ライフサイエンスコーパス: spinal cord injury

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

67 Following traumatic spinal cord injury, acute demyelination of spinal axons

68 Neurodegenerative diseases and spinal cord injury affect approximately 50 million peopl

69 hand dexterity increased in individuals with spinal cord injury after the I-wave protocol.

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

74 individuals with chronic incomplete cervical spinal cord injury and 17 uninjured participants.

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

79 reasing pattern was selectively perturbed in spinal cord injury and glioblastoma.

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

83 ributors to axon growth inhibition following spinal cord injury and limit functional recovery.

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

89 tered miRNA after severe, moderate, and mild spinal cord injury, and SHAM surgery, respectively.

90 Anatomically incomplete spinal cord injuries are often followed by considerable

91 The percentage of spinal cord injury associated with falls increased signi

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.

98 The level of spinal cord injury corresponds to the location of these

99 Spinal cord injury creates physical and chemical barrier

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

103 We present evidence that spinal cord injury directly causes increased risk for ba

104 Spinal cord injuries disrupt bidirectional communication

105 Spinal cord injury disrupts the communication between th

106 yte chemotactic protein-1 was central in non-spinal cord injury dynamic networks.

107 ng the enriched extracellular proteome after spinal cord injury for the first time.

108 stinguish systemic inflammation in traumatic spinal cord injury from blunt trauma.

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

112 raumatic spinal cord injury group versus non-spinal cord injury group.

113 Eight individuals with incomplete spinal cord injury (>1 yr; cervical [n = 6], thoracic [n

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

118 erface that alleviated gait deficits after a spinal cord injury in non-human primates.

119 cord to model the hemorrhage associated with spinal cord injury in the absence of significant mechani

120 car, while also increasing axon growth after spinal cord injury in vivo.

121 They used a rodent model of spinal cord injury, in which human neural progenitor cel

122 on contemporary national trends of traumatic spinal cord injury incidence and etiology are limited.

123 We propose that future drug trials for spinal cord injury include pressure and microdialysis mo

124 Blunt trauma and traumatic spinal cord injury induce systemic inflammation that con

125 ary functional neurogenic immune deficiency (spinal cord injury-induced immune deficiency syndrome, S

126 n of docosahexaenoic acid (DHA) 30 min after spinal cord injury induces neuroplasticity.

127 Dynamic Bayesian network suggested that post-spinal cord injury interleukin-10 is driven by inducible

128 Spinal cord injury interrupts descending motor tracts an

129 Spinal cord injury is characterized by acute cellular an

130 Spinal cord injury is currently incurable and treatment

131 Disability following spinal cord injury is due to failure of axon regeneratio

132 Spinal cord injury is followed by glial scar formation,

133 Therapeutic development for spinal cord injury is hindered by the difficulty in cond

134 of rehabilitation strategies in humans with spinal cord injury is to strengthen transmission in spar

135 Spinal-cord injury is characterized by primary damage as

136 Contusive spinal cord injury leads to a variety of disabilities ow

137 l sufficient to cause pneumonia dependent on spinal cord injury lesion level and investigated whether

138 Thoracic spinal cord injury level was confirmed as an independent

139 Significance statement: Brain and spinal cord injury may lead to permanent disability and

140 ire spinal systems to restore function after spinal cord injury might soon be within reach.

141 We developed a 2-photon laser-induced spinal cord injury model to follow morphological and Ca(

142 and serotonergic fibers in a rat hemisection spinal cord injury model.

143 owth and motor function recovery in a rodent spinal cord injury model.

144 cystic cavities in a clinically relevant rat spinal cord injury model.

145 cystic cavities in a clinically relevant rat spinal cord injury model.

146 rapeutic siRhoA carrier in a rat compression spinal cord injury model.

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

151 Recovery after a spinal cord injury often requires that axons restore syn

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

158 significant quality-of-life issues for many spinal cord injury patients.

