ライフサイエンスコーパス: rise time

1 taCD slowed the wave speed and prolonged the rise time.

2 ased mIPSC amplitude and slowed mIPSC 19-90% rise time.

3 ependent slowing of the macroscopic response rise time.

4 ha4 nAChR subunit was correlated with a slow rise time.

5 ithin a rep-mode was not correlated with its rise time.

6 dity range from 0.5%RH to 85%RH with < 1 sec rise time.

7 were identified based on their amplitude and rise time.

8 nd 20 ms did not vary significantly with the rise time.

9 wed by a second depolarization with a faster rise time.

10 elation between the EPSP half-width and EPSP rise time.

11 : grip strength, standing balance, and chair-rise time.

12 contrasted tone stimuli of 15 ms vs. 185 ms rise time.

13 teers passively listened to tones varying in rise time.

14 cant differences in their mean amplitude and rise times.

15 PSCs at silent synapses; LTP shortened their rise times.

16 little to no effect on current amplitudes or rise times.

17 to elicit action potentials, but with slower rise times.

18 n those produced by ramp stimuli with longer rise times.

19 an increase in miniature EPSC amplitudes and rise times.

20 found in mean amplitude (61 vs. 65 pA), mean rise time (0.58 vs. 0.61 ms), or the first time constant

21 cs of the cholinergic mEPSCs include a rapid rise time (0.6 msec) and decay (tau = 2 msec).

22 lpha7-nAChR responses were kinetically fast (rise time, 0.32 +/- 0.02 ms; decay time, 1.66 +/- 0.18 m

23 ar (mean amplitude, 981 +/- 433 microV; mean rise time, 0.68 +/- 0.18 ms; mean duration, 4.7 +/- 1.7

24 8 +/- 103 pA, n = 7) and kinetically faster (rise time, 0.8 +/- 0.1 ms; decay 11.2 +/- 0.9 ms, n = 7)

25 ) were slightly longer than in basket cells (rise times, 0.4-1.6 ms; half-widths, 2.2-9.7 ms).

26 displayed an approximately threefold slower rise time (1.15 +/- 0.12 ms), 57 % smaller amplitude (29

27 out patches activated currents with a slower rise time (1.5 ms) than those of wild-type channels (0.2

28 and found to display a wide range of 10-90% rise times (1-34 ms), not correlated with amplitude (0.2

29 y isolated alpha3-nAChR responses were slow (rise time, 1.28 +/- 0.35 ms; decay time, 6.71 +/- 1.46 m

30 ring right atrial and endocardial pacing, AP rise time (10%-90% of upstroke) decreased by approximate

31 cell) elicited short-latency IPSPs with fast rise time (10-90%; 2.59 +/- 1.02 ms) and short duration

32 peak amplitude of 1005 +/- 518 microV, fast rise times (10-90%; 0.67 +/- 0.25 ms) and were of short

33 ry potentials that are characterized by fast rise-times (10-90% rise-times < or = 0.75 ms); they are

34 vating currents in response to 5-HT (10-90 % rise time, 103 ms; EC50, 2.34 microM; Hill coefficient,

35 ivation time course (mean +/- S.E.M. 10-90 % rise time 12.5 +/- 1.6 ms; n = 9 patches) for 100 microM

36 Furthermore, the shortest rise time (20-80% of the receptor current response to gl

37 Therefore, the shortest rise time (20-80% of the receptor current response) or t

38 pening rate constants obtained, the shortest rise time (20-80% of the receptor current response) or t

39 The observed shortest rise time (20-80% of the receptor current response), i.e

40 electrical stimulation at 0.1 Hz were rapid (rise time = 49 +/- 2 ms), while the decreases in [Ca(2+)

41 ders did not differ in the percent change of rise time (5.09 +/- 49.13 vs 6.24 +/- 48.06; P = .93) an

42 A, s.e.m., n = 8) and slowest IPSCs (10-90 % rise time, 6.2 +/- 0.6 ms; decay, 20.8 +/- 1.7 ms, n = 8

43 of ~100%, a linear dynamic range of 80 dB, a rise time 60 micros and the ability to measure ac signal

44 mm HEPES at pH 7.4 resulted in faster mIPSC rise time, a 37% reduction in amplitude, and a 48% reduc

45 ent with alkalinization, resulting in faster rise time, a 39% reduction in amplitude, and a 51% reduc

46 ntrol and epileptic mice had similar average rise times, amplitudes, charge transfers, and decay time

47 Action potential (AP) rise time, an indicator of myocardial excitability, is i

48 esolved measurements showed a sub-picosecond rise time and a recovery time of about 66 ps, which sugg

49 ciceptors, decreased AP duration at base, AP rise time and AP fall time, and increased maximum rates

50 showed a similar reciprocal relation between rise time and Ca2+ flux, seen in the initial Ca2+ spike

51 ABT-089 were characterized by faster signal rise time and decay rate.

52 niature IPSCs (mIPSCs) without affecting the rise time and decay time constants.

