ライフサイエンスコーパス: upstroke

1 hich INa is activated to give rise to a fast upstroke.

2 rized resting membrane potential and slow AP upstroke.

3 local Ca(2+) transients that precede the AP upstroke.

4 or a reduction in the amplitude of the spike upstroke.

5 eactivation of INa and thereby drive the EAD upstroke.

6 is significantly longer than the electrical upstroke.

7 tted tip or separating to reduce drag on the upstroke.

8 ned at 50% amplitude (t(F50)) of the optical upstroke.

9 that occurs just before the action potential upstroke.

10 to inversion of their cambered wings during upstroke.

11 uring the downstroke and only 25% during the upstroke.

12 nevertheless very similar epicardial optical upstrokes.

13 reasingly longer delays between AP and Ca2+i upstrokes (9.5 +/- 0.4 to 11.3 +/- 0.4 ms) with increasi

14 maximum rate of rise of the action potential upstroke, a prolongation of the effective refractory per

15 eonatal rat ventricular myocytes had a lower upstroke amplitude (91 +/- 3 vs. control 137 +/- 2 mV) a

16 APs up to several times and increased their upstroke amplitude.

17 These had a rapid upstroke and a short duration and could be blocked with

18 potential that was less negative, and slower upstroke and conduction velocity for rotors in the PV re

19 atrium-selective effects on maximal phase 0 upstroke and conduction velocity.

20 The kinematic symmetry of the hummingbird upstroke and downstroke has led to the assumption that t

21 hat myelin loss does not affect the AP spike upstroke and downstroke kinetics, but dysmyelination red

22 he store Ca2+-ATPases in regulating both the upstroke and downstroke of a Ca2+ spike.

23 was to establish a link between the optical upstroke and exact surface activation time using compute

24 though the specific ion channels used for AP upstroke and repolarization differ.

25 sitive feedback between the action potential upstroke and SCR.

26 ent (I(Ca, L)), which contributes both to AP upstroke and to pacemaker depolarization.

27 s controls the phase of the action potential upstroke and ultimately the final action potential rate.

28 HC-Cre hearts showed faster action potential upstrokes and a more than 2-fold increase in peak I(Na)

29 midal cells reliably encoded the presence of upstrokes and downstrokes in random amplitude modulation

30 performed significantly better at detecting upstrokes and downstrokes of the stimulus compared with

31 epicardial surface results in more rapid AP upstrokes and higher conduction velocities compared with

32 HC-FKBP12 hearts had slower action potential upstrokes and longer action potential durations.

33 ), QTu and RTu dispersion (where u indicates upstroke), and QRST integrals were calculated, and these

34 nduction delays, changes in action potential upstroke, and block of conduction at a lower junction re

35 active channels are recruited during the EAD upstroke, and that nonequilibrium INa dynamics underlie

36 troke, waiting times of SCR events after the upstroke are narrowly distributed, whereas SCR amplitude

37 y smooth muscle, but did not affect the fast upstroke associated with ICC-MY.

38 (2+) release occurs within 2.5 or 5 ms of AP upstroke at 35 degrees C and 25 degrees C, respectively.

39 nly in response to the action potential (AP) upstroke, but also during the DD, and this is augmented

40 ance of LDCAE preceding the action potential upstroke by 98+/-31 ms.

41 ls had diastolic depolarization and multiple upstroke components that corresponded to the separate ex

42 AN had diastolic depolarization and multiple upstroke components, which corresponded to the separate

43 maximum rate of rise of the action potential upstroke, conduction velocity, and diastolic threshold o

44 Before block, depressed upstrokes consisted of two distinct components: the firs

45 nsition between diastolic depolarisation and upstroke, consistent with the activation of INa3.

46 An active upstroke could, therefore, be used to lower stability an

47 endocardial pacing, AP rise time (10%-90% of upstroke) decreased by approximately 50% between 500 and

48 maximal rate of rise of the action potential upstroke, diastolic threshold of excitation, and the sho

49 ations included a prolongation of the action upstroke duration, early upstroke initiation, and reduct

50 PD(50)) and 90% (APD(90)) repolarization and upstroke dV/dt (V(max)) at various cycle lengths were co

51 reduction of action potential amplitude, and upstroke dV/dt.

52 nnels (I(Na)), thereby resulting in a slower upstroke (dV/dt(max)) of the diabetic action potential.

