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1 fect mechanical and electrical properties of heart muscle cells.
2 tential propagation along a linear strand of heart muscle cells.
3 graft rejection in association with death of heart muscle cells.
4 d in Purkinje fibers as compared to ordinary heart muscle cells.
5 the key moiety disrupting the physiology of heart muscle cells.
6 l exerts a direct cardioprotective effect on heart muscle cells, an effect mediated by selective acti
7 can modulate ICa,L, but not ICa,T, in squid heart muscle cells, and that the underlying G protein pa
8 e maturation and pathogenesis of adult human heart muscle cells, and this concept may be expanded to
9 s show that the enhanced force observed when heart muscle cells are maximally activated by calcium is
10 of the L-type calcium current in the type II heart muscle cells, but had no effect on the T-type calc
11 indicate that improving the contractility of heart muscle cells by boosting intracellular calcium han
12 y of human embryonic stem cells (hESCs) into heart muscle cells (cardiomyocytes) is highly sensitive
15 iomyocytes activates PARS and contributes to heart muscle cell death by apoptosis, experiments were p
16 when an atrial chamber fibrillates, and when heart muscle cells die en masse after a heart attack.
18 h immunosuppression might enhance salvage of heart-muscle cells during acute cardiac-allograft reject
20 alcium current in either type of dissociated heart muscle cell, even at concentrations much higher th
23 hypoblast possessed broad capacity to induce heart muscle cells in pregastrula and mid-gastrula epibl
25 in on the actin-containing thin filaments of heart muscle cells, initiating a change in filament stru
27 of viral gene transfer to convert quiescent heart-muscle cells into pacemaker cells, and the success
29 ion, but that loss of all Tln forms from the heart-muscle cell leads to myocyte instability and a dil
32 s show that during and after conversion from heart muscle cells, Purkinje fibers express a unique myo
33 ria and cytoplasmic protein loss in a living heart muscle cell should lead to systolic dysfunction.
34 occur in the terminally differentiated adult heart muscle cells, studies in endomyocardial biopsies f
35 ine factor, endothelin, can induce embryonic heart muscle cells to differentiate into Purkinje fibers
36 ulated increase in ICa,L seen in the type II heart muscle cells was not mediated by a PTX-sensitive G
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