ライフサイエンスコーパス: nerve injury

1 le and female mice, neither before nor after nerve injury.

2 rrb2 reverses chronic neuropathic pain after nerve injury.

3 RGCs) promotes axon regeneration after optic nerve injury.

4 ion and functional recovery after peripheral nerve injury.

5 from acute to chronic pain after peripheral nerve injury.

6 plexes were delivered to DRG neurons without nerve injury.

7 axon-to-soma retrograde signaling following nerve injury.

8 nerve and their dynamics after demyelinating nerve injury.

9 actors maintain active enhancer status after nerve injury.

10 he development of heat hyperalgesia after L5 nerve injury.

11 natomic and functional consequences of optic nerve injury.

12 and elongation of axon re-growth after optic nerve injury.

13 n A1R sensitivity in lamina II neurons after nerve injury.

14 l summation in layer 5 ACC neurons following nerve injury.

15 C survival and axon regeneration after optic nerve injury.

16 n on the localization and pathophysiology of nerve injury.

17 role of GPR84 in a murine model of traumatic nerve injury.

18 n and peripheral nervous system responses to nerve injury.

19 d many Egr2-binding sites lose H3K27ac after nerve injury.

20 n neurons to inhibit axon regeneration after nerve injury.

21 nd in acute-to-chronic pain transition after nerve injury.

22 normalized 638 genes down- or upregulated by nerve injury.

23 silencing and chronic pain development after nerve injury.

24 ally, RtcB is enriched at axon termini after nerve injury.

25 peralgesia at the spinal cord level after L5 nerve injury.

26 increased Panx1 expression in the DRG after nerve injury.

27 ons were reviewed with a particular focus on nerve injury.

28 n controls but there was no difference after nerve injury.

29 tly reduced pain hypersensitivity induced by nerve injury.

30 of the Schwann cell reprogramming induced by nerve injury.

31 myelin and repressing genes that respond to nerve injury.

32 le and requirement of perineurial glia after nerve injury.

33 ardiac damages, coronary vessels and phrenic nerve injury.

34 offers an early warning to impending phrenic nerve injury.

35 naling in retinal ganglion cells after optic nerve injury.

36 dritic arbor of motoneurons before and after nerve injury.

37 lexor hallucis longus (FHL) tendon may cause nerve injury.

38 EGF-B a suitable therapeutic target to treat nerve injury.

39 d mTOR and from mice with or without a prior nerve injury.

40 d cold allodynia remain following peripheral nerve injury.

41 R became upregulated in RGCs following optic nerve injury.

42 responses occurring in RGCs following optic nerve injury.

43 ection of RGCs from degeneration after optic nerve injury.

44 mechanical allodynia, even in the absence of nerve injury.

45 lt sensory neurons in response to peripheral nerve injury.

46 and that it is increased in adult mice after nerve injury.

47 th and a precocious regenerative response to nerve injury.

48 the pathophysiology of metabolically induced nerve injury.

49 ature on the molecular biology of muscle and nerve injury.

50 ntion of neuropathology after trauma-induced nerve injury.

51 c and inflammatory pain following peripheral nerve injury.

52 can support axon regeneration in peripheral nerve injury.

53 through inhibitory molecules associated with nerve injury.

54 mouse SC development, adult homeostasis, and nerve injury.

55 axon regeneration in patients with traumatic nerve injury.

56 n is essential for recovery after peripheral nerve injury.

57 vioral alterations resulting from peripheral nerve injury.

58 ry for mechanical hypersensitivity following nerve injury.

59 n regeneration and functional recovery after nerve injury.

60 e effect on pain hypersensitivity induced by nerve injury.

61 al morphologic activation of microglia after nerve injury.

62 mulate repair in myelin disease or following nerve injury.

63 recruitment, and axon regeneration following nerve injury.

64 ity of myelinated sensory axons that follows nerve injury.

65 ng their actions in neuronal cell death upon nerve injury.

66 es in a neuropathic pain model of peripheral nerve injury.

