ライフサイエンスコーパス: myocardium

1 myofibroblast heterogeneity in the infarcted myocardium.

2 eutrophil to macrophage communication in the myocardium.

3 ontrol function and signalling routes in the myocardium.

4 lesions in both normal and infarcted canine myocardium.

5 as almost undetectable in canine ventricular myocardium.

6 imilar biomechanical properties as native LV myocardium.

7 y with fibrotic genes and protein within the myocardium.

8 1 is dispensable for function of the working myocardium.

9 cleaved caspase-3) were elevated in diabetic myocardium.

10 different organs, including cornea, skin and myocardium.

11 om different regions of the left ventricular myocardium.

12 to augment reverse remodeling of the failing myocardium.

13 ale may contribute to bulk relaxation of the myocardium.

14 lly methylated regions in DNA from liver and myocardium.

15 were significantly higher than in the remote myocardium.

16 of gray-scale values in normal and fibrotic myocardium.

17 limiting the extent of irreversibly injured myocardium.

18 ffect by modulating calcium signaling in the myocardium.

19 vaged myocardium when compared to the remote myocardium.

20 be a viable option for regenerating injured myocardium.

21 iology or cardiotoxic responses of the human myocardium.

22 reinitiate proliferation to replace the lost myocardium.

23 detection of inflammatory macrophages in the myocardium.

24 n transcriptionally distinct from the remote myocardium.

25 and inflammation in postinfarct ventricular myocardium.

26 g cardiomyocytes required to build a working myocardium.

27 tic resistance to diastolic stretch in human myocardium.

28 signaling during pathological insults to the myocardium.

29 tion in patients with >10% to 12.5% ischemic myocardium.

30 in voltage-clamped myocytes from noninfarct myocardium.

31 n the infarcted, the salvaged and the remote myocardium.

32 action potentials (OAPs) in the surrounding myocardium.

33 ributions observed in confocal images of the myocardium.

34 when obtained from the same small volume of myocardium.

35 ak and mitochondrial damage in the senescent myocardium.

36 endocardium is coordinated with that of the myocardium.

37 influence the regenerative potential of the myocardium.

38 d mainly at the border zone of the infarcted myocardium.

39 educed, suggesting recovery toward a healthy myocardium.

40 e and trigger pathological remodeling of the myocardium.

41 al cells that bridge the CCS and surrounding myocardium.

42 f FAP-positive myofibroblasts in the injured myocardium.

43 logy was considered equal to ERP of HB or RV myocardium.

44 am amplitude and histological composition of myocardium.

45 al gene expression patterns in CCC patients' myocardium.

46 to allow sustained drug penetration into the myocardium.

47 ulate repair and remodeling in the infarcted myocardium.

48 ed reduction of sympathetic effectors on the myocardium.

49 nflammation and its negative sequelae on the myocardium.

50 air overall reparative potential for injured myocardium.

51 nslational large animal model of hibernating myocardium.

52 transverse-tubular membranes in ventricular myocardium.

53 re serially measured in infarcted and remote myocardium.

54 tivity but slower force development in human myocardium.

55 e effect of OSAHS treatment with MADs on the myocardium.

56 e to diastolic stretch in human myocytes and myocardium.

57 conduction system or the ventricular working myocardium.

58 brosis and immune cell infiltration into the myocardium.

59 te linked with fibrotic processes within the myocardium.

60 action and HF with reduced ejection fraction myocardium.

61 paths forward toward regenerating the human myocardium.

62 tion and extent of the expanded disorganized myocardium.

63 ough mitigation of its distribution into the myocardium.

64 entricular wall in both normal and infarcted myocardium.

65 els and fibrosis and inflammation within the myocardium.

66 geneous dystrophin expression throughout the myocardium.

67 ct rather than due to cytotoxic infection of myocardium.

68 y, fewer leukocytes migrated to the ischemic myocardium.

69 mpaired inflammation resolution in infarcted myocardium.

70 al ablation catheter in normal and infarcted myocardium.

71 hyroxine and retinol-binding protein, in the myocardium.

