ライフサイエンスコーパス: nerve crush

1 a transient neuropathic pain model (sciatic nerve crush).

2 hat it recovered to supranormal levels after nerve crush.

3 on in restoring the stretch reflex following nerve crush.

4 subtypes examined, they survive after optic nerve crush.

5 3 weeks, and at weeks 10 and 50 after optic nerve crush.

6 suppression was examined in rats after optic nerve crush.

7 etina and optic nerve following intraorbital nerve crush.

8 site of injury in the axon after peripheral nerve crush.

9 zed the recovery of toe spread after sciatic nerve crush.

10 nce when the motor neurons are challenged by nerve crush.

11 chemia, spinal cord compression, and sciatic nerve crush.

12 r enhanced if Zymosan was injected 3 d after nerve crush.

13 tely 50% loss of ganglion cells 1 week after nerve crush.

14 confers neuroprotection on RGCs after optic nerve crush.

15 e degeneration of proprioceptive axons after nerve crush.

16 erfere with apoptotic mechanisms after optic nerve crush.

17 in glutamate-mediated cell death after optic nerve crush.

18 s can block ganglion cell death due to optic nerve crush.

19 pecific PKA inhibitor PKI several days after nerve crush.

20 sh receiving colchicine at the time of optic nerve crush.

21 ual function after experimental glaucoma and nerve crush.

22 ated SNs growing in vitro, or (3) peripheral nerve crush.

23 lly, within 5-7 weeks of retro-orbital optic nerve crush.

24 s of the retina, which increased after optic nerve crush.

25 unofluorescence, which increased after optic nerve crush.

26 ssed in the retina, and was induced by optic nerve crush.

27 na, and that its level decreases after optic nerve crush.

28 sion in the adult rat retina and after optic nerve crush.

29 crease in bcl-xL message shortly after optic nerve crush.

30 cle and then again 7, 10, and 13 weeks after nerve crush.

31 anglion cell axonal regeneration after optic nerve crush.

32 nglion neurons from degeneration after optic nerve crush.

33 , as well as axonal regeneration after optic nerve crush.

34 ation, enhances nerve regeneration following nerve crush.

35 e promotes axon regeneration following optic nerve crush.

36 icantly increases the loss of ChAT following nerve crush.

37 eneration by Pten knockdown (KD) after optic nerve crush.

38 ed analysis of AIS and node disruption after nerve crush.

39 otes axon growth in an animal model of optic nerve crush.

40 d axon loss is delayed in SkpA mutants after nerve crush.

41 -gp130(-/-) compared with control mice after nerve crush.

42 els of experimental optic neuritis and optic nerve crush.

43 retinal neurons of Thy1-CFP mice after optic nerve crush.

44 resulting mice were challenged with sciatic nerve crush.

45 ments may protect RGC health following optic nerve crush.

46 ere imaged weekly for four weeks after optic nerve crush.

47 l animals at 1, 2, 3 and 4 weeks after optic nerve crush.

48 neurite growth and synaptic remodeling after nerve crush.

49 were imaged again prior to unilateral optic nerve crush.

50 gle saline injection immediately after optic nerve crush.

51 ng development and during regeneration after nerve crush.

52 in wild-type and fat-1 mice after a sciatic nerve crush.

53 ed before and at different times after optic nerve crush 1.5 mm behind the eye, followed by TUJ1-posi

54 on cell survival at both 1 and 2 weeks after nerve crush (1 week, 79% vs. 55%; 2 weeks, 60% vs. 31%).

55 Eight days after optic nerve crush, 27,775 +/- 3,332 labeled ganglion cells wer

56 injection of BDNF into normal eyes and optic nerve crush alone showed bell-shaped patterns of change:

57 ntravitreal application of BDNF alone, optic nerve crush alone, and both.

58 However, whether optic nerve crush also damages the structure or function of ph

59 Nerve crush also resulted in decreased TrkB.FL, but the

60 in or even increase the stretch reflex after nerve crush and by difference to nerve transection.

