ライフサイエンスコーパス: myocyte

1 D2 channels in arterial smooth muscle cells (myocytes).

2 icity to calcineurin function in the cardiac myocyte.

3 plasma membrane of human and mouse arterial myocytes.

4 , [Ca(2+)](i), and myogenic tone in arterial myocytes.

5 d the molecular and functional output of VCS myocytes.

6 ine of conditionally immortalized rat atrial myocytes.

7 ging of permeabilized Wistar rat ventricular myocytes.

8 and electrophysiological phenotype of atrial myocytes.

9 ls, including platelets, adipose tissue, and myocytes.

10 s excitation-contraction coupling in cardiac myocytes.

11 C10 domains was expressed in rat ventricular myocytes.

12 f Kv2.1 channels in male and female arterial myocytes.

13 tions, and patch clamping in isolated atrial myocytes.

14 in cultured adult feline and rat ventricular myocytes.

15 oring protein 5 (AKAP5) function in arterial myocytes.

16 (2+)](i), and larger myogenic tone than male myocytes.

17 ential for intracellular Ca(2+) transport in myocytes.

18 ion and cellular stress responses in cardiac myocytes.

19 d I(Kr) in isolated neonatal rat ventricular myocytes.

20 s a component of Ca(2+) signaling in cardiac myocytes.

21 ripts, in healthy and failing hearts, and in myocytes.

22 amount in evaluation of cardiac and skeletal myocytes.

23 urbs mitochondrial ultrastructure in cardiac myocytes.

24 and action potential dynamics in ventricular myocytes.

25 mate ion channel copy numbers for sinus node myocytes.

26 e been studied in detail in isolated cardiac myocytes.

27 Mbp were identified in control human cardiac myocytes.

28 or a mutant LMNA (D300N) protein in cardiac myocytes.

29 t increases in intracellular accumulation in myocytes.

30 r but was still not detected in the AV nodal myocytes.

31 erent between WT (n=18) and R67Q(+/-) (n=16) myocytes.

32 mitochondria-dependent apoptosis in cardiac myocytes.

33 s to induce Ca(2+) sparks in native arterial myocytes.

34 ving maturation of stem cell-derived cardiac myocytes.

35 in tubulated atrial myocytes and ventricular myocytes.

36 ptor (beta3 AR) mediates pump stimulation in myocytes.

37 calcium waves (TCWs) in isolated dog atrial myocytes.

38 are present in both peri-infarct and remote myocytes.

39 based exclusively on data from male arterial myocytes.

40 AP and their integrals covary in individual myocytes.

41 n microscopy we identified, in adult cardiac myocytes, a Na(V)1.5 subpopulation in close proximity to

42 computational model of the human ventricular myocyte action potential, the Cav3 mutation-induced chan

43 In cardiac myocytes, action potentials are initiated by an influx o

44 Ventricular myocytes and tubulated atrial myocytes additionally exhibited early afterdepolarizatio

45 Primary adult rat ventricular myocytes, adeno-associated virus (AAV)-mediated gene del

46 Action potentials of Tbx5-deficient VCS myocytes adopted nodal-specific characteristics, includi

47 In conclusion, altered myocyte adrenergic responses in the peri-infarct but not

48 ese data highlight the importance of altered myocyte adrenergic responses in the peri-infarct region

49 y within the myofilament fraction of cardiac myocytes after exposure to NCA revealed activation of PK

50 Peri-infarct myocytes also had reduced repolarization reserve and inc

51 These myocytes also have reduced repolarization reserve and in

52 as a potential strategy to increase cardiac myocyte and coronary vascular endowment at birth.

53 myocardium is regulated by a combination of myocyte and non-myocyte responses to mechanosensitive pa

54 in increased Ca(2+) influx into ventricular myocytes and a positive inotropic response.

55 and calcium handling in isolated tissues and myocytes and analyzed mitochondrial function by ultrasen

56 ation of region-specific therapies targeting myocytes and autonomic modulation.

57 levated both cAMP and cGMP levels in cardiac myocytes and cardiac fibroblasts, consistent with PDE10A

58 We begin with the myometrium and its myocytes and describe how excitation might initiate and

59 ring static mitochondrial biology in cardiac myocytes and dynamic mitochondrial biology in neurons ar

60 We used isolated adult mouse cardiac myocytes and fibroblasts, as well as preclinical mouse m

61 and translocation of ERK1/2 between cardiac myocytes and fibroblasts.

