ライフサイエンスコーパス: heart muscle

1 for excitation-contraction [EC] coupling in heart muscle).

2 o reconstruct the functional architecture of heart muscle.

3 d in hepatocytes, as well as in skeletal and heart muscle.

4 c cardiomyopathy (FHC), a primary disease of heart muscle.

5 o prevent development of an abnormally large heart muscle.

6 ion and stabilization of its mRNA targets in heart muscle.

7 regulates Ca2+ activation of tension in the heart muscle.

8 the fast transient outward current in mouse heart muscle.

9 have the potential to regenerate functional heart muscle.

10 genic expression inhibits autophagy in mouse heart muscle.

11 Thus, NO acts on the ganglion, but not on heart muscle.

12 This study examined the function of HSP20 in heart muscle.

13 event of excitation-contraction coupling in heart muscle.

14 ds to scarring, with minimal regeneration of heart muscle.

15 tional, and infiltrative deficiencies of the heart muscle.

16 inant-negative mode that impairs function of heart muscle.

17 ending support to the "sliding" mechanism in heart muscle.

18 D signal for skeletal and a 95-kD signal for heart muscle.

19 known to exist and PDE1B is present in human heart muscle.

20 n a 3.6-kb transcript for mouse skeletal and heart muscle.

21 artery disease by imaging the metabolism of heart muscle.

22 process within intact sarcomeres from mouse heart muscle.

23 as a tracer for reference images of the dog heart muscle.

24 includes pancreas, kidney, and skeletal and heart muscle.

25 account for the Pasteur effect in ischaemic heart muscle.

26 ith lung congruent with cerebellum > liver > heart muscle.

27 he regulatory state of the thick filament in heart muscle.

28 variance with previous reports on mammalian heart muscle.

29 empt to target MCP-1 expression to the adult heart muscle.

30 d as a tracer for glucose uptake in ischemic heart muscle.

31 and are especially abundant in epidermis and heart muscle.

32 nisms can also operate in adipose tissue and heart muscle.

33 nitially absent from the cerebral cortex and heart muscle.

34 with both inherited and acquired diseases of heart muscle.

35 ch explains the altered contractility of the heart muscle.

36 ision after tissue damage to regenerate lost heart muscle.

37 ontaining) filaments in intact sarcomeres of heart muscle.

38 benefit from an in vitro surrogate for human heart muscle.

39 ta-adrenergic stimulation on the ventricular heart muscle.

40 hemomechanical energy transducer in striated heart muscle.

41 sfrp1 is strongly induced in differentiating heart muscle.

42 ytes after cardiac injury to regenerate lost heart muscle.

43 d for an artificial means of stimulating the heart muscle.

44 ld result in a hypercontractile state in the heart muscle.

45 tochondrial biogenesis in mouse hindlimb and heart muscles.

46 isomycin also increased glucose transport in heart muscles.

47 osphorylation and glucose uptake in isolated heart muscles.

48 n, which regulates contraction of Drosophila heart muscle [22] and may regulate muscle contractions i

49 cium/calmodulin-dependent protein kinases in heart muscle, acts as an anti-apoptotic factor and is a

50 -binding protein that is expressed solely in heart, muscle, adipose, and mammary tissue, remains to b

51 electrical repolarization (recovery) of the heart muscle after each contraction.

52 By contrast, zebrafish regenerate heart muscle after trauma by inducing proliferation of s

53 calcium-dependent switch for contraction in heart muscle and a potential target for drugs in the the

54 Most prominent among these are direct heart muscle and blood vessel regeneration from transpla

55 broad spectrum of conditions that injure the heart muscle and cause both structural and functional de

56 e to recapitulating the complex structure of heart muscle and might, therefore, be amenable to indust

57 f MCP-1 transcripts and protein in the adult heart muscle and pulmonary vein but not in skeletal musc

58 h RCAS-crescent induces formation of beating heart muscle and represses formation of blood.

