ライフサイエンスコーパス: sci

1 omplete chronic cervical spinal cord injury (SCI).

2 function in humans with spinal cord injury (SCI).

3 lenging complications of spinal cord injury (SCI).

4 function in the rat with spinal cord injury (SCI).

5 store function following spinal cord injury (SCI).

6 rsistent pain induced by spinal cord injury (SCI).

7 tients with subjective cognitive impairment (SCI).

8 iated with high cervical spinal cord injury (SCI).

9 c pain in a rat model of spinal cord injury (SCI).

10 eutic potential to treat spinal cord injury (SCI).

11 24 h and 72 h after the spinal cord injury (SCI).

12 possibility of delayed postoperative SCI (DP-SCI).

13 the risk of immediate postoperative SCI (IP-SCI).

14 ving MCI or subjective cognitive impairment (SCI).

15 issue and function after spinal cord injury (SCI).

16 motor function following spinal cord injury (SCI).

17 athologies and following spinal cord injury (SCI).

18 healing, as occurs after spinal cord injury (SCI).

19 s to treat disabilities and complications of SCI.

20 ion and to restore functional recovery after SCI.

21 Colloid Interface Sci.

22 e immunity may aid functional recovery after SCI.

23 ation to promote locomotor improvement after SCI.

24 ration and survival of injured neurons after SCI.

25 progression in a clinical relevant model of SCI.

26 s (lncRNAs) have never been characterized in SCI.

27 a driver of persistent pain signaling after SCI.

28 enhancing neuroplasticity and recovery after SCI.

29 nvolved in the regulation and progression of SCI.

30 d promotion of functional recovery following SCI.

31 ion structure and dynamics of such an active SCI.

32 tion and edema, and improving recovery after SCI.

33 stem after chronic clinically motor complete SCI.

34 targets for treatment of muscle spasms after SCI.

35 t substantial intrinsic motor recovery after SCI.

36 individuals with chronic clinically complete SCI.

37 urological function and neuropathology after SCI.

38 nduce respiratory recovery in rats following SCI.

39 after NS/PC transplantation, even in chronic SCI.

40 MEPs monitoring on the risk of developing DP-SCI.

41 iscerned from trauma-induced consequences of SCI.

42 elicits a response that could be toxic after SCI.

43 potent neural progenitor cells into sites of SCI.

44 l impairment and spinal cord pathology after SCI.

45 its remarkable effect on acute and subacute SCI.

46 rtical plasticity and partial recovery after SCI.

47 patients with respiratory dysfunction after SCI.

48 nd ACI can also help decrease the risk of DP-SCI.

49 matter sparing and functional recovery after SCI.

50 I/II clinical trial design studies for human SCI.

51 naling may regulate oligodendrogenesis after SCI.

52 R with DAP and MEPs monitoring and had no IP-SCI.

53 vioral recovery after traumatic experimental SCI.

54 mproves repair and functional recovery after SCI.

55 apeutic potential for the treatment of acute SCI.

56 nd neuron-extrinsic barriers to repair after SCI.

57 gically intact whereas 21 (14%) developed DP-SCI.

58 tory muscle paralysis resulted from cervical SCI.

59 ed an unexpected and dramatic decrease after SCI.

60 neficial effects on locomotor recovery after SCI.

61 significant and independent risk factors for SCI.

62 e outgrowth in vitro and axon regrowth after SCI.

63 urement approaches for depression in chronic SCI.

64 on results in significant regeneration after SCI.

65 potassium channel Kv1.1, is decreased after SCI.

66 r reparative role in the post-acute phase of SCI.

67 ns during spasms in a mouse model of chronic SCI.

68 oves motoneuron and locomotor function after SCI.

69 cells contribute to endogenous repair after SCI.

70 are developed as a modality for treatment of SCI.

71 nt and serve as a potential cell therapy for SCI.

72 -) animals partially improves recovery after SCI.

73 is proposal was based on small, midline stab SCI.

74 d may provide a novel therapeutic target for SCI.