62 We used confocal Ca(2+) imaging in myocytes and HEK-RyR2 (ryanodine receptor isoform 2-expr

63 ocardium showed cytoplasmic vacuolization in myocytes and in another patchy interstitial fibrosis.

64 ls and vascular smooth muscle cells, cardiac myocytes and inflammatory cells, like monocyte/macrophag

65 n susceptibility in aged and alcohol-exposed myocytes and intact hearts.

66 tic resistance to diastolic stretch in human myocytes and myocardium.

67 ular hemoprotein highly expressed in cardiac myocytes and oxidative skeletal myofibers.

68 at demonstrate the potential to generate new myocytes and thereby fulfill an essential central criter

69 d delivery of nutrients to the local cardiac myocytes and to augment ATP production by their mitochon

70 Ventricular myocytes and tubulated atrial myocytes additionally exhi

71 h was found to be absent in tubulated atrial myocytes and ventricular myocytes.

72 of JUP(2157del2) in neonatal rat ventricular myocytes) and a robust murine model of ACM (homozygous k

73 potential conduction, contraction of cardiac myocytes, and actin filament-based movement of cardiac c

74 d cause hereditary proteinopathy of neurons, myocytes, and bone.

75 ellular organelles in defined regions of the myocytes, and the functional consequences of that associ

76 ct is more potent in atrial than ventricular myocytes, and this could be explained by our results sho

77 d rise in mitochondrial calcium required for myocyte apoptosis and myocardial failure.

78 e mice, ascending aortic constriction caused myocyte apoptosis, LV dilation, and systolic failure, al

79 Par4-deficient mice showed less myocyte apoptosis, reduced infarct size, and improved fu

80 edistribution of intercalated disk proteins, myocyte apoptosis, release of inflammatory cytokines) an

81 the presence of cleaved caspase-3 suggested myocyte apoptosis.

82 K(+) (SK) channels expressed in ventricular myocytes are dormant in health, yet become functional in

83 calcium (Ca(2+)) cycling dynamics in cardiac myocytes are spatiotemporally generated by stochastic ev

84 od flow are prevented in AKAP5 null arterial myocytes/arteries.

85 is signaling pathway is compartmentalized in myocytes, as it was distinct from atrial natriuretic pep

86 lar Ca(2+) imaging from isolated ventricular myocytes at baseline and after adrenergic stimulation we

87 t that functional diversity among individual myocytes at the microscale may contribute to bulk relaxa

88 As myocyte ATP is consumed in excess of production, [ATP](i

89 n-dependent kinase II activation and altered myocyte bioenergetics.

90 ype 1 (RyR1) supports relaxation of arterial myocytes by unloading Ca(2+) into peripheral nanocourses

91 s were recorded from rabbit and human atrial myocytes by whole-cell-patch clamp.

92 We followed changes in cardiac myocyte Ca(2+) and Na(+) regulation from the formation o

93 aC activation promotes adaptive increases in myocyte Ca(2+) transients and nuclear transcriptional re

94 +) regulation in mut(PG1)JPH2 overexpressing myocytes caused calcium/calmodulin-dependent kinase II a

95 ), a major Ca(2+) signaling mechanism in non-myocyte cells, has recently emerged as a component of Ca

96 In cardiac myocytes, clusters of type-2 ryanodine receptors (RyR2s)

97 The function of ZO-1 in cardiac myocytes (CM) is largely unknown.

98 uated the ultrastructural disorganization of myocytes comparable to VPA.

99 Activation of TRPV1 in vascular myocytes constricted arteries, reduced coronary flow in

100 or TRPML1 channels in regulation of arterial myocyte contractility and blood pressure.

101 n excitation-contraction coupling, impairing myocyte contractility and delaying relaxation, along wit

102 d luminal vacuolization along with decreased myocyte contractility and disrupted Ca(2+) cycling.

103 etween manual and automated observations for myocyte count (r = 0.94, p < 0.001), myocyte diameter (r

104 nduced pluripotent stem cell-derived cardiac myocytes deficient in SCN5A.

105 icle and atrium but also vary between atrial myocytes depending on subcellular structure and electrop

106 of Ca(2+) current was 40 to 70 ms in atrial myocytes (depending on holding potential) so this curren

107 ppaB signaling was also activated in cardiac myocytes derived from a patient with ACM.

