ライフサイエンスコーパス: infarcted myocardium

1 Smad3 regulate repair and remodeling in the infarcted myocardium.

2 rated absence of systolic wall thickening in infarcted myocardium.

3 derived by nuclear transfer cloning restore infarcted myocardium.

4 is under investigation as a means to repair infarcted myocardium.

5 Stem cells are able to regenerate infarcted myocardium.

6 canner after transplantation into normal and infarcted myocardium.

7 ved by stem cells that infiltrate normal and infarcted myocardium.

8 ion and increase their efficacy in repairing infarcted myocardium.

9 0, P<0.001) and relative extent of MO within infarcted myocardium.

10 ctly alters the mechanical properties of the infarcted myocardium.

11 significantly less than that in the core of infarcted myocardium.

12 it is important to differentiate viable from infarcted myocardium.

13 as the source of SCF immunoreactivity in the infarcted myocardium.

14 The immune system orchestrates the repair of infarcted myocardium.

15 NA occurred very early on reperfusion of the infarcted myocardium.

16 uptake and clearance kinetics in reperfused infarcted myocardium.

17 e tissue can be implanted and survive in the infarcted myocardium.

18 dothelial precursor activity in regenerating infarcted myocardium.

19 therefore be responsible for preservation of infarcted myocardium.

20 s remodeling and improves global function in infarcted myocardium.

21 eperfusion showed a significant reduction in infarcted myocardium.

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

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

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

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

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

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

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

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

30 Specific chemokines are upregulated in the infarcted myocardium.

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

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

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

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

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

36 eriologenesis and cardiomyocyte viability in infarcted myocardium.

37 represent a promising strategy for replacing infarcted myocardium.

38 itro and in vivo within sponges, wounds, and infarcted myocardium.

39 aftment of the skeletal myoblasts within the infarcted myocardium.

40 was used to delineate perfusion deficits and infarcted myocardium.

41 after the stem cells were injected into the infarcted myocardium.

42 nt mechanism for characterization of acutely infarcted myocardium.

43 ctional distribution volumes were greater in infarcted myocardium (0.90 +/- 0.05 for gadopentetate di

44 VEGF was injected into the periinfarcted and infarcted myocardium 1 hour after reperfusion.

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

46 levated 23Na image intensity was observed in infarcted myocardium (206+/-37% of remote in dogs, P<0.0

47 1(+) lineage-derived EPDC migration into the infarcted myocardium 5 days post MI, which was inhibited

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

49 In the infarcted myocardium, activation of the inflammatory cas

50 derived angioblasts for revascularization of infarcted myocardium (alone or in conjunction with curre

51 activated neutrophils, activated monocytes, infarcted myocardium and human atheromas.

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

53 CD44 expression was markedly induced in the infarcted myocardium and was localized on infiltrating l

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

55 resonance (MR) contrast agents in reperfused infarcted myocardium, and 2) investigate the effect of i

56 lls generated robust engraftments within the infarcted myocardium, and also stimulated angiogenesis,

57 ced cytokine and chemokine expression in the infarcted myocardium, and impaired phagocytosis of dead

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

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

60 A large proportion of samples from infarcted myocardium are viable at the end of the ischem

61 alize its distribution pattern in reperfused infarcted myocardium as a function of time between onset

62 MTET images clearly depicted infarcted myocardium as brighter than both the normal an

63 Allogeneic MSCs survive in infarcted myocardium as long as 6 months and express mar

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

65 Infarcted myocardium at CT demonstrated a 76.1% reductio

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

67 MI was significantly depressed, not only in infarcted myocardium but also in regions remote from the

68 and decreased neutrophil recruitment in the infarcted myocardium but showed timely repression of inf

69 poptotic cardiomyocytes surrounding areas of infarcted myocardium by terminal deoxynucleotide transfe

70 A 3-dimensional construct of the infarcted myocardium can be rendered by combined epicard

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

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

73 hat optimal TI, relative signal intensity of infarcted myocardium compared with uninfarcted myocardiu

