ライフサイエンスコーパス: retinal damage

1 ion of proliferating MGPCs in the absence of retinal damage.

2 ptors is implicated as a causative factor to retinal damage.

3 used to treat ophthalmic infections without retinal damage.

4 n activator (uPA)] in excitotoxicity-induced retinal damage.

5 -antiplasmin, failed to attenuate KA-induced retinal damage.

6 l-glutamate have been implicated in ischemic retinal damage.

7 nts were inaccurate in the presence of outer retinal damage.

8 offer protection against excitotoxin-induced retinal damage.

9 ived neurotrophic factor (BDNF) reduces this retinal damage.

10 the material in vitreous and variable local retinal damage.

11 in parallel with the increasing severity of retinal damage.

12 stantial, and there was little other obvious retinal damage.

13 damage or by CNTF or FGF2 in the absence of retinal damage.

14 s been reported to play an important role in retinal damage.

15 equired to prevent the voriconazole-mediated retinal damage.

16 diffuse to the posterior segment, triggering retinal damage.

17 ociated with Muller glia and MGPCs following retinal damage.

18 -consuming, and carry risks of infection and retinal damage.

19 uller glia to reenter the cell cycle without retinal damage.

20 trols, as well as to identify early signs of retinal damage.

21 ts and by histopathologic evidence of severe retinal damage.

22 um that was mainly responsible for secondary retinal damage.

23 1 predispose mice to age- and light-mediated retinal damage.

24 in increased susceptibility to light-induced retinal damage.

25 se to intrinsic signals remain despite inner retinal damage.

26 dies against retinal antigens and results in retinal damage.

27 eared to vary with the severity of the laser retinal damage.

28 an important factor in toxoplasmosis-induced retinal damage.

29 eurogenic potential capable of responding to retinal damage.

30 n of photoreceptors or ouabain-induced inner retinal damage.

31 defense mechanism against pressure-mediated retinal damage.

32 betic macular edema without visible signs of retinal damage.

33 issue and was protective from photooxidative retinal damage.

34 filtration, therefore contributing to reduce retinal damage.

35 se provides early evidence of stress-related retinal damage.

36 gy examination was also performed to confirm retinal damage.

37 mice display increased retinal apoptosis and retinal damage.

38 st common and may be due to neurotoxicity or retinal damage.

39 own to block diabetes- and endotoxin-induced retinal damage.

40 response and those that result in extraneous retinal damage.

41 tine, factors besides SAG1 are important for retinal damage.

42 is specifically induced in these cells after retinal damage.

43 part, plays a causative role in KCl-induced retinal damage.

44 to a significant attenuation of KCl-induced retinal damage.

45 eutralizing antibody significantly decreased retinal damage after IR, whereas treatment of retinas or

46 s provide evidence that Hmgb1 contributes to retinal damage after IR.

47 even at relatively low intensities, leads to retinal damage and blindness in wild-type animals.

48 Oxidative stress induces retinal damage and contributes to vision loss in progres

49 dence that Muller glia can proliferate after retinal damage and generate new rods; however, the evide

50 te the mechanism by which alkali burns cause retinal damage and may have importance in designing ther

51 OCT provides objective measures of retinal damage and may offer clues toward understanding

52 g of pathogenic T cells or for effecting the retinal damage and photoreceptor loss typical of EAU.

53 insulin-deficient diabetes, or light-induced retinal damage and protects ganglion cells from apoptosi

54 retinal progenitors that migrate to areas of retinal damage and regenerate lost neurons.

55 istology and ERG analysis revealed increased retinal damage and significant loss of retinal function.

56 l studies, acute blue light exposure induces retinal damage and the use of blue-blocking IOLs lessens

57 cotherapies may well be able to mitigate the retinal damage and vision loss associated with geographi

58 serum RBP4 levels could be a risk factor for retinal damage and vision loss in nondiabetic as well as

59 ation prevented diabetes-induced increase in retinal damage, and increases in VEGF and ICAM-1.

60 he effects of metipranolol, known to prevent retinal damage, and of other antiglaucoma drugs were det

61 nal damage, but the mechanisms that underlie retinal damage are not clearly understood.

62 xicity"), the downstream events that lead to retinal damage are poorly understood.

63 the mechanisms that lead to ischemia-induced retinal damage are poorly understood.

64 ll-deficient mice developed profound RPE and retinal damage at doses that caused minimal effects in w

65 can be specified to avoid not only the inner retinal damage, but also permanent disorganization and s

66 has been proposed to play a pivotal role in retinal damage, but the mechanisms that underlie retinal

67 He may have permanent retinal damage, but this is still unclear because the op

68 Dark-rearing potentiated retinal damage by light.

69 BDNF) rescues photoreceptors from collateral retinal damage caused by photodynamic therapy (PDT).

70 ty of cone arrestin to prevent light-induced retinal damage caused by prolonged activation of the pho

71 ence that AA MS patients exhibit accelerated retinal damage compared to CA MS patients.

