovascularization and capillary tube formation
32 articles to HSV-infected mice led to reduced corneal neovascularization and diminished SK lesions.
33 tial and time-dependent relationship between corneal neovascularization and goblet cell density was a
34 cts of subconjunctival-injected parstatin on corneal neovascularization and inflammation in rats were
35                                VEGF-mediated corneal neovascularization and laser-induced choroidal n
36 TLmap to identify HSV-1 SNPs associated with corneal neovascularization and mean peak percentage weig
37 d to investigate the direct effect of PAF on corneal neovascularization and on the expression of angi
38 sed systemically on rats captopril inhibited corneal neovascularization and showed the antitumor acti
39 GF-A, MMP-2, and MMP-9, that are involved in corneal neovascularization and SK pathogenesis.
40 efficacy of PDT-induced vessel regression in corneal neovascularization, and as such the enhanced eff
41                              Graft survival, corneal neovascularization, and corneal lymphangiogenesi
42                              Graft survival, corneal neovascularization, and corneal lymphangiogenesi
43  solvent evaporation METHOD: Graft survival, corneal neovascularization, and corneal lymphangiogenesi
44                              Graft survival, corneal neovascularization, and corneal lymphangiogenesi
45 th, lung compensatory growth, wound healing, corneal neovascularization, and retinal vascularization.
46 inia virus strain WR results in blepharitis, corneal neovascularization, and stromal keratitis.
47                      IL-6- and VEGF-mediated corneal neovascularization are blocked by TA through the
48 aganirsen significantly reduced the relative corneal neovascularization area after 90 days by 26.20%
49                                         Mean corneal neovascularization area at week 52 (visit 12) wa
50 zumab treatment reduced the extent of stable corneal neovascularization as measured by neovascular ar
51 D5AB1 showed an antiangiogenic effect in the corneal neovascularization assay; however, both were eff
52 ed corneal opacity and developed spontaneous corneal neovascularization at older age.
53                           The differences in corneal neovascularization between matrilysin-deficient
54 inated animals based on survival and reduced corneal neovascularization but displayed similar levels
55                               PAF stimulates corneal neovascularization by a receptor-mediated mechan
56 tor levels for at least 5 weeks, and reduced corneal neovascularization by approximately 40% (P = 0.0
57 eal injection, IL-4 blocked the induction of corneal neovascularization by basic fibroblast growth fa
58  anophthalmia, retinal dysplasia, keratitis, corneal neovascularization, cataracts, and calcification
59  inflammation (CD45), apoptosis (TUNEL), and corneal neovascularization (CD31) were evaluated 27 and
60 -induced retinopathy (OIR) and laser-induced corneal neovascularization (CNV) mouse models in vivo.
61                                              Corneal neovascularization (CNV) was induced by micropel
62                                              Corneal neovascularization (CNV) was induced by suture o
63         Niaspan also significantly increased corneal neovascularization compared with nontreatment co
64 giography (AS-OCTA) to determine severity of corneal neovascularization (CoNV).
65 ere were no Grade 3 or higher corneal edema, corneal neovascularization, corneal staining, conjunctiv
66             Ocular infection with HSV causes corneal neovascularization (CV), an essential step in th
67 The ICP4 gene was previously identified as a corneal neovascularization determinant, validating the v
68 ficant difference in incidence and degree of corneal neovascularization developing after penetrating
69 atory response in the eye that may result in corneal neovascularization during blinding immunopatholo
70              Secondary outcome measures were corneal neovascularization following hydrops and complic
71 showed a persistent 34% to 35% inhibition of corneal neovascularization for up to 4 weeks.
72 J/cm(2) resulted in 30% to 50% regression of corneal neovascularization; however, in these animals, a
73      Application of bevacizumab in mice with corneal neovascularization; however, showed variable pen
74 HR = 2.83, 95% CI 1.63-4.90), 4 quadrants of corneal neovascularization (HR = 2.76, 95% CI 1.56-4.86)
75 ified as the correlate of protection against corneal neovascularization, HSV-1 shedding, and latency
76 n receptor substrate-1 expression, inhibited corneal neovascularization in a previous dose-finding ph
77 horoidal neovascularization and VEGF-induced corneal neovascularization in AIF-deficient mice.
78 lar endothelial growth factor (VEGF)-induced corneal neovascularization in C57BL/6 mice was used to e
79 assays were performed to compare the area of corneal neovascularization in matrilysin-deficient mice
80                                  The area of corneal neovascularization in matrilysin-deficient mice
81                  The mean percentage area of corneal neovascularization in mice 3 weeks after corneal
82 ding tube formation, aortic EC spreading and corneal neovascularization in mice.
83 last growth factor (bFGF) was used to induce corneal neovascularization in mice.
