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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 were identified based on their amplitude and rise time.
7 nd 20 ms did not vary significantly with the rise time.
8 wed by a second depolarization with a faster rise time.
9 elation between the EPSP half-width and EPSP rise time.
10 dity range from 0.5%RH to 85%RH with < 1 sec rise time.
11 e experienced a relatively rapid increase in rise time.
12 : grip strength, standing balance, and chair-rise time.
13 contrasted tone stimuli of 15 ms vs. 185 ms rise time.
14 teers passively listened to tones varying in rise time.
15 cant differences in their mean amplitude and rise times.
16 PSCs at silent synapses; LTP shortened their rise times.
17 little to no effect on current amplitudes or rise times.
18 to elicit action potentials, but with slower rise times.
19 n those produced by ramp stimuli with longer rise times.
20 ast, with lifetimes of 2.5 ns and sub-100 ps rise times.
21 ation of pre-spike feet and slowing of spike rise times.
22 an increase in miniature EPSC amplitudes and rise times.
23 found in mean amplitude (61 vs. 65 pA), mean rise time (0.58 vs. 0.61 ms), or the first time constant
25 lpha7-nAChR responses were kinetically fast (rise time, 0.32 +/- 0.02 ms; decay time, 1.66 +/- 0.18 m
26 ar (mean amplitude, 981 +/- 433 microV; mean rise time, 0.68 +/- 0.18 ms; mean duration, 4.7 +/- 1.7
27 8 +/- 103 pA, n = 7) and kinetically faster (rise time, 0.8 +/- 0.1 ms; decay 11.2 +/- 0.9 ms, n = 7)
29 displayed an approximately threefold slower rise time (1.15 +/- 0.12 ms), 57 % smaller amplitude (29
30 out patches activated currents with a slower rise time (1.5 ms) than those of wild-type channels (0.2
31 and found to display a wide range of 10-90% rise times (1-34 ms), not correlated with amplitude (0.2
32 y isolated alpha3-nAChR responses were slow (rise time, 1.28 +/- 0.35 ms; decay time, 6.71 +/- 1.46 m
33 ring right atrial and endocardial pacing, AP rise time (10%-90% of upstroke) decreased by approximate
34 cell) elicited short-latency IPSPs with fast rise time (10-90%; 2.59 +/- 1.02 ms) and short duration
35 peak amplitude of 1005 +/- 518 microV, fast rise times (10-90%; 0.67 +/- 0.25 ms) and were of short
36 ry potentials that are characterized by fast rise-times (10-90% rise-times < or = 0.75 ms); they are
37 000 shots), repetition rate (> 0.1-Hz), fast rise time (~ 100-ns), and high-energy-delivery efficienc
38 vating currents in response to 5-HT (10-90 % rise time, 103 ms; EC50, 2.34 microM; Hill coefficient,
39 ivation time course (mean +/- S.E.M. 10-90 % rise time 12.5 +/- 1.6 ms; n = 9 patches) for 100 microM
42 pening rate constants obtained, the shortest rise time (20-80% of the receptor current response) or t
44 electrical stimulation at 0.1 Hz were rapid (rise time = 49 +/- 2 ms), while the decreases in [Ca(2+)
45 ders did not differ in the percent change of rise time (5.09 +/- 49.13 vs 6.24 +/- 48.06; P = .93) an
46 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
47 of ~100%, a linear dynamic range of 80 dB, a rise time 60 micros and the ability to measure ac signal
48 mm HEPES at pH 7.4 resulted in faster mIPSC rise time, a 37% reduction in amplitude, and a 48% reduc
49 ent with alkalinization, resulting in faster rise time, a 39% reduction in amplitude, and a 51% reduc
51 nimal pressure transients and submillisecond rise times activate calcium responses in dissociated hum
52 e feature spaces of ring count-amplitude and rise time-amplitude, the size of aggregate has an obviou
53 ntrol and epileptic mice had similar average rise times, amplitudes, charge transfers, and decay time
55 esolved measurements showed a sub-picosecond rise time and a recovery time of about 66 ps, which sugg
56 ciceptors, decreased AP duration at base, AP rise time and AP fall time, and increased maximum rates
57 showed a similar reciprocal relation between rise time and Ca2+ flux, seen in the initial Ca2+ spike
61 rol with tau approximately 400 msec, whereas rise time and decay time were not altered significantly.
