ライフサイエンスコーパス: TLE

1 TLE addition increased linseed oil shelf-life by 31% (Ra

2 TLE addition slowed oil degradation without changing the

3 TLE with hippocampal sclerosis presented a significantly

4 d December 2010, 985 patients underwent 1043 TLE procedures.

5 sing surgically acquired hippocampi from 129 TLE patients, we identify a gene-regulatory network gene

6 17 TLE patients with a lifetime affective diagnosis, 31 TLE

7 In 20 TLE-HS, 19 TLE-G, and 25 healthy controls, we carried out a novel M

8 In 20 TLE-HS, 19 TLE-G, and 25 healthy controls, we carried ou

9 phy distribution of two epilepsy cohorts: 29 TLE subjects with medial temporal sclerosis (TLE-MTS), a

10 ents with a lifetime affective diagnosis, 31 TLE patients with no formal psychiatric history and 30 H

11 medial temporal sclerosis (TLE-MTS), and 50 TLE subjects with normal appearance on MRI (TLE-no).

12 Adding TLE to 80 mg lycopene/kg oil improved linseed oil stabil

13 Although TLE procedural mortality is exceedingly low at high-volu

14 ing levels of Hsp60 in epileptic animals and TLE patients using ELISA.

15 direct competition between beta-catenin and TLE for TCFs as part of an activation-repression switch.

16 for (18)F-FMZ and n = 20 for (18)F-FDG) and TLE patients with mesial temporal sclerosis on MR imagin

17 g, we define two distinct types of Otx2- and TLE-occupied CRMs.

18 nseed oil was extracted by cold pressing and TLE by supercritical CO(2).

19 ion factor (REST) and Groucho (also known as TLE), are considered lineage-specific repressors, it rem

20 with a pair of monozygotic twins affected by TLE and two unaffected siblings born to healthy parents.

21 Compared to 46 controls, TLE-I showed marked bilateral atrophy; in TLE-II atrophy

22 Compared to controls, TLE-HS presented with marked ipsilateral atrophy, T2 hyp

23 artners with the transcriptional corepressor TLE/Groucho (Gro) and inhibits gene expression.

24 and find that occupancy of the corepressor, TLE/Groucho, is a better indicator of tissue-specific ci

25 lophus californianus) that naturally develop TLE after exposure to domoic acid, a neurotoxin that ent

26 y early the FSE individuals who will develop TLE.

27 pitulates earlier developmental roles during TLE acquisition.

28 that astrocytes with mGluR5 signaling during TLE development perform faster glutamate uptake in hippo

29 ects with unilateral temporal lobe epilepsy (TLE) before (n = 29) or after (n = 56) anterior temporal

30 ople worldwide, with temporal lobe epilepsy (TLE) being the most common form.

31 in animal models of temporal lobe epilepsy (TLE) development and patient epilepsy samples.

32 Seizures in temporal lobe epilepsy (TLE) disturb brain networks and lead to connectivity dis

33 R28 in patients with temporal lobe epilepsy (TLE) found increased TSPO ipsilateral to seizure foci.

34 EMENT Development of temporal lobe epilepsy (TLE) generally takes years after an initial insult durin

35 l sclerosis (HS) and temporal lobe epilepsy (TLE) has long been debated.

36 Temporal lobe epilepsy (TLE) is a common and commonly devastating form of human

37 GNIFICANCE STATEMENT Temporal lobe epilepsy (TLE) is a common and devastating form of human epilepsy

38 Temporal lobe epilepsy (TLE) is a common epilepsy syndrome with a complex etiolo

39 Temporal lobe epilepsy (TLE) is a devastating disease in which seizures persist

40 Temporal lobe epilepsy (TLE) is a prevalent neurological disorder resulting in d

41 Temporal lobe epilepsy (TLE) is a prevalent neurological disorder with many pati

42 Temporal lobe epilepsy (TLE) is characterized by recurrent seizures driven by sy

43 Mesial temporal lobe epilepsy (TLE) is characterized by stereotyped origination and spr

44 pilepsy and in these temporal lobe epilepsy (TLE) is common.

45 Temporal lobe epilepsy (TLE) is one of the most common drug-resistant forms of e

46 Temporal lobe epilepsy (TLE) is one of the most common forms of epilepsy.

47 Medial temporal lobe epilepsy (TLE) is the most common form of medication-resistant foc

48 Temporal lobe epilepsy (TLE) is the most common type of drug-resistant epilepsy

49 Temporal lobe epilepsy (TLE) is the most frequent form of focal epilepsies and i

50 nesis occurs in many temporal lobe epilepsy (TLE) models.

