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1 R1 limits the recovery of adult mammals from central nervous system injury.
2 pathway failed to be activated in a model of central nervous system injury.
3 Angiogenesis is a key feature of central nervous system injury.
4 t is considered detrimental to recovery from central nervous system injury.
5 ump-dependent ionic homoeostasis in areas of central nervous system injury.
6 el therapeutic strategies for recovery after central nervous system injury.
7 rkers for axonal damage and other aspects of central nervous system injury.
8 with safe device delivery, and prevention of central nervous system injury.
9 NgR/NgR1) to limit axonal regeneration after central nervous system injury.
10 genesis of neurodegeneration after the acute central nervous system injury.
11 on of tissue reorganization and repair after central nervous system injury.
12 xonal extension and neuronal migration after central nervous system injury.
13 4) has been posited to affect outcomes after central nervous system injury.
14 ator of microglial activation in response to central nervous system injury.
15 ) plays an important role in the response to central nervous system injury.
16 n implicated in the pathophysiology of acute central nervous system injury.
17 eful to promote further recovery after adult central nervous system injury.
18 l extension during development and following central nervous system injury.
19 patients with neurodegenerative diseases or central nervous system injury.
20 rite outgrowth during development, and after central nervous system injury.
21 nsights into mechanisms of and recovery from central nervous system injury.
22 g-term neurologic outcomes in children after central nervous system injury.
23 o GRP-inducing stressors as might occur with central nervous system injury.
24 inhibitory features characteristic of other central nervous system injuries.
25 r development of NgR1-based therapeutics for central nervous system injuries.
26 ellular immune response may be of benefit in central nervous system injury, although T cells may have
27 his discovery may inspire new treatments for central nervous system injuries and neurodegenerative di
31 l injury), myocardial necrosis, the level of central nervous system injury, and the secondary multipl
32 ) serial measurement of S100B as a marker of central nervous system injury; and 4) follow-up head com
33 lion cells (RGCs), used as a common model of central nervous system injury, are particularly vulnerab
35 ce of new cells to replace those lost due to central nervous system injury, as well as a source of tr
36 gle ventricle have multiple risk factors for central nervous system injury, both before and after the
37 ameliorate neurodegenerative dysfunction and central nervous system injuries, but reprogrammed neuron
38 therapy may be helpful in preventing serious central nervous system injury, but studies in children a
39 ith multiple traumas but without evidence of central nervous system injury constituted the control gr
40 pulmonary causes, immaturity, infection, and central nervous system injury decreased, while necrotizi
41 with early-onset IVH followed by significant central nervous system injury had low PPVT-R scores that
42 h early-onset IVH and subsequent significant central nervous system injury had the lowest PPVT-R scor
43 nflammation and edema across the spectrum of central nervous system injury has driven extensive inves
44 the neural stem cell (NSC) response to acute central nervous system injury; however, it is unclear wh
45 ed (LIP) ultrasound on memory impairment and central nervous system injury in a rat model of vascular
48 s issues in the study of axonal growth after central nervous system injury in an attempt to provide g
49 e studies, (2) the mechanism and etiology of central nervous system injury in children with CHD, (3)
51 be an objective tool to assess the degree of central nervous system injury in individuals with PCS an
52 for extracellular nucleotides in response to central nervous system injury including trauma and ische
53 tional recovery when initiated shortly after central nervous system injury, including blockade of mye
54 for the detection and management of ischemic central nervous system injury, including for mild damage
55 to have neuroprotective effects in models of central nervous system injury, including in a contusive
56 results add further strength to the model of central nervous system injury-induced efflux of L-glutam
58 ove beneficial in the treatment of traumatic central nervous system injuries involving the excitotoxi
61 hile on extracorporeal membrane oxygenation, central nervous system injury (odds ratio, 26.5; 95% CI,
64 pathy and do not exhibit motor disturbances, central nervous system injury, or ultrastructural eviden
65 deaths complicated by infection (P=0.04) or central nervous system injury (P<0.001); however, there
68 and clinical researchers in disciplines from central nervous system injury/stroke, mental/addictive d
70 compared to T3D and a restricted pattern of central nervous system injury with damage limited to the
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