ライフサイエンスコーパス: infarcted

1 creened) or when transplanted into normal or infarcted adult mouse hearts (14 EGFP(+) grafts examined

2 ated from normal neonatal, normal adult, and infarcted adult mouse hearts was evaluated.

3 crophages critically determine the repair of infarcted adult murine heart by regulating fibroblast ac

4 magnetic resonance images were acquired in 8 infarcted and 3 healthy pigs.

5 was transferred intramyocardially into four infarcted and four periinfarcted sites.

6 of change in SQUEEZ were calculated for both infarcted and healthy myocardial regions.

7 q analysis of 4,215 leukocytes isolated from infarcted and non-infarcted hearts showed that MI provok

8 Differentiation of fibroblasts from infarcted and noninfarcted hearts into myofibroblasts wa

9 asts, leukocytes, and endothelial cells from infarcted and noninfarcted neonatal (P1) and adult (P56)

10 survived and underwent proliferation in the infarcted and normal hearts, as demonstrated by serial i

11 yocardium (myocytes and microvasculature) in infarcted and peri-infarct/border regions at 21 and 60 d

12 sulas and/or islands of viable myocardium in infarcted and periinfarcted regions and greater number o

13 Collagen deposition also was reduced in the infarcted and remote areas of the Col6a1(-/-) hearts.

14 tracellular volume were serially measured in infarcted and remote myocardium.

15 etic particles of iron oxide occurs with the infarcted and remote myocardium.

16 with the known levels of edema that occur in infarcted and salvaged myocardium, and the finding that

17 served attached to the epicardial surface of infarcted and sham-operated hearts in which a suture was

18 low (P = 0.31), differed between tissue that infarcted and tissue that survived.

19 er the motility of hCSCs in immunosuppressed infarcted animals is controlled by the guidance system t

20 The ME-labeled iCMs were injected into the infarcted area of murine heart and probed by MRI and bio

21 However, injecting the infarcted area of the adult mammalian heart with exogeno

22 ible for the engulfment of dead cells in the infarcted area remain largely unknown.

23 th high spatial resolution spanning from the infarcted area to the remote to identify new regulators

24 In fact, fibroblasts within the infarcted area were largely of epicardial origin.

25 reduction of neuronal nuclear antigen in the infarcted area, although no improvement in neurological

26 -MI leukocyte density, residence time in the infarcted area, and exit from the infarcted injury predi

27 ntour of the bright region exactly match the infarcted area, this level of validation does not exist

28 e (vehicle) along the border of the blanched infarcted area.

29 was detected when moving from healthy toward infarcted area.

30 rganization of the collagenous matrix in the infarcted area.

31 sponse and infiltration of leukocytes to the infarcted area.

32 sults in the generation of dead cells in the infarcted area.

33 athy in the area immediately surrounding the infarcted area; however, the effect was transient, poten

34 , 38 miRNAs were differentially expressed in infarcted areas and 33 miRNAs were aberrantly expressed

35 y decreased cell apoptosis in the border and infarcted areas of the infarcted rat hearts after treatm

36 The down-regulation of miR-21 in the infarcted areas was inhibited by ischemic preconditionin

37 In contrast, remote from the primarily infarcted areas, a marked T2(*)- hypointensity was detec

38 pression was significantly down-regulated in infarcted areas, but was up-regulated in border areas.

39 ligation, iPS cells were delivered to mapped infarcted areas.

40 elevance of TREM2 in the phagocytosis of the infarcted brain and emphasize its role in influencing ne

41 Phagocytosis and infarcted brain tissue resorption was reduced in TREM2 k

42 r nerve growth factor (NGF; P<0.0001) in the infarcted brain.

43 Mice were infarcted by left anterior descending coronary artery li

44 creased and ventricular function enhanced in infarcted calpain 1 knockout hearts.

45 neurons and high mCRP-levels spreading from infarcted core regions matched reduced expression of Abe

46 ed that intramyocardial delivery of BMPCs in infarcted diabetic db/db mice significantly down-regulat

47 s and reducing ventricular remodeling in the infarcted diabetic myocardium.

48 s-mediated impairment of angiogenesis in the infarcted diabetic rat myocardium by proangiogenic gene

49 A single c-kit(+) cell from an infarcted double transgenic adult heart was observed to

50 s of CPCs overexpressing Pim-1 were given to infarcted female mice.