61 times per week starting 1 week before optic nerve crush and continuing for 6 weeks.

62 impaired in CLU(-/-) mice following sciatic nerve crush and impaired regeneration nerve fibers throu

63 Wildtype mice underwent optic nerve crush and intravitreal injection of a control solu

64 death in mice was characterized using optic nerve crush and intravitreal injections of the glutamate

65 ated via MEK/ERK signaling and after sciatic nerve crush and Neto2(-/-) neurons from adult mice have

66 bited features of apoptosis after both optic nerve crush and NMDA injection, including the formation

67 ubulin-positive after injury caused by optic nerve crush and NMDA injection.

68 at eyes and in eyes that received (1) a mild nerve crush and no treatment, (2) a single intravitreal

69 engulfment of synaptic proteins after optic nerve crush and of myelin in two mouse models of demyeli

70 ls from cats that underwent unilateral optic nerve crush and received no treatment or nerve crush com

71 pression promote axonal repair after sciatic nerve crush and spinal cord injury via endocrine or auto

72 during refinement at 1-2 months after optic nerve crush and subsequently returned to baseline over t

73 ptic nerve crush, or immediately after optic nerve crush and then every 2 days for four weeks.

74 of Thy-1 promoter activation following optic nerve crush and whether this effect targets the earlier

75 uadratic terms were fitted to compare TRT of nerve-crushed and control eyes over time.

76 mouse DRG in response to peripheral (sciatic nerve crush) and central axon injuries (dorsal root crus

77 43 cytoplasmic levels in motor neurons after nerve crush, and the relocalization of TDP-43 to the nuc

78 Postnatal day-3 mice were subjected to optic nerve crush, and then retinal ganglion cells (RGCs) were

79 Using mouse optic nerve crush as a model for CNS traumatic injury, we perf

80 In this study, we describe a nerve crush assay in Drosophila melanogaster to study in

81 ce enhanced locomotor recovery after sciatic nerve crush, associated to an improvement in key pro-reg

82 Confirming results after optic nerve crush, astrocytes in glaucomatous optic nerves had

83 ganglion cell (RGC) survival following optic nerve crush based on single-cell RNA-seq analysis.

84 of neuregulin 1 impaired remyelination after nerve crush, but did not affect Schwann cell proliferati

85 also evident in rats with unilateral sciatic nerve crush, but not dorsal rhizotomy, indicating a peri

86 d labeled retinal ganglion cells after optic nerve crush, but remarkable had no influence on their de

87 Optic nerve crush caused rapid (10-20 minutes), irreversible r

88 Optic nerve crush caused RGCs to undergo a superoxide burst.

89 One week following common fibular nerve crush, CES was delivered to the tibial nerve in ha

90 Following nerve crush, CnB(scko) mice have slower degeneration of

91 tic nerve crush and received no treatment or nerve crush combined with intravitreous treatment of the

92 ction velocities consequent to acute sciatic nerve crush compared with wild-type control animals.

93 CpG injection in rats with optic nerve crush conferred significant neuroprotection compar

94 sium channel activity, recordings made after nerve crush demonstrated that the distal stump does not

95 rite extension and synaptic remodeling after nerve crush, demonstrating the importance of cGMP in the

96 laser ophthalmoscope before and after optic nerve crush every week, and fluorescent spots were count

97 Optic nerve crush, excitotoxicity, and elevated intraocular pr

98 Nerve-crushed eyes showed an initial period of thickenin

99 Furthermore, nerve crush failed to activate axonal PKA or stimulate i

100 After sciatic nerve crush, fibrin is deposited and its clearance corre

101 After sciatic nerve crush, functional recovery in vivo was retarded in

102 At 11 d after optic nerve crush, hnRNP K underwent significant translocation

103 y activated in sensory neurons after sciatic nerve crush in adult mice.