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

75 These preliminary data suggest that infarcted myocardium could be accurately diagnosed and d

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

77 The texture of MCE from opacified but infarcted myocardium differed significantly from control

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

79 Matrix-injected infarcted myocardium exhibits an altered inflammatory re

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

81 ogous skeletal myoblast transplantation into infarcted myocardium in a variety of animal models has d

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

83 all patients and in excellent conspicuity of infarcted myocardium in all nine patients with visible i

84 cardial infarction and chemoattracted to the infarcted myocardium in an SDF-1-CXCR4-, HGF-c-Met-, and

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

86 uated whether injection of BMCs restores the infarcted myocardium in mice and whether cell fusion is

87 ected percutaneously into normal and freshly infarcted myocardium in swine.

88 expression is associated with reperfusion of infarcted myocardium in the setting of tissue necrosis,

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

90 Also, infarcted myocardium involved by extensive areas of MO d

91 From local edema, T1 relaxation time of infarcted myocardium is increased, may remain elevated f

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

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

94 t of uncoupling in stable slow conduction in infarcted myocardium, making microreentry possible.

95 tion of unselected BM cells into the acutely infarcted myocardium may induce significant intramyocard

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

97 Among 179 samples from infarcted myocardium, mean k3 after 5 minutes of reperfu

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

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

100 When locally injected in the infarcted myocardium of immunodeficient mice and immunos

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

102 y of transplanting autologous myoblasts into infarcted myocardium of patients undergoing concurrent c

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

104 e and then injected into the border zones of infarcted myocardium of rats.

105 ture contractile phenotype were found in the infarcted myocardium of the PEUU group.

106 peroxidase activity was not different in the infarcted myocardium of the treated group compared with

107 tudy (from 8.8 +/- 1.7% to 43.2 +/- 11.1% of infarcted myocardium; p < 0.05), whereas not important c

108 In the infarcted myocardium, presence of sympathetic nerves and

109 ls genetically enhanced with Akt1 can repair infarcted myocardium, prevent remodeling and nearly norm

110 , the avid binding of 99mTc-duramycin to the infarcted myocardium quickly becomes conspicuous shortly

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

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

113 ted skeletal myoblasts form viable grafts in infarcted myocardium, resulting in enhanced post-MI exer

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

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

116 alone cannot differentiate postischemic from infarcted myocardium; simultaneous data on myocardial pe

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

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

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

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

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

122 ngrafted human and rat cardiomyocytes in the infarcted myocardium up to 14 and 65 days after transpla

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

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

125 cal contractile performance was decreased in infarcted myocardium versus that in remote and adjacent

126 or angioblasts, induce neovascularization of infarcted myocardium via mechanisms involving both cell

127 improved survival and promote repair of the infarcted myocardium via paracrine signaling after trans

128 oFLASH sequence, the signal intensity of the infarcted myocardium was 1,080% +/- 214 higher than that

129 Focal and diffuse uptake of MSCs in the infarcted myocardium was already visible in SPECT/CT ima

130 f CLIO-Cy5.5 by macrophages infiltrating the infarcted myocardium was confirmed by fluorescence micro

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

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

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

134 duction in the total number of BM-MSC in the infarcted myocardium was observed after integrin beta1 b

135 nt nanoparticle CLIO-Cy5.5 by macrophages in infarcted myocardium was studied.

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

137 To visualize the perfusion deficit in the infarcted myocardium, we injected 74 MBq (2 mCi) of (99m

138 chanisms that cause monocyte localization in infarcted myocardium, we studied the impact of ischemia-

139 mediating EPC recruitment and repair to the infarcted myocardium, we used neutralizing antibody to b

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

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

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

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

144 The purpose is to materially support the infarcted myocardium while at the same time repositionin

145 mice exhibited decreased infiltration of the infarcted myocardium with neutrophils and macrophages an

146 We examined whether supplementing infarcted myocardium with skeletal myoblasts would (1) r

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

148 on between normal and acutely or chronically infarcted myocardium, with high sensitivity and specific