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

161 However, in view of recent advances in spinal cord injury research and demand from patients, cl

162 This opens new pathways for investigation in spinal cord injury research.

163 s neurological conditions, such as stroke or spinal cord injury, result in an impaired control of the

164 Acute traumatic spinal cord injury results in disability and use of heal

165 strate that selective blockade of LPA1 after spinal cord injury results in reduced demyelination and

166 Spinal cord injury (SCI) activates macrophages, endowing

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

169 Spasms after spinal cord injury (SCI) are debilitating involuntary mu

170 isms that regulate macrophage function after spinal cord injury (SCI) are poorly understood.

171 People with spinal cord injury (SCI) are predisposed to pressure ulc

172 onths) had reduced functional recovery after spinal cord injury (SCI) associated with impaired induct

173 Spinal cord injury (SCI) at high spinal levels (e.g., ab

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

176 Severe spinal cord injury (SCI) can cause neurological dysfunct

177 Traumatic brain injury (TBI) and spinal cord injury (SCI) can lead to major disability an

178 A major portion of spinal cord injury (SCI) cases affect midcervical levels

179 Traumatic spinal cord injury (SCI) causes a cascade of degenerativ

180 Acute spinal cord injury (SCI) causes systemic immunosuppressi

181 Spinal cord injury (SCI) causes the release of danger si

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

184 Axon regeneration after spinal cord injury (SCI) fails due to neuron-intrinsic m

185 Axon regeneration after spinal cord injury (SCI) fails due to neuron-intrinsic m

186 Traumatic spinal cord injury (SCI) has been shown to trigger struc

187 robust regeneration of this projection after spinal cord injury (SCI) has not been accomplished.

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 t therapy promotes functional recovery after spinal cord injury (SCI) in animal and clinical studies.

191 stability and propulsion after low thoracic spinal cord injury (SCI) in animals and humans.

192 strategy to improve functional outcome after spinal cord injury (SCI) in humans.

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 the communication be

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 Astrogliosis after spinal cord injury (SCI) is a major impediment to functi

199 High-thoracic or cervical spinal cord injury (SCI) is associated with several crit

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

202 Spinal cord injury (SCI) is frequently accompanied by a

203 te after injury, and therefore recovery from spinal cord injury (SCI) is limited.

204 Whether this ability is preserved after spinal cord injury (SCI) is unknown.

205 function or lesion pathology after traumatic spinal cord injury (SCI) is unknown.

206 We recently showed that spinal cord injury (SCI) leads to a decrease in mRNA edi

207 Spinal cord injury (SCI) leads to irreversible neuronal

208 NS trauma and disease.SIGNIFICANCE STATEMENT Spinal cord injury (SCI) leads to profound functional de

209 Spinal cord injury (SCI) lesions present diverse challen

210 sensory or serotonergic axons through severe spinal cord injury (SCI) lesions.

211 IGNIFICANCE STATEMENT Neuropathic pain after spinal cord injury (SCI) may in part be caused by upregu

212 Eight chronic (3-13 years) spinal cord injury (SCI) paraplegics were subjected to l

213 dividual inflammatory complement proteins to spinal cord injury (SCI) pathology is not well understoo

214 Spinal cord injury (SCI) patients develop chronic pain i

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

217 We show that microglia at sites of spinal cord injury (SCI) rapidly produce the danger sign

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

220 Spinal cord injury (SCI) remains one of the most debilit

221 C2 expression in lumbar MNs is reduced after spinal cord injury (SCI) resulting in a depolarizing shi

222 Traumatic spinal cord injury (SCI) results in a cascade of tissue

223 Spinal cord injury (SCI) results in devastating neurolog

224 In this regard, spinal cord injury (SCI), Alzheimer's disease, and other

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

227 Following spinal cord injury (SCI), astrocytes demonstrate long-la

228 fects on promoting neuronal plasticity after spinal cord injury (SCI), but little is known about its