51 Drug-resistant temporal lobe epilepsy (TLE) often requires thorough investigation to define the

52 The effects of temporal lobe epilepsy (TLE) on subcortical arousal structures remain incomplete

53 of individuals with temporal lobe epilepsy (TLE) or AD and correlate with performance on the Mini-Me

54 Although most temporal lobe epilepsy (TLE) patients show marked hippocampal sclerosis (HS) upo

55 ities are present in temporal lobe epilepsy (TLE) patients with a history of affective psychopatholog

56 nce imaging-negative temporal lobe epilepsy (TLE) undergoing standard anterior temporal lobectomy wit

57 efractory unilateral temporal lobe epilepsy (TLE) with hippocampal sclerosis (HS-TLE, n = 26) was stu

58 fect of psychosis on temporal lobe epilepsy (TLE), (2) psychogenic nonepileptic seizures (PNESs) from

59 ficant proportion of temporal lobe epilepsy (TLE), a common, intractable brain disorder, arises in ch

60 In temporal lobe epilepsy (TLE), although hippocampal atrophy lateralizes the focus

61 ilepsy, specifically Temporal Lobe Epilepsy (TLE), and correlate their clinical significance with res

62 ocampal pathology in temporal lobe epilepsy (TLE), but has rarely been evaluated in patients with nor

63 erosis are common in temporal lobe epilepsy (TLE), but little is known about the relationship of hipp

64 pilocarpine model of temporal lobe epilepsy (TLE), exhibited gross expansion of abdominal fat mass an

65 In animal models of temporal lobe epilepsy (TLE), gene therapy treatments based on viral vectors enc

66 perimental models of temporal lobe epilepsy (TLE), interictal-like activity (ILA) precedes SZ1 by sev

67 motes development of temporal lobe epilepsy (TLE), revealing TrkB as a therapeutic target for prevent

68 with severe acquired temporal lobe epilepsy (TLE), the dentate gyrus exhibits sclerosis and GABAergic

69 Temporal lobe epilepsy (TLE), the most common form of acquired epilepsy, is char

70 al pathways in human temporal lobe epilepsy (TLE).

71 n epileptogenesis of temporal lobe epilepsy (TLE).

72 o the development of temporal lobe epilepsy (TLE).

73 with drug-resistant temporal lobe epilepsy (TLE).

74 ve disorder in human temporal lobe epilepsy (TLE).

75 e 1 (HCN1) occurs in temporal lobe epilepsy (TLE).

76 eight patients with temporal lobe epilepsy (TLE).

77 ion resembling human temporal lobe epilepsy (TLE).

78 ific cell therapy in temporal lobe epilepsy (TLE).

79 in rodent models of temporal lobe epilepsy (TLE).

80 ment for intractable temporal lobe epilepsy (TLE).

81 Experimental TLE was provoked by kainic acid-induced status epileptic

82 Experimental TLE was triggered by pilocarpine- or kainic acid-induced

83 on in human (of both sexes) and experimental TLE, and miR-135a regulates dendritic spine number and t

84 sk, is specifically affected in experimental TLE and that the impairment of hippocampal theta activit

85 d MRI hours after FSE predicted experimental TLE.

86 The effect of tomato lycopene-rich extract (TLE) addition on shelf-life of linseed oil was evaluated

87 reased need for transvenous lead extraction (TLE).

88 trophy (R = 0.586 for TLE-MTS, R = 0.283 for TLE-no).

89 elation with measured atrophy (R = 0.586 for TLE-MTS, R = 0.283 for TLE-no).

90 CF/LEFs correlates with their affinities for TLE-Q, rather than direct competition between beta-caten

91 roucho proteins, but the molecular basis for TLE/TCF-dependent repression is unclear.

92 -activated signaling pathway responsible for TLE.

93 ive target for developing new treatments for TLE, hopefully overcoming the pharmacoresistance to trad

94 lls, TLE3, a co-repressor of the Groucho/Grg/TLE family, interacts with FoxA1 and is detected at regu

95 understanding the initiation of Groucho/Grg/TLE mediated gene silencing.

96 corepressor molecules such as Groucho (Gro)/TLE and HDAC1 for activity.

