ライフサイエンスコーパス: myocardium

1 e that are important in healthy and diseased myocardium.

2 reshly isolated cells matches that of intact myocardium.

3 ion to myofibroblasts in pressure-overloaded myocardium.

4 e to the high diastolic stiffness of failing myocardium.

5 platelet recruitment in WT but not PAD4(-/-) myocardium.

6 to allow sustained drug penetration into the myocardium.

7 iac patches with engraftment into native rat myocardium.

8 thus improving cell therapy of the infarcted myocardium.

9 ulate repair and remodeling in the infarcted myocardium.

10 itochondrial quality control in regenerating myocardium.

11 ansion and mechanical function of the atrial myocardium.

12 channel gene expression within adult atrial myocardium.

13 activation of beta1-adrenergic receptors in myocardium.

14 ion within alpha V beta 3-positive infarcted myocardium.

15 PCs), and their potential to recover injured myocardium.

16 force development (Tpk), compared with donor myocardium.

17 haracteristics in the healthy and remodelled myocardium.

18 promising approach to regenerate the injured myocardium.

19 ed reduction of sympathetic effectors on the myocardium.

20 during culture, approaching values of adult myocardium.

21 mumol/L OM but not with 0.5 mumol/L OM in HF myocardium.

22 st, iPLA2gamma predominated in failing human myocardium.

23 s pathologic hypertrophy and fibrosis of the myocardium.

24 r characterized by marked hypertrophy of the myocardium.

25 mice gave specific uptake in the reperfused myocardium.

26 uman mitochondrial phospholipases in failing myocardium.

27 ti-cellular physiology in normal or diseased myocardium.

28 clinical approach to regenerate the injured myocardium.

29 appeared both within the chambers and in the myocardium.

30 observed in WT myocardium were absent in HM myocardium.

31 xtent of myocardial fibrosis in noninfarcted myocardium.

32 d with CD4+ T-lymphocyte infiltration in the myocardium.

33 ceptor kinase 1/2 in the remote noninfarcted myocardium.

34 , extending from the infarct to noninfarcted myocardium.

35 ity of cardiovascular MR to characterize the myocardium.

36 tabolic, and structural consequences for the myocardium.

37 structural and functional changes within the myocardium.

38 GFbeta-Smad2/3 signaling and angiogenesis in myocardium.

39 reperfusion injury via direct effects on the myocardium.

40 crease their efficacy in repairing infarcted myocardium.

41 nI) induces inflammation and fibrosis in the myocardium.

42 it exerts any paracrine effects on the human myocardium.

43 m a network of branching outgrowths from the myocardium.

44 substrate ablation in the thick ventricular myocardium.

45 to the production of oxidized fatty acids in myocardium.

46 r could induce activation of the surrounding myocardium.

47 air overall reparative potential for injured myocardium.

48 system orchestrates the repair of infarcted myocardium.

49 edly up-regulated in the pressure-overloaded myocardium.

50 atherosclerotic plaque and to the infarcting myocardium.

51 h downstream effects on the left ventricular myocardium.

52 he anterior or anterolateral segments of the myocardium.

53 nslational large animal model of hibernating myocardium.

54 transverse-tubular membranes in ventricular myocardium.

55 re serially measured in infarcted and remote myocardium.

56 tivity but slower force development in human myocardium.

57 am amplitude and histological composition of myocardium.

58 A and G-protein receptor kinase sites in the myocardium.

59 embrane caveolae and Cav-3 expression in the myocardium.

60 al gene expression patterns in CCC patients' myocardium.

61 lt CFs for in vitro generation of functional myocardium.

62 matrix or saline was injected into infarcted myocardium 1 week after ischemia-reperfusion in Sprague-

63 chemia, induced capillary rarefaction in the myocardium (163 +/- 14 c/hpf in db vs. 234 +/- 8 c/hpf i

64 lar level as observed in bona fide postnatal myocardium; (3) a positive force-frequency response; (4)

65 ed cardiomyocyte apoptosis in the remodeling myocardium, accompanied by decreased myocardial NOX-2 le

66 suring nonuniformity of the left ventricular myocardium activity distribution.

67 was estimated as the maximum cavity blood-to-myocardium activity ratio.

68 dy, the intensity of (18)F-FDG uptake in the myocardium after acute myocardial infarction correlated

69 ocess that results into a solidified compact myocardium after birth.

