ライフサイエンスコーパス: myocyte

1 active ECC couplons (on average, 17,000 per myocyte).

2 e expressed in arterial smooth muscle cells (myocytes).

3 a1 subunits in arterial smooth muscle cells (myocytes).

4 established mathematical model of the rabbit myocyte.

5 silico model of the adult human ventricular myocyte.

6 d three-dimensional model of the ventricular myocyte.

7 aling in isolated murine primary ventricular myocytes.

8 ing that augments insulin action in skeletal myocytes.

9 nd can trigger action potentials in isolated myocytes.

10 the proximity of beta1 to surface BKalpha in myocytes.

11 thways altered in vivo and by using isolated myocytes.

12 control of respiration by NO within cardiac myocytes.

13 ced early afterdepolarizations in guinea pig myocytes.

14 elayed aftercontractions in HRC null cardiac myocytes.

15 at the beta1 and alpha1B were present in all myocytes.

16 s the cycling of Ca(2+) and Na(+) in cardiac myocytes.

17 gap junction coupling in HF-AS versus CTL-AS myocytes.

18 e increasing organization of the ventricular myocytes.

19 mechanically active in skeletal and cardiac myocytes.

20 l death in embryonic fibroblasts and cardiac myocytes.

21 ial canonical channel 6 (Trpc6), in isolated myocytes.

22 f HCO3(-), impairs O2/CO2 balance in cardiac myocytes.

23 plasma membrane abundance of KV channels in myocytes.

24 tential morphology in guinea pig ventricular myocytes.

25 hat SR Ca content is increased in old atrial myocytes.

26 function is exquisitely regulated in cardiac myocytes.

27 n Kv11.1 tail currents and APs in guinea pig myocytes.

28 of Cx43 protein in PRA versus PRB expressing myocytes.

29 perturbations of O2/CO2 balance in AE3-null myocytes.

30 s (APs) more closely resemble those of human myocytes.

31 kbone for coordinated contraction of cardiac myocytes.

32 ta-adrenergic stimulation in beating cardiac myocytes.

33 a(2+) load alterations vs. control-diet (CD) myocytes.

34 the 5 cardiac ARs in individual ventricular myocytes.

35 rovider of passive tension and elasticity in myocytes.

36 ol/L) and Na(+) current in mouse ventricular myocytes.

37 l of diastolic [Ca(2+) ]i in rat ventricular myocytes.

38 in-A prevented INa increase in CASK-silenced myocytes.

39 ng Fluo-3 in voltage clamped rat ventricular myocytes.

40 ng differentiation and maturation of cardiac myocytes.

41 BTP2 had no effect on normal myocytes.

42 bundance at the surface of mesenteric artery myocytes.

43 content in colon ascendens stent peritonitis myocytes.

44 ion controlling the repolarization of atrial myocytes.

45 et of bursting activity in mouse ventricular myocytes.

46 m concentration were observed in rat cardiac myocytes.

47 resolution to assess coupling of individual myocytes.

48 CC) is strikingly different from ventricular myocytes.

49 e sarcoplasmic reticulum (SR) in ventricular myocytes; a median separation of 20 nm in 2D electron mi

50 Sinoatrial node myocytes act as cardiac pacemaker cells by generating sp

51 How does the myocyte adjust its response to compensate for such chang

52 otassium channels (KATP channels) in cardiac myocytes adjust contractile function to compensate for t

53 lar distribution and preservation in cardiac myocytes after cell isolation are not well documented.

54 candidate loci in neonatal cultured cardiac myocytes after in utero exposure to diesel exhaust and f

55 I reduced surface KV 1.5 protein in isolated myocytes; an effect inhibited by BIM.

56 ailed computational model of the ventricular myocyte and mathematical analysis.

57 iac desmosomes, which leads to detachment of myocytes and alteration of intracellular signal transduc

58 ls (SK, KCa 2) are expressed in human atrial myocytes and are responsible for shaping atrial action p

59 ssium ions outward to repolarize ventricular myocytes and end each beat.

60 Pathological features include loss of myocytes and fibrofatty replacement of right ventricular

61 tagged KCNQ1 and KCNE1 in adult ventricular myocytes and follow their biogenesis and trafficking pat

62 ocesses such as spontaneous beats in cardiac myocytes and glucose-dependent ATP increase in pancreati

63 ns in isolated murine and guinea pig cardiac myocytes and mitochondria.