97 Lef where it monoubiquitylates Groucho (Gro)/TLE.

98 Gro/TLE proteins (TLE1-4) are a family of transcriptional co

99 This modification decreases affinity of Gro/TLE for TCF/Lef.

100 To explore the role of Gro/TLE in more detail we generated an allelic series of kno

101 nvolving XIAP-mediated ubiquitylation of Gro/TLE that facilitates its removal from TCF/Lef, thus allo

102 Here we find that Gro/TLE is not required in ESC for sustaining pluripotency a

103 with this view, we found that one of the Gro/TLE family, TLE4 is expressed heterogeneously in ESCs in

104 ell factors (TCF) and kept silent by Groucho/TLE co-repressors.

105 We identify Groucho/TLE as a functionally relevant substrate, whose ubiquity

106 ctly interfering with the binding of Groucho/TLE to TCF, thereby preventing formation of transcriptio

107 es a previously unrecognized YAP/TAZ-Groucho/TLE interaction to suppress Wnt/TCF-mediated transcripti

108 This C-terminus binds to the Groucho/TLE co-repressor, and also to the Chip/LDB1-SSDP enhance

109 wn as Tle3), encodes a member of the Groucho/TLE family of co-repressors and its function in various

110 nopus tropicalis co-repressor of the Groucho/TLE family, is crucial for regulating the early activity

111 Thus, Groucho/TLE ubiquitylation by Hyd/UBR5 is a key prerequisite tha

112 2 and Drosophila ARID1, and binds to Groucho/TLE.

113 g (MRI) characteristics in patients with HS (TLE-HS) and those with gliosis only (TLE-G).

114 HS-TLE subjects had lateralized atrophy of most temporal lo

115 d from lateralized atrophy common to both HS-TLE and MRI-neg TLE, in comparison to healthy controls (

116 to-occipital fasciculus was found in both HS-TLE and MRI-neg TLE, suggesting a common lateralized eff

117 isease process was uncovered by comparing HS-TLE to unilateral TLE with normal clinical magnetic reso

118 l lobe tracts, and hippocampal volumes in HS-TLE correlated with parahippocampal cingulum and anterio

119 was assessed in first-degree relatives of HS-TLE subjects who did not have epilepsy themselves (HS-1

120 pilepsy (TLE) with hippocampal sclerosis (HS-TLE, n = 26) was studied as an archetype of focal epilep

121 In human TLE and in animal models of TLE, parvalbumin neurons are

122 However, how this translates to human TLE remains unknown.

123 rvations related to network abnormalities in TLE and expand on the notion of underlying aberrant plas

124 cortical atrophy on vertex-wise analysis in TLE before surgery that was bilateral and localized beyo

125 ll subfields in TLE-HS, whereas anomalies in TLE-G were restricted to the subiculum.

126 networked spread of activity and atrophy in TLE from first principles via two simple first order net

127 s, TLE-I showed marked bilateral atrophy; in TLE-II atrophy was ipsilateral; TLE-III showed mild bila

128 of white matter (WM) connectivity changes in TLE may aid the identification of network abnormalities

129 ss all subfields in TLE-HS, while changes in TLE-G were limited to the subiculum.

130 c arousal network functional connectivity in TLE and examine changes after epilepsy surgery.

131 surgery and neuropsychological counseling in TLE.

132 Memory deficits in TLE are associated with specific morphological alteratio

133 reorganization of the dentate gyrus (DG) in TLE may create pathological conduction pathways for sync

134 rize identified GC subpopulation dynamics in TLE, and reveal a specific contribution of abGCs to IEDs

135 responsible for HCN channel dysregulation in TLE are unclear.

136 8b phosphorylation to reduce excitability in TLE.

137 depict the presence and laterality of HA in TLE with accuracy rates that may exceed those achieved w

138 ogic hemisphere to the healthy hemisphere in TLE patients.

139 we investigated the involvement of Hsp60 in TLE using animal and human samples.

140 anterior and posterior default mode hubs in TLE-HS, whereas TLE-G did not differ from controls.

141 DGCs have long been implicated in TLE, because they regulate excitatory signaling through

142 t suggest reduced granule cell inhibition in TLE is not attributable to anatomical loss of PV boutons

143 al regions) that are known to be involved in TLE are the most frequent starting points for seizures i

144 k dysfunction may contribute to morbidity in TLE.

145 ressive cortical atrophy that is observed in TLE and may be potentially neuroprotective.

