ライフサイエンスコーパス: EAD

1 EAD could stem from a defect that prevents binding of Co

2 EAD occurred in 182 (27.6%) cases.

3 EADs are mainly driven by voltage oscillations in the re

4 EADs are promoted by aberrant RyR-mediated Ca(2+) releas

5 EADs disappeared when the pacing cycle length was shorte

6 EADs fired 'out-of-phase' from several sites, propagated

7 EADs occur in the setting of reduced repolarization rese

8 EADs occur randomly, where the likelihood of these event

9 EADs were absent in WT cells before and after isoprotere

10 EADs were especially frequent following temporary cessat

11 EADs were induced in isolated rabbit ventricular myocyte

12 lar action potential recordings that phase 2 EAD can be generated from intact ventricular wall and pr

13 In the presence of phase-2 EADs, the cells may synchronously exhibit the same numbe

14 (2) EADs are reduced in absolute number of occurrence, which

15 azine (5-10 mumol/L) eliminated late phase 3 EAD- and DAD-induced triggered activity as well as isopr

16 ontribute to the development of late phase 3 EAD-induced triggered activity and that this mechanism m

17 700 ms), and the development of late phase 3 EADs and extrasystoles.

18 ced increase in phasic tension, late phase 3 EADs, and extrasystoles that initiate AF.

19 In the presence of phase-3 EADs, regional synchronization leads to propagating EADs

20 +/- 2.6) close to WT (P > 0.05; n = 5); (3) EAD suppression during both spontaneous activity and fol

21 t not its inactive analogue KN-92, abolished EADs and hypokalemia-induced ventricular tachycardia/fib

22 tate inactivation curve completely abolished EADs in myocytes while maintaining a normal Ca(i) transi

23 L-type Ca2+ channels (LTTCs) can activate EADs, and LTCC opening probability (Po) was significantl

24 e development of early afterdepolarisations (EADs), which trigger lethal ventricular arrhythmias.

25 ase 3 early and delayed afterdepolarization (EAD and DAD)-induced triggered activity in SVC sleeves a

26 e role of phase 2 early afterdepolarization (EAD) in producing a trigger to initiate torsade de point

27 ie, by promoting early afterdepolarization (EAD) or delayed afterdepolarization (DAD) or both, is un

28 n slices revealed early afterdepolarization (EAD)-like AP waveforms in CA1 but not in CA3 hippocampal

29 (2)O(2) initiated early afterdepolarization (EAD)-mediated triggered activity that led to sustained V

30 was initiated by early afterdepolarization (EAD)-mediated triggered activity.

31 Early afterdepolarizations (EADs) and delayed afterdepolarizations (DADs) are voltag

32 ol/L) suppressed early afterdepolarizations (EADs) and reduced the increase in TDR induced by the sel

33 quent epicardial early afterdepolarizations (EADs) and spontaneous ventricular tachycardia (VT) in 4

34 shown to induce early afterdepolarizations (EADs) and triggered activity by impairing Na current (I(

35 can give rise to early afterdepolarizations (EADs) and triggered arrhythmia by enhanced forward sodiu

36 Spontaneous early afterdepolarizations (EADs) and ventricular tachycardia/fibrillation occurred

37 s that result in early afterdepolarizations (EADs) are a known trigger for tachyarrhythmias, but the

38 Early afterdepolarizations (EADs) are linked to both triggered arrhythmias and reent

39 al alternans and early afterdepolarizations (EADs) are linked to cardiac arrhythmias.

40 Early afterdepolarizations (EADs) are triggers of cardiac arrhythmia driven by L-typ

41 Early afterdepolarizations (EADs) are voltage oscillations that occur during the rep

42 iac arrhythmias, early afterdepolarizations (EADs) during action potentials(APs) have been extensivel

43 ularly occurring early afterdepolarizations (EADs) in cardiac myocytes are traditionally hypothesized

44 blocker) induced early afterdepolarizations (EADs) in female base myocytes cultured for 1 day if incu

45 f arrhythmogenic early afterdepolarizations (EADs) in isolated cells and poorly coupled tissue.

46 on and prominent early afterdepolarizations (EADs) in neonatal cardiomyocytes expressing the F1486del

47 multiple foci of early afterdepolarizations (EADs) result in beat to beat changes in the origin and d

48 nd to facilitate early afterdepolarizations (EADs) when repolarization reserve is reduced.

