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1 ng regeneration of injured axons relevant to spinal cord injury.
2 enerative failure of sensory axons following spinal cord injury.
3 worsened long-term outcomes after traumatic spinal cord injury.
4 to secondary injury mechanisms in traumatic spinal cord injury.
5 to enable improved functional outcome after spinal cord injury.
6 conditions, including multiple sclerosis and spinal cord injury.
7 deling, and functional recovery in mice with spinal cord injury.
8 accelerates regeneration of zebrafish after spinal cord injury.
9 ospinal circuits limits motor recovery after spinal cord injury.
10 changes in the atrophied cervical cord after spinal cord injury.
11 generative disease and CNS trauma, including spinal cord injury.
12 therapy is currently in clinical testing for spinal cord injury.
13 igration and functional repair in vivo after spinal cord injury.
14 tcomes in patients with tSCI or nontraumatic spinal cord injury.
15 ach appears to merit clinical translation in spinal cord injury.
16 nt future trials targeting acute and chronic spinal cord injury.
17 migration and reversed astroglial fate after spinal cord injury.
18 sticity that improves breathing in models of spinal cord injury.
19 ecruitment of spinal motor neurons following spinal cord injury.
20 ion in conditions such as cerebral palsy and spinal cord injury.
21 different degrees of paralysis and levels of spinal cord injury.
22 ote axonal regeneration and plasticity after spinal cord injury.
23 nassisted hindlimb locomotion after complete spinal cord injury.
24 owth-competent axons after sciatic nerve and spinal cord injury.
25 tor function in humans with paralysis due to spinal cord injury.
26 ectin-1 (Gal-1) promotes axonal growth after spinal cord injury.
27 asticity, and regeneration in the context of spinal cord injury.
28 for cardiovascular functional recovery after spinal cord injury.
29 a large prospective cohort study after human spinal cord injury.
30 for proof-of-concept studies in people with spinal cord injury.
31 te whether ED peptide has similar effects in spinal cord injury.
32 l pressure at 85 to 90mm Hg for a week after spinal cord injury.
33 vements and promotes axon regeneration after spinal cord injury.
34 overing from damage, such as after stroke or spinal cord injury.
35 tegy for ameliorating the adverse effects of spinal cord injury.
36 functional nervous system tissue after major spinal cord injury.
37 participant with quadriplegia from cervical spinal cord injury.
38 euronal survival and axon regeneration after spinal cord injury.
39 icospinal tract (CST), sprout after brain or spinal cord injury.
40 w flexor and extensor muscles after cervical spinal cord injury.
41 during the chronic phase following traumatic spinal cord injury.
42 ar dysfunction often occurs after high-level spinal cord injury.
43 wth of injured pathways in non-human primate spinal cord injury.
44 ian central nervous system trauma, including spinal cord injury.
45 esents the most common form of non-traumatic spinal cord injury.
46 is required for motor sensory recovery after spinal cord injury.
47 diovascular dysfunction following high-level spinal cord injury.
48 ion in multiple preclinical rodent models of spinal cord injury.
49 ented on the membranes of exosomes following spinal cord injury.
50 r patients with movement disorders following spinal cord injury.
51 ants in human patients with tetraplegia from spinal cord injury.
52 circuits mediates functional recovery after spinal cord injury.
53 and recovery of diaphragm function following spinal cord injury.
54 e limbs remain largely intact after complete spinal cord injury.
55 sons with diabetes, indwelling catheters, or spinal cord injury.
56 onship to long-term outcomes after traumatic spinal cord injury.
57 ercome loss of function after, for instance, spinal cord injury.
58 ute a novel therapy for spasticity following spinal cord injury.
59 to novel approaches to develop therapies for spinal cord injury.
60 generative diseases as well as for brain and spinal cord injuries.
61 pathways of protection in heart, brain, and spinal cord injuries.
62 uiding future studies of human subjects with spinal cord injuries.
