ライフサイエンスコーパス: electroretinographic

1 d VPP mice is consistent with histologic and electroretinographic abnormalities determined in previou

2 These electroretinographic abnormalities were correlated with

3 photopsia, minimal funduscopic changes, and electroretinographic abnormalities.

4 All 14 patients had electroretinographic abnormalities.

5 ents displayed a complete absence of vision, electroretinographic amplitude, and PLR at low light int

6 Electroretinographic amplitudes (full-field flash ERG) f

7 ls of IGF-I showed progressive impairment of electroretinographic amplitudes up to complete loss of r

8 On the 21st day, all rats underwent electroretinographic analyses followed by collection of

9 resultant congenic mice was evaluated using electroretinographic analyses.

10 Full-field scotopic electroretinographic analysis (ERG) was performed to mea

11 Both electroretinographic and anatomic methods were used to a

12 Electroretinographic and immunohistochemical analyses of

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

15 type and monogenic controls by histological, electroretinographic, and biochemical analysis.

16 n decrease ischemic damage to the retina, by electroretinographic assessment of visual function and b

17 Unexpectedly, the rate of reduction in electroretinographic B-wave amplitude in eyes infected w

18 nd of each treatment in dark-adapted maximal electroretinographic b-wave amplitude.

19 of either the presence or the absence of an electroretinographic b-wave.

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.

23 Strikingly, these electroretinographic deficits are abrogated in a dose-de

24 However, electroretinographic dysfunction began at 6 months in hi

25 Electroretinographic (ERG) a-wave responses were recorde

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

28 Electroretinographic (ERG) and morphometric analyses wer

29 ssessed by comparing full-field, white-flash electroretinographic (ERG) data obtained before and afte

30 Electroretinographic (ERG) methods were used to determin

31 Electroretinographic (ERG) methods were used to investig

32 To study the development of the electroretinographic (ERG) oscillatory potentials (OPs)

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

35 In a longitudinal design, electroretinographic (ERG) records and digital fundus im

36 ology, we eliminated the rod contribution to electroretinographic (ERG) responses by generating doubl

37 Electroretinographic (ERG) responses in rats treated wit

38 Electroretinographic (ERG) responses of eyes injected wi

39 evaluate the function of the neural retina, electroretinographic (ERG) responses to full-field stimu

40 Rod isolated electroretinographic (ERG) responses to full-field stimu

41 Consistently, the scotopic and photopic electroretinographic (ERG) responses to single-flash sti

42 y, protein expression, retinoid content, and electroretinographic (ERG) responses were evaluated befo

43 Dark-adapted electroretinographic (ERG) responses were twofold greate

44 ull mutations of GRK1 (GRK1 -/-) cone-driven electroretinographic (ERG) responses, including an a-wav

45 Psychophysical and electroretinographic (ERG) studies indicate that patient

46 hotoreceptor status was evaluated by various electroretinographic (ERG) techniques, retinoid analyses

47 immunoblot, immunohistochemistry, TUNEL, and electroretinographic (ERG) techniques.

48 Electroretinographic (ERG) thresholds of mutant fish are

49 al coherence tomography (SD-OCT), full-field electroretinographic (ERG), and color vision testing.

50 Histologic, electroretinographic (ERG), and molecular studies were p

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

53 In contrast to human patients, our electroretinographic examinations of Pde6h(-/-) mice sug

54 To compare retinal function via full-field electroretinographic (ffERG) recordings in 6.5-year-old

55 Electroretinographic findings showed abnormalities in fo

56 clinical manifestations (including abnormal electroretinographic findings).

57 d had no overt ocular defects or decrease in electroretinographic function, up to P28.

58 uated clinically and with psychophysical and electroretinographic measurements of rod and cone functi

59 eterozygously was examined by histologic and electroretinographic measurements.

60 There is neither electroretinographic nor histologic evidence of photorec

61 No demonstrable electroretinographic or histologic changes occurred to s

62 Electroretinographic photoreceptor responses had equal r

63 to assess the physiological role of Panx1 by electroretinographic recordings and also to ensure the s

64 We conducted electroretinographic recordings from dark- and light-ada

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

67 At 12 Hz, electroretinographic response amplitudes and phases prim

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

70 Electroretinographic responses from treated eyes were mo

71 orrelated with the development of visual and electroretinographic responses in the animal.

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

74 Electroretinographic responses to brief ganzfeld flashes

75 Standard clinical 30-Hz flicker electroretinographic responses were also measured.

76 Electroretinographic responses were clearly measurable o

77 Retinal ganglion cell survival and pattern electroretinographic responses were compared in normal c

78 cant changes in ophthalmoscopic findings and electroretinographic responses were detected.

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

82 atrophy and maintained near-normal levels of electroretinographic responses.

83 lecular biological, histological and flicker electroretinographic results have established that mice

84 While the behavioral and electroretinographic results indicate that PLC beta 4 pl

85 Electroretinographic spectral sensitivity analysis showe

86 e in N1 and P1 peak amplitudes on multifocal electroretinographic testing, and change in serum omega-

87 ual acuity or retinal function by multifocal electroretinographic testing.

88 (P = .12) or retinal function by multifocal electroretinographic testing.

89 in temporal tuning (both psychophysical and electroretinographic) were found only within visual fiel