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1 the ATP, Ca2+, and Na+ concentrations in the myoplasmic and mitochondrial matrix compartments.
2 y differential equations (ODEs) for the bulk myoplasmic and network SR [Ca2+], a realistic but minima
3 ordinary differential equations for the bulk myoplasmic and sarcoplasmic reticulum [Ca2+], a realisti
4 el activity plays a critical role in causing myoplasmic Ca(2+) and Na(+) overload both at rest and du
5  excitation-contraction coupling and resting myoplasmic Ca(2+) concentration ([Ca(2+)](rest)) in flex
6                                    Since the myoplasmic Ca(2+) concentration is a critical regulator
7  aging mice exhibit a significant decline in myoplasmic Ca(2+) concentration resulting from a reducti
8              Dantrolene reduces the elevated myoplasmic Ca(2+) generated during malignant hyperthermi
9 t an indirect role for triadin in regulating myoplasmic Ca(2+) homeostasis and organizing the molecul
10  Ca(V)1.1 R174W-expressing myotubes, resting myoplasmic Ca(2+) levels were elevated, and sarcoplasmic
11 nactivation of the Ca(2+) release channel by myoplasmic Ca(2+) likely explains this reduction.
12 ype 1 ryanodine receptor activator, elicited myoplasmic Ca(2+) release in YFP-Rem-expressing myotubes
13 es expressing GFP-alpha(1S)[III-IVa] yielded myoplasmic Ca(2+) transients that activated at approxima
14 ayed by electrically evoked contractions and myoplasmic Ca(2+) transients.
15 ught to play the limited role of maintaining myoplasmic [Ca(2+)] above the critical threshold that ma
16 rt with neurogenically controlled cycling of myoplasmic [Ca(2+)] but rather are driven myogenically b
17 +) sparks are brief, localized elevations of myoplasmic [Ca(2+)] caused by release of increments of C
18               To explore the hypothesis that myoplasmic [Ca(2+)] might similarly rise and fall in con
19                                      Rise in myoplasmic [Ca(2+)] was monitored with antipyrylazo III
20  in the home cage, have chronically elevated myoplasmic[Ca(2+)](rest), and present muscle damage in s
21  a higher level (10-30 microM) than the bulk myoplasmic Ca2+ (peak [Ca2+]i approximately 1 microM).
22 clusion that the age-related decline in peak myoplasmic Ca2+ and specific force is not explained by s
23 el that calculated Ca2+ binding to the major myoplasmic Ca2+ buffers (troponin, ATP and parvalbumin);
24                     Although an elevation in myoplasmic Ca2+ can activate the skeletal muscle ryanodi
25 tected brief, highly localized elevations of myoplasmic Ca2+ concentration (Ca2+ "sparks") initiated
26 tal muscle prevents age-related decreases in myoplasmic Ca2+ concentration and consequently in specif
27 on potential (delta F) appeared to track the myoplasmic Ca2+ transient (delta[Ca2+]) without delay.
28  absence of S100A1 leads to decreased global myoplasmic Ca2+ transients following electrical excitati
29 2+ currents of approximately normal size and myoplasmic Ca2+ transients that were skeletal-type, but
30 as well, the maximal rates of rise of global myoplasmic Ca2+ transients were due primarily to Ca2+ re
31  inactivation of VGCC, assessed by buffering myoplasmic Ca2+ with EGTA in the pipette and using Ca2+
32 indicator expected to be in equilibrium with myoplasmic Ca2+, gave similar values for both the [Ca2+]
33 e generation is roughly proportional to peak myoplasmic Ca2+, we use [Ca2+]i in the model to explore
34  membrane Ca2+-ATPase, mitochondrial uptake, myoplasmic Ca2+-binding proteins and other sources of VG
35 e primed by a physiological level of resting myoplasmic Ca2+.
36                Brief localized elevations in myoplasmic [Ca2+] (Ca2+ sparks) in individual sarcomeres
37                These results exclude reduced myoplasmic [Ca2+] as the cause of the shift in optimum l
38 ch potentiator nitrate was shown to increase myoplasmic [Ca2+] during twitch and tetani, but not to r
39  myosin light chain (MLC) phosphorylation or myoplasmic [Ca2+].
40 , to ascertain whether parvalbumin (Parv), a myoplasmic calcium buffer, could correct the diastolic d
41  RyR2 open probability, Ca2+ sparks, and the myoplasmic calcium concentration ([Ca2+]i) during excita
42 f single SMCs was used to measure changes in myoplasmic calcium concentration (Ca(m)) in response to
43 rdiac contraction in the submaximal range of myoplasmic calcium concentrations.
44                                      In vivo myoplasmic calcium levels in Drosophila flight muscle ha
45 sensitivity to activated calcium release and myoplasmic calcium levels, subsequently affecting mitoch
46  using sharp microelectrodes to preserve the myoplasmic contents.
47  surface potential change that occurs on the myoplasmic face of the T-system membranes when the macro
48 uscle homogenates that contained 0.43 microM myoplasmic FKBP12 and was attenuated by S107.
49 amplitude and half-duration of the change in myoplasmic free [Ca2+] (Delta[Ca2+]) differed significan
50                                          The myoplasmic free [Ca2+] transient elicited by an action p
51 rization-induced (80 mM KCl) accumulation of myoplasmic free Ba2+ and free Ca2+.
52  Ca(2+) that results in chronically elevated myoplasmic free Ca(2+) concentration ([Ca(2+)]i) at rest
53 ator fluorescence (DeltaF), a monitor of the myoplasmic free Ca(2+) transient ([Ca(2+)]), and changes
54 ular Ca2+ regulatory mechanisms to limit net myoplasmic free Ca2+ accumulation in smooth muscle cells
55 ular Ca2+ regulatory mechanisms to limit net myoplasmic free Ca2+ accumulation.
56  differing assumptions: (i) that the resting myoplasmic free Ca2+ concentration ([Ca2+]R) and the tot
57 d Tau cooperatively elevated basal levels of myoplasmic-free calcium, an effect that was accompanied
58           However, the presence of excessive myoplasmic gamma-actin may also contribute to altered ce
59                            During rest, mean myoplasmic Na+ concentration was significantly higher in
60            23Na MR imaging depicts increased myoplasmic Na+ in HyperPP with permanent weakness.
61  measured the osmotic pressure of diffusible myoplasmic proteins in frog (Rana temporaria) skeletal m
62    The mean osmotic pressure produced by the myoplasmic proteins was 9.7 mOsm (4 degrees C).
63  expression was associated with an increased myoplasmic resting [Ca(2+)] ([Ca(2+)](rest)), increased
64 cle cells results in significant increase of myoplasmic resting free Ca(2+) ([Ca(2+)](rest)), suggest
65 and adult fibers had significantly increased myoplasmic resting free Ca(2+).[(3)H]Ryanodine binding s
66 luxes can be represented as occurring in two myoplasmic subcompartments for Ca(2+) distribution, one
67  indicators, estimates were obtained for the myoplasmic value of KD, Ca (the indicator's dissociation
68 fibre differences may reflect differences in myoplasmic viscosity and connectin (titin) isoforms (in
69                             The state of the myoplasmic water was probed by determining the osmotic c

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