ライフサイエンスコーパス: LTM

1 LTM and/or HTM increased gene expression of VEGF, TIMP3,

2 LTM and/or HTM increased inflammation by upregulating TN

3 LTM evolution is unaffected by angiotensin II blockade a

4 LTM improved growth performance on d14, HTM improved gro

5 LTM interacts with the TOPLESS corepressor and with seve

6 LTM is supported by structural synaptic plasticity; howe

7 LTM permitted classification of 131 patients (58%) into

8 LTM was applied to an anti-TNF-alpha antibody, D2E7, whi

9 Since both AD-ITM and AD-LTM require MAPK activity, these collective findings sug

10 some LTM units including a C LTM, all Adelta LTM units (D hair), about 10% of cutaneous LTM Aalpha/be

11 ssible silent nociceptive) units, 5/6 Adelta-LTM (D hair), 13/14 Adelta-nociceptive, 2/9 Aalpha/beta-

12 ceptors: -2.6 nA, -21 pA pF(-1); both Adelta-LTMs and nociceptors: -1.3 nA, approximately -14 pA pF(-

13 at such increased expression does not affect LTM after retrieval.

14 AGXT*LTM expressed in Escherichia coli, as a GST-fusion prote

15 s also were shared in their haplotypes (AGXT*LTM), consistent with a founder effect.

16 Like its normal counterpart, the AGXT*LTM protein was present in the peroxisomes but it was in

17 Although LTM is sustained by structural synaptic plasticity, how

18 Among LTMs, greater practice experience was associated with sl

19 erm memory (LTM) by itself, flies develop an LTM.

20 The use of an LTM assembly that utilizes the principle of resistive wi

21 After scanning, subjects performed an LTM test on words presented during both WM conditions.

22 Together, these results suggest an LTM consolidation model in which transient neural activi

23 There was no difference between CTM and LTM (P =.72) in the rate of coexisting tumor.

24 tent TM, more than 90% with TM (both CTM and LTM) did not have tumor at presentation.

25 haracteristics during walking on the FTM and LTM.

26 d (ii) that facilitated induction of ITM and LTM by CaN inhibition requires MAPK activity.

27 ed that the facilitated induction of ITM and LTM produced by CaN inhibition depends on MAPK activity.

28 ermediate-term and long-term memory (ITM and LTM, respectively) for sensitization also lead to sustai

29 through MAPK, play a pivotal role in LTF and LTM formation.

30 Although L-LTP and LTM are normal in mTOR(+/-) mice, application of a low c

31 Problematically, both LTP and LTM are unaffected in both constitutive and conditional

32 ce indicating that mTORC1 promotes L-LTP and LTM is controversial.

33 Thus, the role of mTORC1 in L-LTP and LTM is unclear.

34 subthreshold for WT mice-prevented L-LTP and LTM only in mTOR(+/-) mice.

35 e and its restoration rescued both L-LTP and LTM.

36 for synapse-specific expression of L-LTP and LTM.

37 of PKMzeta that interferes with both LTP and LTM.

38 sting that appetitive middle-term memory and LTM are mechanistically linked.

39 so required in adult DPM neurons for MTM and LTM formation.

40 Abeta expression detrimental to both MTM and LTM.

41 ral peptides need to be degraded for MTM and LTM.

42 argeting neuropeptides essential for MTM and LTM.

43 -fibre units, including both nociceptive and LTM units, showed Na(v)1.7-LI.

44 in states) may influence both nociceptor and LTM excitability.

45 in states) may influence both nociceptor and LTM excitability.expression and/or properties (e.g. in c

46 ved placebo, nifedipine, or propranolol, and LTM dogs received placebo, atenolol, or amlodipine.

47 Evolution of STM and LTM was attenuated by ICa,L blockers but not beta-blocke

48 ing was associated with both enhanced WM and LTM for faces, as well as baseline activity shifts in a

49 ase A (PKA) activity correlates with Aplysia LTM, the analysis focuses on a positive feedback loop in

50 Appetitive LTM has some mechanistic similarity to aversive LTM in t

51 l motivational drive that enables appetitive LTM retrieval.