104 ls (RGCs) promotes axon regrowth after optic nerve crush in adult mice.

105 motoneurons (MNs) by IA afferents 3 d after nerve crush in anesthetized adult rats.

106 F promotes axonal regeneration after sciatic nerve crush in mice through an unexpected mechanism that

107 After sciatic nerve crush in mice, there was an induction of PA mRNAs

108 nonuclear phagocytes upon unilateral sciatic nerve crush in mice.

109 ganglion cell axon regeneration after optic nerve crush in mice.

110 neration of axons was examined after sciatic nerve crush in pre- and symptomatic SOD1(G93A) mice.

111 , and of lesioned sciatic nerve fibres after nerve crush in rats.

112 d expression of glycolytic genes after optic nerve crush in retinal ganglion cells with the co-deleti

113 After sciatic nerve crush in Sarm1(-/-) mice, axons rapidly extended t

114 ess and visual function are altered by optic nerve crush in the mouse.

115 ates regeneration of optic nerve axons after nerve crush in vivo.

116 from the same Pten-deletion mice after optic nerve crush, in which they differ only in their regenera

117 s muscle showed precise re-innervation after nerve crush, inaccurate regeneration after correct repai

118 a showed that HBO2 significantly reduced the nerve crush-induced allodynia; this anti-allodynic effec

119 ages share gene expression similarities with nerve-crush-induced macrophages(5) and express neurodege

120 Peripheral nerve crush initiates a robust increase in transmission

121 If nerve crush initiates IA EPSP enlargement as proposed by

122 We have now investigated whether a sciatic nerve crush injury alters the behavioral response in rat

123 n two established in vivo models - the optic nerve crush injury and an eIF2B loss of function (LOF) m

124 10 in terminating inflammation after sciatic nerve crush injury and promoting regeneration.

125 Nerve crush injury causes partial leakiness of the blood

126 of sensory nerve regeneration achieved after nerve crush injury compared with untreated diabetic rats

127 RGCs subjected to optic nerve crush injury demonstrated more rapid neurite outgr

128 Furthermore, following a sciatic nerve crush injury in male mice, local NMIIi2 administra

129 nerve regeneration, using a model of sciatic nerve crush injury in mice.

130 inflammation and regeneration after sciatic nerve crush injury in mice.

131 ell as after recovery from atrophy evoked by nerve crush injury in mice.

132 Sciatic nerve crush injury in rats induced expression of the ER

133 al retrograde signaling in response to optic nerve crush injury in vivo.

134 Optic nerve crush injury induced RGC death as expected, demons

135 GC neuronal death in Nf1+/- mice after optic nerve crush injury is also attenuated by rolipram treatm

136 en axonal regrowth into the distal zone of a nerve crush injury is not markedly impaired in cyclin D1

137 Optic nerve crush injury leads to rapid elevation of DLK prote

138 Similarly, in the optic nerve crush injury model, MAB228 and AG490 neutralizes d

139 ied around injured nerves in a mouse sciatic nerve crush injury model, the dExo-loaded pDNH group sig

140 By using optic nerve crush injury models, recent studies have revealed

141 In a sciatic nerve crush injury mouse model, we found that phentolami

142 robead-induced ocular hypertension and optic nerve crush injury paradigms.

143 eatment of adult mice with LiCl after facial nerve crush injury stimulated the expression of myelin g

144 Within 3 days after an optic nerve crush injury to one eye, primary transcript levels

145 One day sciatic nerve crush injury triggered a robust increase in UPR-as

146 Sciatic nerve crush injury triggers sterile inflammation within

147 ever, when combined with retro-orbital optic nerve crush injury, lengthy growth of severed retinal ga

148 s from cell body to axon predominantly after nerve crush injury, suggesting that it encodes a growth-

149 Following optic nerve crush injury, the mpz:egfp transgene was strongly

150 ry recovery occurred in mice after a sciatic nerve crush injury, there was little return of motor fun

151 Using an infraorbital optic nerve crush injury, we show that reducing beta-catenin-d

152 However, optic nerve crush injury-mediated retinal ganglion cell loss e

153 rded early axonal regeneration after sciatic nerve crush injury.

