ライフサイエンスコーパス: left hemisphere

1 here), and fast profiles (all but one in the left hemisphere).

2 rain activation is mostly lateralised to the left hemisphere.

3 eserved contralateral representations in the left hemisphere.

4 illions of cells distributed over the entire left hemisphere.

5 n learning, with a transient bias toward the left hemisphere.

6 ed to be computed in the dominant, typically left hemisphere.

7 4-year follow-up period in the right but not left hemisphere.

8 mory retrieval and semantic judgement in the left hemisphere.

9 onses in temporal-perisylvian areas of their left hemisphere.

10 ls in the region responsive to words, in the left hemisphere.

11 en Broca's and Wernicke's territories in the left hemisphere.

12 as lateral temporal-parietal regions in the left hemisphere.

13 cipital visual areas, predominantly over the left hemisphere.

14 face and tongue are greatly expanded in the left hemisphere.

15 ctural and resting state connectivity in the left hemisphere.

16 se to the Broca's or Wernicke's areas of the left hemisphere.

17 ponding locations in the structurally intact left hemisphere.

18 in the right hemisphere and semantics in the left hemisphere.

19 on and recruitment of eloquent cortex in the left hemisphere.

20 ented on the right producing activity in the left hemisphere.

21 sual analysis, which performed better in the left hemisphere.

22 of which were unilaterally activated in the left hemisphere.

23 nd revealed TOJ activation in the TPJ of the left hemisphere.

24 citation of neural pathways in the undamaged left hemisphere.

25 engthened feedforward connections within the left hemisphere.

26 icits observed after posterior damage to the left hemisphere.

27 Activations were more extensive in the left hemisphere.

28 mporal features (20-50 Hz) lateralize to the left hemisphere.

29 ile following the envelope compared with the left hemisphere.

30 within FC subnetworks mainly driven from the left hemisphere.

31 hening of feedforward connections within the left hemisphere.

32 gions of the fronto-thalamic circuits in the left hemisphere.

33 d or enhanced contralateral dominance in the left hemisphere.

34 e overall predominance of the right over the left hemisphere.

35 hey are also specifically lateralized to the left hemisphere.

36 t majority of behavioral effects seen on the left hemisphere.

37 cingulum and uncinate--predominantly in the left hemisphere.

38 tric gene expression assigns language to the left hemisphere.

39 nal connectivity of these regions within the left hemisphere.

40 terior parietal cortex, predominantly in the left hemisphere.

41 ons, particularly in the memory areas in the left-hemisphere.

42 cerebral commissure connecting the right and left hemispheres.

43 ditory cortical activation in both right and left hemispheres.

44 oteinopathy in the language-dominant (mostly left) hemisphere.

45 irectly introduced to the language-dominant (left) hemisphere.

46 rior limb of the internal capsule (mean ADC: left hemisphere, 1.18 x10(3)mum(2)/sec; right hemisphere

47 ferential permeability between the right and left hemispheres; (2) altered social behavior with incre

48 eir breadth of semantic activation, with the left hemisphere activating a narrow, focused semantic fi

49 , stronger lateralization resulted from more left hemisphere activation in both regions as well as re

50 In contrast to strongly lateralized left hemisphere activations for language in neurotypical

51 Subjects with BDD showed greater left hemisphere activity relative to controls, particula

52 ic representations and highlight a potential left-hemisphere advantage for mnemonic representations.

53 , usually consistent with a reduction in the left hemisphere and a relative increase in the right hem

54 nates of right NAc pcore and pshell onto the left hemisphere and examined structural and resting stat

55 espread temporal/frontal lobe regions of the left hemisphere and expressive aphasia; and (iv) bilater

56 with language and praxis lateralizing to the left hemisphere and spatial attention, face recognition,

57 in December or May/June, lateralized to the left hemisphere and specific to behaviorally relevant st

58 d to identify critical language areas in the left hemisphere and then to quantify each stroke survivo

59 ry inputs (the right visual hemifield in the left hemisphere and vice versa) is a fundamental feature

60 ft hemispheres, hippocampus in the right and left hemispheres and cerebellum.

