ライフサイエンスコーパス: ms

1 e time intervals ranging from 0.25 ms to 2.0 ms at a rate of 0.53 volumes/s.

2 y group (470.4+/-45.0 ms versus 453.3+/-37.0 ms, P=0.004).

3 change between two rounding types was -39.0 ms (95% CI, -50.6 to -27.4 ms; p < 0.001), and at site 2

4 p versus the monotherapy group (470.4+/-45.0 ms versus 453.3+/-37.0 ms, P=0.004).

5 l wall in FD had T2 elevation (FD 58.2+/-5.0 ms versus hypertrophic cardiomyopathy 55.6+/-4.3 ms, chr

6 ignificantly slower saccades (602.9 +/- 50.0 ms versus 578.3 +/- 44.6 ms for controls, P = 0.009) and

7 cm(-3)), an ultra-small time constant (0.01 ms), outstanding specific capacitance (128 mF cm(-2) and

8 rate): spontaneous swallowing 12.02 +/- 1.07 ms vs. ESM 31.66 +/- 98.25 ms, p = 0.301].

9 t repolarization (half-widths: 0.25 +/- 0.08 ms, n = 19 wild-type, 0.60 +/- 0.17 ms, n = 21 Kv3.3KO,

10 MNTB neuron APs (half-width 0.31 +/- 0.08 ms, n = 25) were fast, reliable, and showed no distincti

11 se imaging with a temporal resolution of 0.1 ms and an optical path length sensitivity of <4 pm per p

12 The data obtained at 0.1 ms time resolution exposes transient flow features and t

13 (full width at half-maximal stress: 11 +/- 1 ms) and a high twitch/tetanus ratio (0.91 +/- 0.05), ind

14 ion time was -15.6 ms (95% CI, -29.1 to -2.1 ms; p = 0.023).

15 n-piperaquine did not (mean increase of 22.1 ms [SD 19.2] for dihydroartemisinin-piperaquine vs 20.8

16 : ZT4: 39.7+/-1.9 ms versus ZT14: 33.8+/-3.1 ms, P<0.01).

17 ion (CaTD) at ZT14 (APD(80): ZT4: 45.4+/-4.1 ms; ZT9: 45.1+/-8.6 ms; ZT14: 34.7+/-4.2 ms; ZT21: 49.2+

18 At an average velocity of 6 +/- 1 ms(-1), the average skyrmion Hall angle was measured to

19 tal resolution on the order of 100 mum and 1 ms.

20 CAP imaging with a resolution of <200 um, <1 ms using a non-penetrating flexible nerve cuff electrode

21 We demonstrated high-temporal resolution (<1 ms) opto-electrophysiology without any artifact-induced

22 iological action potentials (e.g., 100 mV, 1 ms) but also exhibit temporal integration close to that

23 of the maximum peak intensity (FW0.1M) of ~1 ms can be achieved for (238)U upon ablation of NIST SRM6

24 obtain 100% sequence coverage in less than 1 ms of digestion time, in sharp contrast to 60% coverage

25 and conformational states and totaling to 1 ms of simulation time.

26 ization reserve and increased BVR (26 +/- 10 ms vs. 9 +/- 7 ms, P < 0.001), correlating with DAD acti

27 oller operates at time delays as small as 10 ms, the fastest steering response observed in any flying

28 lowed the visual stimulus in as little as 10 ms-a delay similar to the human vestibulo-ocular reflex-

29 TMS was delivered 10 ms before the end of TUS to the left M1 hotspot of the f

30 ag coefficients for wind speed scope from 10 ms(-1) to 28 ms(-1).

31 which varies across species from 0.1 to >10 ms.

32 erform chemical modification in less than 10 ms, reporting movements associated to desensitization on

33 obing interactions that last shorter than 10 ms.