59 maintenance of the contractile structures in heart muscle and that its function is regulated by postt

60 The electron microscopic structure of heart muscle and the ultrastructural basis of cardiac co

61 tiate the differentiation process leading to heart muscle and those that define the earliest embryoni

62 ded by a cDNA that is expressed primarily in heart, muscle and adipose tissue.

63 id not show positive effects in diaphragm or heart muscle, and heart pathology was worsened.

64 in-C (MyBP-C) is a key regulatory protein in heart muscle, and mutations in the MYBPC3 gene are frequ

65 lucose transporter found in adipose tissues, heart muscles, and skeletal muscles that is responsible

66 The levels of HK II mRNA in heart, muscle, and adipose tissue are paralleled by HK I

67 lower levels also in kidney, spleen, liver, heart, muscle, and brain.

68 und in the acid-insoluble fraction (>84% for heart, muscle, and liver).

69 wn to utilize fatty acids for energy such as heart, muscle, and liver.

70 ophysical targets of Mbnl proteins in brain, heart, muscle, and myoblasts by using RNA-seq and CLIP-s

71 as BRUNOL3 is expressed predominantly in the heart, muscle, and nervous system.

72 r concentration in fetal liver, gut, kidney, heart, muscle, and skin.

73 The specialized contractile properties of heart muscle are attributable to the expression of cardi

74 events of excitation-contraction coupling in heart muscle are Ca2+ sparks, which arise from one or mo

75 urgical samples of human arteries, veins and heart muscle are proving advantageous in the identificat

76 d passive stiffness in comparison with donor heart muscle as a control.

77 ion with dysfunction of liver, skeletal- and heart muscle as well as brain.

78 of stage XI-XIV blastulas were found to form heart muscle at high frequency with a timing that corres

79 is expressed at a high level in skeletal and heart muscle, at an intermediate level in pancreas and b

80 uscle has a profound capacity to regenerate, heart muscle, at least in mammals, has poor regenerative

81 distal one for the testis, front feet, bone, heart, muscle, brain, spinal cord, and tongue, while die

82 This was confirmed in mice in which the heart-muscle-brain adenine nucleotide translocator isofo

83 ogenous BAT, white adipose tissue (WAT), and heart muscle but, surprisingly, not skeletal muscle.

84 lion is insensitive to L-NA, suggesting that heart muscle (but not the ganglion) produces endogenous

85 Only the mutant mRNA was detected in the heart muscle, but in the skeletal muscle it coexisted wi

86 netics of force development in permeabilized heart muscle, but its role in vivo is unknown.

87 of serine/threonine kinases activated within heart muscle by a variety of agonists.

88 cTnT may participate in tuning the heart muscle by decreasing the speed of XB recruitment s

89 t suppress intracellular calcium handling in heart muscle by interacting with messenger RNA encoding

90 -induced AMPK activation was also blunted in heart muscles by preincubation with either anti-sauvagin

91 and mechanisms contributing to pathological heart muscle calcification remain unknown.

92 st cell-like fate and contribute directly to heart muscle calcification.

93 th a diminution in prostacyclin in infarcted heart muscle, can lead to the development of thrombotic

94 Abnormalities of heart muscle (cardiomyopathies) and/or electrical conduc

95 ker rat hearts, whereas, in obese Zucker rat hearts, muscle carnitine palmitoyltransferase and medium

96 iomyocytes activates PARS and contributes to heart muscle cell death by apoptosis, experiments were p

97 ria and cytoplasmic protein loss in a living heart muscle cell should lead to systolic dysfunction.

98 alcium current in either type of dissociated heart muscle cell, even at concentrations much higher th

99 ion, but that loss of all Tln forms from the heart-muscle cell leads to myocyte instability and a dil

100 y of human embryonic stem cells (hESCs) into heart muscle cells (cardiomyocytes) is highly sensitive

101 s show that the enhanced force observed when heart muscle cells are maximally activated by calcium is

102 indicate that improving the contractility of heart muscle cells by boosting intracellular calcium han

103 The heart muscle cells could be divided into type I and type

104 when an atrial chamber fibrillates, and when heart muscle cells die en masse after a heart attack.