146 g the aberrant neuronal activity observed in TLE.

147 The mean brain-PAD in TLE with inter-ictal psychosis was 10.9 years, which was

148 ise to help elucidate mnemonic processing in TLE.

149 suggesting that affective psychopathology in TLE has a neurobiological correlate, and in this context

150 Genetic reduction in TLE dose resulted in an increase in the expression of pl

151 l-based therapies for neurological repair in TLE require evidence that the transplanted neurons integ

152 Recurrent seizures in TLE are associated with disturbances in ARAS connectivit

153 usly hypothesised that recurrent seizures in TLE may lead to abnormal connections involving subcortic

154 al load of anomalies across all subfields in TLE-HS, whereas anomalies in TLE-G were restricted to th

155 ed network embedding across all subfields in TLE-HS, while changes in TLE-G were limited to the subic

156 is one signaling pathway by which SE induces TLE.

157 pY816 following status epilepticus inhibited TLE and prevented anxiety-like disorder yet preserved ne

158 ples taken from 16 patients with intractable TLE prior to SLAH to test the hypothesis that pre-operat

159 atrophy; in TLE-II atrophy was ipsilateral; TLE-III showed mild bilateral atrophy; whereas TLE-IV sh

160 I findings, 50 patients with EEG lateralized TLE and normal structural Magnetic Resonance Imaging res

161 Both left TLE (LTLE) and right TLE (RTLE) patients had lower verba

162 ccelerated annualized thinning in left (left TLE 0.0192 +/- 0.0014 versus healthy volunteers 0.0032 +

163 ures were compared for 32 subjects with left TLE and 36 age-matched and gender-matched controls along

164 or imaging (DTI) of 22 individuals with left TLE and 39 healthy controls.

165 lumes were analyzed in 24 patients with left TLE and in 24 healthy control subjects.

166 hippocampal atrophy in patients with mesial TLE.

167 TLE subjects with normal appearance on MRI (TLE-no).

168 ed atrophy common to both HS-TLE and MRI-neg TLE, in comparison to healthy controls (n = 76).

169 ciculus was found in both HS-TLE and MRI-neg TLE, suggesting a common lateralized effect of focal sei

170 clinical magnetic resonance imaging (MRI-neg TLE; n = 26, matched for seizure severity).

171 ria were magnetic resonance imaging-negative TLE, standard ECoG performed at the time of surgery, and

172 d ATL in magnetic resonance imaging-negative TLE.

173 (MTS, n = 12) and with normal MR imaging (NL TLE, n = 19).

174 F-FMZ BPND in patients with either MTS or NL TLE, compared with controls subjects.

175 As in patients with nonlesional TLE, these mice developed epilepsy without signs of neur

176 On the basis of TLE binding and comprehensive CRM profiling, we define t

177 ion of genetic factors, the genetic basis of TLE remains largely unknown.

178 One cause of TLE is an episode of de novo prolonged seizures [status

179 ng that mutations in GAL are a rare cause of TLE.

180 nscriptional repressor complex consisting of TLE and the Notch target Hes1.

181 normal DGCs contribute to the development of TLE and also support a role for mossy cell loss.

182 ing mechanisms underlying the development of TLE may identify novel therapeutic targets.

183 a potential mechanism in the development of TLE.

184 d be causally involved in the development of TLE.SIGNIFICANCE STATEMENT Development of temporal lobe

185 All patients had a diagnosis of TLE according to standard clinical criteria.

186 ch signaling and increases the expression of TLE, which could be an important mechanism utilized by c

187 e of defunct PV neurons in the generation of TLE, we permanently inhibited GABA release selectively f

188 A hallmark of TLE is the characteristic loss of layer 3 neurons in the

189 Inactivation of TLE by UBR5-dependent ubiquitylation also involves VCP/p

190 Biologically, loss of TLE-dependent rRNA gene repression coincides with increa

191 However, no animal model of TLE has been shown to specifically replicate this cognit

192 in regions of a kainic acid-induced model of TLE in VGAT-ChR2 transgenic mice.

193 RNA sequencing analysis in a mouse model of TLE using 100 epileptic and 100 control hippocampi shows

194 ology, and network integration in a model of TLE, we retrovirally birthdated either early-born [EB; p

195 enting epileptogenesis in an animal model of TLE.

196 chronic epilepsy in the kainic acid model of TLE.