49 tes had frequent early afterdepolarizations (EADs), a hypothesized mechanism for triggering arrhythmi

50 illations called early afterdepolarizations (EADs), and premature death in paced adult rabbit ventric

51 Ca(2+) overload, early afterdepolarizations (EADs), and torsade de pointes.

52 Epicardial early afterdepolarizations (EADs), often accompanied by spontaneous ventricular tach

53 i) in triggering early afterdepolarizations (EADs), the origins of EADs and the mechanisms underlying

54 lations, such as early afterdepolarizations (EADs), which are associated with lethal arrhythmias.

55 otential causing early afterdepolarizations (EADs).

56 e delayed and/or early afterdepolarizations (EADs).

57 lity, leading to early afterdepolarizations (EADs).

58 o arrhythmogenic early afterdepolarizations (EADs).

59 nt that produces early afterdepolarizations (EADs).

60 hythmias such as early afterdepolarizations (EADs).

61 tiguous susceptible myocytes required for an EAD and a barely suprathreshold DAD to trigger a propaga

62 ween an action potential with and without an EAD) is not sufficient to account for the large variatio

63 sion in the skin of both IAD (p = 0.010) and EAD (p = 0.004), as compared with psoriasis patients.

64 Conversely, IAD (p = 0.019) and EAD (p = 0.002) skin lesions exhibited elevated IL-10 ge

65 SH (4), NAD-beta-Ala-(Arg(11))CCMSH (5), and EAD-beta-Ala-(Arg(11))CCMSH (6) peptides were synthesize

66 herapeutic strategy for suppressing EADs and EAD-mediated arrhythmias.

67 ribute to the AMP deficiency in both IAD and EAD by reducing cytokines that induce AMP.

68 Both MEAF and EAD were independent predictors of transplant survival w

69 lity) of AP duration in cardiac myocytes and EAD-mediated arrhythmias and suggests a novel possible m

70 RNAs, 3- to 6-fold more viral Zta, Rta, and EAD proteins, 3- to 5-fold more viral DNA, and 7- to 9-f

71 locity, AP duration, conduction velocity and EAD incidence, as well as reflection incidence (29.2%, n

72 essing both pacing-induced re-entrant VF and EAD-mediated multifocal VF.

73 The mechanisms of alternans and EADs have been extensively studied under steady-state co

74 e to another, action potential alternans and EADs may occur during the transition between two periodi

75 amical mechanisms of transient alternans and EADs.

76 and a trigger (increased persistent INa and EADs) promotes reflection and arrhythmogenesis.

77 are sufficient to cause APD prolongation and EADs, the predominant characteristic of LQTs.

78 accompanied by aberrant Ca(2+) releases and EADs, which were abolished by inhibition of Ca(2+)/calmo

79 upling promotes complex EAD patterns such as EAD alternans that are not observed for solely voltage-d

80 the past, it has been difficult to associate EADs or reentry with the undulating electrocardiographic

81 Associations between EAD and recipient, donor, and transplant factors were ex

82 Genetic suppression of NCX reduces both EADs and DADs.

83 tes virtually all inward current elicited by EADs, and that this effect occurs at concentrations (40-

84 es in wave propagation patterns initiated by EADs or EAD-induced nonstationary reentrant activity.

85 and the current paradigm holds that cardiac EAD dynamics are dominated by interaction between ICaL a

86 tual Ito-like current (n=1113 trials) caused EADs to reappear over a wide range of Ito conductance (0

87 aMKII activation were ineffective at causing EADs.

88 A key unanswered question is how cellular EADs partially synchronize in tissue, as is required for

89 showed that this bistable switch of cellular EADs provided both a trigger and a functional substrate

90 cally homogeneous tissue models that chaotic EADs synchronize globally when the tissue is smaller tha

91 rcellular clefts, whereas for narrow clefts, EADs were suppressed.

