ライフサイエンスコーパス: pacemaker

1 mplicating prevailing theories of a thalamic pacemaker.

2 the unique molecular make-up of the cardiac pacemaker.

3 n the sinus node forming the primary natural pacemaker.

4 the mouse sinoatrial node (SAN), the cardiac pacemaker.

5 y specialised cells constituting the heart's pacemaker.

6 ts deletion hampers atrial activation by the pacemaker.

7 of circadian phase of the brain's circadian pacemaker.

8 nction of the s-LNvs as the master circadian pacemaker.

9 6 may be a potential modifier of the cardiac pacemaker.

10 of TIM as a modulator of PER function in the pacemaker.

11 nic SND is the implantation of an electronic pacemaker.

12 ementing miniaturized and wirelessly powered pacemakers.

13 gs by atrial burst stimulation via implanted pacemakers.

14 cing the therapeutic potential of biological pacemakers.

15 esult from independent activation by M and E pacemakers.

16 vascular electronic devices, such as cardiac pacemakers.

17 rmed the importance of hub cells as possible pacemakers.

18 e implanted devices included 38 dual-chamber pacemakers, 17 cardiac resynchronization therapy defibri

19 0%), cardiac resynchronization therapy (CRT) pacemakers (4%), and CRT defibrillators (17%), as well a

20 rgitation (8.2% vs. 0.0%, p<0.001) and a new pacemaker (43.7% vs. 8.7%, p<0.001).

21 Cardiac devices included pacemakers (46%), ICDs (30%), cardiac resynchronization

22 oronary obstruction [0.9%], 20 new permanent pacemaker [9.6%], no mortality), and symptomatic improve

23 g SN unmasked ectopic pacemaking in AVRs and pacemaker action potentials were SN-like.

24 hown to be responsible for the generation of pacemaker activity in GI muscles, but this conclusion is

25 Pacemaker activity in longitudinal muscle is an emergent

26 of SK channels could explain arrhythmic SAN pacemaker activity in the atrial-specific Na(+) /Ca(2+)

27 otide-modulated ion channel (HCN) drives the pacemaker activity in the heart, and its malfunction can

28 with age reflects a slowing of the intrinsic pacemaker activity of the sinoatrial node of the heart,

29 the external globus pallidus (GPe) generate pacemaker activity that controls basal ganglia, circuitr

30 Electrical pacemaker activity was reduced in amplitude and increase

31 ar mechanisms that underlie the reduction in pacemaker activity with age and highlight key areas for

32 the consequences of anoctamin-1 knockdown on pacemaker activity, mechanical responses, gastric motili

33 Ano1 may develop with age and contribute to pacemaker activity.

34 n channel that mediates neuronal and cardiac pacemaker activity.

35 intestinal ICC with ageing and contribute to pacemaker activity.

36 ch is the misalignment between the circadian pacemaker and behavioral/environmental cycles, impairs c

37 In conclusion, gastric pacemaker and contractile activity is disordered in type

38 Gaps remain in identifying how pacemaker and extrapacemaker neurons communicate with en

39 nary Resuscitation Registry, and the Swedish Pacemaker and Implantable Cardioverter-Defibrillator (IC

40 A mathematical model of the circadian pacemaker and its response to light was used to demonstr

41 ons, LVEF >35% with the need for a permanent pacemaker and LVEF >35% with late gadolinium enhancement

42 onally distinct subtypes, including putative pacemaker and non-pacemaker populations.

43 if a bacteremia is missed (eg, patient with pacemaker and severe purulent cellulitis).

44 isalignment between the endogenous circadian pacemaker and sleep/wake cycles (circadian misalignment)

45 Overall, 85% received pacemakers and 15% received defibrillators, with one (55

46 Access to pacemakers and defibrillators is problematic in places w

47 d in 1983 to provide tested and resterilized pacemakers and defibrillators to underserved nations; a

48 atrial fibrillation (SCAF) in patients with pacemakers and patients with cryptogenic stroke.

49 ines, the investigators implanted epicardial pacemakers and radiotelemetry units to record cardiac rh

50 he sinoatrial node (SAN; the heart's primary pacemaker), and by the "coupled-clock" system within the

51 not an essential component of the lymphatic pacemaker, and does not exert a strong influence over co

52 r particular SCN neuronal populations act as pacemakers, and if so, by which signalling mechanisms, a

53 iasmatic nucleus (SCN)-the central circadian pacemaker-and the intergeniculate leaflet (IGL) through

54 we investigate a Staphylococcus epidermidis pacemaker-associated endocarditis, in a patient who deve

55 rioventricular-node ablation and ventricular pacemakers at 80 beats/min to control ventricular rate.

