ライフサイエンスコーパス: sci

1 uropathic pain following spinal cord injury (SCI).

2 mice after T9 contusive spinal cord injury (SCI).

3 axotomy that precedes a spinal cord injury (SCI).

4 ic adaptations following spinal cord injury (SCI).

5 lead to spasticity after spinal cord injury (SCI).

6 lish motor control after spinal-cord injury (SCI).

7 recovery in humans with spinal cord injury (SCI).

8 ng-term disability after spinal cord injury (SCI).

9 enic bladder (NB) due to spinal cord injury (SCI).

10 enging diseases, such as spinal cord injury (SCI).

11 ed in people living with spinal cord injury (SCI).

12 ity (BMD) in people with Spinal Cord Injury (SCI).

13 anifested in humans with spinal cord injury (SCI).

14 n humans with incomplete spinal cord injury (SCI).

15 nical model of traumatic spinal cord injury (SCI).

16 in persons with chronic spinal cord injury (SCI).

17 uals in the US live with spinal cord injury (SCI).

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

19 enic bladder (NB) due to spinal cord injury (SCI).

20 plasticity during functional recovery after SCI.

21 ding cause of morbidity in those living with SCI.

22 tenuated mitochondrial dysfunction following SCI.

23 with and without chronic incomplete cervical SCI.

24 d spinal inflammation and fibrosis following SCI.

25 ered upper extremity function after cervical SCI.

26 strategy aids repair of motor circuits after SCI.

27 Maina et al., Sci.

28 rocytes at the injury epicenter 6 weeks post SCI.

29 ks spontaneous activity of nociceptors after SCI.

30 ed pharyngeal epithelium [Rosa et al., 2019, Sci.

31 early diagnosis, prevention and treatment of SCI.

32 motoneurons which leads to spasticity after SCI.

33 d physical impairments in people living with SCI.

34 sion site in rat and pig contusion models of SCI.

35 rehabilitation and assessment of people with SCI.

36 motor pathways on spasticity in humans with SCI.

37 lationship between other sleep disorders and SCI.

38 on pathology and neurological recovery after SCI.

39 arative model to study adaptive responses to SCI.

40 tchalsky model.Arising from: Yaroshchuk, A., Sci.

41 6-722; Kim et al., J Gerontol A Biol Sci Med Sci.

42 are required to produce leg movements after SCI.

43 functional recovery and tissue sparing after SCI.

44 repair strategy for improving recovery from SCI.

45 lear subgroups of humans with motor complete SCI.

46 ivation would enhance axonal outgrowth after SCI.

47 n myelin phagocytosis in mice at 7 days post-SCI.

48 proving the efficacy of stem cell therapy in SCI.

49 erreflexia as a result of chronic incomplete SCI.

50 erreflexia as a result of chronic incomplete SCI.

51 tic muscle in humans with chronic incomplete SCI.

52 male and females with and without incomplete SCI.

53 J Gerontol A Biol Sci Med Sci.

54 d may provide a novel therapeutic target for SCI.

55 ection is a leading cause of mortality after SCI.

56 d to date exhibits spinal scarring following SCI.

57 asymmetrical recovery of elbow muscles after SCI.

58 with and without chronic cervical incomplete SCI.

59 opment of chronic neuropathic pain following SCI.

60 ptors and chronic neuropathic pain following SCI.

61 y with decompressive surgery following acute SCI.

62 ility during postnatal development and after SCI.

63 l ganglia-thalamic circuit over 2 years post-SCI.

64 stress response (Stroth et al., Ann NY Acad Sci 1220:49-59, 2011; Hashimoto et al., Curr Pharm Des 1

65 With delayed post-SCI administration, localization of NPs at the lesion si

66 s a major comorbidity of spinal cord injury (SCI), affecting up to 70-80% of patients.

67 Importantly, SCI also reduces the negative regulation by Galphai of a

68 Here, we present Sub-Compartment Identifier (SCI), an algorithm that uses graph embedding followed by

69 ent of stepping performance after incomplete SCI and are at least partially causative to the observed

70 ve effects after hemisection and compression SCI and can directly affect microglia in these injury mo

71 pathologic angiogenesis and fibrosis in both SCI and EAE.