72 (3); P=0.023) and infarcted left ventricular myocardium (1052.3+/-543.0 versus 340.3+/-160.5 mm(3); P

73 1) describe the pathological spectrum of the myocardium; (2) compare with an alternate viral illness;

74 A volumetric measure of myocardium above a threshold SUV (cardiac metabolic volu

75 We hypothesized that in the infarcted myocardium, activation of TGF-beta/Smad signaling in mac

76 hagy, mitochondrial mass and function in the myocardium after infarction.

77 rk genes are upregulated in the regenerating myocardium after resection.

78 ies were obtained from an adjacent region of myocardium after the CF-LVAD intervention (n=6 ICM, 5 no

79 Diabetic myocardium also had significantly decreased activity of

80 sartan reduced CTGF expression in the remote myocardium, although only sacubitril/valsartan prevented

81 no longer detectable in the left ventricular myocardium, although persistent elevations in serum inte

82 is a key domain of dysfunctional but viable myocardium among others (eg, microvascular dysfunction a

83 d by inflammatory cell infiltration into the myocardium and a high risk of deteriorating cardiac func

84 f the miR-21 targetome in antimiR-21-treated myocardium and a suppression of the inflammatory respons

85 ophages (BMDMs) are recruited to the injured myocardium and are essential for cardiac repair as they

86 s well as preferential microwave coupling to myocardium and blood as opposed to lung and epicardial f

87 ing in vascular smooth muscle cells, kidney, myocardium and brain.

88 enia with the LV epicardial volume (LV(EV)) (myocardium and chamber) estimated from chest CT images i

89 d in the COPDGene Study.Methods: Epicardial (myocardium and chamber) RV volume (RV(EV)), distal pulmo

90 art failure with preserved ejection fraction myocardium and chronic administration of a PDE9a inhibit

91 ailing heart, oxidative stress occurs in the myocardium and correlates with left ventricular dysfunct

92 n of postischemic inflammatory damage of the myocardium and corresponding decline in cardiac function

93 bited fewer suppressive Tregs in the injured myocardium and decreased expression of the gene encoding

94 , causing fibrofatty infiltration within the myocardium and driving major pathological features patho

95 plasminogen activator inhibitor serpine1 in myocardium and endocardium, resulting in increased level

96 in43 (Cx43), the predominate connexin in the myocardium and epithelial tissues, is phosphorylated on

97 ribonucleic acid sequencing (RNA-seq) of the myocardium and genetic deconvolution analysis.

98 ear neutrophils, accumulates within ischemic myocardium and has been linked to adverse left ventricul

99 the vasculature and atherosclerosis, and the myocardium and heart failure.

100 minantly expressed in both mouse ventricular myocardium and hiPSC-CMs, while it was almost undetectab

101 NOD1 was examined in human failing myocardium and in a post-myocardial infarction (PMI) HF

102 e two eicosanoid-lysophospholipids in murine myocardium and in isolated platelets.

103 positive cells were reduced in the infarcted myocardium and in the border zone.

104 Cx43 reduces the levels of total Cx43 in the myocardium and increases Cx43 phosphorylation on sites p

105 nary disease influence the blood flow to the myocardium and its ability to respond to stress; leading

106 balance between the metabolic demands of the myocardium and its oxygen supply, which most often resul

107 through direct actions on both the ischemic myocardium and leukocytes.

108 (TCR-M) cells selectively accumulated in the myocardium and mediastinal lymph nodes (med-LN) of infar

109 improves energy metabolism of the ischaemic myocardium and might improve outcomes and symptoms of pa

110 upregulated and activated in the remodeling myocardium and modulate phenotype and function of all my

111 t accommodates the cyclic deformation of the myocardium and outperforms most existing acellular epica

112 sarcoplasm, and we confirmed this finding in myocardium and reprogrammed cardiomyocytes from patients

113 l CoA was similarly reduced in human failing myocardium and restored to control levels by mechanical

114 Transition zones between healthy myocardium and scar form a spatially complex substrate t

115 sted by indirect immunofluorescence on human myocardium and skeletal muscle in 171 of the 175 ARVC in

116 Monocyte trafficking from the spleen to the myocardium and subsequent phenotype switching to reparat

117 The active material properties of the myocardium and time were features for the LV pressure an

118 apy on the reverse remodeling of the failing myocardium and to discuss the rationale for using a comb

119 Cardiovascular diseases (CVDs) affect the myocardium and vasculature, inducing remodelling of the

120 shown to be selectively concentrated in the myocardium and, using the Langendorff model, to be effec

121 trioventricular junction or left ventricular myocardium) and organs at risk were contoured.