56 lop atrial fibrillation or require permanent pacemakers at a young age.

57 the system width increases the proportion of pacemakers at the boundary.

58 , we demonstrate a fully implanted symbiotic pacemaker based on an implantable triboelectric nanogene

59 europeptide Pdf and have been called 'master pacemakers' because they are essential for circadian rhy

60 through weak field effects distant from the pacemaker, but which are highly effective at recruiting

61 laevis eggs, we find that nuclei define such pacemakers by concentrating cell cycle regulators.

62 Specific regions acted as pacemakers by initiating calcium wave propagation.

63 We show that in zebrafish, pacemaker cardiomyocytes derive from a subset of Nkx2.5+

64 The development and function of the pacemaker cardiomyocytes of the sinoatrial node (SAN), t

65 Pacemaker cardiomyocytes that create the sinoatrial node

66 By discovering the origins of pacemaker cardiomyocytes, we reveal an evolutionarily co

67 SCs) notably results in the creation of hPSC-pacemaker cardiomyocytes, which successfully pace three-

68 isions, which lead to the differentiation of pacemaker cardiomyocytes.

69 c pacemaker program, including activation of pacemaker cell differentiation transcription factors Isl

70 of SAN-specific REs potentially involved in pacemaker cell gene regulation.

71 s and Ca transient decay to insure fail-safe pacemaker cell operation within a wide range of rates.

72 We validated pacemaker cell-specific elements in the SHOX2 and TBX3 l

73 along with smooth myosin heavy chain for the pacemaker cells (previously termed 'atypical' smooth mus

74 lts from electrical remodeling of individual pacemaker cells along with structural remodeling and a b

75 f the regulatory landscape of human SAN-like pacemaker cells and functional assessment of SAN-specifi

76 to lead to a sustained hyperpolarization of pacemaker cells and thereby reduces heart rate.

77 human pluripotent stem cell-derived SAN-like pacemaker cells and ventricle-like cells and identified

78 to a model of the evolutionary emergence of pacemaker cells as neurons using components of innate im

79 ontrolling target gene expression in the SAN pacemaker cells have remained undefined.

80 otypical ANO/SCN/TRPM ion channel-expressing pacemaker cells in the basal metazoan Hydra by using a c

81 Thus, Nkx2-5 defines a population of pacemaker cells in the transitional zone.

82 ived cardiac progenitors produces functional pacemaker cells in vitro, advancing the therapeutic pote

83 19) identify the embryonic origin of cardiac pacemaker cells in zebrafish and implicate Wnt5b in prom

84 Specialized pacemaker cells, termed atypical smooth muscle cells (AS

85 an be explained by the presence of nonfiring pacemaker cells.

86 ncluding thalamocortical neurons and cardiac pacemaker cells.

87 rd of the SSA countries do not have a single pacemaker center, and more than one-half do not have a c

88 hate-dependent regulation (CDR) of the major pacemaker channel HCN4 in the sinoatrial node (SAN) is i

89 the cyclic nucleotide binding domains of HCN pacemaker channel.

90 ated channel HCN2 in the family of so-called pacemaker channels.

91 nophosphate (N (6)-Bnz-cAMP), on murine HCN2 pacemaker channels.

92 Here, we identify a family of voltage-gated "pacemaker" channels, HCNL1, that are exquisitely selecti

93 important for the operation of the circadian pacemaker circuit.

94 d Cl(-) conductance that serves as a primary pacemaker conductance in ICs of the GI tract.

95 The Drosophila circadian pacemaker consists of transcriptional feedback loops sub

96 e sinoatrial node (SAN), the primary cardiac pacemaker, consists of a head domain and a junction/tail

97 the changes in the dual-chamber transvenous pacemaker control group (43% versus 38%, respectively; P

98 Blocking pacemaker current I(f), and disrupting intracellular Ca(

99 cadian clock via the suprachiasmatic nucleus pacemaker, daily TSH secretion profiles are disrupted in

100 ther adjustment for mitral regurgitation and pacemaker/defibrillator (HR: 0.35; 95% CI: 0.23 to 0.54;

101 of vascular complications, bleeding, and new pacemaker/defibrillator implantation demonstrated no sig

102 p = 0.002, respectively) but less frequently pacemakers/defibrillators (1.5% vs. 10.5%; p < 0.001), a

103 Patients with pacemakers/defibrillators, organic valve disease, or pre

104 ffects prosthetic valves and less frequently pacemakers/defibrillators.