53 At the same time, the rise time and decay time of sEPSCs significantly decreas

54 rol with tau approximately 400 msec, whereas rise time and decay time were not altered significantly.

55 antly increased at P12-13; (3) the kinetics (rise time and decay time) of both mEPSCs and mIPSCs acce

56 naptic endings is consistent with the faster rise time and earlier reversal to polarizing currents of

57 on (P2X7-2NbetadelCcys) restored the current rise time and ethidium uptake to WT levels.

58 out significantly affecting their amplitude, rise time and frequency.

59 cidification (from pH 7.4 to 6.8) slowed the rise time and increased current amplitude and total char

60 dose-dependent way the initial slope, 20-80% rise time and measured desensitization rate of the curre

61 PSCs showed no correlation in amplitude and rise time and occurred at relatively low frequencies of

62 periment 2 explored the possible confound of rise time and overall stimulus intensity change (tones w

63 Infiniti had the fastest vacuum rise time and Stellaris had the slowest.

64 hat increasing pH from 7.4 to 8.0 sped mIPSC rise time and suppressed both amplitude of the current a

65 From P0 to P14, both the rise time and the decay time constants were significantl

66 each their maximum amplitude is known as the rise time and this variable is an important perceptual c

67 ndence of activation characterized by slower rise times and a hyperpolarized conductance-voltage rela

68 uminous supernovae that show relatively fast rise times and blue colours, which are incompatible with

69 This study examined AP rise times and conduction velocity as the depolarizing w

70 coil that produces large gradients and short rise times and connects to their clinical system.

71 The variance of 10-90 % rise times and decay kinetics between IPSCs decreased wi

72 The variance of 10-90% rise times and decay kinetics between IPSCs decreased wi

73 These events had slower rise times and decay times than sparks and were more het

74 was also supported by the histograms of the rise times and half-decay times, which revealed modes at

75 synaptic inputs from ADN to MSNs have faster rise times and shorter durations than those to PSNs, sug

76 field pulses induced waves with fast calcium rise times and slow decays, which nucleated in the lamel

77 Multiphasic EPSCs exhibited slower rise times and smaller amplitudes than monophasic EPSCs.

78 k rise times or in the joint distribution of rise times and spatial widths.

79 compound nerve action potentials, latencies, rise times and stimulus thresholds from isolated desheat

80 etween the width of the action potential and rise times and widths at half-amplitude of EPSPs and IPS

81 ynaptic KARs exhibit characteristically slow rise-time and decay kinetics.

82 - 13.1 to 12.8 +/- 3.0 ms at 0 mV for 10-90% rise times) and a 10-mV hyperpolarizing shift (at 0 mV)

83 abilities of connection, amplitude, latency, rise time, and decay time constant of the unitary EPSC w

84 tic properties of the unitary IPSC: latency, rise time, and decay time constant.

85 The amplitude, rise time, and decay time of SSCs were not affected, ind

86 Area, rise time, and duration of these potentials decreased by

87 442 nm illumination, including photocurrent, rise time, and fall time.

88 hese embryos had a smaller amplitude, slower rise time, and slower decay when compared with wild-type

89 2 nAChR subunit was correlated with a medium rise time, and the alpha4 nAChR subunit was correlated w

90 (m gate), the action potentials had a sharp rise time; and for power-law inactivation of the sodium

91 alpha2beta3gamma2 receptors were very fast (rise time approximately 2 ms), whereas events mediated b

92 y alpha6beta3delta receptors were very slow (rise time approximately 20 ms).

93 locity approximately 66 micron/s and average rise time approximately 68 ms) are consistent with a wav

94 e agonist-evoked currents developed rapidly (rise time, approximately 10-25 s), desensitized slowly (

95 The rise times, areas, half-widths, and decay times of sEPSC

96 ntial of -53 +/- 19 mV and a fast component (rise time as fast as 0.85 ms) with a reversal potential

97 should encourage regularity in bedtimes and rise times as a first step in treatment, and carefully m

98 EPSPs underlying each Gaussian and the EPSP rise time but there was a positive correlation between t

99 al cells (PCs) with unchanged amplitudes and rise times, but significantly prolonged decays.

