ライフサイエンスコーパス: conduction time

1 diastolic threshold of excitation and atrial conduction time.

2 ahead of the His) due to the retrograde His conduction time.

3 ained trade-off that reduces both volume and conduction time.

4 nel sign, and median nerve motor and sensory conduction time.

5 lesions on MRI scans or an increase in motor conduction time.

6 s caused an increase in the atrioventricular conduction time.

7 om the pacing site or with a long retrograde conduction time.

8 visual processing across the spectrum of CG conduction times.

9 ing the spectrum of corticogeniculate axonal conduction times.

10 sponsiveness spanning the spectrum of axonal conduction times.

11 e penetration depths, signal amplitudes, and conduction times.

12 t S-QRS (130+/-12 versus 82+/-12 ms), longer conduction time (103+/-14 versus 43+/-13 ms), and slower

13 he wall, (3) sequence of activation, and (4) conduction time across the wall.

14 In contrast, conduction times along CT6 axons were much slower, with

15 Prolongation in transisthmus conduction time and differential pacing techniques are c

16 ram, reflects ventricular depolarization and conduction time and is a risk factor for mortality, sudd

17 recruitment of spinal motor neurons, central conduction time and motor-evoked potential (MEP) latency

18 ections can result in prolonged transisthmus conduction time and reversal in coronary sinus activatio

19 on, but does reveal impairments in brainstem conduction time and temporal processing within the brain

20 Restitution of action potential duration and conduction time and the effective refractory period afte

21 arly PR interval) that reflect longer atrial conduction times and a lower risk of AF.

22 All CT5s had fast-conducting axons (<2 ms conduction time), and nearly all showed step-phase-relat

23 ial node recovery time, increased sinoatrial conduction time, and recurrent sinus pauses.

24 ays and potential imprecision in cross-brain conduction times are especially great in unmyelinated ax

25 Thalamocortical conduction times are short, but layer 6 corticothalamic

26 We show that axonal conduction times are strongly related to multiple visual

27 yceal synaptic terminals and matching axonal conduction times, are evident in several of the major as

28 Orthodromic conduction time around the line to its distal side was l

29 ous sinus rate, and prolongation of AV nodal conduction time as end points of vagal effects, we deter

30 on times shorter than atrioventricular nodal conduction times before adenosine administration.

31 Conduction time between M and epicardial cells increased

32 ing to length, in order to precisely fix the conduction time between the inferior olive and cerebella

33 urons found in superficial layers had longer conduction times, broader spike waveforms, and were more

34 tion velocities to normalize olivocerebellar conduction time, but are consistent with a CF conduction

35 MS patients was left and right central motor conduction time (CMCT) to abductor digiti minimi muscle

36 Central motor conduction time (CMCT), serial MRI of the brain and spin

37 nts of corticomotor threshold, central motor conduction time (CMCT), silent period duration and the a

38 rophysiological study, we measured bi-atrial conduction time (CT) electrogram fractionation at 64 or

39 )), diastolic threshold of excitation (DTE), conduction time (CT), and the shortest S(1)-S(1) permitt

40 tial duration at 90% repolarization (APD90), conduction times (CT) between the pacing site and the ot

41 During AFL, we measured the conduction time, CTi, through the isthmus between the tr

42 icuspid annulus and eustachian ridge and the conduction time, CTni, through the remainder of the righ

43 a quarter-power scaling relationship between conduction time delay and body size.

44 axonal conduction velocity and consequently conduction time delays, or latencies; however, local rul

45 Conduction times during AFL and entrainment were compare

46 slow AVNRT in the same patient, fast pathway conduction times during the 2 types of AVNRT were calcul

47 t whether left atrial (LA) electromechanical conduction time (EMT) and myocardial mechanics were asso

48 s found not to relate simply to the relative conduction times for passage of rhythmic bursts from a c

49 -> EEG direction were closer to the expected conduction times for these pathways than the average del

50 Subtraction of peripheral conduction times gave estimated central delays of locomo

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

52 athy, VT and septal scar, delayed transmural conduction time (>40 ms) and fractionated, late, split,

53 The transisthmus conduction time had limited predictive value for disting

54 p 1 had an abnormally prolonged His-Purkinje conduction time (HV interval, 63+/-11 versus 49+/-6 ms;

55 tion on sensorimotor integration and central conduction time in an asymptomatic population.