64 nse on ischemia/reperfusion (I/R) in cardiac myocytes and mouse hearts.

65 Myocytes and non-myocytes are known to communicate and e

66 Dynamic crosstalk between myocytes and non-myocytes plays a crucial role in stress

67 ed pattern in WT myocytes, whereas CD38(-/-) myocytes and nonpermeabilized WT myocytes showed little

68 croscopy, we demonstrate that in rat cardiac myocytes and other cell types mitochondrial PDE2A2 regul

69 9 promotes pathologic hypertrophy of cardiac myocytes and overall cardiac dysfunction.

70 he cells; they are expressed in human atrial myocytes and responsible for shaping atrial action poten

71 sing latency variance) of Ca waves in nearby myocytes and SR Ca load, whereas the number of Ca wave i

72 gle BK channels and transient BK currents in myocytes and stimulated vasoconstriction via a PKC-depen

73 ntaneous Ca waves are much more common in HF myocytes and these AS myocytes are also poorly coupled,

74 These 'male' and 'female' model myocytes and tissues then were used to predict how vario

75 stimulates TRPM4 currents in cerebral artery myocytes and vasoconstriction of cerebral arteries.

76 in H9c2 cardiac cells, adult rat ventricular myocytes, and human induced pluripotent stem cell-derive

77 had significantly reduced scar size, smaller myocytes, and increased myocyte nuclear density.

78 mechanical properties of normal and diseased myocytes, and to determine whether Orai channels are obl

79 litudes, in chronically stressed ventricular myocytes, and use COS-7 cell expression to probe the und

80 yocardium correlating with oxidative stress, myocyte apoptosis, and the accumulation of proinflammato

81 As a first approximation, sensors inside the myocyte appear to modulate reactive oxygen species while

82 Four distinct myocyte AR phenotypes are defined: 30% of cells with bet

83 much more common in HF myocytes and these AS myocytes are also poorly coupled, enabling local Ca-indu

84 ALE: Junctional membrane complexes (JMCs) in myocytes are critical microdomains, in which excitation-

85 Well-coupled CTL myocytes are effectively voltage-clamped during Ca waves

86 Myocytes and non-myocytes are known to communicate and exert mutual regul

87 tochondrial calcium concentration in cardiac myocytes are largely unknown.

88 Myocytes are responsible for electrical conduction and c

89 The dominant ventricular myocyte ARs present in all cells are the beta1 and alpha

90 ta1 and beta2 are thought to be the dominant myocyte ARs.

91 n the whole rat heart, adult rat ventricular myocytes (ARVMs), and myofibrils from both sexes of rats

92 ecordings were made from isolated guinea pig myocytes as well as from human embryonic kidney 293 (HEK

93 current passed by Kv11.1 channels in cardiac myocytes, as well as the current passed in response to p

94 ter calcein diffusion than in HF, with HF-AS myocyte being slowest.

95 tors, including endothelin-1 (ET-1), inhibit myocyte BK channels, leading to contraction, but mechani

96 The beta2 and beta3 are mostly absent in myocytes but are abundant in nonmyocytes.

97 s the most relevant source for NO in cardiac myocytes, but this nNOS is not located in mitochondria a

98 yndrome in male and female ventricular human myocytes by combining effects of a hormone and a hERG bl

99 In cardiac myocytes Ca(2+) is a crucial regulator of contractile fo

100 ABSTRACT: In atrial myocytes Ca(2+) release during excitation-contraction co

101 their downstream targets, the regulation of myocyte calcium cycling and myofilament activity.

102 of the molecular circuitry governing cardiac myocyte cell cycle regulation is required.

103 cardiac myocytes dominates over that in non-myocyte cell types.

104 propagation of the [Ca(2+) ]i signal to the myocyte centre both in patients with AF and in a rabbit

105 however, the endogenous structure of cardiac myocyte chromatin has never been determined.

106 RATIONALE: During each beat, cardiac myocytes (CMs) generate the mechanical output necessary

107 ire strong and stable connections of cardiac myocytes (CMs) with the extracellular matrix (ECM) to pr

108 gulator of Cx43 expression, GJ formation and myocyte connectivity/synchronization for labour.

109 While cardiac myocytes contain several isoforms of NO synthases, it is

110 Inadequate insulin action in skeletal myocytes contributes to hyperglycemia in diabetes.

111 panied by increased cell cohesion in cardiac myocyte cultures and murine heart slices.