84  aganirsen eye drops significantly inhibited corneal neovascularization in patients with keratitis.
85 ay be useful for the objective evaluation of corneal neovascularization in the future.
86                                              Corneal neovascularization in the matrilysin-deficient m
87 asic fibroblast growth factor (bFGF)-induced corneal neovascularization in vivo and in vitro.
88 receptor Neurokinin-1, significantly reduced corneal neovascularization in vivo.
89 d differentiated EPCs in vitro and augmented corneal neovascularization in vivo.
90 lial cells in vivo, and induce regression of corneal neovascularization in vivo.
91 y treating a chronic ocular disease, such as corneal neovascularization, in a rabbit model without sh
92                                              Corneal neovascularization increases the risk of T cell-
93 thelial growth factor in vitro and inhibited corneal neovascularization induced by basic fibroblast g
94 ng pathway in a murine model of inflammatory corneal neovascularization induced by mechanical injury
95 s can inhibit and cause regression of murine corneal neovascularization induced by mechanical-chemica
96 been sutured into BALB/c recipient beds with corneal neovascularization induced by placement of three
97 characterized murine model of suture-induced corneal neovascularization, insult to the nasal side was
98                                              Corneal neovascularization is a vision-threatening condi
99                                              Corneal neovascularization is critical for the progressi
100                This noninflammatory model of corneal neovascularization is especially advantageous be
101                                              Corneal neovascularization is one of the leading causes
102             The role of VEGF in inflammatory corneal neovascularization is unknown and was investigat
103                                              Corneal neovascularization leads to loss of immune privi
104 uggest that MT1-MMP potentiates bFGF-induced corneal neovascularization, likely by modulating the bFG
105  of endostatin-producing cells, resulting in corneal neovascularization, massive infiltration of effe
106 a basic fibroblast growth factor-induced rat corneal neovascularization model.
107 h and regression were determined in a murine corneal neovascularization model.
108 LB/c) with intact corneas (n = 14), and with corneal neovascularization (n = 14).
109 ndary end points included area of pathologic corneal neovascularization, need for transplantation, ri
110                                              Corneal neovascularization (NV) is a sight-threatening c
111                                              Corneal neovascularization (NV) leads to inflammation an
112                                              Corneal neovascularization (NV) predisposes patients to
113                            For assessment of corneal neovascularization (NV), a quantitative method w
114                  The incidence and degree of corneal neovascularization occurring after penetrating k
115 r: age, sex, risk factors for graft failure (corneal neovascularization, ocular surface disease, glau
116 unctate epithelial keratitis, ulceration, or corneal neovascularization on corneal grafts.
117 n, glaucoma, postoperative steroid response, corneal neovascularization or peripheral anterior synech
118 ial rejection as age </=25 years (P = .017), corneal neovascularization (P = .001), donor trephinatio
119                              A comparison of corneal neovascularization parameters was undertaken bef
120 ects on existing ocular neovascular lesions (corneal neovascularization), PDT monotherapy yielded an
121                                              Corneal neovascularization preceded the appearance of go
122 d 19, in addition to confirming our previous corneal neovascularization QTLs of AngVq1 and AngFq2.
123  demonstrate that scIM gene therapy prevents corneal neovascularization, reduces trauma-induced corne
124                                              Corneal neovascularization represents a key step in the
125 ceived xenografts or cautery manifested less corneal neovascularization than did control animals afte
126 ad a significantly greater effect on induced corneal neovascularization than did TSP-2(-/-), with the
127 ators of the inflammatory and VEGF-dependent corneal neovascularization that follows limbal injury.
128                              The increase in corneal neovascularization was associated with heightene
129  biomicroscopy and fluorescein staining, and corneal neovascularization was confirmed by india ink pe
130 ea, the role of this molecule in controlling corneal neovascularization was examined in this study.
131                                              Corneal neovascularization was induced in Dutch belted r
132                                     Besides, corneal neovascularization was much more extended in SLP
133                                              Corneal neovascularization was present at the time of PK
134  mouse model of suture-induced, inflammatory corneal neovascularization was used to evaluate the lack
135      To determine whether the differences in corneal neovascularization were related to differences i
136 dence that EPCs that contributed to enhanced corneal neovascularization were specifically mobilized f
137 nerves were detected in the areas subject to corneal neovascularization, whereas they persisted in th
138 ls stimulated endothelial cell migration and corneal neovascularization, whereas those from NU cells
139  Using antiangiogenesis treatment to prevent corneal neovascularization, which revokes immune privile
140     PIGF129/VEGF165 heterodimers also induce corneal neovascularization with a maximal vessel length
141          Subconjunctival parstatin inhibited corneal neovascularization, with 200 mug the most effect
142 al neovascularization, growth factor-induced corneal neovascularization, wound healing, and Matrigel

 
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