51 st-infarction, the contractility of targeted infarcted foci and nullified conduction delay in adjacen

52 mly allocated to remain untreated (untreated infarcted group, I) or to receive PY (30 mg.kg(-1).day(-

53 f inhibitory and proresolving signals in the infarcted heart and identification of patients with unco

54 l (GFP(+)c-kit(+) cell) recruitment into the infarcted heart and stem cell-mediated cardiac repair in

55 shown very promising potential to repair the infarcted heart but is severely limited by the poor surv

56 We then analyzed macrophage phenotype in the infarcted heart by flow cytometry and macrophage secreto

57 es with a high spatial resolution across the infarcted heart enabled us to identify gene clusters tha

58 og (Emc10) in cultured endothelial cells and infarcted heart explants.

59 Cardiac stem cells (CSCs) delivered to the infarcted heart generate a large number of small fetal-n

60 nction of adipose stromal cells (ASC) in the infarcted heart has never been compared directly to bone

61 Transplantation of cells into the infarcted heart has significant potential to improve myo

62 rocesses implicated in the adaptation of the infarcted heart have to be dissected in terms of the cri

63 successfully rescued stem cell homing to the infarcted heart in Plg-deficient mice, indicating that C

64 th WT MSC, injection of N1(+/-) MSC into the infarcted heart leads to increased myocardial injury whe

65 Chemokine induction in the infarcted heart mediates recruitment of leukocyte subset

66 ion and to improve pumping efficiency of the infarcted heart offers a promising strategy for making s

67 injected directly in the border zone of the infarcted heart or in corresponding regions of normal he

68 Importantly, depletion of CELF1 in the infarcted heart preserved Cx43 mRNA level and ameliorate

69 Importantly, the ratio of probe uptake in infarcted heart tissue compared to normal tissue was sig

70 continue to find new therapies to regenerate infarcted heart tissue, knowledge of the cellular and mo

71 decrease aberrant remodeling and fibrosis in infarcted heart tissue.

72 e origin of cardiac fibroblasts (CFs) in the infarcted heart to better understand the pathophysiology

73 e effects of cell-specific Smad3 loss on the infarcted heart were studied using histological studies,

74 hCSCs) is a promising approach to repair the infarcted heart, but it is severely limited by the poor

75 In infarcted heart, improper clearance of dying cells by ac

76 In the infarcted heart, Smad3 signaling is activated in both ca

77 generates extensive remuscularization of the infarcted heart.

78 cterize Gal-1 expression and function in the infarcted heart.

79 antation of endothelial cells (ECs) into the infarcted heart.

80 tainment of the inflammatory response in the infarcted heart.

81 ndex to evaluate EC-mediated therapy for the infarcted heart.

82 lation in vitro and transplantation into the infarcted heart.

83 ation of myocardial mass and function in the infarcted heart.

84 tified in atherosclerotic plaques and in the infarcted heart.

85 and enhanced cardiomyocyte apoptosis in the infarcted heart.

86 e in vivo behavior of both cell types in the infarcted heart.

87 e to anoxia and following engraftment in the infarcted heart.

88 nd ameliorated the cardiac phenotypes of the infarcted heart.

89 serve in regenerative medicine to repair the infarcted heart.

90 n of multiple kinds of inflammatory cells in infarcted heart.

91 rdiac function and exacerbated the injury of infarcted heart.

92 tive, and even regenerative functions in the infarcted heart.

93 IL-1 expression is markedly induced in the infarcted heart; however, its role in cardiac injury and

94 hown in serial-transplantation assays in the infarcted heart; these cells created a chimeric organ, c

95 iation of bone marrow cells or isolated from infarcted hearts altered their capacity of efferocytosis

96 e bona fide CPCs and they integrated well in infarcted hearts and emerged de novo into terminally dif

97 PHD2 silencing promotes ADSCs survival in infarcted hearts and enhances their paracrine function t

98 nfarcted hearts, but the mechanisms by which infarcted hearts are more vulnerable to electric shocks

99 Moreover, NK1-expressing PC are abundant in infarcted hearts but not in hearts that developed an inf

100 nmol/liter) for 24 h and re-introduced into infarcted hearts for 2 weeks.

