ライフサイエンスコーパス: LTP

1 LTP enhancement by these drugs is eliminated in mice exp

2 LTP in response to theta-burst stimulation and to 100-Hz

3 LTP is also known to be effectively regulated by extrace

4 LTP of NMDA and AMPA EPSCs after high-frequency stimulat

5 LTP was restored by expression of wild-type Syt7 but not

6 7 (Syt7), but not of either alone, abolished LTP.

7 Strikingly, the NL1 cKO also abolished LTP elicited by activation of L-type Ca(2+)-channels dur

8 AMPA receptor exocytosis, thereby abolishing LTP.

9 leading to transient occlusion of additional LTP-like plasticity.

10 proportions of patients requiring additional LTPs comparing those who were initially treated by ophth

11 Additionally, LTP and LTD are correlated with dendritic spine enlargem

12 Although LTP has suffered considerable growing pains over the yea

13 Here, we analyze LTP in isolated synapses from AD brain using a novel app

14 d NSAID-independent LTP-induced anaphylaxis (LTP-A).

15 ispensable for, the activation of CaMKII and LTP.

16 CA1-3 region is significantly decreased, and LTP inhibition or reversal mediated by NRG1/ErbB signali

17 common mechanism when they impair memory and LTP in mice.

18 extracellular oAbeta and oTau on memory and LTP is dependent upon APP since APP-KO mice were resista

19 ed defects in spatial/associative memory and LTP.

20 ow that generation of plateau potentials and LTP induction in dorsal CA1 neurons depends on the coinc

21 drives increased AMPA receptor recycling and LTP.

22 seizure-induced alterations of both STP and LTP.

23 g prevents the maintenance of LTP as well as LTP-dependent structural modifications of dendritic spin

24 t beta-adrenergic receptors and NA can boost LTP maintenance by regulating translation.

25 tivator of the networks responsible for both LTP and LTD.

26 KOR antagonist provides full rescue of both LTP induction and dopamine release during optogenetic ac

27 ing low-frequency AP-EPSP pairing, with both LTP and LTD absent under control conditions but present

28 Both LTPs are initially cleaved during gastroduodenal proteol

29 group II mGlu receptors was not occluded by LTP induced with high-frequency trains of stimuli.

30 y 40% of food-related anaphylaxis induced by LTPs requires nonsteroidal anti-inflammatory drugs (NSAI

31 Like classical LTP, kainate-receptor-dependent LTP recruits recycling e

32 Induction of classical LTP involves an NMDA-receptor- and calcium-dependent inc

33 1 knockouts have reduced Schaffer collateral LTP, which is rescued by activating OLM neurons with nic

34 demonstrate that TBS evokes corticostriatal LTP, and that optogenetic activation of D1R-SPNs during

35 tructural remodeling of spines and defective LTP in primary neuron cultures and hippocampal slices.

36 ptic MMP-3 supports L-type channel-dependent LTP in the CA1 region, whereas nmdaLTP depends solely on

37 found that L-type calcium channel-dependent LTP in the CA3-CA1 hippocampal projection is critically

38 L-type channel-dependent LTP is known to be impaired by hyaluronic acid digestion

39 se 3 (MMP-3), in contrast to NMDAR-dependent LTP regulated by MMP-9.

40 Additionally, mPFC NMDAR-dependent LTP was also lacking in the n-3-deficient group.

41 inoid/mGlu5-mediated LTD and NMDAR-dependent LTP were lacking in adult n-3-deficient mice.

42 aptic currents and abolished NMDAR-dependent LTP.

43 sufficient to drive NMDA receptor-dependent LTP and LTD, respectively.

44 MPA receptors during NMDA-receptor-dependent LTP at mature hippocampal synapses.

45 ke classical LTP, kainate-receptor-dependent LTP recruits recycling endosomes to spines, enhances syn

46 ing the induction of NMDA-receptor-dependent LTP, Ca(2+) influx stimulates recruitment of synaptic AM

47 rite and show that dendritic spike dependent LTP which is predominant in distal sections can prolong

48 a lower threshold for spike-timing-dependent LTP (t-LTP), a cellular form of learning and memory.

49 duction threshold for spike-timing-dependent LTP (t-LTP).

50 iation (LTP) in the former, timing-dependent LTP is inhibited in the latter.

51 50 Hz) was required to gain timing-dependent LTP.