63 al axons and restore forelimb function after spinal cord injury(1); however, the molecular mechanisms
64 5 (18.88) years) with subacute (ie, 1 month) spinal cord injury (25 patients with neuropathic pain, 1
66 an reveal early inflammation associated with spinal cord injury after thoracic aortic ischemia-reperf
70 or hurdle for functional recovery after both spinal cord injury and cortical stroke is the limited re
71 ired for the development of spasticity after spinal cord injury and during amyotrophic lateral sclero
72 oluntary and spinal reflex integration after spinal cord injury and in recovery of function are broad
73 -cost portable BMI for survivors of cervical spinal cord injury and investigated it as a means to sup
74 fficacy of this reagent in non-human primate spinal cord injury and its toxicological profile have no
76 driver of neuronal dysfunction in models of spinal cord injury and neurodegeneration, the contributi
79 prevalence of adverse events after traumatic spinal cord injury and to evaluate the effects on long-t
80 at motor evoked potentials size increased in spinal cord injury and uninjured participants after the
82 tors has implications for signaling biology, spinal cord injury and, possibly, the evolution of the c
83 te subset is essential during scarring after spinal cord injury, and its arrest results in motor perf
84 ts to people with chronic tetraplegia due to spinal cord injury, and represents a major advance, with
85 city and promote axon regeneration following spinal cord injury, and results from preclinical studies
87 rly complete recovery of neonatal mice after spinal cord injury, and suggest strategies that could be
90 antitative MRI metrics, obtained early after spinal cord injury, are predictive of clinical outcome.
92 cell grafts support axonal growth following spinal cord injury, but a boundary forms between the imp
93 nd corticospinal growth in non-human primate spinal cord injury', by Wang et al. (doi:10.1093/brain/a
94 c remodeling and involves netrin-1 signaling.Spinal cord injury can induce synaptic reorganization an
95 use of their hands because of amputation or spinal cord injury can use prosthetic hands to restore t
96 th chronic tetraplegia, due to high-cervical spinal cord injury, can regain limb movements through co
97 udy participant was a 53-year-old man with a spinal cord injury (cervical level 4, American Spinal In
98 would represent a paradigm shift in the way spinal cord injury clinical trials could be conducted.
99 atent stem cell niche that is reactivated by spinal cord injury contributing new cells to the glial s
100 y protein Nogo-A applied to rats with severe spinal cord injury could prevent development of neurogen
102 llenged by recent findings in rodent model's spinal cord injury, demonstrating its neuroprotection an
103 into endogenous regenerative processes after spinal cord injury, demonstrating that Nrg1 signalling r
107 ility in individuals with traumatic brain or spinal cord injury, glaucoma and ischemia-reperfusion in
108 in and around the glial scar after mammalian spinal cord injury, have been suggested to be key inhibi
109 ered as a new therapeutic option to overcome spinal cord injury-immune depression syndrome and to dec
113 ng this pulmonary and systemic inflammation, spinal cord injury-immune depression syndrome was observ
114 C4ST1/Chst-11 accelerated regeneration after spinal cord injury in larval and adult zebrafish and kno
118 receptor, promotes recovery after traumatic spinal cord injury in mice, a benefit achieved in part b
121 This study investigates the response to spinal cord injury in the gray short-tailed opossum (Mon
126 cell death 1 molecules, improved survival of spinal cord injury infected mice and enhanced interferon
127 spinothalamic tract function-at 1 month post-spinal cord injury is associated with the emergence and
129 like cells are regulated in the aftermath of spinal cord injury is critical to design future manipula
131 nic/intrinsic neural stem cells (NSCs) after spinal cord injury is severely compromised because the h
132 of rehabilitation strategies in humans with spinal cord injury is to strengthen transmission in spar
135 s of time to anaesthetized mice sustaining a spinal cord injury leads to an instantaneous reduction o
137 l sufficient to cause pneumonia dependent on spinal cord injury lesion level and investigated whether
138 etabolic alterations are observed in chronic spinal cord injury, likely reflecting neurodegeneration,
139 tion clinically.SIGNIFICANCE STATEMENT After spinal cord injury, loss of bladder control is common.
141 , and ultra-sensitive detection of brain and spinal cord injury markers in bodily fluids is an unmet
143 early inflammatory response was observed in spinal cord injury mice characterized in lungs by a decr
145 on of neuroimaging biomarkers in centres for spinal cord injury might lead to personalised patient ca
146 growth and functional recovery in vivo in a spinal cord injury model through a unique mechanism of a
152 veral neurological disorders such as stroke, spinal cord injury, multiple sclerosis, amyotrophic late
155 rs for the evaluation of injury severity for spinal cord injury or other forms of traumatic, acute, n
157 The ability to improve motor function in spinal cord injury patients by reactivating spinal centr
159 er, patients with impaired voiding following spinal cord injury, patients undergoing nonurologic surg
160 on's disease, amyotrophic lateral sclerosis, spinal cord injury, peripheral neuropathy, and stroke.
161 nal cord after damage (e.g., after stroke or spinal cord injury), possibly assisting recovery of func
165 us system (CNS) injuries, such as stroke and spinal cord injuries, result in the formation of a prote
166 s neurological conditions, such as stroke or spinal cord injury, result in an impaired control of the
169 ied in 384 patients with clinically complete spinal cord injury (SCI) and consequent anejaculation.