105 cardiac conduction system differentiate from heart muscle cells during embryogenesis.

106 At the cellular level, heart muscle cells generate higher force when stretched,

107 hypoblast possessed broad capacity to induce heart muscle cells in pregastrula and mid-gastrula epibl

108 art transplant model and cytokine-stimulated heart muscle cells in tissue culture.

109 n program during terminal differentiation of heart muscle cells into Purkinje fibers.

110 Contraction and relaxation of heart muscle cells is regulated by cycling of calcium be

111 Personalized heart muscle cells made from stem cells in the laborator

112 Heart muscle cells produce peptide hormones such as natr

113 ine factor, endothelin, can induce embryonic heart muscle cells to differentiate into Purkinje fibers

114 ulated increase in ICa,L seen in the type II heart muscle cells was not mediated by a PTX-sensitive G

115 Internal dialysis of isolated type I heart muscle cells with guanosine 5'-O-(3-thiotriphospha

116 ent but not proliferation of cardiomyocytes (heart muscle cells) during postnatal development.

117 l exerts a direct cardioprotective effect on heart muscle cells, an effect mediated by selective acti

118 can modulate ICa,L, but not ICa,T, in squid heart muscle cells, and that the underlying G protein pa

119 e maturation and pathogenesis of adult human heart muscle cells, and this concept may be expanded to

120 of the L-type calcium current in the type II heart muscle cells, but had no effect on the T-type calc

121 Here, we show that differentiated heart muscle cells, cardiomyocytes, can be induced to pr

122 The heart muscle cells, i.e., the cardiomyocytes, possess a

123 in on the actin-containing thin filaments of heart muscle cells, initiating a change in filament stru

124 s show that during and after conversion from heart muscle cells, Purkinje fibers express a unique myo

125 occur in the terminally differentiated adult heart muscle cells, studies in endomyocardial biopsies f

126 tential propagation along a linear strand of heart muscle cells.

127 graft rejection in association with death of heart muscle cells.

128 d in Purkinje fibers as compared to ordinary heart muscle cells.

129 the key moiety disrupting the physiology of heart muscle cells.

130 fect mechanical and electrical properties of heart muscle cells.

131 h immunosuppression might enhance salvage of heart-muscle cells during acute cardiac-allograft reject

132 of viral gene transfer to convert quiescent heart-muscle cells into pacemaker cells, and the success

133 ity and restoration of dystrophin protein in heart muscle compared with skeletal muscle tissues in DM

134 a greater degree in Purkinje fibers than in heart muscle, consistent with the clinical presentation

135 tissues as diverse as buccal epithelium and heart muscle contain high proportions of clonal mutant m

136 not alter burst duration, spikes per burst, heart muscle contractility, or amplitudes of synaptic po

137 into the sarcoplasmic reticulum, modulating heart muscle contractility.

138 e regulation of overall calcium handling and heart muscle contractility.

139 ), a single-pass membrane protein, regulates heart muscle contraction and relaxation by reversible in

140 etween cMyBP-C, myosin, and actin during the heart muscle contraction.

141 interactions between myosin and actin during heart muscle contraction.

142 trical waves meander erratically through the heart muscle, creating disordered and ineffective contra

143 tablished protein biomarkers associated with heart muscle damage and point-of-care monitoring of both

144 arnosine and anserine in murine skeletal and heart muscle depends on circulating availability of beta

145 pression as a novel mechanism for regulating heart muscle development and function, in particular the

146 catenin signaling are capable of restricting heart muscle development at these relatively late stages

147 rfamily members in regulating early steps of heart muscle development.

148 show that sfrp1 is not only able to promote heart muscle differentiation but is also required for th

149 dogenous Wnt ligand required for controlling heart muscle differentiation via canonical Wnt/beta-cate

150 n unrecognised role in the earliest steps of heart muscle differentiation, and that partial complemen

151 dogenous Wnt signalling inhibitor for normal heart muscle differentiation.

