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1 oderate, or severe nonproliferative diabetic retinopathy).
2 creased visual acuity secondary to radiation retinopathy.
3 ities were present in the absence of visible retinopathy.
4 lomerular filtration rate, or progression of retinopathy.
5 at cells and disease progression in diabetic retinopathy.
6 y vascular effects of RORalpha deficiency in retinopathy.
7 diabetic eyes that do not manifest clinical retinopathy.
8 o develop a rational screening frequency for retinopathy.
9 al complications and vision loss in diabetic retinopathy.
10 aches may enhance early screening for sickle retinopathy.
11 measured by reactive hyperaemia index, or on retinopathy.
12 rs, suppress pathological vascular growth in retinopathy.
13 pathy, 97.9% (94.9%-99.1%) for proliferative retinopathy.
14 severe NPDR or PDR than among those with no retinopathy.
15 ckness compared to patients with no diabetic retinopathy.
16 promised vascular integrity such as diabetic retinopathy.
17 retinal barrier and the damage is related to retinopathy.
18 malities to those seen in diabetic mice with retinopathy.
19 ts with no history of proliferative diabetic retinopathy.
20 ly effective and cost-effective detection of retinopathy.
21 ling codes used in the treatment of diabetic retinopathy.
22 characteristic of non-proliferative diabetic retinopathy.
23 nship was not seen among those with diabetic retinopathy.
24 portant role in the pathogenesis of diabetic retinopathy.
25 reduced in more advanced stages of diabetic retinopathy.
26 es or targets to investigate and inhibit the retinopathy.
27 ion of the blood-retinal barrier in diabetic retinopathy.
28 d recognized risk factors for progression of retinopathy.
29 he medical record for patients with diabetic retinopathy.
30 deep plexus with sickle SC or proliferative retinopathy.
31 y impairs this process and prevents diabetic retinopathy.
32 th adequate UWFA studies demonstrated sickle retinopathy.
33 those with severe nonproliferative diabetic retinopathy.
34 with macroaneurysm, and 1 eye with radiation retinopathy.
35 ge-related macular degeneration and diabetic retinopathy.
36 ermine the presence and severity of diabetic retinopathy.
37 ent of PDR and slows progression of diabetic retinopathy.
38 se model of Matrigel plug and oxygen-induced retinopathy.
39 eferentially protects against oxygen-induced retinopathy.
40 arious ischemic diseases, including ischemic retinopathies.
41 r pathological angiogenesis in proliferative retinopathies.
42 hology of metastatic cancers and age-related retinopathies.
43 alue for the treatment of human RP and other retinopathies.
44 [0.6 million to 13.3 million]), and diabetic retinopathy (2.6 million [0.2 million to 9.9 million]).
45 0.2% (95% CI, 16.3%-24.1%) for those with no retinopathy, 20.4% (95% CI, 15.3%-27.8%) for those with
46 44.8-52.9]), the prevalence was 72.3% for no retinopathy, 25.4% for mild and moderate nonproliferativ
47 nations at 4 years among patients who had no retinopathy, 3 years among those with mild retinopathy,
48 drainage-vitrectomy developed less radiation retinopathy (30.5% and 37.4% after 5 years, P = .001 and
50 o retinopathy, 3 years among those with mild retinopathy, 6 months among those with moderate retinopa
51 ections that were for proliferative diabetic retinopathy), 8.3% to treat retinal vein occlusions, and
52 athy; Retmarker 73.0% (72.0 %-74.0%) for any retinopathy, 85.0% (83.6%-86.2%) for referable retinopat
53 follows: EyeArt 94.7% (94.2%-95.2%) for any retinopathy, 93.8% (92.9%-94.6%) for referable retinopat
54 tinopathy, 85.0% (83.6%-86.2%) for referable retinopathy, 97.9% (94.9%-99.1%) for proliferative retin
55 severe NPDR or PDR relative to those with no retinopathy (adjusted odds ratio [aOR], 3.59; 95% CI, 1.
56 ion loss in eye pathologies such as diabetic retinopathy, age-related macular degeneration, and centr
57 ions to retinopathy of prematurity, diabetic retinopathy, age-related macular degeneration, and glauc
59 tic target in the treatment of proliferative retinopathies and other diseases dependent on pathologic
60 tients without clinical evidence of diabetic retinopathy and 40 eyes of 40 healthy nondiabetic subjec
61 d with the comparator group (52.3% radiation retinopathy and 57.8% neovascular glaucoma after 5 years
62 were recruited (90 patients with no diabetic retinopathy and 90 patients with NPDR) into the study.
