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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
65 hand dexterity increased in individuals with spinal cord injury after the I-wave protocol.
66 an reveal early inflammation associated with spinal cord injury after thoracic aortic ischemia-reperf
67       Rehabilitative exercise in humans with spinal cord injury aims to engage residual neural networ
68 al hydrolase (UCHL-1) biomarker of brain and spinal cord injuries and address the clinical need.
69 individuals with chronic incomplete cervical spinal cord injury and 17 uninjured participants.
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
75 e design and development of therapeutics for spinal cord injury and motor disorders.
76  driver of neuronal dysfunction in models of spinal cord injury and neurodegeneration, the contributi
77 ify their 'regenerative transcriptome' after spinal cord injury and NPC grafting.
78      To investigate what role C5b-9 plays in spinal cord injury and recovery, we generated littermate
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
81      Vertebral LVs remodel extensively after spinal cord injury and VEGF-C-induced vertebral lymphang
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
86 tered miRNA after severe, moderate, and mild spinal cord injury, and SHAM surgery, respectively.
87 rly complete recovery of neonatal mice after spinal cord injury, and suggest strategies that could be
88 ues in healthy animals or safety concerns in spinal cord injury animals.
89        In animals and people with incomplete spinal cord injury, appropriate operant conditioning of
90 antitative MRI metrics, obtained early after spinal cord injury, are predictive of clinical outcome.
91    This has important consequences following spinal cord injury, as neurons fail to regrow.
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
101                                              Spinal cord injury creates physical and chemical barrier
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
104                     We present evidence that spinal cord injury directly causes increased risk for ba
105  neurons, a regeneration-incompetent central spinal cord injury does not.
106 ther potential biomarkers during a traumatic spinal cord injury event.
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
110                               Mouse model of spinal cord injury-immune depression syndrome followed b
111         In patients with spinal cord injury, spinal cord injury-immune depression syndrome induces pn
112                    We aimed to develop a new spinal cord injury-immune depression syndrome mouse mode
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
115              Using a mouse model of ischemic spinal cord injury in male and female mice, we show that
116                                              Spinal cord injury in mammals is thought to trigger scar
117                                This model of spinal cord injury in mice mimics a clinical scenario re
118  receptor, promotes recovery after traumatic spinal cord injury in mice, a benefit achieved in part b
119 erface that alleviated gait deficits after a spinal cord injury in non-human primates.
120 onal sprouting and functional recovery after spinal cord injury in rodents.
121      This study investigates the response to spinal cord injury in the gray short-tailed opossum (Mon
122 new 'neural relays' across sites of complete spinal cord injury in vivo in rodents(1,2).
123                  They used a rodent model of spinal cord injury, in which human neural progenitor cel
124       We propose that future drug trials for spinal cord injury include pressure and microdialysis mo
125 r organs, including the spleen, resulting in spinal cord injury-induced immunodeficiency.
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
128                                              Spinal cord injury is characterized by acute cellular an
129 like cells are regulated in the aftermath of spinal cord injury is critical to design future manipula
130                  Therapeutic development for spinal cord injury is hindered by the difficulty in cond
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
133 ection to spinal motor neurons from ischemic spinal cord injury (ISCI).
134 Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI), examination.
135 s of time to anaesthetized mice sustaining a spinal cord injury leads to an instantaneous reduction o
136                                              Spinal cord injury leads to the disruption of neural cir
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.
140                               After complete spinal cord injury, mammals, including mice, rats and ca
141 , and ultra-sensitive detection of brain and spinal cord injury markers in bodily fluids is an unmet
142            Significance statement: Brain and spinal cord injury may lead to permanent disability and
143  early inflammatory response was observed in spinal cord injury mice characterized in lungs by a decr
144                                              Spinal cord injury mice were more susceptible to methici
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
147            Inhibition of calmodulin in a rat spinal cord injury model with the licensed drug trifluop
148 nitor cells in vitro and host axons in a rat spinal cord injury model.
149 cystic cavities in a clinically relevant rat spinal cord injury model.
150 cystic cavities in a clinically relevant rat spinal cord injury model.
151 rapeutic siRhoA carrier in a rat compression spinal cord injury model.
