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

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

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

6 HFS significantly increased myofibrillar and sarcoplasmi

7 HFS toxicity grade (Common Terminology Criteria for Adve

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

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

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

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

12 Interestingly, Fz5CRD abolishes HFS-induced synapse formation.

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

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

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

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

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

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

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

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

21 Patients completed an HFS diary (HFSD) daily.

22 om an ancient autoproteolytic domain with an HFS motif.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

42 During HFS, significant skin resistance reductions were accompa

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

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

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

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

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

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

49 dopaminergic activation which remains during HFS.

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

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

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

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

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

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

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

57 identical, as were adverse events except for HFS.

58 lation frequency and becomes significant for HFS.

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

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

61 pattern regularization would originate from HFS.

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

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

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

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

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

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

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

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

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

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

72 [26-82] years; 162 women) grade 2 or higher HFS occurred in 33 patients (31.4%) in the pyridoxine ar

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

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

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

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

77 significant predictors of grade 2 or higher HFS.

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

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

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

81 However, following mGluR7 internalization HFS produces presynaptic LTP.

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

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

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

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

86 ter experimental stroke with and without MLR-HFS.

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

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

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

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

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

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

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

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

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

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

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

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

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

100 was manipulated to match baseline intakes of HFS.

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

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

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

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

105 ebo and to identify biomarkers predictive of HFS.

106 folate levels are independent predictors of HFS.

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

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

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

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

111 o had significantly increased food intake on HFS diets.

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

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

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

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

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

117 ical keratolytic agent (ULABTKA) may prevent HFS.

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

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

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

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

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

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

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

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

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

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

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

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

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

131 Sham HFS did not alter EEG activity.

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

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

134 00-700 kHz) and high-frequency sonophoresis (HFS, >1 MHz).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 nsmission during high-frequency stimulation (HFS).

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

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

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

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

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

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

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

172 STN HFS inhibited key brain regions, including the substanti

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

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

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

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

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

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

179 teraction deficits were not corrected by STN-HFS.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 persisted over a longer period of time than HFS.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 These HFS-induced enhancements lasted throughout the recording

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

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

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

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

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

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

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

225 ute after HFS, without reducing responses to HFS.

226 o impaired LTP but not synaptic responses to HFS.

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

228 and caloric loading of B6 mice subjected to HFS.

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

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

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

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

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

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

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

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

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

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

239 When HFS occurred concurrently with reflex blinks, the proced

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

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

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

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

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

245 7 months and then were fed for 1 month with HFS + 5% nopal (HFS + N).

246 BoNT left BR in patients with HFS unchanged.

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