100 5 nm in a stepwise fashion in which the step rise-times can be as long as 80 msec.

101 ast occlusion break surge and similar vacuum rise times compared with the other systems tested.

102 using single values of parameters (e.g. EPSP rise time) consistent with those in the literature.

103 er amplitude events had significantly faster rise times, consistent with their site of generation bei

104 so a close temporal relationship between the rise (time constant approximately 25 s) and fall (time c

105 e was also quicker for bursting stimulation (rise time constant = 1.98 +/- 0.09 s vs. 2.35 +/- 0.20 s

106 SC-like current injections (10-100 pA, 10 ms rise time constant, 5 s decay time constant) in the pres

107 The average values of the rising time constants in CH3SO3- and SO42- were similar

108 Such an order of magnitude difference in rise time could not be attributed to the minute differen

109 e decay of sIPSCs matched for amplitudes and rise times could vary over 10-fold in a given interneuro

110 he kinetic peak parameters including shorter rise time, decay time, and half-width as compared to a b

111 s the spatio-temporal properties (amplitude, rise-time, decay kinetics, and spatial spread) of [Ca2+]

112 IL-17A levels, which rose time-dependently in plasma after CLP, were not affe

113 re insensitive to system filtering, response rise time, desensitization rate and measured variation i

114 erneurons that produce small IPSPs with fast rise-times during quiet sleep are also responsible for t

115 he kinetic parameters (i.e., peak amplitude, rise time, fall time) of Ca2+ sparks were calculated for

116 The fluorescence rise times for both mutants were comparable to the contr

117 The rise-times for the rate of ocular elongation and choroid

118 ease in the yield of M and a decrease in its rise time from 200 &mgr;s to 75 &mgr;s with pK(a) 9.4.

119 cm H2O), using a broad range of inspiratory rise times from 0.05 to 0.4 s.

120 or EPSCs that showed a constant latency and rise time, graded response to increased stimulus intensi

121 rger active sleep-specific IPSPs with 10-90% rise-times > or = 1.00 ms and amplitudes that are intege

122 current and resistance, offset voltage, and rise time have improved by a remarkable 3-4 orders of ma

123 sment demonstrated prolonged field potential rise time in the ARVC-hiPSC-CMs.

124 hydroxyaspartic acid (THA) or Li+, the mEPSC rise time in the presence of KYN was slowed further, ind

125 in bacteriorhodopsin (bR) is found to have a rise time in the submicrosecond time regime and to relax

126 EPSP 10-90 % rise times in bistratified cells (0.7-2 ms) and their wi

127 elicits GABA(A) receptor currents with rapid rise times in hippocampal OPCs.

128 is demonstrated in the distribution of spark rise times in the presence of the channel activator caff

129 arger mEPSCs were not accompanied by briefer rise times, inconsistent with the prediction by, and thu

130 urrent amplitude was reduced and the current rise time increased when choline was co-applied with car

131 I(Nalgt) is decreased by intensity, whereas rise time is increased by duration.

132 For events with 10-90% rise times less than 0.9 ms, no significant differences

133 are characterized by fast rise-times (10-90% rise-times < or = 0.75 ms); they are present in high-gai

134 sion is bipolar, occurs in vacuum, has rapid rise time (<5 ms), and persists for >10 h.

135 Fast activation rise times (< 0.5 ms), hyperpolarized half-activation po

136 Evoked EPSCs had rapid rise times (< 1 s) and decayed monoexponentially (tau =

137 EJPs had short latencies (< 30 ms) and fast rise times (< 60 ms).

138 The 1 N ramp stimuli with a rise time of < or = 20 ms consistently evoked a single,

139 strengths up to 18 G cm(-1) with a gradient rise time of </=295 mus.

140 t at initiation of approximately 2 microm, a rise time of <15 ms, duration <100 ms, and amplitudes of

141 ately 395 nm) leads to green emission with a rise time of 10-15 ps, due to excited-state proton trans

142 maximum gradient amplitude of 45 mT/m and a rise time of 150 musec along all three major axes was us

143 us depolarizations had a latency of 1.2 s, a rise time of 2.5 s, and decayed with an exponential time

144 NR2C channels, which activated with a 10-90% rise time of 3.9 +/- 0.4 ms, faster than other NR2-conta

145 ve oxygen species (ROS) with an average half-rise time of 33 sec.