170 nctional paradox in the context of traumatic spinal cord injury (SCI) and discuss the underlying mech
171 othelial cells in engulfing myelin debris in spinal cord injury (SCI) and experimental autoimmune enc
172 ll (NSPC) grafts can integrate into sites of spinal cord injury (SCI) and generate neuronal relays ac
173 Loss of bladder control is common after spinal cord injury (SCI) and no causal therapies are ava
174 Respiratory complications in patients with spinal cord injury (SCI) are common and have a negative
178 To investigate metabolic changes in chronic spinal cord injury (SCI) by applying MR spectroscopy in
186 didate cellular treatment approach for human spinal cord injury (SCI) due to their unique regenerativ
189 eurotransplantation research to the clinical spinal cord injury (SCI) human population, and few studi
191 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
199 SCI tissue remodeling.SIGNIFICANCE STATEMENT Spinal cord injury (SCI) is characterized by formation o
201 GNIFICANCE STATEMENT Chronic pain induced by spinal cord injury (SCI) is often permanent and debilita
206 NS trauma and disease.SIGNIFICANCE STATEMENT Spinal cord injury (SCI) leads to profound functional de
210 IGNIFICANCE STATEMENT Neuropathic pain after spinal cord injury (SCI) may in part be caused by upregu
212 e a full lower limb perceptual experience in spinal cord injury (SCI) patients, and will ultimately,
213 one of the most devastating forms of trauma, spinal cord injury (SCI) remains a challenging clinical
214 e timing of surgical decompression for acute spinal cord injury (SCI) remains debated, with substanti
218 munity long after SCI.SIGNIFICANCE STATEMENT Spinal cord injury (SCI) significantly disrupts immunity
219 st common symptoms manifested in humans with spinal cord injury (SCI) to date, its mechanisms of acti
220 aralyzed muscles can be reanimated following spinal cord injury (SCI) using a brain-computer interfac
221 illions of patients suffer from debilitating spinal cord injury (SCI) without effective treatments.
222 c neuropathic pain is a major comorbidity of spinal cord injury (SCI), affecting up to 70-80% of pati
224 ays significance roles in recovery following spinal cord injury (SCI), and diabetes mellitus (DM) imp
225 functional recovery and neural repair after spinal cord injury (SCI), as well as axonal regeneration
229 are killed for several weeks after traumatic spinal cord injury (SCI), but they are replaced by resid
231 Spasticity, a common complication after spinal cord injury (SCI), is frequently accompanied by c
234 chanism of inflammation-regulation following spinal cord injury (SCI), orchestrated by CD200-ligand (
238 influence many pathological processes after spinal cord injury (SCI), the intrinsic molecular mechan
241 esolution of inflammation is defective after spinal cord injury (SCI), which impairs tissue integrity
272 c pain and loss of bladder control caused by spinal cord injuries (SCIs) can severely affect quality
273 mber of individuals with cervical incomplete spinal cord injury show limited functional recovery of e
274 ion in conditions such as cerebral palsy and spinal cord injury.SIGNIFICANCE STATEMENT Acquisition of
275 or stimulating axonal regeneration following spinal cord injury.SIGNIFICANCE STATEMENT Injury of peri
276 se data indicate that RN-NSCs grafted into a spinal cord injury site relay supraspinal control of ser
277 visors, urology, multiple sclerosis (MS) and spinal cord injury specialist nurses, and General Practi
279 izes glial activation in an ex vivo model of spinal cord injury, suggesting a new strategy for spinal
281 c spinal cord injury (tSCI) and nontraumatic spinal cord injury - the most common form of which is de
283 s system to restore motor function following spinal cord injury, the role of cortical targets remain
284 turnover to sustain axon regeneration after spinal cord injury through its actin-severing activity.
285 and preclinical research has used models of spinal cord injury to better elucidate the underlying me
288 tients with acute, severe thoracic traumatic spinal cord injuries (TSCIs), American spinal injuries a
289 The study was then extended using GBS and spinal cord injury unrelated patients with similar medic
290 Here we characterized a porcine model of spinal cord injury using a combined behavioural, histolo
291 ipate in neuronal development, angiogenesis, spinal cord injury, viral invasion, and immune response.
295 ic incomplete cervical, thoracic, and lumbar spinal cord injury were randomly assigned to 10 sessions
296 l of the "engineered tissue" was assessed in spinal cord injuries, where hNSC-derived progenitors and
297 in individuals with chronic, motor complete spinal cord injury, which is a key achievement toward th
298 f an individual with traumatic high-cervical spinal cord injury who coordinated reaching and grasping
299 , it presents as a potential therapeutic for spinal cord injury with evidence for behavioural improve