ライフサイエンスコーパス: TMS

1 TMS at 5 Hz was delivered, in up to 40 daily sessions, t

2 TMS degraded visual motion perception when the evoked ph

3 TMS exhibited significant inhibitory effect on G-R NSCLC

4 TMS has provided important insight into the pathophysiol

5 TMS identifies newborns with PNP deficiency, whereas TRE

6 TMS induced caspase-independent apoptosis and autophagy

7 TMS is a valid method for diagnosis of PNP deficiency on

8 TMS modulation of the target and distractor were both pe

9 TMS over both SI and V5/hMT+, but not the PPC site, sign

10 TMS over rightLO but not rightOFA also significantly imp

11 TMS over the aIPS (but not over the other sites) reverse

12 TMS parameters were similar to those used in rat infrali

13 TMS perturbation of the right IPS increased the Flanker

14 TMS to AG disrupted thematic judgments particularly when

15 TMS to the PMv delivered 50 ms after the perturbation (b

16 TMS was applied to one of two targets in the left fronta

17 TMS was either provided after each trial of the ramp pha

18 TMS was given on each trial before stimulus onset either

19 TMS-based transient disruptions to the PMv and aIPS were

20 TMS-evoked responses related to phosphene perception wer

21 tron [bis(NHC)](silylene)Ni(0) complex 1, [((TMS) L)ClSi:-->Ni(NHC)2 ], bearing the acyclic amido-chl

22 During extinction learning (day 2), TMS was paired with one of the conditioned cues but not

23 ms after cue onset, total of four trains (28 TMS pulses).

24 We designed a TMS coil that focuses its effect near the tip of a recor

25 Short-interval intracortical inhibition, a TMS-EMG measure of synaptic GABAAergic inhibition, and o

26 We observed a TMS-locked local oscillatory alpha response lasting seve

27 ject revealed that the generator of abnormal TMS-evoked activity overlapped with the spike and seizur

28 After TMS, symptom reduction was associated with reduced conne

29 onance imaging was acquired before and after TMS therapy in 33 adult outpatients in a prospective ope

30 cally relevant changes in connectivity after TMS, followed by leave-one-out cross-validation.

31 connectivity between auditory cortices after TMS applied over the right AC were negatively related to

32 alpha response lasting several cycles after TMS (but not after sham stimulation).

33 lthy volunteers before and immediately after TMS (continuous theta burst stimulation) to the left or

34 lation and memory tasks also increased after TMS to the left angular gyrus relative to the vertex.

35 TMS-evoked neuronal activity 0.8-1 ms after TMS onset.

36 (GABAAR) modulates early TEPs (<50 ms after TMS), whereas GABA-B receptors (GABABR) play a role for

37 or later TEPs (at approximately 100 ms after TMS).

38 ing hand action was perturbed 25-30 ms after TMS, but our results fail to show any disruption of eye

39 timulus intervals (ISIs) between STN-DBS and TMS that produced cortical facilitation were determined

40 A number of TMS-electromyography (EMG) and TMS-electroencephalography (EEG) studies have identified

41 Here, we used magnetoencephalography and TMS to investigate the effect of attention on specificit

42 n at individualized intensity for 20 min and TMS was performed at rest (before, during, and after tAC

43 s that dopamine activation should antagonize TMS disruption of visual perception.

44 In the first experiment, we applied TMS over the rightOFA, its left homolog (leftOFA), right

45 rted no conscious experience upon awakening, TMS evoked a larger negative deflection and a shorter ph

46 t the sulfur-rich core of the trimeric BACE1 TMS is accessible to metal ions, but copper ions did not

47 Baseline TMS-EEG measures were assessed within 1 week before the

48 Behaviorally, TMS caused a relative slowing of response times to targe

49 only when an optimal timing of 20 ms between TMS pulses [2, 3, 5, 6] was used, not when TMS pulses we

50 We also examined the relationship between TMS-induced interhemispheric signal propagation and anat

51 1,3-dipolar "click" cycloaddition using bis(TMS)butadiyne and other bivalent alkynes.

52 he extent of attentional modulation for both TMS-locked alpha power and N40 amplitude did depend, wit

53 We applied brief TMS bursts (or Sham-TMS) to the dorsal intraparietal sul

54 quent sham-controlled inhibitory theta-burst TMS (TBS) in 40 healthy male volunteers.

55 mTOR pathway was significantly activated by TMS.

56 ation), reflected by a significant detail by TMS site interaction.