34 l droplets of sample are deposited within 10 ms of each other onto the surface of a nanowire EM grid,

35 f symptomatic status (odds ratio for each 10-ms decrease in EMW: 1.37; 95% confidence interval: 1.27

36 sh that pNPP-induced dye blinking at the ~10-ms timescale is responsible for the apparent diffusion e

37 I(Na) activation was examined using 10-ms depolarising, V(1), steps to varying voltages 0-80 mV

38 bles follow a common long (about 300 +/- 100 ms, N = 52) deceleration-reorientation-acceleration patt

39 in OT is visible in the first sniff (50-100 ms) of an odor on each trial, and precedes the motor act

40 cranial magnetic stimulation was applied 100 ms after visual presentation of the object over a regula

41 the grid is vitrified in liquid ethane ~100 ms later.

42 er except for delaying its emergence by >100 ms.

43 lus-driven, and transiently deployed in ~100 ms.

44 decoding with high temporal precision (<100 ms).

45 e CB molecular gate on the time scale of 100 ms is approximately 2 nN.

46 There was an overlap of over 100 ms during which decoding was significant from both presa

47 asuring up to six peptides from a single 100 ms ion mobility separation with the current setup.

48 econd (fs) X-ray pulses in trains spaced 100 ms apart whereas pulses within trains are currently sepa

49 ntained for a very short period of time (100 ms), followed by fast quenching back to room temperature

50 neurons in both areas were active up to 100 ms after the perturbation, suggesting that both SC circu

51 d is apparent in neural responses within 100 ms of speech input.

52 nt and they either undock or fuse within 100 ms.

53 n change detection task, we identified a 100-ms temporal epoch of SC visual activity that is crucial

54 Inhibiting SC during this 100-ms period caused a contralateral detection deficit, wher

55 ; the stationary method requires around 1000 ms to analyze a single image, whereas the mobile app use

56 at full width at half-maximum (FWHM) of 105 ms and a relative standard deviation (%RSD) of 7.7/7.5%

57 ial Duration (APD)80 and APD30 of 152 +/- 11 ms and 71 +/- 6 ms, respectively, and maximum capture ra

58 as interelectrode conduction time of 7 to 11 ms and conduction block (CB) as conduction time >=12 ms.

59 al interaction was present beginning at ~110 ms, even in the absence of an explicit task to think abo

60 onduction block (CB) as conduction time >=12 ms.

61 ations (~400 ms(-2)) and reaction times (~12 ms) to escape approaching predators or environmental thr

62 of right frontal beta (~13 to 30 Hz) at ~120 ms, likely a proxy of right inferior frontal gyrus; then

63 increased frontal theta power (7-9 Hz, ~120 ms) in mid-anterior cingulate cortex (ACC) and a later b

64 (-1) ), and relatively low tau(0) value (121 ms).

65 t alternation at 8 Hz: one scenario per ~125-ms cycle.

66 within a 25 ms tolerance interval in a 1250 ms long spike pattern.

67 ers were exposed to the stimuli briefly (129 ms), warned that clothing cues are non-informative and i

68 e early warning signals occur as much as 130 ms before motion ensues-showing a sharp rise in motion a

69 e resistive force from lower leg muscles 130 ms after the visual motion onset.

70 Within 14 ms, new vesicles are recruited and fully replenish the d

71 pi: 19.2%, P=0.169; mean duration: 590+/-140 ms) and nonsustained focal waves (Endo: 1.2% versus Epi:

72 f right inferior frontal gyrus; then, at 140 ms, there was a broad skeletomotor suppression, likely r

73 rvals (ISIs) were typically between 5 and 15 ms.

74 imescale is comparable to that of geckos (15 ms), and such rapid adhesion switching can be repeated f

75 latency real-time pose estimation (within 15 ms, >100 FPS), with an additional forward-prediction mod

76 SPL (GtSPL) with SAM forms Omega within ~15 ms after mixing.

77 R1s) when the CF input is delayed by 100-150 ms from the first PF input in both cases.

78 epresented in the MEG signal as early as 150 ms after visual stimulus onset.

