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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
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
19 ays and potential imprecision in cross-brain conduction times are especially great in unmyelinated ax
22 yceal synaptic terminals and matching axonal conduction times, are evident in several of the major as
24 ous sinus rate, and prolongation of AV nodal conduction time as end points of vagal effects, we deter
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
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
37 icuspid annulus and eustachian ridge and the conduction time, CTni, through the remainder of the righ
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
44 athy, VT and septal scar, delayed transmural conduction time (>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
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
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
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
58 rmalities of the sinus node, prolongation of conduction times or inducible arrhythmias found at these
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,
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
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
77 ndrites and axons optimizing cable costs and conduction time while keeping the connectivity at the hi
79 AVP induced synaptic failures and increased conduction time without altering the V-M relationship of
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