72 opic data in study participants with chronic SCI and healthy control subjects were prospectively acqu

73 This study shows that SCI and one consequence of SCI (chronic depolarization o

74 ganglia-thalamic circuitry occur early after SCI and progress over time; their magnitude being predic

75 limit the accuracy of outcome prediction in SCI and provide suggestions for how to increase the pred

76 upregulated in the CNS within minutes after SCI and remains elevated.

77 scribe the multi-level mechanisms underlying SCI and several risk factors that promote this health-da

78 influences to spastic muscles in humans with SCI and suggest that these imbalanced contributions are

79 io-metabolic differences as a consequence of SCI and, furthermore, that sex is an underlying factor i

80 the context of traumatic spinal cord injury (SCI) and discuss the underlying mechanisms of the parado

81 gulfing myelin debris in spinal cord injury (SCI) and experimental autoimmune encephalomyelitis (EAE)

82 integrate into sites of spinal cord injury (SCI) and generate neuronal relays across lesions that ca

83 control is common after spinal cord injury (SCI) and no causal therapies are available.

84 on locomotor and histological recovery after SCI, and highlight the importance of using littermate co

85 a systems-wide approach to the treatment of SCI, and identify new targets to mediate complete respir

86 rotocol in people or animals with or without SCI, and it also improved locomotion.

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

88 method that combines combinatorial indexing (sci-) and linear (L) amplification.

89 Sleep disturbances in people living with SCI are associated with significant impairments of dayti

90 Strategies for mitigating the risk of SCI are discussed, drawing on evidence from thoraco-abdo

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

92 d spinal inflammation and fibrosis following SCI as compared to C57BL/6 mice (Mus), which similar to

93 cantly diminished thermal hyperalgesia after SCI as measured by the Plantar test.

94 postnatal Day 7, P7SCI) and nonregenerating (SCI at Day 28, P28SCI) cords +1d, +3d, and +7d after com

95 ifferential gene expression in regenerating (SCI at postnatal Day 7, P7SCI) and nonregenerating (SCI

96 Lastly, we performed an additional sci-ATAC-seq preparation from cultured hippocampal neuro

97 We used sci-ATAC-seq to produce 2346 high-quality single-cell ch

98 assay for transposase accessible chromatin (sci-ATAC-seq); a software suite, scitools, for the rapid

99 Humanized mice receiving a SCI before or after stable engraftment exhibit significa

100 The present results showed that SCI bladders released IGF-1 and TGF-beta1 to stimulate e

101 nsomnia disorder are common conditions after SCI but remain under-recognized, underdiagnosed and ther

102 glia are activated after spinal cord injury (SCI), but their phagocytic mechanisms and link to neurop

103 an increased quality of life for people with SCI by reducing their risk of fractures.

104 bolic changes in chronic spinal cord injury (SCI) by applying MR spectroscopy in the cervical spinal

105 human participant with a clinically complete SCI can use a BCI to simultaneously reanimate both motor

106 Individuals with spinal cord injury (SCI) can face decades with permanent disabilities.

107 More than half of spinal cord injury (SCI) cases occur in the cervical region, leading to resp

108 Together, our data suggest that SCI causes an acquired bone marrow failure syndrome that

109 Indeed, SCI causes excessive proliferation of bone marrow hemato

110 Spinal cord injury (SCI) causes immune dysfunction, increasing the risk of i

111 ns of the spinal cord, which in animals with SCI changed to the lesion site, indicating drastic post-

112 animals with incomplete spinal cord injury (SCI), changing a spinal reflex through an operant condit

113 study shows that SCI and one consequence of SCI (chronic depolarization of resting membrane potentia

114 After spinal cord injury (SCI) chronic inflammation hampers regeneration.

115 In the SCI cohort, lumbosacral epidural electrical stimulation

116 e treatment during the acute phase following SCI could potentially have a positive long-term impact o