79 deteriorated the quality of late-phase (>150 ms from image onset) IT population code and produced com

80 ven among patients with LBBB with QRSd >=150 ms (HR, 0.42 [95% CI, 0.30-0.57]; P<0.001; mean LVEF cha

81 tcomes to patients with LBBB with QRSd >=150 ms (HR, 0.93 [95% CI, 0.67-1.29]; difference in mean LVE

82 election criteria: QRS duration (QRSd) >=150 ms and subjective labeling of left bundle branch block (

83 ong-interval intracortical inhibition(,) 150 ms) receptor activation were recorded from left M1.

84 l representation of the moving dots just 150 ms after they appeared.

85 identified patients with LBBB with QRSd <150 ms with comparable outcomes to patients with LBBB with Q

86 cleus on basal ganglia output; then, at ~160 ms, suppression was detected in the muscle, and, finally

87 h-level models explained later variance (169 ms).

88 +/- 0.08 ms, n = 19 wild-type, 0.60 +/- 0.17 ms, n = 21 Kv3.3KO, p = 0.0001).

89 d constant signals (%RSD = 8.5%, FWHM of 177 ms +/- 8.5%, n = 10 557).

90 nd one novel stimulus simultaneously for 180 ms; then made comparative (Exp.

91 1.6; P=0.01 per decile), QRS duration >=180 ms (OR, 3.5; P=0.02), history of nonsustained VT (OR, 3.

92 muscles (depending on the injury level), 1-2 ms before antidromic potentials were elicited in motor n

93 .7 ms; ZT14: 64.3+/-3.3 ms; ZT21: 74.4+/-1.2 ms, P<0.05 versus other time points).

94 for SC compared with M1 cells (21.7 +/- 11.2 ms vs 25.5 +/- 10.7 ms, respectively, mean +/- SD).

95 l T2 elevation (53.1+/-2.9 versus 50.6+/-2.2 ms, P<0.001).

96 on electro-cardiogram (P=5.53E-24, beta=20.2 ms/allele).

97 arge increase in duration of the EOD to 23.2 ms was accompanied by a small change in size of the papi

98 isomers become protonated in 58 mus and 3.2 ms, respectively, resulting in formation of the blue-abs

99 4.1 ms; ZT9: 45.1+/-8.6 ms; ZT14: 34.7+/-4.2 ms; ZT21: 49.2+/-7.6 ms, P<0.05 versus ZT4 and ZT21; and

100 with the C-terminal domain of CaM in about 2 ms.

101 z, intensity: 2.2 W/cm(2), pulse duration: 2 ms, pulse repetition frequency: 165 Hz, effective radiat

102 tive decrease in DeltaT(2)* (10.4 [3.5-16.2] ms, p < 0.001) and DeltaT(2) (13.4 [6.(2)-18.9] ms; p =

103 ial dissociation as phase difference of >=20 ms between paired endo-epi electrodes.

104 he controllable interval time of at least 20 ms between the lined-up adjacent single cells.

105 T could not be perturbed by a late PHC (<=20 ms ahead of the His) due to the retrograde His conductio

106 nce microscopy with a time resolution of ~20 ms, we could unambiguously distinguish between bursting

107 found that the target evoked N2pc onset ~20 ms earlier when the target location was cued than when i

108 ses allow quantum state storage for up to 20 ms, and are used for few-microsecond single-qubit and tw

109 ms in the left hemisphere, compared with ~20 ms in audio-only.

110 es were most evident at intervals of 100-200 ms and 350-500 ms after stimulus presentation, correspon

111 dence for LAI at longer intervals of 100-200 ms, nor was there any effect of PAS.

112 tions of facial attractiveness after 150-200 ms of cortical processing.

113 uency separation, dissimilarities beyond 200 ms reflected the perceptual status of each tone within t

114 In the first 200 ms after onset, transient patterns of neural activity co

115 ral and dorsal pathways within the first 200 ms.