101 e and restored the functional performance of infarcted hearts for at least 3 months.

102 Within infarcted hearts in the adult, intramyocardial delivery

103 s and enhanced resolution of inflammation in infarcted hearts of apoE(-/-) mice that were treated wit

104 Transplantation of day 20 CMs into the infarcted hearts of immunodeficient mice showed good eng

105 Infarcted hearts receiving intramyocardial injection of

106 Moreover, MFG-E8 administration into infarcted hearts restored cardiac function and morpholog

107 5 leukocytes isolated from infarcted and non-infarcted hearts showed that MI provokes activation of a

108 PCs before their intramyocardial delivery to infarcted hearts was associated with enhanced engraftmen

109 normal and abnormally contracting regions in infarcted hearts were shown to correspond well with noni

110 Defibrillation efficacy is decreased in infarcted hearts, but the mechanisms by which infarcted

111 cytes (hESC-CMs) can improve the function of infarcted hearts, but two critical issues related to the

112 titial but not cardiomyocyte compartments in infarcted hearts, fibroblast-restricted depletion of one

113 In infarcted hearts, NOX5 expression increased, especially

114 diac repair was detected in all cell-treated infarcted hearts, the aggregate volume of the regenerate

115 presses accumulation of Ly6C(low) Mos/Mps in infarcted hearts.

116 rotective effects after transplantation into infarcted hearts.

117 in repair of damaged tissues, including the infarcted hearts.

118 g-1) is beneficial in the repair of diabetic infarcted hearts.

119 lls and angiogenesis in diabetic db/db mouse infarcted hearts.

120 ncreased vulnerability to electric shocks in infarcted hearts.

121 provide functional or structural benefits to infarcted hearts.

122 ownregulated in murine I/R-injured and human infarcted hearts.

123 noted following stem cell transplantation in infarcted hearts.

124 S Ex) possess ability to augment function in infarcted hearts.

125 CSCs may complementarily help the repair of infarcted hearts.

126 ulation of endothelin B receptor only in the infarcted hemisphere 7 days following occlusion.

127 icantly increased at 1 week post MCAO in the infarcted hemisphere of IRL-1620 treated rats as compare

128 The CM+EC+MC ECTs implanted onto infarcted, immune tolerant rat hearts engrafted, display

129 ultimodality characterization of the acutely infarcted, inflamed myocardium may provide multiparametr

130 ime in the infarcted area, and exit from the infarcted injury predict resolving or nonresolving infla

131 Infarcted IP-10(-/-) hearts exhibited accentuated early

132 For qPCR-1, 5 of 98 infarcted lung specimens were positive by qPCR and negat

133 P<0.01), systolic thickening fraction in the infarcted LV wall, and maximum LV dP/dt, as well as lowe

134 SB was quantified as scar percentage (infarcted mass/total left ventricular mass).

135 imately 12-week sham-operated and myocardial infarcted (MI) rats.

136 by fibroblasts isolated from normal (Fb) and infarcted (MI-Fb) hearts.

137 e approach was performed in normal (n=6) and infarcted mice (n=6) as well as healthy human volunteers

138 Infarcted mice also had larger pericardial clusters and

139 Importantly, inhibition of Notch1 in infarcted mice impairs the commitment of resident CPCs t

140 ted that intramyocardial delivery of BMCs in infarcted mice regulates the expression of cardiac miRNA

141 hange in sham-operated mice, OGT deletion in infarcted mice significantly exacerbated cardiac dysfunc

142 myocardial cell administration in normal and infarcted mice.

143 The wall thickness of the infarcted middle anterior septum in the EMU group was si

144 6C(How) monocytes/macrophages populating the infarcted milieu.

145 can remuscularize substantial amounts of the infarcted monkey heart.

146 0 stimulated endothelial cell outgrowth from infarcted mouse heart explants via p38 MAPK-MK2.

147 could survive upon transplantation into the infarcted mouse heart without formation of teratomas.

148 In vivo, injection of CDCs into the infarcted mouse hearts resulted in superior improvement

149 When transplanted into infarcted mouse hearts, 9C-treated fibroblasts were effi

150 In addition, implantation of mCPCs into infarcted mouse myocardium improves cardiac function wit

151 a and MIP-1beta were markedly induced in the infarcted mouse myocardium.