70 these results are consistent with salvage of myocardium after I/R by iPLA2gamma loss of function thro

71 ng mouse cardiomyocytes, representing spared myocardium after injury, and cardiomyocytes generated fr

72 newly formed cardiomyocytes into the remnant myocardium after injury.

73 arrow, but not the myocardium, protected the myocardium against excessive remodeling in response to m

74 arrow, but not the myocardium, protected the myocardium against excessive remodeling of the pressure-

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

76 of CMMPs leads to the preservation of viable myocardium and augmentation of cardiac functions similar

77 ed using the SUVmean of the left ventricular myocardium and blood pool and calculation of target-to-b

78 - 57% higher contrast-to-noise ratio between myocardium and blood.

79 is produced in neuroendocrine cells, and the myocardium and circulating secretoneurin levels provide

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

81 iPSC-CMs can integrate into host myocardium and create a biological pacemaker.

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

83 established a lineage tree for parts of the myocardium and different head and neck muscles.

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

85 terocellular electrotonic coupling in native myocardium and identify tunneling nanotubes as a possibl

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

87 In human atrial myocardium and in both intact wildtype and M2 or M1/3-re

88 S. pneumoniae invades the myocardium and induces cardiac injury with necroptosis a

89 nd increased the concentration of H2S in the myocardium and lung.

90 cond heart field, which is a major source of myocardium and of the pharyngeal arch mesoderm that give

91 emic inflammation in HIV, which involves the myocardium and pericardium, may explain the high rate of

92 with the final aim of salvaging jeopardized myocardium and preventing left ventricular adverse remod

93 s demonstrated by injecting current into the myocardium and recording depolarization in the scar thro

94 y be up-regulated in the pressure-overloaded myocardium and regulate hypertrophy and fibrosis.

95 complexities of insulin signaling within the myocardium and ways in which these pathways are altered

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

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

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

99 sion of pathogenically relevant genes in CCC myocardium, and identify novel potential disease pathway

100 and spleen, moderate uptake in the brain and myocardium, and low uptake in bone and muscle.

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

102 onatal heart is capable of regenerating lost myocardium, and the adult heart is capable of modest sel

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

104 se tissue, urinary bladder, skeletal muscle, myocardium, and visceral pericardium.

105 clude that pneumococci that have invaded the myocardium are an important cause of cardiac damage, pne

106 Conclusion Native T1 and T2 of infarcted myocardium are excellent discriminators between acute an

107 tions of heterocellular communication in the myocardium are hampered by the intricate interspersion o

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

109 od flow and contractile function in ischemic myocardium are well matched, and there is no evidence fo

110 rforming better than those in the epicardial myocardium (areas under the receiver-operating character

111 er differential effects on XB behavior in HF myocardium as evidenced by a greater enhancement in Pdf

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

113 s must aim to improve blood flow to ischemic myocardium as much and as quickly as possible.

114 that uses laser-cut sheets of decellularized myocardium as scaffolds.

115 of NF2 in isolated cardiomyocytes and mouse myocardium at baseline and in response to oxidative stre

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

117 t of both vascular smooth muscle and compact myocardium at later developmental stages in Lb1-null emb

118 ) have been clinically validated to estimate myocardium at risk (MaR) by cardiovascular magnetic reso

119 Reference myocardium at risk was assessed by multidetector compute

120 echniques and protocols for assessing edema, myocardium at risk, infarct size, salvage, intramyocardi

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

122 unction, infarct distribution, infarct size, myocardium at risk, microvascular obstruction, and intra

123 MI by CMR and assessed its implications for myocardium-at-risk (MaR) quantification both in patients

124 maller differences exist for diseases of the myocardium, atrial fibrillation, aortic and peripheral a

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

126 ss contributed to stiffness of failing human myocardium because of reduced titin distensibility.

127 metric appearance, granular sparkling of the myocardium, biatrial enlargement, thickening of the mitr

128 fibrofatty replacement of right ventricular myocardium; biventricular involvement is often observed.

129 er in HF myocardium when compared with donor myocardium, both prior to and after OM incubations.

130 Both strains efficiently invaded the myocardium, but cardiac damage was entirely dependent on

131 < .001 vs day 1) were similar to surrounding myocardium by day 20 (P = .409).

