ライフサイエンスコーパス: HFS

1 HFS also caused a prolonged activation of the translatio

2 HFS diets also resulted in decreased expression of essen

3 HFS mice elicited a 70% increased susceptibility to AF.

4 HFS of m836 resulted in a 5-fold loss of affinity, where

5 HFS of the STN, but not of other nearby regions surround

6 HFS selectively activates the PKB-TSC2-mTOR cascade caus

7 HFS significantly increased myofibrillar and sarcoplasmi

8 HFS toxicity grade (Common Terminology Criteria for Adve

9 HFS-TB studies included log-phase growth studies under a

10 There were 22 HFS-TB studies published, of which 12 were combination t

11 Grade 1-3 HFS was lower in the diclofenac group than in the placeb

12 Grade 2 or 3 HFS was observed in 3.8% of participants in the diclofen

13 differ (P = 0.877): HFD [3781 (2513, 5050)], HFS [4006 (2711, 5302), and UF [4315 (3027, 5603)].Highe

14 es that examined the same parameters as in 8 HFS-TB studies.

15 Interestingly, Fz5CRD abolishes HFS-induced synapse formation.

16 ched on, and persists for several days after HFS is stopped.

17 to prestimulus values within 30-40 min after HFS was applied in the presence of mAb 1.9.

18 tion, beginning with the second minute after HFS, without reducing responses to HFS.

19 Within minutes after HFS, the expression of multiple translational proteins,

20 al studies published at least 6 months after HFS-TB experiments' quantitative predictions.

21 Twenty clinical studies were published after HFS-TB experiments predicted optimal drug exposures and

22 erformed a literature search to identify all HFS-TB experiments published between 1 January 2000 and

23 inhibitor tetrahydrolipstatin did not alter HFS-induced striatal LTD.

24 Patients completed an HFS diary (HFSD) daily.

25 Recently, an HFS utilizing the Anomalous Nernst Effect (ANE) has been

26 om an ancient autoproteolytic domain with an HFS motif.

27 s 127.3 +/- 18.4 nmol/min/mg; P = 0.026) and HFS mice (0.10 +/- 0.04 DeltaF/F0 x ms(-1) vs 0.06 +/- 0

28 Moreover, a component of basal and HFS-induced ERK activity depended on PI3K, indicating th

29 insulin resistance occurred in both HFS and HFS+Resv diets compared with SD.

30 y of permeability enhancement due to IFS and HFS treatments are different.

31 G) wave activities were also measured around HFS in conjunction with VPL neuron recordings.

32 loys, revealing their numerous advantages as HFS materials.

33 amide transport inhibitor, AM404, attenuated HFS-LTP, an effect reversed by the CB1 receptor antagoni

34 In contrast, an adult-like BLA HFS-induced decrease in spike probability of mPFC neuron

35 s not prevented by treatments known to block HFS-induced LTD, including antagonism of metabotropic gl

36 le for degrading anandamide, failed to block HFS-LTP alone or in combination with cOA.

37 ERK inhibitors blocked HFS-induced phosphorylation of all three proteins at sit

38 tion and insulin resistance occurred in both HFS and HFS+Resv diets compared with SD.

39 inhibition of L- and N-type VOCCs induced by HFS by 30 and 33%, respectively.

40 odil, both blocked LTPs that were induced by HFS or TBS.

41 amplitude of the population spike induced by HFS, both declined gradually and returned to prestimulus

42 significantly blocked LTP and PTP induced by HFS, but not when TBS was used.

43 lity or the EEG slow-wave pattern induced by HFS.

44 ion, ERK mediated the stimulation of mTOR by HFS.

45 cl mice fed with high fat-high sucrose chow (HFS), multifunctionality of CD8 + splenic and tumor-infi

46 epresenting a typical western diet, named CL-HFS, successfully induces male mouse non-alcoholic steat

47 n and hepatic fibrosis in normal diet- or CL-HFS-fed mice.

48 l and metabolic mediators contributing to CL-HFS-induced non-alcoholic steatohepatitis.

