ライフサイエンスコーパス: ms

1 ms peri-stimulus) and polysynaptic (35-1,000 ms peri-stimulus) activity with temporarily (<35 ms) ele

2 l stimuli with varying ITDs (0, +/-0.4, +/-1 ms) was recorded using multichannel electroencephalograp

3 access to TMS-evoked neuronal activity 0.8-1 ms after TMS onset.

4 at 60 beats per minute, 2 V amplitude, and 1 ms pulse width, restoring mean arterial pressure from 0

5 oximately 1 nS that decay in approximately 1 ms and mildly voltage-dependent NMDA receptor EPSCs of a

6 eceptor, approximately 1 nS, approximately 1 ms; NMDA receptor, approximately 0.6 nS, approximately 7

7 orders of magnitude from extremely fast (<1 ms) at pH 8 to very slow (>300 ms) at pH 7.

8 The ASSR paradigm (1 ms, 85 dB clicks in 250-0.5 s trains at a frequency of 4

9 periments conducted at seismic slip rates (1 ms(-1)) show that phyllosilicates can facilitate co-seis

10 e demonstrate that, at seismic slip rates (1 ms(-1)), similar calcite gouges with pre-existing phyllo

11 quired for fusion within the approximately 1-ms timescale of neurotransmitter release.

12 low, ranging from <5% for short pulses (1/10 ms long) to approximately 20% for longer stimuli (100/10

13 outcomes were similar for short pulses (1/10 ms long: 0% success) but improved for longer stimuli (10

14 1 mapping values (1264+/-10 versus 1184+/-10 ms, P<0.001), and impaired cardiac energetic status (pho

15 -component dC20:1 control bilayer (65 +/- 10 ms), implying lipid redistribution.

16 mes in the two-component bilayers (95 +/- 10 ms for dC18:1+dC22:1 and 195 +/- 20 ms for dC16:1+dC24:1

17 isometric force generation, approximately 10 ms after the start of electrical stimulation in frog mus

18 of latency relaxation (LR), approximately 10 ms after the start of stimulation, when the myosin filam

19 roviding fair resolution in approximately 10 ms and FAIMS scans in under 5 s.

20 a total measurement time of approximately 10 ms per particle.

21 10 mV) and short duration voltage pulses (10 ms), which have the net effect of reducing the capacitiv

22 lysis of ionized lipids occurred rapidly (10 ms) without prior mass-selection.

23 ance protocol employing three sequential, 10 ms voltage steps (-10 mV, -20 mV, -30 mV) in an alternat

24 a fast decaying population (T2 less than 10 ms) and a larger population with T2 greater than 1000 ms

25 oximately 10000) at short analysis times (10 ms) is desirable.

26 e, nonoscillatory events reoccurring with 10 ms precision.

27 re often than expected by chance and with 10 ms precision.

28 lor and transitions within approximately 100 ms into a sharper tuned profile in more posterior ventra

29 derlying the immature P1 ( approximately 100 ms) response peak with reduced activity in the auditory

30 ency instability is lower than 10(-6) at 100 ms integration time.

31 OmpLA populates an ensemble of slowly (>100 ms) interconverting and conformationally heterogeneous u

32 t salience is represented much earlier (<100 ms following stimulus onset) than previously estimated.

33 e-locked) responses at early latencies (<100 ms post-stimulus) and more abundant induced (non-phase-l

34 was found at an average auditory lag of 100 ms, but this varied widely between individuals.

35 tudy, we introduced a constant delay (of 100 ms) between actions and action-associated sounds, and we

36 ibitory response lasting on the order of 100 ms.

37 beled release sites of dopamine spanning 100 ms to seconds that correlate with protrusions but not pr

38 pulse trains (300 ms at 20 Hz) starting 100 ms after cue onset, total of four trains (28 TMS pulses)

39 uccess) but improved for longer stimuli (100 ms: 54% success; 1000 ms: 90% success).

40 Gain was apparent within 100 ms of stimulus onset, and a quantitative model based on

41 ediate a fast inhibition observed within 100 ms of the first pulse, whereas D2 autoreceptors in DAN t

42 proximately 20% for longer stimuli (100/1000 ms).

