ライフサイエンスコーパス: TLE

1 TLE corepressors interact and modulate the activity of a

2 TLE patients showed greater asymmetry.

3 TLE-1 and BBC3/PUMA were identified as direct targets of

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 by attempting replication in a cohort of 339 TLE patients of European origin.

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

13 Presurgical brain PET scans of 75 TLE patients were examined using a display/analysis tool

14 mpus, the temporoammonic pathway, exhibits a TLE-associated transformation from a spatially restricte

15 tion of the HES1 transcription factor from a TLE-dependent repressor to an activator required for neu

16 Knockdown of Gro3, a TLE homolog in zebrafish, cooperated with AML1-ETO to ca

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

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

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

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

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

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

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

24 and potentially other signaling pathways by TLE corepressors leads to a more malignant phenotype.

25 ocampi from the pilocarpine model of chronic TLE.

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

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

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

29 y early the FSE individuals who will develop TLE.

30 f acutobin, a purified thrombin-like enzyme (TLE), isolated from the snake venom of Deinagkistrodon a

31 oups: (i) those with temporal lobe epilepsy (TLE) and mesial temporal sclerosis (MTS) (MTS-TLE); (ii)

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

33 ogically intractable temporal lobe epilepsy (TLE) carries risk for post-operative naming decline.

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

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

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

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

38 been associated with temporal lobe epilepsy (TLE) in humans and in animal models of TLE.

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

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

41 Human temporal lobe epilepsy (TLE) is associated with bioenergetic abnormalities inclu

42 used animal model of temporal lobe epilepsy (TLE) is characterized by behavioural and biochemical alt

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

44 Temporal lobe epilepsy (TLE) is commonly caused by hippocampal sclerosis and is

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 Temporal lobe epilepsy (TLE) is the most common form of epilepsy, affecting appr

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

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

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

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

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

53 ical improvement for temporal lobe epilepsy (TLE) patients, but prognostic value for identifying pati

54 ic brain tissue from temporal lobe epilepsy (TLE) patients.

55 the population, with temporal lobe epilepsy (TLE) the most common variant in adults.

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

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

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

61 medically refractory temporal lobe epilepsy (TLE), but may be complicated by amnestic syndromes.

62 nts and animals with temporal lobe epilepsy (TLE), but whether these changes are important for epilep

63 n in rat, a model of temporal lobe epilepsy (TLE), causes degeneration of the hippocampal CA3 pyramid

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 In animal models of temporal lobe epilepsy (TLE), neurosteroid sensitivity of GABA(A) receptors on d

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

69 mmonly precede human temporal lobe epilepsy (TLE), suggesting that transcriptional dysregulation of H

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

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

72 ired in experimental temporal lobe epilepsy (TLE), the most common form of epilepsy in adults.

73 Temporal lobe epilepsy (TLE), traditionally thought to develop largely due to en

74 n epileptogenesis of temporal lobe epilepsy (TLE).

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

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

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

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

79 eight patients with temporal lobe epilepsy (TLE).

80 T 1A) play a role in temporal lobe epilepsy (TLE).

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

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

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

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 reased need for transvenous lead extraction (TLE).

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

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

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

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

91 -activated signaling pathway responsible for TLE.

92 Seizure events resulting from TLE are characterized by aberrant hippocampal mossy fibe

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

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

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

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

97 The Groucho (Gro)/TLE/Grg family of corepressors operates in many signalin

98 ivity of Grg5, an atypical member of the Gro-TLE family of co-repressors.

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

100 Gro/TLE proteins recognize a wide range of transcriptional r

101 Although Gro/TLE/Grgs disrupt activator complexes and recruit histone

102 epressor activity, and a direct role for Gro/TLE/Grg binding and altering chromatin structure has not

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

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

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

106 Groucho-related (Gro/TLE/Grg) corepressors meditate embryonic segmentation, d

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

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

109 ctor-beta/BMP-SMAD, SRC/YES-YAP, and GROUCHO/TLE).

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

111 of association with the corepressors Groucho/TLE or Sin3.

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

113 A subset of Groucho/TLE family members that lack the C-terminal WD40 domains

114 t as dominant-negative regulators of Groucho/TLE proteins, yet such a role has not been conclusively

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

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

117 Transcriptional co-repressors of the Groucho/TLE family are important regulators of development in ma

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

119 this report, we demonstrate that the Groucho/TLE family protein, Grg4, interacts with Pax2 to suppres

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

121 se1 (PARP-1) sensor component of the groucho/TLE-corepressor complex mediating dismissal of the corep

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

123 2 and Drosophila ARID1, and binds to Groucho/TLE.

