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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 altered the phosphorylation level of cTnI in heart muscle cells and characterized the structural and
8  can modulate ICa,L, but not ICa,T, in squid heart muscle cells, and that the underlying G protein pa
9 e maturation and pathogenesis of adult human heart muscle cells, and this concept may be expanded to
10                                  Conversely, heart muscle cells are inactivated when they shorten dur
11 s show that the enhanced force observed when heart muscle cells are maximally activated by calcium is
12 ctural changes in the myofilaments of intact heart muscle cells associated with activation of myocard
13 of the L-type calcium current in the type II heart muscle cells, but had no effect on the T-type calc
14 indicate that improving the contractility of heart muscle cells by boosting intracellular calcium han
15      Here, we designed a mouse in which only heart muscle cells can be infected with a SARS-CoV-2 str
16 hibitory kinase cascade that represses adult heart muscle cell (cardiomyocyte) proliferation and rene
17 y of human embryonic stem cells (hESCs) into heart muscle cells (cardiomyocytes) is highly sensitive
18                       Here, we show that rat heart muscle cells (cardiomyocytes) undergo a 63% decrea
19            Here, we show that differentiated heart muscle cells, cardiomyocytes, can be induced to pr
20                                          The heart muscle cells could be divided into type I and type
21 iomyocytes activates PARS and contributes to heart muscle cell death by apoptosis, experiments were p
22    A further role for MAP4K4 was proposed in heart muscle cell death triggered by cardiotoxic anti-ca
23 tive therapeutic target in DOX-induced human heart muscle cell death.
24 when an atrial chamber fibrillates, and when heart muscle cells die en masse after a heart attack.
25             No current treatment reactivates heart muscle cell division to prevent this decline.
26 cardiac conduction system differentiate from heart muscle cells during embryogenesis.
27 h immunosuppression might enhance salvage of heart-muscle cells during acute cardiac-allograft reject
28 ent but not proliferation of cardiomyocytes (heart muscle cells) during postnatal development.
29 alcium current in either type of dissociated heart muscle cell, even at concentrations much higher th
30                       At the cellular level, heart muscle cells generate higher force when stretched,
31                                          The heart muscle cells, i.e., the cardiomyocytes, possess a
32 hypoblast possessed broad capacity to induce heart muscle cells in pregastrula and mid-gastrula epibl
33 art transplant model and cytokine-stimulated heart muscle cells in tissue culture.
34 in on the actin-containing thin filaments of heart muscle cells, initiating a change in filament stru
35 n program during terminal differentiation of heart muscle cells into Purkinje fibers.
36  of viral gene transfer to convert quiescent heart-muscle cells into pacemaker cells, and the success
37                Contraction and relaxation of heart muscle cells is regulated by cycling of calcium be
38 ion, but that loss of all Tln forms from the heart-muscle cell leads to myocyte instability and a dil
39                                 Personalized heart muscle cells made from stem cells in the laborator
40 nzyme, pyruvate kinase muscle isozyme M2, in heart muscle cells of juvenile and adult pig models afte
41                                              Heart muscle cells produce peptide hormones such as natr
42 s show that during and after conversion from heart muscle cells, Purkinje fibers express a unique myo
43 ytes towards terminally differentiated adult heart muscle cells remain obscure.
44 ria and cytoplasmic protein loss in a living heart muscle cell should lead to systolic dysfunction.
45 occur in the terminally differentiated adult heart muscle cells, studies in endomyocardial biopsies f
46                                    Mammalian heart muscle cells, termed cardiomyocytes, are one such
47 ine factor, endothelin, can induce embryonic heart muscle cells to differentiate into Purkinje fibers
48   Increased venous filling stretches relaxed heart muscle cells, triggering a stronger contraction in
49 ulated increase in ICa,L seen in the type II heart muscle cells was not mediated by a PTX-sensitive G
50         Cardiac mitochondria from mice whose heart muscle cells we engineered deficient in the mitoch
51         Internal dialysis of isolated type I heart muscle cells with guanosine 5'-O-(3-thiotriphospha