92 ycling play a key role in generating complex EAD and DAD dynamics observed experimentally in cardiac

93 and 4) Ca-voltage coupling promotes complex EAD patterns such as EAD alternans that are not observed

94 recipients were monitored for complications, EAD (defined by postoperative day 7 bilirubin >10 mg/dL

95 Also, for normal transverse coupling, EADs develop in the endocardial region rather than in th

96 After cryoablation, EADs from surviving epicardium (~1 mm) fired at the same

97 tal myasthenic syndrome, EP AChE deficiency (EAD), the normal asymmetric species of AChE are absent f

98 hypokalemia to induce bradycardia-dependent EADs at a long pacing cycle length of 6 s, when native r

99 Early after-depolarization (EAD), or abnormal depolarization during the plateau phas

100 tilide produced early after depolarizations (EADs) and arrhythmias, whereas verapamil, vanoxerine and

101 ams/ml) induced early after depolarizations (EADs) in cells in the M (20%) but not epicardial or endo

102 in the form of early after depolarizations (EADs).

103 atch leading to early after-depolarizations (EADs) and reflection of impulses in monolayers of well-p

104 e likelihood of early after-depolarizations (EADs).

105 n infections in extrinsic atopic dermatitis (EAD) may be because of the suppression of anti-microbial

106 isolated SHR ventricular myocytes developed EADs and triggered activity to the same extent as NR ven

107 Early Alzheimer's disease (EAD) is the intermediary stage between mild cognitive im

108 Further, simulations of a cell displaying EADs electrically connected to a cell with normal action

109 afts with entinostat, ATRA, and doxorubicin (EAD) resulted in significant tumor regression and restor

110 t are not observed for solely voltage-driven EADs.

111 erang' during an AP and like ellipses during EADs, with V(m) preceding Ca2+iby 9.2 +/- 1.4 (n = 6) an

112 nism that causes voltage oscillations during EADs, depending on the amplitude and kinetics of the L-t

113 ents undergoing early allograft dysfunction (EAD) (p < 0.05).

114 Early allograft dysfunction (EAD) after living donor liver transplantation (LDLT) has

115 the categorical early allograft dysfunction (EAD) classification, MEAF is a continuous score, based o

116 fold more viral IE Zta and Rta and early (E) EAD protein than did cells infected with the parental wi

117 ; optical mapping revealed that the earliest EADs fired at the base.

118 How early (EADs) and delayed afterdepolarizations (DADs) overcome e

119 In conclusion, overload elicits EADs originating from either ventricular or Purkinje fib

120 e equalized TG and WT LTCC Po and eliminated EADs, whereas a peptide antagonist of the Na+/Ca2+ excha

121 ergic stimulation is independent of enhanced EAD frequency.

122 Eventually, EADs and triggered activity ensued, giving rise to inter

123 l number of cells that synchronously exhibit EADs are needed to result in arrhythmia triggers and sub

124 t influence membrane voltage (V) can explain EAD intermittency.

125 nt (INa), but not late INa, are required for EAD initiation.

126 X current reversal as an indicator event for EADs, the model identified counterintuitive ionic change

127 molecular and biophysical and mechanism for EADs and impaired survival in adult cardiomyocytes.

128 still require synchronization mechanisms for EADs and DADs to overcome the robust protective effects

129 responsible for LQTS, and elevated risks for EADs may depend on genotypes, such as exercise in LQT1 v

130 ral heterogeneities provided a substrate for EADs, retrograde propagation along the same pathway (ref

131 nine left ventricles, they produced frequent EADs in rabbits, in which more pronounced QT prolongatio

132 y slowed repolarization, leading to frequent EADs and electrocardiographic QT prolongation.

133 Away from EAD origins, V(m) coincided with or preceded Ca2+i.

134 tography-electroantennographic detection (GC-EAD) by orders of magnitude through a technique known as

135 circumstances a more sensitive and robust GC-EAD instrument will result from the application of this

136 polarization reserve was reduced to generate EADs and random ion channel or path cycle length fluctua

137 However, EAD occurrence was reduced to 62 +/- 7.1%, 44 +/- 9.7%,

138 However, EADs are also frequent in the rapidly repolarizing mouse

139 However, EADs emerge upon simultaneous activation of both LCCs an

140 gional differences in I(Ca,L) density and in EAD susceptibility were analyzed in epicardial left vent

141 to be excessively covalently bound by HNE in EAD inferior parietal lobule (IPL) compared to age-relat

142 ssion of AD, and is the first to identify in EAD identical brain proteins previously identified as HN

143 The role of I(Ca,L) in EAD formation was directly assessed using the dynamic cl

144 gate excessively HNE-bound brain proteins in EAD compared to those in control.

