ライフサイエンスコーパス: SNL

1 SNL also significantly increased HVACC currents in small

2 SNL decreases total I(K(Ca)) in axotomized (L5) neurons,

3 SNL induced a slow (>3 d) and persistent (>21 d) activat

4 SNL led to increased immunoreactivity for met-enkephalin

5 SNL was followed by bilateral upregulation of mGluR1 in

6 SNL-enhanced kalirin immunofluorescence was coincident w

7 SNL-evoked mechanical hypersensitivity was attenuated, a

8 SNL-induced neuropathic pain was assessed behaviorally u

9 Thus it is expected that DNA-mediated 2D SNL structures open new avenues for designing miniaturiz

10 validation cohort included 492 patients (50% SNL, 35% LT, 15% expired).

11 gle-center cohort included 147 patients (58% SNL, 32% LT, 10% expired), while the PALFSG validation c

12 on: the carboxyl-terminal three amino acids (SNL) and the cyclic nucleotide-binding domain, respectiv

13 In addition, SNL did not alter the density of serotonergic fibers or

14 Additionally, SNL L4 neurons developed shoulders following transients

15 nced Ca(2+) buffering by neurons in adjacent SNL L4 neurons.

16 rily induced in spinal cord astrocytes after SNL.

17 en cisternae in the dorsal spinal cord after SNL.

18 persensitivity was induced in rats 2 d after SNL and lasted for >14 d.

19 p38 was activated between 5 hr and 3 d after SNL and returned to baseline within 5 d.

20 ar changes following 1, 3, 6, and 14 d after SNL injury and demonstrated that specific molecular chan

21 Treatment starting 1 or 7 d after SNL was ineffective.

22 y if it was started before but not 7 d after SNL.

23 er SNL and returned to baseline by 1 d after SNL.

24 nsetron in rats between 14 and 30 days after SNL and assessed effects on thermal and mechanical hyper

25 es from neuropathic rats 3 and 10 days after SNL displayed smaller EPSCs with prolonged latency, less

26 uced in injured L5 DRG neurons 14 days after SNL.

27 ized with CXCL13 and was downregulated after SNL.

28 dose (10 microg) now became effective after SNL.

29 drug effect was significantly enhanced after SNL (p<0.05).

30 ated p38 was transiently elevated 5 hr after SNL and returned to baseline by 1 d after SNL.

31 tile allodynia or thermal hyperalgesia after SNL, but it increases cold allodynia 6h after applicatio

32 Adjacent neurons (L4 after SNL) exhibit increased I(K(Ca)) current.

33 tivation was found in spinal microglia after SNL, which had fallen to near basal level by 21 d.

34 g patterns in uninjured L4 DRG neurons after SNL, in the presence or absence of TTX, were not affecte

35 tly upregulated in spinal cord neurons after SNL, resulting in spinal astrocyte activation via CXCR5

36 s are increased in adjacent L4 neurons after SNL.

37 e identified in injured L5 DRG neurons after SNL.

38 pregulated in uninjured L4 DRG neurons after SNL.

39 eurons, with larger increases observed after SNL relative to CCI.

40 lyzed for total and phosphorylated p38 after SNL alone or SNL combined with etanercept pretreatment.

41 hyperexcitability and neuropathic pain after SNL.

42 ivity by Cdk5-mediated phosphorylation after SNL contributes nerve injury-induced tactile allodynia.S

43 C-fiber-evoked dorsal horn potentials after SNL, which was prevented by mGluR1 antagonist AIDA [(RS)

44 SNL, showing that upregulation of SOCE after SNL is driven by store depletion.

45 These data indicate that after SNL treatment, phosphorylated p38 levels in spinal cord

46 ured DRG neurons are sensitized to TNF after SNL.

47 was resistant (>40%) to 100 microm TTX after SNL, whereas both A- and C-fiber components of sciatic n

48 ewise, Cdk5 expression was upregulated after SNL in the DRG.

