ライフサイエンスコーパス: APD

1 APD (spearman r = 0.25, p < 0.05), UI (spearman r = 0.38

2 APD and calcium handling were assessed by live cell imag

3 APD decreased during the stressful parts of the film cli

4 APD depends on several preceding diastolic intervals (DI

5 APD in both LWHs and LANG hearts dropped steadily during

6 APD is less sensitive to changes in other IKr gating par

7 APD variations were associated with decreased transient

8 APDs also initiate blood digestion as components of mult

9 APDs have been considered as virulence factors of Trypan

10 xperiments, while the model predicted 10.06% APD shortening with 29.33% block of INaL.

11 -1) + alpha(2)CL(n-2)) showed that alpha(1) (APD restitution slope) is largest and heterogeneous in L

12 ed to shorter (-16.3%) and prolonged (+6.5%) APD(90) in response to hyperpolarizing and depolarizing

13 fects on AP features (RMP, V (max), APD(50), APD(90) (AP duration at 50 and 90% of repolarization), a

14 t 50 and 90% of repolarization), and APD(50)/APD(90)) after including them in the hiPSC-CM mathematic

15 uM) caused a 28.67% block of INaL and 12.57% APD shortening in experiments, while the model predicted

16 on of intracellular Ca(2+) release abolished APD alternans, indicating that [Ca(2+)]i dynamics have a

17 By adapting APD-AED method in the case of UAE, the intensive optimum

18 using carbenoxolone only minimally affected APD distribution in confluent cells.

19 itive to inactivation shifts, which affected APD and SD1 concordantly; (4) activation shifts of the s

20 Q-T interval of the electrocardiogram alter APD stability, and modulate responsiveness to pharmacolo

21 n InP substrate to design and demonstrate an APD with low k-value.

22 The internal gain of an APD can improve system signal-to-noise ratio (SNR).

23 the pacing threshold for both SR Ca(2+) and APD alternans (188+/-15 and 173+/-12 ms; P<0.05 versus b

24 concordant but not discordant SR Ca(2+) and APD alternans.

25 Results show that LV/RV APD and APD adaptation heterogeneities promote unidirectional bl

26 an vernakalant, which increased both APD and APD dispersion.

27 covered DYS and nNOS, and normalised APD and APD rate-dependency.

28 ressed or completely eliminated both CaT and APD alternans in single atrial myocytes and atrial T-wav

29 3 ms and 93+/-6 versus 76+/-4 ms for CaT and APD alternans, respectively, P<0.05), suggesting increas

30 racted great attention for monitoring DA and APD levels but none of the methods developed so far aime

31 AF is linked to atrial APD heterogeneity and APD reduction due to progressive remodelling.

32 tations produced distinct effects on IK1 and APD shortening.

33 INa-L block with lidocaine shortened QTc and APD more at 6.5 hours than at 50 minutes (QTc) or 30 min

34 Dofetilide monotonically increased QTc and APD throughout 6.5-hour exposure.

35 ration at 50 and 90% of repolarization), and APD(50)/APD(90)) after including them in the hiPSC-CM ma

36 Unlike conduction velocity slowing and APD heterogeneity, the magnitude of APD alternans was gr

37 PDs in LWHs were longer at all workloads and APD reductions during deoxygenation were blunted in both

38 eral preceding diastolic intervals (DIs) and APDs, which complicates the prediction of alternans.

39 s (SNPs) in 180 mCRC patients (Angiopredict [APD] cohort) treated with combined BVZ + chemotherapy an

40 optimal kinetic profile for D(2)R antagonist APDs that avoids EPS.

41 egrees offcut from the [110] do not show any APDs, whereas samples grown on the exactly oriented subs

42 i-arrhythmic strategies that increase atrial APD without increasing its dispersion are effective in t

43 Amiodarone increased atrial APD and reduced APD heterogeneity and was more effective

44 gene deletion or inhibition shortened atrial APD and increased atrial fibrillation inducibility in vi

45 stenance of rotors in AF is linked to atrial APD heterogeneity and APD reduction due to progressive r

46 Both typical and atypical APD administration induced neuroanatomical remodeling of

47 The typical and atypical APDs do not differ in improving psychopathology in non-T

48 operties of a series of typical and atypical APDs in a novel time-resolved fluorescence resonance ene

49 tively correlated in SZ patients on atypical APDs and in NCs; this correlation was stronger in SZ pat

50 tively correlated in SZ patients on atypical APDs; this correlation was significantly stronger than t

51 and hyperprolactinemia relative to atypical APDs such as clozapine.