43 es, representations dynamically change >1000 ms before stabilizing.

44 or longer stimuli (100 ms: 54% success; 1000 ms: 90% success).

45 larger population with T2 greater than 1000 ms.

46 fects 143 ms (95% CI, 136-150) early and 111 ms (95% CI, 104-118) late.

47 ation (69+/-32 versus 39+/-29 versus 21+/-12 ms; P=0.0005) compared with RV or left ventricle.

48 versus 89%, P<0.05) than QRS duration >/=120 ms.

49 racy for the apparent motion task (ISI = 120 ms) was evident in the phase of theta oscillations (6-7

50 reflex pathways with delays of at least 120 ms.

51 onset, median (interquartile range) 96 (121) ms and 48 (72) ms, respectively.

52 idence interval [CI], 152-163) early and 125 ms (95% CI, 120-130) late.

53 necrotic myocardium were identified as 1251 ms and 1400 ms, respectively, with prediction accuracy o

54 the DN evoked relatively late effects (>130 ms) in other nodes of the DN, as well as FPN and SN.

55 mmHg) than in LWHs without TOLB (109 +/- 14 ms, P = 0.005; 65 +/- 6.5 mmHg, P = 0.01).

56 se figures were significantly lower (mean 14 ms; 95% CI, 6-22; P<0.001) among fetuses with heart defe

57 ects in the occipital module between 100-140 ms, coinciding with the P100 visually evoked potential,

58 Short-latency (80-140 ms) striatal responses to a first target determined cons

59 =1 (odds ratio, 6.7; P=0.01), and QRS </=140 ms (odds ratio, 7.7; P<0.001).

60 ocardium were identified as 1251 ms and 1400 ms, respectively, with prediction accuracy of 96.7% (95%

61 Using the proposed threshold of 1400 ms, the volume of irreversibly damaged tissue was in goo

62 <0.001) among fetuses with heart defects 143 ms (95% CI, 136-150) early and 111 ms (95% CI, 104-118)

63 compared with those having a QRSD 120 to 149 ms (HR: 0.85; 95% CI: 0.80 to 0.92) and 150 to 179 ms (H

64 ingle LV breakthrough at the septum (38+/-15 ms post-QRS onset); (2) prolonged right-to-left transsep

65 4-9) ms mmHg(-1) ] compared to NC [11 (8-15) ms mmHg(-1) ; P = 0.002].

66 mulus modulated ERP amplitude between 20-150 ms over left fronto-central scalp region.

67 CS-TS inter-stimulus intervals (ISIs: 40-150 ms).

68 ns with this slower time constant of ca. 150 ms, indicating that the almost fully folded protein reta

69 TCs are most pronounced during the first 150 ms after stimulation and are mediated by glomerular laye

70 e-locked) responses at later latencies (>150 ms post-stimulus).

71 continuum increased their firing rates 150 ms after stimulus onset and these firing rates covaried

72 athreshold PMv and rM1 conditioning at a 150-ms ISI, while site-specific, intensity-dependent facilit

73 correlated with actual sex ratios after 1500 ms exposures to groups of simultaneous voices.

74 ange: 53-104; 18th year of life: median: 151 ms, range: 107-187).

75 arget was decoded at a later time-point, 151 ms after saccade offset.

76 ut heart defects, the mean T2* value was 157 ms (95% confidence interval [CI], 152-163) early and 125

77 igher in LWHs perfused with TOLB (199 +/- 16 ms; 92 +/- 5.3 mmHg) than in LWHs without TOLB (109 +/-

78 with a half-removal time of approximately 16 ms, which suggests the neck has low resistance.

79 erstimulus interval decreased from 500 to 16 ms there was an approximate 79% reduction in the FEF res

80 ccade, albeit with a slower time course (162 ms) and poorer signal strength.

81 for distorted (vs natural) stimuli from 170 ms post stimulus.

82 not in those with LBBB and a QRSD 150 to 179 ms (adjusted HR for death: 1.06; 95% CI: 0.95 to 1.19).

83 : 0.85; 95% CI: 0.80 to 0.92) and 150 to 179 ms (HR: 0.87; 95% CI: 0.81 to 0.93).