116 esaccadic stimulus remained present for ~200 ms after the saccade, transcending retinotopic specifici

117 was now only significant in the early (<200 ms) foreperiod.

118 opsin 2-expressing pyramidal neurons, or 200 ms silencing of Archeorhodopsin T-expressing pyramidal n

119 ual cells integrated global motion over ~200 ms, and responses were tuned to direction.

120 Bigeminal PVCs (200 ms coupling) were applied for 12 weeks to induce PVC-CM

121 of early processing (i.e., earlier than ~200 ms); nor did it influence the decodability of stimulus i

122 ls to make odor-guided decisions within ~200 ms, but animals routinely engage in bouts of high-freque

123 us transitions) are expressed early (102-207 ms poststimulus), while high-level PEs (about transition

124 ly, the behavioral time of stopping was ~220 ms.

125 ing from 450 ms before stimulus onset to 225 ms after onset were measured to quantify gaze stability.

126 th multiple time intervals ranging from 0.25 ms to 2.0 ms at a rate of 0.53 volumes/s.

127 heir QTc shortened from 492+/-37 to 423+/-25 ms [P<0.001]; their Schwartz score went from 3.0 to 0.06

128 ng 12.02 +/- 1.07 ms vs. ESM 31.66 +/- 98.25 ms, p = 0.301].

129 with more than 85% of the spikes within a 25 ms tolerance interval in a 1250 ms long spike pattern.

130 tality outcomes for pulse durations up to 25 ms, which appears to be the ideal duration to minimize r

131 nd PAR TEPs across a wide time range (15-250 ms), however the signals were correlated after ~80 ms, s

132 for interstimulus intervals shorter than 250 ms.

133 es than matched objects are, but within ~250 ms, the representation transforms, and they become equiv

134 sensory cortical activity within the 112-252 ms time window was significantly reduced in the individu

135 of ~15 dB and a propagation velocity of 255 ms(-1), an approximately 25% reduction from free-field p

136 sterior visual and parietal cortex from ~260 ms after stimulus onset.

137 line widths, continues to increase beyond 27 ms.

138 th a significantly higher bond lifetime (270 ms) compared to that for H3 (36 ms).

139 ency): spontaneous swallowing 119.35 +/- 273 ms(2) vs. ESM 99.83 +/- 194.58 ms(2), p = 0.301; SD1 (st

140 ted by later components (152-199 and 215-277 ms) of single-trial responses.

141 ts for wind speed scope from 10 ms(-1) to 28 ms(-1).

142 mptomatic LQTS (-52 +/- 38 ms vs. -18 +/- 29 ms; p < 0.0001).

143 uced postural responses that were later (290 ms) and had smaller amplitudes compared to when visual m

144 s eel, especially when U was higher than 0.3 ms(-1).

145 cle were 5 +/- 2 mL/100 g/min and 21.1 +/- 3 ms respectively.

146 , which produced a short biphasic EOD of 1.3 ms duration, shows small papillae (average area 136 mum(

147 3.3 ms; ZT9: 72.7+/-2.7 ms; ZT14: 64.3+/-3.3 ms; ZT21: 74.4+/-1.2 ms, P<0.05 versus other time points

148 ZT4 and ZT21; and CaTD(80): ZT4: 70.1+/-3.3 ms; ZT9: 72.7+/-2.7 ms; ZT14: 64.3+/-3.3 ms; ZT21: 74.4+

149 ersus hypertrophic cardiomyopathy 55.6+/-4.3 ms, chronic myocardial infarction 53.7+/-3.4 ms and heal

150 s; p = 0.04) and 10 (69 +/- 4 ms to 62 +/- 3 ms; p < 0.001) miles.

151 ely after running 3 (65 +/- 3 ms to 62 +/- 3 ms; p = 0.04) and 10 (69 +/- 4 ms to 62 +/- 3 ms; p < 0.

152 reased immediately after running 3 (65 +/- 3 ms to 62 +/- 3 ms; p = 0.04) and 10 (69 +/- 4 ms to 62 +

153 magnetic stimulation (TMS) of fM1 was 15-30 ms.