52 influences Abeta levels and function during LTP and memory.

53 GMP affects Abeta levels and function during LTP.

54 of two molecules with known functions during LTP, including 3'UTR APA of Notch1 and intronic APA of C

55 ependent exocytosis of AMPA receptors during LTP, and thereby delineate a simple mechanism for the re

56 Early LTP (less than 1 h) had initially been explained either

57 can rapidly recruit new AMPARs during early LTP remains unknown.

58 erfunction, which likely drives the enhanced LTP.

59 This effect could contribute to enhanced LTP and the maintenance of augmented excitatory synaptic

60 hereas increasing their probability enhances LTP.

61 ere, we show that postsynaptically expressed LTP is induced selectively in the CS-specific auditory p

62 We identified extensive LTP-induced APA changes, including a general trend of 3'

63 Second, we conducted FASS-LTP analysis in two well-characterized Alzheimer's disea

64 rs of cAMP and cGMP signaling pathways, FASS-LTP identified vardenafil and Bay-73-6691 (phosphodieste

65 single-synapse long-term potentiation (FASS-LTP).

66 First, we demonstrate that FASS-LTP is simple, sensitive, and models electrically induce

67 Third, we used FASS-LTP for drug evaluation in human synaptosomes.

68 Pru p 3 can be used as a marker allergen for LTP sensitization also in Central European patients.

69 es and that NL1 specifically is required for LTP induced by postsynaptic Ca(2+)-elevations, a functio

70 ma-2/3/4, as a critical CaMKII substrate for LTP.

71 rsal CA1 neurons have a higher threshold for LTP induction and require coincident timing of excitator

72 orsoventral differences in the threshold for LTP induction could account for the differences in scale

73 p recordings, we show that the threshold for LTP induction is higher in dorsal CA1 neurons and that a

74 persed inputs and have a lower threshold for LTP.

75 ce that ensemble integration may result from LTP but also from cell-autonomous changes in membrane ex

76 Furthermore, LTP initiated by activation of group II mGlu receptors w

77 Furthermore, LTP requires inhibition of SK channels by mGluR1, which

78 pathway with a presynaptic form of GABAergic LTP, while interneurons of stratum radiatum, despite rec

79 lb prevented the socially relevant GABAergic LTP and impaired memory formation after STFP.

80 olfactory bulb slices elicited the GABAergic LTP in mitral cells by enhancing postsynaptic GABA recep

81 The GABAergic LTP is mimicked with PKA or PKC activation.

82 ing the excitation/inhibition balance, MC-GC LTP enhances GC output at the associative MC-GC recurren

83 s at muscle afferent synapses drives greater LTP following repetitive stimulation.

84 ntaining AD brain extracts block hippocampal LTP, augment glutamate release probability, and disrupt

85 agonist isoproterenol to enhance hippocampal LTP, and this effect is absent in slices treated with ei

86 ar more bioactive: they impaired hippocampal LTP, decreased neuronal levels of beta2-adrenergic recep

87 In rodents, hippocampal LTP may be induced through electrical stimulation of the

88 How LTP, induced postsynaptically, engages these extracellul

89 Furthermore, synaptic loss and impaired LTP at hippocampal CA3 region of P301S mice were attenua

90 ivation of D1R-SPNs during induction impairs LTP.

91 trongly support a critical role of CaMKII in LTP maintenance and memory storage.

92 from AD brain are intrinsically defective in LTP.

93 ased synapses are intrinsically defective in LTP.

94 s demonstrate a key role for the retromer in LTP and provide insights into how retromer malfunction i

95 cond messenger cGMP exerts a central role in LTP mechanisms, here we studied whether cGMP affects Abe

96 otein kinase A (PKA) play important roles in LTP and spine structural plasticity.

97 nts of NSAID-dependent and NSAID-independent LTP-induced anaphylaxis (LTP-A).

98 ) thus converge on NMDA receptor independent LTP induction in O/A interneurons.

99 c complex-spike bursting and does not induce LTP at ventral SC synapses.

100 eta-burst pattern, shown to optimally induce LTP.

101 try-based method to track chemically induced LTP by detecting surface AMPA receptors in isolated syna

102 , sensitive, and models electrically induced LTP recorded in intact circuitries.

103 tic transmission in the BLA, and (3) induces LTP of cortical-amygdala circuits.

