ライフサイエンスコーパス: upstroke

1 rized resting membrane potential and slow AP upstroke.

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

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

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

5 upracoracoideus recovers the wing during the upstroke.

6 eactivation of INa and thereby drive the EAD upstroke.

7 is significantly longer than the electrical upstroke.

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

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

10 y by 18% by decreasing the duration of their upstroke.

11 that occurs just before the action potential upstroke.

12 to inversion of their cambered wings during upstroke.

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

14 nevertheless very similar epicardial optical upstrokes.

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

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

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

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

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

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

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

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

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

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

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

26 A correlation between AP upstroke and I(Na) transients was identified and drug-in

27 potentials were more depolarized with slower upstroke and reduced peak amplitude.

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

29 sitive feedback between the action potential upstroke and SCR.

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

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

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

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

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

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

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

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

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

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

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

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

42 (2+) release occurs within 2.5 or 5 ms of AP upstroke at 35 degrees C and 25 degrees C, respectively.

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

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

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

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

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

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

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

50 ed by downstrokes, while relatively inactive upstrokes cost almost no aerodynamic power.

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

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

53 on activates Ca(V) 3.2 channels, causing the upstroke depolarization phase of slow waves.

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

55 ant circle bifurcation with action potential upstroke driven by Ca(V)1.2.

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

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

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

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

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

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

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

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

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

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

66 ng the supracoracoideus tendon to assist the upstroke-improving the pectoralis work loop efficiency s

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

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

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

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

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

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

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

74 The upstroke is transient and followed by a long-duration pl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

91 roteins that are responsible for the initial upstroke of an action potential in excitable cells.

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

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

94 tage-gated sodium (Na(V)) channels drive the upstroke of the action potential and are comprised of a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 nel, hNa(V)1.5, is responsible for the rapid upstroke of the cardiac action potential and is target f

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

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

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

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

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

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

116 the key depolarizing current that drives the upstroke of the skeletal muscle action potential.

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

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

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

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

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

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

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

124 d conduction velocity (- 27 6%, p < 10(-3)), upstroke rate (- 13 4%, p = 0.002), and action potential

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

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

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

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

129 we show correlations between I(Na) block and upstroke slowing after treatment with flecainide or quin

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

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

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

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

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

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

136 Action potential upstroke velocities in isolated ventricular myocytes fro

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

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

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

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

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

142 ential duration and reduced action potential upstroke velocity (V(max)).

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

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

145 the effects of lidocaine on action potential upstroke velocity and conduction velocity in our model a

146 altered in Akita mice due to a reduction in upstroke velocity and increases in AP duration.

147 hat acting on hiPSC-CMs low action potential upstroke velocity and lack of IK1 may restore pre-MI act

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

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

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

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

152 ll effects on action potential threshold and upstroke velocity but substantially reduced the peak and

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

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

155 ential duration, and reduced maximum phase 0 upstroke velocity compared with wild type.

156 xpression increased maximal action potential upstroke velocity in human inducible pluripotent stem ce

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

158 rts showed a decrease in ventricular maximum upstroke velocity of the action potential and conduction

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

160 bulin detyrosination and ventricular maximum upstroke velocity of the action potential.

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

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

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

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

165 eased cellular INa, maximal action potential upstroke velocity, and action potential amplitude in Scn

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

167 th a lower maximum contractile force, slower upstroke velocity, and immature mitochondrial function c

168 membrane potential, faster action potential upstroke velocity, greater incidence of delayed afterdep

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

170 es stretch-induced slowing of conduction and upstroke velocity.

171 ion potential duration and decreased maximum upstroke velocity.

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

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

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

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

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

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

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