154 SD alone (37 [58%] female, mean QTc 466+/-30 ms, 16 [25%] patients were symptomatic before diagnosis

155 AF termination or cycle length slowing >=30 ms.

156 ieved the spatial (75 um) and temporal (<=30 ms) control required to resolve folding and self-cleavag

157 nalysis of vesicles released by trains of 30 ms depolarizations revealed that most releasable vesicle

158 A single 30 ms step to 0 mV was sufficient to deplete the membrane-p

159 sed temporal stability of transient (100-300 ms lifetime) and recurrent states of network activation

160 2 95% CI); LAT was 230 milliseconds (160-300 ms 95% CI); ACV was 3.70 mm/sec (2.21-5.18 mm/sec 95% CI

161 ggerated (more different from baseline) ~300 ms after initial physical stimulations.

162 goal-driven, and deployed in a slower (~300 ms) and sustained manner [4].

163 ss than the prematurity of the PHC (mean, 32 ms; range, 18-54 ms).

164 the saturated wind speed threshold is 22.33 ms(-1) when regressed from drag coefficient, and it is 2

165 unequivocal ECG abnormalities (QTc, 472+/-33 ms).

166 ties with positive genotyping (QTc, 482+/-35 ms).

167 later beta power suppression (13-22 Hz, ~350 ms) in prefrontal and auditory cortex.

168 t pronounced at response latencies up to 350 ms, and in both planum temporale and Heschl's gyrus.

169 ifetime (270 ms) compared to that for H3 (36 ms).

170 to those with asymptomatic LQTS (-52 +/- 38 ms vs. -18 +/- 29 ms; p < 0.0001).

171 hreshold at implant was 0.62+/-0.21 V at 0.4 ms which remained stable during follow-up at 0.65+/-0.68

172 in the piriform cortex (before: 47.7 +/- 1.4 ms; 18-24 h: 82.3 +/- 13.4 ms).

173 ore: 47.7 +/- 1.4 ms; 18-24 h: 82.3 +/- 13.4 ms).

174 ticity, reveal time constants (tau(1) = 27.4 ms, tau(2) = 725 ms) that closely match those from a bio

175 g types was -39.0 ms (95% CI, -50.6 to -27.4 ms; p < 0.001), and at site 2, the performance stop sign

176 ms, chronic myocardial infarction 53.7+/-3.4 ms and healthy volunteers 48.9+/-2.5 ms, P<0.001), but w

177 s to 62 +/- 3 ms; p = 0.04) and 10 (69 +/- 4 ms to 62 +/- 3 ms; p < 0.001) miles.

178 ells without DAPs peaked sharply at around 4 ms and varied only minimally across that group.

179 trical intravascular stimulation at 20 Hz, 4 ms pulse width, and <=20 mA.

180 nics in the nanoscale with fast response (<4 ms) and high resolution (~0.78 nm).

181 NREM sleep attenuation, such that late (>40 ms) responses in all monitored regions diminished during

182 ng steering responses lagged by more than 40 ms.

183 e over lateral-occipital electrodes (250-400 ms), which also increased with higher numbers.

184 em to achieve impressive accelerations (~400 ms(-2)) and reaction times (~12 ms) to escape approachin

185 whereas the mobile app uses only around 400 ms per image.

186 king of Pyr neurons to a subsequent tone 400 ms later.

