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1 vements and promotes axon regeneration after spinal cord injury.
2 overing from damage, such as after stroke or spinal cord injury.
3 tegy for ameliorating the adverse effects of spinal cord injury.
4 functional nervous system tissue after major spinal cord injury.
5 participant with quadriplegia from cervical spinal cord injury.
6 euronal survival and axon regeneration after spinal cord injury.
7 icospinal tract (CST), sprout after brain or spinal cord injury.
8 ediated remyelination of central axons after spinal cord injury.
9 management of patients with acute traumatic spinal cord injury.
10 eved through rehabilitation after incomplete spinal cord injury.
11 Es) can mitigate the pathological effects of spinal cord injury.
12 ecruitment of spinal motor neurons following spinal cord injury.
13 pathology and impedes neuronal repair after spinal cord injury.
14 yelination and functional recovery following spinal cord injury.
15 nts were recruited within 72 hours of severe spinal cord injury.
16 and in-hospital mortality of acute traumatic spinal cord injury.
17 routing as well as functional recovery after spinal cord injury.
18 tact cortical structures, such as those with spinal cord injury.
19 after crush and of supraspinal tracts after spinal cord injury.
20 otential therapeutic target for treatment of spinal cord injury.
21 ewiring facilitate functional recovery after spinal cord injury.
22 licated in the neurodegenerative response to spinal cord injury.
23 a novel suppressor of CNS axon repair after spinal cord injury.
24 ost functions after stroke, brain trauma and spinal cord injury.
25 tricting tissue damage and neural loss after spinal cord injury.
26 city that improves behavioral recovery after spinal cord injury.
27 m might be useful for the treatment of acute spinal cord injury.
28 demyelination and functional deficits after spinal cord injury.
29 otal of 63,109 patients with acute traumatic spinal cord injury.
30 edes functional recovery in a mouse model of spinal cord injury.
31 on that restored locomotion after paralyzing spinal cord injury.
32 therapy for restoring sensory function after spinal cord injury.
33 a LPA1 contributes to secondary damage after spinal cord injury.
34 omic neuropathy, traumatic brain injury, and spinal cord injury.
35 rafted into adult immunodeficient rats after spinal cord injury.
36 ef periods of hypoxia in humans with chronic spinal cord injury.
37 res may be a key pharmacotherapeutic goal in spinal cord injury.
38 ikely exaggerated in patients with traumatic spinal cord injury.
39 evel in nine of nine patients with traumatic spinal cord injury.
40 s in secondary axonal degeneration following spinal cord injury.
41 c brain injury, subarachnoid hemorrhage, and spinal cord injury.
42 n CNS injury models of cerebral ischemia and spinal cord injury.
43 oteoglycans (CSPGs) inhibit repair following spinal cord injury.
44 Patients with severe traumatic spinal cord injury.
45 sulfate proteoglycans (CSPGs) produced after spinal cord injury.
46 also singularly promotes regeneration after spinal cord injury.
47 andidate experimental treatments to clinical spinal cord injury.
48 pressure from 12 subjects without traumatic spinal cord injury.
49 site can be measured safely after traumatic spinal cord injury.
50 y elicited by a peripheral lesion and not by spinal cord injury.
51 europrotection in rats subjected to ischemic spinal cord injury.
52 ion in conditions such as cerebral palsy and spinal cord injury.
53 ote axonal regeneration and plasticity after spinal cord injury.
54 nassisted hindlimb locomotion after complete spinal cord injury.
55 tor function in humans with paralysis due to spinal cord injury.
56 migration and reversed astroglial fate after spinal cord injury.
57 ectin-1 (Gal-1) promotes axonal growth after spinal cord injury.
58 asticity, and regeneration in the context of spinal cord injury.
59 a large prospective cohort study after human spinal cord injury.
60 for proof-of-concept studies in people with spinal cord injury.
61 sticity that improves breathing in models of spinal cord injury.
62 l pressure at 85 to 90mm Hg for a week after spinal cord injury.
63 bution of blood components to the outcome of spinal-cord injury.
64 herapeutic treatment for traumatic brain and spinal cord injuries.
65 cells also promise to be useful for treating spinal cord injuries.