49 tective effect of dermorphin-saporin against SNL-induced pain was blocked by beta-funaltrexamine, a s

50 RVM dermorphin or saporin did not alter SNL-induced experimental pain, and no pretreatment affec

51 In nerve injury models, AXO, PSNL, CCI, and SNL caused changes to the largest number of gait indices

52 ecreased by 5-HT2CR knockdown in control and SNL conditions to a similar degree.

53 chondrial Ca(2+) release in most Control and SNL L4 neurons, this usually failed to release mitochond

54 neuregulins blocked the effects of GDNF and SNL-CM, suggesting that both neuregulin and GDNF are req

55 t significantly different in non-injured and SNL-injured DRG neurons.

56 lectrophysiology in naive, sham-operated and SNL rats demonstrated that application of ice to recepti

57 increased both innocuous (sham-operated and SNL rats) and noxious (SNL rats) receptive field sizes o

58 els of endocannabinoids in sham-operated and SNL rats.

59 ly target SNL GABA neurons, and CeA->SNL and SNL dopamine neurons respond similarly to salient stimul

60 y, central corneal epithelial thickness, and SNL.

61 ile and thermal hypersensitivity, as well as SNL-induced upregulation of spinal dynorphin.

62 3 in the spinal cord persistently attenuated SNL-induced neuropathic pain.

63 RT((R)); Ellex Pty Ltd, Adelaide, Australia) SNL or sham treatment to the study eye at 6-monthly inte

64 Autochthonous SNL meat showed a higher nutraceutical quality compared

65 Autochthonous SNL raw and cooked meat showed a higher endogenous antio

66 mitochondrial Ca(2+) buffering in axotomized SNL L5 neurons but enhanced Ca(2+) buffering by neurons

67 Because SNL-CM and GDNF-like molecules stimulated the formation

68 Treatment starting 2 d before SNL with the TNF antagonist etanercept (1 mg, i.p., ever

69 Comparisons were made between SNL rats and a sham-operated group.

70 RVM lidocaine blocked SNL-induced tactile and thermal hypersensitivity on post

71 aments 1-75 g) were markedly reduced in both SNL and control groups.

72 sis that the rescued penumbra is affected by SNL.

73 d STIM1 and Orai1 levels were not altered by SNL, showing that upregulation of SOCE after SNL is driv

74 hyperalgesia and tactile allodynia caused by SNL but had no significant effect on the normal nocicept

75 mized neurons from rats made hyperalgesic by SNL lost sensitivity to the myristoylated form of autoca

76 y with the degree of hyperalgesia induced by SNL in the rats from which the neurons were isolated.

77 CXCR5 expression induced by SNL was required for the SNL-induced activation of spina

78 d the mechanical hypersensitivity induced by SNL.

79 iceptive neuron hyperexcitability induced by SNL.

80 control of mGluR1 upregulation triggered by SNL.

81 between WT and KO mice and were unchanged by SNL injury.

82 In contrast, SNL had no effect on DNA methylation levels around the C

83 In contrast, SNL induces a delayed (>3 d) activation of p38 in the L5

84 ibiting neurotransmitter release from either SNL DANs or cortical afferents to SNL resulted in impair

85 eceive mainly inhibitory input, establishing SNL DANs as a physiologically distinct dopaminergic subp

86 leukemia inhibitory factor (LIF)-expressing SNL feeders, frequently had two Xas.

87 In fact, SNL cells were found to express 100-fold higher levels o

88 al and mechanical hypersensitivity following SNL.

89 mal and mechanical pain thresholds following SNL were increasingly reversed over the days after injur

90 failed to release mitochondrial Ca(2+) from SNL L5 neurons.

91 r of CaMKII, whereas axotomized neurons from SNL animals that failed to develop hyperalgesia showed n

92 d ectopic in an ex vivo DRG preparation from SNL rats.

93 Enhanced, evoked CGRP release from SNL rats was blocked by anti-dynorphin A(1-13) antiserum

94 rom BLA to CeA recorded in brain slices from SNL rats using whole-cell patch-clamp conditions.

95 rkedly enhanced in lumbar spinal tissue from SNL rats when compared with sham-operated controls.

96 Furthermore, SNL induced a rapid (<12 h) but transient activation of

97 Furthermore, SNL induced CXCR5 expression in spinal astrocytes, and n

98 es with the rank order being AXO>PSNL=CCI >> SNL.