146 Fast rising mIPSCs (mIPSCFR) had a 10-90 % rise time of 410 +/- 50 micros, an amplitude of 68 +/- 6

147 ponents of synaptic drive: a slow component (rise time of 9.6 +/- 2.1 ms) with a reversal potential o

148 The rise time of [Ca(2+)](i) signals in NM neurons did not c

149 ing conditions, averaged mEPSCs had a 10-90% rise time of about 0.3 ms.

150 Additionally, amplitude and rise time of action potentials were reduced compared wit

151 ilibrium affinity of the antagonist, and the rise time of AMPA receptor miniature EPSCs (mEPSCs) was

152 t reasonably rapid response time (10 --> 90% rise time of approximately 1.2 min for a transient event

153 rise from transient depolarizations having a rise time of approximately 10 msec.

154 be used for bipolar temperature jumps with a rise time of approximately 100 microseconds.

155 The practical limit seems to be a rise time of approximately 20 microseconds.

156 to quantify occlusion break surge and vacuum rise time of current phacoemulsification systems used in

157 uthenium oxide (RuOx) NPs as an example, the rise time of current-time transients for NP impacts is c

158 s confers a strong voltage dependence to the rise time of currents.

159 The width, area and rise time of excitatory postsynaptic potentials (EPSPs)

160 We report that the rise time of firing rates of cells in striate and extras

161 lux measured as the reciprocal of the 10-90% rise time of free [Ca2+]i showed a linear correlation wi

162 The frequency, amplitude, and rise time of gamma-aminobutyric acid (GABA)(A) receptor-

163 It is found that each continuum has a rise time of less than 80 ns and a decay time component

164 In addition, the amplitude, duration, and rise time of macroscopic I(Ca)-induced Ca2+ transients a

165 ents increased quantal size the mean 20-80 % rise time of MEPPs recorded with an extracellular electr

166 The amplitude and rise time of miniature endplate potentials were also inc

167 However, the frequency, amplitude, and rise time of miniature IPSCs were normal.

168 at vertebrate central synapses, because the rise time of mPSCs was constant regardless of the amplit

169 ely 12 ms, as compared to 19 ms for the mean rise time of puffs, and their spatial extent is approxim

170 The effect of agonist concentration on the rise time of the current showed that the extracellular N

171 ate of pore expansion appears to control the rise time of the flux to its maximum value.

172 e and back to the ground state, and that the rise time of the K590 intermediate is determined by vibr

173 n channels closure in the dark, shortens the rise time of the light response directly, and accelerate

174 The rise time of the PPII signals is approximately 250 ns, c

175 oltage-activated channels that shortened the rise time of the receptor potential and (2) some calyces

176 Also under both conditions, the rise time of the response to intense light was slower by

177 e bundle's initial position and the size and rise time of the stimulus; the twitch was largest over t

178 ated the effects of KYN on the amplitude and rise time of the synaptic responses when driven by gluta

179 The rise time of V(m) determines the required duration of a

180 on counting from a high speed photodetector (rise time of ~1 ns) and applied to remove ringing distor

181 a1beta1gamma2 receptors (reflected in 10-90% rise times of 0.5 versus 1.0 ms, respectively), and deac

182 cerebellar molecular layer interneurons with rise times of 2 ms, comparable to flash duration.

183 muM (n = 6 animals, 3-4 injections each) and rise times of 22 +/- 2 s.

184 The rise times of all of the flares were less than one minut

185 The rise times of EPSPs from different SR axons were not sig

186 The rise times of EPSPs underlying the first, and all, fitte

187 DAR miniature currents (minis) were lost and rise times of NMDAR evoked currents increased in mutant

188 This would suggest that the rise times of synaptic currents through native Ca2+-perm

189 Second, they delayed the rise times of the 5-15 nM (+L264) and 30 nM (S252F) ACh

190 The rise times of the amplitudes of the two components were

191 d TES with no significant differences in the rise times of the evoked EPSPs.

192 Kv1.1 channel resulted in a decrease in the rise times of the macroscopic current (e.g. from 51.7 +/

193 The SQ cage compounds show "rise times" of 700-1000 fs and low anisotropy (~0.1) in

194 Both signals showed a rise time on the order of seconds, similar to those obse

195 nd fall time) in A-fibre neurons and with AP rise time only in positive C-fibre neurons.

196 hypothesis that a short inspiratory pressure rise time or a low PaCO2 level promotes inspiratory lary

197 reversibly, they should not have a preferred rise time or amplitude.

198 taneous Ca(2+) events without changing their rise time or amplitude.

199 oxin without affecting their mean amplitude, rise time or decay time constant.