67 ological in neurodegenerative conditions and nerve injuries.

68 ve reserve or on the outcome of second optic nerve injuries.

69 stently observed in glaucoma and other optic nerve injuries.

70 g in excitatory neurons following peripheral nerve injuries.

71 therapies to improve outcomes of peripheral nerve injuries.

72 After nerve injury, adult sensory neurons can regenerate perip

73 Nerve injury after radiofrequency ablation was greatest

74 Nerve injury also upregulated CSF1 in motoneurons, where

75 We conclude that, following peripheral nerve injury, an immediate acute immune response occurs

76 eat ENL aiming to prevent the development of nerve injuries and deformities in leprosy.

77 ntly delays axonal degeneration from various nerve injuries and in multiple species; however, the mec

78 tenance of adult nervous systems, both after nerve injuries and in neurodegenerative diseases.

79 Peripheral nerve injuries and neuropathies lead to profound functio

80 readily dedifferentiate following peripheral nerve injury and become repair cells.

81 Nerve injury and bone cancer caused a rapid-onset and lo

82 in expression of two factors associated with nerve injury and cell stress, activating transcription f

83 Using a well-known form of nerve injury and combining behavioral analysis, calcium

84 cers as a function of cell type-specificity, nerve injury and development.

85 gainst ER stress, in mouse models of sciatic nerve injury and found that ablation of the transcriptio

86 pace and degree of nerve regeneration after nerve injury and hindlimb transplantation.

87 ulated ion channel expression in response to nerve injury and inflammation results in enhanced neuron

88 ing triggers cold allodynia and up-regulates nerve injury and inflammatory markers in dorsal root gan

89 alcium channels is upregulated after sensory nerve injury and is also the therapeutic target of gabap

90 itro and ameliorate a critical-sized sciatic nerve injury and its associated defects in a murine mode

91 cortical circuits also accompany peripheral nerve injury and may represent additional therapeutic ta

92 r spinal cord trauma, ischemic stroke, optic nerve injury and models of multiple sclerosis.

93 to visualize nerves during surgery to avoid nerve injury and monitor nerve degeneration and regenera

94 e imaging techniques to diagnose and monitor nerve injury and regeneration are being developed, and h

95 molecular mechanisms involved in pain, itch, nerve injury and regeneration.

96 T lymphocytes infiltrate the DRG after nerve injury and release leukocyte elastase (LE), which

97 ng both development and following peripheral nerve injury and repair.

98 ral nerve can mimic the effect of peripheral nerve injury and significantly increase the number of se

99 icacy of hMDSPC-based therapy for peripheral nerve injury and suggest that hMDSPC transplantation has

100 2 expression is upregulated after peripheral nerve injury and that Celf2 mutant mice are defective in

101 long-distance axon regeneration after optic nerve injury and uncover a novel and important KLF9-JNK3

102 reduces pathologic pain after inflammation, nerve injury, and cancer but not baseline pain.

103 that cold allodynia induced by inflammation, nerve injury, and chemotherapeutics is abolished in mice

104 ses mechanical allodynia after chemotherapy, nerve injury, and diabetic neuropathy, but this blockade

105 nterventions included myocardial infarction, nerve injury, and hematoma.

106 Egr2 expression is lost after nerve injury, and many Egr2-binding sites lose H3K27ac a

107 first sensory synapse induced by peripheral nerve injury, and presynaptic NMDARs might be a novel ta

108 in RGCs, including in a mouse model of optic nerve injury, and show that the same pathway is active i

109 Runx2, a transcription factor induced after nerve injury, and we show that Runx2 is required for act

110 adaptor protein DAP12 was required for both nerve injury- and intrathecal CSF1-induced upregulation

111 ensitivity in the mouse models of peripheral nerve injury- and paclitaxel-induced neuropathic pain.

112 Although tissue and nerve injuries are well-described causes of pain hyperse

113 contrast, enhancers that lose H3K27ac after nerve injury are enriched for binding sites of the Sox10

114 ying the diminished MOR expression caused by nerve injury are not clear.