61 he same linguistic functions as those in the left-hemisphere and only indirectly contribute to preser

62 e effect of lesion location (in the affected left hemisphere) and grey matter density (in the unaffec

63 insula, and extending into occipital cortex (left hemisphere) and orbitofrontal cortex (right hemisph

64 (three tasks selected to probe the right or left hemisphere), and (11)C-flumazenil positron emission

65 er parieto-frontal network in the right than left hemisphere, and a significant correlation between t

66 ly, Broca's area is most often larger in the left hemisphere, and functional imaging studies in human

67 la, medial frontal gyrus, hippocampus in the left hemisphere, and right cerebellum.

68 The P1 and N1 latencies were shorter in the left hemisphere, and the N1 and P2 amplitudes were large

69 s of interhemispheric inhibition, we applied left hemisphere anodal-excitatory and right hemisphere c

70 lation between attentional control and FA in left hemisphere anterior corona radiata, as well as the

71 tentional control and FA within a ROI in the left hemisphere anterior corona radiata.

72 articipants showed greater activation in the left hemisphere anterior extent of MT/V5 when motion wor

73 In addition, we found over the left hemisphere, anterior to primary auditory cortex, a

74 The integrity of the left hemisphere appears predictive of a better clinical

75 operties of a secondary auditory area in the left hemisphere, are capable to predict future song copy

76 1 subjects with focal hemisphere lesions (15 left hemisphere) as well as 16 normal controls on a batt

77 effects in several association tracts of the left hemisphere, as well as in the lateral aspect of the

78 There was a left-hemisphere association of motor ability in the cont

79 Paired-pulse TMS was delivered to the left hemisphere at the following interstimulus intervals

80 hree characteristics: greater atrophy of the left hemisphere; atrophy of anterior components of the p

81 In the left hemisphere, attending to the stimulus also resulted

82 peech has long been considered the domain of left-hemisphere auditory areas.

83 es by rate-specialized neurons in right- and left-hemisphere auditory cortex.

84 ctor of longitudinal aphasia severity in the left hemisphere [beta = -0.630, t(-3.129), P = 0.011].

85 lly specific relationships, primarily in the left hemisphere, between atrophy and impairments in lang

86 Individuals suffering from posterior left hemisphere brain injury often exhibit temporal proc

87 reorganize to the right-hemisphere following left-hemisphere brain damage.

88 case of the high grade glioma (HGG) only the left hemisphere Broca's area was activated (LI=1).

89 controls, syntactic processing co-activated left hemisphere Brodmann areas 45/47 and posterior middl

90 real-life narrative is not localized to the left hemisphere but recruits an extensive bilateral netw

91 network and language-related regions in the left hemisphere but to attention networks in the right h

92 this specific error type in 45 patients with left hemisphere chronic stroke.

93 in antipsychotic-treated vs HC's in a larger left hemisphere cluster (100 voxels, CCLAV = 0.01).

94 itory-speech-to-brain delay of ~70 ms in the left hemisphere, compared with ~20 ms in audio-only.

95 Dendritic length measurements in the left hemisphere confirm that males have greater overall

96 he control sample demonstrating rapid within-left hemisphere connectivity increases and the traumatic

97 Here, we show that mPFC neurons in the left hemisphere control stress effects on social behavio

98 eached levels of smoothness (associated with left hemisphere control), acceleration time (associated

99 and found the amount of FOXP2 protein in the left hemisphere cortex of 4-year-old boys was significan

100 f different, but overlapping, regions of the left hemisphere cortex, such that the distribution of ti

101 ask-based functional MRI voxel activation in left hemisphere cortical regions for verb generation (fr

102 Patients with left hemisphere damage and concomitant aphasia usually h

103 r integrity and performance in patients with left hemisphere damage and healthy participants to ask w

104 in differentiating between individuals with left hemisphere damage and right hemisphere damage where

105 amage produce different effects on movement: Left hemisphere damage produces deficits in specifying f

106 e right hemisphere in aphasia recovery after left hemisphere damage remains unclear.

107 ts indicated a double dissociation; although left hemisphere damage was associated with greater error

108 the right hemisphere has been observed after left hemisphere damage.