197 tochemistry, was increased in a rat model of TLE.

198 sis in male rats in the pilocarpine model of TLE.

199 ation is reduced in the kainic acid model of TLE.

200 hin CA1 pyramidal cells in a rodent model of TLE.

201 opment (epileptogenesis) in animal models of TLE could enable the identification of predictive biomar

202 In human TLE and in animal models of TLE, parvalbumin neurons are selectively lost in the sub

203 ulum of TLE patients and in animal models of TLE.

204 pairments has never been tested in models of TLE.

205 Unfortunately, the clinical outcomes of TLE cannot be determined based only on current diagnosti

206 and mood dysfunction in the chronic phase of TLE.

207 a therapeutic with promise for prevention of TLE caused by status epilepticus in humans.

208 kB as a therapeutic target for prevention of TLE.

209 are silenced by TCF-mediated recruitment of TLE/Groucho proteins, but the molecular basis for TLE/TC

210 Multiple reports of TLE procedural outcomes exist; however, data regarding p

211 sion or potentially ameliorating severity of TLE whereby transient inhibition of TrkB-PLCgamma1 signa

212 eurons has been observed in the subiculum of TLE patients and in animal models of TLE.

213 ed light on future therapeutic treatments of TLE.

214 ith HS (TLE-HS) and those with gliosis only (TLE-G).

215 ure gene therapy trials in pharmacoresistant TLE patients.

216 +/- 0.0016 mm/year, P < 0.0001) presurgical TLE cases.

217 ectly comparing the post- versus presurgical TLE groups on vertex-wise analysis, the areas of postope

218 kinase is one molecular mechanism promoting TLE.

219 w hope as a therapeutic agent for refractory TLE.

220 ves for offering early surgery in refractory TLE.

221 cessing Battery in 145 unilateral refractory TLE patients undergoing epilepsy surgery, a validation s

222 a validation set of 55 unilateral refractory TLE patients, and 39 age- and sex-matched healthy volunt

223 Information regarding TLE long-term outcomes may help guide cardiovascular imp

224 images from 121 patients with drug-resistant TLE across 3 independent epilepsy centers were used to t

225 the presurgical evaluation of drug-resistant TLE, providing information complementary to (18)F-FDG PE

226 Both left TLE (LTLE) and right TLE (RTLE) patients had lower verbal (LTLE 44 +/- 11; RT

227 0.0013 mm/year, P < 0.0001) and right (right TLE 0.0198 +/- 0.0016 versus healthy volunteers 0.0037 +

228 r was used to discriminate left versus right TLE, hippocampal asymmetry achieved 94% classification a

229 TLE subjects with medial temporal sclerosis (TLE-MTS), and 50 TLE subjects with normal appearance on

230 regulator of full-length PRH by sequestering TLE proteins that function as PRH co-repressors.

231 Several TLEs are expressed in a dynamic manner throughout embryo

232 Since TLE is a neuronal network disorder, DKI may be well suit

233 f Groucho/transducin-like enhancer of Split (TLE) and led to increased amounts of a transcriptional r

234 o Groucho/Transducin-Like Enhancer of split (TLE) proteins that function as co-repressors by interact

235 h Groucho/Transducin-Like Enhancer of Split (TLE) to block Wnt/T-cell factor (TCF)-mediated transcrip

236 f the hippocampus, which could help stratify TLE patients into those at high versus low risk of presu

237 Twelve pre-surgical TLE patients (7 MRI-negative) and age-matched healthy vo

238 ed histone H4 tails, suggesting that the TCF/TLE tetramer complex promotes structural transitions of

239 9 years, which was significantly higher than TLE without psychosis (5.3 years).

240 Group comparison revealed that TLE patients with lifetime affective morbidity showed si

241 Taken together, our results suggest that TLE activity is essential for early differentiation wher

242 This study suggests that TLE involves altered structural connectivity in a networ

243 functional connectivity profiles across the TLE spectrum.

244 ription of individual variability across the TLE spectrum.

245 olume or structural connectivity between the TLE groups.

246 rior cingulate cortex (sACC) than either the TLE-only or the HVs (p<0.001).

247 ngly supports GAL as the causal gene for the TLE in this family.

248 Furthermore, the TLE Q tetramer, not the dimer, binds to chromatin, speci

249 In the TLE patients, we map the trans-acting genetic control of

250 Structure-based mutation of the TLE tetramer interface shows that dimers cannot mediate

251 ermine the relationship of these findings to TLE.