52 ation is negatively correlated with baseline APD and positively correlated with PCL.

53 aT responses; however, a pronounced biphasic APD response occurred, with initial prolongation (50.9 +

54 We determined the biphasic APD response in mouse was partly due to dynamic changes

55 Kv7.1 and NS1643 for Kv11.1) abolished both APD and CaT alternans in field-stimulated and current-cl

56 ng AF than vernakalant, which increased both APD and APD dispersion.

57 tween normal and SZ cases, nor influenced by APD, in any region tested.

58 longer detect any anti-Dsg3 clones in PV1 by APD.

59 pparent increase in Kv3.1b protein levels by APDs in SZ neocortex was confirmed in laboratory rodents

60 SZ neocortex, a deficit that is restored by APDs.

61 ) within the mammalian myocardium can change APD and the Q-T interval of the electrocardiogram alter

62 tion on pacing history and tau characterizes APD accommodation, which is an exponential change of APD

63 nterior cingulate cortex (ACC) after chronic APD treatment, regardless of the APD administered.

64 egion-specific structural effects of chronic APD treatment on the rat cortex, primarily but not exclu

65 etric findings and demonstrated that chronic APD treatment had no effect on the total number of neuro

66 d in laboratory rodents treated with chronic APDs.

67 es of APD as a function of two previous CLs (APD(n) = C + alpha(1)CL(n-1) + alpha(2)CL(n-2)) showed t

68 eridol (HAL)) and atypical (clozapine (CLZ)) APDs on the neuroanatomy of wild-type (WT) and dopamine

69 n on the exactly oriented substrates contain APDs.

70 zophrenia and related disorders than current APDs.

71 sets and the Antimicrobial Peptide Database (APD)3 benchmark dataset.

72 With JNJ-303, ISO decreased APD significantly more in the epicardium as compared to

73 d power density and absorbed energy density (APD-AED) and response surface methodology (RSM).

74 ucine-derived 4-alkyl-l-proline derivatives (APDs) in their structures.

75 f patients on automated peritoneal dialysis (APD) is increasing worldwide and may be guided by clinic

76 automated pipeline to extract AAA diameter (APD), undulation index (UI) and radius of curvature (RC)

77 able states consisting of APs with different APDs, and caused multiple hysteretic dynamics.

78 ceptibility to VT/VF secondary to discordant APD alternans.

79 IgG(+) repertoire by antibody phage display (APD) and PCR indicated that six clonal lines persisted i

80 ance (FD) data and amplitude-phase-distance (APD) data, from which we construct 3D depth profiles of

81 characterise and quantify antiphase domains (APDs) in GaP thin films grown on different (001) Si subs

82 Haloperidol is a typical antipsychotic drug (APD) associated with an increased risk of extrapyramidal

83 h has shown that chronic antipsychotic drug (APD) treatment further decreases cortical gray matter an

84 ut only in cases without antipsychotic drug (APD) treatment; Kv3.1 levels are normal in antipsychotic

85 hanisms of action of the antipsychotic drug (APD), clozapine, is of great importance, as clozapine is

86 evidence suggests that antipsychotic drugs (APD) might affect brain structure directly, particularly

87 st clinically available antipsychotic drugs (APDs) bind dopamine D2 receptors (D2R) at therapeutic co

88 Atypical antipsychotic drugs (APDs) have been hypothesized to show reduced extrapyrami

89 Current antipsychotic drugs (APDs) show efficacy with positive symptoms, but are limi

90 All FDA-approved antipsychotic drugs (APDs) target primarily dopamine D2 or serotonin (5-HT2A)

91 ed hippocampal neurons, antipsychotic drugs (APDs) were proposed to accumulate in synaptic vesicles b

92 lopment of new atypical antipsychotic drugs (APDs), with better tolerability due to more selective do

93 ith typical or atypical antipsychotic drugs (APDs).

94 Increased AP duration (APD) and beat-to-beat alternations in AP morphology lowe

95 nduction velocity and increased AP duration (APD) heterogeneity in STIM1-KD.

96 rical restitution (ER), the way AP duration (APD) senses changes in preceding cycle length (CL), has

97 (TOLB) to identify the level of AP duration (APD) shortening attributed to KATP channel activation.