66 enesis in the mouse models of oxygen-induced retinopathy and laser-induced choroid neovascularization
67 enesis in the mouse models of oxygen-induced retinopathy and laser-induced choroid neovascularization
68 Five- and 10-year freedom from radiation retinopathy and optic neuropathy rates were higher in th
69 and appears to promote experimental diabetic retinopathy and that Muller cells orchestrate inflammato
70 an diseases including proliferative diabetic retinopathy and wet age-related macular degeneration.
71 diabetes mellitus patients with no diabetic retinopathy and with non-proliferative diabetic retinopa
72 tive retinopathy, or progression of diabetic retinopathy), and nerve events (a composite of new loss
73 inopathy, 6 months among those with moderate retinopathy, and 3 months among those with severe nonpro
74 7.7) microL/min in the diabetic eyes without retinopathy, and 44.4 (8.3) microL/min in age-matched he
76 cluding retinopathy of prematurity, diabetic retinopathy, and age-related macular degeneration, as we
77 cluding retinopathy of prematurity, diabetic retinopathy, and age-related macular degeneration, threa
78 a set of images from patients with malarial retinopathy, and found it compares favourably with the r
79 determinant in the pathogenesis of diabetic retinopathy, and inhibition of sEH can prevent progressi
82 macular degeneration, glaucoma, and diabetic retinopathy, are ideal candidates for home monitoring pr
83 012 Preferred Practice Patterns for Diabetic Retinopathy as 91 answerable clinical research questions
84 ntial treatment strategy for STGD1 and other retinopathies associated with complement dysregulation.
85 dies in 25 cases of acute zonal occult outer retinopathy (AZOOR) identified using the classification
87 nt microalbuminuria (not reported), incident retinopathy, bodyweight, insulin dose, and endothelial f
88 55%, 40%, 44%, and 30% reported, blindness, retinopathy, cataracts, glaucoma, and double vision resp
90 elopment of microalbuminuria, progression of retinopathy, changes in the glomerular filtration rate,
97 y factors associated with prevalent diabetic retinopathy (DR) among Chinese American adults with type
98 generation in the initial stages of diabetic retinopathy (DR) and 2) the presence of neurodegeneratio
99 ivo function of microRNAs (miRs) in diabetic retinopathy (DR) and age-related macular degeneration (A
100 ral human visual disorders, such as diabetic retinopathy (DR) and age-related macular degeneration (A
101 studies on the relationship between diabetic retinopathy (DR) and cardiovascular disease (CVD) focuse
102 cular diseases; cataract, glaucoma, diabetic retinopathy (DR) and dry eye disease (DED) was assessed.
104 the United States, severe forms of diabetic retinopathy (DR) are significantly associated with a gre
105 mal (NL), 183 glaucoma (GL), and 18 diabetic retinopathy (DR) at Tilganga Institute of Ophthalmology,
107 e of diabetes, annual screening for diabetic retinopathy (DR) by expert human grading of retinal imag
110 the prevalence and risk factors for diabetic retinopathy (DR) in the Singapore Epidemiology of Eye Di
111 Ophthalmic screening to check for diabetic retinopathy (DR) is important to prevent vision loss in
115 nty-six eyes of 69 patients with no diabetic retinopathy (DR) or mild or moderate nonproliferative DR
116 ssion after stratifying by baseline diabetic retinopathy (DR) severity and adjusting for age, sex, ra
117 Diabetic Retinopathy Study (ETDRS) diabetic retinopathy (DR) severity scale (DRSS) grade during the
118 esults regarding the progression of diabetic retinopathy (DR) were neutral with liraglutide (LEADER)
119 tes (HEs) are the classical sign of diabetic retinopathy (DR) which is one of the leading causes of b
120 tal of 143 diabetic eyes-27 with no diabetic retinopathy (DR), 47 with nonproliferative DR (NPDR), 51
122 y (OCTA) may have value in managing diabetic retinopathy (DR), but there is limited information on th
123 ized controlled trials for managing diabetic retinopathy (DR), including diabetic macular edema (DME)
124 s, under chronic diseases including diabetic retinopathy (DR), mitophagy dysregulation and NLRP3 infl
125 of exudative maculopathy including diabetic retinopathy (DR), retinal vein occlusion (RVO), and neov
133 (DSM) may affect his or her risk of diabetic retinopathy (DR); however, few studies have examined thi
134 cular degeneration [AMD], cataract, diabetic retinopathy [DR], and glaucoma) and the overlap between
136 visual acuity (VA; Early Treatment Diabetic Retinopathy [ETDRS] letters) from baseline to 24 weeks.