57 d either directly because of facilitation by TMS or indirectly through reduced interference from the

58 rimotor area and they were least impaired by TMS.

59 ion and activation of EGFR were inhibited by TMS in G-R cells.

60 eam of AMPK, was significantly suppressed by TMS.

61 (chloro)(silyl)nickel(II) complex 3, {[cat((TMS) L)Si](Cl)Ni<--:BH(NHC)2 }, via the cleavage of two

62 the importance in accurately characterizing TMS effects on seizure suppression due to the heterogene

63 , bearing the acyclic amido-chlorosilylene ((TMS) L)ClSi: ((TMS) L=N(SiMe3 )Dipp; Dipp=2,6-Pr(i)2 C6

64 cyclic amido-chlorosilylene ((TMS) L)ClSi: ((TMS) L=N(SiMe3 )Dipp; Dipp=2,6-Pr(i)2 C6 H4 ) and two NH

65 By contrast, TMS measures of cortical excitability and physiological

66 In contrast, TMS to pMTG disrupted thematic judgments for weak but no

67 Critically, TMS over the LPFC eliminated these fluctuations while le

68 rmined to be a cinchona alkaloid derivative (TMS-quinine or Me-quinidine).

69 y quality, population sampled, study design, TMS parameters and outcome measures.

70 This reaction, catalyzed by diphenylprolinol TMS ether, proceeds through an aromatic iminium intermed

71 tep method catalyzed by (S)-diphenylprolinol TMS ether, which joins two sequential domino reactions,

72 Regulating the evolution of distinctive TMSs is highly desirable but remains challenging to date

73 of anion-regulated evolution of distinctive TMSs, providing a new pathway for enhancing performances

74 etic stimulation and electroencephalography (TMS-EEG).

75 This is the first study to evaluate TMS-associated changes in connectivity in patients with

76 The following K values were evaluated: TMS topography (flattest K within first 9 rings, average

77 Both left and right FEF TMS caused marked attenuation of alpha modulation in the

78 Additionally, right FEF TMS enhanced gamma modulation in left visual cortex.

79 results showed that spatiotemporally focused TMS may enhance extinction learning and/or consolidation

80 ted within the 25-125 ms epoch that followed TMS.

81 n each trial we applied 10 Hz bursts of four TMS (or Sham) pulses to the intraparietal sulcus (IPS).

82 Low-frequency TMS to left parietal cortex increases low-frequency osci

83 With the use of hand-portable GC-TMS instrumentation, membranes cut with dimensions 40 mm

84 phy toroidial ion trap mass spectrometry (GC-TMS) instrumentation was shown to push detection limits

85 pt, the first ever, entirely on-site TFME-GC-TMS analysis was performed at a construction impacted la

86 Global TMS ether deprotection in the presence of oxygen and sub

87 used connectivity imaging findings to guide TMS targeting and compared the evoked responses to singl

88 However, TMS-evoked activity of individual neurons has remained l

89 Critically, however, TMS disruption of M1 activity selectively impaired conso

90 all of which can be linked to various human TMS responses recorded at the level of spinal cord and m

91 A control experiment revealed that identical TMS pulses at identical frequencies caused no change in

92 These results implicate TMS as a promising approach for reversing the adverse ne

93 Importantly, TMS-locked alpha power was suppressed during deployment

94 as yet unidentified ascaroside components in TMS-derivatized crude nematode exometabolome extracts.

95 Systematic variation in TMS location revealed that this response could also be e

96 irmed a previous finding in which individual TMS SI1mV (stimulus intensity for 1 mV MEP amplitude) se

97 IPS-TMS abolished the visual induced response suppression in

98 IPS-TMS relative to Sham-TMS increased activation in the par

99 Importantly, IPS-TMS abolished target-evoked activation increases in the

100 Our results demonstrate that IPS-TMS exerts profound directional causal influences not on

101 mained largely inaccessible due to the large TMS-induced electromagnetic fields.