66 site in a dorsal column hemisection model of spinal cord injury, a population of transplanted cells m
70 an reveal early inflammation associated with spinal cord injury after thoracic aortic ischemia-reperf
71 Besides obvious motor and sensory paralysis, spinal cord injury also induces a functional SCI-IDS ('i
72 8 patients who had isolated severe traumatic spinal cord injury (American Spinal Injuries Association
73 suggests that, following traumatic brain and spinal cord injuries and stroke, GFAP and its breakdown
75 e validation cohorts of 356 patients without spinal cord injury and 85 traumatic spinal cord injury p
76 of patients with nerve damage resulting from spinal cord injury and are of significant interest for t
77 or hurdle for functional recovery after both spinal cord injury and cortical stroke is the limited re
78 ired for the development of spasticity after spinal cord injury and during amyotrophic lateral sclero
80 oluntary and spinal reflex integration after spinal cord injury and in recovery of function are broad
81 -cost portable BMI for survivors of cervical spinal cord injury and investigated it as a means to sup
82 ia is the leading cause of death after acute spinal cord injury and is associated with poor neurologi
84 driver of neuronal dysfunction in models of spinal cord injury and neurodegeneration, the contributi
85 xploited to enhance spontaneous repair after spinal cord injury and other central nervous system diso
86 oved understanding of the pathophysiology of spinal cord injury and the factors that prevent nerve an
87 at motor evoked potentials size increased in spinal cord injury and uninjured participants after the
88 ts to people with chronic tetraplegia due to spinal cord injury, and represents a major advance, with
92 holds considerable promise as a therapy for spinal cord injury, but the optimal source of these cell
93 t functions in patients affected by brain or spinal cord injury, by providing the brain with a non-mu
94 c remodeling and involves netrin-1 signaling.Spinal cord injury can induce synaptic reorganization an
95 th chronic tetraplegia, due to high-cervical spinal cord injury, can regain limb movements through co
96 udy participant was a 53-year-old man with a spinal cord injury (cervical level 4, American Spinal In
97 would represent a paradigm shift in the way spinal cord injury clinical trials could be conducted.
100 llenged by recent findings in rodent model's spinal cord injury, demonstrating its neuroprotection an
101 into endogenous regenerative processes after spinal cord injury, demonstrating that Nrg1 signalling r
102 ntrast, permanent mitochondrial damage after spinal cord injury depends on calcium influx and mitocho
109 cantly elevated in thoracocervical traumatic spinal cord injury group versus non-spinal cord injury g
110 amma were significantly reduced in traumatic spinal cord injury group versus non-spinal cord injury g
111 raumatic spinal cord injury group versus non-spinal cord injury group, whereas interleukin-1beta, sol
114 ve factors to promote regeneration following spinal cord injury has been promising, yet, few strategi
115 pinal Injuries Association grade C traumatic spinal cord injury, higher spinal cord perfusion pressur
116 As we show here in an in vivo paradigm for spinal cord injury in mice, 5-nonyloxytryptamine and vin
117 receptor, promotes recovery after traumatic spinal cord injury in mice, a benefit achieved in part b
119 cord to model the hemorrhage associated with spinal cord injury in the absence of significant mechani
122 on contemporary national trends of traumatic spinal cord injury incidence and etiology are limited.
125 ary functional neurogenic immune deficiency (spinal cord injury-induced immune deficiency syndrome, S
127 Dynamic Bayesian network suggested that post-spinal cord injury interleukin-10 is driven by inducible
134 of rehabilitation strategies in humans with spinal cord injury is to strengthen transmission in spar
137 l sufficient to cause pneumonia dependent on spinal cord injury lesion level and investigated whether
147 veral neurological disorders such as stroke, spinal cord injury, multiple sclerosis, amyotrophic late
148 been successfully described in patients with spinal cord injury, multiple sclerosis, Guillain-Barre d
149 f pneumonia in patients after motor complete spinal cord injury (odds ratio = 1.35, P < 0.001) indepe
150 rt disease (odds ratio, 7.35; p < 0.001) and spinal cord injury (odds ratio, 8.85; p = 0.008) strongl
152 , and the impact of treatment strategies for spinal-cord injury on hemorrhage-related injury can be e
153 rs for the evaluation of injury severity for spinal cord injury or other forms of traumatic, acute, n
154 ic neurological disorders than in those with spinal cord injury or spina bifida; this difference in m
155 The ability to improve motor function in spinal cord injury patients by reactivating spinal centr
156 systemic inflammatory responses of traumatic spinal cord injury patients versus patients without spin
157 without spinal cord injury and 85 traumatic spinal cord injury patients, individuals with plasma ind
159 had a motor complete, but sensory incomplete spinal cord injury regained voluntary movement after 7 m
160 2012, the incidence rate of acute traumatic spinal cord injury remained relatively stable but, refle
163 s neurological conditions, such as stroke or spinal cord injury, result in an impaired control of the
165 strate that selective blockade of LPA1 after spinal cord injury results in reduced demyelination and
167 ied in 384 patients with clinically complete spinal cord injury (SCI) and consequent anejaculation.