108 apabilities of our device to support cardiac myocytes derived from human induced pluripotent stem cel

109 Cs prevented Ca2+ alternans in human cardiac myocytes derived from induced pluripotent stem cells dur

110 us calcium release activity in human cardiac myocytes derived from induced pluripotent stem cells, re

111 Cs were cocultured with normal human cardiac myocytes derived from induced pluripotent stem cells.

112 se activity (n=14, P<0.013) in human cardiac myocytes derived from induced pluripotent stem cells.

113 ly correlated in both healthy rabbit and pig myocytes, despite high overall cell-to-cell variability.

114 ons for myocyte count (r = 0.94, p < 0.001), myocyte diameter (r = 0.97, p < 0.001), endomysial fibro

115 uring endocardial ablation partially rescued myocyte differentiation, maturation and function.

116 M) can be objectively measured, fibrosis and myocyte disarray are difficult to assess.

117 hypertrophy on echocardiogram, SCD occurred, myocyte disarray was found on autopsy heart, and tissue

118 inhibited concentric hypertrophy in cultured myocytes; disruption of anchoring in vivo using an adeno

119 xtacrine signaling receptor, is expressed on myocytes during embryonic and fetal myogenesis and on na

120 whole heart and Ca(2+) transients in single myocytes during the former stage.

121 some of the Ang II-induced changes in atrial myocyte electrophysiology and preventing fibrosis throug

122 fects of normal and diseased cardiac MSCs on myocyte electrophysiology remain unclear.

123 Thus, TRPV1 activation in vascular myocytes enables a persistent depolarizing current, lead

124 atine (PCr) plays a vital role in neuron and myocyte energy homeostasis.

125 at exercise and mTg are each associated with myocyte enhancer factor (MEF) 2 and estrogen-related rec

126 egulated kinase 5 (ERK5) via upregulation of myocyte enhancer factor 2 (MEF2) induces KLF2 expression

127 Furthermore, we identified the myocyte enhancer factor 2 C (MEF2C) transcription factor

128 s the activation of the transcription factor myocyte enhancer factor 2C (MEF2C) and promotes the tran

129 The transcription factor, myocyte enhancer factor-2 (MEF2), is required for normal

130 he prohypertrophic transcription factor (TF) myocyte enhancer factor-2 (MEF2).

131 Myocyte enhancer factor-2B (MEF2B) has the unique capabi

132 ) channel Ca(V)1.2 is essential for arterial myocyte excitability, gene expression and contraction.

133 Experiments were performed in isolated rat myocytes exposed to simulated hypokalemia conditions (re

134 Myocytes express low levels of MHC class I (MHC I), perh

135 In adult rat ventricular myocytes expressing wild-type SERCA, H(2)O(2) caused a 2

136 Adult rat ventricular myocytes expressing wild-type SERCA2b or a redox-insensi

137 These effects were greater in left atrial myocytes from Ang II-treated NPR-C(-/-) mice.

138 close correlation was lost in heart failure myocytes from both species.

139 a rod-like protein(2) that protects striated myocytes from contraction-induced injury(3,4).

140 functional investigation of SOCE in cardiac myocytes from healthy mice (wild type; WT) and from a ge

141 Single adult cardiac myocytes from mice treated with AAV9-M7.8L showed partia

142 and single-nucleus transcriptomes of cardiac myocytes from murine HF models and human patients with H

143 rrent, I(p), was measured in voltage-clamped myocytes from noninfarct myocardium.

144 In myocytes from SERCA knock-in mice, basal SERCA activity

145 so increased I(p) significantly to levels of myocytes from sham-operated rabbits.

146 om the peri-infarct region, in comparison to myocytes from the remote region, had more DADs, associat

147 rtant signalling enzymes determining cardiac myocyte function and phenotype.

148 ncentration regulate many aspects of cardiac myocyte function.

149 anscription factor Myogenin (Myog) regulates myocyte fusion during development, but its role in adult

150 on, myogenic commitment and differentiation, myocyte fusion, and myotube maturation.

151 Thus, beyond controlling myocyte fusion, Myog influences the MuSC:niche relations

152 predicted response of the adult ventricular myocyte given the same genetic mutation.

153 e reduction of PGI activity directly affects myocyte growth by regulating mTOR activation.

154 ion of the mechanisms governing asymmetrical myocyte growth could provide new therapeutic targets for

155 r protein-1)-dependent enhancers that direct myocyte growth in width.

156 g deltaB exhibited more severe HF, eccentric myocyte growth, and nuclear changes.

157 R proteostasis are challenged during cardiac myocyte growth.

158 emonstrating a role for ATF6 in compensatory myocyte growth.

159 chitecture should be used to assess striated myocytes has not been fully explored.