105 ntation depth alone were not associated with pacemaker dependency (odds ratio, 0.79 [95% CI, 0.60-1.0

106 ion depth alone, are predictive of long-term pacemaker dependency after TAVR, thus influencing device

107 sess the rate and the possible predictors of pacemaker dependency after TAVR.

108 ta exist on anatomic factors predisposing to pacemaker dependency after TAVR.

109 Pacemaker dependency at 30 days and 1 year and all-cause

110 e analysis, independent predictors of 30-day pacemaker dependency included left ventricular outflow t

111 Of these, 44.6% (50 of 112) were pacemaker dependent at 30 days and 46.7% (36 of 77) at 1

112 rgoing pacemaker implantation after TAVR are pacemaker-dependent at midterm follow-up.

113 Pacemaker-dependent patients comprised 27% of all MRI ex

114 median follow-up of 28.1 (11.7-48.6) months, pacemaker-dependent patients did not show a worse surviv

115 Pacemaker-dependent patients received asynchronous pacin

116 nts who have non-MRI-conditional devices, in pacemaker-dependent patients with ICDs, and in patients

117 asmatic nucleus (SCN), the central circadian pacemaker, disrupts the timing of feeding, resulting in

118 lying molecular mechanism defining these two pacemaker domains remains elusive.

119 prachiasmatic nucleus (SCN) acts as a master pacemaker driving circadian behavior and physiology.

120 ereafter, the hippocampal activity acts as a pacemaker, entraining the other territories to their dis

121 of baroreflex, chemoreflex and carbachol on pacemaker entrainment and electrical conduction across t

122 nt a python implementation of the Epigenetic Pacemaker (EPM), a conditional expectation maximization

123 A suite of Atlantic Pacemaker experiments successfully reproduces the WTP mu

124 ent discharges of dopamine neurons (tonic or pacemaker firing) determine the motivation to respond to

125 mitotic entry and propose that it acts as a pacemaker for cell cycle.

126 the fastest intrinsic rhythm should act as a pacemaker for the process.

127 uggest that the Atlantic Ocean acts as a key pacemaker for the western Pacific decadal climate variab

128 eract with interneurons to act as excitatory pacemakers for the V1 gamma rhythm.

129 cle contractility) and reduced expression of pacemaker gene programs (neuronal, Wnt signaling, calciu

130 a neurochemically and topologically specific pacemaker hub that determines the emergent properties of

131 Pacemaker hyperpolarization-activated cyclic nucleotide-

132 underwent atrioventricular node ablation and pacemaker implant demonstrated clear improvement in LVEF

133 In 11 of these countries, the first pacemaker implant in the country was through the mission

134 ion, no differences in the rate of permanent pacemaker implant were observed.

135 er next-generation implant materials such as pacemakers, implantable sensors, or prosthetic devices i

136 life-threatening arrhythmia, implantation of pacemaker/implantable cardioverter defibrillator, acute

137 ere aortic regurgitation (3.5% vs. 0.5%) and pacemaker implantation (17.4% vs. 6.1%).

138 ever, BAV was associated with lower rates of pacemaker implantation (2.9% versus 8.0%; P<0.001) and b

139 lation, 8 patients (36%) underwent permanent pacemaker implantation (atrio-ventricular blocks-5; sinu

140 cular conduction disease requiring permanent pacemaker implantation (PPMI).

141 th, rehospitalization for heart failure, and pacemaker implantation after a TAVR procedure.

142 Less than half of the patients undergoing pacemaker implantation after TAVR are pacemaker-dependen

143 (53.5% men; median age, 81 years) underwent pacemaker implantation after TAVR.

144 TAVR was also associated with lower rates of pacemaker implantation after the procedure (relative ris

145 e 2/3 were lower, whereas those of permanent pacemaker implantation and moderate/severe paravalvular

146 ACURATE neo bioprosthesis, was new permanent pacemaker implantation at 30 days.

147 ence and time course for developing HF after pacemaker implantation for cAVB.

148 identified patients undergoing dual-chamber pacemaker implantation from 2008 to 2014.

149 lectrophysiological testing, and pre-emptive pacemaker implantation have been described.

150 s in 2 and severe bradyarrhythmias requiring pacemaker implantation in 2.