154 enhanced regrowth of axons after an in vivo nerve crush injury.

155 in the lumbar spinal cord, following sciatic nerve crush injury.

156 le enhances motor nerve regeneration after a nerve crush injury.

157 leration in recovery of force after an acute nerve crush injury.

158 nflammation and delayed RGC loss after optic nerve crush injury.

159 ilarly protected from degeneration following nerve crush injury.

160 n vivo in mice of both sexes following optic nerve crush injury.

161 l regeneration following retro-orbital optic nerve crush injury.

162 that remyelination is severely delayed after nerve-crush injury.

163 inal profile of RGC degeneration after optic nerve crush is characterized by a two-phase exponential

164 Better recovery following nerve crush is commonly attributed to superior reconnect

165 generation of the distal nerve stump after a nerve crush is greatly delayed when there is increased p

166 nsgenic rats and transplanted into a sciatic nerve crush lesion which transects all axons.

167 Eleven eyes from 11 nerve crush mice (baseline age 76 +/- 11.8 days) and eig

168 We have used the adult mouse facial nerve crush model and adult-onset conditional disruption

169 reductant, would protect RGCs in a rat optic nerve crush model of axotomy.

170 By using an optic nerve crush model that results in the death of the major

171 wth in vivo, by showing that in a peripheral nerve crush model there is less neurite outgrowth from R

172 A cat optic nerve crush model was combined with standard histologic

173 ting axonal regeneration in vivo in an optic nerve crush model when given intraocularly without lens

174 In the optic nerve crush model, 37%, 87%, and 93% of Rbpms-positive c

175 ls independent of dissociation with an optic nerve crush model.

176 TCEP is neuroprotective of RGCs in an optic nerve crush model.

177 odels of photoreceptor degeneration and in a nerve crush model.

178 Two weeks after nerve crush, morphological analysis of distal nerve segm

179 ir macrophage recruitment 1 and 7 days after nerve crush; neither did intraneural injections of CNTF

180 We found that after nerve crush, neuromuscular junction reinnervation was si

181 To address this role, we performed nerve crush on embryonic day 15 chick retina-optic nerve

182 MMPs in axonal regeneration following optic nerve crush (ONC) in adult zebrafish, which fully recove

183 ased survival of retinal neurons after optic nerve crush (ONC) in rodent models of visual system inju

184 In adult mice, optic nerve crush (ONC) injury by severing retinal ganglion ce

185 Next, we performed optic nerve crush (ONC) injury on wild-type (WT) mice and show

186 etinal ganglion cells (RGCs) following optic nerve crush (ONC) injury, albeit not to a clinically use

187 r example, a model of axon injury, the optic nerve crush (ONC), kills ~80% of RGCs after 2 weeks.

188 etinal ganglion cells (RGCs) following optic nerve crush (ONC), which severs their axons and leads to

189 ed with RGC loss in the mouse model of optic nerve crush (ONC).

190 normal retina and that is activated by optic nerve crush (ONC).

191 th chronic (bead occlusion) and acute (optic nerve crush, ONC) rat models to characterize disease res

192 mparable to that exhibited by rats receiving nerve crush only.

193 ibited an anti-allodynic effect, compared to nerve crush-only control rats.

194 reby T cells that infiltrate the brain after nerve crush or contusion actually protect neurons from i

195 Thus, peripheral axotomy-by nerve crush or during removal of DRGs--induces a transcr

196 es to 8-10% of normal following both sciatic nerve crush or permanent transection injury and only beg

197 t CNTFRalpha, even when challenged by facial nerve crush or the injection-associated trauma, thereby

198 a, most RBPMS cells are lost following optic nerve crush or transection at 3 weeks, and all Brn3a-, S

199 istochemical studies have shown that sciatic nerve crush or transection induces upregulation of the i

200 Twenty-eight days after nerve crush or transection, there was a dramatic decreas

201 ered either one time immediately after optic nerve crush, or immediately after optic nerve crush and

202 2, 3, 10, and 50, respectively, after optic nerve crush (P < 0.001; n = 5).