152 were the predominant sources of Emc10 in the infarcted murine heart.

153 e proliferation, whereas poorly regenerative infarcted murine hearts did not.

154 on in both cultured human cardiomyocytes and infarcted murine hearts.

155 were injected into the myocardium of a nude infarcted murine model and followed over 1 year for func

156 ed muscle, human atherosclerotic plaque, and infarcted myocardium (rat and human) and its colocalizat

157 yocardial matrix or saline was injected into infarcted myocardium 1 week after ischemia-reperfusion i

158 1(+) lineage-derived EPDC migration into the infarcted myocardium 5 days post MI, which was inhibited

159 nterparts, cardiopoietic hMSC delivered into infarcted myocardium achieved superior functional and st

160 In patients with infarcted myocardium and reduced FDG uptake (n = 18), a

161 ow that Ly-6C(high) monocytes infiltrate the infarcted myocardium and, unlike Ly-6C(low) monocytes, d

162 Conclusion Native T1 and T2 of infarcted myocardium are excellent discriminators betwee

163 rage in the neovessels of the border zone of infarcted myocardium are severely impaired in db/db mice

164 yocardium, and improved regional function of infarcted myocardium at 1 year post-treatment.

165 rtery ligation, CCR1-MSCs accumulated in the infarcted myocardium at significantly higher levels than

166 ent yields improved structural remodeling of infarcted myocardium compared with control BMCs.

167 Results Native T1 of infarcted myocardium decreased from 1286 msec +/- 99 at

168 The environment of the failing and infarcted myocardium drives resident and transplanted MS

169 Matrix-injected infarcted myocardium exhibits an altered inflammatory re

170 NA, and total protein levels were reduced in infarcted myocardium in ADAM17 knockdown mice.

171 sibility of CrEST measurement in healthy and infarcted myocardium in animal models in vivo on a 3-T c

172 he first time that injection of EMU into the infarcted myocardium increases neovascularization and pr

173 ow survival of the transplanted cells in the infarcted myocardium is possibly a primary reason for fa

174 ombination of microRNAs (miR combo) into the infarcted myocardium leads to direct in vivo reprogrammi

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

176 SCs from TLR4(-/-) and WT male mice into the infarcted myocardium of female WT mice and evaluated inf

177 quently, we injected MSCs or saline into the infarcted myocardium of mice and evaluated LV remodeling

178 and VEGF, respectively) and delivered to the infarcted myocardium of rats.

179 ngraftment and survival of stem cells in the infarcted myocardium remain problematic in cell-based th

180 nocyte and/or macrophage infiltration of the infarcted myocardium shown by prior histologic studies.

181 l regeneration and functional improvement in infarcted myocardium than transplanted cardiac fibroblas

182 ts CD133(+)/c-kit(+) cell recruitment to the infarcted myocardium thereby mediating cardiac repair in

183 hypothesis that MSCs regenerate chronically infarcted myocardium through mechanisms comprising long-

184 rcted myocardium to remote myocardium and of infarcted myocardium to blood plateaued at around 1.9 an

185 after contrast injection, and the ratios of infarcted myocardium to remote myocardium and of infarct

186 ss-linking within decellularized healthy and infarcted myocardium using second harmonic generation (S

187 ave hampered attempts at revascularizing the infarcted myocardium using systemic delivery of proangio

188 (18)F-FDG uptake in the infarcted myocardium was highest in areas with transmura

189 eased in CMI and AMI (P<0.05), and T2 of the infarcted myocardium was increased in AMI (P<0.001) but

190 elative to the remote territories, T1 of the infarcted myocardium was increased in CMI and AMI (P<0.0

191 The ability of IGF-1R(+) hCSCs to regenerate infarcted myocardium was then compared with that of unse

192 The patients' core and border zones of infarcted myocardium were analyzed and followed for CVE.

193 ificantly increased capillary density in the infarcted myocardium which was associated with enhanced

194 The population of c-kit-positive cells in infarcted myocardium with the EMU injection increased si

195 In the infarcted myocardium, activation of the inflammatory cas

196 Within the infarcted myocardium, CD4 KO mice displayed higher total

197 ive M2 macrophages (F4/80(+)CD206(+)) in the infarcted myocardium, compared with mononuclear- and sal

198 e kinase, known as solMER, was identified in infarcted myocardium, implicating a natural mechanism of

199 When transplanted into infarcted myocardium, neonatal-derived CDCs had a signif

200 In the infarcted myocardium, presence of sympathetic nerves and

201 Two days after direct injection into the rat infarcted myocardium, Sfrp2 inhibited MI-induced type I

202 actor-kappaB activation (DNA binding) in the infarcted myocardium, which could underlie the suppresse

203 ardiac repairs and neovascularization in the infarcted myocardium, which were absent in Kit(W)/Kit(W-

204 therefore be responsible for preservation of infarcted myocardium.

