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1 acterized by deep refractoriness to seizure (silent period).
2 did not affect the duration of the cortical silent period.
3 de with voluntary facilitation and a shorter silent period.
4 physiology occurring during the seizure-free silent period.
5 status) and 4.3+/-0.7 late (14 days) in the silent period.
6 terval intracortical inhibition and cortical silent period.
7 xplained by a decrease in the density of the silent periods.
8 t bursts of RNA synthesis followed by longer silent periods.
9 nerve response (16 x baseline) followed by a silent period (1-2 s) during which another stimulus evok
10 = 0.01) and the post-motor evoked potential silent period (101 ms; SEM +/- 10) was significantly sho
11 fore conversion, P<.01); (2) an electrically silent period (267+/-45 ms); (3) "organized atrial fibri
12 lices when depolarized during their normally silent period and (2) bursting when depolarized in nonrh
13 t zolpidem reduced hyperexcitability in both silent period and chronically epileptic cells, but was m
14 rtical inhibition was measured with cortical silent period and intracortical inhibition paradigms.
15 al intracortical inhibition and the cortical silent period) and GABAA (short-interval intracortical i
16 thresholds, input/output curves or cortical silent period between patients with secondary and primar
17 between respiratory and syringeal control of silent periods between sound units and wing movement cyc
18 eurons that alternate bursting activity with silent periods, but the mechanism underlying this vital
19 ed by gamma-aminobutyric acid-A receptors in silent period cells differed markedly from controls.
20 or-evoked potentials (MEPs) and the cortical silent period (CSP) evoked by a single-pulse TMS, short-
23 shold, central motor conduction time (CMCT), silent period duration and the amplitude of compound mus
27 racortical inhibition and prolonged cortical silent period during voluntary activity of an intrinsic
28 onal coinactivation: the occurrence of brief silent periods during which all neurons in the local net
29 igms, such as trace conditioning, in which a silent period elapses between the offset of the conditio
34 ements of their display with atypically long silent periods in their song, potentially avoiding adver
36 ion of the reflex occurred within a cortical silent period induced by transcranial magnetic stimulati
37 spheric inhibition (IHI) and the ipsilateral silent period (iSP), whilst excitability of CTS pathways
41 vements of the display are synchronized with silent periods of song, but it is unknown how this coord
43 tracortical facilitation (ICF), the cortical silent period (SP) and spinal reciprocal inhibition (RI)
45 rhythmic CS discharges were interleaved with silent periods, suggesting that apamin- and CTX-sensitiv
47 tials and decreased duration of the cortical silent period (the latter only in the conditioned group)
52 asynchronous state) and (2) "filling-in" of silent periods with low-frequency (2-4 Hz) activity (beg
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