203 In a nerve crush paradigm, mitochondrial clusters form sequen

204 Ultimately, we found that optic-nerve crush pathologically upregulated activity in amacr

205 ion and RGC survival following partial optic nerve crush (pONC) injury.

206 microg of colchicine within 3 days of optic nerve crush (post-crush; PC) recovered vision after some

207 A cohort of mice not exposed to the nerve crush procedure served as control.

208 Seven days after the nerve crush procedure, rats were treated with HBO2 at 3.

209 ntravitreal injection of MT-I/II after optic nerve crush promotes axonal regeneration.

210 When gross trauma was minimized (by a nerve-crushing rather than nerve-cutting procedure), reg

211 However, after nerve crush, reflex muscle forces during stretch do reco

212 ganglion cell (RGC) degeneration after optic nerve crush remained unaffected upon microglia depletion

213 Optic nerve crush rescued the circadian period of Myk/+ behavi

214 Sciatic nerve crush resulted in a patchy but marked tactile allo

215 Sciatic nerve crush resulted in increased LAR protein expression

216 Analysis of the sciatic nerve at 11 d after nerve crush showed that the number of regenerating axons

217 Electron microscopy of the site of nerve crush shows abundant regenerating axons crossing t

218 g of RGCs in control mice subjected to optic nerve crush significantly decreased following their trea

219 Macrophages at the nerve crush site are molecularly distinct from macrophag

220 After optic nerve crush, staining for multiple markers of regenerati

221 age was not observed at any time after optic nerve crush, suggesting that axon damage alone is insuff

222 reserving retinal ganglion cells after optic nerve crush than the NMDA antagonist MK801.

223 generate RGC axons more robustly after optic nerve crush than wild-type littermates under normal cond

224 In mutant mice, after sciatic nerve crush, the axons showed impaired regeneration.

225 At one week after optic nerve crush, the proportion of fluorescent retinal neuro

226 Eight days after nerve crush, the total number of back-labeled RGCs was e

227 sualized by gel zymography showed that after nerve crush, the upregulation of PA activity in the tPA

228 One week after optic nerve crush, these cells started to die, progressing to

229 was examined by performing repeated sciatic nerve crushes to delay regenerating axons from reaching

230 ague Dawley rats were subjected to a sciatic nerve crush under anesthesia and mechanical thresholds w

231 In rats, optic nerve crush was performed on one side and a sham operati

232 nas at 1 and 4 days after intraorbital optic nerve crush was used in a modification of the differenti

233 Acute optic nerve crush was used to examine neuronal atrophy in the

234 mice aged 6 to 9 months (n = 5) before optic nerve crush, weekly after crush for 3 weeks, and at week

235 maining in the vehicle group following optic nerve crush were 36 +/- 8, 18 +/- 6, 13 +/- 10, 12 +/- 4

236 When BDNF and nerve crush were combined, trkB-FL levels reached 90% of

237 ponding retinal areas before and after optic nerve crush were compared, and the fluorescent spots wer

238 Adult rats with sciatic nerve crush were immediately and systemically injected B

239 NT-3 in recovery from nerve injury, sciatic nerve crushes were performed in young adult mice.

240 tic nerve after spinal cord injury and optic nerve crush, which is accompanied by upregulation of reg

241 raised in the retina immediately after optic nerve crush, whilst levels were suppressed in regenerati

242 s of fluorescent spots was found after optic nerve crush with 18.6% +/- 2.3%, 11.3% +/- 3.4%, 8.8% +/

243 h intact nerves, but was found after sciatic nerve crush with peripheral regeneration.