160 Female myocytes have larger Ca(V)1.2 clusters, larger [Ca(2+)](

161 Cardiac myocytes have multiple cell autonomous mechanisms that f

162 nduced pluripotent stem cell-derived cardiac myocytes (hiPSC-CM) demonstrated that ERRgamma activates

163 umol/mg tissue/min), increased inflammation, myocyte hypertrophy (WT, 19.8 mum; CatA-TG, 21.9 mum), c

164 ic constriction and exercise-induced cardiac myocyte hypertrophy and impaired cardiac function, demon

165 differentiation and neonatal rat ventricular myocyte hypertrophy are inhibited by mAKAPbeta signaloso

166 se calcineurin is a key regulator of cardiac myocyte hypertrophy in disease.

167 We report that asymmetrical cardiac myocyte hypertrophy is modulated by SRF (serum response

168 terations in Ca(2+) handling at baseline and myocyte hypertrophy were present throughout the left ven

169 cise, both of which promote adaptive cardiac myocyte hypertrophy with preserved cardiac function.

170 ular disease, including heart contractility, myocyte hypertrophy, arterial stiffness, and systemic re

171 a) is required for induction of pathological myocyte hypertrophy, despite calcineurin Aalpha expressi

172 t contributes to increased oxidative stress, myocyte hypertrophy, ECM remodeling, and inflammation, i

173 2D-dependent gene expression and ventricular myocyte hypertrophy.

174 regulatory pathway controlling pathological myocyte hypertrophy.

175 Here, using murine ventricular myocytes, immunoblotting, proximity ligation as-says, an

176 erized by asymmetrical growth of the cardiac myocyte in mainly width or length, respectively.

177 g HEK 293 cells and neonatal rat ventricular myocytes in low osmolarity (LO) medium and then recorded

178 annels, which biases the electrically active myocytes in the hyperpolarization (negative) direction.

179 in width versus length of adult ventricular myocytes in vitro and in vivo.

180 In 11 rabbit atrial myocytes in which EADs were generated either by increasi

181 rocesses that extend well beyond the cardiac myocyte, including important roles for pericardial const

182 NCA treatment of cardiac myocytes induced translocation of PKA and phosphatases t

183 process, with rapid pacing in canine atrial myocytes inducing oxidative injury through the induction

184 hanisms by which lipin 1 deficiency leads to myocyte injury and for testing potential therapeutic app

185 rrant cardiac remodeling, heart failure, and myocyte injury and repair.

186 Histology demonstrated 48% myocyte injury in the HESP group compared with 49% in im

187 We hypothesized that edema and myocyte injury would be chronically associated and have

188 mechanisms connecting lipin 1 deficiency to myocyte injury.

189 icular arrhythmias by disrupting ventricular myocyte intercalated disk (ID) nanodomains rich in cardi

190 t Na(+) channels are highly clustered at the myocyte intercalated disk, facilitating formation of Na(

191 se to atrial stretch is secreted from atrial myocytes into the circulation, where it stimulates vasod

192 irming mAKAPbeta as a nodal regulator in the myocyte intracellular signaling network.

193 ors (myoblasts) to terminally-differentiated myocytes is a critical step in skeletal muscle developme

194 hat generation of oxidative injury in atrial myocytes is a frequency-dependent process, with rapid pa

195 g gene expression in the majority of cardiac myocytes is essential.

196 wn substrate, but the functional role of the myocytes is less well known.

197 reticulum calcium ATPase (SERCA) in cardiac myocytes is modulated by an inhibitory interaction with

198 fibroblasts, neonatal myocytes, or adult LV myocytes isolated from "redox dead" (Cys17Ser) PKARIalph

199 Myocytes isolated from the peri-infarct region have more

200 Myocytes isolated from the peri-infarct region, in compa

201 Kcne5 deletion increased mean ventricular myocyte K(V) current density in the apex and also in the

202 In contrast, in male myocytes, Kv2.1 channels regulate membrane potential but

203 sion of Kv2.1 protein is higher than in male myocytes, Kv2.1 has conductive and structural roles.

204 ls control membrane potential but, in female myocytes, Kv2.1 plays dual electrical and Ca(V)1.2 clust

205 At the myocyte level, homogeneously large or small RyR clusters

206 Furthermore, fusiform myocyte-like cells forming reticulated pathways were loc

207 tch clamping, in vitro tachypacing of atrial myocytes, lucigenin chemiluminescence assay, immunoblott

208 and gamma are critical regulators of cardiac myocyte maturation, serving as transcriptional activator

209 computed in real-time (every 50 us) based on myocyte membrane potential.