200 sence of a mode in the distribution of spark rise times or in the joint distribution of rise times an

201 o alter the frequency of occurrence, 10-90 % rise times or peak amplitude of events.

202 to alter the frequency of occurrence, 10-90% rise times or peak amplitude of events.

203 ells without altering event amplitude, area, rise time, or decay.

204 id not change their mean conductance, 10-90% rise time, or frequency of occurrence.

205 The ramp stimuli with shorter rise times produced larger responses than those produced

206 The observed ~450-attosecond step rise time provides an upper limit for the carrier-induce

207 nhibitory responses evoked by 1 N ramps with rise times ranging between 2.5 and 20 ms did not vary si

208 rt ventilation is not altered by inspiratory rise times ranging from 0.05 to 0.4 s or by moderate hyp

209 ffects of tissue depth and pacing rate on AP rise time reduce conduction safety and myocardial excita

210 x detector mechanism sensitive to changes in rise time, relatively independently of sound intensity c

211 of peak enhancement (PE), enhancement curve rise time (RT) and wash-in-rate (WiR).

212 They also had significantly longer rise times (RTs) and fall times (FTs) in all CV ranges.

213 ulation of synapses that had EPSCs with fast rise times, short latencies, and monophasic decays, cons

214 s excited, green fluorescence appears with a rise time shorter than the instrument time resolution (

215 scan line appeared attenuated, whereas their rise times slowed down only slightly.

216 timulus intensity change (tones with shorter rise times sound louder).

217 esponded with a shorter duration and shorter rise-time spike burst as sniff frequency increased, refl

218 The shorter 15 ms rise time stimuli elicited an N1b over central frontal e

219 nificantly greater amplitude than the 185 ms rise time stimuli.

220 ing in a bimodal distribution of the 10-90 % rise times, suggesting two distinct populations of event

221 ons of L-Glu revealed slow voltage-dependent rise-times, suggesting that polyamines additionally bind

222 late current (MEPC) amplitude (A(c)), 20-80% rise time (t(r)), and 90-33% fall-time (t(f)) was determ

223 old faster than GCaMP3 with Ca(2+) decay and rise times, t1/2, of 3.3 ms and 0.9 ms, respectively, ma

224 The different inspiratory pressure rise times tested did not alter the phasic inspiratory a

225 r II/III (distal location) had longer 10-90% rise times than IPSPs evoked from layer V/VI stimulating

226 is concluded that the large IPSPs with slow rise-times that are observed in motoneurons during activ

227 its were individually correlated with a fast rise time, the alpha2 nAChR subunit was correlated with

228 The rise time (time to peak) of fAMPAsEPSCs was 1.5+/-1.05 m

229 he AHPslow in nodose neurons displays a slow rise time to peak (0.3-0.5 s) and a long duration (3-15

230 Rise time to vacuum limits of 400 and 600 mmHg was asses

231 lso observable for both the 15 ms and 185 ms rise time tones when the same stimuli served as deviant

232 We obtained a 20-80% rise time (tr) of approximately 80 micros at 22 degrees

233 nds after the initial rectangular phase) and rise time (tr; the time required for the porated membran

234 ion protocols, including stimuli with finite rise time, trains of ligand or voltage steps, and global

235 The rise time was 1.2 +/- 0.5 ms and the width at half-ampli

236 perometric traces of exocytosis based on the rise time was developed.

237 was greatly delayed (approximately 50 s) and rise time was doubled in comparison to cells not subject

238 Vacuum rise time was evaluated for Infiniti, WhiteStar Signatur

239 amidal cells; no change in IPSC amplitude or rise time was observed.

240 ive stimulus threshold was increased and the rise time was slower in slices from scrapie-infected mic

241 authors found that regularizing bedtimes and rise times was often sufficient to bring about improveme

242 ll stimulus intensity between short and long rise times was perceptually matched.

243 ion required to cause a half-maximum effect (rise-time) was estimated.

244 IPSC latency and rise time were also strongly dependent on the presynapti

245 The spark amplitude and rise time were found to be highly dependent on the conce

246 The depth-dependent changes in rise time were larger at higher pacing rates.

247 The 10-90% rise times were 0.7 and 0.6 ms, respectively.

248 EPSP rise times were consistent with the majority of the syna

249 N1b amplitude differences to the contrastive rise times were still observed, suggesting that N1b may

250 e in a single spark); 4), prolonged Ca spark rise time (which implies that CaMKII either delays RyR c

251 tively, for R305S and R342S) in fluorescence rise times with water as an electron donor.