ライフサイエンスコーパス: retinal injury

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

2 f cortical reorganization following acquired retinal injury.

3 ges also underlie MG reprogramming following retinal injury.

4 2 expression can effectively reduce ischemic retinal injury.

5 rovide an efficacious treatment for ischemic retinal injury.

6 ls injected intravitreally in mice eyes with retinal injury.

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

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

9 islocated lens material and surveillance for retinal injury.

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

11 ction against retinal pigment epithelium and retinal injury.

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

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

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

15 notype of microglia activated in response to retinal injury.

16 r exogenous agonists can ameliorate ischemic retinal injury.

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

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

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

20 subset of Muller glia that proliferate after retinal injury.

21 distinct phases of the cellular response to retinal injury.

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

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

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

25 re development of new diagnostic methods for retinal injuries.

26 mans treated for retinal detachment or other retinal injuries.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 Outer retinal injury has been well described in glaucoma.

51 After retinal injury in mammals, the retinal pigment epitheliu

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

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

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

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

56 Retinal injury is a common cause of profound and intract

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

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

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

60 After retinal injury, recombination showed tuba1a expression i

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

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

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

64 Retinal injuries secondary to handheld laser devices may

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

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

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

68 Retinal injuries that affect the photoreceptors and/or t

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

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

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

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

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