99 erentially target SNL GABA neurons, and CeA->SNL and SNL dopamine neurons respond similarly to salien

100 CeA->SNL neural responses to appetitive and aversive stimuli

101 CeA->SNL terminal activation elicited reinforcement when link

102 However, SNL treatment may have a role in slowing progression for

103 However, SNL-induced upregulation of GFAP was not attenuated by s

104 In SNL rats, subthreshold doses of TNF synergized with nerv

105 oads, the releasable mitochondrial Ca(2+) in SNL L5 neurons was less than Control while it was increa

106 ike firing, and increased burst activity) in SNL rats.

107 lus oligomycin elevated resting [Ca(2+)]c in SNL L4 neurons more than in Control neurons.

108 s the subsequent RIM1alpha/CaV2.2 cascade in SNL-induced neuropathic pain.

109 ion of 5-HT2CR in non-GABAergic BLA cells in SNL rats.

110 neurones, which was significantly greater in SNL rats than naive and sham-operated rats.

111 of JWH-133 reversed pain hypersensitivity in SNL rats, but had no effect in sham control rats.

112 tor (GDNF)-like molecules were identified in SNL-CM and recombinant forms of GDNF, neurturin, and art

113 ays of metabolism have greater importance in SNL rats.

114 less than Control while it was increased in SNL L4 neurons.

115 nuated evoked responses of spinal neurons in SNL rats but did not alter hindpaw levels of endocannabi

116 ic currents in spinal dorsal horn neurons in SNL rats, but not in sham control rats; intrathecal inje

117 tsynaptic currents of dorsal horn neurons in SNL rats.

118 acilitating mechanically-evoked responses in SNL rats.

119 Due to the collective plasmonic responses in SNL, these ultrathin 2D films display rapid and reversib

120 resulted in a 72% reduction of GLU uptake in SNL rats compared to sham controls in the ipsilateral L5

121 t is tempting to speculate that peri-infarct SNL could represent a new therapeutic target.

122 L5 SNL induced BIP upregulation in the neuron of superficia

123 arkedly altered on days 3, 7, or 14 after L5 SNL in L5 spinal cord or DRG.

124 neurons from hyperalgesic rats following L5 SNL.

125 Subthreshold nanosecond laser (SNL) treatment has shown promise in preclinical studies

126 ANs) in the substantia nigra pars lateralis (SNL) project to the tail of striatum, where they contrib

127 in the SNR, substantia nigra pars lateralis (SNL), and VTA.

128 ates, a series of single-nanoparticle-layer (SNL) plasmonic films is fabricated.

129 ber of nerves/mm(2)), subbasal nerve length (SNL, total length of nerves/mm(2)) and subbasal nerve br

130 s of spinal neurons in spinal nerve ligated (SNL) rats or hindpaw levels of endocannabinoids.

131 0.02) more neurones of spinal nerve-ligated (SNL) rats responded to brush compared with the sham cont

132 thic pain produced by spinal nerve ligation (SNL) (L5).

133 sts in rats following spinal nerve ligation (SNL) but not sham operation.

134 Axonal injury by spinal nerve ligation (SNL) elevated SOCE and I(CRAC).

135 ad received L5 and L6 spinal nerve ligation (SNL) immediately before injection.

136 sensory neurons after spinal nerve ligation (SNL) in mice.

137 perexcitability after spinal nerve ligation (SNL) in rat.

138 Spinal nerve ligation (SNL) in rats significantly increased mRNA and protein le

139 following unilateral spinal nerve ligation (SNL) in rats.

140 oblotting showed that spinal nerve ligation (SNL) induced a delayed and sustained increase in CB2 exp

141 Furthermore, spinal nerve ligation (SNL) induced persistent neuropathic pain and MCP-1 upreg

142 Spinal nerve ligation (SNL) injury in rats pretreated with RVM dermorphin-sapor

143 al consequences of L5 spinal nerve ligation (SNL) injury.

144 Using the spinal nerve ligation (SNL) model of neuropathic pain, we found that CXCL13 was

145 ceral pain, and a rat spinal nerve ligation (SNL) model of neuropathic pain.