53 the endocardial myocytes results in a faster upstroke (dV/dt(max)).

54 o of 1.7+/-0.1, whereas the action potential upstroke ([dV(m)/dt](max)) and duration decreased to 1.6

55 at negative time lags and a slower positive upstroke for positive time lags.

56 the downstroke, nearly matching the relative upstroke forces produced by hummingbirds.

57 Surprisingly, the pigeon's upstroke generated aerodynamic forces that were approxim

58 ) supported the later phase of the depressed upstroke, ICa(L) enhanced conduction and delayed block b

59 tract such information from the shape of the upstroke in optical mapping recordings.

60 A prolonged S-wave upstroke in V1 through V3 is the most frequent ECG findi

61 ewly proposed criterion of "prolonged S-wave upstroke in V1 through V3" > or =55 ms was the most prev

62 of leading-edge vortex, active and inactive upstrokes, in addition to the use of rotational mechanis

63 ation of the action upstroke duration, early upstroke initiation, and reduction in signal amplitude i

64 theoretical studies suggest that the optical upstroke is sensitive to the subsurface orientation of t

65 al nature of the optical signal, the optical upstroke is significantly longer than the electrical ups

66 maximal rate of rise of the action potential upstroke, leading to the development of atrial-specific

67 horizontal stroke plane; other forms of the upstroke may make a small positive contribution to stabi

68 is to clarify the interpretation of optical upstroke morphologies and reconcile the results obtained

69 he quantitative relationship between optical upstroke morphology and subsurface wavefront orientation

70 ntal studies have indicated that the optical upstroke morphology reflects the orientation of the subs

71 eometry of a whole guinea pig heart, optical upstroke morphology reveals the 3D wavefront orientation

72 We discovered that OAP upstroke morphology was highly sensitive to the transmur

73 To characterize the upstroke morphology, we use V(F)(*), the fractional leve

74 lues in 95% of pixels, and 80% of all Ca(i)T upstrokes occurred during the initial 25% of the excitat

75 Two aspects of the regenerative upstroke of a spike were differently affected by SERCA i

76 ansient sodium current that flows during the upstroke of action potential, we show that resurgent sod

77 ium channels underlie the rapid regenerative upstroke of action potentials and are modulated by cytop

78 d sodium channels (Na(v)) underlie the rapid upstroke of action potentials in excitable tissues.

79 age-gated sodium channels initiate the rapid upstroke of action potentials in many excitable tissues.

80 produces most of the current underlying the upstroke of action potentials in these neurons.

81 +) currents (Na(V)1.6/1.7) contribute to the upstroke of action potentials.

82 ve voltages, PD-307243 induced an I(to)-like upstroke of hERG current.

83 ly peak of the junctional current during the upstroke of the action potential (AP) due to GJ channel

84 hannel NaV1.5 is responsible for the initial upstroke of the action potential in cardiac tissue.

85 Voltage-gated sodium channels control the upstroke of the action potential in excitable cells of n

86 ated sodium channels are responsible for the upstroke of the action potential in most excitable cells

87 to understand variations in the shape of the upstroke of the action potential in order to identify st

88 -gated sodium channels (Na(V)s) underlie the upstroke of the action potential in the excitable tissue

89 G current activation began shortly after the upstroke of the action potential waveform.

90 The former appears to be responsible for the upstroke of the action potential, while the latter may a

91 depend on the L-type calcium current for the upstroke of the action potential, would also be somewhat

92 annel, SCN5A, is responsible for the initial upstroke of the action potential.

93 nitial slow pre-potential preceding the fast upstroke of the action potential.

94 ides a rapid depolarizing current during the upstroke of the action potential.

95 ides a rapid depolarizing current during the upstroke of the action potential.

96 tage-gated sodium (NaV) channels control the upstroke of the action potentials in excitable cells.

97 After the upstroke of the Ca(2+) transient, LCSs were detected whi

98 Na(v)1.5-dependent activity regulates rapid upstroke of the cardiac action potential.

99 erogeneities in the appearance of the second upstroke of the epicardial action potential, and discret

100 o carry the largest inward charge during the upstroke of the nociceptor action potential (approximate

101 y via reverse Na(+)-Ca2+ exchange during the upstroke of the normal cardiac action potential might tr

102 h allow significant calcium entry during the upstroke of the presynaptic action potential, and extrem

103 ar ejection time was measured from the rapid upstroke of the pulmonary artery pressure curve to the d

104 ated a very specific limited time during the upstroke of the T-wave to be the critical time for injur

105 dium ions to enter the cell, inducing a fast upstroke of the transmembrane potential.