187 references of membrane-bound K-Ras4B in 1.45-ms aggregate time of atomistic molecular dynamics simula

188 he central cortex (Cz electrode) between 450 ms and 750 ms post-stimulation, whereas the highest acti

189 ng of saccades and blinks occurring from 450 ms before stimulus onset to 225 ms after onset were meas

190 nt QT prolongation (>460 ms in women or >450 ms in men) in the intensive versus standard glycemic con

191 e the risk of incident QT prolongation (>460 ms in women or >450 ms in men) in the intensive versus s

192 of the PHC required to perturb AVNRT was 48 ms (range, 28-70 ms) and the advancement less than the p

193 LQTS patients with a QTc>=480 ms (n=120) had a significantly higher QTc-PRS (89.3+/-6.

194 RS (89.3+/-6.7) than patients with a QTc<480 ms (n=303, 87.6+/-7.4, difference-in-mean, 1.7+/-0.8, P<

195 ort-interval intracortical inhibition(,) 2.5 ms) and GABA(B) (long-interval intracortical inhibition(

196 7+/-3.4 ms and healthy volunteers 48.9+/-2.5 ms, P<0.001), but when LGE was present there was also gl

197 to an average QT prolongation of 60.5+/-40.5 ms from a baseline QTc of 473.7+/-35.9 ms to a peak QTc

198 HVC, which typically adds between 1 and 7.5 ms for each link within the sequence.

199 laxation time of the human tissue T1 = 810.5 ms.

200 lerating to zero velocity in approximately 5 ms at accelerations as high as 5.5 gravities.

201 tially decaying pulses of about 2,000 V in 5 ms.

202 responses at an interstimulus interval of 5 ms (PA-CBI), whereas the maximum effect on AP responses

203 eveal that the cells reorient in less than 5 ms, an order of magnitude faster than reported so far fo

204 We next used 5 ms optical activation of Channelrhodopsin 2-expressing p

205 was either constant or was changing every 50 ms according to different statistical distributions.

206 re of successive differences, proportion >50 ms of normal-to-normal R-R intervals, and the calculated

207 re of successive differences, proportion >50 ms, high-frequency power, low-frequency power), and both

208 of successive differences and proportion >50 ms.

209 lore whether the long apparent lifetime (~50 ms) of the Cu(B)(+)-CO complex generated upon photolysis

210 With this approach, even a single 50 ms pulse of light is able to significantly inhibit seizu

211 y reported, with state dwell-times in the 50 ms range, and report the kinetics of an intermediate tra

212 ident at intervals of 100-200 ms and 350-500 ms after stimulus presentation, corresponding to time pe

213 chronized during preinspiration (for ~50-500 ms), which can trigger inspiratory bursts that propagate

214 wer decreased in a stepwise fashion from 500 ms onward, first from CR to IR and then from IR to AR.

215 lpha power patterns revealed that late (>500 ms latency) in the cue-to-target foreperiod, only EEG al

216 osed with severe LQT2 (rate-corrected QT>500 ms).

217 thermal shock heating (i.e., ~1,650 K, ~500 ms).

218 ychloroquine developed a QTc interval of 500 ms or greater, but the proportion of patients with this

219 -band (12-30 Hz), ramping up slowly over 500 ms after stimulus onset and peaking at ~800 ms, around r

220 nd scalp potentials approximately 300 to 500 ms after article onset, predominantly over bilateral pos

221 in barrel activity were preceded within 500 ms by whisker movements: at least 55% of barrel activity

222 activity increased significantly within 500 ms of whisker movements, especially after twitches.

223 window) with near 100% efficiency using a 52 ms SWIFT isolation, followed by in-cell fragmentation by

224 um yields up to 20 % and lifetimes up to 520 ms.

225 turity of the PHC (mean, 32 ms; range, 18-54 ms).

226 19.35 +/- 273 ms(2) vs. ESM 99.83 +/- 194.58 ms(2), p = 0.301; SD1 (standard deviation of the instant

227 formance stop signal reaction time was -15.6 ms (95% CI, -29.1 to -2.1 ms; p = 0.023).

228 73.7+/-35.9 ms to a peak QTc of 532.6+/-31.6 ms.