75 em cells or neuroprotective astrocytes after SCI.

76 mission at a cortical and spinal level after SCI.

77 tion, compared with low-thoracic level (Th9) SCI.

78 n that can be therapeutically targeted after SCI.

79 gonist referred to as maresin 1 (MaR1) after SCI actively propagates resolution processes at the lesi

80 ral improvement after traumatic experimental SCI, administrated no combined interventions, and report

81 d in individuals with incomplete or complete SCI (affecting lower limbs' somatosensation), with respe

82 of locomotor functions in rats with moderate SCI, along with reduction of swelling, concomitant compr

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

84 izes the inactivity of single-chain insulin (SCI) analogs (in which the A and B chains are directly l

85 omotor recovery after traumatic experimental SCI and (ii) to estimate the likelihood of reporting bia

86 ges in 30 individuals with chronic traumatic SCI and 31 healthy controls.

87 s or polydendrocytes) also proliferate after SCI and accumulate in large numbers among astrocytes in

88 um (ER) stress occurs in the early stages of SCI and affects prognosis and cell survival.

89 individuals with chronic incomplete cervical SCI and age-matched controls needed to suppress (NOGO) o

90 a novel meningeal cell type that responds to SCI and could lead to new therapeutic insights for neuro

91 phage-specific transcriptional profile after SCI and highlight the lipid catabolic pathway as an impo

92 phage-specific transcriptional profile after SCI and highlight the lipid catabolic pathway as an impo

93 g is required for persistent SA months after SCI and long after isolation of nociceptors is surprisin

94 ir and may be a novel therapeutic target for SCI and other CNS pathologies.

95 hway in mediating spontaneous recovery after SCI and support a focus on spared corticospinal neurons

96 tential of the first human RGMa antibody for SCI and uncovers a new role for the RGMa/Neogenin pathwa

97 with clinically complete spinal cord injury (SCI) and consequent anejaculation.

98 es in recovery following spinal cord injury (SCI), and diabetes mellitus (DM) impairs endothelial cel

99 a significant pathophysiological role after SCI, and may provide a novel therapeutic target for SCI.

100 ransgenic mice promotes motor recovery after SCI, and recombinant viral overexpression of LOTUS enhan

101 flammation in a clinically relevant model of SCI, and suggests that rIL-37 may have therapeutic poten

102 ptor is essential for repair responses after SCI, and the potential mechanisms of this beneficial eff

103 s were systemically administered after acute SCI, and were detected in serum, cerebrospinal fluid, an

104 iding NG2(+) pericytes are required for post-SCI angiogenesis, which in turn is needed for fibrotic s

105 DRG membranes isolated from SCI animals revealed a novel alteration in the regulatio

106 ansmission in humans with chronic incomplete SCI are also present in the preparatory phase of upcomin

107 Effective pharmacological treatments for SCI are not currently available.

108 leading causes of death in humans following SCI are respiratory complications secondary to paralysis

109 cations in patients with spinal cord injury (SCI) are common and have a negative impact on the qualit

110 Spasms after spinal cord injury (SCI) are debilitating involuntary muscle contractions th

111 acrophage function after spinal cord injury (SCI) are poorly understood.

112 and neural repair after spinal cord injury (SCI), as well as axonal regeneration after optic nerve c

113 PM, propagated inflammatory resolution after SCI, as revealed by accelerated clearance of neutrophils

114 After SCI, astrocyte-specific trkB.T1 KO mice showed reduced h

115 Following spinal cord injury (SCI), astrocytes demonstrate long-lasting reactive chang

116 Spinal cord injury (SCI) at high spinal levels (e.g., above thoracic level 5

117 After SCI, axon growth and circuit reorganization are determin

118 he amplitude of spontaneous activity (SA) in SCI bladder muscle strips.