52 Furthermore, appetitive LTM requires activity in the dorsal paired medial neuron

53 However, appetitive LTM is completely disrupted by the radish mutation that

54 On average, LTMs showed slower baseline respiration rate (RR) than C

55 has some mechanistic similarity to aversive LTM in that it can be disrupted by cycloheximide, the dC

56 -4.6 nA,-33 pA pF(-1); cutaneous Aalpha/beta LTMs: -2.2 nA, -20 pA pF(-1); Abeta-nociceptors: -2.6 nA

57 9 Aalpha/beta-nociceptive, 10/18 Aalpha/beta-LTM cutaneous and 0/9 Aalpha/beta-muscle spindle afferen

58 Of the Aalpha/beta-LTM units, muscle spindle afferents had the fastest CV a

59 eptive, 10 C-, 8 Adelta- and 178 Aalpha/beta-LTM, 18 C- and 19 Adelta- unresponsive, and 4 C-cooling

60 or sharp/pricking-type pain) and Aalpha/beta-LTMs (tactile sensations and proprioception).

61 or sharp/pricking-type pain) and Aalpha/beta-LTMs (tactile sensations and proprioception).

62 evidence for specific dissociations between LTM and LTP.

63 a heat-shock promoter was reported to block LTM, whereas overexpression of an activator isoform (dCR

64 t into LTM, whereas CaMKIIalpha-HM4D blocked LTM formation.

65 rapamycin reduces L-LTP and partially blocks LTM, recent genetic and pharmacological evidence indicat

66 roup experienced greater gains in total body LTM (0.45 kg; 95% CI: 0.07, 0.84 kg), leg LTM (0.22 kg;

67 timulus-guided visuospatial attention and by LTM-guided visuospatial attention.

68 also present in some LTM units including a C LTM, all Adelta LTM units (D hair), about 10% of cutaneo

69 Positive units included 1/1 C-LTM, 6/6 C-nociceptive, 4/4 C-unresponsive (possible sil

70 ors: -1.3 nA, approximately -14 pA pF(-1); C-LTMs: -0.4 nA, -7.6 pA pF(-1); and C-nociceptors: -0.26

71 the magnitude of a previously characterized LTM trace, which is manifested as increased calcium infl

72 r inhibition of DNMT eliminates consolidated LTM.

73 20E either enhanced or suppressed courtship LTM, depending on the timing of its administration.

74 a LTM units (D hair), about 10% of cutaneous LTM Aalpha/beta-units, but no muscle spindle afferent un

75 ernable ring, while 2 (Aalpha/beta cutaneous LTMs) had weakly stained rings.

76 onsolidated into protein-synthesis-dependent LTM remains unclear.

77 l outcomes were compared between 3 different LTM subgroups.

78 ve model for the role of dCREB in Drosophila LTM.

79 fundamental mechanism underlying Drosophila LTM.

80 We found that the swing phase during LTM walking was slightly enhanced as well as some specif

81 talk between these two brain regions during LTM formation.

82 ehensively identified genes regulated during LTM consolidation.

83 uts from these MBONs are all required during LTM retrieval.

84 KII autophosphorylation is in fact to enable LTM formation after a single training trial, possibly by

85 se a specific function for CaMK2N1; enabling LTM maintenance after retrieval by inhibiting T286 autop

86 2-a transgene originally reported to enhance LTM carries a mutation that produces a translational rea

87 r isoform (dCREB2-a) was reported to enhance LTM.

88 nverted early LTP into late LTP and enhanced LTM.

89 processing in the reorder condition enhanced LTM by strengthening inter-item associations.

90 ther mTORC2 or actin polymerization enhances LTM.

91 rtial training cannot subsequently establish LTM.

92 w that it impairs maintenance of established LTM, but only if retrieval occurs.

93 synapses after retrieval of contextual fear LTM.

94 Three of 36 A-fibre LTM units exhibited CGRP-LI; all were Aalpha/beta-fibre

95 determines effective training intervals for LTM formation.

96 essential intertrial signaling mechanism for LTM induction.

97 tivation, a necessary signaling molecule for LTM induction, at 45 min after a single TS.