252 d glutamatergic excitation and ultimately to TLE.

253 memory in rats, we show that kainate-treated TLE rats exhibit a selective impairment of the "what-whe

254 ific MGE cell grafting approach for treating TLE.

255 ed an allelic series of knockout ESCs of two TLE genes expressed most dynamically in early differenti

256 ive study of consecutive patients undergoing TLE at a single, high-volume center.

257 uch as elderly patients and those undergoing TLE for infectious indications and device system upgrade

258 ied clustering to 114 consecutive unilateral TLE patients using 1.5T MRI profiles derived from surfac

259 uncovered by comparing HS-TLE to unilateral TLE with normal clinical magnetic resonance imaging (MRI

260 E-III showed mild bilateral atrophy; whereas TLE-IV showed hypertrophy.

261 sterior default mode hubs in TLE-HS, whereas TLE-G did not differ from controls.

262 vity increases across all subfields, whereas TLE-G presented with dentate gyrus hypertrophy, focal in

263 ion of network abnormalities associated with TLE and the phenotypic characterisation of the disease.

264 ion of network abnormalities associated with TLE by revealing connectivity abnormalities that are not

265 Humans with TLE display loss of PV interneurons in the dentate gyrus

266 l VWRPY motif that mediates interaction with TLE/Gro corepressor proteins.

267 the hilus of the dentate gyrus of mice with TLE and evaluated graft differentiation, mossy fiber spr

268 epileptiform discharges (IEDs) in mice with TLE as well as sharp-wave ripples (SPW-Rs) in healthy mi

269 A total of 22 patients with TLE (12 males, 10 females, 22-57 age range) underwent ei

270 unctional MRI recordings in 27 patients with TLE (67% right sided) and 27 matched controls to examine

271 ntralateral to seizure foci in patients with TLE ([11C]PBR28: 2%-6%; [11C]DPA-713: 4%-9%).

272 Twenty-three patients with TLE and 11 age-matched controls were scanned with [11C]P

273 ging data were analyzed for 34 patients with TLE and 116 control subjects.

274 We examined 26 adult patients with TLE and 26 matched control participants and used resting

275 the epileptogenic side in all patients with TLE and also on the contralateral side in three patients

276 fraction (fP) was measured in patients with TLE and controls using FreeSurfer software and T1-weight

277 rotation was observed in three patients with TLE and four control subjects.

278 greater Ammon horn atrophy in patients with TLE and hippocampal sclerosis.

279 is paper presented AE in a few patients with TLE and normal MRI.

280 uneus, and occipital cortex in patients with TLE as compared with healthy subjects.

281 vide new insights for why some patients with TLE continue to experience postoperative seizures if pat

282 Overall, patients with TLE demonstrate impaired connectivity in thalamic arousa

283 Before surgery, patients with TLE demonstrated abnormal thalamo-occipital functional c

284 An independent dataset of 47 patients with TLE from 3 other epilepsy centers was used to assess the

285 mpal asymmetries discriminated patients with TLE from control subjects with high sensitivity (86.7%-8

286 Patients with TLE had 22%-45% reduced (P < .01) distant connectivity i

287 All eight patients with TLE had hippocampal abnormalities on the epileptogenic s

288 Patients with TLE had unilateral temporal seizure foci based on ictal

289 increased in both animals and patients with TLE in affected tissues, and in plasma in response to ep

290 tion on interictal EEG-fMRI in patients with TLE retrospectively confirmed the epileptogenic zone.

291 ity was significantly lower in patients with TLE than controls (p<0.05, paired t-test), particularly

292 8 VT to fp ratio was higher in patients with TLE than in controls for all ipsilateral temporal region

293 Side-to-side asymmetry in patients with TLE was calculated as the ratio of ipsilateral to contra

294 Adult and pediatric patients with TLE who underwent standard ATL between January 1, 1990,

295 ntralateral to seizure foci in patients with TLE, suggesting ongoing inflammation.

296 itors into the dentate gyrus in rodents with TLE, but the scarcity of human fetal cells limits applic

297 ompared with healthy controls, subjects with TLE demonstrated pathological changes in circumscribed r

298 Subregional data in individual subjects with TLE were compared with data in control subjects to detec

299 Linseed oils with and without TLE addition were characterized for moisture, color, ref

300 ndogenous hilar interneurons in mice without TLE.