104 CaMKII activation is sufficient for inducing LTP and sLTP.

105 n gephyrin in response to protocols inducing LTP of inhibitory synaptic responses (iLTP).

106 ed that, during the expression of inhibitory LTP, the increase of gephyrin density at postsynaptic si

107 pathway striatal projection neurons inhibits LTP while reducing dopamine release.

108 KT1, but not AKT2 or AKT3, is required for L-LTP through regulating activity-induced protein synthesi

109 se (AD), late long-term potentiation (LTP; L-LTP) and its associative plasticity mechanisms such as s

110 tors (RyRs) in these neurons reestablished L-LTP and STC.

111 rn of synaptic input to achieve long-lasting LTP and memory storage.

112 rgic receptor will likely block long-lasting LTP in response to strong stimulation.

113 athways underpins most forms of long-lasting LTP.

114 s later stages of learning will result in M1 LTP-like plasticity modifications.

115 te mushroom spine density and high-magnitude LTP in the SO layer.

116 , and -10 are gatekeepers for high-magnitude LTP.

117 dherins has no effect on the lower-magnitude LTP typically observed in the SR layer, demonstrating th

118 sera revealed IgE-binding proteins matching LTP and/or profilin.

119 Currently available techniques to measure LTP are time-intensive and require highly specialized ex

120 recruitment of AMPA receptors that mediates LTP.

121 In hippocampi of aged (21-28 months) mice, LTP was relayed to unstimulated synapses, blemishing its

122 Moreover, LTP and memory formation, but not basal transmission, ar

123 interaction is required not only for normal LTP induction but also for the maintenance of synaptic s

124 in patients with LTP-A and those with NSAID-LTP-A of the IFN-gamma pathway, IgG receptors, and ADORA

125 To expand and facilitate the analysis of LTP, here we use a flow cytometry-based method to track

126 , disrupted the MMP-3-dependent component of LTP.

127 Moreover, the cGMP-induced enhancement of LTP and memory was disrupted by blockade of Abeta, sugge

128 , prevents the cGMP-dependent enhancement of LTP and memory.

129 bitors, respectively) as potent enhancers of LTP in synaptosomes from AD cases.

130 However, direct evidence of LTP deficits in human AD brain has been elusive, primari

131 s a critical mechanism for the expression of LTP and hippocampal learning.

132 synaptic transmission and the expression of LTP are dependent upon an AMPAR anchoring mechanism that

133 ptic transmission and impaired expression of LTP.

134 of the fundamental questions in the field of LTP is why different molecules are critical for long-las

135 um interneurons, displayed a Hebbian form of LTP that was mimicked by PKC activation.

136 ng a critical role for MMP-3 in this form of LTP.

137 e hippocampal slices these distinct forms of LTP are specifically regulated by different metalloprote

138 ppocampal CA3-CA1 pathway, distinct forms of LTP depend on NMDA receptors (nmdaLTP) or L-type voltage

139 dict the occurrence of long-lasting forms of LTP for multiple experimental protocols.

140 cules are critical for long-lasting forms of LTP induced by diverse experimental protocols.

141 whereas it did not prevent the generation of LTP in the slices from males.

142 G expression and prevented the generation of LTP.

143 Here the rich history of LTP is reviewed.

144 The impairment of LTP due to VPS35 knockdown was mechanistically independe

145 A selective impairment of LTP was observed in layer II horizontal connections of E

146 ope, little is known about the importance of LTP sensitization.

147 neurons for 1-2 min during the induction of LTP and structural LTP (sLTP) of dendritic spines inhibi

148 contribute to the preferential induction of LTP at hyperpolarized potentials.

149 tion plays an important role in induction of LTP by integrating Ca(2+) signals, and it greatly promot

150 Moreover, the induction of LTP was associated with an increase in MMP-3 expression

151 but the positive associative interaction of LTP and LTD, cross-capture, was altered in these mice.

152 approximately 300 d of age, the magnitude of LTP increased in Tg(CJD) mice but decreased in PrP KO mi

153 RNF10 silencing prevents the maintenance of LTP as well as LTP-dependent structural modifications of

154 Whereas, occlusion of LTP-like plasticity over M1 occurred only during late, b

155 MP (Epac) together predict the occurrence of LTP in response to strong stimulation (multiple trains o

156 s with LTP-A was mirrored by the presence of LTP-specific IgG1 and IgG3.