122 n) for LV blood cavity, 0.89 +/- 0.03 for LV myocardium, and 0.62 +/- 0.08 for LV trabeculation (mean

123 blood flow, expressed as relative to remote myocardium, and absolute blood flow was not statisticall

124 reperfusion-induced arrhythmias in the adult myocardium, and compares the effect of acute (perfusion

125 post-gadolinium T1 measurements of blood and myocardium, and diastolic function was assessed by echoc

126 ut embryonic stem cells and engineered human myocardium, and human samples were used to validate the

127 Aldosterone (Aldo) promotes fibrosis in myocardium, and MR (mineralocorticoid receptor) antagoni

128 s a third mechanism for PEC translocation to myocardium, and observed a fourth mechanism in which PEC

129 ined to segment the left ventricular cavity, myocardium, and right ventricle by processing an incomin

130 induced opening of the mPTP in failing human myocardium, and the highly selective pharmacological blo

131 ed from different regions of the ventricular myocardium are known to vary significantly.

132 d modulation of XB behavior in failing human myocardium are unclear.

133 ac myofibroblasts in the pressure-overloaded myocardium are, at least in part, because of suppression

134 Instead of characterizing the myocardium as homogenous tissue and using important yet

135 d uniform and robust across all areas of the myocardium as well as in the coronary arteries.

136 tural and functional recovery of the failing myocardium, as only a small fraction of VAD-supported pa

137 eased BK activity favors the survival of the myocardium at ischemia/reperfusion.

138 (I/R) myocardial tissue composition (edema, myocardium at risk, infarct size, salvage, intramyocardi

139 lycystic kidney disease derive directly from myocardium-autonomous abnormalities.

140 diac involvement was also detected in D2-mdx myocardium based on both decreased function and myocardi

141 yocardial energetic demands increase and the myocardium becomes energy deficient.

142 tiate between the salvaged and the infarcted myocardium, but ECV was significantly higher in the latt

143 r essential for the formation of the working myocardium, but it was generally thought to be detriment

144 per se threatens metabolic resilience in the myocardium by causing broad-ranging disruption to mitoch

145 < .001 vs day 1) were similar to surrounding myocardium by day 20 (P = .409).

146 ibroblasts in the heart begin to remodel the myocardium by depositing excess extracellular matrix, re

147 chestrates neutrophil recruitment to injured myocardium by promoting adhesion of neutrophils to coron

148 olaldehyde (dopegal) damages neurons and the myocardium by protein cross-linking, resulting in conglo

149 Bordering areas of the infarcted myocardium can also experience impaired blood supply and

150 Immune cell infiltration in the myocardium can have adverse effects in the heart and con

151 point that proposes that the adult mammalian myocardium can undergo a low level of new cardiomyocyte

152 Following viral infection of the myocardium, cDCs accumulated in the heart coincident wit

153 ucture were assessed in right ventricle (RV) myocardium collected from patients with RV hypertrophy w

154 These findings in human myocardium confirm studies in rodents where contractile

155 In failing myocardium, confocal laser microscopy revealed alpha-B c

156 The myocardium consists of numerous cell types embedded in o

157 ing that physical contact of the PE with the myocardium constitutes a third mechanism for PEC translo

158 o regions of myocardial injury; however, the myocardium contained only a small proportion of total MS

159 (18)F-FOL shows specific uptake in inflamed myocardium containing macrophages expressing FR-beta, wh

160 oise ratio (SNR) for each sequence and blood-myocardium contrast for the cine sequences were assessed

161 all of the measured parameters and decreased myocardium damage during whole heart coronary ligation e