98 ependent changes in ventricular AP duration (APD), and variations in APD at a fixed heart rate are bo

99 showed gradual prolongation of AP duration (APD), and were annihilated without AP configuration chan

100 Effects of mutations on AP duration (APD), conduction velocity (CV), effective refractory per

101 g long QT syndrome 3) prolonged AP duration (APD); however, using GS-967 to inhibit I(NaL) sufficient

102 the cardiac action potential (AP) duration (APD) is a well-known arrhythmogenic mechanism.

103 monotonic decreases in AP and CaT duration (APD, CaTD), and a monotonic increase in CaT amplitude.

104 fferences in mean action potential duration (APD(80)) between groups; however, isoproterenol (ISO) si

105 SR Ca(2+) and action potential duration (APD) alternans occurred in-phase, but SR Ca(2+) alternan

106 t (kiCa) produced action potential duration (APD) alternans seen clinically at slower pacing rates.

107 strated shortened action-potential duration (APD) and abbreviated refractory period in the SQTS-hiPSC

108 had the shortest action potential duration (APD) and Ca(2+) transient duration (CaTD) at ZT14 (APD(8

109 hanism to prolong action potential duration (APD) and cause LQT9.

110 ulting changes in action potential duration (APD) and its short term variability (SD1) were measured.

111 such as decreased action potential duration (APD) and plateau height-were found when hCMs were couple

112 d chromatography; action potential duration (APD) and rate dependent adaptation were assessed by sing

113 ent that prolongs action potential duration (APD) and triggering proarrhythmic early afterdepolarizat

114 olongation of the action potential duration (APD) at 50% and 90% repolarization in UNx EPI cardiomyoc

115 pping techniques, action potential duration (APD) at 80% of repolarization was longer in CKD rats (78

116 y function of the action potential duration (APD) at different cycle lengths.

117 rmined transmural action potential duration (APD) before and after 100 nmol/L apamin administration i

118 that CO prolongs action potential duration (APD) by inhibiting a subset of inward-rectifying potassi

119 responding longer action potential duration (APD) in cardiomyocytes incubated with L5 in vitro.

120 ge on ventricular action potential duration (APD) in conscious healthy humans has not been reported.

121 n groups, because action potential duration (APD) in T2DM failed to undergo progressive adaptation to

122 d prolongation of action potential duration (APD) in TAC and leptin-treated sham animals, whereas, fo

123 lternation in the action potential duration (APD) of myocytes, i.e. alternans, is believed to be a di

124 gs (shortens) the action potential duration (APD) of that beat.

125 (AP) morphology, action potential duration (APD) restitution and conduction velocity (CV) restitutio

126 the slope of the action potential duration (APD) restitution curve, by reducing the propensity of AP

127 tilide effects on action potential duration (APD) were studied in canine left ventricular subendocard

128 nges that prolong action potential duration (APD) within the border zone (BZ) of chronically infarcte

129 s in contraction, action potential duration (APD), and magnitude of the Ca(2+) transient (CaT).

130 utation prolonged action potential duration (APD), produced steepened action potential duration resti

131 ng alternation in action potential duration (APD), which is considered to be a precursor of ventricul

132 RG) and shortened action-potential duration (APD).

133 heterogeneity of action potential duration (APD).

134 ural gradients of action potential duration (APD).

135 dent reduction in action potential duration (APD).

136 of cardiomyocyte action potential duration (APD).

137 normal changes in action potential duration (APD).

138 al for cardiocyte action potential duration (APD).

139 14 +/- 0.6 cm/s, Action Potential Duration (APD)80 and APD30 of 152 +/- 11 ms and 71 +/- 6 ms, respe

140 used to measure action potential durations (APDs) in the presence of the IKs blocker JNJ-303 and the

141 nans is Ca(2+) -driven, electromechanically (APD-Ca(2+) ) concordant alternans becomes electromechani

142 is synaptic corelease is expected to enhance APD antagonism of D2Rs where and when dopaminergic trans

143 neous in LQT2 but uniform in LQT1, enhancing APD dispersion under long CL(n-1) in LQT2.

144 4 in nearly every parameter assessed (except APD(80): ZT4: 39.7+/-1.9 ms versus ZT14: 33.8+/-3.1 ms,

145 In current-clamp experiments, APD and CaT alternans strongly correlated in time and ma

146 Fitting APD with a function of two previous APDs and CLs permitt

147 ors in structural changes observed following APD administration in clinical populations.