152 veral neurological disorders such as stroke, spinal cord injury, multiple sclerosis, amyotrophic late
153                                    Traumatic spinal cord injury occurs when an external physical impa
154                                    Following spinal cord injury, oligodendrocyte loss and an inhibito
155 rs for the evaluation of injury severity for spinal cord injury or other forms of traumatic, acute, n
156             Upon testing clinical samples of spinal cord injury patients and healthy controls, both p
157     The ability to improve motor function in spinal cord injury patients by reactivating spinal centr
158  significant quality-of-life issues for many spinal cord injury patients.
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
162                                              Spinal cord injury remains a scientific and therapeutic
163                          Tissue repair after spinal cord injury requires the mobilization of immune a
164  cerebellar ataxia, Alzheimer's disease, and spinal cord injury, respectively.
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
167                                              Spinal cord injury results in locomotor impairment attri
168                                    Traumatic spinal cord injury results in severe and irreversible lo
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
175                                 Spasms after spinal cord injury (SCI) are debilitating involuntary mu
176 isms that regulate macrophage function after spinal cord injury (SCI) are poorly understood.
177                                              Spinal cord injury (SCI) at high spinal levels (e.g., ab
178  To investigate metabolic changes in chronic spinal cord injury (SCI) by applying MR spectroscopy in
179                             Individuals with spinal cord injury (SCI) can face decades with permanent
180                            More than half of spinal cord injury (SCI) cases occur in the cervical reg
181                                    Traumatic spinal cord injury (SCI) causes a cascade of degenerativ
182                                              Spinal cord injury (SCI) causes immune dysfunction, incr
183                                        Acute spinal cord injury (SCI) causes systemic immunosuppressi
184                                        After spinal cord injury (SCI) chronic inflammation hampers re
185                                              Spinal cord injury (SCI) disrupts critical physiological
186 didate cellular treatment approach for human spinal cord injury (SCI) due to their unique regenerativ
187                      Axon regeneration after spinal cord injury (SCI) fails due to neuron-intrinsic m
188               Most studies targeting chronic spinal cord injury (SCI) have concluded that neural stem
189 eurotransplantation research to the clinical spinal cord injury (SCI) human population, and few studi
190                                              Spinal cord injury (SCI) impairs the flow of sensory and
191 t therapy promotes functional recovery after spinal cord injury (SCI) in animal and clinical studies.
192  nm pulse emission) on the spinal cord after spinal cord injury (SCI) in rats.
193  the loss of neuron-derived monoamines after spinal cord injury (SCI) in rats.
194                                              Spinal cord injury (SCI) induces a centralized fibrotic
195                                              Spinal cord injury (SCI) interrupts descending projectio
196                 The inflammatory response to spinal cord injury (SCI) involves localization and activ
197 STATEMENT Pain sensitization associated with spinal cord injury (SCI) involves poorly understood mala
198                                              Spinal cord injury (SCI) is a common cause of disability
199 SCI tissue remodeling.SIGNIFICANCE STATEMENT Spinal cord injury (SCI) is characterized by formation o
200                       Chronic pain caused by spinal cord injury (SCI) is notoriously resistant to tre
201 GNIFICANCE STATEMENT Chronic pain induced by spinal cord injury (SCI) is often permanent and debilita
202            The goal of stem cell therapy for spinal cord injury (SCI) is to restore motor function wi
203      Whether this ability is preserved after spinal cord injury (SCI) is unknown.
204 function or lesion pathology after traumatic spinal cord injury (SCI) is unknown.
205 or muscle injury, but the Acomys response to spinal cord injury (SCI) is unknown.
206 NS trauma and disease.SIGNIFICANCE STATEMENT Spinal cord injury (SCI) leads to profound functional de
207                                              Spinal cord injury (SCI) leads to wide-spread neurodegen
208                                              Spinal cord injury (SCI) lesions present diverse challen
209 sensory or serotonergic axons through severe spinal cord injury (SCI) lesions.
