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1 ggable targets for treating victims of acute nervous system injury.
2 urodegenerative disorders, including central nervous system injury.
3 axon initial segment is a common event after nervous system injury.
4 r axonal damage and other aspects of central nervous system injury.
5 growth during development, and after central nervous system injury.
6 s the recovery of adult mammals from central nervous system injury.
7 failed to be activated in a model of central nervous system injury.
8     Angiogenesis is a key feature of central nervous system injury.
9 sidered detrimental to recovery from central nervous system injury.
10 ndent ionic homoeostasis in areas of central nervous system injury.
11 ribe a previously unrecognized mechanism for nervous system injury.
12 peutic strategies for recovery after central nervous system injury.
13 e device delivery, and prevention of central nervous system injury.
14 ) to limit axonal regeneration after central nervous system injury.
15 tion may limit functional outcomes following nervous system injury.
16  functional recovery following many types of nervous system injury.
17 of neurodegeneration after the acute central nervous system injury.
18 ssue reorganization and repair after central nervous system injury.
19 tension and neuronal migration after central nervous system injury.
20 een posited to affect outcomes after central nervous system injury.
21 microglial activation in response to central nervous system injury.
22 an important role in the response to central nervous system injury.
23 ated in the pathophysiology of acute central nervous system injury.
24 promote further recovery after adult central nervous system injury.
25 ion during development and following central nervous system injury.
26 s with neurodegenerative diseases or central nervous system injury.
27 into mechanisms of and recovery from central nervous system injury.
28 larger issue of network remodeling following nervous system injury.
29 eurologic outcomes in children after central nervous system injury.
30 ducing stressors as might occur with central nervous system injury.
31 city and improve motor control after central nervous system injuries.
32 ory features characteristic of other central nervous system injuries.
33 egulated along pain-signaling pathways after nervous system injuries.
34 hey may be beneficial in repairing mammalian nervous system injuries.
35 pment of NgR1-based therapeutics for central nervous system injuries.
36 nt of neuropathic pain after SCI and related nervous system injuries.
37                                After central nervous system injury, a rapid cellular and molecular re
38 nd debilitating outcome of traumatic central nervous system injury, affecting up to 80% of individual
39 immune response may be of benefit in central nervous system injury, although T cells may have either
40 elopment and have important implications for nervous system injuries and diseases because disruption
41 very after brachial plexus avulsion or other nervous system injuries and diseases.
42  an attractive strategy for the treatment of nervous system injuries and neurodegenerative and demyel
43 ead to development of therapeutics to combat nervous system injuries and neurodegenerative diseases.
44 overy may inspire new treatments for central nervous system injuries and neurodegenerative diseases.
45                      Muscle spasticity after nervous system injuries and painful low back spasm affec
46                                              Nervous system injury and disease have broad effects on
47                                   In central nervous system injury and disease, apolipoprotein E (APO
48  inhibitors that limit recovery from central nervous system injury and disease.
49 logy of MS as well as the cascade of central nervous system injury and might facilitate early detecti
50 deviate reparative programming after central nervous system injury and offer a new therapeutic target
51 immune equilibrium by stroke in both central nervous system injury and repair responses.
52 ping our understanding of basic mechanism of nervous system injury and repair.
53 vated during embryogenesis or in response to nervous-system injury and disease.
54 reverse neurologic deficits, prevent further nervous system injury, and optimize overall oncologic th
55  neuronal excitability, axon outgrowth after nervous system injury, and protein folding in neurodegen
56 ), myocardial necrosis, the level of central nervous system injury, and the secondary multiple system
57  measurement of S100B as a marker of central nervous system injury; and 4) follow-up head computed to
58 ls (RGCs), used as a common model of central nervous system injury, are particularly vulnerable to me
59 0% of all fatalities, second only to central nervous system injury as a cause of death.
60 w cells to replace those lost due to central nervous system injury, as well as a source of trophic mo
61             The specific mechanisms by which nervous system injury becomes a chronic pain state remai
62 ricle have multiple risk factors for central nervous system injury, both before and after the Fontan
63 te neurodegenerative dysfunction and central nervous system injuries, but reprogrammed neurons are di
64 may be helpful in preventing serious central nervous system injury, but studies in children are lacki
65 y could provide a rapid diagnosis of central nervous system injury caused by infections.