157 By contrast, similar regulation of LTP is absent in ventral CA1 neurons.

158 We investigated the role of LTP sensitization in Central European patients displayin

159 as molecular switches for specific types of LTP.

160 ase occluded the effect of MMP-3 blockade on LTP, further confirming a critical role for MMP-3 in thi

161 ts, taken together with prior experiments on LTP, strongly support a critical role of CaMKII in LTP m

162 onastrol, a small-molecule Eg5 inhibitor, on LTP in hippocampal slices and synapse loss in neuronal c

163 iological effect of the cyclic nucleotide on LTP and memory is dependent upon Abeta.

164 anism how CaMKII can indeed mediate not only LTP but also LTD through regulated substrate selection;

165 Hz but vanished >50 Hz or <1 Hz (where only LTP or LTD occurred).

166 We show that the ability of MOR to oppose LTP is rapidly impaired by sustained D1LR activation via

167 In contrast to the CA3-CA1 pathway, LTP in the mossy fiber-CA3 projection did not depend on

168 KEY MESSAGE: Pru p 3, a peach LTP, is located in pollinated flower styles and secretin

169 There, peach LTP (Pru p 3) seems to be the primary sensitizer, wherea

170 are lobbying to obtain privileges to perform LTP and other laser procedures.

171 inhibition or knock-out impaired late-phase LTP in the CA3-CA1 pathway.

172 Interestingly, late-phase LTP was also decreased by MMP-9 blockade.

173 9 were inhibited, both early- and late-phase LTP was impaired.

174 napse and induction of long-term plasticity (LTP) in M1, leading to transient occlusion of additional

175 d for normal short-term synaptic plasticity, LTP, and spatial learning and memory in mice.

176 electrical stimulation induced postsynaptic LTP.

177 ), develop defective long-term potentiation (LTP) and aged mice display spatial learning and memory d

178 Long-term potentiation (LTP) and depression (LTD) at glutamatergic synapses are

179 Both long-term potentiation (LTP) and depression (LTD) of excitatory synapse strength

180 for the induction of long-term potentiation (LTP) and is generally neuroprotective, while calpain-2 a

181 ergic synapses, both long-term potentiation (LTP) and long-term depression (LTD) can be induced at th

182 ectional changes are long-term potentiation (LTP) and long-term depression (LTD) forms that relay on

183 r the maintenance of long-term potentiation (LTP) and long-term memory (LTM).

184 ta are necessary for long-term potentiation (LTP) and memory.

185 KII is necessary for long-term potentiation (LTP) and memory.

186 enhance hippocampal long-term potentiation (LTP) and memory.

187 NT: Various types of long-term potentiation (LTP) are correlated with distinct phases of memory forma

188 c changes induced by long-term potentiation (LTP) are thought to underlie memory formation.

189 plasticity (STP) and long-term potentiation (LTP) at perforant path-DG synapses in naive rats.

190 f Calstabin2 reduced long-term potentiation (LTP) at the hippocampal CA3-CA1 connection, increased me

191 Long-term potentiation (LTP) at the Schaffer collateral-commissural synapses in

192 lting suppression of long term potentiation (LTP) by Abeta oligomers was prevented.

193 Remarkably, long-term potentiation (LTP) can override the masking effect of the GFP tag.

194 associative synaptic long-term potentiation (LTP) due to saturation after sleep deprivation.

195 for the induction of long-term potentiation (LTP) elicited by theta-burst stimulation in field CA1 of

196 napse specificity of long-term potentiation (LTP) ensures that no interference arises from inputs irr

197 ts the expression of long-term potentiation (LTP) evoked by high-frequency stimulation of Schaffer co

198 nce the discovery of long-term potentiation (LTP) in 1973, thousands of papers have been published on

199 oth the induction of long-term potentiation (LTP) in hippocampal CA1 pyramidal cells and hippocampal-

200 receptor independent long-term potentiation (LTP) in hippocampal stratum oriens-alveus (O/A) interneu

201 atal fibres produces long-term potentiation (LTP) in striatal projection neurons when measured using

202 essed development of long-term potentiation (LTP) in the CA1-subiculum, but not in the CA3-CA1 pathwa

203 essed development of long-term potentiation (LTP) in the CA1-subiculum, but not in the CA3-CA1 pathwa