49 Combining HFS with feedback from the lid movement was critical for

50 The HCs and SZs had comparable HFS-driven electroencephalographic visual steady state r

51 In contrast, HFS acutely increased phosphorylation of PKB at Ser473 5

52 In contrast, HFS-induced LTP increased monotonically with drug concen

53 We found that cortical HFS increases calcium (Ca(2+)) levels in striatal astroc

54 mice fed with a obesogenic and diabetogenic HFS diet were administered with either water or two CBC

55 Bl/6J mice fed with a high-fat sucrose diet (HFS) for 2 (n = 42) or 12 (n = 39) weeks.

56 hepatic steatosis in high-fat-sucrose diet (HFS) induced obese mice.

57 During HFS, significant skin resistance reductions were accompa

58 During HFS, the lack of functional ASICs in synaptic transmissi

59 In naive slices, mGluR7 activation during HFS generates MF-SLIN LTD, depressing presynaptic releas

60 hermore, application of synthetic AEA during HFS in field recordings of slices from P12-P14 rats allo

61 t skin resistance reductions measured during HFS correlated significantly greater with subharmonic th

62 ncentration of glutamate rose quickly during HFS, remained elevated for the duration of stimulation,

63 LTD whereas blocking the CB1 receptor during HFS in animals P16-P34 resulted in expression of LTP.

64 isingly, inhibition of NMDA receptors during HFS "uncovered" a persistent form of depression.

65 dopaminergic activation which remains during HFS.

66 d control brain slices tetanized with either HFS or TBS gave similar levels of LTP and post tetanic s

67 In total, 47 of 152 patients experienced HFS (30.9%), 39.5% with the new ointment and 22.4% in th

68 e compared to controls when animals were fed HFS diets.

69 was increased on the surface of fibroblasts HFS-13 compared with the mock-infected sample of the sam

70 Following HFS, the EEG shifted to a continuous large-amplitude, sl

71 Following HFS, the ongoing firing rate and stimulus-evoked (brush,

72 e loop, rendezvous in the striatum, and, for HFS, positively overlap (reinforcement), thus causing la

73 identical, as were adverse events except for HFS.

74 However, ideal materials for HFS not only require a large transverse thermopower but

75 lation frequency and becomes significant for HFS.

76 cally stimulated with either high frequency (HFS; 6x10 repetitions of 3 s-bursts at 100 Hz to mimic r

77 Islets from HFS+Resv monkeys were morphologically similar to SD.

78 pattern regularization would originate from HFS.

79 Selective Fil VGCC depression results from HFS-induced mGluR7 activation leading to persistent P/Q-

80 rade 1 was comparable, but time to any-grade HFS was significantly longer in the urea group (P = .03)

81 ence and time to onset of grade 2 or greater HFS in patients receiving pyridoxine vs placebo and to i

82 itudes, and unlike YS, COC, and SHAM groups, HFS in the IL induced persistent LTP in the NAc shell.

83 ichlorosilane (TFS) or hexyltrichlorosilane (HFS) assembled on surfaces of the arrays served as therm

84 m the short-term potentiating effect of HFS (HFS/LFS), there was an initial transient (<10 min) enhan

85 omparable between treatment arms except HFSR/HFS (44% v 14%).

86 foot skin reaction/hand- foot syndrome (HFSR/HFS; 90% v 66%); grade 3 to 4 toxicities were comparable

87 he time to onset (days) of grade 2 or higher HFS and identification of biomarkers predictive of HFS,

88 could prevent the onset of grade 2 or higher HFS in 210 patients scheduled to receive single-agent ca

89 point was the incidence of grade 2 or higher HFS in patients receiving pyridoxine.

90 [26-82] years; 162 women) grade 2 or higher HFS occurred in 33 patients (31.4%) in the pyridoxine ar

91 he study on development of grade 2 or higher HFS or cessation of capecitabine.

92 he median time to onset of grade 2 or higher HFS was not reached in both arms.

93 significant predictors of grade 2 or higher HFS.

94 ted with increased risk of grade 2 or higher HFS.

95 vent or delay the onset of grade 2 or higher HFS.

96 However, HFS delivered to MF synapses on cells loaded with the PK

97 vitro and abolished the occurrence of AF in HFS mice.

98 BR in HFS was also measured before and after BoNT.

99 ny-forming units/mL below the day 0 level in HFS-Mab.

100 es associated with efficacy were the same in HFS-TB as in patients for all drugs examined.

101 o-Ps by absorbing those HFS photons (induced HFS transitions).