210 IGNIFICANCE STATEMENT Neuropathic pain after spinal cord injury (SCI) may in part be caused by upregu
211                         Humans with cervical spinal cord injury (SCI) often recover voluntary control
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
215                                              Spinal cord injury (SCI) remains one of the biggest chal
216                                              Spinal cord injury (SCI) remains one of the most debilit
217                            Traumatic primary spinal cord injury (SCI) results in paralysis below the
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
223                              In this regard, spinal cord injury (SCI), Alzheimer's disease, and other
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
226                                    Following spinal cord injury (SCI), astrocytes demonstrate long-la
227       Spontaneous remyelination occurs after spinal cord injury (SCI), but the extent of myelin repai
228                Microglia are activated after spinal cord injury (SCI), but their phagocytic mechanism
229 are killed for several weeks after traumatic spinal cord injury (SCI), but they are replaced by resid
230         In people or animals with incomplete spinal cord injury (SCI), changing a spinal reflex throu
231      Spasticity, a common complication after spinal cord injury (SCI), is frequently accompanied by c
232                                        After spinal cord injury (SCI), meningeal ILC2s are activated
233                                    Following spinal cord injury (SCI), newly formed endothelial cells
234 chanism of inflammation-regulation following spinal cord injury (SCI), orchestrated by CD200-ligand (
235                                 Months after spinal cord injury (SCI), respiratory deficits remain th
236                                           In spinal cord injury (SCI), the initial damage leads to a
237                                    Following spinal cord injury (SCI), the innate immune response of
238  influence many pathological processes after spinal cord injury (SCI), the intrinsic molecular mechan
239                                           In spinal cord injury (SCI), timely therapeutic interventio
240              Also, in rat T9-T10 hemisection spinal cord injury (SCI), we demonstrated that the tailo
241 esolution of inflammation is defective after spinal cord injury (SCI), which impairs tissue integrity
242 ical deficits and long-term disability after spinal cord injury (SCI).
243 subjects with neurogenic bladder (NB) due to spinal cord injury (SCI).
244 ethod to treat challenging diseases, such as spinal cord injury (SCI).
245 of a million individuals in the US live with spinal cord injury (SCI).
246 e commonly encountered in people living with spinal cord injury (SCI).
247 of bone mineral density (BMD) in people with Spinal Cord Injury (SCI).
248 st common symptoms manifested in humans with spinal cord injury (SCI).
249 f a spastic muscle in humans with incomplete spinal cord injury (SCI).
250 promotes recovery of function in humans with spinal cord injury (SCI).
251 measures in a preclinical model of traumatic spinal cord injury (SCI).
252 e (TG) was performed in persons with chronic spinal cord injury (SCI).
253 y associated with persistent pain induced by spinal cord injury (SCI).
254 examine their therapeutic potential to treat spinal cord injury (SCI).
255 cytes that protect tissue and function after spinal cord injury (SCI).
256 he recovery of hand motor function following spinal cord injury (SCI).
257 rious neurological pathologies and following spinal cord injury (SCI).
258  and impaired wound healing, as occurs after spinal cord injury (SCI).
259 d in humans with incomplete chronic cervical spinal cord injury (SCI).
260 the recovery of hand function in humans with spinal cord injury (SCI).
261  among the most challenging complications of spinal cord injury (SCI).
262 o improve locomotor function in the rat with spinal cord injury (SCI).
263  the potential to restore function following spinal cord injury (SCI).
264 subjects with neurogenic bladder (NB) due to spinal cord injury (SCI).
265 opment of chronic neuropathic pain following spinal cord injury (SCI).
266 paring in Bmal1(-/-) mice after T9 contusive spinal cord injury (SCI).
267 ioning sciatic nerve axotomy that precedes a spinal cord injury (SCI).
268 rly capable of plastic adaptations following spinal cord injury (SCI).
269  promotes functional recovery in humans with spinal cord injury (SCI).
270 oride extruder KCC2 lead to spasticity after spinal cord injury (SCI).
271 ndamental to reestablish motor control after spinal-cord injury (SCI).
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
278                             In patients with spinal cord injury, spinal cord injury-immune depression
279 izes glial activation in an ex vivo model of spinal cord injury, suggesting a new strategy for spinal
280                             After paralyzing spinal cord injury the adult nervous system has little a
281 c spinal cord injury (tSCI) and nontraumatic spinal cord injury - the most common form of which is de
282                     After CNS trauma such as spinal cord injury, the ability of surviving neural elem
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
286                                  Appropriate spinal cord injury treatment at individual centers.
287        Spinal cord MRI findings in traumatic spinal cord injury (tSCI) and nontraumatic spinal cord i
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.
292        As rats are used extensively to model spinal cord injury, we asked if the S1 CST response is c
293                   Eight weeks post contusive spinal cord injury, we built a peripheral nerve graft br
294 normal muscle tone in awake female mice with spinal cord injuries were investigated.
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
300 PCMS without exercise in 13 individuals with spinal cord injury with similar characteristics.

 
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