106 The upstroke phase of Ca(2+) transients in ICC-MY appeared t

107 tly higher when shocks were delivered in the upstroke phase of manual chest compression.

108 hen electrical shock is delivered during the upstroke phase of manual chest compression.

109 These consisted of a rapidly propagating upstroke phase that initiated a sustained plateau phase,

110 nt-voltage (I-V) relationships during the AP upstroke; rapid recovery of AP excitability during the r

111 uction velocity and maximum action potential upstroke rate of rise dV/dt (max) of shock-induced activ

112 VF* at which the rate of rise of the optical upstroke reaches the maximum linearly depends on phi.

113 loped theoretical predictions of the optical upstroke shape dependence on phi.

114 g slowed sinus automaticity, reduced phase 0 upstroke slope, and prolonged action potential duration.

115 to the rate of rise of the action potential upstroke, suggesting that increases in spike threshold r

116 ncided with the maximal slope of the optical upstroke (t(F)*) for a broad range of optical attenuatio

117 ion (LDCAE) relative to the action potential upstroke to detect the Ca2+ clock.

118 um rate of rise of the action potential (AP) upstroke (V(max)), diastolic threshold of excitation (DT

119 rphology heterogeneity, with reduced maximum upstroke velocities (dV/dt) and prolonged AP durations.

120 reduced Na(+) currents and action potential upstroke velocities compared with hiPSC-derived cardiomy

121 Action potential upstroke velocities in isolated ventricular myocytes fro

122 control 137 +/- 2 mV) and decreased maximum upstroke velocity (70 +/- 10 vs. control 163 +/- 15 V s(

123 on velocity, and normalized action potential upstroke velocity (dV/dt(max)) significantly decreased i

124 Maximum upstroke velocity (dV/dt(max)) was 153+/-14 V/s, and con

125 s stimulated by current pulses had a maximum upstroke velocity (dV/dtmax) of 118 +/- 14 V s(-1) in co

126 ivated, contributing to low action potential upstroke velocity (V(max)), slow conduction, and reentry

127 ANP increased AP upstroke velocity (Vmax), AP duration, and ICa,L similar

128 g correlations between cycle length, maximum upstroke velocity and action potential amplitude, and ce

129 tion potential measurements showed a reduced upstroke velocity and longer action potential duration i

130 ecreased sodium current and action potential upstroke velocity and significantly prolonged action pot

131 and significantly increased action potential upstroke velocity because of a 2-fold increase in sodium

132 id not affect cardiomyocyte action potential upstroke velocity but markedly reduced action potential

133 ne potential, increased duration and reduced upstroke velocity compared to surrounding myocytes, sugg

134 ne potential, and increased action potential upstroke velocity compared with green fluorescent protei

135 clamp reveals that Nav1.5 contributes to the upstroke velocity of APs, whereas Nav1.9, which remains

136 line (HL-1) increased hyperpolarization and upstroke velocity of the action potential.

137 on front (i.e., threshold for activation and upstroke velocity of the initiating beat) of currently a

138 Action potential maximal upstroke velocity was diminished in the rapid pacing gro

139 tion rate that is independent of the maximum upstroke velocity, a parameter that can vary significant

140 ations, depolarized cells, and increased MPO upstroke velocity, amplitude and frequency.

141 amplitude, maximum diastolic potential, peak upstroke velocity, and conduction velocity.

142 by impaired impulse formation, as AP maximum upstroke velocity, whole-cell sodium current magnitude/p

143 depolarization, and after-shock increase in upstroke velocity.

144 was >3.2 micromol/L within < 32 ms of the AP upstroke (versus peak [Ca(2+)](i) of 1.1 micromol/L at 8

145 maximum rate of rise of the action potential upstroke, Vmax.

146 Ca(2+) releases during the action potential upstroke, waiting times of SCR events after the upstroke

147 Local calcium upstroke was delayed (23.9+/-4.9 versus 10.3+/-1.7 milli

148 contribution may be diminished by an active upstroke with a low advance ratio and more horizontal st

149 ating parallel to myocardial fibers produced upstrokes with VF*<0.5, consistent with theoretical pred