115 erve ligation resulted in a delayed onset of nerve injury-associated mechanical hypersensitivity.

116 actors as important regulators of tumor- and nerve injury-associated pain.

117 egeneration in superimposed acute peripheral nerve injury attributable to tissue-damaging inflammator

118 After peripheral nerve injury, axons are able to regenerate, although spe

119 tinal ganglion cell death in models of optic nerve injury, but the mechanism of action remains unclea

120 pattern and are upregulated following optic nerve injury, but the presence of Nogo-A does not inhibi

121 tein 2 (Igfbp2), that become activated after nerve injury, but without activation of a primary regula

122 modeling of neuromuscular synapses following nerve injury by their guidance of axonal reinnervation.

123 Peripheral nerve injury can trigger neuropathic pain in adults but

124 Chronic pain after arthritis, nerve injury, cancer, and chemotherapy is associated wit

125 Nerve injury causes a long-lasting reduction in K(+) cha

126 Our findings demonstrate that a peripheral nerve injury causes activated microglia within reward ci

127 Nerve injury causes down-regulation of MORs in the dorsa

128 However, how nerve injury causes this downregulation is still elusive

129 xia in a mouse model of traumatic peripheral nerve injury, causing painful mononeuropathy.

130 n acute slices showed that, 1 week after the nerve injury, cholinergic modulation of layer 5 (L5) pyr

131 Cranial nerve injury (CNI) was 5.5% in the CEA group, while CAS

132 t an impairment of functional recovery after nerve injury compared to 2-month-old animals.

133 Nerve injury consistently increased the enrichment of th

134 to enhance Schwann cell reprogramming after nerve injury could be used to foster effective remyelina

135 In this study, we investigated whether nerve injury could upregulate connexin-43 to sustain lat

136 ed maintenance of peripheral axons following nerve injury, demonstrating a role for TMEM184b in axon

137 Following nerve injury, denervated Schwann cells (SCs) convert to

138 cells, whether transplanted before or after nerve injury, develop into inhibitory neurons, are activ

139 In conclusion, medial and lateral plantar nerve injuries did not occur more frequently, even after

140 t microglial inhibitors, given 3 weeks after nerve injury, effectively reduced mechanical allodynia,

141 In mice lacking Ehmt2 in DRG neurons, nerve injury failed to reduce the expression level of MO

142 However, nerve injury had no effect on the DNA methylation level

143 eatment is beneficial in humans with sensory nerve injury has not been tested.

144 ur understanding of the biology of metabolic nerve injury has rapidly expanded over the past several

145 Current approaches for treating peripheral nerve injury have resulted in promising, yet insufficien

146 the S1 cortex appears within days following nerve injury; however, the underlying cellular mechanism

147 In this study, we performed optic nerve injury in adult naked mole-rats, the longest livin

148 ubstantially inhibits myelin clearance after nerve injury in both male WT and Ccr2(-/-) mice, highlig

149 s the pathways that contribute to peripheral nerve injury in DN.

150 s required for pain-like responses following nerve injury in mice, and a potential therapeutic target

151 After nerve injury in mice, miR-21-5p is upregulated in DRG ne

152 is critical for pain-like effects following nerve injury in mice, perhaps via a GPCR-mediated activa

153 es in endplate structure following traumatic nerve injury in MMP3 knockout mice.

154 We found that nerve injury in rats induced a long-lasting reduction in

155 might be a good target for the treatment of nerve injury in the aged.

156 ere we demonstrate that chemotherapy-induced nerve injury in the bone marrow of mice is a crucial les

157 al root ganglia (DRGs) neurons after sciatic nerve injury in the rat.

158 derstand the mechanism of recovery following nerve injury in this species we investigated the process

159 tions and hastened recovery after peripheral nerve injury in wild type mice.