98 smission from MB-V3 neurons is necessary for LTM retrieval; and (v) RNAi-mediated down-regulation of

99 related with effective training patterns for LTM.

100 ortens the inter-trial interval required for LTM induction, whereas overexpression of constitutively

101 ing that CaMKII activity is not required for LTM storage.

102 thesized that these enzymes are required for LTM to support the increased expression of a family of g

103 rain are reported now as essential sites for LTM formation, while mushroom bodies are claimed to be u

104 Tests for LTM and its dependence on NO were performed routinely 24

105 to random Brownian or ATP-dependent forces (LTM).

106 a massed training protocol, but cannot form LTM after a single trial.

107 ation as well as long-term memory formation (LTM).

108 ase of new items, which are independent from LTM retrieval, masked priming reduced PRC activity and p

109 Left ventricular epicardial myocytes from LTM or sham control dogs were dissociated, and ICa,L was

110 (3.7%) patients had CTM, and 155 (14.4%) had LTM; 15 (1.4%) had tumors visible at US.

111 of 27 patients had CTM, and one of seven had LTM.

112 ory (LTM), and hSyn-HM4D completely impaired LTM formation.

113 oteins (ORBs) in any of these MBONs impaired LTM.

114 ion of CaMK2N2 in dorsal hippocampus impairs LTM formation, but not LTM maintenance, suggesting that

115 rotein translation) in MB-V3 neurons impairs LTM.

116 g protein synthesis in MB-V3 neurons impairs LTM; (ii) MB-V3 neurons show enhanced neural activity af

117 Neither the target of Notch activity in LTM formation nor the underlying mechanism of regulation

118 plicating alphaCaMKII autophosphorylation in LTM formation rather than storage.

119 contrast, produced the anticipated block in LTM formation.

120 ysone signaling is reduced were defective in LTM, and that an elevation of 20E levels was associated

121 of the mutants tested revealed a deficit in LTM compared to the robust LTM observed in control flies

122 tch-clamp experiments, peak ICa,L density in LTM and control were equivalent, but activation was more

123 ntial part of the neural network involved in LTM formation.

124 ntrinsic and synaptic plasticity involved in LTM formation.

125 at a number of these targets are involved in LTM.

126 the requirement of a secreted TrkB ligand in LTM formation at molecular, synaptic, and behavioral lev

127 and time constants of inactivation longer in LTM (P<0.05).

128 y whether there is a prior representation in LTM, and not whether the stimulus involves letters or fa

129 get-predictive spatial information stored in LTM triggers spatiotopic modulation of preparatory activ

130 nhibition (trandolapril) were also tested in LTM.

131 d in various biological processes, including LTM.

132 duced LTF in the CNS, and tail shock-induced LTM but is not necessary for short-term synaptic facilit

133 vel two-trial training pattern which induces LTM in Aplysia, we show that the first of two training t

134 n of resting intervals required for inducing LTM is regulated by activity levels of the protein tyros

135 By using a paradigm that integrates LTM and attentional orienting, we first demonstrate that

136 Intensive LTM training after hemisection was found to change featu

137 (STM) but not LTM, can be consolidated into LTM by exposing animals to novel but not familiar enviro

138 mation of a subthreshold learning event into LTM, whereas CaMKIIalpha-HM4D blocked LTM formation.

139 brain consolidates early labile memory into LTM.

140 dy LTM (0.45 kg; 95% CI: 0.07, 0.84 kg), leg LTM (0.22 kg; 95% CI: 0.02, 0.42 kg), and muscle strengt

141 was divided into classic (CTM) and limited (LTM) on the basis of the presence of five or more microl

142 3 treatments supplemented with 0 (NTM), low (LTM) and high (HTM) TM levels in the same basal diet.

143 d through lean red meat on lean tissue mass (LTM), muscle size, strength and function, circulating in

144 e (including low-threshold mechanoreceptive (LTM) and cooling units).

145 ceptive than low threshold mechanoreceptive (LTM) neurons showed Nav1.8-LI, and nociceptive neurons h

146 nd cutaneous low-threshold mechanoreceptive (LTM) neurons, 50 had no discernable ring, while 2 (Aalph

147 nociceptive, low threshold mechanoreceptive (LTM) or unresponsive unit.