146 behaviors in the rat spinal nerve ligation (SNL) model.

147 the rat hot plate and spinal nerve ligation (SNL) models of acute and neuropathic pain, respectively,

148 as the hot plate and spinal nerve ligation (SNL) models of acute and neuropathic pain.

149 amined the effects of spinal nerve ligation (SNL) on the number of neurons in the rostral ventromedia

150 he fourth lumbar (L4) spinal nerve ligation (SNL) or chronic constriction injury (CCI) of the sciatic

151 Spinal nerve ligation (SNL) produced expected tactile and thermal hyperesthesia

152 rats induced by L5/L6 spinal nerve ligation (SNL) via electrophysiological and neurochemical approach

153 ve transection (SNT), spinal nerve ligation (SNL), and chronic constriction injury (CCI).

154 made hyperalgesic by spinal nerve ligation (SNL), basal K(ATP) channel activity was decreased, and s

155 After spinal nerve ligation (SNL), both wild-type (WT) and KO mice demonstrated decre

156 als in rats receiving spinal nerve ligation (SNL), but not in uninjured rats.

157 behavior after L5/L6 spinal nerve ligation (SNL), implicating a critical functional role of Na(V)1.8

158 ats, we reported that spinal nerve ligation (SNL), in addition to causing allodynia, enhances the Rab

159 hy, unilateral lumbar spinal nerve ligation (SNL), to characterize the distribution of alpha(2)delta-

160 lammatory pain and L5 spinal nerve ligation (SNL)-induced neuropathic pain in rats.

161 R) activation in a L5 spinal nerve ligation (SNL)-induced rat neuropathic pain model.

162 allodynia induced by spinal nerve ligation (SNL).

163 y in rats after L5-L6 spinal nerve ligation (SNL).

164 tion injury (CCI) and spinal nerve ligation (SNL).

165 ) neurons after L5/L6 spinal nerve ligation (SNL).

166 r pain behavior after spinal nerve ligation (SNL).

167 re induced in rats by spinal nerve ligation (SNL).

168 wnregulated following spinal nerve ligation (SNL).

169 tested in rats after spinal nerve ligation (SNL).

170 root ganglia after L5 spinal nerve ligation (SNL).

171 We observed that spinal nerve ligation (SNL, L5) in male Sprague Dawley rats resulted in behavio

172 ated and neuropathic (spinal nerve ligation, SNL) rats using in vivo electrophysiology to elucidate t

173 nerve ligation; PSNL, spinal nerve ligation; SNL or chronic constriction injury; CCI).

174 ement precision beyond the shot-noise limit (SNL) by taking advantage of the infinite-dimensional Hil

175 dium conditioned by the SNL fibroblast line (SNL-CM) is able to stimulate primary cultures of rat typ

176 al trajectory or survival with native liver (SNL).

177 s DRGs with injured spinal nerves) of living SNL rats.

178 WNS, FNW, HNA, FNS, SNK, GNV, HNH, SNY, LNW, SNL, NNF, DNA, GNS, and FNR showed no deamidation.

179 Selective neuronal loss (SNL) in the rescued penumbra could account for suboptima

180 mus lumborum muscles from Suino Nero Lucano (SNL) and a modern crossbred (CG) pig.

181 issimus dorsi muscle from Suino Nero Lucano (SNL) and a modern crossbred (CG) pigs, before and after

182 antitative (11)C-flumazenil (FMZ)-PET to map SNL in the non-infarcted tissue and assess its relations

183 In WT mice, SNL upregulated lumbar dynorphin content on day 10, but

184 so includes a C-terminal PDZ-binding motif (-SNL).

185 the electrophysiological responses of naive, SNL-injured, or adjacent uninjured DRG to TNF (0.1-1000

186 Ligation of the L5 spinal nerve (SNL) on one side in adult rats produces an early onset a

187 r tight ligation of L5 and L6 spinal nerves (SNL).

188 hrough tight ligation of L5/6 spinal nerves (SNL).