132 arious types has been reported to create new myocardium by the direct conversion of these progenitor

133 Delivery of H2S to the myocardium by ultrasound targeted hs-MB destruction atte

134 onduction (propagation) within the mammalian myocardium can change APD and the Q-T interval of the el

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

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

137 The mechanical properties of myocardium change regionally and over time after myocard

138 ike macrophages predominantly in the injured myocardium, compared to the control.

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

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

141 that in WT mice, but the iPLA2beta-KO mouse myocardium contained more parasite pseudocysts.

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

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

144 HIV infection may involve the pericardium, myocardium, coronary arteries, pulmonary vasculature, an

145 gulation of atypical G protein Gbeta5 in the myocardium correlating with oxidative stress, myocyte ap

146 ansplantation, patient-derived bioartificial myocardium could provide functional support and ultimate

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

148 Results Native T1 of infarcted myocardium decreased from 1286 msec +/- 99 at baseline t

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

150 rrelated with a greater volume of denervated myocardium (defect of the positron emission tomography n

151 Experiments with permeabilized human myocardium demonstrate that OM increases calcium sensiti

152 f static stress conditioning, the engineered myocardium demonstrated increases in contractility (0.63

153 me-wide map of miR targeting events in human myocardium, detecting 4000 cardiac Ago2 binding sites ac

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

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

156 ntations and also to study remodeling of the myocardium due to volume unloading.

157 tion to illustrate changes that occur to the myocardium due to volume unloading.

158 g the activation of KATP channels in working myocardium during high-stress situations is crucial to t

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

160 ile abnormalities in the ischemic and remote myocardium during one week after MI.

161 milieu, and reduced parasite load within the myocardium during the acute phase.

162 rotein signatures in the ischemic and remote myocardium early after I/R and might have implications f

163 cardiomyocyte maturation in engineered human myocardium (EHM) toward an adult phenotype under defined

164 tiates between infarcted versus noninfarcted myocardium, even in patients with stable ischemic heart

165 HF myocardium exhibited impaired contractile function as ev

166 Matrix-injected infarcted myocardium exhibits an altered inflammatory response, re

167 The engineered human myocardium exhibits Frank-Starling-type force-length rel

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

169 ly sourced macrophages isolated from failing myocardium expressed different genes in a pattern distin

170 logy for the engineering of macroscale human myocardium for disease modeling and heart repair from em

171 cells were isolated from fresh, dissociated myocardium for quantitative reverse transcription polyme

172 the expression of beta-catenin and Nanog in myocardium from AMI mice.

173 the role of titin strain in LDA, we isolated myocardium from either WT or homozygous mutant (HM) rats

174 METHODS AND Immunoblot analysis of myocardium from end-stage HF patients (n=12) and non-HF

175 apacity to repair and regenerate the damaged myocardium from ischemic injury.

176 -influx inhibitors on relaxation in isolated myocardium from patients with HHD and HFpEF.

177 ion and relaxation are prolonged in isolated myocardium from patients with HHD and HHD+HFpEF.

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

179 ss induced CHOP and apoptotic signatures and myocardium from subjects with dilated cardiomyopathy sho

180 Pitx2 mutant myocardium had increased levels of reactive oxygen speci

181 Whereas dysregulation of autophagy in the myocardium has been implicated in a variety of cardiovas

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

183 ived from decellularized porcine ventricular myocardium has been shown to halt the post-infarction pr

184 Analysis of myocardium has revealed mechanistic insights into arrhyt

185 Alterations in the remote myocardium have also been neglected, disregarding its co

186 in post-MI remodeling of nonischemic remote myocardium, however, remain unclear.

187 e in cardiac lactate to the left ventricular myocardium, implying a direct myocardial effect, though

188 ing cysts contribute to PEC translocation to myocardium in a CDC42-dependent manner.

189 that is diffuse in nature and affecting the myocardium in a rather uniform and global distribution i

190 logic and noncardiomyocyte function of human myocardium in end-stage heart failure (HF).