152 -MHC gene in cardiac myocyte cultures and in heart muscle directly injected with plasmid DNA.

153 hmogenic cardiomyopathy (AC) is an inherited heart muscle disease associated with point mutations in

154 HIV infection is the development of primary heart muscle disease associated with severe global left

155 Dilated cardiomyopathy is a form of heart muscle disease characterized by impaired systolic

156 cardiomyopathy (HCM) is an important genetic heart muscle disease for which prevalence in the general

157 right ventricular cardiomyopathy (ARVC) is a heart muscle disease of unknown etiology that causes arr

158 icular cardiomyopathy (ARVC) is a hereditary heart muscle disease that causes sudden cardiac death (S

159 should be relevant to the acquired forms of heart muscle disease that HCM models.

160 cataracts and skeletal myopathies, including heart muscle diseases (cardiomyopathy).

161 the healthy heart and their disturbances in heart muscle diseases are described.

162 he pharmacological treatment of skeletal and heart muscle diseases rely on direct sarcomeric modulato

163 heart tissue engineering and in the study of heart muscle diseases.

164 hmogenic right ventricular cardiomyopathy, a heart muscle disorder associated with ventricular arrhyt

165 Dilated cardiomyopathy (DCM) is a heart muscle disorder characterized by atrial and ventri

166 trictive cardiomyopathy (RCM) is an uncommon heart muscle disorder characterized by impaired filling

167 ntricular cardiomyopathy (ARVC) is a primary heart muscle disorder resulting from desmosomal protein

168 rdiomyopathy (ARVC) is an autosomal dominant heart muscle disorder that causes arrhythmia, heart fail

169 rrhythmogenic cardiomyopathy is an inherited heart muscle disorder, predisposing to sudden cardiac de

170 ents afflicted with ischemic and nonischemic heart muscle disorders.

171 he vertebrate heart to form, surrounding the heart muscle during embryogenesis and providing signalin

172 cesses fail to work properly or effectively, heart muscle dysfunction can occur with or without accom

173 al benefits, and teratoma risk of engineered heart muscle (EHM) in a chronic myocardial infarction mo

174 stem cells (PSCs) and deployed as engineered heart muscle (EHM) may overcome all of these formidable

175 However, forming Engineered Heart Muscle (EHM) typically requires >1 million cells p

176 Tissue engineered heart muscles (EHMs) were generated by casting human emb

177 ohydrate ketogenic diet) to demonstrate that heart muscle engages a metabolic response that limits ke

178 in a number of embryonic tissues, including heart muscle, epidermis and neuroepithelium.

179 Skeletal and heart muscle excitability is based upon the pool of avai

180 Heart muscle excitation-contraction (E-C) coupling is go

181 We show that Xenopus anterior lymph heart muscle expresses skeletal muscle markers such as m

182 f Hh signaling and upon en1 knockdown, lymph heart muscle fails to develop, despite the normal develo

183 happens when plaque forms in an artery, when heart muscle fibers cross-link and weaken, when an atria

184 g complex, has been shown to be required for heart muscle formation in mouse.

185 d non-canonical Wnt signalling in regulating heart muscle formation.

186 NOx is formed in heart muscle from NO; NO originates through the activity

187 Engineered heart muscles from TTS-iPSC-CMs showed an impaired force

188 rdiac contractility due to direct changes in heart muscle function independent of vascular disease.

189 chrome c oxidase (COX) subunits VIa and VIIa heart/muscle (H) and ubiquitous (L) isoforms.

190 sgenic mice, the contractile defect in human heart muscle has not been studied.

191 The engineering of 3-dimensional (3D) heart muscles has undergone exciting progress for the pa

192 d the three troponin subunits found in human heart muscle, how the isoform profiles of these proteins

193 tablished model of pressure overload-induced heart muscle hypertrophy caused by transverse aortic con

194 ing, as a marker of complement activation in heart muscle in a murine model of myocardial IRI.