112 While assays to detect myocyte death are used to diagnose a heart attack (acute

113 ocks CaMKII- or ISO-induced mPTP opening and myocyte death in vitro and rescues heart hypertrophy in

114 e (synchrony of Ca release in populations of myocytes) determine DAD features in cardiac tissue using

115 pathways regulated by TBX5 in human cardiac myocyte development.

116 Myomerger deficient myocytes differentiate and harbour organized sarcomeres

117 ating that the function of miR-29 in cardiac myocytes dominates over that in non-myocyte cell types.

118 sidered cardiomyopathies because of electric myocyte dysfunction.

119 esult in myocyte hypertrophy with changes in myocyte electrical and mechanical phenotype.

120 Hearts of Glyco(Lo) mice had larger myocytes, enhanced cardiac function, and higher capillar

121 The Myocyte Enhancer Factor 2 (MEF2) transcription factors s

122 tor), SRF (serum response factor), and MEF2 (myocyte enhancer factor 2) play critical roles in the me

123 Psychiatric Genomics Consortium, and report myocyte enhancer factor 2C (MEF2C) motif enrichment in s

124 the activity-dependent transcription factor, Myocyte enhancer factor-2C (Mef2c), differentially regul

125 evels, effects likely to preserve functional myocyte excitation-contraction coupling.

126 KEY POINTS: In atrial myocytes excitation-contraction coupling is strikingly d

127 FRD myocytes exhibited enhanced SR Ca(2+) spontaneous events

128 ALE: It is unknown whether every ventricular myocyte expresses all 5 of the cardiac adrenergic recept

129 A sequencing were performed in adult cardiac myocytes following development of pressure overload-indu

130 pective markers of atrial versus ventricular myocyte formation from hPSCs and their use in directed d

131 c myocytes from wild-type but not in cardiac myocytes from ATF6 knockout mice.

132 o I-1c gene transfer in isolated left atrial myocytes from both pigs and rats increased calcium trans

133 te electrophysiology and calcium dynamics in myocytes from control rats (SHAM) and aortic-banded rats

134 te electrophysiology and calcium dynamics in myocytes from control sham operated rats and aortic-band

135 We show that myocytes from fructose-rich diet (FRD) animals exhibit a

136 Isolated myocytes from HFD-fed mice also displayed a reduced cont

137 tein inactivation with pertussis toxin or in myocytes from M2- or M1/3-muscarinic receptor knockout m

138 and transverse-tubule imaging of ventricular myocytes from MCM-Speg(fl/fl) mice post HF revealed both

139 In freshly-isolated myocytes from rat cerebral resistance arteries, FaLM sho

140 field focusing on the withdrawal of cardiac myocytes from the cell cycle during the transition from

141 stressor, tunicamycin, and by I/R in cardiac myocytes from wild-type but not in cardiac myocytes from

142 METHODS AND We studied ventricular myocytes from wild-type mice, mice with alpha1A and alph

143 ced increase in Ca(2+) transients in cardiac myocytes from WT but not CD38(-/-) mice.

144 Using single atrial myocytes from young and old Welsh Mountain sheep, we sho

145 ze electrotonic conduction occurs across non-myocyte gaps in the heart and is partly mediated by Conn

146 the adult mammalian heart lacks a definable myocyte-generating progenitor cell of biological signifi

147 ses revealed interactions within the cardiac myocyte genome at 5-kb resolution, enabling examination

148 eptor (FGFR) 4 thereby inducing hypertrophic myocyte growth and the development of left ventricular h

149 and global differential gene expression for myocyte growth, amino acid biosynthesis, and oxidative s

150 Hypertrophied myocytes had increased STIM1 expression and activity, wh

151 th restricted diffusion for Na(+) in cardiac myocytes has been inferred from a transient peak electro

152 earts containing mostly post-mitotic cardiac myocytes have lost this ability.

153 The histological features of HCM include myocyte hypertrophy and disarray, as well as interstitia

154 ated PE-mediated/FAK-dependent initiation of myocyte hypertrophy in vivo Collectively, these findings

155 cal increases in cardiac afterload result in myocyte hypertrophy with changes in myocyte electrical a

156 ting increased calcineurin/NFAT signaling in myocyte hypertrophy.