191 metabolism can be detected in the blood and myocardium in human PAH and are associated with in vivo

192 diac macrophages residing in the nonischemic myocardium in mice with chronic heart failure after coro

193 characterize PW1-expressing cells in the LV myocardium in normal and ischemic conditions 7 days afte

194 The noninvasive assessment of altered myocardium in patients with genetic mutations that are a

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

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

197 Ly6C(hi) monocyte/macrophage subset into the myocardium in response to pressure overload.

198 Both iPSCs and iPSC-EVs preserved viable myocardium in the infarct zone, whereas reduction in apo

199 rats exhibited smaller scars and more viable myocardium in the risk region, along with improved left

200 e electromechanical dysfunction of human HCM myocardium in vitro.

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

202 fission to impact all cell types within the myocardium, including cardiac myocytes, cardiac fibrobla

203 tural and functional properties of postnatal myocardium, including: (1) rod-shaped cardiomyocytes wit

204 ice, Streptococcus pneumoniae can invade the myocardium, induce cardiomyocyte death, and disrupt card

205 As the myocardium is a highly oxidative tissue, mitochondria pl

206 owing injury, and this failure to regenerate myocardium is a leading cause of heart failure and death

207 Considering that parasite persistence within myocardium is a necessary and sufficient condition for t

208 Given that the myocardium is an obligate aerobic tissue and consumes la

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

210 ping analysis confirms that the newly formed myocardium is derived from pre-existing cardiomyocytes.

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

212 heart fills with blood during diastole, the myocardium is stretched and oxidants are produced.

213 isease, S. pneumoniae can gain access to the myocardium, kill cardiomyocytes, and form bacterium-fill

214 systolic loading sequence of the ventricular myocardium likely affects its coupling with the left atr

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

216 Previously silent recessive defects of the myocardium may predispose to acute heart failure present

217 rventions that influence autonomic inputs to myocardium may prevent AF.

218 Thus, (18)F-FDG uptake in infarcted myocardium may represent a novel biosignal of myocardial

219 resulted from inclusion of right ventricular myocardium (n=37; 38.1%), LV trabeculations (n=5; 5.2%),

220 gene expression and anatomic description of myocardium obtained at the time of coronary artery revas

221 e observed that pneumococcal invasion of the myocardium occurred soon after development of bacteremia

222 in full width at half maximum of the canine myocardium of 13% +/- 5%, similar to cardiac gating but

223 ethanol or acetic acid was injected into the myocardium of 8 swine using MRI-conspicuous needle cathe

224 S. pneumoniae was detected in the myocardium of all NHPs with acute severe pneumonia.

225 croptosis and apoptosis were detected in the myocardium of both acutely ill and convalescent NHPs.

226 d reverses mitochondrial abnormalities in LV myocardium of dogs with advanced HF.

227 LR4(-/-) and WT male mice into the infarcted myocardium of female WT mice and evaluated infarct size,

228 There may be changes in the myocardium of incident HD patients over a 6-month period

229 e injected MSCs or saline into the infarcted myocardium of mice and evaluated LV remodeling and funct

230 exhibit high in vivo specific binding to the myocardium of non-human primates.

231 ncreased T cell infiltration in the fibrotic myocardium of nonischemic HF patients, as well as the pr

232 Mitochondria prepared from the myocardium of Nrf2 knockout mice are more sensitive to p

233 One unique remodeling event in the myocardium of obese and diabetic rodents is an increase

234 scular dysfunction and over-expressed in the myocardium of patients with myocardial infarction (MI).

235 genase activity could be assessed within the myocardium of perfused hearts using NADH ED-FRAP.

236 17 in the lungs of wild-type mice and in the myocardium of transgenic mice with cardiomyocyte-specifi

237 (18)F]-17 showed specific binding to PDE5 in myocardium of transgenic mice; however [(18)F]-17 showed

238 I rescued Treg infiltration into the injured myocardium of YAP/TAZ mutants and decreased fibrosis.

239 erentiation between ischemic scar and normal myocardium on cine MR images in both subgroups: Teta1, P

240 =45% on the acute scans could predict viable myocardium on the follow-up scan.

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

242 in strained cell cultures and in the failing myocardium (P<0.05).