145 into connecting HNE-bound brain proteins in EAD to those previously identified in MCI and AD, since

146 hat there is an overlap of brain proteins in EAD with previously identified oxidatively modified prot

147 trotonic effects may play a critical role in EAD-mediated arrhythmogenesis.

148 KII activation may be an important factor in EADs caused by oxidative stress.

149 previous study explains slow fluctuations in EADs, which may underlie intermittency of EAD trains and

150 t complex effects on EADs, but cannot induce EADs of significant amplitude without the participation

151 mol/L), or a combination were used to induce EADs, DADs, and triggered activity.

152 micromol/L, n=5), prevented H(2)O(2)-induced EADs and DADs, and the selective CaMKII peptide inhibito

153 sing Ca influx via I(Ca,L), H(2)O(2)-induced EADs were also frequently followed by DADs in response t

154 /L) for 5 to 15 minutes consistently induced EADs that were suppressed by the I(Na) blocker tetrodoto

155 g bradycardia, the emergence of H2O2-induced EADs was correlated with a shift in the timing of NCX cu

156 easured slow-rate dependence of H2O2-induced EADs.

157 the whole heart, suggesting that ISO-induced EADs are genotype specific.

158 Pacing-induced EADs were enhanced by re-introduction of normal Tyrode s

159 both dl-sotalol and azimilide rarely induced EADs in canine left ventricles, they produced frequent E

160 der several experimental conditions inducing EADs, including oxidative stress with hydrogen peroxide,

161 nd intercellular coupling strongly influence EAD development during interventions or disorders that p

162 Ca(2+) entry through Ca(V)1.2 and inhibiting EADs.

163 smic reticulum Ca(2+) release, and initiated EADs below the ICaL activation range (-47 +/- 0.7 mV).

164 t ventricular myocytes revealed intermittent EADs, with slow fluctuations between runs of APs with EA

165 ling and computer simulations to investigate EAD synchronization and arrhythmia induction in tissue m

166 riments in isolated myocytes, that irregular EAD behavior is dynamical chaos.

167 l/L) increased APD more than dl-sotalol, its EADs often failed to propagate transmurally, probably be

168 NR ventricular myocytes, except with larger EAD amplitude.

169 During 6-s pacing cycle length, EADs were blocked by the Ito blocker 4-aminopyridine, bu

170 tective negative feedback mechanism, masking EADs.

171 e H(2)O(2)) and suppressed H(2)O(2)-mediated EADs by reducing the number of foci, causing VF to termi

172 interactions between coupled cells modulates EAD formation, cell connectivity was reduced by RNA sile

173 quilibrium reactivation of INa drives murine EADs.

174 This suggests that murine EADs exhibit unique dynamics, which are key for interpre

175 nonequilibrium INa dynamics underlie murine EADs.

176 In well-coupled myocardium, EAD formation in the subendocardium can be the source of

177 though the uncoupled cells exhibit either no EAD or only a single EAD, when these cells are coupled t

178 ion with lower [K(+)](o), while there was no EAD formation in littermate control (LMC) or LQT1 myocyt

179 nously exhibit the same number of EADs or no EADs with a very small dispersion of refractoriness, or

180 Upon reducing I Kr, the APs without EADs (no-EAD response) showed gradual prolongation of AP duration

181 smural dispersion of repolarization, but not EADs, in intact arterially perfused wedges of canine lef

182 anscriptional silencing of RAR-beta Notably, EAD was the most effective combination in inducing diffe

183 This novel EAD mechanism is observed only in association with marke

184 Among putative causes of EAD after LDLT are excessive portal pressure and/or flow

185 in EADs, which may underlie intermittency of EAD trains and consequent arrhythmias.

186 erved and exhibit an increased likelihood of EAD formation.

187 the Hopf-homoclinic bifurcation mechanism of EAD-mediated triggered activity, and raise the possibili

188 Here we introduce a cell culture model of EAD propagation consisting of monolayers of cultured neo

189 Our objective was to evaluate patterns of EAD after LDLT.

190 arization (TDR) to transmural propagation of EAD and the maintenance of TdP was also evaluated.

191 less concerning the possible relationship of EAD HNE-modified brain proteins with HNE-modified protei

192 Risk of EAD was associated with left lobe grafts, lower graft we

193 The symptoms of EAD mirror the disease advancement between the two phase

194 ransplant survival was compared with that of EAD in univariable and multivariable models by means of

195 tage oscillations that are characteristic of EADs.