160 ion factor Sox11 as a key player after optic nerve injury-in DLK signaling of RGC cell death, and in

161 r the promotion of functional recovery after nerve injury.In vitroandin vivoanalysis of GSK3 single k

162 Pathophysiological responses to peripheral nerve injury include alterations in the activity, intrin

163 hic pain results from numerous mechanisms of nerve injury including infectious diseases, complication

164 Nerve injury increased activity of euchromatic histone-l

165 We found that nerve injury increased dimethylation of Lys9 on histone

166 Nerve injury increased ionized calcium binding adapter m

167 Peripheral nerve injury increased Kcna2 antisense RNA expression in

168 Here, we report that peripheral nerve injury increases expression of the DNA methyltrans

169 Our findings suggest that nerve injury increases Panx1 expression levels in the DR

170 A preconditioning nerve injury increases the levels of amphoterin protein

171 layed axon degeneration following peripheral nerve injury, indicating that it participates in the deg

172 We found that peripheral nerve injury induced de novo expression of colony-stimul

173 The fact that peripheral nerve injury induced de novo GRP expression in DRG neuro

174 Unexpectedly, however, peripheral nerve injury induced significant GRP expression in a het

175 n injury of the sciatic nerve and suppressed nerve injury-induced activation of microglia.

176 Nerve injury-induced downregulation of voltage-gated pot

177 tatory interneurons contribute to tissue and nerve injury-induced heat and mechanical pain and that t

178 , but reflex responsiveness to noxious heat, nerve injury-induced heat hypersensitivity, and tissue i

179 inct Panx1 inhibitors blocked development of nerve injury-induced hypersensitivity and partially reli

180 g BH4 production only in these cells reduces nerve injury-induced hypersensitivity without affecting

181 We showed here that blocking nerve injury-induced increase in G9a rescued Kcna2 mRNA

182 ing or blocking Schwann cell NOX1 attenuated nerve injury-induced macrophage infiltration, oxidative

183 derived from docosahexaenoic acid, prevents nerve injury-induced mechanical allodynia and ongoing pa

184 neuron deletion of Csf1 completely prevented nerve injury-induced mechanical hypersensitivity and red

185 mechanical withdrawal thresholds and loss of nerve injury-induced mechanical hypersensitivity, but re

186 Blocking this increase prevents nerve injury-induced methylation of the voltage-dependen

187 evels are suppressed in the spinal cord in a nerve injury-induced neuropathic pain mouse model.

188 spared nerve injury (SNI) model of traumatic nerve injury-induced neuropathic pain was used, and an N

189 Although microglia have been implicated in nerve injury-induced neuropathic pain, the manner by whi

190 glion (DRG) neurons, which may contribute to nerve injury-induced neuropathic pain.

191 a potential mechanism underlying trigeminal nerve injury-induced orofacial hypersensitivity, we used

192 omized DRG and attenuated the development of nerve injury-induced pain hypersensitivity.

193 neurons that resembles both inflammation and nerve injury-induced pain states.

194 gic epidermal nerve fibers in a rat model of nerve injury-induced pain.

195 or Ehmt2 knockout in DRG neurons normalized nerve injury-induced reduction in the inhibitory effect

196 we describe the distribution, phenotype, and nerve injury-induced regulation of NECAB1/NECAB2 in mous

197 ive spinal cord prevented the development of nerve-injury-induced mechanical hypersensitivity.

198 Nerve injury induces changes in gene transcription in do

199 Mechanistically, peripheral nerve injury induces DNA demethylation and upregulation

200 Peripheral nerve injury induces increased expression of thrombospon

201 As compared with inflammation, nerve injury induces much more robust morphologic activa

202 Peripheral nerve injury induces permanent alterations in spinal cor

203 Nerve injury inducing nociceptive hypersensitivity also

204 Neuropathic pain caused by peripheral nerve injury is a debilitating neurological condition of

205 Peripheral nerve injury is a major neurological disorder that can c

206 Nerve injury is an unusual but not rare complication of

207 e whether, in humans, chronic pain following nerve injury is associated with altered ongoing function