162 n humans, T2 relaxation time in the ischemic myocardium declines significantly from early after reper

163 he high density and the opaque nature of the myocardium, deep three dimensional (3D) imaging is diffi

164 t sites (0.88 +/- 0.74 mV) were localized to myocardium demonstrating CMR scar and abnormal innervati

165 After ischemic injury to the myocardium, dendritic cells (DC) respond to cardiomyocyt

166 nteratrial shunts; and finally targeting the myocardium directly by cell therapy in an attempt to reg

167 The environment of the failing and infarcted myocardium drives resident and transplanted MSCs toward

168 In fixed ventricular myocardium, dual-axis electron tomography was used for t

169 t aetiologies, including inflammation of the myocardium due to an infection (mostly viral); exposure

170 lycan within the extracellular matrix of the myocardium during early development and in the aftermath

171 eased in response to RIPC and to protect the myocardium during ischemic cardioplegic arrest.

172 vere EHS results in metabolic changes in the myocardium, emerging only after 9-14 days.

173 Postcardiopulmonary resuscitation, the myocardium exhibited increased reactive oxygen species a

174 D Global transcriptome profiling from murine myocardium exposed to doxorubicin identified 5 different

175 have the potential to regenerate functional myocardium following myocardial infarction.

176 c resonance (CMR) mapping to interrogate the myocardium following ST-segment elevation myocardial inf

177 e T1-weighted images was used to segment the myocardium for automated myocardial T2 and ECV quantific

178 Left ventricular myocardium from 37 patients (a group of patients with di

179 In human ventricular myocardium from patients with end-stage HF, we found hig

180 fraction were more fibrotic and elastic than myocardium from patients with HF with preserved ejection

181 Post hoc subgroup analysis revealed that myocardium from patients with HF with reduced ejection f

182 omeostasis have not been studied in isolated myocardium from patients with hypertensive heart disease

183 nd COX IV (cytochrome C oxidase) activity in myocardium from patients with valvular or ischemic heart

184 7 and P14, DUSP5 expression increases in the myocardium from the LV base to its apex; after this peri

185 The adult myocardium has a limited regenerative capacity following

186 In recent years, the myocardium has been rediscovered under the lenses of imm

187 te proliferation and heart function in adult myocardium has not been studied previously.

188 tion and a direct effect of hypoxemia on the myocardium have been proposed, the latter of which may p

189 d to neutrophil infiltration in the ischemic myocardium in an infarct size-independent manner.

190 y applied to surgically disrupted epicardial myocardium in canines.

191 -ribonucleic acid (antimiR) molecules to the myocardium in larger organisms is challenging, though, a

192 proved approaches to revascularizing damaged myocardium in patients with ischemic heart disease.

193 result of increased myeloid invading injured myocardium in response to MI.

194 hypertrophy, greater preservation of viable myocardium in the infarct zone, and superior left ventri

195 useful for delineating IMAT dense regions of myocardium, in postinfarct cardiomyopathy.

196 ssion of TRalpha1 and TRbeta1 in ovine fetal myocardium increases with age, although TRalpha1 levels

197 (99m)Tc-NOET therefore traps in myocardium independently of the mitochondrial perturbati

198 e extracellular volume (ECV) fraction of the myocardium, indexed ECV (iECV) to body surface area and

199 ightened macrophage numbers in the infarcted myocardium, inflamed lung regions, and atherosclerotic p

200 rotection by salvage of the infarct-affected myocardium is an unmet yet highly desired therapeutic go

201 ption (STAT)5 activation in left ventricular myocardium is associated with RIPC s cardioprotection.

202 acrine signaling from the endocardium to the myocardium is crucial for initiating early differentiati

203 ctive refractory period (ERP) of the working myocardium is different than the ERP of the HB, we hypot

204 or the direct cardioprotective effect at the myocardium is inhibited by propofol.

205 How trabeculations resolve to form compact myocardium is poorly understood.

206 Remodelling of the myocardium is regulated by a combination of myocyte and

207 In the heart, the growth of the myocardium is tightly coupled to that of the endocardium

208 e electrophysiological properties of injured myocardium is unknown.