109 sphere areas supports aphasia recovery after left hemisphere damage.

110 l neglect syndrome), but only for right (not left) hemisphere damage.

111 onger in patients with right- as compared to left-hemisphere damage and were independent of lesion vo

112 ues, whereas average volume elsewhere in the left hemisphere deviated from control values by only 8%.

113 In the left hemisphere, differential visual processing occurred

114 cessed bilaterally in auditory cortex, but a left hemisphere dominance emerges when the input is inte

115 sistently suggest that the normal pattern of left hemisphere dominance of language processing is sign

116 e right middle cerebral arteries, indicating left hemisphere dominance.

117 s for auditory recognition and that there is left-hemisphere dominance for processing information der

118 ns, the approximately 0.5 Hz coupling became left-hemisphere dominant, compared with bilateral coupli

119 raphy imaging shows a clinically concordant, left-hemisphere-dominant pattern of deposition in primar

120 maging showed that microstructural damage to left hemisphere dorsal tracts--the superior longitudinal

121 identify a structural brain marker-volume of left hemisphere dorsolateral prefrontal cortex-associate

122 r MEDH in functionally eloquent areas of the left-hemisphere due to GBM in the right-hemisphere may b

123 ith right-side onset of motor symptoms (RPD, left hemisphere dysfunction) would be impaired at local

124 ght-hemisphere dysfunction; RPD, predominant left-hemisphere dysfunction) would display distinct patt

125 a common network strongly lateralized to the left hemisphere especially during planning but also acti

126 erior temporal atrophy, predominantly in the left hemisphere, especially along the superior temporal

127 The left hemisphere exhibited load-dependent activity only f

128 ocampal and fusiform gyri, and predominantly left hemisphere extra-temporal activations within the in

129 nts with schizophrenia by a reduction in the left hemisphere (F = 7.7, df 1,32, P < 0.01).

130 span (right hemisphere: F = 7.69, P < 0.001; left hemisphere: F = 8.69, P < 0.001).

131 zure onset with temporal lateralization, and left hemisphere focus with a unilateral right pattern.

132 and must subsequently be transferred to the left hemisphere for language processing than when it is

133 sphere for fight-or-flight processes and the left hemisphere for performing structured motor sequence

134 for different aspects of motor control: the left hemisphere for predicting and accounting for limb d

135 misphere, affording it an advantage over the left hemisphere for the activation of distantly related

136 200 ms, ISI and this difference was over the left-hemisphere for linguistic probes and over the right

137 may prevent fronto-parietal networks in the left hemisphere from resolving the activity imbalance wi

138 Recovery of left hemisphere frontoparietal metabolic activity was fu

139 rrelated with chunk concatenation, whereas a left-hemisphere frontoparietal network was correlated wi

140 tegrated from signs using the same classical left hemisphere frontotemporal network used for speech i

141 etry was attributable to a right slower than left hemisphere growth rate mapped in COS patients (P =

142 responses, suggesting that most ACFs in the left hemisphere had greater resilience against reduced c

143 spitalization for schizophrenia, MMN indexed left hemisphere Heschl gyrus gray matter volume, consist

144 Only schizophrenia evinced longitudinal left hemisphere Heschl gyrus reduction (P=.003), highly

145 ispheres, the basal ganglia in the right and left hemispheres, hippocampus in the right and left hemi

146 ht-hemisphere tangle density despite greater left-hemisphere hypoperfusion and atrophy during life.

147 sities in another and frontal atrophy of the left hemisphere in a third patient.

148 riginate more often in the right than in the left hemisphere in both callosotomized and healthy adult

149 indings challenge consensus that because the left hemisphere in neglect is pathologically over-excite

150 ally depends on posterior brain areas of the left hemisphere in proficient adult readers.

151 This establishes the unique role of the left hemisphere in syntax, a core component in human lan

152 Broca's area was present- in 2 cases in the left hemisphere, in 1 case in the right hemisphere and i

153 p, particularly along the mesial wall of the left hemisphere, in the same region where we previously

154 ht temporal cortex, (2) increased HFA in the left hemisphere including the medial temporal lobe (MTL)

155 es of human brain functions in the right and left hemispheres, including sensory, motor, and language

156 isphere, and the cuneus and precuneus in the left hemisphere, independent of familial risk.