117 y protein Nogo-A applied to rats with severe SCI could prevent development of neurogenic lower urinar

118 se they were among the highest quality acute SCI datasets available and contained highly granular dat

119 cluster analysis, we show that in male rats SCI decreases opioid responsiveness in vitro within a sp

120 ticity in 33 individuals with motor complete SCI (determined by clinical examination) without preserv

121 re accurate sub-compartment predictions when SCI-determined sub-compartments are used as labels for t

122 Four weeks after SCI, detrusor sphincter dyssynergia had developed in all

123 diabetes and 330 892 with type 2 diabetes in SCI-Diabetes between 2006 and 2015.

124 Clinical Practice Research Datalink) and the SCI-Diabetes dataset (Scottish Care Information-Diabetes

125 In T2D participants from CPRD and SCI-Diabetes, pooled hazard ratios for CVD associated wi

126 d among 27 900 (27%) CPRD-T2D, 101 362 (31%) SCI-Diabetes-T2D, and 75 520 (19%) CPRD-controls.

127 Over 3 years follow-up (SCI-Diabetes: 6 years), CVD events occurred among 27 900

128 s 63 years and 28% had cardio-renal disease (SCI-Diabetes: 62 years; 35% cardio-renal disease).

129 proper immune function, we hypothesize that SCI disrupts bone marrow hematopoiesis.

130 SCI disrupts neural circuitry to vital organs in the bod

131 Spinal cord injury (SCI) disrupts critical physiological systems, including

132 After SCI, DRG neurons show hyperactivity and chronic depolari

133 There have been 6 cases of SCI during pancreas transplantation since 2002.

134 This SCI effect is mimicked in nociceptors from naive animals

135 o single therapy will be sufficient to treat SCI effectively and that a combination of cell-based, re

136 y an ex vivo rat model of SCI mimicking post-SCI environment in vivo and by delivering S-220 via a se

137 rcise was used; 3 participants with complete SCI exercised in the system for 1 hour twice-weekly for

138 We used sci-fate to study the cortisol response in >6,000 single

139 We anticipate that sci-fate will be broadly applicable to quantitatively ch

140 atorial indexing and messenger RNA labeling (sci-fate), which uses combinatorial cell indexing and 4-

141 e in body fat percentage in both sexes, with SCI females disproportionately affected in percent body

142 eter during systole (LVIDs) was decreased in SCI females more than in SCI males.

143 iratory motor functional recovery in chronic SCI following 2 weeks of spinal neuroplasticity.

144 s self-administered daily in 10 persons with SCI for 4 months with monthly blood testing to quantify

145 The mainstay of early treatment for SCI for all cases was blood pressure control.

146 n to have a positive effect in patients with SCI: gait training by means of non-invasive, surface fun

147 heart failure disease status and used the G-SCI (Genotype-independent Signal Correlation and Imbalan

148 ional effects on metabolic information after SCI have been little studied.

149 efforts to promote axonal regeneration after SCI have involved multiple strategies that have been onl

150 cessfully capture cell type differences from sci-Hi-C data in the form of "chromatin topics." We furt

151 rent single-cell combinatorial indexed Hi-C (sci-Hi-C) libraries from five human cell lines (GM12878,

152 Spinal cord injury (SCI) impairs the flow of sensory and motor signals betwe

153 al cord ischemia (SCI) in 4/8 (50%), with no SCI in group 3 (P = 0.033).

154 ivered by the gel at 3 weeks after contusion SCI in male adult rats, resulted in significantly better

155 NT-3-mediated recovery after a T9 contusive SCI in mice.

156 hough diabetes mellitus is a risk factor for SCI in other types of major surgery, SCI is not widely r

157 The risk of SCI in pancreas transplantation was estimated using the

158 The risk of SCI in pancreas transplantation was estimated using the

159 ings, there is approximately a 1:440 risk of SCI in pancreas transplantation.

160 im of this study was to quantify the risk of SCI in pancreatic transplantation.