137 photographs from 7 Early Treatment Diabetic Retinopathy fields were graded in a masked manner using
141 ly important for the development of diabetic retinopathy; however, the interplay between these cells
142 tinopathy, 93.8% (92.9%-94.6%) for referable retinopathy (human graded as either ungradable, maculopa
144 genes associated with the different forms of retinopathies in general do not overlap despite their ov
147 This case report describes a proliferative retinopathy in a 16 year-old patient with co-inheritance
150 ein paxillin, growth factor-induced ischemic retinopathy in the murine oxygen-induced retinopathy mod
151 mmendations regarding screening for diabetic retinopathy include annual dilated retinal examinations
152 ly causes vision impairment in proliferative retinopathies, including retinopathy of prematurity.
154 claim codes used during the care of diabetic retinopathy is a necessary precursor to fully understand
155 oidal angiogenesis, including oxygen-induced retinopathy, laser-induced choroidal neovascularization,
156 cular edema in patients with various initial retinopathy levels (no retinopathy or mild, moderate, or
158 s already in development for targeting these retinopathies may also prove useful for the treatment of
159 These findings suggest that pediatric sickle retinopathy may be more prevalent than previously suspec
161 hological angiogenesis in the oxygen-induced retinopathy mouse model by promoting glycolysis in endot
162 malaria parasites are innocent bystanders in retinopathy-negative CM and the etiology of the coma is
167 can be classified as retinopathy-positive or retinopathy-negative, based on the presence or absence o
168 and cerebrovascular morbidity and mortality; retinopathy, nephropathy, and neuropathy; and harms.
171 ) progression from nonproliferative diabetic retinopathy (NPDR) to PDR based on graded fundus photogr
172 mild and moderate nonproliferative diabetic retinopathy (NPDR), and 2.3% for severe NPDR or prolifer
176 pairment at all ages in 2015 due to diabetic retinopathy (odds ratio 2.52 [1.48-3.73]) and cataract (
177 The Children's Hospital of Philadelphia Retinopathy of Prematurity (CHOP ROP) model uses birth w
178 and The Children's Hospital of Philadelphia Retinopathy of Prematurity (CHOP-ROP) postnatal weight g
179 edicine Approaches to Evaluating Acute-Phase Retinopathy of Prematurity (e-ROP) Study telemedicine sy
180 edicine Approaches to Evaluating Acute-Phase Retinopathy of Prematurity (e-ROP) study was conducted f
181 medicine study) and the Postnatal Growth and Retinopathy of Prematurity (G-ROP) Study (a multicenter
183 eveloped to improve diagnostic competency in retinopathy of prematurity (ROP) by ophthalmologists-in-
184 on retinal image grading of fellow eyes for retinopathy of prematurity (ROP) features (stage, zone a
189 625 mg) is increasingly used to treat type 1 retinopathy of prematurity (ROP), but there remain conce
195 e the rate from the best quartile for severe retinopathy of prematurity and severe intraventricular h
196 ment concepts for diagnosis and treatment of retinopathy of prematurity and to provide interpretation
197 tamin A deficiency, perinatal infections and retinopathy of prematurity as well as specialist pediatr
200 m, birth weight percentile, gestational age, retinopathy of prematurity occurrence, maternal age at c
204 many vision-threatening diseases, including retinopathy of prematurity, diabetic retinopathy, and ag
206 injury on postnatal ultrasonography, severe retinopathy of prematurity, necrotizing enterocolitis, o
207 were no differences in chronic lung disease, retinopathy of prematurity, or NDI among survivors.