157 athways to all calculated PFC regions in the left hemisphere, indicating stronger pathways for person

158 ession abilities associated with blurring in left hemisphere inferior frontal cortex and temporal pol

159 that better language outcome following early left hemisphere injury relies on the contribution of the

160 ch is typically more severe after right than left hemisphere injury, includes deficits of spatial att

161 ntral tegmental areas and nucleus accumbens, left-hemisphere insula, orbitofrontal cortex, and ventro

162 Lateralization of language to the left hemisphere is considered a key aspect of human brai

163 ory, which predicts that the right-eye (i.e. left-hemisphere) is used to categorize stimuli while the

164 We evaluated 331 patients with left hemisphere ischemic stroke with various spelling te

165 o controls before training comprised damaged left hemisphere language areas, right precentral and sup

166 language homologues compensate for damage in left hemisphere language areas, the current prevailing t

167 epsy (n = 21, 5-12 years, nine females) with left hemisphere language dominance.

168 s characterised by dysfunction of the normal left hemisphere language network and also implicates abn

169 measures of directed connectivity across the left hemisphere language network revealed a continuous i

170 yndrome that causes a gradual atrophy of the left hemisphere language network, leading to impairments

171 These findings suggest that left-hemisphere language processing emerges from early b

172 Moreover, the left hemisphere lateralization of this operation remains

173 Asymmetry in the form of left-hemisphere lateralization is a striking characteris

174 Finally, we show that the more left hemisphere-lateralized the pedunculopontine nucleus

175 ontribute to language function after a focal left hemisphere lesion.

176 he differential deficits induced by right or left hemisphere lesions to enhance post-stroke rehabilit

177 Thirty-eight stroke patients (16 with left-hemisphere lesions) underwent MRI anatomical brain

178 ng known that language is lateralized to the left hemisphere (LH) in most neurologically healthy adul

179 ioral data in 21 human patients with chronic left hemisphere (LH) lesions and a range of language imp

180 ablished that in human speech perception the left hemisphere (LH) of the brain is specialized for pro

181 of the unambiguous conditions; however, the left hemisphere (LH) showed less facilitation for the we

182 onal targets across the visual field; in the left hemisphere (LH), IPS0-2 codes primarily contralater

183 In adults, color CP is lateralized to the left hemisphere (LH), whereas in infants, it is laterali

184 eralization per se but rather on patterns of left-hemisphere (LH) and right-hemisphere (RH) activatio

185 ior temporal white matter connections of the left hemisphere likely involved in semantic and lexical

186 sphere, these responses were stronger in the left-hemisphere MD regions.

187 a more anterior word-selective region in the left hemisphere (mid OTS) was consistent with a single c

188 rior-posterior topography of P3 amplitude at left hemisphere, midline, and right hemisphere scalp loc

189 ion with perceiving actions in videos, while left-hemisphere MNS showed a supramodal association with

190 at asymmetric NPTN expression may render the left hemisphere more sensitive to the effects of NPTN mu

191 f 1.53 x 10(5) neurons/mm(3) (greater in the left hemisphere), more glia (72% of all cells) than neur

192 features of human hand movements within the left-hemisphere motor network.

193 Largely left-hemisphere MZS showed a supramodal association with

194 Greater post-stroke left hemisphere network fragmentation and higher modular

195 posed to rely on areas outside the classical left-hemisphere network for alphabetic reading.

196 While healthy controls activated a left-hemisphere network of correlated activity including

197 together, and the degree of fragmentation of left hemisphere networks.

198 al regions of the right hemisphere (with the left hemisphere not analyzed given artifacts arising fro

199 th normally developing controls, significant left-hemisphere occipitotemporal deficits in cortical th

200 Compared with controls, left-hemisphere occipitotemporal thickness correlations

201 peech (happy, angry, sad and neutral) in the left hemisphere of 21 two-month-old infants using diffus

202 r synaptic activity in the right than in the left hemisphere of females, mediating timely neuroendocr

203 , neocortical NFTs were more numerous in the left hemisphere of PPA/AD.