148 is predicted to be primarily responsible for APD prolongation, although increased I(Ca,L) and late I(

149 rom unipolar electrograms as a surrogate for APD (n=19) were recorded from right and left ventricular

150 ns of the extraction, i.e. 70% EtOH, 30mL/g, APD of 0.22W/mL, AED of 450J/mL are able to achieve simi

151 ditions of MAE obtained at 80% EtOH, 50mL/g, APD of 0.35W/mL, AED of 250J/mL can be used to determine

152 Among the first- and second-generation APDs that we tested, clozapine exhibited the lowest effi

153 ed 3,901 patients of which 1,819 (46.6%) had APD as their first modality.

154 operty, resulting in rapid and heterogeneous APD shortening.

155 n only in LQT2 rabbits through heterogeneous APD restitution and the short-term memory, underscoring

156 However, if APD accommodation is small (tau </= 250 ms), increase in

157 cross-correlation based approaches to image APDs.

158 -hiPSC-CCSs revealed shortened APD, impaired APD-rate adaptation, abbreviated wavelength of excitatio

159 ncrease arrhythmias rely on small changes in APD and Q-T intervals as criteria for safety pharmacolog

160 A 20% decrease in APD dispersion by Type C hMSCs compared to hEAG1-active

161 +/-5.6% versus ZT14: 22.7+/-9.5% decrease in APD, P<0.01).

162 arts, resulting in a significant increase in APD(80) dispersion in the DBH-Sap group.

163 LRP1 rs12150220 and AA for SRL rs13334970 in APD KRAS wild-type patients (HR = 4.44, 95% CI:1.23-16.1

164 ricular AP duration (APD), and variations in APD at a fixed heart rate are both reliable biomarkers o

165 ng kinetics at the D2 receptor may result in APDs with improved therapeutic profile.Atypical antipsyc

166 We found that JNJ-303 alone did not increase APD.

167 , which led to decreased IhERG and increased APD.

168 conclusion, short-long RR pattern increased APD dispersion only in LQT2 rabbits through heterogeneou

169 nd additional E-4031 significantly increased APD.

170 e that this characteristic pattern increases APD dispersion in LQT2, thereby promoting arrhythmia.

171 iarrhythmic effect is hampered by increasing APD variance.

172 Pacing-induced APD and CaT alternans were studied in single rabbit atri

173 We investigated APD dispersion and its dependence on two previous cycle

174 For the case of large APD accommodation (tau >/= 290 ms), increase in alpha le

175 why a short-long combination causes a larger APD dispersion in LQT2 but not in LQT1 rabbits.

176 long RR pattern was associated with a larger APD dispersion in LQT2 but not in LQT1 rabbits.

177 Because many APDs are dopamine (DA) D2 receptor (D2R) antagonists, su

178 cyclase, a recent study has shown that many APDs affect not only G(i/o)- but they can also influence

179 their effects on AP features (RMP, V (max), APD(50), APD(90) (AP duration at 50 and 90% of repolariz

180 Bazett formula-corrected, Arclight-measured APD(90) of CACNA1C-p.R518C hiPSC-CMs was significantly l

181 ours than at 50 minutes (QTc) or 30 minutes (APD) dofetilide administration.

182 ata indicate that parasites express multiple APD isoenzymes of various functions that can now be spec

183 ation recovered DYS and nNOS, and normalised APD and APD rate-dependency.

184 nd disopyramide, but not sotalol, normalized APD and suppressed arrhythmia induction.

185 ally discordant SR Ca(2+) alternans, but not APD alternans, the pacing threshold for discordance, or

186 reening where competitive binding of a novel APD and DA to a dopamine D3 receptor (D3R) was investiga

187 ic parameters may allow development of novel APDs based on the haloperidol scaffold with improved sid

188 The multivariate analyses of APD as a function of two previous CLs (APD(n) = C + alph

189 rents leading to different primary causes of APD prolongation, which suggests the use of mutation-spe

190 mmodation, which is an exponential change of APD over time once basic cycle length (BCL) changes.

191 A definition of APD stability is also proposed, based on successive APD

192 ac stability, as manifested by the degree of APD alternans.

193 he computational model to test the degree of APD prolongation induced by small electrical perturbatio

194 dominated by steady-state rate dependence of APD (type 1), intermediate rates (~5 ms/beat) lead to a

195 ers characterizing whether the dependence of APD on previous DIs or CLs is strong (typical for voltag

196 Here, alpha quantifies the dependence of APD restitution on pacing history and tau characterizes

197 ges to tissue excitability and dispersion of APD in mutation conditions.

198 , contributes to the structural diversity of APD precursors.