161 f the transcriptomic changes occurring after SCI in this model.

162 des, however, suggest differently: following SCI in various animal models (lamprey, chick, rodents, n

163 opathologic changes of spinal cord ischemia (SCI) in 4/8 (50%), with no SCI in group 3 (P = 0.033).

164 on the spinal cord after spinal cord injury (SCI) in rats.

165 act for broadly improving quality of life of SCI individuals.

166 ition of ERK downstream of C-Raf also blocks SCI-induced hyperexcitability and depolarization, withou

167 urotrophin-3 (NT-3) to lumbar MNs attenuated SCI-induced lumbar MN dendritic atrophy and enabled func

168 rugs are first line analgesics used to treat SCI-induced neuropathic pain, but their efficacy is very

169 represent a pharmacological target to treat SCI-induced neuropathic pain.

170 SCI-induced pain in a rat model has been shown to depend

171 individuals with incomplete chronic cervical SCI influenced in parallel the excitability cortical and

172 Spinal cord injury (SCI) interrupts descending projections and denervates lu

173 Surgical decompression within 24 h of acute SCI is associated with improved sensorimotor recovery.

174 Sequestration of HSPCs in bone marrow after SCI is linked to aberrant chemotactic signaling that can

175 tor for SCI in other types of major surgery, SCI is not widely recognized in transplantation.

176 Spinal cord injury (SCI) is a common cause of disability, which often leads

177 Spinal cord ischemia (SCI) is a rare but devastating condition that can occur

178 Chronic pain caused by spinal cord injury (SCI) is notoriously resistant to treatment, particularly

179 Chronic pain induced by spinal cord injury (SCI) is often permanent and debilitating, and usually re

180 of stem cell therapy for spinal cord injury (SCI) is to restore motor function without exacerbating p

181 t the Acomys response to spinal cord injury (SCI) is unknown.

182 We anticipate that sci-L3 assays can be applied to fully characterize recom

183 The sci-L3 method adopts a 3-level (3) indexing scheme that

184 We demonstrate the generalizability of sci-L3 with proof-of-concept demonstrations of single-ce

185 Here, we describe sci-L3, a single-cell sequencing method that combines co

186 a co-assay of the genome and transcriptome (sci-L3-RNA/DNA).

187 equencing (sci-L3-WGS), targeted sequencing (sci-L3-target-seq), and a co-assay of the genome and tra

188 We apply sci-L3-WGS to profile the genomes of >10,000 sperm and s

189 ions of single-cell whole-genome sequencing (sci-L3-WGS), targeted sequencing (sci-L3-target-seq), an

190 d initial eastward exploration, resulting in SCI landfall(s) and return voyaging, with colonization a

191 nditioning-dependent axon regeneration after SCI leading to improved functional recovery.

192 Spinal cord injury (SCI) leads to wide-spread neurodegeneration across the n

193 0; Dahl TW, Stevenson DJ (2010) Earth Planet Sci Lett 295:177-186].

194 s) was decreased in SCI females more than in SCI males.

195 Influencing the local microenvironment after SCI may provide a strategy to modulate inflammation and

196 55(7):716-722; Kim et al., J Gerontol A Biol Sci Med Sci.

197 J Gerontol A Biol Sci Med Sci.

198 were 18 male study participants with chronic SCI (median age, 51 years; range, 30-68 years) and 11 ma

199 Loss of mitochondrial homeostasis after SCI, mediated primarily by oxidative stress, is consider

200 Finally, preliminary in vivo tests on SCI mice revealed good handling of the CS solution loadi

201 ional capacity of HSPCs is still impaired in SCI mice.

202 Since manipulating SCI microenvironment properties, such as mechanical and

203 axonal outgrowth by an ex vivo rat model of SCI mimicking post-SCI environment in vivo and by delive

204 lesion site in a clinically relevant severe SCI model, significantly improves motor outcomes.

205 edictive, translational value of preclinical SCI models.