196 al approach to investigate the dependence of EADs on the biophysical properties of the L-type Ca(2+)

197 We conclude that the irregular dynamics of EADs is intrinsically chaotic, with random fluctuations

198 as an important player in the generation of EADs.

199 PD prolongation and reduced the incidence of EADs in LQT2 myocytes.

200 may synchronously exhibit the same number of EADs or no EADs with a very small dispersion of refracto

201 The occurrence of EADs during a train of action potentials was reduced by

202 igated, and mechanisms for the occurrence of EADs on a beat-to-beat basis have been proposed.

203 engthening AP duration and the occurrence of EADs promote DADs by increasing intracellular Ca loading

204 The occurrence of EADs was also drastically reduced in hetKO.

205 afterdepolarizations (EADs), the origins of EADs and the mechanisms underlying Torsade de Pointes (T

206 At the origins of EADs, Ca2+ipreceded V(m) and phase maps traced clockwise

207 otalol facilitated transmural propagation of EADs that initiated multiple episodes of spontaneous TdP

208 m leading to the concealing and revealing of EADs in LQT3 models.

209 ers eliminated Purkinje fibres as sources of EADs.

210 a coupling strength-dependent suppression of EADs consistent with the experimental results.

211 n Scn5a+/Delta hearts through suppression of EADs.

212 states, forming a bistable on-off switch of EADs.

213 pathetic tone can be an effective trigger of EADs in LQT2 perfused hearts.

214 imulation demonstrated a high-risk window of EADs in LQT2 during ISO perfusion owing to mismatch in t

215 tigate the effects of Ca-voltage coupling on EAD and DAD dynamics.

216 to accounts for these paradoxical effects on EADs by influencing the dynamic evolution of repolarizat

217 ous Ca waves also exhibit complex effects on EADs, but cannot induce EADs of significant amplitude wi

218 ve propagation patterns initiated by EADs or EAD-induced nonstationary reentrant activity.

219 such as period 2 or chaos when alternans or EADs occur in pathological conditions.

220 elicited spontaneous Ca2+iand V(m) spikes or EADs (3.5 +/- 1.9 Hz) during the AP plateau (n = 6).

221 MEAF outperformed EAD as predictor of transplant survival, either when use

222 icular or Purkinje fibres and 'out-of-phase' EAD activity from multiple sites generates TdP, evident

223 als (APs), V(m) oscillations on AP plateaux (EADs) then ventricular tachycardia (VT).

224 curve combining both lipid levels predicted EAD with 82% accuracy.

225 agonists BayK8644 and isoproterenol produce EAD bursts that are suppressed by the LTCC blocker nitre

226 tion, is not by itself sufficient to produce EADs.

227 potential duration prolongation and produced EADs, in particular, at slow pacing rates.

228 ssociated mutant channels, myocytes produced EADs for wide intercellular clefts, whereas for narrow c

229 e of intermediate Ito properties can promote EADs by influencing the temporal evolution of other curr

230 releases caused by RyR hyperactivity promote EADs and underlie the enhanced triggered activity throug

231 increased sodium current(INa) would promote EADs, we employed adenoviral transfer of Nav1.5 (Ad-Nav1

232 also impairs I(Na) inactivation and promotes EADs, we hypothesized that CaMKII activation may be an i

233 tions concur that I(Ca,L) elevation promotes EADs and is an important determinant of long QT type 2 a

234 pokalemia plays a critical role in promoting EAD-mediated arrhythmias by inducing a positive feedback

235 egional synchronization leads to propagating EADs, forming PVCs in tissue.

236 or global cellular CaMKII inhibition reduced EADs and improved cell survival to control levels in WT

237 ion of the terminal phase of repolarization (EADs) were observed during interventions increasing cont

238 al properties of the native I(Ca,L) restored EAD occurrence in myocytes challenged by H(2)O(2) or hyp

239 The data show EAD formation in superfused canine pulmonary veins, enha

240 e previously identified in MCI and AD, since EAD is a transitional stage between MCI and late-stage A

241 cells exhibit either no EAD or only a single EAD, when these cells are coupled to form a tissue, more

242 In six EAD patients, we found no mutations in ACHET.

243 er, only LQT2 myocytes developed spontaneous EADs following perfusion with lower [K(+)](o), while the

244 In summary, EAD formation is genotype specific, such that EADs can b

245 hanger current, also hypothesized to support EADs, was ineffective.