205 s remodeling and improves global function in infarcted myocardium.

206 eperfusion showed a significant reduction in infarcted myocardium.

207 ite, creatine, was used to identify areas of infarcted myocardium.

208 , we found infiltration of CD4(+) T cells in infarcted myocardium.

209 ng, apelin expression was upregulated in the infarcted myocardium.

210 tation, fibrosis, and hypertrophy of the non-infarcted myocardium.

211 vivin-mediated anti-apoptotic pathway in the infarcted myocardium.

212 d by increases in arteriole formation in the infarcted myocardium.

213 and, therefore, their efficacy in repairing infarcted myocardium.

214 e marrow-derived progenitor cells (BMPCs) in infarcted myocardium.

215 Specific chemokines are upregulated in the infarcted myocardium.

216 elivered to inflamed tissue, such as acutely infarcted myocardium.

217 tment and thus improving cell therapy of the infarcted myocardium.

218 re than doubled myocardial blood flow in the infarcted myocardium.

219 fibrosis were analyzed in the border zone of infarcted myocardium.

220 Smad3 regulate repair and remodeling in the infarcted myocardium.

221 accumulation within alpha V beta 3-positive infarcted myocardium.

222 ion and increase their efficacy in repairing infarcted myocardium.

223 The immune system orchestrates the repair of infarcted myocardium.

224 dothelial precursor activity in regenerating infarcted myocardium.

225 Explantation of infarcted neonatal and adult heart tissue to scid mice,

226 ted on LGE images and with 90 (29%) rated as infarcted on cine images.

227 PET images, compared with 93 (30%) rated as infarcted on LGE images and with 90 (29%) rated as infar

228 In 306 segments, 97 (32%) were rated as infarcted on PET images, compared with 93 (30%) rated as

229 C)-negative tissue, normally associated with infarcted or ischemic tissue.

230 farct size (19.2% to 14.2% of left ventricle infarcted, P=0.01), whereas placebo did not (17.7% to 15

231 This was associated with a decrease in infarcted papillary muscle-to-mitral annulus tethering d

232 l was significantly reduced in the whole non-infarcted penumbra (P < 0.01) but not within the functio

233 An overlap between non-infarcted penumbra and functional magnetic resonance ima

234 However, although the non-infarcted penumbra as a whole was affected by selective

235 Following image coregistration, the non-infarcted penumbra comprised all acutely ischaemic voxel

236 However, whether the non-infarcted penumbra is capable of neuronal activation, an

237 suggest that 1-3 months after stroke the non-infarcted penumbra is capable of neuronal activation, co

238 esonance imaging activation clusters and non-infarcted penumbra was mapped, and binding potential val

239 magnetic resonance imaging responses and non-infarcted penumbra, and tested the hypothesis that the f

240 lly infarcted tissue, and the eventually non-infarcted penumbra, were determined by performing voxel-

241 ession model that included the volume of non-infarcted penumbra.

242 RDN in the infarcted pig model leads to reduction of postinfarction

243 In a pivotal randomized study, 7 infarcted pigs received 300,000 CDCs/kg (approximately 1

244 tered percutaneously into the endocardium of infarcted pigs.

245 ffect of intramyocardial delivery of CSCs to infarcted porcine hearts.

246 ional computational model of the chronically infarcted rabbit ventricles to characterize the arrhythm

247 eneic CDCs survived at similar levels in the infarcted rat heart 1 week after delivery, but few synge

248 ion, and attenuate adverse remodeling in the infarcted rat heart, without deleterious immunological s

249 sis in the border and infarcted areas of the infarcted rat hearts after treatment with Ad-miR-21.