195 echanisms of mesodermal commitment to create heart muscle in mammals are largely unknown.

196 , adult zebrafish vigorously regenerate lost heart muscle in response to injury.

197 so required for the formation of normal size heart muscle in the embryo.

198 enon that describes an intrinsic property of heart muscle in which increased cardiac filling leads to

199 hese studies is proregenerative responses in heart muscle induced by systemic chemical suppression of

200 lustrate that the cells of the lens, retina, heart muscle, inner ear, and bone are dependent on XylT2

201 Optical control of the heart muscle is a promising strategy for cardiology beca

202 Heart muscle is characterized by a regular array of prot

203 e creatine kinase (MCK) gene in skeletal and heart muscle is controlled in part by a 5' tissue-specif

204 Compared with the adult, neonatal heart muscle is less sensitive to deactivation by acidic

205 Heart muscle is metabolically versatile, converting ener

206 layer lines in x-ray diffraction patterns of heart muscle is not due to an inherently more disordered

207 Although heart muscle is particularly sensitive to metabolic stre

208 ABSTRACT: Contraction of heart muscle is triggered by a transient rise in intrace

209 Contraction of heart muscle is triggered by calcium binding to the acti

210 luding the ATP synthase beta subunit and the heart-muscle isoform of the adenine nucleotide transloca

211 .523delC, p.Q175RfsX38), which codes for the heart-muscle isoform of the adenine nucleotide transloca

212 We have mapped the gene for the heart/muscle isoform of cytochrome c oxidase (COX) subun

213 mined the mitochondria from mice lacking the heart/muscle isoform of the adenine nucleotide transloca

214 e generated 'knockout' mice deficient in the heart/muscle isoform of the adenine nucleotide transloca

215 As a result, heart muscle isolated from bag3(-/-) mice exhibited myof

216 the pore channel was commonly unoccupied in heart muscle-isolated cardiac cells, yet a dense materia

217 ac growth; simultaneously, blood flow to the heart muscle itself is increased, and reserve blood flow

218 dominantly in postmitotic tissues, including heart, muscle, kidney, and brain.

219 7/BL 6 mouse tissues including brain, liver, heart, muscle, kidney, and testis.

220 pt indicated its occurrence in liver, brain, heart, muscle, kidney, lung, testis, and spleen.

221 orylation and maximal activation of BCKDC in heart, muscle, kidneys, and liver with reduction in plas

222 , which is recognized by the protein kinase, heart muscle kinase and can be specifically labeled with

223 ence, an antibody recognition epitope, and a heart muscle kinase site, was engineered and expressed i

224 d to isolate a full-length human cDNA from a heart muscle library.

225 impulse-conducting Purkinje cells within the heart muscle lineage and also may provide a basis for ti

226 C16 was only expressed in testis, and not in heart, muscle, liver, ovaries, or eggs, whereas the mRNA

227 lect adult tissues, TIMP3 mRNA is present in heart, muscle, liver, skin, intestine and ovaries.

228 Cardiomyocytes, the cells of the heart muscle, lose nearly all of their proliferative cap

229 (Does a Drug Allopurinol Reduce Heart Muscle Mass and Improve Blood Vessel Function in P

230 s targeting CRM1-dependent nuclear export in heart muscle may have salutary effects on cardiac functi

231 Thus, MCP-1 expression in the heart muscle may provide a model to investigate myocardi

232 Skeletal and heart muscle mitochondria of the CAP(R) mice were enlarg

233 solution which could allow the creation of a heart muscle model, enabling the growth of cardiac cells

234 nes features of EHM and cardiospheres: Micro-Heart Muscle (muHM) arrays, in which elongated muscle fi

235 The vertebrate heart muscle (myocardium) develops from the first heart

236 iogenic mesoderm begin to differentiate into heart muscle (myocardium).