206 Few days after SCI, neonatal rats developed behavioral signs of spastic

207 the increased activity of T-type channels in SCI-nociceptors and chronic neuropathic pain following S

208 rexcitable state and spontaneous activity of SCI-nociceptors have been proposed as a possible underly

209 y the injury plays a primary role in driving SCI-nociceptors to a hyperexcitable state and contribute

210 by the injury plays a major role in driving SCI-nociceptors to a hyperexcitable state and for promot

211 ing ionic mechanisms responsible for driving SCI-nociceptors to a hyperexcitable state and for trigge

212 firing in response to current injections in SCI-nociceptors to a level similar to sham-nociceptors.

213 d voltages during the interspike interval in SCI-nociceptors, with a modest contribution (~10-15%) fr

214 rvations, animals and humans with incomplete SCI often show various degrees of spontaneous motor reco

215 Humans with cervical spinal cord injury (SCI) often recover voluntary control of elbow flexors an

216 ore, this shows the significant influence of SCI on cerebral function and neuroscience research.

217 We examined the effects of SCI on functional recovery, cardiac structure and functi

218 of timing of decompressive surgery for acute SCI on long-term neurological outcomes.

219 enhancing and/or accelerating recovery after SCI or in other disorders.

220 rtunity to enhance functional recovery after SCI or in other disorders.

221 data indicate that Bmal1 deficiency improves SCI outcome, in part by reducing BSCB disruption and hem

222 We found that SCI participants showed similar MEPs and maximal volunta

223 A total of 66.7% of the SCI participants showed symptoms of spasticity, whereas

224 Eight SCI participants were control subjects.

225 , but not sham-TESS, in control subjects and SCI participants, suggesting a subcortical origin for th

226 timated from 182 MRI datasets acquired in 17 SCI patients and 21 healthy controls at baseline (1-mont

227 t and well tolerated in preventing R-UTIs in SCI patients.

228 nt and well-tolerated in preventing R-UTI in SCI patients.

229 splantation caused no difference compared to SCI + PBS group.

230 In SCI + PBS rat bladders, cystometry showed increased peak

231 sham and SCI plus phosphate-buffered saline (SCI + PBS), human embryonic kidney 293 (HEK293) cells, a

232 As a proof of concept, we applied sci-Plex to screen three cancer cell lines exposed to 18

233 Here, we introduce "sci-Plex," which uses "nuclear hashing" to quantify glob

234 Four groups were studied: sham and SCI plus phosphate-buffered saline (SCI + PBS), human em

235 We show that SCI-predicted sub-compartments have distinct epigenetic

236 rized RMP and nociceptor hyperactivity after SCI, providing a self-reinforcing mechanism to persisten

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

238 rent recorded from nociceptors isolated from SCI rats showing TTA-P2-induced CPP (responders) was ~6

239 Importantly, only SCI rats that received EI-tPA primed hiNPC demonstrated

240 ly improve the endogenous ability of chronic SCI rats to fight off pneumonia, a common cause of hospi

241 rent recorded from nociceptors isolated from SCI rats without TTA-P2-induced CPP (non-responders).

242 otube based scaffold that, once implanted in SCI rats, improves motor function recovery.

243 nd molecular changes in spinal cord-injured (SCI) rats were investigated.

244 decompression for acute spinal cord injury (SCI) remains debated, with substantial variability in cl

245 Spinal cord injury (SCI) remains one of the biggest challenges in the develo

246 Sci Rep 8:14432, 2018), might also account for IOG.

247 trapping limit (Bhattacharya and John in Nat Sci Rep 9:12482, 2019).

248 ed hydrogel that has suitable properties for SCI repair.

249 While most SCI research focuses on central neural pathway responses

250 Months after spinal cord injury (SCI), respiratory deficits remain the primary cause of m

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

252 e lesion site to minimize the impact of post-SCI response.

253 py for Mo2 and Mo4 initiated in persons with SCI resulted in a robust and favorable change in the ser

254 Cervical SCI results in rVRG axon damage, PhMN denervation, and c

255 s that the recovery of biceps after cervical SCI results, at least in part, from increased reticulosp

256 Traumatic primary spinal cord injury (SCI) results in paralysis below the level of injury and

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

258 r to the rat results, pig contusion model of SCI showed greater NP localization at the lesion site.