119 myelination occurs after spinal cord injury (SCI), but the extent of myelin repair and identity of th

120 n occur after incomplete spinal cord injury (SCI), but the pathways underlying this remain poorly und

121 ecovery after incomplete spinal cord injury (SCI), but the pathways underlying this remain poorly und

122 al weeks after traumatic spinal cord injury (SCI), but they are replaced by resident progenitor cells

123 eceptor (BDNF), contributes to gliosis after SCI, but little is known about the effects of trkB.T1 on

124 on growth and reduce neuroinflammation after SCI by acting on both neurons and macrophages.

125 bitor in promoting functional recovery after SCI by dampening inflammatory cytokines, thus pointing t

126 ould be differentiated from bvFTD, svPPA and SCI by limb apraxia.

127 SCI caused a small but significant increase in the expre

128 Traumatic spinal cord injury (SCI) causes a cascade of degenerative events including c

129 Acute spinal cord injury (SCI) causes systemic immunosuppression and life-threaten

130 The emerging understanding of how SCI cell biology differs across lesion compartments is f

131 Here, we review SCI cell biology, which varies considerably across three

132 endothelial cells and pericytes 1 day after SCI compared to non-diabetic rats.

133 r voluntary contractions in individuals with SCI compared with controls.

134 progressively deteriorates proportionally to SCI completeness.

135 ns suggest that reticulospinal outputs after SCI contribute to hand motor tasks involving gross finge

136 itability of inhibitory DH interneurons post-SCI could provide a neurophysiological mechanism of cent

137 nal axons at injury epicenter 3 months after SCI, demonstrating that these resident cells are a major

138 f the pathobiology of events following acute SCI, developing integrated approaches aimed at preventin

139 e pronounced after high-thoracic level (Th1) SCI disconnecting adrenal gland innervation, compared wi

140 We found that (i) complete SCI disrupts the influence of postural changes on the re

141 ate the possibility of delayed postoperative SCI (DP-SCI).

142 ral stem cells (hCNS-SCns) at 9 or 30 d post-SCI (dpi) resulted in extensive donor cell migration, pr

143 tment approach for human spinal cord injury (SCI) due to their unique regenerative potential and auto

144 ospinal tract to hand control in humans with SCI during gross finger manipulations and suggest that t

145 uction of gut dysbiosis in naive mice before SCI (e.g., via oral delivery of broad-spectrum antibioti

146 ortic clamp interval (ACI) nor absence of IP-SCI eliminate the possibility of delayed postoperative S

147 el for the formation and resolution of toxic SCI entanglements on eukaryotic genomes is proposed.

148 ermediate layers of the superior colliculus (SCi), evoked robust pupil dilation even in the absence o

149 Compared to controls, individuals with SCI exhibited decreased cord area, reduced grey matter (

150 ts in corticospinal transmission after human SCI extend to the preparatory phase of upcoming movement

151 Axon regeneration after spinal cord injury (SCI) fails due to neuron-intrinsic mechanisms and extrac

152 Axon regeneration after spinal cord injury (SCI) fails due to neuron-intrinsic mechanisms and extrac

153 ocedure that was striving to transition from sci-fi novels to science.

154 ero-dimensional model calculations show that sCI from biogenic volatile organic compounds composed th

155 ng can promptly detect spinal cord ischemia (SCI) from aortic clamping during open thoracoabdominal a

156 Traumatic spinal cord injury (SCI) has been shown to trigger structural atrophic chang

157 of this projection after spinal cord injury (SCI) has not been accomplished.

158 reveal that humans with incomplete cervical SCI have an altered ability to modulate corticospinal ex

159 Previous studies of SCI have usually focused on few genes and pathways at a

160 tudies targeting chronic spinal cord injury (SCI) have concluded that neural stem/progenitor cell (NS

161 ons at the sub-chronic and chronic stages of SCI, highlighting the temporal regulation of pathologica

162 research to the clinical spinal cord injury (SCI) human population, and few studies have investigated

163 spinal cord injury also induces a functional SCI-IDS ('immune paralysis'), sufficient to propagate cl

164 neumonia to investigate whether the systemic SCI-IDS is functional sufficient to cause pneumonia depe

165 d injury-induced immune deficiency syndrome, SCI-IDS) may account for the enhanced infection suscepti

166 lencing of this reflex circuitry blocks post-SCI immune suppression.