189 projections to the lateral substantia nigra (SNL) that contribute to appetitive and aversive learning

190 oscintigraphy (LSG) for sentinel lymph node (SNL) mapping in a woman with a breast mass presents an u

191 y passage Xa/Xi hiPSC lines generated on non-SNL feeders were converted into Xa/Xa hiPSC lines after

192 us (sham-operated and SNL rats) and noxious (SNL rats) receptive field sizes of WDR neurones.

193 In the absence of SNL, pharmacological stimulation of 5-HT(2A)R with TCB-2

194 both male and female mice in the absence of SNL.

195 ength differently, we purified components of SNL-CM to identify the additional contributing factor(s)

196 ior similar to that seen on feeder layers of SNL fibroblasts.

197 A predictive model of SNL versus LT or death was created using logistic regres

198 d rats or the contralateral sciatic nerve of SNL rats.

199 ater PO period the proportion of neurones of SNL rats responsive to prod was significantly (P = 0.007

200 morphin-saporin did not prevent the onset of SNL-induced tactile and thermal hypersensitivity, but th

201 funiculus (DLF) did not prevent the onset of SNL-induced tactile and thermal hypersensitivity, but th

202 magnitude of the evoked neuronal response of SNL rats at PO days 7-10 was comparable to that of the s

203 In addition, neuronal responses of SNL rats to mechanical punctate stimuli and the C fibre-

204 brush- and prod-evoked neuronal responses of SNL rats were significantly smaller (P = 0.05 and P = 0.

205 We aimed to evaluate the safety of SNL treatment in iAMD and its efficacy for slowing progr

206 Previous studies of SNL used single-photon emission tomography (SPECT), did

207 ehaviors and increased sensory thresholds of SNL rats, but had no effect in sham controls.

208 Chronic PGB treatment of SNL animals, at a dose that alleviated allodynia, marked

209 ure trials to examine the potential value of SNL treatment for slowing progression in intermediate AM

210 Xa/Xa hiPSC lines after several passages on SNL feeders, and supplementation with recombinant LIF ca

211 al and phosphorylated p38 after SNL alone or SNL combined with etanercept pretreatment.

212 III, or IV of the dorsal horn in the CCI or SNL models.

213 g of WDR neurones in naive, sham-operated or SNL rats but inhibited mechanically-evoked responses of

214 ) criteria, and grouped by clinical outcome (SNL, LT, or death).

215 reversed neuropathic pain in WT mice at post-SNL day 10 (when dynorphin was upregulated) but not on p

216 KO mice showed a return to baselines by post-SNL day 10.

217 n dynorphin was upregulated) but not on post-SNL day 2; intrathecal MK-801 reversed SNL-pain at both

218 tivity on post-SNL days 6-12 but not on post-SNL day 3.

219 eversed to baseline levels beginning on post-SNL day 4.

220 eversed to baseline levels beginning on post-SNL day 4.

221 tactile and thermal hypersensitivity on post-SNL days 6-12 but not on post-SNL day 3.

222 er failure score) was created that predicted SNL versus LT or death with greater accuracy (C statisti

223 A model using these variables predicted SNL versus LT or death with high accuracy (accuracy [0.7

224 The CHLA-acute liver failure score predicts SNL versus LT or mortality in PALF using admission labor

225 he pathogenesis of cold allodynia in the rat SNL model, but it is a potential mechanism for the analg

226 here participants were randomized to receive SNL or sham treatment in 1 eye at 6-monthly intervals up

227 rticipants were randomly assigned to receive SNL or sham treatment to the study eye at 6-month interv

228 In rats receiving SNL, we found that the number of RVM neurons decreased b

229 ion rate to late AMD between those receiving SNL and sham treatment were observed.

230 t with the TNF antagonist etanercept reduced SNL-induced allodynia by almost 50%.

231 NA expression (10 mug, 10 mul; i.t.) reduced SNL-induced allodynia, kalirin and pNR2B expression, as

232 te, starting before the SNL surgery, reduces SNL-induced mechanical allodynia from day 1 to day 10, w

233 nto the L5 DRG prevented but did not reverse SNL-induced mechanical allodynia.

234 post-SNL day 2; intrathecal MK-801 reversed SNL-pain at both times.