209 d by Sox17 and required for nurturing of the myocardium, is responsible for the reduction in NOTCH-re

210 ambient temperature changes compared to the myocardium, it was hypothesized that heart mitochondria

211 tification of PET signal in the hypoperfused myocardium, K (1) (rate constant for transfer from arter

212 ferential expression of p38gamma MAPK in the myocardium, little is known about its function in the he

213 axis cine cardiac MRI: LV trabeculations, LV myocardium, LV papillary muscles, and the LV blood cavit

214 uantification of LV end-diastolic volume, LV myocardium mass, LV trabeculation, and trabeculation mas

215 Dysfunctional myocardium may persist, in part, from ongoing inflammati

216 In failing myocardium, microtubules elevate stiffness over the typi

217 l infarction), and nonischemic injury to the myocardium (myocarditis) and the progression to heart fa

218 tricular junction (n=5) and left ventricular myocardium (n=20) of intact animals.

219 Results: The myocardium of 10 of 18 immunized rats showed focal macro

220 yperpolarized (13)C MRS was performed on the myocardium of 8 sham-operated control rats and 8 rats wi

221 a source of free radicals, decreased in the myocardium of conditioned cases.

222 However, at 9-14 days, the myocardium of female mice developed marked elevations in

223 The results demonstrate that the myocardium of female mice is vulnerable to a slowly emer

224 the sarcomeric proteoform alterations in the myocardium of HCM patients undergoing septal myectomy we

225 , 2.1 +/- 1.1), whereas uptake in the remote myocardium of immunized rats and controls was low (SUV(m

226 A and protein expression were reduced in the myocardium of mice with streptozotocin-induced diabetes

227 ycation-end product-modified proteins in the myocardium of old mice (>=20months) compared with young

228 inding protein 1 (XBP1s), was reduced in the myocardium of our rodent model and in humans with HFpEF.

229 The myocardium of patients with cardiac sarcoidosis showed m

230 In atrial myocardium of patients with SDB, increased CaMKII-depend

231 at restore electrical conduction in diseased myocardium, offering potential long-term restorative sol

232 tructures that can be adjacent to the atrial myocardium, often within millimeters of the energy sourc

233 RI group with ischemia in at least 6% of the myocardium or in the FFR group with an FFR of 0.8 or les

234 including ratio of noncompacted to compacted myocardium (P<0.001) and left ventricular ejection fract

235 esults: (68)Ga-FAPI-04 uptake in the injured myocardium peaked on day 6 after coronary ligation.

236 ble to the uptake in the remote noninfarcted myocardium (PET image-derived ratio of infarct uptake to

237 In the myocardium, PKARIalpha (type-1 protein kinase A) can be

238 Geometrical structure of the myocardium plays an important role in understanding the

239 ence of activated fibroblasts in the injured myocardium predicts the quality of cardiac remodeling af

240 In early PAH LV myocardium proteins that may be linked to an increase in

241 muscle is biomechanically similar to native myocardium remains unknown.

242 The normal function of the human myocardium requires the proper generation and utilizatio

243 aracterized by fibrofatty replacement of the myocardium, resulting in heart failure and sudden cardia

244 a tissue volume of ~7 mm(3) in the adult rat myocardium, revealing a fixed level of intrinsic relaxat

245 Pulsed field ablation (PFA) can be myocardium selective, potentially sparing the esophagus

246 Samples of human left atrial myocardium showed a positive correlation between Rac1 ac

247 In 1 patient, the surrounding myocardium showed cytoplasmic vacuolization in myocytes

248 Remote myocardium showed decreased contractility at 120 min- an

249 Electron microscopy of myocardium showed irregular, convoluted intercalated dis

250 ll embryos revealed failure of outflow tract myocardium specification, whereas right ventricular myoc

251 besity-prone ALX deficient mice had impaired myocardium strain.

252 travenously administered MSCs engraft in the myocardium, studies have mainly utilized direct myocardi

253 c cardiomyopathy in comparison to nonfailing myocardium, suggesting a clinical relevance of HIPK2 in

254 ssing multiple important targets to maximize myocardium supplied by ITAs improved long-term survival.