210 ardiac ventricular myocytes, sense the local myocyte metabolic state and communicate a negative feedb

211 monstrate the pivotal roles of local cardiac myocyte metabolism and K(ATP) channels and the minor rol

212 established cardiomyopathy, restored cardiac myocyte mitochondrial membrane potential and flavoprotei

213 Cardiac myocyte mitochondrial metabolic activity was assessed as

214 ts into our previously developed ventricular myocyte model consisting of a three-dimensional Ca(2+) r

215 Furthermore, we developed a novel numerical myocyte model of Ca(2+) alternans that incorporates Ca(2

216 y, we developed a spatiotemporal ventricular myocyte model that integrates mitochondria-related Ca(2+

217 nsional physiologically-detailed ventricular myocyte model, and a coupled map lattice model.

218 to our knowledge, spatiotemporal ventricular myocyte model, incorporating properties of mitochondrial

219 These results show that TRPV1 in arteriolar myocytes modulates regional blood flow and systemic bloo

220 esponsible for modulating changes in cardiac myocyte morphology that occur secondary to pathological

221 R67Q(+/-) myocytes (n=10) under adrenergic stimulation showed freq

222 R67Q(+/-) myocytes (n=5) demonstrated prolonged action potential d

223 Both R67Q(+/-) (n=8) and WT myocytes (n=9) demonstrated typical n-shaped I(K1) IV re

224 AR-selective agonists given in vivo increase myocyte Na(+)-K(+) pump activity and reverse organ conge

225 e monitored Ca(2+) transients in ventricular myocytes near the adenovirus-injection sites in Langendo

226 imary cultures of Pam (0-Cre-cKO/cKO) atrial myocytes (no Cre recombinase, PAM floxed) were transduce

227 ockdown in cultured neonatal rat ventricular myocytes (NRVMs) impaired protein folding in the ER and

228 r O(2) partial pressures and capillary blood-myocyte O(2) diffusion across a ~100-fold range of muscl

229 ating from rest to exercise, increased blood-myocyte O(2) flux occurs predominantly via elevating red

230 enhanced steady-state inactivation in atrial myocytes of patients with SDB consistent with significan

231 (small ubiquitin-like modifier 1) protein in myocytes of resistance-size arteries.

232 rdant or discordant Ca2+alternans in cardiac myocytes or spatially concordant or discordant Ca2+ and

233 iate into osteochondrogenic cells instead of myocytes or tenocytes.

234 ck-out mouse embryonic fibroblasts, neonatal myocytes, or adult LV myocytes isolated from "redox dead

235 Myocyte orientation was assessed using structure tensor

236 Our results show that myocyte orientations are an important determinant of arr

237 ssess the importance of natural variation in myocyte orientations on cardiac arrhythmogenesis using 3

238 were performed to investigate the effects of myocyte orientations on the following: 1) ventricular ac

239 elective inhibitor TP-10, attenuated cardiac myocyte pathological hypertrophy induced by Angiotensin

240 er mice specific for progenitors of skeletal myocytes (Pax7(+) and MyoD(+)) and VSMCs (Prrx1(+) and N

241 nd isoproterenol, but did not affect cardiac myocyte physiological hypertrophy induced by IGF-1 (insu

242 we show that the increased SR load in atrial myocytes predisposes these cells to subcellular Ca waves

243 The molecular mechanisms determining myocyte preferential growth in width versus length remai

244 al nanostructure of TT in rabbit ventricular myocytes, preserved at different stages of the dynamic c

245 f exogenous PAM in Pam (Myh6-cKO/cKO) atrial myocytes produced a dose-dependent rescue of proANP cont

246 in which EphA7 expression on differentiated myocytes promotes commitment of adjacent myoblasts to te

247 the thiol-oxidizing agent diamide on cardiac myocyte protein phosphorylation and oxidation.

248 gest that the NCA-mediated effect on cardiac myocyte protein phosphorylation orchestrates alterations

249 hmias in vivo and their relation to regional myocyte remodelling.

250 a phase of the cardiac cycle that underlies myocyte repolarization detectable on the electrocardiogr

251 egulated by a combination of myocyte and non-myocyte responses to mechanosensitive pathways, which ca

252 Inducible myocyte-restricted STIM1-KD (STIM1 knockdown) was achiev

253 mulation of L-type Ca2+ channels in arterial myocytes resulting in increased vasoconstriction.