102 Repeated pairing of STN-DBS and M1-TMS at short ( approximately 3 ms) and medium ( approxim

103 ring of subthalamic nucleus (STN)-DBS and M1-TMS at specific time intervals will lead to plasticity i

104 rtical transcranial magnetic stimulation (M1-TMS) at specific times can induce cortical plasticity in

105 Based on phosphene mapping, TMS double pulses were applied at one of various delays

106 Electropositive groups X (X = H, Me, TMS, TES) gave preferentially the linear isomer (regiois

107 , we focused on NREM sleep only and measured TMS-evoked EEG responses before awakening the subjects a

108 y used methoximated-trimethylsilylated (MeOx-TMS) derivatives, covering elemental composition, typica

109 On the other hand, MO-TMS derivatives were not significantly affected by water

110 rmate (MCF) and methoxime-trimethylsilyl (MO-TMS) derivatives of metabolites were evaluated using gas

111 Moreover, TMS disruption of VWFA activity decreased their tactile

112 formed with an initial turnover rate of 1 N(TMS)3/min, ultimately reaching a turnover number of appr

113 notion was supported by previous noninvasive TMS studies of human motor cortex indicating a reduction

114 he alpha band (8-13 Hz), predicted occipital TMS phosphenes, whereas higher-frequency beta-band (13-2

115 view data that have elucidated the action of TMS and TES, concentrating mainly on the most direct evi

116 ce, very little is known about the action of TMS at the cellular level let alone what effect it might

117 Spectral analyses of TMS-evoked responses in frontal cortex revealed non-line

118 addressed this issue through the analyses of TMS-evoked responses recorded over a 29 h sleep deprivat

119 atients, before and after a 5-week course of TMS.

120 , Albouy et al. (2017) examine the effect of TMS on oscillations in the brain during the manipulation

121 For comparison purposes, the effect of TMS over M1 was monitored when subjects tracked an exter

122 activation can partially block the effect of TMS.

123 tion, confirming the neural effectiveness of TMS stimulation.

124 areas; and (iii) elicit stronger effects of TMS on these motor regions.

125 flex conditioning and directional effects of TMS), we show that a specific set of excitatory inputs t

126 that this inhibition is due to expectancy of TMS or a possible need to cancel the prepared response.

127 id not differ statistically as a function of TMS site (i.e., number of free associates produced or di

128 A number of TMS-electromyography (EMG) and TMS-electroencephalograph

129 twork, and salience network as predictors of TMS response and suggest their involvement in mechanisms

130 Indeed, the frequency profile of TMS-evoked potentials (TEPs) closely resembles that of o

131 redox-catalyzed 2-fold arylation reaction of TMS-terminated alkynols.

132 This result implies a specificity of TMS at the dendritic level that could in principle be ex

133 We conclude that modern trials of TMS in functional disorders are part of a repeating cycl

134 It can be argued that use of TMS or peripheral stimulation to produce movement of a f

135 neglected previously in the construction of TMSs.

136 , there are often multiple existing forms of TMSs, which are of different natures and catalytic model

137 anions on the creation of different types of TMSs are investigated for the first time.

138 ined in the same volunteers by using offline TMS over right IPS and right MFG.

139 y spiking within the first 6 ms depending on TMS-induced current orientation and a multiphasic spike-

140 Online TMS over rTPJ also impacted on participants' explicit be

141 s from visual to motor cortices using paired-TMS with an ISI in the range 18-40 ms.

142 Both frontal and parietal TMS elicited a low-amplitude electroencephalographic (EE

143 n of phosphenes after occipital and parietal TMS.

144 Hz) power (but not phase) predicted parietal TMS phosphenes.

145 at positions 5 and 5' with thienyl, phenyl, TMS-ethynyl, and vinyl groups is reported herein.

146 Based on a pre-TMS functional MRI (fMRI) experiment we selected the lef

147 Online double-pulse TMS over rTPJ 300 ms (but not 50 ms) after target appear

148 tor-evoked responses (PMEPs) to single-pulse TMS as a measure of cortical excitability.

149 Here, we examine the effect of single-pulse TMS on dendritic activity in layer 5 pyramidal neurons o

150 ency disturbance of grip force, single-pulse TMS should also quickly disrupt ongoing eye motion.

151 In a single-pulse TMS study carried on 16 Met (Val/Met and Met/Met) and 16

152 We translated human single-pulse TMS to rodents and unveiled time-grained evoked activiti

153 For 2a (R = TMS), a 1,3-silyl shift gave an intermediary disilene, w

154 Recent TMS work has also revealed markers of motor inhibition d

155 Repetitive TMS (rTMS) pulse frequency is recognized as one of the m

156 to receive one of five cerebellar repetitive TMS (rTMS) interventions (Sham, 1 Hz, 5 Hz, 10 Hz and 20

157 the motor account, we found that repetitive TMS pulses impaired participants' global sensitivity to

158 hile participants rested in the MRI scanner (TMS/BOLD imaging).