84 with CRT-D, and those with a QRSD 150 to 179 ms and LBBB had only a modest improvement.

85 BBB, whereas patients with a QRSD 150 to 179 ms without LBBB had no improvement in survival with CRT-

86 Ablating fractionated electrograms (117+/-18 ms; 44+/-13% of tachycardia cycle length) within the car

87 effect in the frontal module between 140-180 ms, suggesting that the differences found constitute an

88 urvival in those with LBBB and a QRSD >/=180 ms (adjusted HR for death: 0.78; 95% CI: 0.68 to 0.91),

89 those with LBBB, patients with a QRSD >/=180 ms had a greater adjusted survival benefit with CRT-D ve

90 were greatest in patients with a QRSD >/=180 ms with or without LBBB, whereas patients with a QRSD 15

91 ibrillators (CRT-D) have a very wide (>/=180 ms) QRS complex duration (QRSD).

92 a defect relaxation time constant of 10-0.2 ms, which decreases monotonically with increasing temper

93 o be 26.9 ms, 4.6 ms (fraction 22%) and 33.2 ms (fraction: 78%), respectively.

94 d long T2 relaxation times were 24.7 ms, 4.2 ms (fraction 15%) and 30.4 ms (fraction 85%) respectivel

95 n at 0.1 Hz were rapid (rise time = 49 +/- 2 ms), while the decreases in [Ca(2+) ]m occurred more slo

96 ic axons can exhibit conduction delays of <2 ms to 40-50 ms.

97 cilia with a spatiotemporal resolution of 2 ms and <16 nm.

98 nizations are essentially completed within 2 ms and occur without channel opening at low proton conce

99 than 9 weeks, whereas a short-lasting (10-20 ms) central peak was observed for EMG-EMG synchronizatio

100 5 +/- 10 ms for dC18:1+dC22:1 and 195 +/- 20 ms for dC16:1+dC24:1) were increased relative to the sin

101 escape from a single budding profile in 5-20 ms and from three concatenated ILVs in 80-200 ms.

102 screte "sub-events" over an approximately 20 ms interval.

103 tivation preceded vibrissa stimulation by 20 ms.

104 ptic responses to inputs at intervals </= 20 ms is increased by apamin, suggesting a role for the inh

105 oral summation of inputs at intervals </= 20 ms.

106 ccurred with precision on the order of </=20 ms, showing that long repeated patterns of subthreshold

107 IR-IIb window with short exposure time of 20 ms for rare-earth based probes.Fluorescence imaging in t

108 occurred with a precision on the order of 20 ms.

109 roscopy sequence: 24 echo time steps with 20-ms increments).

110 RTD in all phases, except for 0-200 ms in PFs, significantly decreased in KEs (11-42%) and P

111 e development (RTD: 0-30, 0-50, 0-100, 0-200 ms) were also measured.

112 posterior negativity emerging around 180-200 ms.

113 sion through the reaction region (ca. 20-200 ms), representing a 50-1000-fold improvement in performa

114 s and from three concatenated ILVs in 80-200 ms.

115 ined responses in later time windows (85-200 ms).

116 resentation at several time points after 200 ms.

117 rmation followed similarly approximately 200 ms later suggests that this earlier neural response cont

118 ites and were characterized by an early (200 ms) posterior negativity and a later (>300 ms) parietal

119 th regular auditory pure tones (1000 Hz, 200 ms duration), with 11% of the tones deviating in both du

120 y 23000) with a transient length of only 200 ms.

121 rk and perceptual accuracy was strongest 200 ms before stimulus presentation, and it greatly diminish

122 wards, from which a sample was revealed 2000 ms later.

123 n (isovolumic relaxation time: control, 0.21 ms [interquartile range, 0.12-0.35] versus FGR, 0.35 ms

124 on and behavior: 40 kHz/300 ms and 66 kHz/21 ms.

125 imately 2% between delay times of 16 and 211 ms, which may have implications for other IM experiments

126 rrent with decay time constants of up to 225 ms, and small-amplitude hyperpolarization-activated curr

127 nd a neural signature of the unique hues 230 ms after stimulus onset at a post-perceptual stage of vi

128 For delays ranging from 16 to 33 231 ms, the collision cross sections of native-like, 7+ cyto

129 n potential duration; median, 275 versus 241 ms; P=0.014).