124 tochemistry in hippocampi from three groups: TLE with hippocampal sclerosis (HS; n = 17), epileptic h

125 We report 10 right-handed TLE patients with left hippocampal sclerosis who underwe

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

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

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

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

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

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

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

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

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

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

136 In TLE brain specimens, CD45-positive leukocytes were detec

137 In TLE, it appears that collaboration before publication is

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

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

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

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

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

143 < 0.05) BP reductions were also detected in TLE patients with normal MR images (n = 6), in mesial te

144 re anterior propagation of EEG discharges in TLE.

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

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

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

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

149 Despite this potential importance in TLE, these pathways have received little study.

150 pyramidal neuron dendrites was increased in TLE because of decreased availability of A-type potassiu

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

152 ise to help elucidate mnemonic processing in TLE.

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

154 sensitivity of synaptic GABA(A) receptors in TLE.

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

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

157 - neuronal stimulation, such as that seen in TLE.

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

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

160 initiation and/or propagation of seizures in TLE.

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

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

163 ed to an increased seizure susceptibility in TLE, strategies that restrain the aberrant mossy fiber s

164 pus may contribute to depressive symptoms in TLE patients.

165 Our study shows that in TLE patients, reductions of 5-HT 1A receptor binding in

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

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

168 erosis (MTS) (MTS-TLE); (ii) lesional TLE (l-TLE); or (iii) extratemporal epilepsy (ETE).

169 (CI), 0.8-5.9 ms; P = 0.01], patients with l-TLE had prolongation of T2 relaxation time by a mean of

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

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

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

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

174 ral sclerosis (MTS) (MTS-TLE); (ii) lesional TLE (l-TLE); or (iii) extratemporal epilepsy (ETE).

175 corepressor that is homologous to mammalian TLE proteins.

176 Eleven patients with mesial TLE and 13 control subjects were examined with multisect

177 hippocampal atrophy in patients with mesial TLE.

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

179 LE) and mesial temporal sclerosis (MTS) (MTS-TLE); (ii) lesional TLE (l-TLE); or (iii) extratemporal

180 Unsurprisingly, in patients with MTS-TLE, T2 relaxation time in the sclerotic hippocampus was

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

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

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

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

185 d ATL in magnetic resonance imaging-negative TLE.

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

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

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

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

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

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

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

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

194 a potential mechanism in the development of TLE.

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

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

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

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

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

200 tudies in the adult rat pilocarpine model of TLE found reduced expression of GABR alpha1 subunits and

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

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

203 ovide initial evidence that post-SE model of TLE might serve as a model of the comorbidity of epileps

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

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

206 dent also in the pilocarpine animal model of TLE.

207 chronic epilepsy in the kainic acid model of TLE.

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

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

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

211 epsy (TLE) in humans and in animal models of TLE.

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

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

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

215 kB as a therapeutic target for prevention of TLE.

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

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

218 mpal interactions underlying the seizures of TLE.

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

220 ed light on future therapeutic treatments of TLE.

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

222 ure gene therapy trials in pharmacoresistant TLE patients.

223 FoxG1 has two potential TLE binding sites: an N-terminal eh1 motif and a C-termi

224 Thirty-five patients with refractory TLE undergoing pre-surgical evaluation for temporal lobe

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

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

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

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

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

230 Several TLEs are expressed in a dynamic manner throughout embryo

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

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

233 l Groucho/transducin-like enhancer of split (TLE) protein, and induces cell death with characteristic

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

235 the region typically removed with 'standard' TLE resection.

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

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

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

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

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

241 functional connectivity profiles across the TLE spectrum.

242 ription of individual variability across the TLE spectrum.

243 olume or structural connectivity between the TLE groups.

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

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

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

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

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

249 enhancer, followed by stable binding of the TLE-1 and HDAC1 corepressors.

250 tment of transcriptional corepressors of the TLE/Groucho family.

251 perceived to be important for preventing the TLE development after the hippocampal injury.

252 nt of co-repressor proteins belonging to the TLE family of chromatin-binding proteins.

253 PW domains of HES1, which associate with the TLE/Groucho corepressors.

254 This study is the first to implicate the TLEs as potential tumor suppressor genes in myeloid leuk

255 a model in which haploinsufficiency of these TLEs overcomes the negative survival and antiproliferati

256 ermine the relationship of these findings to TLE.

257 d glutamatergic excitation and ultimately to TLE.

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

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

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

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

262 ampal involvement in the seizures underlying TLE.

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

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

265 ting transcription factor, Hesx1, acting via TLE/Reptin/HDAC1 corepressor complexes.

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

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

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

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

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

271 s modified in hippocampi of individuals with TLE.

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

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

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

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

276 ceptor antagonist, to study 22 patients with TLE and 10 control subjects.

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

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

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

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

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

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

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

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

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 of association of genetic polymorphisms with TLE by attempting replication in a cohort of 339 TLE pat

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

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

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

300 ndogenous hilar interneurons in mice without TLE.