229 des (602.9 +/- 50.0 ms versus 578.3 +/- 44.6 ms for controls, P = 0.009) and reduced saccade accuracy

230 .6 ms; ZT14: 34.7+/-4.2 ms; ZT21: 49.2+/-7.6 ms, P<0.05 versus ZT4 and ZT21; and CaTD(80): ZT4: 70.1+

231 D)80 and APD30 of 152 +/- 11 ms and 71 +/- 6 ms, respectively, and maximum capture rate (MCR) of 3.9

232 APD(80): ZT4: 45.4+/-4.1 ms; ZT9: 45.1+/-8.6 ms; ZT14: 34.7+/-4.2 ms; ZT21: 49.2+/-7.6 ms, P<0.05 ver

233 by delivering nonarcing, nonbarotraumatic 6 ms, 200 J direct current IRE applications via a custom n

234 ition drifts, and with only approximately 60 ms latency.

235 val): spontaneous swallowing 16.99 +/- 15.65 ms vs. ESM 44.74 +/- 138.85 ms, p = 0.312; HF (high freq

236 essed from drag coefficient, and it is 22.65 ms(-1) when regressed from the medium number of drag coe

237 identified a Left Mid Frontal (LMF; 400-650 ms) component over left-lateralised medial frontal sites

238 s-light noise, with short response time (<66 ms), excellent UV photoresponsivity (4.7 A W(-1) for tri

239 nced phosphorescence lifetimes (reaching 0.7 ms) and increased circularly polarized emission (CPL) ac

240 M1 cells (21.7 +/- 11.2 ms vs 25.5 +/- 10.7 ms, respectively, mean +/- SD).

241 aTD(80): ZT4: 70.1+/-3.3 ms; ZT9: 72.7+/-2.7 ms; ZT14: 64.3+/-3.3 ms; ZT21: 74.4+/-1.2 ms, P<0.05 ver

242 ry lag for phrenic nerve stimulation of 23.7 ms (p < 0.001 vs null hypothesis of <88ms).

243 mparable duration to the younger stage (24.7 ms) but featured a prominent increase in size of the pap

244 ithromycin; 440.6+/-24.9 versus 439.9+/-24.7 ms, P=0.834).

245 ea (to 73 +/- 22 muVs) and SDAT (to 26 +/- 7 ms) than BiV (to 93 +/- 26 muVs and 31 +/- 7 ms; both p

246 ms) than BiV (to 93 +/- 26 muVs and 31 +/- 7 ms; both p < 0.05) and LVs+RV pacing (to 108 +/- 37 muVs

247 and increased BVR (26 +/- 10 ms vs. 9 +/- 7 ms, P < 0.001), correlating with DAD activity.

248 the maximum effect on AP responses was at 7 ms (AP-CBI), suggesting that CB-M1 pathways with differe

249 red to perturb AVNRT was 48 ms (range, 28-70 ms) and the advancement less than the prematurity of the

250 with reduced early beta power (18-26 Hz, ~70 ms) in auditory and motor areas, presumably reflecting a

251 eptal VA interval during tachycardia was <70 ms in 3, 1 had spontaneous atrioventricular dissociation

252 by an auditory-speech-to-brain delay of ~70 ms in the left hemisphere, compared with ~20 ms in audio

253 inactivation of Ca(2+) current was 40 to 70 ms in atrial myocytes (depending on holding potential) s

254 me constants (tau(1) = 27.4 ms, tau(2) = 725 ms) that closely match those from a biological synapse.

255 cortex (Cz electrode) between 450 ms and 750 ms post-stimulation, whereas the highest activation for

256 A weighted QTc-PRS (range, 0-154.8 ms) was calculated for each patient, and the FHS (Framin

257 ] for dihydroartemisinin-piperaquine vs 20.8 ms [SD 17.8] for dihydroartemisinin-piperaquine plus mef

258 (to 108 +/- 37 muVs; p < 0.05; and 29 +/- 8 ms; p = 0.05).

259 crease at 52 h compared with baseline of 8.8 ms [SD 18.6] vs 0.9 ms [16.1]; p<0.01) but adding mefloq

260 rminal domain of CaM more slowly, in about 8 ms.

