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1 ement of retinal function as measured by the electroretinogram.
2 .9 +/- 5.6 to 45.8 +/- 15.2 muV for photopic electroretinogram.
3 eld photopic negative response (PhNR) of the electroretinogram.
4 asis for cone dystrophy with supernormal rod electroretinogram.
5 s and decreased retinal function measured by electroretinogram.
6 that was reflected in the slow decay of the electroretinogram.
7 ing S- and M-opsins and a preserved photopic electroretinogram.
8 g in abnormal visual function as measured by electroretinogram.
9 ons to this generalization, for example, the electroretinogram.
10 ear identical derived rod responses from the electroretinogram.
11 tern blot analysis, histologic analysis, and electroretinogram.
12 demonstrated in rAAV.sFLT-1-treated eyes by electroretinogram.
13 unction can be assessed using the multifocal electroretinogram.
14 electro-oculogram light rise, and a reduced electroretinogram.
15 syndrome (SARDS) exhibiting a nonrecordable electroretinogram.
16 eservation of visual function as measured by electroretinogram.
17 and increased the amplitude of the photopic electroretinogram.
18 pharmacological treatment through multifocal-electroretinogram.
19 d increased a-wave amplitude of the scotopic electroretinogram.
20 at reported for visual fields and full-field electroretinograms.
21 educed amplitudes and prolonged latencies in electroretinograms.
22 s to estimates of rod function from in vitro electroretinograms.
23 ones, concomitant with reduced cone-mediated electroretinograms.
24 y ranges from structural defects to abnormal electroretinograms.
25 plete loss of visual function as measured by electroretinograms.
26 compromised maximal voltage response in the electroretinograms.
27 aturated fatty acids and severely attenuated electroretinograms.
28 change in the a and b waves of bright-flash electroretinograms.
32 electron microscopy, rhodopsin measurement, electroretinogram activity, and visual acuity, indicatin
34 95% confidence interval [CI] 5.6-10.6), cone electroretinogram amplitude declined exponentially at a
36 USH2A patients lose visual field and cone electroretinogram amplitude faster than patients with RH
37 hout the study duration and exhibited higher electroretinogram amplitude, thicker photoreceptor layer
40 nd tritan thresholds, pattern and full-field electroretinogram amplitudes and implicit times, and mul
41 nths of pioglitazone significantly increased electroretinogram amplitudes in type 2 diabetic obese ra
43 onsyndromic USH2A patients had 30 Hz-flicker electroretinogram amplitudes that were significantly hig
44 isplay scattered OS disorganization, reduced electroretinogram amplitudes, and progressive photorecep
48 function was evaluated 8 weeks later by the electroretinogram and compared with photoreceptor cell l
50 ed retinal stimulus processing by full-field electroretinogram and found impaired photoreceptor funct
51 9.4 +/- 4.6 to 57.6 +/- 8.8 muV for scotopic electroretinogram and from 10.9 +/- 5.6 to 45.8 +/- 15.2
60 attenuation of visual function with abnormal electroretinograms and reduced retinal rhodopsin levels.
