ライフサイエンスコーパス: cardiac contraction

1 ultrastructural) architecture, which enables cardiac contraction.

2 sin that pull on actin filaments to generate cardiac contraction.

3 etic stimulation on the rate and strength of cardiac contraction.

4 rom each other with concurrent initiation of cardiac contraction.

5 activity, Ca(2+) signalling and arterial and cardiac contraction.

6 pping of mRNAs encoding proteins involved in cardiac contraction.

7 ynaptic transmission, neural plasticity, and cardiac contraction.

8 studies used lidocaine perfusion to abolish cardiac contraction.

9 y abdominal palpation until the cessation of cardiac contraction.

10 n heart failure, while hyperglycemia impairs cardiac contraction.

11 rotein kinase A (PKA) activation to regulate cardiac contraction.

12 the cardiac action potential and initiating cardiac contraction.

13 a(2+) efflux across the sarcolemma following cardiac contraction.

14 s in decapping of critical mRNAs involved in cardiac contraction.

15 nd valves, is not dependent on blood flow or cardiac contraction.

16 ficant enhancement of in vitro parameters of cardiac contraction.

17 ortant role in ion homeostasis and regulates cardiac contraction.

18 Troponin is essential for the regulation of cardiac contraction.

19 allosterically involved in calcium-mediated cardiac contraction.

20 gulatory complex that is required for normal cardiac contraction.

21 culation, and dictate the rate and rhythm of cardiac contraction.

22 nin tail region, modulates the regulation of cardiac contraction.

23 acellular Ca2+ concentration and strengthens cardiac contraction.

24 Na,K-ATPase isoform in Ca2+ signaling during cardiac contraction.

25 in heart and regulates the rate and force of cardiac contraction.

26 was completely preserved because of greater cardiac contraction.

27 anges in sarcoplasmic reticulum function and cardiac contraction.

28 (type-2 ryanodine receptor) is essential for cardiac contraction.

29 gle crossbridges can contribute to increased cardiac contraction.

30 h demands a higher ATP production to sustain cardiac contraction.

31 ation to augmented Ca2+ influx and increased cardiac contraction.

32 ovel biomechanical forces upon initiation of cardiac contractions.

33 ntact with their target despite the vigorous cardiac contractions.

34 owed the heartbeat and produced fibrillatory cardiac contractions.

35 e, MLC2, is recognized as a key regulator of cardiac contraction, a MLCK that is preferentially expre

36 Gaskell's elucidation of the sequence of cardiac contraction and atrioventricular block and his c

37 determination of the presence or absence of cardiac contraction and breathing.

38 Impaired cardiac contraction and dilated cardiomyopathy were obse

39 ies demonstrate essential roles for Dicer in cardiac contraction and indicate that miRNAs play critic

40 alcium-dependent regulatory system mediating cardiac contraction and inotropy.

41 Because cardiac contraction and intracardiac hemodynamic forces

42 d leads to heart failure by interfering with cardiac contraction and intracellular transport is a den

43 ms involved in the opposing effects of NO on cardiac contraction and investigated whether NO modulate

44 AMP accumulation, yet play distinct roles in cardiac contraction and myocyte apoptosis.

45 Cardiac contraction and relaxation are regulated by conf

46 through the same second messenger regulates cardiac contraction and relaxation dependent on its subc

47 Cardiac contraction and relaxation dynamics result from

48 ng the dephosphorylation state of cMyBP-C on cardiac contraction and relaxation in experimental heart

49 The normal influence of heart rate (HR) on cardiac contraction and relaxation in the mouse remains

50 e troponin complex and is a key regulator of cardiac contraction and relaxation.

51 of Ca(2+) channels, allowing fine control of cardiac contraction and rhythmicity in cardiac tissue wh

52 lating evidence indicates a crucial role for cardiac contraction and the resulting fluid forces in sh

53 heart failure by increasing the strength of cardiac contraction and, more recently, is used for hear

54 erbb2 mutants, tnnt2a morphants, which lack cardiac contractions and flow, and myh6 morphants, which

55 Cardiac contractions and hemodynamic forces are essentia

56 ) channel Ca(V) 1.2 governs gene expression, cardiac contraction, and neuronal activity.

57 ) channel Ca(V)1.2 controls gene expression, cardiac contraction, and neuronal activity.

58 3 forms showed delayed ARVC5 onset, improved cardiac contraction, and reduced ECG abnormalities compa

59 l artificial-intelligence-derived metrics of cardiac contraction, and their relationship with MACE wa

60 ghts into the role of the myosin filament in cardiac contraction, assembly, and disease.