204 that were confined almost exclusively to the left hemisphere of the brain and that involved almost it

205 , language is processed predominantly by the left hemisphere of the brain, but we do not know how or

206 connections within and between the right and left hemisphere of the reading network of patients with

207 In the left hemispheres of PSCs we found a negative correlation

208 sphere was not correlated with damage in the left-hemisphere or with performance.

209 The correlation between the right and left hemispheres' ORP (R/L ORP) was calculated.

210 al (right hemisphere p = 0.032, r(2) = 0.31, left hemisphere p = 0.032, r(2) = 0.32) and right basola

211 ea (right hemisphere p = 0.032, r(2) = 0.38, left hemisphere p = 0.032, r(2) = 0.35) each displayed s

212 ADC maturation occurred earlier in the left hemisphere (P < .001) in several regions, including

213 only a 1.3% per year trend for growth in the left hemisphere (P = 0.066).

214 1755, associating with thinner cortex in the left hemisphere (P=1.12 x 10(-)(7)), particularly in the

215 Second, regions in the left hemisphere (particularly within temporal and subcor

216 As expected, deaf signers engaged left-hemisphere perisylvian language areas during the pe

217 Nonetheless, a single region in the left hemisphere (posterior OTS) contained spatial channe

218 ges lower-order, intact resources within the left hemisphere (posterior to their lesion locations) to

219 Neural connectivity was reduced in a left-hemisphere pre-language region, and the degree to w

220 under both movement conditions namely in the left hemisphere precentral gyrus (BA 4), the left hemisp

221 e correlation between total PANESS score and left hemisphere primary motor and premotor white matter

222 triking pattern of underconnectivity between left-hemisphere pSTS and distributed nodes of the dopami

223 Lesion-symptom mapping showed that specific left hemisphere regions related to different language ab

224 n these two groups occurred in homologues of left hemisphere regions that sustained task activation.

225 g a model language network consisting of six left hemisphere regions, the DCM analysis demonstrated r

226 ho stutter exhibited deactivation over these left hemisphere regions.

227 re activation in homologous regions to those left-hemisphere regions typically involved in the young.

228 symmetry in the brain's coding of space: the left hemisphere represents the right side, whereas the r

229 ater diagnosed as autistic display deficient left hemisphere response to speech sounds and have abnor

230 ility of patients with strokes affecting the left hemisphere revealed that meaningless gestures can b

231 erent clustering results, with LSE capturing left hemisphere/right hemisphere affinity structure and

232 The left hemisphere's dominance in processing social communi

233 ust responses than the American listeners at left hemisphere scalp sites that probably index activity

234 nvoluntary orienting were more frequent with left-hemisphere seeds.

235 The left hemisphere seems to perform faster processing to re

236 We studied 45 patients, all with a left hemisphere seizure focus (mean age 22.8, seizure on

237 t, only patients with parietal damage in the left hemisphere showed a clear deficit in movement adapt

238 vs. the right cerebral hemisphere, with the left hemisphere showing a preference to interact more ex

239 calization judgments of two individuals with left hemisphere somatosensory damage subsequent to strok

240 thermore, our lateralization results suggest left hemisphere specificity for the processing of phonol

241 that the recovery of speech production after left hemisphere stroke not only depends on the integrity

242 sed lesion-symptom mapping with data from 71 left hemisphere stroke participants to assess the critic

243 10 healthy adults and 10 individuals with left hemisphere stroke participated.

244 We report data from 43 left hemisphere stroke patients in two action recognitio

245 lesion-symptom mapping (VLSM) in a series of left hemisphere stroke patients to identify brain region

246 miliar and novel objects was assessed in six left hemisphere stroke patients, two of whom exhibited d

247 s, 27 patients (aged 59 +/- 11 years) with a left hemisphere stroke performed behavioural assessments

248 anisms underlying recovery of language after left hemisphere stroke remain elusive.