159 om score (TSS), and total medication scores (TMS) were significantly lower than pharmacotherapy group

160 requires the BACE1 transmembrane sequences (TMSs) and cytoplasmic domains, with residues Ala(463) an

161 We applied brief TMS bursts (or Sham-TMS) to the dorsal intraparietal sulcus (IPS) 100 ms aft

162 IPS-TMS relative to Sham-TMS increased activation in the parietal cortex regardle

163 arge neutral zwitterionic compounds [(Ge9{Si(TMS)3}2)(t)Bu2P]M(NHC(Dipp)) (M: Cu, Ag, Au) (4-6), in w

164 ction with the bis-silylated cluster [Ge9{Si(TMS)3}2](2)(-) yields the novel cluster compound [Ge9{Si

165 ated clusters [Ge9{Si(TMS)3}3](-) or [Ge9{Si(TMS)3}2](2-) with dialkylhalophosphines R2PCl (Cy, (i)Pr

166 -) yields the novel cluster compound [Ge9{Si(TMS)3}2P(t)Bu2](-) (3).

167 sphine (t)Bu2PCl does not react with [Ge9{Si(TMS)3}3](-) due to steric crowding.

168 Reactions of silylated clusters [Ge9{Si(TMS)3}3](-) or [Ge9{Si(TMS)3}2](2-) with dialkylhalophos

169 roups and the tris-silylated cluster [Ge9{Si(TMS)3}3](-) yield the novel neutral cluster compounds [G

170 the novel neutral cluster compounds [Ge9{Si(TMS)3}3PR2] (R: Cy (1), (i)Pr (2)) with discrete Ge-P ex

171 Through the use of model compounds (H-Si(TMS)3 and H-Si(OTMS)3), nanoparticles (H-SiNPs), and pla

172 he TMS-evoked potential (TEP) after a single TMS pulse.

173 ition of the left amygdala induced by single TMS pulses to the right dorsolateral prefrontal cortex;

174 troduction of active transition metal sites (TMSs) in carbon enables the synthesis of noble-metal-fre

175 , during non-rapid eye movement (NREM) sleep TMS elicits a larger positive-negative wave, fewer phase

176 ivity via transcranial magnetic stimulation (TMS) abolished the adaptation of M100 attenuation, while

177 combined transcranial magnetic stimulation (TMS) and electroencephalography (EEG).

178 gle-pulse transcranial magnetic stimulation (TMS) applied to visual cortical area V5/MT to reduce the

179 oncurrent transcranial magnetic stimulation (TMS) as a causal perturbation approach to investigate th

180 cation of transcranial magnetic stimulation (TMS) as a research and clinical tool in the field of epi

181 Transcranial magnetic stimulation (TMS) at beta frequency has previously been shown to incr

182 gle-pulse transcranial magnetic stimulation (TMS) concurrent with fMRI to examine whether predictive

183 -invasive transcranial magnetic stimulation (TMS) delivered twice a week over a four-week period can

184 essed via transcranial magnetic stimulation (TMS) during maximum voluntary contraction (MVC) and cort

185 series of transcranial magnetic stimulation (TMS) experiments to examine in detail the specificity of

186 Transcranial magnetic stimulation (TMS) has been shown to modulate multiple brain functions

187 Transcranial magnetic stimulation (TMS) has emerged as an important technique in cognitive

188 have used transcranial magnetic stimulation (TMS) in humans to demonstrate the participation of the a

189 CM with a transcranial magnetic stimulation (TMS) intervention that transiently perturbed the LPFC.

190 Transcranial magnetic stimulation (TMS) is a widely used non-invasive tool to study and mod

191 Transcranial magnetic stimulation (TMS) is widely used in clinical interventions and basic

192 at paired transcranial magnetic stimulation (TMS) near ventral premotor cortex (PMv) and primary moto

193 Transcranial magnetic stimulation (TMS) of human occipital and posterior parietal cortex ca

194 epetitive transcranial magnetic stimulation (TMS) of the dorsolateral prefrontal cortex (DLPFC) is an

195 ndergoing transcranial magnetic stimulation (TMS) of the RLPFC versus two prefrontal control regions.

