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1 d VPP mice is consistent with histologic and electroretinographic abnormalities determined in previou
5 ents displayed a complete absence of vision, electroretinographic amplitude, and PLR at low light int
7 ls of IGF-I showed progressive impairment of electroretinographic amplitudes up to complete loss of r
13 irculating antiretinal antibodies along with electroretinographic and visual field abnormalities.
14 terized by progressive visual loss, abnormal electroretinographic and visual field findings in the pr
16 n decrease ischemic damage to the retina, by electroretinographic assessment of visual function and b
20 dent fundus lesions developed accompanied by electroretinographic changes consistent with defects in
21 mpany, Princeton, NJ) produces histologic or electroretinographic changes in the rabbit retina up to
22 development of systemic glucose intolerance, electroretinographic defects, or microvascular disease.
26 inal ischemia, as measured by a cessation of electroretinographic (ERG) activity, was induced in anes
27 days after ischemic injury, morphometric and electroretinographic (ERG) analyses were used to assess
29 ssessed by comparing full-field, white-flash electroretinographic (ERG) data obtained before and afte
33 formed binocularly, using DTL electrodes and electroretinographic (ERG) protocols with flash strength
34 function and structure were evaluated using electroretinographic (ERG) recordings and immunohistoche
36 ology, we eliminated the rod contribution to electroretinographic (ERG) responses by generating doubl
39 evaluate the function of the neural retina, electroretinographic (ERG) responses to full-field stimu
42 y, protein expression, retinoid content, and electroretinographic (ERG) responses were evaluated befo
44 ull mutations of GRK1 (GRK1 -/-) cone-driven electroretinographic (ERG) responses, including an a-wav
46 hotoreceptor status was evaluated by various electroretinographic (ERG) techniques, retinoid analyses
49 al coherence tomography (SD-OCT), full-field electroretinographic (ERG), and color vision testing.
51 deficiency (CNGA3-/- mice) were evaluated by electroretinographic (ERG), morphometric, and Western bl
52 opia, reduced central vision, nystagmus, and electroretinographic evidence of ON bipolar cell dysfunc
54 To compare retinal function via full-field electroretinographic (ffERG) recordings in 6.5-year-old
58 uated clinically and with psychophysical and electroretinographic measurements of rod and cone functi
63 to assess the physiological role of Panx1 by electroretinographic recordings and also to ensure the s
65 lities in IRBP-/- mice were more severe, and electroretinographic recordings revealed a marked loss i
66 the rescue of cone function as indicated by electroretinographic recordings using natural noise stim
68 ction, detected as a deficit in the scotopic electroretinographic response, was improved in this tran
69 hanges in the RPE, and a deficit in scotopic electroretinographic response, which is reflective of im
72 ompleted before eye opening and the onset of electroretinographic responses on postnatal day 13 (P13)
73 RR was present, others may have dark-adapted electroretinographic responses that are within normal ra
77 Retinal ganglion cell survival and pattern electroretinographic responses were compared in normal c
79 ht-adapted cone-isolated (Wratten 26 filter) electroretinographic responses were measured as a functi
80 ent, and all patients had severely decreased electroretinographic responses with predominant rod impa
81 -treated Ins2(Akita) mice exhibited impaired electroretinographic responses, characterized by reduced
83 lecular biological, histological and flicker electroretinographic results have established that mice
86 e in N1 and P1 peak amplitudes on multifocal electroretinographic testing, and change in serum omega-
89 in temporal tuning (both psychophysical and electroretinographic) were found only within visual fiel
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