249 egression lesion-symptom mapping (LSM) of 73 left hemisphere stroke survivors (male and female human

250 l anatomical whole-brain connectomes from 90 left hemisphere stroke survivors using diffusion MR imag

251 Thirty-two left hemisphere stroke survivors with aphasia underwent

252 To confirm this result, 10 chronic left hemisphere stroke survivors with no history of apha

253 ognition tests were obtained from 67 chronic left hemisphere stroke survivors.

254 to language production abilities in chronic left hemisphere stroke, and that these areas may undergo

255 h in 52 speakers during the acute stage of a left hemisphere stroke.

256 participants with aphasia due to unilateral left hemisphere stroke.

257 reasoning test) in 64 patients with chronic left hemisphere stroke.

258 o receptive language outcome following early left hemisphere stroke.

259 he sSTR support sensory discrimination after left hemisphere stroke.

260 ontributes to aphasia outcomes after chronic left hemisphere stroke.

261 th speech comprehension impairment following left hemisphere stroke: (1) phonological training using

262 Here, we analysed longitudinal change in 28 left-hemisphere stroke patients, each more than a year p

263 ho were investigated at least 1 year after a left-hemisphere stroke.

264 f the disorder following right compared with left hemisphere strokes.

265 cessing is considered to be dominated by the left hemisphere, studies have indicated that both left a

266 d 8 right-handed patients who had suffered a left-hemisphere subcortical ischemic stroke with paresis

267 left hemisphere precentral gyrus (BA 4), the left hemisphere superior parietal lobe (BA 7), and the b

268 ned present in a large cluster involving the left hemisphere temporal and precuneus regions.

269 rived from a steeper decline with age in the left hemisphere than in the right on the mesial surface.

270 and PFt and this cluster was greater in the left hemisphere than in the right.

271 reveal a frontal-subcortical circuit in the left hemisphere that is simultaneously associated with e

272 dorsal and ventral processing streams in the left hemisphere that underlie core linguistic abilities

273 ionally defined visual word form area in the left hemisphere that was activated for words relative to

274 In an intermediate region in the left hemisphere, the response was significantly higher t

275 In the left hemisphere, the supramarginal gyrus was thinner in

276 locations: the frontal lobe in the right and left hemispheres, the basal ganglia in the right and lef

277 etwork, which is robustly lateralized to the left hemisphere, these responses were stronger in the le

278 Reduced neural integrity in the left-hemisphere through brain damage or healthy ageing r

279 o stutter that were found primarily in major left hemisphere tracts (e.g. superior longitudinal fasci

280 Patients with left hemisphere tumors generally performed worse than th

281 ical surface area of planum temporale in the left hemisphere (usually asymmetrically larger) was posi

282 ns by supporting disrupted processing in the left hemisphere via interhemispheric connections.

283 In the left hemisphere, visual and sentential constraints joint

284 predictors including preinjury intelligence, left hemisphere volume loss, and dorsolateral PFC volume

285 Higher Abeta load in the left hemisphere was associated with reduced glucose meta

286 on, hypothalamus, and septum/striatum of the left hemisphere was correlated with social status.

287 For each subject, the SLF of the left hemisphere was reconstructed from diffusion tensor

288 Even when the left hemisphere was relatively spared, subjects with dis

289 In the left hemisphere, we find that CA1-entorhinal connectivit

290 s, FD values of the lesion-free areas of the left hemisphere were associated with better FM scores; w

291 toward risky bets, while it increased in the left hemisphere when participants were biased away from

292 in the anterior and posterior regions of the left hemisphere, whereas damage to the posterior portion

293 onal connectivity is better preserved in the left hemisphere while prefrontal DTI fiber pathways are

294 The magnitude of left hemisphere white matter disturbances mediated the s

295 Reduced left hemisphere white matter was associated with slower

296 urban youth by disrupting the development of left hemisphere white matter, whereas postnatal PAH expo

297 l delta brushes which were associated in the left hemisphere with ipsilateral BOLD activation in the

298 dic Creutzfeldt-Jakob disease, mainly in the left hemisphere, with a strong trend (P=0.06) towards re

299 an elicit larger responses in the right than left hemisphere within these areas, depending on task de

300 In an intermediate region, only in the left hemisphere, words and emblems evoked a stronger res