61 lamine release resulting in the formation of cardiac contraction bands may represent the cause of dea

62 ein C (cMyBP-C) has a key regulatory role in cardiac contraction, but the mechanism by which changes

63 Isoflurane and propofol are known to depress cardiac contraction, but the molecular mechanisms involv

64 fraction by 16% and the energy efficiency of cardiac contraction by 1%.

65 crease in heart rate affects the strength of cardiac contraction by altering the Ca(2+) transient as

66 Regulation of cardiac contraction by neurotransmitters and hormones is

67 we compare two genetic approaches to control cardiac contractions by modulating the levels of the ess

68 Control over cardiac contractions can be achieved pharmacologically o

69 We show that this lack of early cardiac contraction defects is due, at least in part, to

70 that enables quantitative analysis of normal cardiac contraction, disease phenotypes, and pharmacolog

71 we observed pulses that were coincident with cardiac contraction documented by esophageal echocardiog

72 y regulator of the kinetics and amplitude of cardiac contraction during beta-adrenergic stimulation a

73 ns of continual Ca2+ transients that mediate cardiac contraction during each heartbeat.

74 f the FTO-dependent cardiac m6A methylome in cardiac contraction during heart failure and provides a

75 Tolerance was defined as the persistence of cardiac contraction for the duration of evaluation (125-

76 el unexpected role of BDNF in regulating the cardiac contraction force independent of the nervous sys

77 cemaker provides effective pacing to restore cardiac contraction from a nonbeating heart and have the

78 eart muscle and the ultrastructural basis of cardiac contraction have been reviewed.

79 afeguard the splicing of genes essential for cardiac contraction, highlighting the importance of SF c

80 art development, we investigated the role of cardiac contraction in chamber maturation, focusing on t

81 despread mis-splicing of genes essential for cardiac contraction in double-KO mice, underscoring the

82 reorientation of myofiber aggregates during cardiac contraction in patients with dilated cardiomyopa

83 hip between this faster motility and altered cardiac contraction in patients with HCM is discussed.

84 nC) is the regulatory protein that initiates cardiac contraction in response to Ca(2+) TnC binding Ca

85 ion of the mutant protein and a disabling of cardiac contraction in the submaximal range of myoplasmi

86 complex regulatory mechanisms that fine-tune cardiac contraction, in which myosin not only generates

87 Cardiac contraction is modulated by the phosphorylation

88 ation of cardiac contraction, we showed that cardiac contraction is required for trabeculation throug

89 Cardiac contraction is triggered by the release of Ca(2+

90 isoforms play key roles in the regulation of cardiac contraction, ischemic preconditioning, and hyper

91 cardiovascular system, including effects on cardiac contraction, relaxation, and energetics.

92 es cGMP formation, which, in turn, modulates cardiac contraction/relaxation by a) altering cardiomyoc

93 Given that cardiac contraction requires a continuous supply of ATP

94 at forced Notch activation in the absence of cardiac contraction rescues efnb2a and nrg1 expression.

95 tent increases in cAMP signals for sustained cardiac contraction response; and arrestin acts as an ag

96 our findings describe an essential role for cardiac contraction-responsive transcriptional changes i

97 , including humans, have a positive FFR, and cardiac contraction strength increases with heart rate.

98 cium signaling in cardiomyocytes to maintain cardiac contraction, sufficient stroke volume, and adequ

99 defect in the primary mechanism controlling cardiac contraction, switching between different conform

100 ed by elevations of cytosolic calcium during cardiac contraction (systole).

101 e critical free energy of ATP hydrolysis for cardiac contraction that is consistent with these findin

102 hat seems to contribute to the regulation of cardiac contraction through interactions with either myo

103 myosin in the primed state prior to onset of cardiac contraction, thus increasing the number of heads

104 in HCTnT can perturb the proper response of cardiac contraction to changes in pH.

105 myosin binding protein C (cMyBP-C) modulates cardiac contraction via direct interactions with cardiac

106 otential importance of stretch activation in cardiac contraction, we examined the effects of cMyBP-C

107 By genetic and pharmacological ablation of cardiac contraction, we showed that cardiac contraction

108 omyocyte excitation/contraction coupling and cardiac contraction were evaluated in isolated mouse and

109 etected micromovements of the head following cardiac contraction (what we have described as "headpuls

110 cytosolic Ca(2+) to physiologically augment cardiac contraction, whereas excessive betaAR activation

111 process lags 2-3 months behind the onset of cardiac contraction, which may be a prerequisite for car

112 There were more pronounced impairments of cardiac contraction with greater eccentric cardiac hyper

113 adation line enables non-invasive control of cardiac contractions with high spatial and temporal spec

114 amplitude and frequency analysis of physical cardiac contraction, with nonlinear analysis of the cont