66 iple traumas but without evidence of central nervous system injury constituted the control group.
67 y causes, immaturity, infection, and central nervous system injury decreased, while necrotizing enter
68              Lower GA, lower BW, and central nervous system injury emerged as significant risk factor
69 t strategies for both central and peripheral nervous system injury from cancer therapies is a major u
70 ly-onset IVH followed by significant central nervous system injury had low PPVT-R scores that decline
71 onset IVH and subsequent significant central nervous system injury had the lowest PPVT-R scores initi
72 ion and edema across the spectrum of central nervous system injury has driven extensive investigation
73 al stem cell (NSC) response to acute central nervous system injury; however, it is unclear whether th
74  ultrasound on memory impairment and central nervous system injury in a rat model of vascular dementi
75 te (FBP) has been shown to attenuate central nervous system injury in adult animals.
76 ration and functional recovery after central nervous system injury in adult mammals.
77  in the study of axonal growth after central nervous system injury in an attempt to provide guidance
78 s, (2) the mechanism and etiology of central nervous system injury in children with CHD, (3) perioper
79 as potential biomarkers for ischemic central nervous system injury in humans.
80 jective tool to assess the degree of central nervous system injury in individuals with PCS and to dis
81 ked, functional recovery after acute central nervous system injury in rats, suggesting that inhibitin
82 s limited information on the pathogenesis of nervous system injury in these infections.
83 acellular nucleotides in response to central nervous system injury including trauma and ischemia have
84 ecovery when initiated shortly after central nervous system injury, including blockade of myelin-deri
85 detection and management of ischemic central nervous system injury, including for mild damage associa
86 neuroprotective effects in models of central nervous system injury, including in a contusive spinal c
87 add further strength to the model of central nervous system injury-induced efflux of L-glutamate thro
88                        Patients with central nervous system injuries, injury requiring medical care i
89 ficial in the treatment of traumatic central nervous system injuries involving the excitotoxic action
90                                              Nervous system injury is a frequent result of cancer the
91          Manganese is known to cause central nervous system injury leading to parkinsonism and to con
92  have hypothesized that irreversible central nervous system injury may up-regulate proinflammatory me
93 covery of mammalian axonal projections after nervous system injury observed to date, highlighting an
94 extracorporeal membrane oxygenation, central nervous system injury (odds ratio, 26.5; 95% CI, 7.3-96.
95                                      Central nervous system injury often results in a pervasive inhib
96                                              Nervous system injury or disease leads to activation of
97 ay offer therapeutic opportunities following nervous system injury or disease where myelin inhibits n
98 he circulation, cardiac dysfunction, central nervous system injury, or sepsis.
99 d do not exhibit motor disturbances, central nervous system injury, or ultrastructural evidence of mi
100 complicated by infection (P=0.04) or central nervous system injury (P<0.001); however, there were inc
101           These findings may suggest central nervous system injury potentially related to COVID-19 in
102                                      Central nervous system injury re-initiates neurogenesis in anamn
103 ntribution to neurodegenerative diseases and nervous system injuries, recent studies have revealed un
104  clinical symptoms of central and peripheral nervous system injury remain incompletely understood.
105          SC receptors that detect peripheral nervous system injury remain incompletely understood.
106 limits functional repair following a central nervous system injury remains a challenge.
107 growth and functional recovery after central nervous system injury remains elusive.
108 the mechanism underlying its role in central nervous system injury remains unclear.
109                Functional regeneration after nervous system injury requires transected axons to recon
110 cond-order dorsal horn sensory neurons after nervous system injury, showing that SCI can trigger chan
111 ical researchers in disciplines from central nervous system injury/stroke, mental/addictive disorders
112 oke pain in patients with chronic pain after nervous system injury than in patients without somatosen
113 ly recognize and clear cellular debris after nervous system injury to maintain brain homeostasis, but
114                               Covert central nervous system injury was numerically lower with TG both
115 ce of cumulative end organ damage or central nervous system injury was observed.
116 rotective cytokine in models of ischemic and nervous system injury, where it reduces neuronal apoptos
117 uropathological conditions and acute central nervous system injury, which has driven therapeutic inte
118 d to T3D and a restricted pattern of central nervous system injury with damage limited to the hippoca

 
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