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1 sing three well-established rodent models of optic nerve injury.
2 hat could promote robust axon regrowth after optic nerve injury.
3 ocytes incorporate into the glial scar after optic nerve injury.
4 nd stimulates robust axon regeneration after optic nerve injury.
5 ote functional recovery after spinal cord or optic nerve injury.
6  regulatory and therapeutic candidates after optic nerve injury.
7 ells (RGCs) promotes axon regeneration after optic nerve injury.
8  the anatomic and functional consequences of optic nerve injury.
9 ation and elongation of axon re-growth after optic nerve injury.
10 tic RGC survival and axon regeneration after optic nerve injury.
11 te pathway, enhanced axon regeneration after optic nerve injury.
12 t3 signaling in retinal ganglion cells after optic nerve injury.
13 rative responses occurring in RGCs following optic nerve injury.
14 d protection of RGCs from degeneration after optic nerve injury.
15 eficiency delayed RGC death after mechanical optic nerve injury.
16 rodegeneration above that normally seen with optic nerve injury.
17 ce cell survival and axon regeneration after optic nerve injury.
18 ntiation and promotes RGC survival following optic nerve injury.
19 ene expression changes associated with early optic nerve injury.
20  of retinal ganglion cells in vivo following optic nerve injury.
21 TF) was observed within the retina following optic nerve injury.
22 l but not regeneration in vivo 2 weeks after optic nerve injury.
23 eutic approach to enhance RGC survival after optic nerve injury.
24 GCs) promotes robust axon regeneration after optic nerve injury.
25 ation in the glaucomatous eye, and following optic nerve injury.
26 t and robust regenerative response following optic nerve injury.
27 ls (RGCs) regenerating their axons following optic nerve injury.
28 n regulating adult RGC axon plasticity after optic nerve injury.
29  to regenerate long axons beyond the site of optic nerve injury.
30  is no effective treatment for this ischemic optic nerve injury.
31 sed RGC axon re-extension or sprouting after optic nerve injury.
32 rrelate with either IOP level or severity of optic nerve injury.
33 n of ephrin-A expression in conjunction with optic nerve injury.
34 after metamorphosis, to be reexpressed after optic nerve injury.
35  neuroprotectant in primate-sized eyes after optic nerve injury.
36 opment of novel and effective treatments for optic nerve injury.
37 and reestablish functional connections after optic nerve injury.
38 yes of rodents of either sex with or without optic nerve injury.
39  mouse RGCs promoted axon regeneration after optic nerve injury.
40 romotes retinal ganglion cell survival after optic nerve injury.
41 inal ganglion cells (RGCs) in a rat model of optic nerve injury.
42 xamine changes occurring in the retina after optic nerve injury.
43     NgR became upregulated in RGCs following optic nerve injury.
44 in more than 1000 proteins at 1 or 5 d after optic nerve injury.
45 -eye differences of 4 mum or greater support optic nerve injury.
46 ing of how or why activity changes following optic nerve injury.
47 thway activity, regulates RGC survival after optic nerve injury.
48  consistently observed in glaucoma and other optic nerve injuries.
49 ic nerve reserve or on the outcome of second optic nerve injuries.
50 ere, we investigated axonal plasticity after optic nerve injury and found that macrophages recruited
51 portome' from RGC somas to their axons after optic nerve injury and identified transport failure of a
52 ted in a reproducible and transient ischemic optic nerve injury and long-term axonal loss.
53 r after spinal cord trauma, ischemic stroke, optic nerve injury and models of multiple sclerosis.
54 etinas from one group of eyes with extensive optic nerve injury and on RGCL isolated by laser capture
55  loss is fastest during the first week after optic nerve injury and slower in subsequent weeks.