56 gnment has a direct influence on the central conduction time in an asymptomatic population.

57 0 mumol/L) markedly prolonged postpacing SAN conduction time in HF by 206 +/- 99 milliseconds (versus

58 the conduction anisotropy and the transmural conduction time in pig ventricles.

59 may be due to the progressive maturation of conduction time in the afferent visual pathways, with th

60 ow and fast pathways, as well as the altered conduction time in the slow pathway parallel with changi

61 the heart (P-R interval or atrioventricular conduction time) in response to selective stimulation of

62 uggesting that CB-M1 pathways with different conduction times interact with AP and PA networks.

63 rior bodies of C2-C7), central somatosensory conduction time (latency) (N13-N20), and amplitudes of p

64 tter outcomes across all measures except VEP conduction time; male sex, which predicted worse outcome

65 P27, frontal N30 potentials (P < 0.001), and conduction time N13-N20 (P = 0.004).

66 SPS patients had normal central motor conduction times, normal thresholds for motor evoked pot

67 After a RF conduction time of 2 seconds, the individual areas of th

68 ion delay (CD) was defined as interelectrode conduction time of 7 to 11 ms and conduction block (CB)

69 ebellar cortex may have differences in spike conduction time of a few milliseconds, and that submilli

70 -mediated increase in atrioventricular nodal conduction time of isolated perfused guinea pig hearts f

71 The fastest axons have conduction times of 1-5 ms across the neocortex and <1 m

72 erves improved on the basis of faster median conduction times of 3.1 and 3.0 ms and 3.3 and 3.4 ms, r

73 Here, we investigate (1) how axonal conduction times of corticogeniculate (CG) neurons are r

74 rmalities of the sinus node, prolongation of conduction times or inducible arrhythmias found at these

75 <0.003), and longer septal electromechanical conduction time (P<0.01).

76 Local conduction times parallel and perpendicular to fiber ori

77 ximately 90 min, increasing peripheral motor conduction time (PMCT) by approximately 35% (assessed by

78 ss by reducing action potential duration and conduction time restitution in a dose-dependent fashion,

79 The stimulus to His bundle conduction times (SH) at both sites (SH(P) and SH(A), re

80 inus node dysfunction, prolongs intra-atrial conduction time, shortens atrial refractoriness, and per

81 adenosine effect and resulted in dormant AP conduction times shorter than atrioventricular nodal con

82 iform across the broad spectrum of CG axonal conduction times.SIGNIFICANCE STATEMENT Corticothalamic

83 othalamic axons display an enormous range of conduction times, some exceeding 40-50 ms.

84 terminalis, found that the action potential conduction time taken and conduction distance increased

85 and female rabbits, and measure their axonal conduction times, thalamic inputs and receptive field pr

86 arget, is unaffected, consistent with normal conduction times through the His-Purkinje system measure

87 s study was to relate abnormalities of motor conduction time to the presence of spinal cord MRI lesio

88 Intercycle interval (ICI) and wave front conduction time (WCT) were determined for the first 5 po

89 Given minimum motor and sensory conduction time, we estimate that the loud sound reduced

90 CG conduction times were also significantly related to visu

91 CG axonal conduction times were strongly related to modulated firi

92 ) by decreasing p to 0.65, whereas q, N, and conduction times were unaffected.

93 ved in most patients, but the infra-His (HV) conduction times were usually abnormal.

94 ndrites and axons optimizing cable costs and conduction time while keeping the connectivity at the hi

95 n an optimal manner which requires tuning of conduction time with millisecond precision.

96 AVP induced synaptic failures and increased conduction time without altering the V-M relationship of