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1 diastolic threshold of excitation and atrial conduction time.
2 ained trade-off that reduces both volume and conduction time.
3 nel sign, and median nerve motor and sensory conduction time.
4 lesions on MRI scans or an increase in motor conduction time.
5 s caused an increase in the atrioventricular conduction time.
6 om the pacing site or with a long retrograde conduction time.
7 e penetration depths, signal amplitudes, and conduction times.
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 t S-QRS (130+/-12 versus 82+/-12 ms), longer conduction time (103+/-14 versus 43+/-13 ms), and slower
12 he wall, (3) sequence of activation, and (4) conduction time across the wall.
13                                 In contrast, conduction times along CT6 axons were much slower, with
14 ram, reflects ventricular depolarization and conduction time and is a risk factor for mortality, sudd
15 on, but does reveal impairments in brainstem conduction time and temporal processing within the brain
16 Restitution of action potential duration and conduction time and the effective refractory period afte
17    All CT5s had fast-conducting axons (<2 ms conduction time), and nearly all showed step-phase-relat
18 ial node recovery time, increased sinoatrial conduction time, and recurrent sinus pauses.
19 ays and potential imprecision in cross-brain conduction times are especially great in unmyelinated ax
20                              Thalamocortical conduction times are short, but layer 6 corticothalamic
21                          We show that axonal conduction times are strongly related to multiple visual
22 yceal synaptic terminals and matching axonal conduction times, are evident in several of the major as
23                                  Orthodromic conduction time around the line to its distal side was l
24 ous sinus rate, and prolongation of AV nodal conduction time as end points of vagal effects, we deter
25 on times shorter than atrioventricular nodal conduction times before adenosine administration.
26                                              Conduction time between M and epicardial cells increased
27 ing to length, in order to precisely fix the conduction time between the inferior olive and cerebella
28 urons found in superficial layers had longer conduction times, broader spike waveforms, and were more
29 tion velocities to normalize olivocerebellar conduction time, but are consistent with a CF conduction
30 MS patients was left and right central motor conduction time (CMCT) to abductor digiti minimi muscle
31                                Central motor conduction time (CMCT), serial MRI of the brain and spin
32 nts of corticomotor threshold, central motor conduction time (CMCT), silent period duration and the a
33 rophysiological study, we measured bi-atrial conduction time (CT) electrogram fractionation at 64 or
34 )), diastolic threshold of excitation (DTE), conduction time (CT), and the shortest S(1)-S(1) permitt
35 tial duration at 90% repolarization (APD90), conduction times (CT) between the pacing site and the ot
36                  During AFL, we measured the conduction time, CTi, through the isthmus between the tr
37 icuspid annulus and eustachian ridge and the conduction time, CTni, through the remainder of the righ
38                                              Conduction times during AFL and entrainment were compare
39 slow AVNRT in the same patient, fast pathway conduction times during the 2 types of AVNRT were calcul
40 t whether left atrial (LA) electromechanical conduction time (EMT) and myocardial mechanics were asso
41 s found not to relate simply to the relative conduction times for passage of rhythmic bursts from a c
42 -> EEG direction were closer to the expected conduction times for these pathways than the average del
43                    Subtraction of peripheral conduction times gave estimated central delays of locomo
44 athy, VT and septal scar, delayed transmural conduction time (&gt;40 ms) and fractionated, late, split,
45 p 1 had an abnormally prolonged His-Purkinje conduction time (HV interval, 63+/-11 versus 49+/-6 ms;
46 0 mumol/L) markedly prolonged postpacing SAN conduction time in HF by 206 +/- 99 milliseconds (versus
47 the conduction anisotropy and the transmural conduction time in pig ventricles.
48  may be due to the progressive maturation of conduction time in the afferent visual pathways, with th
49 ow and fast pathways, as well as the altered conduction time in the slow pathway parallel with changi
50  the heart (P-R interval or atrioventricular conduction time) in response to selective stimulation of
51        SPS patients had normal central motor conduction times, normal thresholds for motor evoked pot
52                                   After a RF conduction time of 2 seconds, the individual areas of th
53 ebellar cortex may have differences in spike conduction time of a few milliseconds, and that submilli
54 -mediated increase in atrioventricular nodal conduction time of isolated perfused guinea pig hearts f
55                       The fastest axons have conduction times of 1-5 ms across the neocortex and <1 m
56 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
57          Here, we investigate (1) how axonal conduction times of corticogeniculate (CG) neurons are r
58 rmalities of the sinus node, prolongation of conduction times or inducible arrhythmias found at these
59 <0.003), and longer septal electromechanical conduction time (P<0.01).
60                                        Local conduction times parallel and perpendicular to fiber ori
61 ximately 90 min, increasing peripheral motor conduction time (PMCT) by approximately 35% (assessed by
62 ss by reducing action potential duration and conduction time restitution in a dose-dependent fashion,
63                   The stimulus to His bundle conduction times (SH) at both sites (SH(P) and SH(A), re
64 inus node dysfunction, prolongs intra-atrial conduction time, shortens atrial refractoriness, and per
65  adenosine effect and resulted in dormant AP conduction times shorter than atrioventricular nodal con
66 iform across the broad spectrum of CG axonal conduction times.SIGNIFICANCE STATEMENT Corticothalamic
67 othalamic axons display an enormous range of conduction times, some exceeding 40-50 ms.
68  terminalis, found that the action potential conduction time taken and conduction distance increased
69 arget, is unaffected, consistent with normal conduction times through the His-Purkinje system measure
70 s study was to relate abnormalities of motor conduction time to the presence of spinal cord MRI lesio
71     Intercycle interval (ICI) and wave front conduction time (WCT) were determined for the first 5 po
72              Given minimum motor and sensory conduction time, we estimate that the loud sound reduced
73                                           CG conduction times were also significantly related to visu
74                                    CG axonal conduction times were strongly related to modulated firi
75 ) by decreasing p to 0.65, whereas q, N, and conduction times were unaffected.
76 ved in most patients, but the infra-His (HV) conduction times were usually abnormal.
77 ndrites and axons optimizing cable costs and conduction time while keeping the connectivity at the hi
78 n an optimal manner which requires tuning of conduction time with millisecond precision.
79  AVP induced synaptic failures and increased conduction time without altering the V-M relationship of

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