167 nal reflex mediating immunosuppression after SCI, implying that therapeutic normalization of the gluc

168 ation of astrocytes was also confirmed after SCI in astrocyte-specific trkB.T1 KO mice; using mechani

169 an H9 NSCs that were implanted into sites of SCI in immunodeficient rats over a period of 1.5 years.

170 drenal axis activation, we report that acute SCI in mice induced suppression of serum norepinephrine

171 ), Olig2+, and P0+ cells following contusion SCI in mice.

172 after clinically relevant impact-compression SCI in rats, and importantly, also in the injured human

173 induces recovery of diaphragm function after SCI in the adult rat model.

174 unctional recovery after spinal cord injury (SCI) in animal and clinical studies.

175 derived monoamines after spinal cord injury (SCI) in rats.

176 o chronic pathophysiological consequences of SCI, including pain, that are promoted by persistent hyp

177 Data in this study show that SCI increases intestinal permeability and bacterial tran

178 ction in motor complete spinal cord injured (SCI) individuals is poor.

179 aN expression and localization after injury, SCI induced upregulation of the native regulator of CaN

180 rongly suggest that CaN inhibition underlies SCI-induced dysfunction of Kv3.4 and the associated exci

181 phylactic adrenalectomy completely prevented SCI-induced glucocorticoid excess and lymphocyte depleti

182 cavenger, to the site of injury can mitigate SCI-induced oxidative stress and tissue damage.

183 The occurrence of SCI-induced SA in a large fraction of DRG neurons and th

184 The present study demonstrates that SCI-induced SA requires continuing activity of adenylyl

185 Spinal cord injury (SCI) induces a centralized fibrotic scar surrounded by a

186 Spinal cord injury (SCI) interrupts the communication between brain and body

187 inflammatory response to spinal cord injury (SCI) involves localization and activation of innate and

188 tization associated with spinal cord injury (SCI) involves poorly understood maladaptive modulation o

189 decrease the risk of immediate postoperative SCI (IP-SCI).

190 We report that inflammation after SCI is dysregulated in part due to inappropriate synthes

191 r, these data show that TLR4 signaling after SCI is important for OL lineage cell sparing and replace

192 that ependymal contribution of progeny after SCI is minimal, local and dependent on direct ependymal

193 e in Galphai inhibition of AC activity after SCI is novel for any physiological system and potentiall

194 igh-thoracic or cervical spinal cord injury (SCI) is associated with several critical clinical condit

195 g.SIGNIFICANCE STATEMENT Spinal cord injury (SCI) is characterized by formation of astrocytic and fib

196 L) death after traumatic spinal cord injury (SCI) is followed by robust neuron-glial antigen 2 (NG2)-

197 ility is preserved after spinal cord injury (SCI) is unknown.

198 athology after traumatic spinal cord injury (SCI) is unknown.

199 ommon complication after spinal cord injury (SCI), is frequently accompanied by chronic pain.

200 largest cerebral artery after high-thoracic SCI, leading to increased stiffness and possibly impaire

201 SCI leads to oligodendrocyte death and demyelination, an

202 e.SIGNIFICANCE STATEMENT Spinal cord injury (SCI) leads to profound functional deficits, though subst

203 d that astrocytes and non-astrocyte cells in SCI lesions express multiple axon-growth-supporting mole

204 axon-specific growth factors not present in SCI lesions, plus growth-activating priming injuries, st

205 rming astrocytes and inhibitory molecules in SCI lesions.

206 Spinal cord injury (SCI) lesions present diverse challenges for repair strat

207 gic axons through severe spinal cord injury (SCI) lesions.