62 antly increased at P12-13; (3) the kinetics (rise time and decay time) of both mEPSCs and mIPSCs acce
63 naptic endings is consistent with the faster rise time and earlier reversal to polarizing currents of
65 and response speed (i.e., propagation delay, rise time and fall time) of the optocouplers were charac
68 cidification (from pH 7.4 to 6.8) slowed the rise time and increased current amplitude and total char
69 dose-dependent way the initial slope, 20-80% rise time and measured desensitization rate of the curre
70 PSCs showed no correlation in amplitude and rise time and occurred at relatively low frequencies of
71 periment 2 explored the possible confound of rise time and overall stimulus intensity change (tones w
78 hat increasing pH from 7.4 to 8.0 sped mIPSC rise time and suppressed both amplitude of the current a
80 each their maximum amplitude is known as the rise time and this variable is an important perceptual c
81 ndence of activation characterized by slower rise times and a hyperpolarized conductance-voltage rela
82 uminous supernovae that show relatively fast rise times and blue colours, which are incompatible with
88 was also supported by the histograms of the rise times and half-decay times, which revealed modes at
89 synaptic inputs from ADN to MSNs have faster rise times and shorter durations than those to PSNs, sug
90 field pulses induced waves with fast calcium rise times and slow decays, which nucleated in the lamel
93 compound nerve action potentials, latencies, rise times and stimulus thresholds from isolated desheat
94 etween the width of the action potential and rise times and widths at half-amplitude of EPSPs and IPS
96 - 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)
97 abilities of connection, amplitude, latency, rise time, and decay time constant of the unitary EPSC w
103 hese embryos had a smaller amplitude, slower rise time, and slower decay when compared with wild-type
104 2 nAChR subunit was correlated with a medium rise time, and the alpha4 nAChR subunit was correlated w
105 uM) enhanced sEPSP amplitudes, frequencies, rise-times, and half-widths preferentially in PT neurons
106 (m gate), the action potentials had a sharp rise time; and for power-law inactivation of the sodium
107 alpha2beta3gamma2 receptors were very fast (rise time approximately 2 ms), whereas events mediated b
109 locity approximately 66 micron/s and average rise time approximately 68 ms) are consistent with a wav
110 e agonist-evoked currents developed rapidly (rise time, approximately 10-25 s), desensitized slowly (
112 ntial of -53 +/- 19 mV and a fast component (rise time as fast as 0.85 ms) with a reversal potential
113 should encourage regularity in bedtimes and rise times as a first step in treatment, and carefully m
114 itation-power thresholds, exceptionally long rise time at threshold, and a dominant excited-state abs
115 we found reductions in muscle twitch tension rise times, becoming faster than controls, suggesting th
116 and placebo for the primary outcome of chair rise time (beta = 0.579; 95% CI -1.080-2.239 p = 0.494).
118 EPSPs underlying each Gaussian and the EPSP rise time but there was a positive correlation between t
122 using single values of parameters (e.g. EPSP rise time) consistent with those in the literature.