237 ials of the kidney enzyme in comparison with heart muscle Na(+),K(+)-ATPase, in agreement with experi

238 d by progressive inflammatory destruction of heart, muscles, nerves, and gastrointestinal (GI) tract

239 fter gastrulation, with major defects in the heart muscle, neuroepithelium and skin epithelium, all o

240 al ribonucleic acids have been identified in heart muscle of a subset of patients with myocarditis an

241 leg (p = 0.038), diaphragm (p = 0.042), and heart muscles (p < 0.001).

242 ys an essential role in healthy and diseased heart muscle, particularly in Ca(2+)-induced Ca(2+) rele

243 role of 111In-antimyosin in the detection of heart muscle pathology, radiation dose estimates were ma

244 with the highest level of expression in the heart, muscle, peripheral blood leukocytes, and brain.

245 unrecognized structural element close to the heart muscle plasma membrane at the intercalated disc wh

246 sophila mesoderm into visceral, somatic, and heart muscle precursors.

247 evels are in contrast preserved in the aging heart muscle, presumably due to its incessant aerobic ac

248 rp1 controls the size of the differentiating heart muscle primarily by regulating cell fate within th

249 h in the United States in large part because heart muscle regenerates poorly.

250 hts into the fundamental pathways that drive heart muscle regeneration have begun to arise as well as

251 xide synthase (NOS) is strongly expressed in heart muscle relative to other muscles.

252 events driving deleterious calcification of heart muscle remains elusive.

253 f cardiac signaling, the function of PKD1 in heart muscle remains unclear.

254 Heart muscle requires a constant supply of oxygen.

255 Excitation-contraction coupling in heart muscle requires the activation of Ca(2+)-release c

256 generating zebrafish retina, caudal fin, and heart muscle revealed additional candidate genes potenti

257 ow measureable specific binding of F-Dapa in heart, muscle, salivary glands, liver, or brain.

258 Mice deficient in the heart/muscle specific isoform of the adenine nucleotide

259 two nuclear genes, one (COX7AH) producing a heart/muscle-specific isoform and the other (COX7AL) a f

260 Here, we show that heart/muscle-specific knockdown of MED13 or MED12, anoth

261 t level of expression in testis, followed by heart muscle, spleen and prostate.

262 Contracting slow and heart muscles stretched under load could employ this enh

263 The level of p204 in mouse heart muscle strongly increased during differentiation;

264 the adult chicken liver but not in the adult heart, muscle, testis, or brain.

265 corporated in a patient to a higher level in heart muscle than skeletal muscle, causing X-linked dila

266 diomyopathy (HCM) is an inherited disease of heart muscle that can be caused by mutations in sarcomer

267 Myocarditis is inflammation of the heart muscle that can follow various viral infections.

268 Cardiomyopathies are disorders affecting heart muscle that usually result in inadequate pumping o

269 In isolated heart muscles, the AMPK activator 5-aminoimidazole-4-car

270 Compared with postmitotic cardiac cells from heart muscle, these proliferative and differentiating st

271 to develop strategies for restoring healthy heart muscle through the regeneration and repair of dama

272 rdiogenic mesoderm later differentiates into heart muscle tissue (myocardium) and non-muscular heart

273 ration, and assembly of these cells into the heart muscle tissue, the pacemaker and conduction system

274 lize with I-band titin N2A epitopes in adult heart muscle tissues.

275 The inability of heart muscle to regenerate by replication of existing ca

276 e for delivering oxygen to the anaemic fetal heart muscle using contrast-enhanced echocardiography.

277 ls to generate replacement cells for damaged heart muscle, valves, vessels and conduction cells holds

278 plicing activity is inhibited postnatally in heart muscle via expression of a nuclear dominant negati

279 humans is higher in skeletal muscle than in heart muscle, we propose that the hnRNP G/Tra2beta ratio

280 In contrast, histograms of contracting heart muscle were peaked and asymmetric, suggesting that

281 lower in the cerebral cortex, cerebellum and heart muscle, whereas Bcl-x was not downregulated in any