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1 about 30 microM (perhaps 100-1,000 times the resting level).
2 st depletions analyzed were to 8+/-6% of the resting level.
3 e SR depletion was to 20+/-10% (s.d.) of the resting level.
4 t membrane potentials more negative than the resting level.
5 uced yet always higher than the preocclusion resting level.
6 n, which is followed by a slow return to the resting level.
7 st and during exercise was below the control resting level.
8 [Ca2+]i has been completely restored to its resting level.
9 d to increase their precision estimates from resting levels.
10 cellular free calcium concentrations towards resting levels.
11 g [Ca2+]i elevations and clamping [Ca2+]i to resting levels.
12 e phagosome although [Ca(2+)](i) remained at resting levels.
13 in(-1), P<0.01) increased from the depressed resting levels.
14 l was able to effectively restore [Ca2+]i to resting levels.
15 lowed the recovery of [Ca(2+)](cyto) towards resting levels.
16 rophic muscles compared with those at normal resting levels.
17 ncrease in fluorescence (L(0)) compared with resting levels.
18 h internal calcium strongly buffered to near resting levels.
19 ackground discharge rates were comparable to resting levels.
20 ading to a slow return of Ca(i) and Na(i) to resting levels.
21 lular Ca2+ that slowly recovered to baseline resting levels.
22 ollowed by a steady-state augmentation above resting levels.
23 ased 8.4-fold (P = .002) and returned to the resting level 5 minutes after exercise, whereas the lact
24 rkinje cells fire a single type of spikes at resting level, a subset of small Purkinje cells fire sma
25 e, whereas reversal of glucose uptake toward resting levels after exercise/contraction was markedly f
26 BA defects, leading to reduced intracellular resting levels and induced surface levels of CTLA-4.
27 ion, the rate of actively returning force to resting levels, and passive release of force "relaxation
28 d (>30 s) even when [Ca(2+)](c) had regained resting levels, and was not prevented by kinase or phosp
31 responses to arterial pressure changes below resting levels but normal initial responses to upright t
33 osolic Ca2+ concentration was clamped at the resting level by a high concentration of a selective Ca2
36 ensuing 2 h, whereas ATP levels decayed to a resting level; consequently, resting extracellular UDP-g
37 suggest that by buffering [Ca(2+)](ER) near resting levels, CRT may prevent InsP(3) from depleting t
39 g intraterminal Ca2+ to approximately normal resting levels does not eliminate the modulation, sugges
41 rease was due to a rise of intra-WPB pH from resting levels, estimated as pH 5.45+/-0.26 (s.d., n=144
43 , the entire axonal arborization returned to resting level in a spatially uniform manner during the D
51 ation in low [Cl] media as is NKCC1, but the resting level of activity is higher in h1r2A0.7 and acti
52 his discrepancy may be the difference in the resting level of Ang II, which may be lower in well-trai
58 ling caused by a progressive increase in the resting level of Ca(2+), which may influence cognition b
60 hloride with prestin, we determined that the resting level of chloride in OHCs is near or below 10 mm
61 GABAergic system, it is conceivable that the resting level of cortical GABAergic tone directly relate
64 take capacity are impaired, and an increased resting level of free intracellular Ca(2+) is accompanie
72 release without increasing [Ca2+]i, although resting levels of calcium are required, suggesting alter
74 ition and thus do not contribute markedly to resting levels of CSNA and HR, but when disinhibited, th
79 ing restraint were due to the differences in resting levels of HR, since both control and chronically
80 ows 2-Cys Prxs to act as floodgates, keeping resting levels of hydrogen peroxide low, while permittin
81 n to its homeostatic role of maintaining low resting levels of intracellular calcium ([Ca2+](i)), the
86 d Phase 2 were a result of the elevations in resting levels of MAP, but even when differences in rest
89 normal left ventricular function, and normal resting levels of NT-pro-BNP and BNP who were referred f
91 ents with focal limb dyskinesias showed that resting levels of regional cerebral blood flow after ora
92 responses to mental stress, despite elevated resting levels of sympathetic activity, but they do have
95 uff occlusion sustained blood pressure above resting levels only when the leg had intact sensation.
96 tely 20-30 s with thrombin present either to resting levels or to a maintained elevated level of 2.0
98 by 2 degrees C with CO(2) /pH normalized to resting levels, there was a marked cerebral uptake of mi
99 plication is that an increase in ICAM-1 from resting levels to those on inflamed endothelium effectiv
100 ls were unchanged in the training group, but resting levels were significantly (p < 0.001) reduced (a
101 levels of MAP, but even when differences in resting levels were taken into account, HR remained elev
102 es in endoplasmic reticulum calcium near the resting level, whereas a threshold of calcium depletion
103 ic Ca2+ concentration to the pre-stimulation resting level, which was attained long before the endopl
104 ccur with slight elevations of calcium above resting levels, which implies that inhibition should be
105 is prevented by buffering [Ca(2+)] at normal resting levels while in wildtype PNs mGluR1 EPSCs are en
106 etics of other early signals and returned to resting levels while nonspecific desensitization remaine
108 CETNO decreased and V NO increased above resting levels with increasing exercise intensity during