ライフサイエンスコーパス: retinal injury

1 anatomic ganglion cell loss suggests a focal retinal injury.

2 ction against retinal pigment epithelium and retinal injury.

3 re, conserved in the steady state and during retinal injury.

4 functions in a mouse model of laser-induced retinal injury.

5 f cortical reorganization following acquired retinal injury.

6 ges also underlie MG reprogramming following retinal injury.

7 2 expression can effectively reduce ischemic retinal injury.

8 rovide an efficacious treatment for ischemic retinal injury.

9 ls injected intravitreally in mice eyes with retinal injury.

10 f HDAC2 isoform in a mouse model of ischemic retinal injury.

11 rms were consistent with inner but not outer retinal injury.

12 islocated lens material and surveillance for retinal injury.

13 ollected from the animals 3 months after the retinal injury.

14 eans of monitoring recovery of laser-induced retinal injury.

15 s may provide a novel treatment for ischemic retinal injury.

16 time intervals after light- or laser-induced retinal injury.

17 notype of microglia activated in response to retinal injury.

18 r exogenous agonists can ameliorate ischemic retinal injury.

19 ia-reperfusion injury in an in vivo model of retinal injury.

20 mine the role of CD40 in the pathogenesis of retinal injury.

21 subset of Muller glia that proliferate after retinal injury.

22 distinct phases of the cellular response to retinal injury.

23 cycle occurs within the first 24 hours after retinal injury.

24 c time period in adulthood, and to long-term retinal injury.

25 ants can regenerate normally following acute retinal injury.

26 adult mice to generate neurons from MG after retinal injury.

27 re development of new diagnostic methods for retinal injuries.

28 mans treated for retinal detachment or other retinal injuries.

29 [0.03%]), retinal dystrophy (3 [0.1%] vs 0), retinal injury (5 [0.2%] vs 0), and retinal toxicity (3

30 We set out to assess the dynamics of retinal injury after acute optic neuritis (ON) and their

31 biochemical, and immunological components of retinal injury after alkali burn and explored a novel ne

32 e clinical appearance mirrors that in severe retinal injury after blunt ocular trauma in humans, and

33 s) protection against corneal aberration and retinal injury after pilocarpine delivery using dual-fun

34 was upregulated in Muller cells in models of retinal injury and aging, and CCR1 expression was correl

35 t on microglia involvement in the context of retinal injury and disease.

36 delivery frequently caused focal columns of retinal injury and intraretinal hemorrhages from retinal

37 amage and improves functional outcomes after retinal injury and may be a useful adjunctive treatment

38 pects of the pathophysiology of nonperfusion retinal injury and may improve therapy in patients with

39 , suggesting the possibility of long-lasting retinal injury and neuronal inflammation after primary b

40 photobiomodulation may enhance recovery from retinal injury and other ocular diseases in which mitoch

41 ic oxide (NO) production can cause ischaemic retinal injury and result in blindness.

42 and structural outcomes in animal models of retinal injury and retinal degenerative disease.

43 he temporal changes in gene expression after retinal injury and to relate these changes to the inflam

44 OCT in diagnosing and managing laser-induced retinal injuries, and the importance of timely surgical

45 The Wnt pathway is activated by retinal injury, and prolonging the endogenous Wnt signal

46 Weight drop did not cause reproducible retinal injury, and the energy threshold for retinal inj

47 tence to Muller glia in fish and birds after retinal injury are not expressed in mammals.

48 the photoreceptor rescue effect elicited by retinal injury as well as by injection of exogenous bFGF

49 Within 4 h after retinal injury, ascl1a is induced in Muller glia.

50 ays that can promote neuronal survival after retinal injury, but the intrinsic survival mechanisms in

51 Muller glia respond to retinal injury by a reactive gliosis, but only rarely do

52 brafish are Muller glia (MG) that respond to retinal injury by dedifferentiating into a cycling popul

53 developing and characterizing a rat model of retinal injury caused by blunt ocular trauma.

54 c Th1/Th17 responses and were protected from retinal injury compared with the mice that received PBS

55 Dynamics of acute retinal injury (consisting of abnormal intraretinal ligh

56 of FGFR1 mRNA occurred within 12 hours after retinal injury/detachment, but then declined to near bas

57 ansgene in mice, with the goal of minimizing retinal injury during the subretinal delivery of rAAV-me

58 After both light-induced and laser-induced retinal injury, enhanced migration of microglia is detec

59 In control animals, 7 days after ischemic retinal injury, ERG a- and b-wave amplitudes were signif

60 Outer retinal injury has been well described in glaucoma.

61 After retinal injury in mammals, the retinal pigment epitheliu

62 glial cells (astrocytes and Muller cells) to retinal injury in mice that lack glial fibrillary acidic

63 ogical repair occurs following neurovascular retinal injury in the oxygen-induced retinopathy neonata

64 ng CNS regeneration, we recently showed that retinal injury induces tuba1a gene expression in Muller

65 phthalmitis, increased intraocular pressure, retinal injury, intraocular hemorrhage, traumatic catara

66 Retinal injury is a common cause of profound and intract

67 in the inner nuclear layer, suggesting that retinal injury is more widespread than previously apprec

68 ptor (Oprm1), to be neuroprotective in three retinal injury models.

69 expression of Ikzf1/4 in MG in vivo, without retinal injury, mostly generates iONL cells that share m

70 ducible pattern of changes in the context of retinal injuries or degenerations.

71 ggest that MSC-Exos ameliorate laser-induced retinal injury partially through down-regulation of MCP-

72 After retinal injury, recombination showed tuba1a expression i

73 Laser-induced retinal injuries resulted in circulating anti-retinal an

74 n immune response is elicited after an acute retinal injury resulting in circulating anti-retinal ant

75 Ischemia-reperfusion retinal injury results in generation of highly chemotact

76 Retinal injuries secondary to handheld laser devices may

77 An increased incidence of retinal injuries secondary to handheld lasers has been r

78 Sixteen children (24 eyes) with retinal injuries secondary to handheld lasers were ident

79 We previously found that in zebrafish, retinal injury stimulates Muller glia to generate multip

80 Here, we report that retinal injury stimulates mycb and mych expression and t

81 Previous studies reported that retinal injury stimulates pSmad3 signaling in injury-res

82 h are the top cellular processes affected by retinal injury, suggesting that Mycb and Mych are potent

83 oprotective in a transient ischemia model of retinal injury, suggesting the possible use of AQP4 inhi

84 Retinal injuries that affect the photoreceptors and/or t

85 us opioid administration can reduce ischemic retinal injury was determined by pretreating rats with m

86 retinal injury, and the energy threshold for retinal injury was similar to that for rupture.

87 e patients identified to have handheld laser retinal injuries were included at 2 academic centers.

88 crotizing inflammatory response, infiltrate, retinal injuries with calcification and focal gliosis, r

89 Blunt ocular trauma causes severe retinal injury with death of neuroretinal tissue, scarri

90 o the inferior sclera created a reproducible retinal injury, with central sclopetaria retinae, retina

91 Upon retinal injury, zebrafish Muller glia (MG) transition fr