204 pression switches to long-term potentiation (LTP) in the former, timing-dependent LTP is inhibited in

205 eriments showed that long-term potentiation (LTP) in the hippocampus, which is dependent on intracell

206 Although long-term potentiation (LTP) in the lateral amygdala (LA) plays an essential rol

207 Long-term potentiation (LTP) in the rat hippocampus is the most extensively stud

208 Long-term potentiation (LTP) is a rapid and persistent increase in synaptic tran

209 Long-term potentiation (LTP) is an activity-dependent and persistent increase in

210 Long-term potentiation (LTP) is widely perceived as a memory substrate and in th

211 ciatic nerve induced long-term potentiation (LTP) of C-fiber-evoked potentials, revealing a constitue

212 pression of synaptic long-term potentiation (LTP) of C-fiber-evoked potentials.

213 Long-term potentiation (LTP) of excitatory synaptic transmission has long been c

214 cate that persistent long-term potentiation (LTP) of excitatory synaptic transmission onto ventral te

215 We found that long-term potentiation (LTP) of mossy fiber input invoked a large increase in gr

216 llowing induction of long-term potentiation (LTP) of mouse hippocampal CA3-CA1 synapses.

217 s known to exhibit a long-term potentiation (LTP) of synaptic efficacy through a combination of presy

218 glomerulus-specific long-term potentiation (LTP) of synaptic strength selectively at the GABAergic c

219 , phenomena known as long-term potentiation (LTP) or long-term depression (LTD), respectively.

220 ticity mechanisms of long-term potentiation (LTP) or of long-term depression (LTD) were assessed usin

221 zed, their effect on long-term potentiation (LTP) remains unknown.

222 ong-lasting forms of long-term potentiation (LTP) represent one of the major cellular mechanisms unde

223 ) receptor-dependent long-term potentiation (LTP) shapes neural circuits and mediates learning and me

224 and higher-magnitude long-term potentiation (LTP) than SR synapses.

225 -independent form of long-term potentiation (LTP) that requires postsynaptic brain-derived neurotroph

226 ease the duration of long-term potentiation (LTP), a form of hippocampal synaptic plasticity.

227 damental property of long-term potentiation (LTP), but it is not known if learning is mediated by syn

228 ggerated hippocampal long-term potentiation (LTP), consistent with deficits in hippocampus-mediated b

229 siological surrogate long-term potentiation (LTP), effects that may be mediated by intra-neuronal oli

230 We show that long-term potentiation (LTP), in the CA1 region of hippocampal slices from this

231 or (NMDAR)-dependent long-term potentiation (LTP), remains unclear.

232 virtually abolished long-term potentiation (LTP), whereas it did not prevent the generation of LTP i

233 iated by fast-acting long-term potentiation (LTP), which relies on the precise timing of neural activ

234 depression (LTD) and long-term potentiation (LTP).

235 anti-Hebbian form of long-term potentiation (LTP).

236 ation of hippocampal long-term potentiation (LTP).

237 for the induction of long-term potentiation (LTP).

238 in the late phase of long-term potentiation (LTP).

239 ident by a decreased long-term potentiation (LTP).

240 re unable to sustain long-term potentiation (LTP).

241 s disease (AD), late long-term potentiation (LTP; L-LTP) and its associative plasticity mechanisms su

242 tic transmission but long-term-potentiation (LTP) of synaptic signals in HIL cells.

243 ic plasticity (e.g., long-term potentiation [LTP]) is considered the cellular correlate of learning.

244 The ability of MOR both to prevent LTP and to modulate mechanical and thermal pain threshol

245 T-type currents pharmacologically prevented LTP induced by high-frequency stimulation of glutamaterg

246 gurations: the low temperature plasma probe (LTP) and the dielectric barrier discharge for soft ioniz

247 rall survival (OS), local tumor progression (LTP), postoperative complications, and hospital stay and

248 Mediterranean area, lipid transfer proteins (LTPs) are important causes of plant-food allergies often

249 icking vesicles and lipid transfer proteins (LTPs)].

250 forms of peach leaf lipid transfer proteins( LTP), so the recognition frequency of some LTP isoform b

251 There were 1150 eyes that received LTP (83.1%) by an ophthalmologist and 234 eyes (16.9%) t

252 asing the probability of NMDA spikes reduces LTP, whereas increasing their probability enhances LTP.