157 d L-type Ca(++) currents (rabbit ventricular myocytes, IC50=66.5+/-4 mumol/L) and IK1 (HEK cells expr

158 ing BKalpha and beta1 surface trafficking in myocytes, identify mechanisms involved, and determine fu

159 myocytes (PdCMs) are similar to conventional myocytes in morphological, electrical and contractile pr

160 ption of myo18b is restricted to fast-twitch myocytes in the zebrafish embryo; consistent with this,

161 deled the Holt-Oram syndrome in iPSC-cardiac myocytes in vitro and uncovered novel pathways regulated

162 Targeted deletion of miR-29 in cardiac myocytes in vivo also prevents cardiac hypertrophy and f

163 sis for CO-induced arrhythmias in guinea pig myocytes in which action potentials (APs) more closely r

164 lar organ composed of cardiomyocytes and non-myocytes including fibroblasts, endothelial cells and im

165 f STIM1 in cultured adult feline ventricular myocytes increased diastolic spark rate and prolonged AP

166 -type action potentials of PMCA1(cko) atrial myocytes increased significantly under Ca(2+) overload c

167 lammatory molecules, immune cells may induce myocyte inflammation, adversely regulate myocyte metabol

168 rs of inflammation, endothelial dysfunction, myocyte injury and stress, and kidney function.

169 he end of perfusion, and histology showed no myocyte injury.

170 abolished the protection against H/R-induced myocytes injury by AS-1.

171 ln forms from the heart-muscle cell leads to myocyte instability and a dilated cardiomyopathy.

172 s the number of Ca wave initiation sites per myocyte is less important.

173 trial natriuretic peptide secreted by atrial myocytes is a major adipogenic factor operating at a low

174 namic CpG and non-CpG methylation in cardiac myocytes is confined to A compartments.

175 The desmin network's pivotal role in myocytes is evident since mutations in the human desmin

176 the calcium signalling apparatus in cardiac myocytes is unknown.

177 and contractility measurements performed or myocytes isolated for patch-clamp electrophysiology.

178 -I) and in colon ascendens stent peritonitis myocytes isolated from mutant mice that have the ryanodi

179 d Ca(2+) transients from cardiac ventricular myocytes isolated from rabbit hearts.

180 eserved in colon ascendens stent peritonitis myocytes isolated from transgenic mice expressing a calc

181 nthases (NOSs) are also expressed in cardiac myocytes, it is unclear whether they control respiration

182 In adult ventricular myocytes, KCNE1 maintains a stable presence on the cell

183 Myocyte KV currents are inhibited by vasoconstrictors, i

184 ngly different from ventricle because atrial myocytes lack a transverse tubule membrane system: Ca(2+

185 In many species atrial myocytes lack a transverse tubule system, dividing the s

186 ibuted to perturbed Ca2+ handling in cardiac myocytes leading to spontaneous Ca2+ release and delayed

187 ricular (LV) relaxation, restoration forces, myocyte lengthening load, and atrial function, culminati

188 At the cardiac myocyte level, colon ascendens stent peritonitis cells s

189 nic Cl(-)/HCO3(-) transporter in ventricular myocytes, linking the critical roles of Slc26a6 in regul

190 Isolated patch-clamped rabbit ventricular myocytes loaded with Fluo-4 to image intracellular Ca we

191 The pathological characteristic of ARVC is myocyte loss with fibrofatty replacement.

192 In uMSC-myocytes, lower amino acid concentrations and global dif

193 stages of cardiomyocytes and supporting non-myocytes may be a critical factor for promoting function

194 sparate diseases that have in common altered myocyte mechanics.

195 type IV collagen and effects of fibrosis on myocyte membrane indicated the possible interaction betw

196 p experiments using native cerebral arterial myocytes, membrane stretch-induced cation currents were

197 uce myocyte inflammation, adversely regulate myocyte metabolism, and contribute to insulin resistance

198 muscle inflammation and negatively regulate myocyte metabolism, leading to insulin resistance.

199 Mechanistically, we found cardiac myocyte miR-29 to de-repress Wnt signaling by directly t

200 of APs observed in a paced human ventricular myocyte model by decreasing and/or increasing the rapid

201 hannels were integrated into the O'Hara-Rudy myocyte model modified to include dynamic drug-hERG chan

202 Using computer simulations of a ventricular myocyte model, we show that initiation and termination a

203 into a physiologically detailed ventricular myocyte model.

204 Quantitative assessment of myocyte morphology revealed significantly enhanced myocy

205 a3 were detected in only approximately 5% of myocytes, mostly in different cells.