123 er amplitude events had significantly faster rise times, consistent with their site of generation bei
124 so a close temporal relationship between the rise (time constant approximately 25 s) and fall (time c
125 e was also quicker for bursting stimulation (rise time constant = 1.98 +/- 0.09 s vs. 2.35 +/- 0.20 s
127 SC-like current injections (10-100 pA, 10 ms rise time constant, 5 s decay time constant) in the pres
129 Such an order of magnitude difference in rise time could not be attributed to the minute differen
130 e decay of sIPSCs matched for amplitudes and rise times could vary over 10-fold in a given interneuro
131 he kinetic peak parameters including shorter rise time, decay time, and half-width as compared to a b
132 s the spatio-temporal properties (amplitude, rise-time, decay kinetics, and spatial spread) of [Ca2+]
133 to 100% charge collection efficiency and ns rise times demonstrated, achieving "thin" detector perfo
135 re insensitive to system filtering, response rise time, desensitization rate and measured variation i
136 erneurons that produce small IPSPs with fast rise-times during quiet sleep are also responsible for t
137 he kinetic parameters (i.e., peak amplitude, rise time, fall time) of Ca2+ sparks were calculated for
140 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.
142 or EPSCs that showed a constant latency and rise time, graded response to increased stimulus intensi
143 rger active sleep-specific IPSPs with 10-90% rise-times > or = 1.00 ms and amplitudes that are intege
144 veningness, a preference for later sleep and rise times, has been associated with a number of negativ
145 current and resistance, offset voltage, and rise time have improved by a remarkable 3-4 orders of ma
147 hydroxyaspartic acid (THA) or Li+, the mEPSC rise time in the presence of KYN was slowed further, ind
148 in bacteriorhodopsin (bR) is found to have a rise time in the submicrosecond time regime and to relax
151 is demonstrated in the distribution of spark rise times in the presence of the channel activator caff
152 arger mEPSCs were not accompanied by briefer rise times, inconsistent with the prediction by, and thu
154 urrent amplitude was reduced and the current rise time increased when choline was co-applied with car
156 etric first ground-wave peak due to a longer rise time, larger peak current, weaker decay of electrom
158 are characterized by fast rise-times (10-90% rise-times < or = 0.75 ms); they are present in high-gai
165 t at initiation of approximately 2 microm, a rise time of <15 ms, duration <100 ms, and amplitudes of
166 ately 395 nm) leads to green emission with a rise time of 10-15 ps, due to excited-state proton trans
167 maximum gradient amplitude of 45 mT/m and a rise time of 150 musec along all three major axes was us
168 y (NEP of 82 pW[Formula: see text]) and fast rise time of 17 nanoseconds (setup-limited), among other
169 us depolarizations had a latency of 1.2 s, a rise time of 2.5 s, and decayed with an exponential time
170 NR2C channels, which activated with a 10-90% rise time of 3.9 +/- 0.4 ms, faster than other NR2-conta
172 Fast rising mIPSCs (mIPSCFR) had a 10-90 % rise time of 410 +/- 50 micros, an amplitude of 68 +/- 6
173 ponents of synaptic drive: a slow component (rise time of 9.6 +/- 2.1 ms) with a reversal potential o
177 ilibrium affinity of the antagonist, and the rise time of AMPA receptor miniature EPSCs (mEPSCs) was
178 t reasonably rapid response time (10 --> 90% rise time of approximately 1.2 min for a transient event
182 to quantify occlusion break surge and vacuum rise time of current phacoemulsification systems used in
183 uthenium oxide (RuOx) NPs as an example, the rise time of current-time transients for NP impacts is c
187 lux measured as the reciprocal of the 10-90% rise time of free [Ca2+]i showed a linear correlation wi
190 In addition, the amplitude, duration, and rise time of macroscopic I(Ca)-induced Ca2+ transients a
191 ents increased quantal size the mean 20-80 % rise time of MEPPs recorded with an extracellular electr
194 at vertebrate central synapses, because the rise time of mPSCs was constant regardless of the amplit
195 ely 12 ms, as compared to 19 ms for the mean rise time of puffs, and their spatial extent is approxim