151 arch 2018, and who did not require permanent pacemaker implantation pre-discharge, were discharged wi

152 time, whereas rates of cardiac tamponade and pacemaker implantation significantly increased.

153 Consecutive patients undergoing pacemaker implantation up to 30 days after TAVR between

154 Need for permanent pacemaker implantation was significantly higher with the

155 The 30-day rates of new permanent pacemaker implantation were 10.5% in the ACURATE neo gro

156 Rehospitalization for heart failure and pacemaker implantation were more frequently reported in

157 Higher rates of prosthetic regurgitation and pacemaker implantation were seen after TAVR.

158 rillation, atrioventricular heart block, and pacemaker implantation).

159 is associated with conduction abnormalities, pacemaker implantation, atrial fibrillation (AF), and ca

160 the background population; the composite of pacemaker implantation, atrioventricular block, and sino

161 In consecutive patients during HB pacemaker implantation, programmed HB pacing was deliver

162 ated with a lower incidence of new permanent pacemaker implantation.

163 re found highest in the patient who required pacemaker implantation.

164 onduction abnormalities leading to permanent pacemaker implantation.

165 tentially life-threatening complications and pacemaker implantation.

166 nd chronic (6 months to 4 years) phases post-pacemaker implantation.

167 f residual aortic regurgitation and need for pacemaker implantation.

168 drome, the most common reason for electronic pacemaker implantation.

169 developed to treat these conditions without pacemaker implantation.

170 mark (n=2 824 199 individuals; 5397 incident pacemaker implantations), individuals with at least 1 fi

171 There were no deaths, strokes, or permanent pacemaker implantations.

172 f-contained right ventricular single-chamber pacemakers implanted by using a femoral percutaneous app

173 oring antegrade conduction with a biological pacemaker in a porcine model of RV PICM.

174 s demonstrates a competent 24-hour molecular pacemaker in Bmal1 knockouts.

175 t of retinal ganglion cells to the circadian pacemaker in the suprachiasmatic nucleus (SCN) in the br

176 The central pacemaker in the suprachiasmatic nucleus (SCN) is consid

177 enting unnecessary implantation of permanent pacemakers in otherwise healthy young individuals.

178 In a preclinical model, pacemaker-induced cardiomyopathy can be prevented, and r

179 Cardiac conduction blocks and risk for pacemaker insertion cluster within families.

180 east 1 first-degree relative with history of pacemaker insertion had a multivariable-adjusted 1.68-fo

181 tionally, we assessed familial clustering of pacemaker insertion in the Danish general population.

182 clustering of cardiac conduction defects and pacemaker insertion in the FHS (Framingham Heart Study).

183 history of conduction system disturbance or pacemaker insertion should trigger increased awareness o

184 rrogated to assess the relations of parental pacemaker insertion with offspring pacemaker insertion.

185 lete bundle branch block (QRS, >=0.12 s), or pacemaker insertion with the occurrence of cardiac condu

186 ular block, complete bundle branch block, or pacemaker insertion, and 1471 age- and sex-matched contr

187 ny electrocardiographic conduction defect or pacemaker insertion, the offspring had a 1.62-fold odds

188 tio, 95% CI, 1.49-1.89) risk of undergoing a pacemaker insertion.

189 parental pacemaker insertion with offspring pacemaker insertion.

190 major vascular complications, new permanent pacemaker insertions, or moderate or severe paravalvular

191 was not performed because the patient had a pacemaker; instead, CT of the lower extremity was perfor

192 was not performed because the patient had a pacemaker; instead, CT of the lower extremity was perfor

193 his study, procedural success was tracked by pacemaker interrogation in the atrioventricular junction

194 microRNA (miR-370-3p), downregulation of the pacemaker ion channel, HCN4, and downregulation of the c

195 positioning and strongly influence whether a pacemaker is more likely to be at a boundary or an inter

196 The power consumption of these pacemakers is reduced to uW-level by a novel integrated

197 Endocardial pacemaker leads and right ventricular (RV) pacing are we

198 ing medical tubing, Foley catheters, cardiac pacemaker leads, and soft robots on massive scales are f

199 r computational model reproduced the regular pacemaker-like spiking pattern, action potential shape,

200 r import, nuclear positioning determines the pacemaker location.

201 esponsible for this process - termed leading pacemaker (LP) shift - have not been investigated fully.

202 ith concomitant caudal shifts of the leading pacemaker (LP) site within the sinoatrial node (SAN).