61 dly disrupts retinal function as assessed by electroretinograms and vision as assessed by optomotor b
62 ation of Mfn2 and Mlh1 and retinal function (electroretinogram), and the retinopathy continued to pro
64 ity, automated visual field testing, pattern electroretinogram, and spectral-domain optical coherence
66 receptor potential (ERP), a component of the electroretinogram arising from photoisomerization-induce
69 ight adaptation, as evidenced by an impaired electroretinogram b-wave from cones, whereas a dopamine
70 RGS11 produced delays in the ON-BPC-derived electroretinogram b-wave, but no changes in the photorec
75 sing homozygous Nmnat1(V9M) mutant mice, the electroretinogram becomes undetectable and the pupillary
78 ce restricted peripheral vision and scotopic electroretinogram confirmed the diagnosis of retinitis p
79 as indicated by the loss of ON transients in electroretinograms, consistent with a neurotransmission
80 ice showed nonprogressive b-wave deficits on electroretinograms, consistent with compromised BP cell
81 Based on single-photoreceptor recordings, electroretinograms, cortical recordings, and visual beha
82 while Prph2Y/+ animals exhibited a cone-rod electroretinogram defect, Prph2Y/+/Rom1-/- animals displ
86 nd/or macular pigment mottling, and abnormal electroretinograms demonstrating mixed cone and rod dysf
87 retinal function, measured by the multifocal electroretinogram, differs between males and females wit
88 ch as early visual impairment as assessed by electroretinogram, disorganization of lamination and api
90 As a group, CSNB1 patients have a normal electroretinogram (ERG) a-wave, indicative of photorecep
93 rea (V4e white test light) and in full-field electroretinogram (ERG) amplitudes to 0.5- and 30-Hz whi
94 expression, endogenous retinoid levels, and electroretinogram (ERG) analyses were performed on Lrat(
97 uter nuclear layer (ONL) and functionally by electroretinogram (ERG) analysis, 5 to 7 days after expo
100 n the etiology of psychiatric disorders, and electroretinogram (ERG) anomalies have been reported in
106 e impairment of night vision, absence of the electroretinogram (ERG) b-wave, and variable degrees of
108 Amplitude reduction of >50% in the relevant electroretinogram (ERG) component or a peak time shift o
109 mune retinopathy based on clinical features, electroretinogram (ERG) findings, and serum antiretinal
110 Goldmann perimetry, and full-field standard electroretinogram (ERG) from all patients were registere
111 s were classified on the basis of full-field electroretinogram (ERG) Fundus autofluorescence (FAF) an
113 wed nonspecific retinal inflammation, and an electroretinogram (ERG) illustrated decreased amplitude
114 the impact of KCNJ10 mutations on the human electroretinogram (ERG) in four unrelated patients with
117 and photopic negative response (PhNR) of the electroretinogram (ERG) noninvasively with an electrode
123 ouse, which lacks GPR179 and has a no b-wave electroretinogram (ERG) phenotype, to demonstrate that d
125 To evaluate the diagnostic potential of the electroretinogram (ERG) photostress test and the focal c
131 eal injection (IVI) of 25 pmol MTX increased electroretinogram (ERG) response and rhodopsin level in
132 localization of cone opsin, loss of photopic electroretinogram (ERG) responses and loss of cone cells
137 y biochemically, by recording single rod and electroretinogram (ERG) responses, by intracellular free
140 e known to contribute to the mammalian flash electroretinogram (ERG) via activity of third-order reti
145 group were investigated by monocular pattern electroretinogram (ERG), L&M (long and medium wavelength
146 assessed by restoration of the cone-mediated electroretinogram (ERG), optomotor responses, and cone o
147 d examining gene message and protein levels, electroretinogram (ERG), retinal morphology and ultrastr
148 ent in normal numbers, and the a-wave of the electroretinogram (ERG)--reflecting their physiological
149 , brain, and male reproductive organs and by electroretinogram (ERG)-based studies of the retina and
158 ing Gng13(-/-) knockout (KO) mice, recording electroretinograms (ERG) and performing immunocytochemic
159 in the retina, and the scotopic and photopic electroretinograms (ERG) and retinal morphology in wild-
160 athy were recruited, and photopic full-field electroretinograms (ERG) were performed at baseline and
161 no adverse effects on the eye as assessed by electroretinograms (ERG), corneal and retinal tomography
163 sual acuity, constricted fields, and reduced electroretinograms (ERGs) 5 years before death correlate
169 nction was assessed with serial dark-adapted electroretinograms (ERGs) optimized for detection of the
170 However, we find further variability in cone electroretinograms (ERGs) ranging from normal to absent
181 ual acuity loss early in life, nondetectable electroretinograms (ERGs), and little or no detectable v
183 ver, each patient had recordable and similar electroretinograms (ERGs), which demonstrated absent con
188 ith dark-adapted electroretinograms (monthly electroretinograms [ERGs]), and cataract formation with