246 e) could enhance repolarization and suppress EADs.

247 Whereas sufficiently large Ito can suppress EADs, a wide range of intermediate Ito properties can pr

248 se surrounding tissue to conduct or suppress EADs are poorly understood.

249 Pase activity can either promote or suppress EADs due to the complex effects of Ca on ionic current p

250 The actions of ranolazine to suppress EADs and reduce TDR suggest that, in addition to its ant

251 ese properties could be designed to suppress EADs.

252 ation or larger pedestals tended to suppress EADs.

253 owerful therapeutic strategy for suppressing EADs and EAD-mediated arrhythmias.

254 coupling can no longer globally synchronize EADs, resulting in regions of partial synchronization th

255 These regional partially synchronized EADs then form premature ventricular complexes that prop

256 tion as the likely mechanism for terminating EAD bursts.

257 ion, and lower levels of IL-4 and IL-13 than EAD.

258 Computer modeling revealed that EAD generation by hypokalemia (with or without dofetilid

259 bel immunofluorescence assays suggested that EAD protein expression was activated even better than ZT

260 AD formation is genotype specific, such that EADs can be elicited in LQT2 myocytes simply by lowering

261 The EAD formation was prevented by ryanodine (10 microM) or

262 The EAD is a physiological recording from the antenna of an

263 The EAD-like waveforms of Scn8a(N1768D/+) CA1 hippocampal ne

264 um reactivation of INa and thereby drive the EAD upstroke.

265 y inactive channels are recruited during the EAD upstroke, and that nonequilibrium INa dynamics under

266 Thus, the EAD-induced arrhythmias with repolarisation reserve atte

267 These EAD bursts exhibited a key dynamical signature of the du

268 These EADs were abolished by caffeine and tetrodotoxin (but no

269 y that this mechanism may also contribute to EAD formation in clinical settings such as long QT syndr

270 anges in LCC gating properties contribute to EAD generation.

271 enhanced cell differentiation in response to EAD triple therapy.

272 oorly coupled tissue are more susceptible to EAD development than epicardial or endocardial cells.

273 ne (0.05-3 muM) prolonged the AP, leading to EADs and reflection.

274 Cellular studies point to EADs as a triggering mechanism for arrhythmias but sugge

275 prolong action potentials and predisposes to EADs.

276 ch contributes to the enhanced propensity to EADs and TdP in female hearts.

277 l area of contiguous myocytes susceptible to EADs or DADs was surrounded by unsusceptible tissue.

278 mpared to results obtained using traditional EAD recording techniques.

279 ase of the action potential (AP) can trigger EADs.

280 different high-risk conditions that trigger EADs using transgenic rabbit models of LQT1 and LQT2, wh

281 depolarizing electrotonic current to trigger EADs and reflection.

282 prenaline (ISO) prolonged APDs and triggered EADs in LQT1 myocytes in the presence of lower [K(+)](o)

283 or of transplant loss than the commonly used EAD classification.

284 ells before and after isoproterenol, whereas EAD frequency was unaffected by isoproterenol in TG mice

285 orphic arrhythmias; and 2) determine whether EADs may initiate nonstationary reentry, giving rise to

286 Risk factors associated with EAD after LDLT include: graft type and size, preoperativ

287 ays was 5.2 times higher for recipients with EAD versus those without EAD (P < 0.001).

288 teomics analysis of brain from subjects with EAD and even less concerning the possible relationship o

289 Simulations in 2-dimensional tissue with EAD-mediated multifocal VF showed progressive reduction

290 tatic cells also responded to treatment with EAD.

291 nihilation caused a transition to an AP with EADs as a new stable steady state.

292 h slow fluctuations between runs of APs with EADs present or absent.

293 pendent plateau oscillations consistent with EADs.

294 iations in action potential duration without EAD presence do not cause large dispersion of refractori

295 for recipients with EAD versus those without EAD (P < 0.001).

296 ting in 2 stable AP states, with and without EADs (ie, bistability).

297 Upon reducing I Kr, the APs without EADs (no-EAD response) showed gradual prolongation of AP

298 that propagate into recovered tissue without EADs.