203 ces can potentially be mitigated by leadless pacemaker (LP) therapy by eliminating the presence of a

204 12%) developed H-AVB necessitating permanent pacemaker <2 days post-TAVR, 1 died pre-discharge, and 1

205 e cardioverter defibrillators, biventricular pacemakers, mechanical circulatory support, and transpla

206 on downregulates fundamental sinoatrial cell pacemaker mechanisms to lower heart rate, including sarc

207 ength in AVRs, indicating a role for SN-like pacemaker mechanisms.

208 one accessory pathway ablation; 17 (19%) had pacemakers (median age at implantation 36 years; IQR: 27

209 ts had LVH, 29% had AF, 21% required de novo pacemakers (median age at implantation 37 years; IQR: 29

210 n, endovascular baroreflex amplification and pacemaker-mediated cardiac neuromodulation therapy have

211 heterotrimer action in GIRK-channel induced pacemaker membrane hyperpolarization.

212 cently developed a formalism inspired by the Pacemaker model of evolution that accounts for varying r

213 has started to decrease (2.75% to 2.3%), but pacemaker need is unchanged (10.9% to 10.8%).

214 derlies the functional differences among the pacemaker neuron subgroups.

215 Pacemaker neurons exert control over neuronal circuit fu

216 Unexpectedly, these prototypical pacemaker neurons express a rich set of immune-related g

217 t entrainment pathway is mediated by central pacemaker neurons in the brain.

218 genic cellular or synaptic mechanisms, i.e., pacemaker neurons or inhibition.

219 emonstration that Rh7 functions in circadian pacemaker neurons represents, to our knowledge, the firs

220 oting upstream neurons is a set of circadian pacemaker neurons that activates dFB neurons via direct

221 Central pacemaker neurons that perceive light entrain a distribu

222 ing factor-immunoreactive (PDF-ir) circadian pacemaker neurons with somata in the lamina (PDFLAs) or

223 s an additional light-sensing pathway in fly pacemaker neurons.

224 hin the pigment dispersing factor (PDF) cell-pacemaker neurons; only mir-92a peaks during the night.

225 cal properties regardless of the conditional pacemaker node's tuning, and that node's outputs are dom

226 verturning Circulation-the strongest oceanic pacemaker of the Atlantic Ocean and perhaps the entire E

227 es of the sinoatrial node (SAN), the leading pacemaker of the heart, are tightly controlled by a cons

228 The sinus node (SAN) is the primary pacemaker of the human heart, and abnormalities in its s

229 The circadian pacemaker of the Madeira cockroach, Rhyparobia (Leucopha

230 Pyruvate kinase (PK) is the main "pacemaker" of the EDP, and its activity is also relevant

231 ll patients with an indication for permanent pacemaker or cardiac resynchronization therapy that unde

232 lant use is common among patients undergoing pacemaker or defibrillator surgery.

233 tries who received a resterilized and reused pacemaker or defibrillator, the incidence of infection o

234 strength of 1.5 tesla for patients who had a pacemaker or implantable cardioverter-defibrillator (ICD

235 ole in modulating the frequency of the ionic pacemaker or the amplitude of spontaneous contractions.

236 Patients who have pacemakers or defibrillators are often denied the opport

237 dopamine neurons fire action potentials in a pacemaker pattern in the absence of synaptic input, the

238 Our results are consistent with circadian pacemaker period being relatively unaffected by Abeta pa

239 t implantable cardio-defibrillator/permanent pacemaker placements (n = 8; 27.6%).

240 implantable cardio-defibrillators/permanent pacemaker placements within 12 months of discharge.

241 btypes, including putative pacemaker and non-pacemaker populations.

242 cardiac valve surgery requiring a permanent pacemaker (PPM) are poorly characterized.

243 The incidence of permanent pacemaker (PPM) implantation is higher following mitral

244 ve replacement and often result in permanent pacemaker (PPM) implantation.

245 settings, for example as in vivo biological pacemaker, preclinical drug safety screening tool or ult

246 a novel role of CDR of HCN4 for the central pacemaker process in the sinoatrial node.

247 uropeptide sNPF, released from s-LNv and LNd pacemakers, produces Ca(2+) activation in the DN1 group

248 ical Wnt5b signaling to initiate the cardiac pacemaker program, including activation of pacemaker cel

249 The interplay between V2a interneuron pacemaker properties and their organized connectivity pr

250 the prime generator of tremor because of the pacemaker properties of ION neurons, but structural and

251 chical connectivity that acts in tandem with pacemaker properties to provide an ignition and gear-shi

252 In Drosophila, key pacemaker proteins PERIOD (PER) and TIMELESS (TIM) are p

253 l, national, and institutional standards for pacemaker qualification and credentials are lacking.