208 Neuropathic pain following peripheral nerve injury is associated with hyperexcitability in dam

209 Nerve injury is associated with microvascular disturbanc

210 Reinnervation timing after nerve injury is critical for favorable axonal regenerati

211 learance of axonal and myelin debris after a nerve injury is directed primarily by inflammatory CCR2(

212 ponse in infant male rats and mice following nerve injury is due to an active, constitutive immune su

213 lated inflammatory response after peripheral nerve injury is essential for axon regeneration and reco

214 als in the spinal cord after an experimental nerve injury is increased in the inbred DA strain compar

215 w that neuropathic pain following early life nerve injury is not absent but suppressed by neuroimmune

216 cold hypersensitivity induced by peripheral nerve injury is reduced in eIF4E(S209A) and Mnk1/2(-/-)

217 id proinflammatory response after peripheral nerve injury is required for clearance of tissue debris

218 Peripheral nerve injury leads to various injury-induced responses i

219 d large DRG neurons in control rats and that nerve injury markedly increased the number of Panx1-immu

220 n levels of neuropeptides, ion channels, and nerve injury markers associated with neuropathic and/or

221 hypothesized that neuropathic pain-inducing nerve injury may elicit neuronal alterations that recapi

222 A-Seq data analyses indicate that peripheral nerve injury may result in highly selective mRNA enrichm

223 Conversely, in the absence of nerve injury, mimicking this increase reduces the Kcna2

224 ysis to investigate the relationship between nerve injury, mitochondrial localization, and axon regen

225 s in oxaliplatin-treated rats and the spared nerve injury model (SNI).

226 iceptive effects in the chronic constriction nerve injury model of neuropathic pain and carrageenan m

227 Here, we use the murine spared-nerve injury model of neuropathic pain to investigate th

228 ted hypersensitivity generated by the spared nerve injury model of neuropathic pain was reversed by i

229 tinociceptive effects in a rat model (spared nerve injury model) of persistent neuropathic pain.

230 eptors and modulators after the onset of the nerve injury model, these results suggest that disruptio

231 erent microglia phenotypes in a murine optic nerve injury model.

232 ficial dorsal horn synapses in a rat partial nerve-injury model of neuropathic pain.

233 te Freund's adjuvant) or neuropathic (spared nerve injury) model of persistent pain, we observed that

234 l and thermal hypersensitivity in peripheral nerve injury models of neuropathic pain.

235 ns (NAc) neurons in mouse and rat peripheral nerve injury models of neuropathic pain.

236 otected from hypersensitivity in two sciatic nerve injury models.

237 chronic constriction injury (CCI) and spared nerve injury models.

238 However, following the second optic nerve injury, most patients' vision fell to the pretreat

239 here is consensus that, distal to peripheral nerve injury, myelin and Remak cells reorganize to form

240 regulated by myelinating Schwann cells after nerve injury, myelin debris was present in autophagosome

241 of regeneration associated genes upon optic nerve injury nor the increased regenerative potential of

242 Motor and/or sensory nerve injuries occurred after seven procedures (1.1%).

243 When nerve injury occurs, the axon and myelin fragments dista

244 Traumatic peripheral nerve injuries often produce permanent functional defici

245 nerve might mimic the stimulatory effect of nerve injury on the regenerative state of the primary se

246 nder pathophysiological conditions following nerve injury or diabetic neuropathy, the slightest touch

247 derate to severe chronic pain resulting from nerve injury or disorder, affects 6.9%-10% of the global

248 roup developed permanent recurrent laryngeal nerve injury or hyperparathyroidism.

249 namic mechanical hypersensitivity induced by nerve injury or inflammation in mice by ablating a group

250 the spinal neurons vulnerable to peripheral nerve injury or neuropathic pain stimuli.

251 ming of the Schwann cell transcriptome after nerve injury, our results have highlighted a novel epige

252 Furthermore, nerve injury persistently increased excitatory synaptic

253 As expected, nerve injury produced an early and stable decrease in se

254 dent pathway activated by TSP4 or peripheral nerve injury promotes exaggerated presynaptic excitatory

255 Nerve injury provokes the loss of many proprioceptive IA

256 in both oxaliplatin-treated rats and spared nerve injury rats.