206 heart failure typically arises from cardiac myocyte necrosis/apoptosis, associated with the patholog

207 Cardiac myocytes normally initiate action potentials in response

208 logical property of neonatal rat ventricular myocyte (NRVM) cultures.

209 d scar size, smaller myocytes, and increased myocyte nuclear density.

210 rs includes lamina-associated protein LAP-1, myocyte nuclear envelope protein Syne1, BetaM itself, he

211 neously nor do they physically colocalize in myocyte nuclei.

212 Here, we report that cardiac myocytes of heterozygous mice carrying a catecholaminerg

213 and a loss of functional KV 1.5 channels in myocytes of pressurized arteries.

214 ed, and determine functional significance in myocytes of small cerebral arteries.

215 ABSTRACT: Smooth muscle cells (myocytes) of resistance-size arteries express several di

216 ximal +34-mV shift in neonatal mouse cardiac myocytes or Chinese hamster ovary (CHO) cells expressing

217 ytes were much more frequent in HF (10.8% of myocytes, P<0.05 versus CTL).

218 Cardiac myocyte passive tension was significantly increased 1 ho

219 Dynamic crosstalk between myocytes and non-myocytes plays a crucial role in stress/injury-induced h

220 omains, and LQT3-associated mutant channels, myocytes produced EADs for wide intercellular clefts, wh

221 Also, the exact nature of various putative myocyte-producing progenitor cells remains elusive and u

222 growth factor receptor ERBB2 is critical for myocyte proliferation and trabeculation.

223 To (re)initiate cardiac myocyte proliferation in adult mammalian hearts, a thoro

224 bians leading to the hypothesis that cardiac myocyte proliferation is a major driver of heart regener

225 n after cardiac damage, induction of cardiac myocyte proliferation is an attractive therapeutic optio

226 a linker element between passive and active myocyte properties.

227 In mutant myocytes, ranolazine inhibited the enhanced late Na(+) c

228 ed cardiac function, and higher capillary-to-myocyte ratios.

229 ouse hearts containing proliferating cardiac myocytes regenerate even extensive injuries, whereas adu

230 not elicit cKit(+) cardiac stem cell-derived myocyte regeneration.

231 ctive is to understand how adult ventricular myocytes regulate the IKs amplitudes under basal conditi

232 ing ubiquitin-tagged proteins within cardiac myocytes related to proteasome dysfunction and impaired

233 first evidence of human infant adipocyte- or myocyte-related alterations in cellular metabolic pathwa

234 n pathological hypertrophy and is central to myocyte remodeling.

235 ibilities have been proposed: differentiated myocyte replication and progenitor/immature cell differe

236 thylation in embryonic stem cells or cardiac myocytes, respectively, does not alter genome-wide chrom

237 a(2+) ]SR ; fluo-5N) Ca(2+) in rabbit atrial myocytes revealed that Ca(2+) release from j-SR resulted

238 However, most of these myocytes seem to recover and do not elicit cKit(+) cardi

239 How does the cardiac myocyte sense changes in preload or afterload?

240 k initiation after Ca(2+) release in cardiac myocytes should inhibit further Ca(2+) release during th

241 TAC myocytes showed a higher incidence of triggered activiti

242 s CD38(-/-) myocytes and nonpermeabilized WT myocytes showed little or no staining, without striation

243 The majority of HF myocytes showed remarkable t-system remodeling, particul

244 e morphology revealed significantly enhanced myocyte size compared with patients with ICM.

245 N, activating transcription factor 2 (ATF2), myocyte-specific enhancer factor 2A (MEF2A), and SRY-Box

246 elated IFN-I milieu downregulates microglial myocyte-specific enhancer factor 2C (Mef2C).

247 in of chromatin with GPR98, including MEF2C (Myocyte-specific enhancer factor 2C).

248 LRRK2 also inhibited myocyte-specific enhancer factor 2D activity, which is r

249 in combination with activated fibroblast- or myocyte-specific GRK2 ablation-each initiated after myoc

250 mma, germ-line iPLA2gamma(-/-) mice, cardiac myocyte-specific iPLA2gamma transgenic mice, and wild-ty

251 A novel cardiac myocyte-specific Speg conditional knockout (MCM-Speg(fl/

252 ts that complex with the sarcomere, altering myocyte stiffness, contractility, and mechanosignalling.