199 ular AP model, I investigate the dynamics of APD at high pacing rate under sinusoidally, saw-tooth, a

200 ation, such as shortening of APD and loss of APD rate-dependency, but had no effect in patients with

201 overed a marked increase in the magnitude of APD alternans during rapid pacing, and the emergence of

202 wing and APD heterogeneity, the magnitude of APD alternans was greater (by 80%, P<0.05) in VT/VF(+) v

203 The percentages of APD prolongation in the last 4 hearts at 2000 ms PCL aft

204 The arrhythmogenic potential of APD prolongation was also tested as a basis for comparis

205 itution curve, by reducing the propensity of APD alternans, converting discordant to concordant alter

206 y atrial fibrillation, such as shortening of APD and loss of APD rate-dependency, but had no effect i

207 id and spatially heterogeneous shortening of APD preceded the onset of arrhythmias in T2DM.

208 Limiting the use of APD in disadvantaged population may be unethical.

209 beat-to-beat and short-term variabilities of APD.

210 t that differential intracellular actions of APDs at their common G protein-coupled receptor (GPCR) t

211 last reaction in the biosynthetic pathway of APDs, catalyzed by F(420)H(2)-dependent Apd6 reductases,

212 which we can further assess the potential of APDs as targets for novel effective intervention strateg

213 oup divided by treatment response or type of APDs.

214 The effect of mental challenge on APD was not secondary to emotionally induced altered res

215 SD1 more than expected by its dependency on APD; (2) mIKr completely reversed APD and SD1 changes ca

216 ) are predicted to have negligible effect on APD, whereas blunted Ca(2+) -dependent inactivation of I

217 of the same magnitude had marginal impact on APD, but only when reducing mIKr, they significantly inc

218 interest was the probability to start PD on APD.

219 le modulating role of altered respiration on APD, the subjects then repeated the same breathing patte

220 an American patients less likely to start on APD (Odds ratio 0.74 CI95% 0.58-0.94) compared to Whites

221 cational levels were more likely to start on APD (Odds ratio 3.70, CI95% 2.25-6.09) compared to illit

222 length thresholds to induce CaT alternans or APD alternans were longer in CKD rats than normal rats (

223 of psychiatric disorders compared with other APDs.

224 At 50% perfusate oxygenation, APD and LVDP were significantly higher in LWHs perfused

225 At rapid pacing, APD maps show areas of conduction block in the failing h

226 ion of aspartic cathepsin D-like peptidases (APDs) has been often discussed as an antiparasite interv

227 The percent APD prolongation is negatively correlated with baseline

228 tions to fabricate avalanche photodetectors (APDs) with a sensitive mid-infrared light detection (4 m

229 ndium gallium arsenide avalanche photodiode (APD) detectors operated in Geiger mode.

230 employed a solid-state avalanche photodiode (APD)-based detector for real-time, high-sensitivity beta

231 Avalanche photodiodes (APDs) are essential components in quantum key distributi

232 endence of the DI on the immediate preceding APD (i.e. feedback).

233 Fitting APD with a function of two previous APDs and CLs permitted us to estimate lambdaalt along wi

234 Ca2+ homeostasis which drives proarrhythmic APD alternans in patients with AF.

235 Additionally, SNS produced APD(80) prolongation in the apex of control but not DBH-

236 iPSC-CMs paced at 1 Hz confirmed a prolonged APD(90) (689+/-29 ms; n=10) compared with the patient's

237 Apamin prolonged APD from 363 ms (95% confidence interval [CI], 341-385)

238 beat-to-beat AP alternations, but prolonged APD and failed to suppress CaT alternans.

239 hosphoinositide 3-kinase and INa-L prolonged APD acutely but no additional prolongation occurred on c

240 also detected in experiments with prolonged APD, they were often not sustained because of the subseq

241 hibition of Kir2.2 and Kir2.3 by CO prolongs APD in myocytes, cardiac Kir2.2 and Kir2.3 are promising

242 We were able to image and quantify APDs by relating the asymmetrical intensity distribution

243 Amiodarone increased atrial APD and reduced APD heterogeneity and was more effective in terminating

244 lular cleft narrowing or expansion regulates APD prolongation; in contrast, modulating the bulk inter

245 P)3.1 channel inhibition reverses AF-related APD shortening.

246 ility; conversely, the rabbit heart requires APD shortening to produce optimal inotropic responses.

247 Moreover, I(NaL) inhibition also restored APD and repolarization stability in heart failure.

248 -967 to inhibit I(NaL) sufficiently restored APD to control in both cases.

