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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
7 aging mice exhibit a significant decline in myoplasmic Ca(2+) concentration resulting from a reducti
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
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
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
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);
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
38 ch potentiator nitrate was shown to increase myoplasmic [Ca2+] during twitch and tetani, but not to r
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
45 sensitivity to activated calcium release and myoplasmic calcium levels, subsequently affecting mitoch
47 surface potential change that occurs on the myoplasmic face of the T-system membranes when the macro
49 amplitude and half-duration of the change in myoplasmic free [Ca2+] (Delta[Ca2+]) differed significan
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
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
61 measured the osmotic pressure of diffusible myoplasmic proteins in frog (Rana temporaria) skeletal m
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
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