208 ntary motor control in key muscles below the SCI level, as measured by EMGs, resulting in marked impr

209 Our data show that at 7 d after SCI, macrophages are best described as foam cells, with

210 Our data show that at 7 d after SCI, macrophages are best described as foam cells, with

211 T Neuropathic pain after spinal cord injury (SCI) may in part be caused by upregulation of the brain-

212 After spinal cord injury (SCI), meningeal ILC2s are activated in an IL-33-dependen

213 Conversely, feeding SCI mice commercial probiotics (VSL#3) enriched with lac

214 After dorsal column SCI, miR-155 KO mouse spinal cord has reduced neuroinfla

215 findings indicate that chronic pain in a rat SCI model depends upon hyperactivity in dorsal root gang

216 enotypes and improved functional recovery in SCI model.

217 ently deliver pbeta-Gal in a rat compression SCI model.

218 I RNA editing in stab wound injury (SWI) and SCI models and showed that the apparent under-editing ob

219 improve pain and bladder function in rodent SCI models.

220 ll fate mapping strategy in different murine SCI models.

221 plantation for chronic SCI, we used thoracic SCI mouse models to compare manifestations secondary to

222 fter complete T3 spinal cord transection (T3-SCI, n = 15) or sham injury (Sham, n = 10), rats were sa

223 Following spinal cord injury (SCI), newly formed endothelial cells, located only at th

224 Following SCI, newly formed endothelial cells located within the e

225 ndently associated with decreased risk of DP-SCI (odds ratio = 0.14; 95% confidence interval: 0.03, 0

226 fluence of high-thoracic (T3 spinal segment) SCI on cerebrovascular structure and function, as well a

227 pathway from the frontal cortex through the SCi operates in parallel with frontal inputs to arousal

228 ion-regulation following spinal cord injury (SCI), orchestrated by CD200-ligand (CD200L) expressed by

229 that the dual and opposing roles of C5aR on SCI outcomes primarily relate to its expression on CNS-r

230 benefited from extended monitoring had no DP-SCI (p = 0.003).

231 ght chronic (3-13 years) spinal cord injury (SCI) paraplegics were subjected to long-term training (1

232 s remained unchanged compared to baseline in SCI participants but were suppressed in control subjects

233 Reaction times were prolonged in SCI participants compared with control subjects and stim

234 We found that although SCI participants voluntarily responded to all tasks, rea

235 g neurological disorders and the majority of SCI patients are in the chronic phase.

236 lucocorticoid and catecholamine imbalance in SCI patients could be a strategy to prevent detrimental

237 nce that serum NfL is of prognostic value in SCI patients for the first time.

238 Serum NfL concentrations in SCI patients show a close correlation with acute severit

239 and markedly improve the quality of life for SCI patients.

240 perceptual experience in spinal cord injury (SCI) patients, and will ultimately, lead to a higher rat

241 l cerebrovascular clinical conditions in the SCI population.

242 zation of this switch within an ultra-stable SCI promises to circumvent insulin's complex global cold

243 in areas with stronger competition (highest SCI quartile [0.87-0.92]; p=0.0081) than in areas with w

244 eath and increased the number of DPCs in the SCI rat spinal cord even 7 weeks after transplantation.

245 Inosine (1 mM) delivered intravesically to SCI rats during conscious cystometry significantly decre

246 by us demonstrated an improvement in NDO in SCI rats following chronic systemic treatment with the p

247 al role on the integrity of BSCB in diabetic SCI rats, leading to improved prognosis.

248 or lowered the adverse effect of diabetes on SCI, reduced EB dye extravasation, and limited the loss

249 the integrity of BSCB in diabetic rats after SCI remains unclear.

250 stating forms of trauma, spinal cord injury (SCI) remains a challenging clinical problem.

251 Spinal cord injury (SCI) remains one of the most debilitating neurological d

252 Importantly, SCI removal in anaphase requires condensin and coincides

253 s highlight new roles for TLR4 in endogenous SCI repair and emphasize that altering the function of a

254 ards a new direction of immunomodulation for SCI repair.