198 e were no other causes of an electronegative electroretinogram identified in any of the affected pati
201 o sign of vitreous inflammation and abnormal electroretinogram in at least 1 eye), and a negative fam
202 recording electrodes; the maturation of the electroretinogram in preterm infants and in the first ye
204 cal modifications for performing a pediatric electroretinogram, including the possible need for sedat
205 red at 4 weeks of age, although a full-field electroretinogram indicated a visual response was still
214 functional recovery evidenced by multifocal-electroretinogram (mfERG) and microperimetry (MP1) after
216 nship between DE development and: multifocal electroretinogram (mfERG) implicit time (IT) Z-score, mf
219 l parameters of surgical success, multifocal electroretinogram (mfERG), and histopathologic analyses
221 charts, 10-2 visual fields (VFs), multifocal electroretinograms (mfERG), and spectral-domain optical
223 sitivity, retinal function with dark-adapted electroretinograms (monthly electroretinograms [ERGs]),
224 Although the technique for performing an electroretinogram must be modified for young children, w
225 ematic forward genetic Drosophila screen for electroretinogram mutants lacking synaptic transients id
226 statistically significant differences in the electroretinograms obtained between the linezolid-inject
229 at flash responses measured by trans-retinal electroretinogram or single-cell suction electrode recor
230 croscopy parameters, retina cell counts, and electroretinogram parameters were compared between the g
233 mice were longitudinally tested with pattern electroretinogram (PERG) and spectral-domain optical coh
235 eliability, and dynamic range of the pattern electroretinogram (PERG) as a tool to monitor progressiv
236 ical response of RGC was measured by pattern electroretinogram (PERG) in 43 C57BL/6J mice 4 to 6 mont
237 optical coherence tomography (OCT), pattern electroretinogram (PERG) or frequency-doubling technolog
239 ommon inbred mouse strains using the pattern electroretinogram (PERG), a sensitive measure of RGC fun
240 avioral abnormalities was made using pattern electroretinogram (PERG), magnetic resonance imaging (MR
241 d structure were evaluated using the pattern electroretinogram (pERG), spectral domain optical cohere
243 The authors retrospectively analyzed pattern electroretinograms (PERG) recorded twice a year in 32 gl
246 pamine in vision using electrophysiological (electroretinogram), psychophysical (optokinetic tracking
252 t of functional roles in the photoreceptors, electroretinogram recordings demonstrate impaired respon
254 tion in NCKX2-deficient (Nckx2(-/-)) mice by electroretinogram recordings revealed normal photopic b-
258 s but display reduced "on-off" transients in electroretinogram recordings, indicating a failure to ev
259 rget cones and rescue both the cone-mediated electroretinogram response and visual acuity in the Gnat
262 restored rod morphology and the rod-derived electroretinogram response, but cone photoreceptors were
263 ght-blindness models with an electronegative electroretinogram response, which is also characteristic
264 enously expressed rod or cone Talpha rescued electroretinogram responses (ERGs) in mice lacking funct
265 ubretinal delivery of PDE6alpha' rescues rod electroretinogram responses and preserves retinal struct
267 ent, one fourth of the mice showed increased electroretinogram responses in the transplanted eyes.
269 se of vitreo-macular traction and multifocal electroretinogram responses showed a significant increas
272 e exhibited absence of scotopic and photopic electroretinogram responses, a phenotype that resembles
273 nd no statistically significant influence on electroretinogram responses, and used in conjunction wit
276 sion testing, light sensitivity testing, and electroretinograms (retinal imaging and fundus photograp
279 examination, dilated fundus examination, and electroretinograms showed no evidence of vitritis, uveit
283 induced negative-masking behavior and normal electroretinogram, suggesting an intact retina light res
284 e was bilateral and in the context of normal electroretinograms therefore indicates generalized dysfu
285 and the size and density of RPE melanosomes, electroretinograms to study retinal function, and retrog
286 cted individuals, nonrecordable rod-specific electroretinogram traces were recovered after prolonged
288 gatively affected in glaucoma, including the electroretinogram, visual evoked potential, visual spati
289 The visual field was severely decreased and electroretinogram was undetectable in most cases; howeve
295 of neurophysiological responses (multifocal electroretinogram) were decreased in all eccentricity ri
296 f retinal degeneration, and a non-recordable electroretinogram with negligible amplitudes in both eye
297 d photophobia, reduced amplitude of the cone electroretinogram with normal rod responses, normal fund
298 ng to abnormalities of scotopic and photopic electroretinograms with decreased b-wave amplitude as th