168 Respiratory complications in patients with spinal cord injury (SCI) are common and have a negative
172 onths) had reduced functional recovery after spinal cord injury (SCI) associated with impaired induct
174 ne B (epoB), decreased scarring after rodent spinal cord injury (SCI) by abrogating polarization and
175 g therapies targeting improved recovery from spinal cord injury (SCI) by enhancing OL survival and/or
182 preclinical traumatic brain injury (TBI) and spinal cord injury (SCI) data sets mined from the Visual
183 didate cellular treatment approach for human spinal cord injury (SCI) due to their unique regenerativ
187 robust regeneration of this projection after spinal cord injury (SCI) has not been accomplished.
189 eurotransplantation research to the clinical spinal cord injury (SCI) human population, and few studi
190 t therapy promotes functional recovery after spinal cord injury (SCI) in animal and clinical studies.
197 STATEMENT Pain sensitization associated with spinal cord injury (SCI) involves poorly understood mala
200 SCI tissue remodeling.SIGNIFICANCE STATEMENT Spinal cord injury (SCI) is characterized by formation o
201 e oligodendrocyte (OL) death after traumatic spinal cord injury (SCI) is followed by robust neuron-gl
208 NS trauma and disease.SIGNIFICANCE STATEMENT Spinal cord injury (SCI) leads to profound functional de
211 IGNIFICANCE STATEMENT Neuropathic pain after spinal cord injury (SCI) may in part be caused by upregu
213 dividual inflammatory complement proteins to spinal cord injury (SCI) pathology is not well understoo
215 e a full lower limb perceptual experience in spinal cord injury (SCI) patients, and will ultimately,
216 occurs in a significant portion of traumatic spinal cord injury (SCI) patients, resulting in debilita
218 -based therapies are routinely integrated in spinal cord injury (SCI) rehabilitation programs because
219 one of the most devastating forms of trauma, spinal cord injury (SCI) remains a challenging clinical
221 C2 expression in lumbar MNs is reduced after spinal cord injury (SCI) resulting in a depolarizing shi
225 ays significance roles in recovery following spinal cord injury (SCI), and diabetes mellitus (DM) imp
226 functional recovery and neural repair after spinal cord injury (SCI), as well as axonal regeneration
228 fects on promoting neuronal plasticity after spinal cord injury (SCI), but little is known about its
230 ntaneous recovery can occur after incomplete spinal cord injury (SCI), but the pathways underlying th
231 tes to spontaneous recovery after incomplete spinal cord injury (SCI), but the pathways underlying th
232 are killed for several weeks after traumatic spinal cord injury (SCI), but they are replaced by resid
236 Spasticity, a common complication after spinal cord injury (SCI), is frequently accompanied by c
238 and in vivo models of relevance to traumatic spinal cord injury (SCI), new data indicate that stochas
240 r, its role as a neuroprotective agent after spinal cord injury (SCI), or the involvement of the estr
241 chanism of inflammation-regulation following spinal cord injury (SCI), orchestrated by CD200-ligand (
243 ctivity (NDO) is a well known consequence of spinal cord injury (SCI), recognizable after spinal shoc
244 ablility occurs in primary nociceptors after spinal cord injury (SCI), suggesting that SCI pain also
246 influence many pathological processes after spinal cord injury (SCI), the intrinsic molecular mechan
251 esolution of inflammation is defective after spinal cord injury (SCI), which impairs tissue integrity
276 c pain and loss of bladder control caused by spinal cord injuries (SCIs) can severely affect quality
278 ion in conditions such as cerebral palsy and spinal cord injury.SIGNIFICANCE STATEMENT Acquisition of
279 or stimulating axonal regeneration following spinal cord injury.SIGNIFICANCE STATEMENT Injury of peri
280 visors, urology, multiple sclerosis (MS) and spinal cord injury specialist nurses, and General Practi
281 disrupted and may be improved by therapy in spinal cord injury, stroke, and Parkinson's disease.
283 cord injury patients versus patients without spinal cord injury, suggesting a key role for inducible
285 s system to restore motor function following spinal cord injury, the role of cortical targets remain
286 types rapidly respond to tissue damage after spinal cord injury to form a structurally and chemically
287 sex-stratified incidence of acute traumatic spinal cord injury; trends in etiology and in-hospital m
288 The study was then extended using GBS and spinal cord injury unrelated patients with similar medic
289 Here we characterized a porcine model of spinal cord injury using a combined behavioural, histolo
290 at DHA could exert its beneficial effects in spinal cord injury via neuroplasticity enhancement.
291 ipate in neuronal development, angiogenesis, spinal cord injury, viral invasion, and immune response.
292 In 1993, the estimated incidence of acute spinal cord injury was 53 cases (95% CI, 52-54 cases) pe
293 pressure from the 18 patients with traumatic spinal cord injury was significantly higher than average
296 f an individual with traumatic high-cervical spinal cord injury who coordinated reaching and grasping
298 y, unreliable physical examination, head and spinal cord injury with an AGSW underwent immediate lapa
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