235 esponses but potently prevented and reversed SNL-induced mechanical allodynia, a major symptom of neu

236 -1/CB neurons were also detected in the SNC, SNL, and VTA.

237 Central corneal SND, SNL, and SNBD were reduced by 84.6%, 82.6%, and 89.2%, r

238 < .0001) and positively correlated with SND, SNL, and SNBD (rho = 0.63, 0.66, and 0.56, respectively;

239 CR neurons were distributed in the SNC, SNR, SNL, and VTA.

240 Intrathecal D-JNKI-1 also suppressed SNL-induced phosphorylation of the JNK substrate, c-Jun,

241 mechanism, CeA inputs preferentially target SNL GABA neurons, and CeA->SNL and SNL dopamine neurons

242 ; and a downstream site where the C-terminal SNL (Ser-Asn-Leu) tripeptide of the channel interacts wi

243 nsion study to the LEAD Study confirmed that SNL treatment did not significantly reduce the overall r

244 Here, we show that SNL DANs fire irregularly, achieve rapid maximal firing

245 mmunoprecipitation-qPCR analysis showed that SNL increased enrichment of two activating histone marks

246 scope in situ hybridization also showed that SNL substantially increased CB2 mRNA levels, mostly in m

247 These results suggest that SNL leads to hypoglutamatergic neurotransmission in the

248 The SNL L4 neurons showed decreased transient peak and area

249 This microinjection also alleviated the SNL-induced increases in the levels of phosphorylated ex

250 a the intrathecal route, starting before the SNL surgery, reduces SNL-induced mechanical allodynia fr

251 Lesions of the DLF also blocked the SNL-induced increase in spinal dynorphin content, which

252 of somatic cells, medium conditioned by the SNL fibroblast line (SNL-CM) is able to stimulate primar

253 pression induced by SNL was required for the SNL-induced activation of spinal astrocytes and microgli

254 ith a significantly higher proportion in the SNL and CCI models, compared with SNT.

255 tric field distribution between AuNPs in the SNL film, based on which responsive surface-enhanced Ram

256 was slightly higher for participants in the SNL group compared with the sham treatment group in the

257 In the SNL model, mechanical allodynia failed to develop 1 and

258 astrocytes of the spinal dorsal horn in the SNL model.

259 NA into the ipsilateral L4 DRG mitigated the SNL-induced nociceptive hypersensitivities in both male

260 ng SNL showed a time-related reversal of the SNL-induced experimental pain to preinjury baseline leve

261 scending influences can underlie some of the SNL-induced plasticity at the spinal level.

262 9.1 dB enhancement of the precision over the SNL at N = 12 is achieved, which is only 1.7 dB away fro

263 of spinal RIM1alpha expression reversed the SNL-induced allodynia and increased spontaneous EPSC (sE

264 a 60-month period in those randomized to the SNL compared with the sham group (adjusted hazard ratio

265 area compared to control neurons, while the SNL L5 neurons showed increased shoulder level.

266 rom either SNL DANs or cortical afferents to SNL resulted in impaired auditory threat conditioning.

267 uditory and temporal association cortices to SNL DANs, but not SNc DANs.

268 -HT) neurons decreased by 35% ipsilateral to SNL.

269 spinal cord was 15-30% lower, ipsilateral to SNL.

270 bust functional corticonigral projections to SNL DANs which directly regulate threat behaviors.

271 e DLF-lesioned or dermorphin-saporin-treated SNL rats did not exhibit enhanced capsaicin-evoked CGRP-

272 targeting signal, the C-terminal tripeptide 'SNL'.

273 or saporin, in animals previously undergoing SNL showed a time-related reversal of the SNL-induced ex

274 Admission variables associated with SNL included albumin (odds ratio [OR], 16; P < 0.01), am

275 study eye was not significantly delayed with SNL treatment (hazard ratio, 0.83; 95% confidence interv

276 or the 70 participants (24.0%) with RPD with SNL treatment.

277 o late AMD was not slowed significantly with SNL treatment compared with sham treatment (adjusted haz

278 y, progression was slowed significantly with SNL treatment for those without coexistent RPD (adjusted