257 Peripheral nerve injury reduces NECAB2, but not NECAB1, expression

258 ntly, diagnosis and monitoring of peripheral nerve injury relies on clinical and electrodiagnostic in

259 However, full functional recovery after nerve injuries remains poor.

260 ndings explain how DLK specifically mediates nerve injury responses and reveal a novel cellular mecha

261 Additionally, nerve injury resulted in a potentiation of the intrinsic

262 ld-type mice, following transient peripheral nerve injury, reversed the overexpression of genes in mu

263 After nerve injury, Schwann cells convert to a phenotype speci

264 After peripheral nerve injury, Schwann cells transition from axon myelina

265 Nerve injury score was significantly greater (P<0.001) a

266 Nerve injury significantly increased the enrichment of t

267 Using the spared nerve injury (SNI) model of neuropathic pain in Long-Eva

268 persistent neuropathic pain using the Spared Nerve Injury (SNI) model of neuropathic pain.

269 nisms of mPFC deactivation in the rat spared nerve injury (SNI) model of neuropathic pain.

270 to define their gene profiling in rat spared nerve injury (SNI) model of neuropathic pain.

271 The spared nerve injury (SNI) model of traumatic nerve injury-induc

272 ediated analgesia specifically in the spared nerve injury (SNI) model.

273 reversed tactile allodynia in a mouse spared-nerve injury (SNI) model.

274 ork properties between rats receiving spared nerve injury (SNI) vs. sham injury, at 5 days (n = 11 SN

275 elopment of SC lineage and during peripheral nerve injury, so we sought to study their functional pro

276 Surprisingly, optic nerve injury stimulated the expression of Socs3 and Sfpq

277 excitatory synapses in the dorsal horn after nerve injury suggest that new generation PAMs of the A1R

278 namic mechanical hypersensitivity induced by nerve injury, suggesting that these neurons may be a cel

279 or in the rotarod, water maze and peripheral nerve injury tests was possibly affected by its prominen

280 se a series of neural and glial events after nerve injury that result in the generation of altered th

281 ause several such pathologies co-occur after nerve injury, that no single pathology is uniquely neces

282 However, in a significant proportion of nerve injuries, the likelihood of spontaneous regenerati

283 e transplants were performed before or after nerve injury, the MGE cells developed into mature neuron

284 sufficient to recover hypersensitivity after nerve injury; this rescue required expression of a Panx1

285 localize treatments for neuropathic pain and nerve injury to injured nerves.

286 ind that DLK-activating insults ranging from nerve injury to neurotrophin deprivation result in both

287 Sciatic nerve injury triggered generation of two-chain SorCS2 in

288 e response in the spinal dorsal horn, infant nerve injury triggers an anti-inflammatory immune respon

289 endent anion channel 1 (VDAC1) after sciatic nerve injury triggers Schwann cell demyelination via ERK

290 Nerve injury triggers the conversion of myelin and non-m

291 Finally, nerve injury upregulated CXCL12 in lumbar L4-L6 DRGs, an

292 Following nerve injury, upregulation of the alpha2delta-1 subunit

293 d a greater inhibition of eEPSC amplitude of nerve-injury versus control animals in both lamina I and

294 Moreover, cooling-induced analgesia after nerve injury was abolished in both genotypes.

295 Mechanical hyperalgesia after spared nerve injury was also reduced in C5aR(-/-) mice compared

296 The role of IL-10 in nerve injury was assessed using IL-10-null mice.

297 In addition to Wallerian degeneration, nerve injury was significantly aggravated (P = 0.032) af

298 All nerve injuries were recorded.

299 In contrast to adult nerve injury, which triggers a proinflammatory immune re

300 lated in the dorsal root ganglia (DRG) after nerve injury, which was further validated for its mouse