130 ion symmetrically distributed within a +/-25 ms time window.

131 (st-LTP and st-LTD) were confined to a +/-25 ms time-window.

132 h-resolution atomic force microscopy with 25 ms resolution.

133 easure, a positive component peaking at 250 ms was found - a distraction positivity.

134 ollection of four complementary views in 250 ms, doubling speed and improving information content rel

135 with a low relaxation time constant of 0.27 ms.

136 ling, which rapidly decreases from 8 to 0.3 ms with increasing temperature.

137 +/- 3 years, QTc before treatment 331 +/- 3 ms) received HQ therapy (584 +/- 53 mg/day).

138 rect (I) waves in corticospinal neurons (4.3 ms; I-wave protocol) or at an interstimulus interval in-

139 alf-lives spanning 9 orders of magnitude: <3 ms to 6.5 months.

140 ted, ongoing hand action was perturbed 25-30 ms after TMS, but our results fail to show any disruptio

141 s on a slower timescale of tau2 = 610 +/- 30 ms depending on H3O(+) adsorption.

142 layer V pyramidal neurons is induced at +30 ms, a normally ineffective timing interval for t-LTP ind

143 ed sampling of membrane conductance every 30 ms.

144 e for rapid, time-resolved monitoring (</=30 ms) of IC-modulated membrane conductance.

145 ect features a response latency of a mere 30 ms and provided the foundation for the quantitative audi

146 nductance decreased by 76 +/- 7.5% within 30 ms of switching from solutions containing 0 to 1 M Ca(2+

147 0-, approximately 100-, and approximately 30-ms modulation periods) and identified the stimuli while

148 ring of many neurons over periods of 100-300 ms reoccurs during behavior and during periods of quiesc

149 EPN was scored as the mean activity (225-300 ms after picture onset) at occipital and parieto-occipit

150 tween excitation and inhibition in the 6-300 ms epoch, all of which can be linked to various human TM

151 and change cues were implemented (0 and 300 ms) in order to vary task difficulty.

152 mely fast (<1 ms) at pH 8 to very slow (>300 ms) at pH 7.

153 0 ms) posterior negativity and a later (>300 ms) parietal positivity in the time domain and an increa

154 e window covering the act of inhibition (300 ms-350 ms).

155 ps with respiration and behavior: 40 kHz/300 ms and 66 kHz/21 ms.

156 m/z 173.919) with a transient length of 300 ms.

157 Online double-pulse TMS over rTPJ 300 ms (but not 50 ms) after target appearance selectively d

158 us, while there was no difference in the 300 ms delay condition.

159 infralimbic cortex: brief pulse trains (300 ms at 20 Hz) starting 100 ms after cue onset, total of f

160 than in controls (1031+/-74 versus 954+/-32 ms, P<0.001) and female patients had higher RV T1 compar

161 etect>/=16, and a fast VT zone of 240 to 320 ms.

162 height was associated with increases of 4.33 ms (0.76-7.96; P=0.02) in PR interval and 2.57 ms (1.33-

163 antly faster in group B patients (257 +/- 34 ms vs. 328 +/- 72 ms in group A; p = 0.003).

164 s immediately after landing was 7-10% (30-34 ms) slower than mean preflight values, but results retur

165 or return in a biphasic manner (taufast = 34 ms, tauslow = 2.5 s).

166 rquartile range, 0.12-0.35] versus FGR, 0.35 ms [interquartile range, 0.20-0.46]; P=0.04).

167 ions evoked amplitude-dependent direct (5-35 ms peri-stimulus) and polysynaptic (35-1,000 ms peri-sti

168 eri-stimulus) activity with temporarily (<35 ms) elevated propagation velocities along the perisomati

169 of noise compensation starting at around 350 ms after stimulus onset, indicating that noise compensat

170 w covering the act of inhibition (300 ms-350 ms).

171 The average lifetime of the MCA is 36 ms and the free energy difference to the TSA-like form i

172 ve and the aortic valve artifact was 19+/-37 ms.