254 In vitro REEP5 depletion in mouse cardiac myocytes results in SR/ER membrane destabilization and l

255 nergy transfer biosensor imaging of cultured myocytes revealed that Ca(2+) levels and calcineurin act

256 al Ca(2+) imaging of long QT syndrome type 2 myocytes revealed that GS967 shortened Ca(2+) transient

257 atrial fibrosis, and the disorganization of myocyte's ultrastructure.

258 Using a myocyte-selective genetic ablation mouse model of the es

259 TP)), hugely abundant in cardiac ventricular myocytes, sense the local myocyte metabolic state and co

260 Cardiac myocyte-specific CIP4 gene deletion in mice attenuated p

261 Cardiac myocyte-specific deletion of Atf6 (ATF6 cKO [conditional

262 onged the median survival time 2-fold in the myocyte-specific Lmna-deleted mice.

263 defects of subcellular components in cardiac myocytes, specifically in the dyadic cleft, which includ

264 icrotubule density or detyrosination reduced myocyte stiffness, particularly at diastolic strain rate

265 n the protein titin, the main determinant of myocyte stiffness.

266 establish a mechanistic link between atrial myocyte structural remodeling in HF and AF.

267 of proteins involved in calcium handling in myocytes, such as the cardiac ryanodine receptor (RyR2),

268 dence for self-duplication of multinucleated myocytes, suggesting a more complex picture of polyploid

269 dSTORM images of myocyte surfaces demonstrated that both FKBP12 and 12.6

270 e showed using glycoside blockade in healthy myocytes that increases in SR Ca(2+) content and Ca(2+)

271 apex and also in the subpopulation of septal myocytes that lack fast transient outward current ( I(to

272 c human-pluripotent-stem-cell-derived cardio-myocytes that were genome-edited via CRISPR to create an

273 lel myofibrils and give cardiac and skeletal myocytes their distinct striated appearance.

274 nd it also has a structural role in arterial myocytes to enhance clustering of Ca(V)1.2 channels.

275 was further characterized by the adhesion of myocytes to stimulated endothelial cells, phagocytic act

276 The contribution of myocytes to the reduced atrophy remains largely unknown.

277 encing dataset from neonatal rat ventricular myocytes transduced with Etv1 showed reciprocal changes.

278 Neonatal ventricular myocytes treated with miR-294 showed elevated expression

279 in to quantify how titin-based forces define myocyte ultrastructure and mechanics.

280 CaT alternans were studied in rabbit atrial myocytes using combined Ca(2+) imaging and electrophysio

281 t for arrhythmia termination in human atrial myocytes using dynamic clamp.

282 chaperone that enhances protein folding and myocyte viability during reductive ER stress.

283 nhibiting mitochondrial function and cardiac myocyte viability using SAMbetaA, a rationally-designed

284 K(+) (SK) channels expressed in ventricular myocytes (VMs) are dormant in health, yet become functio

285 , LV mass can vary in response to changes in myocyte volume, edema, or fibrosis.

286 te of proANP secretion by Pam (Myh6-cKO/cKO) myocytes was a major contributor to its reduced levels.

287 tion, proANP secretion by Pam (Myh6-cKO/cKO) myocytes was unaffected.

288 lico subcellular model of rabbit ventricular myocyte, we show that the high dimensional nonlinear pro

289 , I(Kr) and I(NaL) integrals in each control myocyte were highly correlated in both healthy rabbit an

290 Primary adult rat ventricular myocytes were studied for morphology and intracellular s

291 Cultured cardiac myocytes were subjected to different stresses in vitro.

292 Cardiac myocytes were the most commonly used cell type (37.0%).

293 In female myocytes, where expression of Kv2.1 protein is higher th

294 zed to the intercalated discs in ventricular myocytes, where K(V)2.1 was also detected in both Kcne5(

295 en genotypes was assessed in fura2-loaded LV myocytes, whereas I/R-injury was assessed ex vivo.

296 ve activity in normal and failing dog atrial myocytes which occurs during the action potential (AP) a

297 ensity electric mapping, isolation of atrial myocytes, whole-cell patch clamping, in vitro tachypacin

298 ration was measured in adult rat ventricular myocytes with a genetically targeted fluorescent probe,

299 beta-Adrenergic stimulation of HFpEF myocytes with isoprenaline (isoproterenol) failed to eli

300 elease from the sarcoplasmic reticulum in LV myocytes, without affecting intrinsic ryanodine receptor