148 nor C-fibre low threshold mechanoreceptive (LTM) units (n = 3) had CGRP-LI.

149 by cutaneous low threshold mechanoreceptors (LTMs).

150 ciceptive or low-threshold-mechanoreceptors (LTMs) and as having C-, Adelta- or Aalpha/beta-conductio

151 resentations in subjects long-term memories (LTM) and that face stimuli used in prior experiments wer

152 the formation of long-term olfactory memory (LTM).

153 Both the formation of long-term memory (LTM) and dendritic spine growth that serves as a physica

154 Both the formation of long-term memory (LTM) and late-long-term potentiation (L-LTP), which is t

155 ddle-term memory (MTM) and long-term memory (LTM) and that their expression is required in the mushro

156 selectively impaired both long-term memory (LTM) and the late phase of hippocampal long-term potenti

157 study of humans engaged in long-term memory (LTM) and working memory tasks.

158 is not capable of inducing long-term memory (LTM) by itself, flies develop an LTM.

159 of ventricular pacing and long-term memory (LTM) by ventricular pacing for 21 days.

160 n Morris Water Maze (MWM), long-term memory (LTM) contextual fear testing, and rotarod test when comp

161 mTORC2 (A-443654) reverses long-term memory (LTM) deficits in both aged mice and flies.

162 om neuroimaging studies of long-term memory (LTM) encoding have contributed to the view that the vent

163 trials in the induction of long-term memory (LTM) for sensitization in Aplysia californica.

164 tic facilitation (LTF) and long-term memory (LTM) for sensitization in Aplysia.

165 iate-term memory (ITM) and long-term memory (LTM) for tail shock-induced sensitization in Aplysia wit

166 DLPFC should contribute to long-term memory (LTM) formation by strengthening associations among items

167 11A is required for social long-term memory (LTM) formation during adolescence and adulthood.

168 ture involved in olfactory long-term memory (LTM) formation.

169 EC) that are necessary for long-term memory (LTM) formation.

170 not affect contextual fear long-term memory (LTM) formation.

171 APK isoforms important for long-term memory (LTM) formation.

172 on working memory (WM) and long-term memory (LTM) has not yet been investigated.

173 ormal short-term (STM) and long-term memory (LTM) in a novel object recognition task, but exhibit imp

174 t role in the formation of long-term memory (LTM) in adults, implying that memory formation requires

175 eviously, we reported that long-term memory (LTM) in Aplysia can be reinstated by truncated (partial)

176 use LTF is a substrate for long-term memory (LTM) in Aplysia, we examined the requirement of a secret

177 shown to be necessary for long-term memory (LTM) in Aplysia.

178 for middle-term (MTM) and long-term memory (LTM) in the dorsal paired medial (DPM) neurons, a pair o

179 ity.SIGNIFICANCE STATEMENT Long-term memory (LTM) induced by repeated trials spaced over time is know

180 A property of long-term memory (LTM) induction is the requirement for repeated training

181 Consolidation of long-term memory (LTM) is a complex process requiring synthesis of new mRN

182 Long-term memory (LTM) is believed to be stored in the brain as changes in

183 y (STM) is intact, whereas long-term memory (LTM) is significantly impaired.

184 trials in the formation of long-term memory (LTM) is widely appreciated, surprisingly little is known

185 tion of aversive olfactory long-term memory (LTM) requires multiple training sessions pairing odor an

186 Creating long-term memory (LTM) requires new protein synthesis to stabilize learnin

187 mporoparietal junction and long-term memory (LTM) retrieval processes are localized to the left later

188 buted to the recovery of a long-term memory (LTM) signal.

189 itial learning defect, but long-term memory (LTM) specifically is abolished under these training cond

190 tophosphorylation mediates long-term memory (LTM) storage.

191 Short-term memory (STM) or long-term memory (LTM) was evaluated in rutabaga (rut) and dunce (dnc) mut

192 grate information coded in long-term memory (LTM) with ongoing perceptual processing remain unknown.

193 eshold learning event into long-term memory (LTM), and hSyn-HM4D completely impaired LTM formation.