253 dentified pharmacological agents that rescue LTP in AD, thus opening up a new avenue for drug screeni

254 but not GluA2, lacking the ATD fails to show LTP.

255 ( LTP), so the recognition frequency of some LTP isoform by our patient sera was 42%.

256 Our results suggest that input-specific LTP in the LA contributes to fear memory specificity, en

257 conditioning is mediated by synapse-specific LTP in the amygdala, allowing animals to discriminate st

258 Both st-LTP and st-LTD required NMDA receptors, but st-LTP also

259 P and st-LTD required NMDA receptors, but st-LTP also required reinforcing signals mediated by mGluRs

260 nt long-term potentiation and depression (st-LTP and st-LTD) were confined to a +/-25 ms time-window.

261 Importantly, st-LTP and st-LTD were significantly larger than LTP and LT

262 Because EPSPs led APs in st-LTP while APs led EPSPs in st-LTD, STDP was Hebbian in n

263 of co-released dynorphin and KOR on striatal LTP.

264 onged, weak LTD stimuli versus brief, strong LTP stimuli.

265 n during the induction of LTP and structural LTP (sLTP) of dendritic spines inhibited these forms of

266 uld provide the basis for protocols to study LTP in both healthy and diseased human brains, a previou

267 naptic strength and the maximal attainable t-LTP magnitude remain unchanged after cocaine exposure.

268 GluN2A-containing NMDA receptors to drive t-LTP at extended timing.

269 to facilitate coincidence detection during t-LTP induction.

270 a normally ineffective timing interval for t-LTP induction in saline-exposed mice.

271 but not single, daily cocaine injections, t-LTP in layer V pyramidal neurons is induced at +30 ms, a

272 threshold for spike-timing-dependent LTP (t-LTP), a cellular form of learning and memory.

273 threshold for spike-timing-dependent LTP (t-LTP).

274 ther show that the cocaine facilitation of t-LTP induction is caused by sensitized D1-cAMP/protein ki

275 pre-post spike pairs, indicating a reduced t-LTP induction threshold.

276 This cocaine-induced, extended-timing t-LTP lasts for approximately 1 week after terminating coc

277 ide dynorphin is responsible for reduced TBS LTP and illustrate a physiological phenomenon whereby he

278 At 30 and 120 min after TBS-LTP, vesicles were decreased only in presynaptic boutons

279 n using a novel approach that allows testing LTP in cryopreserved brain.

280 TP and st-LTD were significantly larger than LTP and LTD obtained by modulating the frequency and dur

281 raphy, and immunofluorescence, we found that LTP induction was associated with an increase in MMP-3 e

282 Our results showed that LTP sensitization represents a risk factor for severe al

283 The LTP is representative of a DBD with one covered electrod

284 Blocking hemichannel activity reduced the LTP of these excitatory synaptic currents triggered by h

285 ptor activation, and that BDNF rescues theta-LTP and cocaine-associated memory deficits in BAF53b tra

286 Further experiments indicate that theta-LTP in the NAc is dependent on TrkB receptor activation,

287 This LTP is input specific and selectively expressed at MC-GC

288 collaterals, and that CN2097 attenuates this LTP impairment.

289 presynaptic activity, which actually led to LTP in PE animals, whereas LTD was still observed in con

290 tion in stratum radiatum specifically led to LTP of the paired pathway in adult mice (P75).

291 privileges to perform laser trabeculoplasty (LTP).

292 , whereas PKMzeta is essential for wild-type LTP and long-term memory, persistent PKCiota/lambda acti

293 ed ability of ventral SC synapses to undergo LTP.

294 residues 39-40, 56-57 and 79-80, with wheat LTP being more resistant to cleavage than its peach orth

295 rom the entorhinal cortex to the DG, whereas LTP in HILs may facilitate the temporal coordination of

296 ory fear conditioning, it is unknown whether LTP is induced selectively in the neural pathways convey

297 Differential regulation in patients with LTP-A and those with NSAID-LTP-A of the IFN-gamma pathwa

298 of the IgG receptor (CD64) in patients with LTP-A was mirrored by the presence of LTP-specific IgG1

299 r OS (36.7% vs. 44.6%, p = 0.4289) or 5-year LTP (73.3% vs. 67.9%, p = 0.8897) between CT-RFA and L-R

300 d considerable growing pains over the years, LTP has finally come of age.