102 However, following mGluR7 internalization HFS produces presynaptic LTP.

103 iate high frequency stimulation-induced LTP (HFS-LTP) in mice over 2-months of age, which involves ca

104 INTERPRETATION: MLR-HFS can improve disordered locomotor function in a roden

105 f high-frequency stimulation of the MLR (MLR-HFS) on gait impairment in a rodent stroke model.

106 Simultaneous to the onset of MLR-HFS, a significantly higher walking speed and improvemen

107 ter experimental stroke with and without MLR-HFS.

108 2 weeks post-adult stress after BLA and mPFC HFS, respectively.

109 of antidiabetic (NHS) or anticoagulant (NHS, HFS) medications and cessation of antihypertensive medic

110 en were fed for 1 month with HFS + 5% nopal (HFS + N).

111 s DNA double-strand breaks (DSBs) in normal (HFS) and cancer (LNCaP, A549) cells.

112 rning-induced synaptic potentiation occluded HFS-induced LTP, we conclude that inhibitory avoidance t

113 period immediately after the application of HFS (the induction phase of LTP).

114 Capecitabine dose reductions because of HFS were less frequent in the diclofenac group (3.8%) th

115 ods were used to examine the consequences of HFS versus sham HFS conditioning on individual wide-dyna

116 s inhibitor actinomycin-D before delivery of HFS to MF input also caused a rapid decay of MF potentia

117 Consistent with these data, delivery of HFS to MFs synapsing onto L-M interneurons loaded with P

118 y end points included time to development of HFS greater than grade 1, evaluation of capecitabine dos

119 gel for 12 weeks or until the development of HFS, whichever occurred earlier.

120 y from the short-term potentiating effect of HFS (HFS/LFS), there was an initial transient (<10 min)

121 Pe and GPi underlie the beneficial effect of HFS in the STN in Parkinson's disease and further suppor

122 h and further improving the effectiveness of HFS in robotic surgical applications and tasks such as t

123 EA may be the key factor in the emergence of HFS-induced striatal LTD.

124 to show a 20% reduction of the incidence of HFS with the new ointment.

125 domains of GRF1 are key to the induction of HFS-LTP by GRF proteins.

126 was manipulated to match baseline intakes of HFS.

127 r of Ras proteins, causes a specific loss of HFS-LTP in the medium spiny neurons in the direct pathwa

128 theses suggest that the therapeutic merit of HFS stems from increasing the regularity of the firing p

129 naptic pools of BDNF can act within 2 min of HFS to support the formation of a postsynaptic form of L

130 gavage from week 6 to week 14 (end-point) of HFS feeding.

131 d identification of biomarkers predictive of HFS, including baseline folate and vitamin B12 levels, a

132 ebo and to identify biomarkers predictive of HFS.

133 folate levels are independent predictors of HFS.

134 ince 2011, with urea cream for prevention of HFS in patients treated with capecitabine.

135 The primary end point was prevention of HFS of any grade within 6 weeks of treatment as indicate

136 g might also occur if any external source of HFS frequencies is nearby, thus many p-Ps convert to o-P

137 id signaling, properties similar to those of HFS-LTD.

138 On HFS diets, on the other hand, all the subcongenic mice h

139 o had significantly increased food intake on HFS diets.

140 ozygous control mice were fed either chow or HFS diets, and their post-mortem fat pads were weighed.

141 burst or high-frequency stimulation (TBS or HFS).

142 (SMB), HFS technique outperformed all other HFS techniques.

143 gar diet in combination with either placebo (HFS) or resveratrol (HFS+Resv) for 24 months, and pancre

144 b component scores from baseline to the post-HFS assessments were compared between groups.

145 cal for this facilitation because presenting HFS immediately after the blink did not alter subsequent

146 ical keratolytic agent (ULABTKA) may prevent HFS.

147 s superior to the new ointment at preventing HFS over the first 6 weeks of treatment with capecitabin

148 e efficacy of a ULABTKA cream for preventing HFS symptoms in patients receiving capecitabine.

149 Celecoxib prevents HFS by inhibiting cyclooxygenase-2 (COX-2) that is upreg

150 urons, because stimulation of the previously HFS-treated SO evoked altered blinks in both eyelids, wh

151 r depression, depending on whether a priming HFS train has been applied.