253 These findings suggest that myocyte stretch, fibroblast stretch, and matrix stiffeni

254 that mutated desmin already markedly impedes myocyte structure and function at pre-symptomatic stages

255 METHODS AND Knockdown of ATF6 in cardiac myocytes subjected to I/R increased reactive oxygen spec

256 Direct observation of MTs in working myocytes suggests a spring-like function, one that is su

257 the abundance of functional channels at the myocyte surface.

258 ve been identified, which may promote either myocyte survival or death or, most interestingly, both.

259 raction amplitudes were smaller in CD38(-/-) myocytes than in the WT.

260 ted mechanism of glucose sensing in skeletal myocytes that contributes to homeostasis and therapeutic

261 l design, such as receptor overexpression in myocytes that do not express the AR normally.

262 ly-adapted membrane invaginations in cardiac myocytes that facilitate the synchronous release of Ca(2

263 n electrophysiological alterations in atrial myocytes that may promote AF.

264 arcomere, the structural unit of the cardiac myocytes, the Frank-Starling mechanism consists of the i

265 In cardiac myocytes, there are several Ca(2+) -sensitive potassium

266 initial ion circumstances within ventricular myocytes, these multi-stable AP states might increase th

267 stic triggered activity in a one-dimensional myocyte tissue model.

268 iled mathematical model of mouse ventricular myocytes to disclose the key mechanisms underlying the c

269 work provides structural evidence in cardiac myocytes to indicate the formation of microdomains betwe

270 current beyond steady state on reexposure of myocytes to K(+) after a period of exposure to K(+)-free

271 STIM1 can associate with Orai in cardiac myocytes to produce a Ca(2+) influx pathway that can pro

272 osely associated with the ability of cardiac myocytes to proliferate.

273 Exposure of hypertrophied myocytes to the Orai channel blocker BTP2 caused a reduc

274 Failure of trabecular myocytes to undergo appropriate cell cycle withdrawal le

275 cells as well as in neonatal rat ventricular myocytes treated with the muscarinic agonist carbachol.

276 significantly prolonged in PMCA1(cko) atrial myocytes under basal conditions, with Ca(2+) overload le

277 rial permeability transition pore in cardiac myocytes under stress.

278 Spontaneous calcium (Ca) waves in cardiac myocytes underlie delayed afterdepolarizations (DADs) th

279 rk (LCS) activity in intact isolated cardiac myocytes using fast confocal line scanning with improved

280 ded from freshly isolated rabbit ventricular myocytes using whole-cell patch clamp.

281 In ventricular cardiac myocytes (VCM), Gbeta5 deficiency provided substantial p

282 aturic hormone that directly targets cardiac myocytes via FGF receptor (FGFR) 4 thereby inducing hype

283 vity regulate internal Ca release in cardiac myocytes via Na/Ca exchange.

284 CO induces arrhythmias in guinea pig cardiac myocytes via the ONOO(-)-mediated inhibition of Kv11.1 K

285 increased in fructose-rich diet mouse (FRD) myocytes vs. control diet (CD) mice, in the absence of s

286 The number of EdU(+) cardiac myocytes was increased in CBSC- versus vehicle- treated

287 Calcium release in HF myocytes was restricted to regions proximal to the sarco

288 3W) in patient-specific iPSC-derived cardiac myocytes, we demonstrated that the knockout strategy ame

289 the patch-clamp technique in beating cardiac myocytes, we identified a neuronal NO synthase (nNOS) as

290 electrophysiology and rat cerebral arterial myocytes, we monitored STOCs in the presence and absence

291 gical inhibition of iNOS in isolated cardiac myocytes, we reveal that an increase of expression and a

292 Furthermore, ventricular myocytes were found to be an important source of cardiac

293 These AS myocytes were much more frequent in HF (10.8% of myocyte

294 In CTL hearts, 1.4% of myocytes were poorly synchronized with neighboring cells

295 phy due to polymicrobial sepsis and cultured myocytes were used for mechanistic analyses.

296 entricle can be captured by data from single myocytes when these results are expressed as 'repolariza

297 ining of CD38, with a striated pattern in WT myocytes, whereas CD38(-/-) myocytes and nonpermeabilize

298 gene and were shown to bind ATF6 in cardiac myocytes, which increased catalase promoter activity.

299 nzymatically digested to isolate ventricular myocytes, which were subsequently fixed at 0, 3, and 8 h

300 Membrane permeabilization of cardiac myocytes with saponin and/or Triton X-100 increased NAAD