229 Spontaneous remyelination occurs after spinal cord injury (SCI), but the extent of myelin repai

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

233 After a spinal cord injury (SCI), CNS axons fail to regenerate,

234 After spinal cord injury (SCI), CNS axons fail to regenerate,

235 Following spinal cord injury (SCI), immune-mediated secondary proc

236 Spasticity, a common complication after spinal cord injury (SCI), is frequently accompanied by c

237 After spinal cord injury (SCI), meningeal ILC2s are activated

238 and in vivo models of relevance to traumatic spinal cord injury (SCI), new data indicate that stochas

239 Following spinal cord injury (SCI), newly formed endothelial cells

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 (

242 After spinal cord injury (SCI), poor ability of damaged axons

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

245 Following spinal cord injury (SCI), the innate immune response of

246 influence many pathological processes after spinal cord injury (SCI), the intrinsic molecular mechan

247 In patients with subacute spinal cord injury (SCI), the motor system undergoes pro

248 In spinal cord injury (SCI), the severity of disease is qua

249 Also, in rat T9-T10 hemisection spinal cord injury (SCI), we demonstrated that the tailo

250 After an incomplete spinal cord injury (SCI), we know that plastic reorganiz

251 esolution of inflammation is defective after spinal cord injury (SCI), which impairs tissue integrity

252 ragm paralysis associated with high cervical spinal cord injury (SCI).

253 tributions to chronic pain in a rat model of spinal cord injury (SCI).

254 strongly induced at 24 h and 72 h after the 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 g treatment of neural tissue damage, such as spinal cord injury (SCI).

258 d with negative outcomes in individuals with spinal cord injury (SCI).

259 unctional recovery in animal models of adult spinal cord injury (SCI).

260 a in secondary pathology following contusive spinal cord injury (SCI).

261 e loss of descending 5-HT projections due to spinal cord injury (SCI).

262 canonical signaling Wnts are increased after spinal cord injury (SCI).

263 ic acid, plays a role in the pathogenesis of spinal cord injury (SCI).

264 ion of corticospinal tract (CST) axons after spinal cord injury (SCI).

265 macrophages and assess their viability after spinal cord injury (SCI).

266 ubcortical damage due to incomplete cervical spinal cord injury (SCI).

267 rious neurological pathologies and following spinal cord injury (SCI).

268 and impaired wound healing, as occurs after spinal cord injury (SCI).

269 y associated with persistent pain induced by spinal cord injury (SCI).

270 d in humans with incomplete chronic cervical spinal cord injury (SCI).

271 the recovery of hand function in humans with spinal cord injury (SCI).

272 among the most challenging complications of spinal cord injury (SCI).

273 examine their therapeutic potential to treat spinal cord injury (SCI).

274 o improve locomotor function in the rat with spinal cord injury (SCI).

275 the potential to restore function following spinal cord injury (SCI).

276 c pain and loss of bladder control caused by spinal cord injuries (SCIs) can severely affect quality

277 Spinal cord injuries (SCIs) often result in permanent da

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.

282 e used as a standardized tool for future CST spinal cord injury studies.

283 cord injury patients versus patients without spinal cord injury, suggesting a key role for inducible

284 After paralyzing spinal cord injury the adult nervous system has little a

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

294 Eight weeks post contusive spinal cord injury, we built a peripheral nerve graft br

295 ed, whereas patients with isolated brain and spinal cord injuries were excluded.

296 f an individual with traumatic high-cervical spinal cord injury who coordinated reaching and grasping

297 In controls and mice with spinal cord injuries with spasticity, spinal-to-sciatic

298 y, unreliable physical examination, head and spinal cord injury with an AGSW underwent immediate lapa

299 (Sac2) gene deletion promoted recovery from spinal cord injury with no side effects.

300 The acronym SCIWORA (Spinal Cord Injury Without Radiographic Abnormality) was