243 cardium versus 20.4+/-10.6% left ventricular myocardium, P<0.0001) and corresponded to the area at ri

244 is a defining property of pectinated atrial myocardium (PAM) and the ventricular conduction system (

245 1) with readings obtained in the endocardial myocardium performing better than those in the epicardia

246 In the infarcted myocardium, presence of sympathetic nerves and tissue ab

247 ssion of TNC in the bone marrow, but not the myocardium, protected the myocardium against excessive r

248 ssion of TNC in the bone marrow, but not the myocardium, protected the myocardium against excessive r

249 biomaterials as an implantable hiPSC-derived myocardium provides a path to realize sustainable myocar

250 However, the mechanisms by which injured myocardium recruits suppressive immune cells remain larg

251 IMAT dense regions of myocardium reliably identified using endocardial mapping

252 anges, or imaging evidence of loss of viable myocardium) required for the diagnosis of spontaneous ac

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

254 , BODIPY was capable of penetrating into the myocardium, resulting in a transmural gradient.

255 The power in the myocardium sarcomere is generated by two bipolar arrays

256 Atrial myocardium secretome induces the adipogenic differentiat

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

258 Remote myocardium showed decreased contractility at 120 min- an

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

260 activate the PKG/PLN pathway in the ischemic myocardium, suggesting that the combination of both phar

261 T2 relaxation time in the myocardium (T2 mapping) and the extent of edema on T2-we

262 Moreover, myocardium that is remote from ischemic area also become

263 s are 100- to 400-mum-thick slices of living myocardium that retain the native multicellularity, arch

264 high capacity to regenerate damaged or lost myocardium through proliferation of cardiomyocytes spare

265 ne-6 and is an important mechanism of remote myocardium to adapt to the increased mechanical demands

266 netic resonance in tissue characterizing the myocardium to be combined with the unique metabolic insi

267 t understood as the final common response of myocardium to diverse genetic and environmental insults.

268 nd may impair the responsiveness of ischemic myocardium to proangiogenic factors.

269 Volumes of interest were drawn on LV myocardium to quantify mean SUV.

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

271 onance (CMR) imaging is used to evaluate the myocardium, valves, coronary arteries, pericardium, also

272 lar system by means of directly altering the myocardium, vasculature, and metabolism.

273 cement extent (33.2+/-16.2% left ventricular myocardium versus 20.4+/-10.6% left ventricular myocardi

274 ammatory) phenotype that occurred within the myocardium very shortly after BALB/c mice infection.

275 hat mediates AMPK activation in the ischemic myocardium via an interaction with AMPK upstream LKB1.

276 ical coupling between the scar and uninjured myocardium was demonstrated by injecting current into th

277 (18)F-FDG uptake in the infarcted myocardium was highest in areas with transmural scar, an

278 Myocardium was obtained from subjects undergoing LVAD pl

279 interactions in the setting of healthy adult myocardium was predicted by coupling and fusing these hM

280 more than one-third of the left ventricular myocardium was replaced by fibrosis, mainly of replaceme

281 (18)F-FDG uptake in normal myocardium was scored according to a scale ranging from

282 uses, microvascular blood flow per volume of myocardium was twice that of control fetuses at rest, du

283 ependent changes in structure observed in WT myocardium were absent in HM myocardium.

284 ificity and localization of m21G6 to injured myocardium were confirmed using fluorescently labeled m2

285 e clonal T-cell populations infiltrating the myocardium were identical to those present in tumors and

286 cutoff values for oedematous versus necrotic myocardium were identified as 1251 ms and 1400 ms, respe

287 To create EHTs, sections of porcine myocardium were laser-cut into ribbon-like shapes, decel

288 of force generation (pCa50) was higher in HF myocardium when compared with donor myocardium, both pri

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

290 ested the function of these two Tln forms in myocardium where Tln2 is the dominant isoform in postnat

291 stellate lesions with patchy areas of normal myocardium, whereas acetic acid caused homogeneous circu

292 ity was elevated in neonatal FNIP1-deficient myocardium, whereas AMPK-dependent unc-51-like autophagy

293 gnal mainly confined to the left ventricular myocardium, whereas the [1-(13)C]lactate signal appeared

294 R2-mediated transmural depolarization of the myocardium, which causes a block of voltage-dependent Na

295 ions to force-bearing states in remodeled HF myocardium, which may extend the systolic ejection time

296 vivo study, we demonstrate that left atrial myocardium with increased gadolinium uptake has lower lo

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

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

299 sion of CD8(+) and CD4(+) T cells in failing myocardium, with increased Th1, Th2, Th17, and Treg CD4(

300 dia is associated with channels of surviving myocardium within scar characterized by fractionated and