254 gs indicate the LP region is defined by both pacemaker rate and capacity to drive activation.

255 enomenon whereby acetylcholine slows central pacemaker rate disproportionately, enabling caudal cells

256 r differences between centers and studies in pacemaker rates post-TAVR.

257 re matching, and mean and maximal biological pacemaker rates were 45 and 75 beats per minute.

258 y outcomes (eg, aortic valve reintervention, pacemaker rates) were more closely concordant between tr

259 matched controls of dual-chamber transvenous pacemaker recipients.

260 the firing rate of action potentials in the pacemaker region of the heart and in pain-sensitive (noc

261 ts in LP site from the central SAN to caudal pacemaker regions, which were positive for HCN4 and rece

262 te from the central SAN to one or two caudal pacemaker regions.

263 Here, we show that such waves initiate at pacemakers, regions that oscillate faster than their sur

264 ications, basic function/programming, common pacemaker-related issues, and remote monitoring, which a

265 maker to its 24.84-h rhythm and altering the pacemaker's phase-relationship to sleep in a manner that

266 There are many countries where pacemaker services do not meet one-hundredth of the nati

267 ates what standards should be set to develop pacemaker services in a resource-constrained continent,

268 Both presently manufactured leadless pacemakers show similar complications, which are mostly

269 rtholog of a noncoding region with candidate pacemaker-specific REs in the SHOX2 locus resulted in se

270 Putative pacemaker-specific REs were identified up to 1 Mbp upstr

271 a genome-wide collection of candidate human pacemaker-specific REs, including the loci of SHOX2, TBX

272 The symbiotic pacemaker successfully corrects sinus arrhythmia and pre

273 The central circadian pacemaker (Suprachiasmatic Nuclei, SCN) maintains the ph

274 t was comparable to dual-chamber transvenous pacemaker systems.

275 basis for future wirelessly powered leadless pacemakers that address various cardiac resynchronizatio

276 rk is coordinated by the principal circadian pacemaker, the hypothalamic suprachiasmatic nucleus (SCN

277 iological dissection of the master circadian pacemaker, the suprachiasmatic nuclei (SCN).

278 he brain, including to the central circadian pacemaker, the suprachiasmatic nucleus (SCN).

279 ession of an underlying infradian affective "pacemaker." The authors attempted to determine which con

280 potential strategies for biological cardiac pacemaker therapy.

281 y two possible mechanisms: either a unitary "pacemaker" timing signal is imposed on the hippocampal s

282 ycle oscillator model of the human circadian pacemaker to estimate circadian phase in 25 nursing and

283 es, by periodically entraining the circadian pacemaker to its 24.84-h rhythm and altering the pacemak

284 lpha1-A(R)-dependent induction of persistent pacemaker-type firing of dorsal raphe neurons and regula

285 4 +/- 0.4 beats/min; p = 0.01), lower backup pacemaker utilization (45 +/- 2.6% vs. 94.6 +/- 1.4%; p

286 .1 +/- 0.4 beats/min; p = 0.05), less backup pacemaker utilization (53 +/- 8.2% vs. 95 +/- 1.6%; p =

287 A pacemaker was implanted in 17.5% of patients.

288 New permanent pacemaker was placed in 46 (18.3%).

289 With their flexible form factors, two pacemakers were implanted epicardially on the right and

290 r tachyarrhythmias in 17 (2%), and permanent pacemakers were implanted in 181 (21%).

291 Pacemakers were implanted in all animals for continuous

292 In 64 missions, a total of 542 permanent pacemakers were implanted.

293 -nucleotide-gated potassium channel 1 (HCN1) pacemakers were required for systemic ketamine to induce

294 to show that once a conditional respiratory pacemaker, which can be tuned across oscillatory and non

295 the solar day is largely enabled by a neural pacemaker, which is directly responsive to certain envir

296 In mammals, the central circadian pacemaker, which is located in the hypothalamic suprachi

297 ned or epicardial leads, and dependence on a pacemaker with an implantable cardioverter defibrillator

298 In one case, a pacemaker with less than 1 month left of battery life re

299 about the sex differences with biventricular pacemakers with respect to ventricular remodeling and re

300 ctions are driven by an intrinsic electrical pacemaker, working through an unknown underlying ionic m