196 ffects of transcranial magnetic stimulation (TMS) on task performance, but it is unclear whether thes

197 ndergoing transcranial magnetic stimulation (TMS) over the cortical motor representation of the left

198 effect of transcranial magnetic stimulation (TMS) over the hand area of the primary motor cortex (M1)

199 means of transcranial magnetic stimulation (TMS) over the hand area of the primary motor cortex (M1)

200 We used transcranial magnetic stimulation (TMS) over the occipital cortex to interfere with attenti

201 eta-burst transcranial magnetic stimulation (TMS) over the PPC, but not the dorsal premotor cortex, e

202 applying transcranial magnetic stimulation (TMS) over the primary motor cortex, we investigated whet

203 Transcranial magnetic stimulation (TMS) studies in humans have shown that many behaviors en

204 fMRI) and Transcranial Magnetic Stimulation (TMS) study.

205 epetitive transcranial magnetic stimulation (TMS) therapy can modulate pathological neural network fu

206 RI-guided transcranial magnetic stimulation (TMS) to assess whether temporary disruption of the left

207 gle-pulse transcranial magnetic stimulation (TMS) to co-localise pharyngeal and thenar representation

208 , we used transcranial magnetic stimulation (TMS) to examine the physiological basis and behavioral r

209 ffered by transcranial magnetic stimulation (TMS) to explore the impact of pre-morbid individual diff

210 gle-pulse transcranial magnetic stimulation (TMS) to interfere with postmovement activity in M1 in tw

211 , we used transcranial magnetic stimulation (TMS) to interrupt processing in the OPA while subjects p

212 ired with transcranial magnetic stimulation (TMS) to primary motor cortex (M1) at specific intervals

213 , we used transcranial magnetic stimulation (TMS) to probe the excitability of distinct sets of excit

214 RI-guided transcranial magnetic stimulation (TMS) to shed light on the role of the occipital face are

215 , we used transcranial magnetic stimulation (TMS) to test the effects of a single oral dose of 50 and

216 Here, transcranial magnetic stimulation (TMS) was used to establish a causal yet dissociable role

217 ble-pulse transcranial magnetic stimulation (TMS) while moving a single tactile point across the fing

218 ng online transcranial magnetic stimulation (TMS) with computational modeling of behavioral responses

219 employed transcranial magnetic stimulation (TMS) with simultaneous electroencephalographic (EEG) rec

220 epetitive transcranial magnetic stimulation (TMS) with subsequent magnetoencephalography.

221 nhibitory transcranial magnetic stimulation (TMS) would reduce appetitive neuromodulation in a manner

222 Using transcranial magnetic stimulation (TMS), 25 motor-evoked potentials (MEPs) were recorded be

223 sics, and transcranial magnetic stimulation (TMS), all within the same human participants, we show th

224 Using transcranial magnetic stimulation (TMS), we applied a novel cortico-cortical paired associa

225 sponse to transcranial magnetic stimulation (TMS)--an approach that has proven helpful in assessing o

226 fMRI and transcranial magnetic stimulation (TMS).

227 orders is transcranial magnetic stimulation (TMS).

228 ng paired transcranial magnetic stimulation (TMS).

229 ations by transcranial magnetic stimulation (TMS).

230 sue using transcranial magnetic stimulation (TMS).

231 gle-pulse transcranial magnetic stimulation (TMS).

232 ing using transcranial magnetic stimulation (TMS).

233 navigated transcranial magnetic stimulation (TMS).

234 indices of increased net synaptic strength (TMS intensity to elicit a predefined amplitude of motor-

235 During subsequent TMS sessions, observers performed the same task, with hi

236 Using a combined tACS-TMS approach, we demonstrate that driving gamma frequenc

237 B1 inhibitor 2,3',4,5'-tetramethoxystilbene (TMS) every third day for 4 weeks.

238 rol, (Z)3,4,5,4'-trans-tetramethoxystilbene (TMS) which selectively elevated the intracellular calciu

239 signals for perception of stiffness and that TMS alters the synchronization between the two signals c

240 We therefore argue that TMS-locked and spontaneous oscillations are of common ne

241 We conclude that TMS directly activates fibers within the upper cortical

242 STATEMENT The present work demonstrates that TMS disruption of M1 activity impairs the consolidation

243 We find that TMS causes GABAB-mediated inhibition of sensory-evoked d

244 We found that TMS to the right AC, but not the left, resulted in wides

245 onsistent with our prediction, we found that TMS to the right OPA impaired spatial memory for boundar

246 We found that TMS-induced disruption of the motor lip representation m

247 These results support the idea that TMS-EEG could be a useful biomarker in epilepsy in gray

248 Results revealed that TMS did not influence adaptation to the new visuomotor r

249 The findings show that TMS-induced network modulation occurs, even in the absen

250 tatus, stimulation, and word type, such that TMS increased the disadvantage for spelling-sound atypic

251 These results suggest that TMS probes theta phase-reset by attentional reorienting

252 Additional features are the TMS protecting group and halo-induced ipso-desilylation

253 Crucially, the TMS pulse was delivered when all the subjects exerted th

254 negative peak around 100 milliseconds in the TMS-evoked potential (TEP) after a single TMS pulse.