152 with a high frequency stimulation protocol (HFS-LTP) in the dorsal striatum, but also for its revers

153 on with either placebo (HFS) or resveratrol (HFS+Resv) for 24 months, and pancreata were examined bef

154 The same HFS failed to evoke visible side effects such as steppin

155 ynaptic potentiation in response to the same HFS that induces LTD in naive slices.

156 ylbenzeneacetic acid] (100 microm), the same HFS that induces MF LTP in naive slices triggered NMDAR-

157 subjected to hypocaloric feeding schedules (HFS) exhibit compulsive behavioral responses involving f

158 entification tool, Hybrid Feature Screening (HFS), to construct a candidate feature set for downstrea

159 sts of two steps: human framework selection (HFS) and specificity-determining residue optimization (S

160 A Heat Flux Sensor (HFS) facilitates the visualization of heat flow, unlike

161 d point was the incidence of moderate/severe HFS symptoms in the first treatment cycle, based on the

162 percentage of patients with moderate/severe HFS symptoms was not different between groups, being 13.

163 Sham HFS did not alter EEG activity.

164 examine the consequences of HFS versus sham HFS conditioning on individual wide-dynamic range thalam

165 r, DKO mice showed normal LTP after a single HFS at 200 Hz or two compressed HFSs at 100 Hz.

166 m relevancy minimum redundancy-Boruta (SMB), HFS technique outperformed all other HFS techniques.

167 00-700 kHz) and high-frequency sonophoresis (HFS, >1 MHz).

168 ng those with a history of hemifacial spasm (HFS), facial palsy, traumatic brain injury, intracranial

169 m a group of patients with hemifacial spasm (HFS).

170 s spontaneously by emitting hyperfine split (HFS) photons, which also drops 3gamma/2gamma ratio hence

171 One spring ('HFS') exhibited statistically significant, coupled micro

172 High-frequency deep brain stimulation (HFS) is clinically recognized to treat parkinsonian move

173 Brief high-frequency EC stimulation (HFS; 100 Hz, 1 sec) induced APV-sensitive short-term pot

174 TP by high-frequency electrical stimulation (HFS) in rat hippocampal slices.

175 ns by high-frequency electrical stimulation (HFS) of the subthalamic nucleus (STN), we investigated t

176 posure to visual high-frequency stimulation (HFS) ( approximately 8.8 Hz, 2 minutes) designed to indu

177 Ac core pathway, high-frequency stimulation (HFS) had no effect on eLFP in VNS-treated animals, signi

178 f LTP induced by high frequency stimulation (HFS) in hippocampal slices.

179 sts also blocked high-frequency stimulation (HFS) induced LTP formation in the BLA.

180 High-frequency stimulation (HFS) of BLA and mPFC depressed evoked spike probability

181 erved that brief high frequency stimulation (HFS) of cortical afferents innervating the dorsolateral

182 emonstrated that high-frequency stimulation (HFS) of cortical inputs induced long-term depression (LT

183 cacy produced by high-frequency stimulation (HFS) of glutamatergic afferents to the rat dorsolateral

184 High-frequency stimulation (HFS) of neocortical afferents produced a rapid and stabl

185 High frequency stimulation (HFS) of nociceptors produced a persistent increase in sy

186 hat results from high-frequency stimulation (HFS) of the afferent pathway.

187 ASIC-1as during high-frequency stimulation (HFS) of the presynaptic nerve terminal leads to a PcTx1-

188 eparately during high frequency stimulation (HFS) of the STN (16 patients, 31 sides) and following dr

189 High frequency stimulation (HFS) of the STN improved treadmill walking immediately a

190 n the STN during high-frequency stimulation (HFS) of the STN.

191 tudy showed that high-frequency stimulation (HFS) of the subthalamic nucleus (STN) improved treadmill

192 ) after a single high-frequency stimulation (HFS) or two spaced HFSs at 100 Hz.

193 singly, the same high-frequency stimulation (HFS) protocol induces presynaptically expressed LTP and

194 the same type of high-frequency stimulation (HFS) that induces LTP at MF synapses on pyramidal cells.

195 Moreover, high-frequency stimulation (HFS) that typically triggers asynchronous release and re

196 ctivation during high-frequency stimulation (HFS) triggers presynaptic LTD due to persistent P/Q-type

197 and administered high-frequency stimulation (HFS) via implanted electrodes at the subthalamic nucleus

198 d, 90 min later, high-frequency stimulation (HFS) was applied to the medial perforant path.