173 d fire with short burst duration (median, 38 ms) preferentially at the trough of both CA1 theta and s

174 of 615 MOmega and a mean time constant of 38 ms.

175 e proportion (0-20 of 40) and precision (0-4 ms jitter) of synchrony of inhibitory inputs, along with

176 s not significant (Baseline septal T1 1277.4 ms, follow up 1271.5 p = 0.504).

177 nductance cycle (current half-decay time 2-4 ms depending on voltage).

178 th >/=10 inhibitory inputs active within 2-4 ms of each other.

179 were 24.7 ms, 4.2 ms (fraction 15%) and 30.4 ms (fraction 85%) respectively.

180 racy for the two-flash fusion task (ISI = 40 ms) was evident in the phase of alpha oscillations (8-10

181 y when conditioning PMv, rM1 and SMA at a 40-ms ISI, with larger effects after PMv conditioning.

182 rget was signaled by longer-latency (200-400 ms) striatal activity.

183 Between approximately 50 and 400 ms after stimulus onset, face-selective sources in right

184 crease in theta activity between 200 and 400 ms.

185 event-related potential at approximately 400 ms (N400), which showed the typical enhancement to seman

186 nd early transient effects approximately 400 ms before the UP of lexical competition in left supramar

187 encoding appeared early ( approximately 400 ms) during the encoding of congruent words.

188 encoding appeared early ( approximately 400 ms) during the encoding of congruent words.

189 with average durations of approximately 400 ms, which are more prevalent during fast versus slow mov

190 curring as early as 50 ms and as late as 400 ms after the phoneme onset.

191 curring as early as 50 ms and as late as 400 ms after the phoneme onset.

192 dent main frequency and duration (30 kHz/400 ms in juveniles, 22 kHz/900 ms in adults).

193 tion, and QTc interval were 156, 88, and 402 ms, respectively.

194 idence interval: 396, 399) to 404 (403, 404) ms.

195 ar activation duration (median, 52 versus 42 ms; P=0.007) and prolonged mean epicardial activation-re

196 hows a fast response time ( approximately 45 ms) and a significantly high photoresponsivity ( approxi

197 e hydrated Rb(+)ions reside tau1 = 104 +/- 5 ms at a given location, but this is dependent on the hyd

198 2.6 ms; ischemia/reperfusion, 1115.0+/-140.5 ms; P<0.001; n=14/13), which were later associated with

199 s) into larger FCC crystals, captured at 2.5 ms time resolution using a fast electron camera.

200 short-lived (lifetimes approximately 0.2-2.5 ms) Hoogsteen (HG) bps.

201 PI mouse images of a 512 ng bolus and a 21.5 ms acquisition time allow for capturing the flow of an i

202 during the earliest events in unfolding, 3.5 ms before secondary structure is disrupted.

203 terstimulus interval in-between I-waves (3.5 ms; control protocol) on separate days in a randomized o

204 This occurred across an interval of 30 +/- 5 ms (equivalent to 1 m degrees C).

205 to take place across an interval of 54 +/- 5 ms corresponding to an estimated full-width of only 1 m

206 r, occurs in vacuum, has rapid rise time (<5 ms), and persists for >10 h.

207 Conversely, the exact same 5 ms pairing in stratum oriens potentiated both pathways,

208 he pre-post delay was shortened from 10 to 5 ms, which selectively potentiated paired radiatum pathwa

209 A low-amplitude, broad-duration (40-50 ms) central peak of EMG-EMG synchronization was observed

210 exhibit conduction delays of <2 ms to 40-50 ms.

211 ge of conduction times, some exceeding 40-50 ms.

212 suppression was measured between -50 and 50 ms from saccadic onset.

213 d continuous, 6 ms on/off micropulse, and 50 ms on/off long pulse.

214 amplitude, input-output relationship and 50 ms paired-pulse facilitation were unchanged following CO

215 le neural responses occurring as early as 50 ms and as late as 400 ms after the phoneme onset.

216 at different times occurring as early as 50 ms and as late as 400 ms after the phoneme onset.