259 ther the recovery of limb function following SCI.SIGNIFICANCE STATEMENT Accumulating evidence support

260 ibutes to chronic neuropathic pain following SCI.SIGNIFICANCE STATEMENT Chronic neuropathic pain is a

261 ovascular regulation and immunity long after SCI.SIGNIFICANCE STATEMENT Spinal cord injury (SCI) sign

262 I.SIGNIFICANCE STATEMENT Spinal cord injury (SCI) significantly disrupts immunity, thus increasing su

263 performed calcium imaging of NSPC grafts in SCI sites in vivo and in adult spinal cord slices.

264 equencing (ChIA-PET) data, we confirmed that SCI sub-compartment prediction outperforms HMM.

265 cal centrality and clustering performance of SCI sub-compartment predictions are superior to those of

266 theoretical basis for clinical therapy after SCI, such as mitochondrial transplantation.

267 tinjury time point (i.e., 3 d after complete SCI) sufficiently diminishes maladaptive plasticity with

268 d/or functional recovery in animal models of SCI that are pushing toward clinical translation.

269 s can promote systemic chronic inflammation (SCI) that can, in turn, lead to several diseases that co

270 In spinal cord injury (SCI), the initial damage leads to a rapidly escalating c

271 s of long-term peripheral complications from SCI, the cardio-metabolic consequences and divergences i

272 In rodents, at 7 days after SCI, the level of phagocytosed myelin within Iba1-positi

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

274 ces spasticity in humans with motor complete SCI; this knowledge might help the rehabilitation and as

275 In spinal cord injury (SCI), timely therapeutic intervention is critical to inh

276 ho/mI ratios were lower in participants with SCI (tNAA/mI: -26%, P = .003; tCho/mI: -18%; P = .04) th

277 muscle stimulation which enables users with SCI to safely stand and exercise.

278 anifested in humans with spinal cord injury (SCI) to date, its mechanisms of action remain poorly und

279 egies will probably be necessary to optimize SCI treatment.

280 e S, House J, Willer R (2015) Proc Natl Acad Sci USA 112:15838-15843] showed that higher income indiv

281 [Ufimtsev IS, Levitt M (2019) Proc Natl Acad Sci USA, 10.1073/pnas.1821512116], we presented a method

282 18870; Raupach et al. [2007], Proc Natl Acad Sci USA, 104, 10288-10293).

283 2007 (Canadell et al. [2007], Proc Natl Acad Sci USA, 104, 18866-18870; Raupach et al. [2007], Proc N

284 be reanimated following spinal cord injury (SCI) using a brain-computer interface (BCI) to enhance m

285 l) for six months in patients with NB due to SCI, using clean intermittent self-catheterization, and

286 rol) for 6 months in patients with NB due to SCI, using clean intermittent self-catheterization, and

287 promising therapeutic potential of S-220 in SCI, via beneficial effects on neurons and glia after in

288 SCI was induced at T10 via contusion.

289 Bladder function of rats with SCI was repeatedly assessed by urodynamic examination in

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

291 In rodent contusion SCI, we demonstrate that DHA (500 nmol/kg) administered

292 eviously, in a rat contusion model of severe SCI, we demonstrated extravasation and retention of intr

293 In a rat model of C2 hemisection SCI, we expressed the axon guidance molecule, brain-deri

294 ransmission in different brain regions after SCI, which present evidence for the alternation of brain

295 nced in participants with chronic incomplete SCI with lesser recovery.

296 We found that participants with SCI with spasticity showed small corticospinal responses

297 ho underwent decompressive surgery for acute SCI within these datasets were included.

298 at the lesion site, and the time window post-SCI within which NPs localize at the lesion site.

299 suffer from debilitating spinal cord injury (SCI) without effective treatments.

300 een applied to reduce inflammation following SCI, yet was discontinued due to an unfavorable risk-ben