199 in responses to high-frequency stimulation (HFS), as well as in long-term potentiation (LTP).

200 (LTD) following high-frequency stimulation (HFS), in contrast to MF-pyramid (PYR) synapses, where lo

201 cell soma during high-frequency stimulation (HFS), intracellular injections of the Ca(2+) chelator BA

202 larization or by high-frequency stimulation (HFS), known to induce synapse formation, raises the leve

203 re induced using high frequency stimulation (HFS), versus theta burst stimulation (TBS).

204 loss, transforms high-frequency stimulation (HFS)-induced long-term potentiation (LTP) into long-term

205 not cOA blocked high frequency stimulation (HFS)-LTP.

206 mpal area CA1 by high-frequency stimulation (HFS).

207 nsmission during high-frequency stimulation (HFS).

208 tigue induced by high-frequency stimulation (HFS).

209 he VOCC, we used high-frequency stimulation (HFS).

210 mulation but not high-frequency stimulation (HFS).

211 s LTD induced by high-frequency stimulation (HFS-LTD) and requires elevated postsynaptic calcium and

212 by high-frequency sciatic nerve stimulation (HFS) at intensities recruiting C-fibers.

213 pses by high-frequency synaptic stimulation (HFS).

214 ns of low-intensity, high-frequency stimuli (HFS) to the supraorbital branch of the trigeminal nerve

215 trates that a brief high frequency stimulus (HFS) train can induce a switch in the direction of the e

216 STN HFS inhibited key brain regions, including the substanti

217 STN HFS prevented the re-escalation of heroin intake after a

218 stimulation of the subthalamic nucleus (STN HFS) for heroin addiction.

219 us (STN), we investigated the effects of STN HFS on neuronal activity of the internal and external se

220 to examine the therapeutic effects that STN HFS may have on relapse in humans with heroin addiction.

221 ired to explore the circuitry engaged by STN-HFS, as well as other potential stimulation sites.

222 omotor activity, which was unaffected by STN-HFS.

223 teraction deficits were not corrected by STN-HFS.

224 d electrodes at the subthalamic nucleus (STN-HFS).

225 Our data show STN-HFS suppresses excessive self-grooming in two autism-lik

226 We found that STN-HFS significantly suppressed excessive self-grooming in

227 lteration of the S1' subsite of stromelysin (HFS:L214Y/V215A) to resemble matrilysin increases activi

228 e and protein substrates, while stromelysin (HFS) has a broader specificity.

229 if any information exists as to whether such HFS conditioning that produces spinal LTP affects sensor

230 pellets high in content of fat and sucrose (HFS), pure sucrose, and pure fat (Crisco), during the fi

231 rbated upon feeding a high fat-high sucrose (HFS) diet.

232 rodents were fed a high-fat, refined-sugar (HFS) diet, insulin resistance developed along with aspec

233 Hand-foot syndrome (HFS) is a common adverse effect of capecitabine treatmen

234 Hand-foot syndrome (HFS) is a dose-limiting side effect of capecitabine.

235 Hand-foot syndrome (HFS) is a dose-limiting toxicity of capecitabine for whi

236 Hand-foot syndrome (HFS) is a frequently occurring adverse event associated

237 hyperbilirubinemia, and hand foot syndrome (HFS) on the troxacitabine plus ara-C combination.

238 continuous process for High Fructose Syrup (HFS) production was established with the adsorbed GICA u

239 We then used the hollow fiber system (HFS) model of intracellular tuberculosis to identify opt

240 ew of literature on the hollow fiber system (HFS) model, murine model, and guinea pig model of tuberc

241 persisted over a longer period of time than HFS.

242 These data support the concept that HFS conditioning of the sciatic nerve, which leads to sp

243 Here, we demonstrate that HFS-induced LTP at these MF-interneuron synapses require

244 Indeed we report that HFS persistently depresses voltage-gated calcium channel

245 We recently showed that HFS-induced striatal LTD requires retrograde signalling

246 The data suggest that HFS produce LTP- and long-term depression (LTD)-like eff

247 The HFS spectrum lies in a broad range of microwaves, from 0

248 The HFS step involved generation of a library of m836 antige

249 The HFS-TB model is highly accurate at forecasting optimal d

250 The HFS-TB model is highly accurate at identifying optimal d

251 The HFS-TB model offers the ability to perform PK/PD studies

252 In CD8 + splenic T cells from the HFS mice, glycolysis/basal respiration ratio was signifi

253 s that utilized quantitative output from the HFS-TB.