196 The effect of agonist concentration on the rise time of the current showed that the extracellular N
198 e and back to the ground state, and that the rise time of the K590 intermediate is determined by vibr
199 n channels closure in the dark, shortens the rise time of the light response directly, and accelerate
201 oltage-activated channels that shortened the rise time of the receptor potential and (2) some calyces
203 e bundle's initial position and the size and rise time of the stimulus; the twitch was largest over t
204 ated the effects of KYN on the amplitude and rise time of the synaptic responses when driven by gluta
206 on counting from a high speed photodetector (rise time of ~1 ns) and applied to remove ringing distor
208 om donor excitations is characterized with a rise time of ~9 ps, while that from acceptor excitations
209 a1beta1gamma2 receptors (reflected in 10-90% rise times of 0.5 versus 1.0 ms, respectively), and deac
210 ide synthase, have ultra-fast kinetics (half-rise times of 2 ms) and the highest sensitivity for neur
216 DAR miniature currents (minis) were lost and rise times of NMDAR evoked currents increased in mutant
221 Kv1.1 channel resulted in a decrease in the rise times of the macroscopic current (e.g. from 51.7 +/
223 ivity and total charge, while decreasing the rise-times of optically-evoked GABA(A) receptor-mediated
227 hypothesis that a short inspiratory pressure rise time or a low PaCO2 level promotes inspiratory lary
231 sence of a mode in the distribution of spark rise times or in the joint distribution of rise times an
238 nhibitory responses evoked by 1 N ramps with rise times ranging between 2.5 and 20 ms did not vary si
239 rt ventilation is not altered by inspiratory rise times ranging from 0.05 to 0.4 s or by moderate hyp
240 ffects of tissue depth and pacing rate on AP rise time reduce conduction safety and myocardial excita
242 x detector mechanism sensitive to changes in rise time, relatively independently of sound intensity c
243 /- 2.3 vs 21 seconds +/- 8.7 [P < .001]) and rise time (right hemisphere, 3.5 seconds +/- 1.7 vs 11 s
246 ulation of synapses that had EPSCs with fast rise times, short latencies, and monophasic decays, cons
247 s excited, green fluorescence appears with a rise time shorter than the instrument time resolution (
251 esponded with a shorter duration and shorter rise-time spike burst as sniff frequency increased, refl
254 ing in a bimodal distribution of the 10-90 % rise times, suggesting two distinct populations of event
255 ons of L-Glu revealed slow voltage-dependent rise-times, suggesting that polyamines additionally bind
256 late current (MEPC) amplitude (A(c)), 20-80% rise time (t(r)), and 90-33% fall-time (t(f)) was determ
257 old faster than GCaMP3 with Ca(2+) decay and rise times, t1/2, of 3.3 ms and 0.9 ms, respectively, ma
260 r II/III (distal location) had longer 10-90% rise times than IPSPs evoked from layer V/VI stimulating
261 is concluded that the large IPSPs with slow rise-times that are observed in motoneurons during activ
262 its were individually correlated with a fast rise time, the alpha2 nAChR subunit was correlated with
265 he AHPslow in nodose neurons displays a slow rise time to peak (0.3-0.5 s) and a long duration (3-15
267 lso observable for both the 15 ms and 185 ms rise time tones when the same stimuli served as deviant
269 nds after the initial rectangular phase) and rise time (tr; the time required for the porated membran
270 ion protocols, including stimuli with finite rise time, trains of ligand or voltage steps, and global
271 ortic velocity (v(p)), peak velocity squared/rise time (v(p)(2)/T), peak (+ dv(p)/dt or v'(p)) and me
274 was greatly delayed (approximately 50 s) and rise time was doubled in comparison to cells not subject
277 ive stimulus threshold was increased and the rise time was slower in slices from scrapie-infected mic
278 authors found that regularizing bedtimes and rise times was often sufficient to bring about improveme
287 N1b amplitude differences to the contrastive rise times were still observed, suggesting that N1b may
288 e in a single spark); 4), prolonged Ca spark rise time (which implies that CaMKII either delays RyR c