194 LTP), a cellular model for long-term memory (LTM), requires de novo protein synthesis.

195 hly proficient in auditory long-term memory (LTM).

196 tures for the formation of long-term memory (LTM).

197 nts that possess defective long-term memory (LTM).

198 t role in the formation of long-term memory (LTM).

199 tization, a simple form of long-term memory (LTM).

200 ntial for the formation of long-term memory (LTM).

201 athway in the formation of long-term memory (LTM).

202 stent memory identified as long-term memory (LTM).

203 erm potentiation (LTP) and long-term memory (LTM).

204 , synaptic plasticity, and long-term memory (LTM).

205 etry (MTC) and laser tracking microrheology (LTM) are described.

206 Latent linear trajectory modeling (LTM) was applied to identify patients with a similar tra

207 Long Term Video-EEG Monitoring (LTM) is the gold standard for diagnosis.

208 Long-term monitoring (LTM) of groundwater remedial projects is costly and time

209 d with I(h) and I(h) density for all non-MSA LTMs, and for Adelta-nociceptors.

210 Look-through mutagenesis (LTM) is a multidimensional mutagenesis method that simul

211 ansmission of food preference (STFP), but no LTM 24 h post training.

212 Importantly, PDE11A KO mice show normal LTM for nonsocial odor recognition.

213 l hippocampus impairs LTM formation, but not LTM maintenance, suggesting that CaMKII activity is not

214 hich induces short-term memory (STM) but not LTM, can be consolidated into LTM by exposing animals to

215 exposure to IMD and TMX affected STM but not LTM.

216 Compared to NTM, LTM reduced area under the curve (AUC) of FPD lesion sco

217 to some extent, the temporary activation of LTM.

218 might be important for repetitive aspects of LTM formation, such as memory consolidation.

219 shortly afterwards, blocks consolidation of LTM and prevents its subsequent induction by truncated t

220 Thus, the consolidation of LTM depends on two functionally distinct phases of prote

221 n of genes regulated during consolidation of LTM.

222 Here, we explore how the contents of LTM optimize perception by modulating anticipatory brain

223 g, we first demonstrate that the contents of LTM sharpen perceptual sensitivity for targets presented

224 n visual cortex according to the contents of LTM.

225 An electrophysiological correlate of LTM was also blocked by PTIO, showing that the dependenc

226 cked by PTIO, showing that the dependence of LTM on NO is amenable to analysis at the cellular level

227 transgene failed to show any enhancement of LTM.

228 on is necessary for the normal expression of LTM.

229 of sleep did not result in the formation of LTM after massed training.

230 s as a molecular switch for the formation of LTM in fear conditioning.

231 ication of DOX might impair the formation of LTM via the p38 MAPK pathway.

232 f the Arc/Arg3.1 ODN showed an impairment of LTM (tested approximately 24 later), but no deficit in S

233 We also found a comparable impairment of LTM in dTORC2-deficient flies, highlighting the evolutio

234 Both the consolidation and maintenance of LTM depend on DNA methylation.

235 anism that contributes to the persistence of LTM.

236 olateral prefrontal cortex was predictive of LTM for words studied on both reorder and rehearse trial

237 e supported by the temporary reactivation of LTM representations.

238 ng protein (CREB), an essential regulator of LTM formation.

239 , a higher proportion of nociceptive than of LTM neurones was positive, and the median relative stain

240 xtended neural network involved in olfactory LTM: (i) inhibiting protein synthesis in MB-V3 neurons i

241 e enhancing effect of CREB overexpression on LTM formation is shown to be specific in terms of bioche

242 ffective for enhancing the effects of PRT on LTM and muscle strength and reducing circulating IL-6 co

243 nificant difference between no TM and CTM or LTM (P </=.001) in the rate of coexisting tumor.

244 tients with tumor at presentation had CTM or LTM.

245 nd observe whether training regimens (FTM or LTM) can induce durable changes in the parameters of loc

246 istinct connections is associated with WM or LTM benefits.

247 est of postreactivation long-term memory (PR-LTM).

248 reactivation (PR)-STM are intact, whereas PR-LTM is significantly impaired.