217 Here, we found that brief (50 ms) visual stimulus re-exposure during a repetitive foil

218 of the tones deviating in both duration (50 ms) and frequency (1200 Hz) while watching a silent movi

219 greatly attenuated after a short latency (50 ms) following burst-like PFC electrical stimulation, and

220 ouble-pulse TMS over rTPJ 300 ms (but not 50 ms) after target appearance selectively decreased partic

221 Typically, when T2 follows T1 within 100-500 ms, it is often not perceived (i.e., the attentional bli

222 ertain duration), with the temporary 200-500 ms periods of irresponsiveness to sensory input making t

223 Data points were recorded every 250-500 ms (>8 data points/peak), effectively eliminating under

224 latter frequency shifts normalized to a 500 ms lifetime, and these values increase nearly linearly w

225 e biases in decisions made approximately 500 ms later.

226 r inhibition that peaks at approximately 500 ms.

227 disappeared when they were separated by 500 ms, and were partly recovered (evident for our measure o

228 entity at different times over the first 500 ms after stimulus onset.

229 re of the neural substrate for the first 500 ms of word recognition.

230 ), brief tetanic contraction (100 Hz for 500 ms) evoked rapid onset vasodilatation (ROV) in FAs that

231 a stimulus did not stimulate the RF for 500 ms.

232 the majority of cells preset at -80 mV, 500 ms depolarizing current injections to cells led to a bri

233 n the AV and VA maps at each time point (500 ms window after stimulus) and then correlated with two a

234 dow of performance monitoring processes (500 ms-600 ms).

235 Ps) initiated with variable delay (up to 500 ms) after ACh application, but not by subthreshold depol

236 formation that can be decoded within 110-518 ms of a sniff, and maximally within the theta frequency

237 ditis and healthy controls was 86% for T2>52 ms, 78% for native T1>981 ms, 74% for extracellular volu

238 tivity to sensory information of 350 and 550 ms for 1st and 2nd order systems respectively).

239 (0.76-7.96; P=0.02) in PR interval and 2.57 ms (1.33-3.83; P<0.0001) in QRS duration but was not rel

240 (5.4+/-2.8 versus 2.0+/-2.8 versus 1.1+/-1.6 ms; P=0.007) and activation recovery intervals prolongat

241 T1 day 1: permanent ligation, 1280.0+/-162.6 ms; ischemia/reperfusion, 1115.0+/-140.5 ms; P<0.001; n=

242 tion times were estimated to be 26.9 ms, 4.6 ms (fraction 22%) and 33.2 ms (fraction: 78%), respectiv

243 The 6 ms on and 6 ms off micropulse transverse 3-dimensional ultrasound is

244 ied in the 3 runs and included continuous, 6 ms on/off micropulse, and 50 ms on/off long pulse.

245 ow high-frequency spiking within the first 6 ms depending on TMS-induced current orientation and a mu

246 The 6 ms on and 6 ms off micropulse transverse 3-dimensional u

247 atosensory evoked potentials increased 50-60 ms after stimulation (P1) for both suprathreshold and su

248 tral deflection that peaked approximately 60 ms after the response.

249 kPa(-1) ), response time ( approximately 60 ms), and good mechanical stability.

250 duration is adjustable on-demand between 60 ms and 5.5 s.

251 e generated at a high frequency of 17 Hz (60 ms in period) and the pulse duration is adjustable on-de

252 ebo, patients exhibited PPI deficits with 60 ms prepulse intervals; these deficits were 'rescued' by

253 performance monitoring processes (500 ms-600 ms).

254 e and decay time for the 1(st) order is 7.62 ms and 6.75 ms, and for the 2(nd) order is 0.75 ms and 3

255 single mode centered about approximately 650 ms into a fast decaying population (T2 less than 10 ms)

256 pared with males (1051+/-79 versus 1017+/-68 ms, P=0.02).

257 ment, which reduced the latency delay by 1.7 ms/eye (95% CI 0.5-2.9; p=0.0048) when analysing the tri

258 short and long T2 relaxation times were 24.7 ms, 4.2 ms (fraction 15%) and 30.4 ms (fraction 85%) res

259 eptor, approximately 0.6 nS, approximately 7 ms) and depressed moderately.

260 imately 0.6 nS that decay in approximately 7 ms.