250 After delivery into infarcted rat hearts, the gel was efficiently infiltrate

251 Myocardial infarcted rats and aorto-caval fistulated rats were used

252 afted poly(disulfide amine) (ABP) polymer in infarcted rats preserves cardiac geometry and systolic f

253 Afferent inputs were attenuated from the infarcted region (19% in control vs. 7% in MI; P = 0.03)

254 d over the entire slice (P=0.038) and in the infarcted region (P=0.0086) was significantly higher in

255 increase of microvasculature density in the infarcted region (P=0.0105 versus vehicle).

256 closely related miRNAs, is regulated in the infarcted region of the heart in response to ischemia-re

257 Emc10 protein abundance was increased in the infarcted region of the left ventricle and in the circul

258 Afferent neural signals from the infarcted region to IC neurons are attenuated, while tho

259 y redistribution of myocardial work from the infarcted region to the viable tissue.

260 in part, to enhanced neoangiogenesis in the infarcted region via upregulation of the ER target gene

261 thelial growth factor receptor type 2 in the infarcted region.

262 endogenous c-Kit(+) progenitor cells to the infarcted region.

263 sion coefficient (ADC), decreases within the infarcted region.

264 own to correspond well with noninfarcted and infarcted regions as detected by delayed enhancement car

265 ntense regions with the intricate contour of infarcted regions by delayed-enhancement MRI.

266 motes cellular hypertrophy in the border and infarcted regions coupled with an upregulation of hypert

267 sity and preserved cardiomyocyte size in the infarcted regions suggesting CCs role in protective para

268 Myocardial work in infarcted regions was zero.

269 ence between contours of T2-hyperintense and infarcted regions, and the transmural-extent of these re

270 d nullified conduction delay in adjacent non-infarcted regions.

271 issue from preserved myocardial regions into infarcted regions.

272 cells of each type per heart) was tested in infarcted SCID (severe combined immunodeficiency)-Beige

273 as the correlation with number of transmural infarcted segments by delayed enhancement imaging.

274 therapy led to improved regional function of infarcted segments compared with control patients.

275 Strain recovery is impaired in infarcted segments with intramyocardial hemorrhage or mi

276 The infarcted side of the brain had marked elevation of TNF-

277 re injected into the border zone of subacute infarcted syngeneic Fischer rat hearts and compared with

278 C-flumazenil (FMZ)-PET to map SNL in the non-infarcted tissue and assess its relationship with acute-

279 xo reduce the number of CD68+ Mvarphi within infarcted tissue and modify the polarization state of Mv

280 on the makeup and the ensuing effect on the infarcted tissue during the chronic phase remain unexplo

281 e models, activated B-lymphocytes infiltrate infarcted tissue in the weeks after stroke.

282 ip between the acutely silent but eventually infarcted tissue volume and early neurological course wa

283 n out of proportion to the amount of overtly infarcted tissue, and how decreased delivery of oxygen a

284 es of both the acutely silent but eventually infarcted tissue, and the eventually non-infarcted penum

285 IK-5001 is assumed to permeate the infarcted tissue, cross-linking into a hydrogel and form

286 blood perfusion, and brain metabolism in the infarcted tissue.

287 via its conjugation to Hoechst for targeting infarcted tissue.

288 al avenue for selectively targeting drugs to infarcted tissue.

289 ranscriptional regulation pattern across the infarcted tissue.

290 ligation by mitigating adverse remodeling of infarcted tissue.

291 Compared to healthy ECM, infarcted tissues demonstrate a significant increase in

292 The uptake of radioactivity in infarcted tissues was confirmed by autoradiography and h

293 30 mg.kg(-1).day(-1)) in the supplied water (infarcted treated group, I + PY).

294 arcts and induces fibrotic remodeling of the infarcted ventricle contributing to the development of d

295 maintaining the structural integrity of the infarcted ventricle.

296 different degrees of Mfb infiltration in the infarcted ventricles determines susceptibility to arrhyt

297 Strain differentiates between infarcted versus noninfarcted myocardium, even in patien

298 Ability to discriminate infarcted versus noninfarcted segments by late gadoliniu

299 ence of small capillaries and venules in the infarcted zones by CD31 staining.

300 Myocyte apoptosis within the infarcted zones was initially greater in the Col6a1(-/-)