255 facilitates a new level of insight into the TMS-brain interaction that is vital for developing this

256 rgic inhibition, and other components of the TMS-evoked EEG response remained unaffected.

257 de of the N45, a GABAAergic component of the TMS-evoked EEG response.

258 re the initiation of MST treatment using the TMS-EEG measures of cortical inhibition (ie, N100 and lo

259 When the TMS was targeted to the same cortical sites that had bec

260 mer interface of the sulfur-rich core of the TMSs.

261 In this TMS-fMRI study, participants attended to the left visual

262 We used near-threshold TMS with concurrent EEG recordings to measure how oscill

263 tution by cyanide upon treatment with TMSCN (TMS=trimethylsilyl).

264 irect in vivo electrophysiological access to TMS-evoked neuronal activity 0.8-1 ms after TMS onset.

265 Relative to TMS to a control site (vertex), disruption of the left a

266 Analyses used a priori seeds relevant to TMS, posttraumatic stress disorder, or MDD (subgenual an

267 , we assessed the alpha-like EEG response to TMS of the visual cortex during periods of high and low

268 reliability, inter-individual sensitivity to TMS accounted for a modest percentage of the variance in

269 The results show that TBI rats subjected to TMS therapy showed significant increases in the evoked-f

270 and if they are differentially vulnerable to TMS perturbation.

271 Taken together, TMS showed promising anti-cancer activity by mediating c

272 discusses the application of trimethylsilyl (TMS)-4,4'-desmethylsterols derivatives chromatographic f

273 Thus, finely tuned TMS treatment has great potential to become a powerful a

274 paired adaptation to a new force field under TMS parietal perturbation; (2) defective control of dire

275 paration, focusing on studies that have used TMS to monitor changes in the excitability of the cortic

276 We used TMS to quantify motor cortical excitability and physiolo

277 on (DBS) of the BG with M1 stimulation using TMS.

278 rticospinal responsiveness was monitored via TMS-evoked potentials (MEPs) during a 25% MVC.

279 her, we built group-level maps that weighted TMS-induced electric fields and diffusion magnetic reson

280 n TMS pulses [2, 3, 5, 6] was used, not when TMS pulses were delivered synchronously.

281 This effect did not take place when TMS was delivered over adjacent dorsal premotor cortex o

282 reduced skin conductance responses, whereas TMS to target 2 had no effect.

283 However, it is unclear whether TMS-locked and spontaneous oscillations are produced by

284 h minimal overcorrections were achieved with TMS flattest K (mean -0.68+/-0.60 D, 73% within +/-0.50

285 oms of both disorders can be alleviated with TMS therapy.

286 were less able to update prior beliefs with TMS delivered at 300 ms after target onset.

287 found that repeated pairing of STN-DBS with TMS at short ( approximately 3 ms) and medium ( approxim

288 tinction recall (day 3), the cue paired with TMS to target 1 showed significantly reduced skin conduc

289 d experiment, we combined this paradigm with TMS applied over either the right aIPS, pSTS, and the ri

290 e then combined the adaptation paradigm with TMS.

291 R chemical shifts in DMSO are presented with TMS as the calculated reference and with empirical scali

292 tromagnetic machines, and more recently with TMS and TENS.

293 d in Apoe(-/-)/Cyp1b1(+/+) mice treated with TMS and in Apoe(-/-)/Cyp1b1(-/-) mice and by concurrent

294 changes were inhibited in mice treated with TMS and in Apoe(-/-)/Cyp1b1(-/-) mice.

295 poe(-/-)/Cyp1b1(+/+) mice; mice treated with TMS or Apoe(-/-)/Cyp1b1(-/-) mice had reduced AAAs.

296 s of various targeted reactions related with TMSs.

297 Z-TMS also inhibited proliferation of erlotinib-resistant

298 Z-TMS exhibited hepatoprotective effects against DEN/CCl4-

299 In conclusion, Z-TMS appears to be a unique therapeutic agent targeting H

300 trated that (Z)-3,5,4'-trimethoxystilbene (Z-TMS) exhibits potent antitumor and anti-HCV activities w