255 In the pressure-overloaded myocardium, TGF-beta/Smad3-activated cardiac fibroblasts

256 c valve disease, promotes remodelling of the myocardium that can progress to heart failure with prese

257 on of structural/molecular changes in atrial myocardium that correlate with myocardial injury and pre

258 nal to noise ratio compared with surrounding myocardium that makes it feasible to identify coronary m

259 structure-function relationship of diseased myocardium that will help pave the way toward more effec

260 lopment as it functions to induce trabecular myocardium, the first heart tissue to form, and is the s

261 The amount of infarcted myocardium, the so-called infarct size, has long been kn

262 Sulfs reduced HS sulfation in the infarcted myocardium, thereby diminishing Vegfa (vascular endothel

263 rdiomyocytes, ventricular trabeculation, and myocardium thickening were also impaired in a non-cell-a

264 gions of FCGRT in samples of human liver and myocardium tissue, and we examined the impact of FCGRT m

265 c activation (ie, charge density) across the myocardium to guide ablation of atrial arrhythmias.

266 Three readers independently delineated the myocardium to investigate inter- and intraobserver repro

267 The endocardium interacts with the myocardium to promote proliferation and morphogenesis du

268 cise and reproducible results than the blood myocardium tracing algorithm.

269 In the developing heart, the myocardium transitions from a simple epithelium to an in

270 Hypoxic myocardium trapped [(64)Cu][Cu(ATSM)] despite no evidenc

271 Reperfusion of the ischemic myocardium triggers a complex inflammatory response that

272 iently activate Notch signaling within adult myocardium using a doxycycline-inducible genetic system

273 Quantification of FDG-avid myocardium using cardiac metabolic volume is proposed as

274 wall motion abnormalities in the jeopardized myocardium versus both groups at day 42.

275 ed for the segmentation of the LV cavity and myocardium via a novel FCN architecture.

276 In the patient study, the thickness of myocardium wall was reduced on average by 21%.

277 he presence of reparatory macrophages in the myocardium was also impaired in S100A9(-/)(-) mice with

278 The presence of viable myocardium was associated with improvement in left ventr

279 istribution of quinidine into perfused mouse myocardium was decreased by almost an order of magnitude

280 Uptake of (18)F-FOL in inflamed myocardium was efficiently blocked by a nonlabeled FR-be

281 Percent ischemic myocardium was estimated from a 17-segment model.

282 Myocardium was obtained from subjects undergoing LVAD pl

283 The left ventricular myocardium was segmented using standard clinical nuclear

284 ium specification, whereas right ventricular myocardium was specified but failed to properly differen

285 sed on the differences in ERP between HB and myocardium, was formulated, assessed, and found as diagn

286 lyzing macrophages lodged within the healthy myocardium, we discovered that they actively took up mat

287 In aged myocardium, we found that, compared with WT Cx43, mutant

288 responses (MBRs) between normal and ischemic myocardium were compared with mixed model analysis.

289 identification of pathological substrates of myocardium were evaluated according to EMB results.

290 ctice change whereby patients with high-risk myocardium were identified on daily rounds.

291 d ECV in both the infarcted and the salvaged myocardium were significantly higher than in the remote

292 ECV was also higher in the salvaged myocardium when compared to the remote myocardium.

293 e, yet more CD3(+) T cells infiltrated their myocardium when compared with TAC-operated cMy-mOVA mice

294 re is arrhythmia originating deep within the myocardium where it is inaccessible to conventional endo

295 erentiate between the infarcted and salvaged myocardium, whereas ECV could differentiate between the

296 Most cell subsets are found within the myocardium, whereas mast cells are found also in the epi

297 of both proteins in the clinically affected myocardium, which demonstrated a combined respiratory ch

298 Replacing lost myocardium with new tissue is a major goal of regenerati

299 diomyopathy (DCM) is a condition of abnormal myocardium with unknown sheetlet function.

300 on the structural 3D modeling of the viable myocardium within areas of dense scar.