254 a and increased intestinal occludin-1 in the HFS + N group.

255 on each of these zones was then used in the HFS model, with observed half-lives of 4.08 +/- 0.66 for

256 Imipenem demonstrated biologic effect in the HFS-Mab and in patients.

257 inamide, and ethambutol were the same in the HFS-TB as in patients.

258 mplex with IL-13 were obtained for m836, the HFS variant chosen for SDRO, and one of the highest-affi

259 As in aged wild-type mice, the HFS-LTP in the young adult CaMKII(DeltaSNO) mice require

260 executed an evidence-based evaluation of the HFS-TB for predictive accuracy.

261 ical studies, the predictive accuracy of the HFS-TB was 94.4% (95% CI, 84.3%-99.9%), and bias was 1.8

262 However, the predictive accuracy of the HFS-TB, or any other nonclinical DDT such as an animal m

263 lutamic acid (EGLU; 50 microM) prevented the HFS-dependent switch from synaptic facilitation to depre

264 e sampling from the same unit over time, the HFS-TB vastly improves statistical power and facilitates

265 the affinity up to 100-fold compared to the HFS antibody.

266 greater visual steady state responses to the HFS predicted greater N1b potentiation in HCs but not in

267 These HFS-induced enhancements lasted throughout the recording

268 many p-Ps convert to o-Ps by absorbing those HFS photons (induced HFS transitions).

269 the induction of LTP by TBS, as compared to HFS, may be responsible for this resistance of TBS-induc

270 receptors is the only factor contributing to HFS-induced LTP.

271 All clinical studies were published prior to HFS-TB experiments.

272 e to the postnatal switch in the response to HFS.

273 hypothalamic and neuroendocrine responses to HFS throughout the light-dark cycle suggests uncoupling

274 NF potentiation of the synaptic responses to HFS was unaltered.

275 BDNF effect on PPF and synaptic responses to HFS, suggesting that BDNF regulates neurotransmitter rel

276 ute after HFS, without reducing responses to HFS.

277 o impaired LTP but not synaptic responses to HFS.

278 ion of caloric loading in B6 mice subject to HFS, characterized by increased meal size and duration,

279 and caloric loading of B6 mice subjected to HFS.

280 Time to HFS greater than grade 1 was comparable, but time to any

281 o hollow fiber system model of tuberculosis (HFS-TB) is able to recapitulate concentration-time profi

282 e hollow fiber system model of tuberculosis (HFS-TB) is designed to perform pharmacokinetics/pharmaco

283 e hollow fiber system model of tuberculosis (HFS-TB), in tandem with Monte Carlo experiments, represe

284 o hollow fiber system model of tuberculosis (HFS-TB), in tandem with Monte Carlo experiments, was int

285 epend on postsynaptic depolarization, unlike HFS-induced LTD.

286 By using HFS films, it was possible to selectively deposit two so

287 diet with 5% sucrose in the drinking water (HFS) for 7 months and then were fed for 1 month with HFS

288 by pharmacological inhibition, enabling weak HFS to induce L-LTP.

289 aF/F0 x ms(-1); P = 0.0076 in 2- and 12-week HFS mice, respectively).

290 DLTs were HFS, rash, and mucositis on the troxacitabine plus idaru

291 When HFS occurred concurrently with reflex blinks, the proced

292 When HFS preceded the blink, however, this treatment suppress

293 Whereas HFS most often induces striatal long-term potentiation (

294 n but increased UCP3 mRNA 11.7-fold, whereas HFS had no significant effect on UCP3 mRNA.

295 ng glucagon and glucagon-like peptide 1 with HFS diets.

296 glutamate receptors as induction of LTP with HFS and caused a spatially restricted increase in the am

297 7 months and then were fed for 1 month with HFS + 5% nopal (HFS + N).

298 BoNT left BR in patients with HFS unchanged.

299 milder severity in contrast to patients with HFS.

300 pplication of Zn(2+) (50-100 microm) without HFS induced a long-lasting potentiation of synaptic tran