261 centrations >90th percentile, QT increased 7 ms across the CC and TT genotypes: 397 (95% confidence i

262 n partition coefficient (p < 0.001), and 4.7-ms increment in native T1 (p = 0.001).

263 h precisely-actuated, millisecond-length (70 ms), uniform-intensity UV pulses, delivered through eigh

264 lation of the FPN and SN evoked a rapid (<70 ms) response that was predominantly higher within the SN

265 Optimized GC-qMS parameters (dwell time 70 ms, 2 most abundant ions) resulted in standard deviation

266 nent (corresponding to the P3b, from 550-700 ms) sensitive to outcome devaluation.

267 oup B patients (257 +/- 34 ms vs. 328 +/- 72 ms in group A; p = 0.003).

268 interquartile range) 96 (121) ms and 48 (72) ms, respectively.

269 and 6.75 ms, and for the 2(nd) order is 0.75 ms and 3.87 ms, respectively.

270 time for the 1(st) order is 7.62 ms and 6.75 ms, and for the 2(nd) order is 0.75 ms and 3.87 ms, resp

271 ed desensitization kinetics (from 5.5 to 775 ms), whereas it only had a minor effect on deactivation

272 of the fluctuations was in the range 0.2-0.8 ms.

273 re to an extensional flow field for 0.36-1.8 ms, at concentrations as low as 0.5 mg mL(-1) In additio

274 tion of the aortic valve artifact was 39+/-8 ms with amplitude of 0.12+/-0.07 mV (range, 0.06-0.36 mV

275 low beta oscillatory activity as early as 80 ms after T1, indicating that the attentional blink to T2

276 dependent facilitation was detected at an 80-ms ISI.

277 was detected rapidly ( approximately 200-800 ms from the onset of the event boundary) and was specifi

278 sensory alternatives were presented 750-800 ms before as peripheral "targets" that specified the sti

279 AAT increased with age (neonates: median: 81 ms, range: 53-104; 18th year of life: median: 151 ms, ra

280 ion occurring with a time constant of ca. 85 ms, but slower protection is observed around a reverse t

281 ensive equilibrium pulling simulations (0.86 ms total) on eleven RNA sequences (hairpins and duplexes

282 monstrate a spin coherence time (T2) of 0.87 ms, five orders of magnitude longer than typical exchang

283 and for the 2(nd) order is 0.75 ms and 3.87 ms, respectively.

284 s, with a lifetime ranging from 0.23 to 0.89 ms over a broad range of viscosities (0.6-1200 cP).

285 o relaxation times were estimated to be 26.9 ms, 4.6 ms (fraction 22%) and 33.2 ms (fraction: 78%), r

286 N and HTN patients [5(3-8), 4 (2-7), 6 (4-9) ms mmHg(-1) ] compared to NC [11 (8-15) ms mmHg(-1) ; P

287 nd stimulation was provided approximately 90 ms prior to movement onset in each group.

288 a detection limits and a response time of 90 ms is demonstrated.

289 SIGNIFICANCE STATEMENT We found long (>/=900 ms), repeated, subthreshold patterns of activity in CA1

290 tion (30 kHz/400 ms in juveniles, 22 kHz/900 ms in adults).

291 of nine recordings, we discovered long (900 ms) reoccurring subthreshold fluctuations or "repeats."

292 was 86% for T2>52 ms, 78% for native T1>981 ms, 74% for extracellular volume fraction >0.24, and 100

293 stored in the conduction band of TiO2 on an ms-s time scale, and we propose that they lead to furthe

294 of sugar repuckering dynamics at the mus and ms timescale accompanying transitions between non-helica

295 mutation leads to altered dynamics on a mus-ms time scale and deactivates both of the divalent catio

296 ll states undergo significant amounts of mus-ms time scale dynamics, only the MCA samples a dominant

297 the main allosteric binding site, retain mus-ms motions.

298 hat apo-thrombin is highly dynamic, with mus-ms motions throughout the molecule.

299 -scale, low-cost production of male-sterile (ms) female lines necessary for hybrid wheat seed product

300 measured to capture motions across the ps to ms timescale.

301 nanobody-coupled states to extensive mus-to-ms timescale dynamics when bound to a full agonist.