249 g-term mindfulness meditation practitioners (LTMs, n = 31) and a matched group of non-meditators (Con

250 ormance, FFA connectivity with MFG predicted LTM improvements.

251 thesis: an early phase that appears to prime LTM; and a later phase whose successful completion is ne

252 ing on-line processing, and this may promote LTM for associations between items.

253 ingle training trial, possibly by regulating LTM consolidation-specific transcription.

254 aled a deficit in LTM compared to the robust LTM observed in control flies.

255 and precocious doming of the vegetative SAM LTM encodes a kelch domain-containing protein, with no l

256 positive Nav1.8-LI was also present in some LTM units including a C LTM, all Adelta LTM units (D hai

257 set of MB neurons is converted into a stable LTM through protein synthesis in dendrites of MB-V3 neur

258 emory in the MB are consolidated into stable LTM at a few postsynaptic MBONs through sequential ORB-r

259 in alphaCaMKII autophosphorylation can store LTM after a massed training protocol, but cannot form LT

260 reorder trials was predictive of subsequent LTM.

261 a more general role in promoting successful LTM formation.

262 tal cortex (VLPFC) contributes to successful LTM formation, whereas the dorsolateral prefrontal corte

263 eptor blockade nor ACE inhibition suppressed LTM.

264 ional repressor, and the crammer and tequila LTM-specific mutations.

265 and tested their short (STM) and long-term (LTM) olfactory memories.

266 e significantly greater for nociceptive than LTM units in all CV groups.

267 ng intensity was greater in nociceptive than LTM units.

268 could reflect increased fluency rather than LTM retrieval per se.

269 ntense immunoreactivity in their somata than LTM neurons.

270 training, we provided further evidence that LTM formation depends on an intact NO-cGMP pathway.

271 significant improvement would indicate that LTM training maximizes the contribution of spinal locomo

272 Here, we report that LTM can be induced by partial training after disruption

273 We now report that LTM can be induced with only two spaced training trials

274 Biochemical analysis reveals that LTM-inducing training regimens generate repetitive waves

275 Here we show that LTM for sensitization also requires MAPK activity.

276 Here, we show that LTM storage and synaptic change can be dissociated.

277 ng was partially suppressed, suggesting that LTM functions to suppress SP in the vegetative SAM In ag

278 ts) in the same enclosure on the FTM and the LTM, the changes in averaged locomotor characteristics m

279 ory-specific patterns of activity during the LTM task, these patterns were not reinstated in PFC duri

280 memory trace was defective in all 26 of the LTM mutants.

281 ) to regularly train cats for 6 weeks on the LTM to determine whether such regular training improves

282 emispinalized and trained for 6 weeks on the LTM, whereas the 3 other cats were hemispinalized and tr

283 In addition, we find evidence that the LTM for sensitization persists covertly after its appare

284 We reasoned that the LTM-trained classifier would be able to decode delay-per

285 bservations elevate the significance of this LTM trace given that 26 independent mutants all exhibit

286 Thus, this LTM/combinatorial beneficial mutagenesis strategy genera

287 rt the view that the DLPFC may contribute to LTM through its role in active processing of relationshi

288 pothesized that the DLPFC does contribute to LTM, but under specific circumstances.

289 pport the view that the DLPFC contributes to LTM formation through its role in organization of inform

290 ian oscillation, both of which are linked to LTM formation.

291 s on the rungs of a moving ladder treadmill (LTM); (2) to assess the capability of cats after a unila

292 paper introduces a method (ladder treadmill [LTM]) to study the locomotor ability of cats with an int

293 vide a narrow molecular window for two-trial LTM formation.

294 row permissive training window for two-trial LTM is accompanied by an equally narrow window of transi

295 We report the novel finding that, under LTM-guided attention, both RH and LH IPS0-2 exhibit bila

296 long-term synaptic plasticity that underlies LTM.

297 system Lymnaea, we investigate here whether LTM formation is associated with specific changes in the

298 ryonal cell in one), nine (5.8%) of 155 with LTM (seminoma in six, mixed germ cell in one, Leydig cel

299 ith CTM and one (2%) of the 65 patients with LTM had tumor at presentation (P =.004).

300 Patients with LTM have a lower prevalence of associated malignancy tha