249 endency on APD; (2) mIKr completely reversed APD and SD1 changes caused by IKr blockade; (3) repolari

250 king short QT syndrome), and E-4031 reverted APD shortening.

251 During sinus rhythm, APD was shorter in LWHs compared to LANG hearts.

252 Results show that LV/RV APD and APD adaptation heterogeneities promote unidirect

253 termine the formation of the fully saturated APD moiety of lincomycin versus the unsaturated APD moie

254 the methods developed so far aimed to screen APD candidates.

255 nversely, pretreatment with GS-967 shortened APD (mimicking short QT syndrome), and E-4031 reverted A

256 duces regionally heterogeneous and shortened APD; these respectively facilitate initiation and mainte

257 Lidocaine shortened APD equally during acute and chronic moxifloxacin superf

258 ng of the SQTS-hiPSC-CCSs revealed shortened APD, impaired APD-rate adaptation, abbreviated wavelengt

259 isoproterenol (ISO) significantly shortened APD(80) in DBH-Sap but not control hearts, resulting in

260 We design InGaAs/AlInAs SL APDs with three different SL periods (4 ML, 6 ML, and 8

261 tice avalanche photodiodes (InGaAs/AlInAs SL APDs) on InP substrate to design and demonstrate an APD

262 Therefore, in the striatum, APDs are released with DA in response to action potentia

263 bility is also proposed, based on successive APD changes introduced in an AP sequence by a premature

264 idth of the intercellular cleft can suppress APD prolongation and EADs in the presence of Na(+) chann

265 s with improved performance for various SWIR APD application.

266 associated with slow conduction rather than APD prolongation form a potent substrate for arrhythmoge

267 SD1 may be more sensitive than APD in detecting IKr-dependent repolarization abnormalit

268 Here, we present data that demonstrate that APDs act independently of dopamine at an intracellular p

269 of D2R to the cell surface and suggest that APDs can act as pharmacological chaperones at D2R.

270 The APD and L-type calcium channel biophysical properties we

271 The APD prolongation was mediated by an increase of L-type c

272 onlinear functional relationship between the APD and the preceding diastolic interval (DI).

273 lop a mathematical framework to describe the APD signal using an autoregressive stochastic model, and

274 Here, the APD cyamemazine (CYAM) is visualized directly by two-pho

275 In the APD cohort IL8 rs4073 any A carriers, compared to TT car

276 ter chronic APD treatment, regardless of the APD administered.

277 , whereas, following TAC, leptin reduced the APD towards control values.

278 serve attenuation might be attributed to the APD variability caused by multi-stability in cardiac AP

279 Monitoring of these APD candidates in biological fluids is of great importan

280 m-selective K(2P)3.1 currents contributes to APD shortening in patients with chronic AF, and K(2P)3.1

281 te I(Na) by Cav3-S141R contribute equally to APD prolongation.

282 s a paradoxical resistance of T2DM hearts to APD adaptation.

283 y diastolic [Ca(2+)]SR alternans and lead to APD alternans.

284 explored CL range includes values leading to APD alternans under constant pacing.

285 s promoting conduction slowing as opposed to APD prolongation mark the chronic phase.

286 3KO mice had larger striatal volume prior to APD administration, coupled with increased glial and neu

287 Exposure to APDs early in development causes dose-dependent developm

288 ons of SZ and in the therapeutic response to APDs.

289 With TOLB, APDs in LWHs were longer at all workloads and APD reduct

290 cific cardiac models revealed that transient APD prolongation in mouse allowed for greater and more r

291 stronger than that in SZ patients on typical APDs or in NCs.

292 SZ patients on atypical rather than typical APDs or in NCs.

293 moiety of lincomycin versus the unsaturated APD moiety of PBDs, providing molecules with optimal sha

294 Using APD, UI and RC as three input variables, the area under

295 f a mental challenge protocol on ventricular APD in conscious humans.

296 fects of GS-458967 on guinea pig ventricular APD.

297 n a disturbance of Ca(2+) signaling, whereas APD alternans are a secondary consequence, mediated by C

298 with the PCL, but negatively correlated with APD when PCL is fixed.

299 nce imaging in rats treated chronically with APDs, we used automated analysis techniques to map the r

300 nd Ca(2+) transient duration (CaTD) at ZT14 (APD(80): ZT4: 45.4+/-4.1 ms; ZT9: 45.1+/-8.6 ms; ZT14: 3