ライフサイエンスコーパス: nerve crush

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

2 3 weeks, and at weeks 10 and 50 after optic nerve crush.

3 suppression was examined in rats after optic nerve crush.

4 etina and optic nerve following intraorbital nerve crush.

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

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

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

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

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

10 confers neuroprotection on RGCs after optic nerve crush.

11 e degeneration of proprioceptive axons after nerve crush.

12 erfere with apoptotic mechanisms after optic nerve crush.

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

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

15 pecific PKA inhibitor PKI several days after nerve crush.

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

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

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

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

20 unofluorescence, which increased after optic nerve crush.

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

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

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

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

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

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

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

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

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

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

31 resulting mice were challenged with sciatic nerve crush.

32 ual function after experimental glaucoma and nerve crush.

33 ments may protect RGC health following optic nerve crush.

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

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

36 neurite growth and synaptic remodeling after nerve crush.

37 were imaged again prior to unilateral optic nerve crush.

38 anglion cell axonal regeneration after optic nerve crush.

39 gle saline injection immediately after optic nerve crush.

40 ng development and during regeneration after nerve crush.

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

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

43 icantly increases the loss of ChAT following nerve crush.

44 hat it recovered to supranormal levels after nerve crush.

45 on in restoring the stretch reflex following nerve crush.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 43 cytoplasmic levels in motor neurons after nerve crush, and the relocalization of TDP-43 to the nuc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 Optic nerve crush, excitotoxicity, and elevated intraocular pr

83 Nerve-crushed eyes showed an initial period of thickenin

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

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

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

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

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

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

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

91 nonuclear phagocytes upon unilateral sciatic nerve crush in mice.

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

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

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

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

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

97 Peripheral nerve crush initiates a robust increase in transmission

98 If nerve crush initiates IA EPSP enlargement as proposed by

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

100 10 in terminating inflammation after sciatic nerve crush injury and promoting regeneration.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 ilarly protected from degeneration following nerve crush injury.

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

124 rded early axonal regeneration after sciatic nerve crush injury.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 2, 3, 10, and 50, respectively, after optic nerve crush (P < 0.001; n = 5).

159 In a nerve crush paradigm, mitochondrial clusters form sequen

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

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

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

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

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

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

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

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

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

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

170 Sciatic nerve crush resulted in increased LAR protein expression

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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