72 caspase-independent apoptosis contribute to retinal damage during murine cytomegalovirus (MCMV) reti

73 sion strikingly increased with the extent of retinal damage, especially at the photoreceptors, in con

74 cient diet rats exhibited protection against retinal damage from either intermittent or hyperthermic

75 tamate have been suggested to play a role in retinal damage in a number of blinding diseases such as

76 tive in preventing or reducing light-induced retinal damage in all transgenic rats.

77 on of plasminogen activators might attenuate retinal damage in blinding retinal diseases in which hyp

78 a can serve as a source of new neurons after retinal damage in both fish and birds.

79 hondria initiate the subsequent irreversible retinal damage in experimental uveitis.

80 There was no evidence of retinal damage in eyes treated with insulin and FGF2.

81 These changes seem consistent with retinal damage in human glaucoma (focal field defects),

82 eneration in fish but is not expressed after retinal damage in mice.

83 Although glutamate can cause retinal damage in part by hyperstimulating its receptors

84 Retinal damage in teleosts, unlike mammals, induces robu

85 Light-induced retinal damage in transgenic rats depends on the time of

86 tion factor Ascl1 is upregulated in MG after retinal damage in zebrafish and is necessary for regener

87 Following retinal damage, in which MGPCs are known to form, mTor s

88 retina which may contribute to ameliorating retinal damage induced by HFD.

89 retinal glial cells contribute critically to retinal damage induced by RD and provide a new avenue fo

90 In the absence of retinal damage, insulin, IGF1 and FGF2 induced pS6 in Mu

91 tis (EAU), recent work has demonstrated that retinal damage involves oxidative stress early in uveiti

92 The time course of light-induced T17M retinal damage is biphasic, with an initial decline in r

93 Visual field loss due to retinal damage is considered irreversible, and methods a

94 The experiments confirmed that the retinal damage is not mediated by direct effect of the a

95 precisely how inefficient autophagy promotes retinal damage is unclear.

96 In conclusion, we propose that central retinal damage leads to enhanced peripheral vision by se

97 ensity (20 000 lux for 30 min) light-induced retinal damage (LIRD) as compared with WT, indicating im

98 ansient amplification of Wnt signaling after retinal damage may unlock the latent regenerative capaci

99 Retinal damage models suggested that rod cell death indu

100 LB(gld) mice, correlating with the increased retinal damage observed in BALB(gld) mice.

101 Retinal damage occurred as a direct result of total aver

102 d in Muller glia in response to NMDA-induced retinal damage or by CNTF or FGF2 in the absence of reti

103 No differences in retinal damage or parasite growth were observed, indicat

104 ession levels of Pax2 are increased by acute retinal damage or treatment with growth factors.

105 To assess retinal damage, outer nuclear layer (ONL) thickness was

106 jection-induced retinal detachment can cause retinal damage, particularly when SR vector bleb include

107 m permissible exposure safety limit produces retinal damage preceded by a transient reduction in the

108 infiltration in the inner retina, leading to retinal damage primarily localized to the ganglion cells

109 of the retina showed no evidence of residual retinal damage resulting from the colchicine injections

110 nflammatory protein production, leukostasis, retinal damage, signs of anterior uveitis, and uncouplin

111 retinal pigment epithelium (RPE) may lead to retinal damage similar to that associated with the early

112 After either kainate- or colchicine-induced retinal damage, some of the newly generated cells expres

113 Although high levels of glutamate induce retinal damage, subtoxic levels of glutamate directly st

114 Much of the retinal damage that characterizes the disease results fr

115 rovides an alternative rod-dominant model of retinal damage that shares a surprising number of featur

116 In the postnatal retina, acute retinal damage transiently induces transitin expression

117 g potential therapeutic approaches to reduce retinal damages upon DR progression.

118 expressing mononuclear cells contributing to retinal damage via recruitment of CD4(+) T cells.

119 Retinal damage was also observed but only from postnatal

120 Retinal damage was assessed by immunolocalization studie

121 Retinal damage was assessed by measuring outer nuclear l

122 Retinal damage was assessed in quail fed a carotenoid-de

123 The degree of retinal damage was assessed morphologically by measuring

124 ere measured to assess retinal function, and retinal damage was evaluated by light microscopy.

125 In this study, the potential of retinal damage was investigated by using radiant exposur

126 x metalloproteinases in excitotoxin-mediated retinal damage was investigated.

127 rix metalloproteinase (MMP)-9 in KCl-induced retinal damage was investigated.

128 Progressive retinal damage was quantified by direct counting of rod

129 No clinically apparent warning of outer retinal damage was seen in the SD-OCT images of long-ter

130 However, retinal damage was still evident at 6 months after supra

131 he inflamed retina, CD4(+) T cells can cause retinal damage when they are not properly regulated.

132 that IL-8 is upregulated upon laser-induced retinal damage, which recapitulates enhanced vasculariza

133 This demonstrates that inner retinal damage, without extensive photoreceptor damage,

134 The decreasing width of the retinal damage zone suggests that photoreceptors migrati