255 esion sites, achieving a major unmet goal of SCI research and offering new possibilities for clinical

256 ith anatomically incomplete chronic cervical SCI responded to a startle stimulus, a test that engages

257 Here we show that SCI resulted in an upregulation of histone deacetylase 3

258 On gentle agitation, the SCI retained full activity for >140 days at 45 degrees C

259 cell flow cytometry image analysis following SCI revealed CD200L-dependent direct interaction between

260 yte cultures and a computational analysis of SCI RNA-seq data further supported the possibility that

261 scriptomes of single cells or nuclei, termed sci-RNA-seq (single-cell combinatorial indexing RNA sequ

262 The data generated by sci-RNA-seq constitute a powerful resource for nematode

263 We applied sci-RNA-seq to profile nearly 50,000 cells from the nema

264 In this model, a loop defined by the SCI's B and C domains encircles the C-terminal segment o

265 We propose a model of the SCI's IR-bound state based on molecular-dynamics simulat

266 clusion chromatography revealed only limited SCI self-assembly and aggregation in the concentration r

267 ingle-cell combinatorial indexed sequencing (SCI-seq) as a means of simultaneously generating thousan

268 improving neurological recovery after acute SCI.SIGNIFICANCE STATEMENT Inflammation is a protective

269 1 may provide a novel therapeutic target for SCI.SIGNIFICANCE STATEMENT Neuropathic pain after spinal

270 l mechanism of pain sensitization induced by SCI.SIGNIFICANCE STATEMENT Pain sensitization associated

271 combination with cell transplantation after SCI.SIGNIFICANCE STATEMENT The interaction of transplant

272 n that can be therapeutically targeted after SCI.SIGNIFICANCE STATEMENT The intrinsic molecular mecha

273 SCI similarly induced concurrent Kv3.4 current attenuati

274 of dilation closely resembled that evoked by SCi stimulation.

275 inhibition increased in controls but not in SCI subjects during NOGO trials and decreased in both gr

276 pain and neurological dysfunction following SCI, suggesting that trkB.T1 may provide a novel therape

277 t longitudinally after a C3/C4 dorsal column SCI that bilaterally ablated the dorsal corticospinal tr

278 tic mapping of motor cortex after a cervical SCI that interrupts most corticospinal transmission but

279 Following spinal cord injury (SCI), the innate immune response of microglia and infilt

280 ological processes after spinal cord injury (SCI), the intrinsic molecular mechanisms that regulate t

281 In spinal cord injury (SCI), the severity of disease is quantified by clinical

282 After T3-SCI, the MCA had more collagen I (42%), collagen III (24

283 We find that, months after the imposition of SCI, the spinal cord below the site of injury is in a ch

284 ely sprout into gray matter structures after SCI; therefore, it has been proposed that the reticulosp

285 n an individual with chronic, motor complete SCI throughout 3.7 years of activity-based interventions

286 Transcriptome analysis of SCI tissue at day 1 identified the survival factor Tox3

287 ytes and glia play fundamental roles in post-SCI tissue remodeling.SIGNIFICANCE STATEMENT Spinal cord

288 m to ablate proliferating NG2(+) cells after SCI to better understand their role in repair.

289 nes in the sub-chronic and chronic stages of SCI using RNA-Sequencing.

290 tes exacerbates the disruption of BSCB after SCI via inducing ER stress, and inhibition of ER stress

291 cells, functional recovery of mice following SCI was impaired.

292 n rat T9-T10 hemisection spinal cord injury (SCI), we demonstrated that the tailored scaffolding main

293 derlying the proresolving actions of MaR1 in SCI, we found that this SPM facilitated several hallmark

294 In murine models of SCI, we report robust corticospinal axon regeneration, f

295 effect of NS/PC transplantation for chronic SCI, we used thoracic SCI mouse models to compare manife

296 with and without incomplete chronic cervical SCI were tested.

297 ation is defective after spinal cord injury (SCI), which impairs tissue integrity and remodeling and

298 ssures, inward remodelling occurred after T3-SCI with a 40% reduction in distensibility (both P < 0.0

299 n analog, a 57-residue single-chain insulin (SCI) with multiple acidic substitutions.

300 sured by use of a spatial competition index [SCI], with a score of 0 indicating weakest competition a