261 que monkeys and found that even fleeting (~8 ms duration) stimulus presentations can robustly trigger

262 owever the signals were correlated after ~80 ms, suggesting early peaks reflect site-specific activit

263 otide d[TTAGGGTTAG] to POT1 is both fast (80 ms) and strong (-10.1 +/- 0.3 kcal mol-1).

264 High-level features followed 80 ms later, providing key insights into how the brain make

265 r findings suggest that early TEP peaks (<80 ms) from PFC and PAR reflect stimulation site specific a

266 ms after stimulus onset and peaking at ~800 ms, around response selection and production.

267 , using ultrahigh-field (7 T) ultrafast (802 ms) fMRI optimized for single-participant-level detectio

268 er the full +/-1 g dynamic range (1 g = 9.81 ms(-2)).

269 16.99 +/- 15.65 ms vs. ESM 44.74 +/- 138.85 ms, p = 0.312; HF (high frequency): spontaneous swallowi

270 odels explained earlier vERP variability (88 ms after image onset), whereas high-level models explain

271 red with baseline of 8.8 ms [SD 18.6] vs 0.9 ms [16.1]; p<0.01) but adding mefloquine to dihydroartem

272 er assessed (except APD(80): ZT4: 39.7+/-1.9 ms versus ZT14: 33.8+/-3.1 ms, P<0.01).

273 -40.5 ms from a baseline QTc of 473.7+/-35.9 ms to a peak QTc of 532.6+/-31.6 ms.

274 han in males (106.8 +/- 8.4 vs 110.2 +/- 7.9 ms, p < 0.00001).

275 p < 0.001) and DeltaT(2) (13.4 [6.(2)-18.9] ms; p = 0.001) was found on carotid MR imaging at 48 hrs

276 ide 2-methythio-N(6)-(isopentenyl)adenosine (ms(2)i(6)A).

277 APC-ms are composed of individual high-aspect-ratio silica m

278 Here we provide a detailed protocol for APC-ms synthesis and use for human T-cell activation, and di

279 eracting T cells assemble the individual APC-ms microrods into a biodegradable 3D matrix.

280 Compared to conventional methods, APC-ms facilitates several-fold greater polyclonal T-cell ex

281 rotocol describes the facile assembly of APC-ms in ~4 h and rapid expansion or enrichment of relevant

282 tly, we developed APC-mimetic scaffolds (APC-ms), which present signals to T cells in a physiological

283 2 x 2, [x(1) = the age(y), x(2) = the NEG-C (ms)].

284 The extended ms-PAF method enabled the adjustment of current water qu

285 ultisubstance-Potentially Affected Fraction (ms-PAF) to a nonchemical stressor, elevated sea surface

286 The RO(2):GFR (ms/mL/min) was calculated as RO(2) (T2*, ms) divided by

287 amic compression (ns) or fast laser heating (ms).

288 eart rate variability (HRV) [rMSSD, SD1, HF (ms(2))] and skin conductance were evaluated before and d

289 rate (HR) variability (HRV) (rMSSD, SD1, HF [ms(2)]) were evaluated before and during recovery from e

290 collagen I and detect collagen I-induced mus-ms time-scale dynamics in the beta(2)m backbone.

291 tive conformation of DHFR sampled on the mus-ms timescale.

292 conformational changes occurring on the mus-ms timescale.

293 Iron normalizes ms(2)t(6)A37 and proinsulin lysine incorporation, restor

294 hort-lived conformational states over the ns-ms timescale.

295 r short/long term plasticity in the order of ms/minutes, respectively.

296 ing and rejection of noncognate TCs on a sub-ms timescale is essential to enable incorporation of the

297 FR (ms/mL/min) was calculated as RO(2) (T2*, ms) divided by GFR (mL/min).

298 ensive study at different time scales (fs to ms) to determine the effect of competitive reactions on

299 motions spanning a dynamic range from ns to ms.

300 ylthiolation of t(6)A37 in tRNA(Lys)(UUU) to ms(2)t(6)A37.