56 omotes long-distance axon regeneration after optic nerve injury and uncover a novel and important KLF
57 the secondary degeneration of RGCs following optic nerve injury, and is associated with JNK signaling
58 death in RGCs, including in a mouse model of optic nerve injury, and show that the same pathway is ac
59 ina, their regulated response to retinal and optic nerve injury, and the effects of altered neurotrop
60 ) are unable to regenerate their axons after optic nerve injury, and they soon undergo apoptotic cell
61  accounts for visual function deficits after optic nerve injury, but how axonal insults lead to neuro
62 ows retinal ganglion cell death in models of optic nerve injury, but the mechanism of action remains
63 n-like pattern and are upregulated following optic nerve injury, but the presence of Nogo-A does not
64 xon regeneration and neuronal survival after optic nerve injury by activating mammalian target of rap
65 icant impact on ganglion cell survival after optic nerve injury, combined treatment of the eye and br
66 , the main neuronal population that survives optic nerve injury, express CXCR4 instead.
67 icroscopy, including masked determination of optic nerve injury grade (ONIG; 1, normal; 5, severe, di
68 vided measurements that correlated well with optic nerve injury grade, only the Tono-Pen documented s
69      The loss of RGCs expressing Thy-1 after optic nerve injury has an initial phase of rapid decline
70 c mechanisms involved in the pathogenesis of optic nerve injury has contributed to the use of empiric
71                  In this study, we performed optic nerve injury in adult naked mole-rats, the longest
72                                        After optic nerve injury in mature mammals, retinal ganglion c
73 ondary RGC degeneration occurs after orbital optic nerve injury in monkeys.
74 drinking water, was tested for its effect on optic nerve injury in rats with ocular hypertension.
75 tinal ganglion cells (RGCs) after calibrated optic nerve injury in rats.
76 n of the outer retina was not detected after optic nerve injury in the presence of significant RGC de
77 transporter changes occur with two models of optic nerve injury in the rat.
78 ncreased axon growth both in vitro and after optic nerve injury in vivo.
79 scription factor Sox11 as a key player after optic nerve injury-in DLK signaling of RGC cell death, a
80         Other newer techniques for assessing optic nerve injury include optical coherence tomography,
81                                              Optic nerve injury induces progressive loss in the numbe
82 iment suggests that primary RGC death due to optic nerve injury is associated with secondary death of
83          Results suggest that in vivo DTI of optic nerve injury may be used as a noninvasive tool for
84 erse, a final common pathway for irreparable optic nerve injury may exist.
85 reserve the GCL and rescue vision using this optic nerve injury model would not require additional st
86 f different microglia phenotypes in a murine optic nerve injury model.
87  between our data and reports of retinal and optic nerve injury models in mice, rats, and monkeys.
88 ons in our non-regenerating and regenerating optic nerve injury models, a finding that is inconsisten
89                            Differences among optic nerve injury models, as well as effects on "untrea
90                However, following the second optic nerve injury, most patients' vision fell to the pr
91 uction of regeneration associated genes upon optic nerve injury nor the increased regenerative potent
92                    If ROS have a role in the optic nerve injury of LHON, then increasing mitochondria
93 les axon regeneration in mice and rats after optic nerve injury or peripheral nerve injury, yet the m
94                                    Following optic nerve injury, plasticin expression is elevated tra
95                                              Optic nerve injury produced a significant decrease in th
96                                              Optic nerve injury provokes a sustained CCAAT/enhancer b
97 retina and optic nerve, we characterized the optic nerve injury response and subsequent recovery.
98 ar response to injury.SIGNIFICANCE STATEMENT Optic nerve injury results in death and degeneration of
99 n promoting ganglion cell survival following optic nerve injury results, in part, due to drug-induced
100 3CR1(+) and CCR2(+) monocytes infiltrate the optic nerve injury site and remain present for months.
101                                Surprisingly, optic nerve injury stimulated the expression of Socs3 an
102 sed after excitotoxic injury to RGC somas or optic nerve injury to RGC axons, and reactivation of thi
103                                              Optic nerve injury triggers reduction of Thy-1 promoter
104               Finally, in an animal model of optic nerve injury, we observed early glial activation a
105 and device dependent, supports demyelinating optic nerve injury when done with appropriate technical
106  ganglion cells (RGCs) at 1 and 5 days after optic nerve injury with and without a cocktail of strong

 
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