208 fection more than 3 days after birth, severe retinopathy of prematurity, severe intraventricular hemo
209 al insufficiency (UPI) increases severity of retinopathy of prematurity, we developed a composite rat
218 local failure, death, enucleation, radiation retinopathy, optic neuropathy, and best-corrected visual
219 ood of progression to proliferative diabetic retinopathy or clinically significant macular edema in p
220 ity of progression to proliferative diabetic retinopathy or clinically significant macular edema was
221 rom no retinopathy to proliferative diabetic retinopathy or clinically significant macular edema was
222 retinal examinations to detect proliferative retinopathy or clinically significant macular edema, bot
223 er 31, 2014, using the search terms diabetic retinopathy OR macular edema AND stroke OR cerebrovascul
224 with various initial retinopathy levels (no retinopathy or mild, moderate, or severe nonproliferativ
225 atio [OR], 2.58; 95% CI, 1.39-4.81; P=.003), retinopathy (OR, 2.24; 95% CI, 1.11-4.50; P = .02), and
226 us images and classified them as healthy (no retinopathy) or having DR, identifying relevant cases fo
228 or vitrectomy, development of proliferative retinopathy, or progression of diabetic retinopathy), an
229 on the progression to proliferative diabetic retinopathy (PDR) and the impact of FAc on changes in Ea
231 epresent worsening of proliferative diabetic retinopathy (PDR) in eyes treated with panretinal photoc
233 n (PRP) when managing proliferative diabetic retinopathy (PDR), with or without concomitant baseline
237 cular edema [DME] and proliferative diabetic retinopathy [PDR]) have a higher risk of CVD will allow
239 re considered central to the pathogenesis of retinopathy-positive CM, their contribution to retinopat
240 Cerebral malaria (CM) can be classified as retinopathy-positive or retinopathy-negative, based on t
241 TGF-beta signaling may protect against rapid retinopathy progression and should not be a target of in
242 te recent advances in therapeutics, diabetic retinopathy remains a leading cause of vision impairment
243 sed on standard screening techniques, sickle retinopathy reportedly occurs in 10% of adolescents with
245 tive), 99.6% (97.0%-99.9%) for proliferative retinopathy; Retmarker 73.0% (72.0 %-74.0%) for any reti
248 nt in contralateral PCME (RR 19.5), diabetic retinopathy (RR 13.1), retinal vein occlusion (RR 12.9),
249 evaluate self-reported adherence to diabetic retinopathy screening examinations among diabetic subjec
252 e clinical importance of changes in diabetic retinopathy severity score (DRSS) in patients with diabe
254 pared with standard Early Treatment Diabetic Retinopathy Study (ETDRS) 7-field photographs (ETDRS pho
255 f FAc on changes in Early Treatment Diabetic Retinopathy Study (ETDRS) diabetic retinopathy (DR) seve
256 nts with 15 or more Early Treatment Diabetic Retinopathy Study (ETDRS) letter score change, mean cont
258 in patients with Early Treatment of Diabetic Retinopathy Study (ETDRS) level 20-35 than in patients w
263 ty (VA) measured on Early Treatment Diabetic Retinopathy Study charts, injection episodes, and compli
264 uity of at least 72 Early Treatment Diabetic Retinopathy Study letter score (20/40 Snellen equivalent
265 yes was 47.8 (16.9) Early Treatment Diabetic Retinopathy Study letter score (approximately 20/100 Sne
267 [<5, 5-9, or >/=10; Early Treatment Diabetic Retinopathy Study letters] in BCVA) after treatment with
268 ategories of no DR (Early Treatment Diabetic Retinopathy Study levels 10-15; n = 154), mild to modera
269 drusen area in the Early Treatment Diabetic Retinopathy Study Report (ETDRS) grid (P = 2.29 x 10(-11
271 tinopathy severity (Early Treatment Diabetic Retinopathy Study scale) were associated with increased
274 orrected electronic Early Treatment Diabetic Retinopathy Study VALS (scores range from 0-100; higher
275 r tufts in the mouse model of oxygen-induced retinopathy, suggesting a role for Cavin-2 in pathogenic
276 ts in the retina of mice with oxygen-induced retinopathy, suggesting that RUNX1 upregulation is a hal
277 ction of neovascular tufts in oxygen-induced retinopathy, supporting the feasibility of targeting RUN
278 ibution around the 5 North Carolina Diabetic Retinopathy Telemedicine Network sites by zip code and t
279 participating in the North Carolina Diabetic Retinopathy Telemedicine Network, (2) the locations of p
281 t insights into the pathogenesis of diabetic retinopathy that will further guide us toward rationally
282 .5 million to 15.4 million), and by diabetic retinopathy to 3.2 million (0.2 million to 12.9 million)
284 echanisms of monogenic as opposed to complex retinopathies, using AMD as an example of the latter.
285 ciated with ocular hypertension, hemorrhagic retinopathy, vitreous hemorrhage, combined traction and
286 lar edema (DME), vision-threatening diabetic retinopathy (VTDR), defined as the presence of severe no
292 could be a therapeutic target for preventing retinopathy, we used a pharmacologic approach (SM16, a s
293 -laser treated active proliferative diabetic retinopathy were recruited from 22 UK ophthalmic centres
295 chieved acceptable sensitivity for referable retinopathy when compared with that of human graders and
296 TATION: Patients with proliferative diabetic retinopathy who were treated with intravitreal afliberce
297 dy by assessing the association of worsening retinopathy with objectively measured functional outcome
300 and 2 years and cumulative probabilities for retinopathy worsening through 2-year without adjustment
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