ライフサイエンスコーパス: ischemic myocardium

1 nsequently, fewer leukocytes migrated to the ischemic myocardium.

2 levels in cultured endothelial cells and in ischemic myocardium.

3 that is able to prevent lipotoxicity in the ischemic myocardium.

4 rated that postconditioning in dogs salvaged ischemic myocardium.

5 iated with preservation of ATP levels in the ischemic myocardium.

6 y may be combined with gene therapy to treat ischemic myocardium.

7 anisms subtend the survival capacity of this ischemic myocardium.

8 ovide a novel adjunctive approach to protect ischemic myocardium.

9 es infarct size, and increases blood flow to ischemic myocardium.

10 enhances bone marrow cell incorporation into ischemic myocardium.

11 a NOGA mapping injection catheter to target ischemic myocardium.

12 that interventions that inhibit SDH protect ischemic myocardium.

13 er-based transendocardial delivery of ABM to ischemic myocardium.

14 than systolic shortening identifies acutely ischemic myocardium.

15 potential of IPPA as a noninvasive marker of ischemic myocardium.

16 ropoietin gene to control gene expression in ischemic myocardium.

17 a result of increased A3AR signaling in the ischemic myocardium.

18 trol of angiogenic factor gene expression in ischemic myocardium.

19 ialized blood via retroperfusion to severely ischemic myocardium.

20 165 significantly improves blood flow to the ischemic myocardium.

21 TCEC in SRI closely quantifies the extent of ischemic myocardium.

22 % of neutrophil infiltration into previously ischemic myocardium.

23 lateral perfusion and myocardial function in ischemic myocardium.

24 investigated for therapeutic angiogenesis in ischemic myocardium.

25 e that phVEGF(165) GTx augments perfusion of ischemic myocardium.

26 red by AAV vector can induce angiogenesis in ischemic myocardium.

27 mportant therapeutic angiogenic responses in ischemic myocardium.

28 crophage activation, was not detected in the ischemic myocardium.

29 limited engraftment on transplantation into ischemic myocardium.

30 imits damage during the revascularization of ischemic myocardium.

31 promotes the growth of new blood vessels in ischemic myocardium.

32 ng slow conduction in normal nodal cells and ischemic myocardium.

33 zes recovery during the revascularization of ischemic myocardium.

34 trical stability independently of salvage of ischemic myocardium.

35 were the primary source of TNF-alpha in the ischemic myocardium.

36 of viability occurred during reperfusion of ischemic myocardium.

37 mote infiltration of monocytes into formerly ischemic myocardium.

38 ronary sinus, thus redistributing blood into ischemic myocardium.

39 sess the affinity of 99mTc glucarate for the ischemic myocardium.

40 180448 (2) with improved selectivity for the ischemic myocardium.

41 lecular species predominantly accumulated in ischemic myocardium.

42 igh concentrations during the reperfusion of ischemic myocardium.

43 se over fat as an oxidative substrate in the ischemic myocardium.

44 hnique for relieving angina in patients with ischemic myocardium.

45 itment and macrophage activation in the post-ischemic myocardium.

46 active oxygen species-mediated mechanisms in ischemic myocardium.

47 n [TIMI] </=2), 9% had >5% and 3.6% had >10% ischemic myocardium.

48 lium-dependent vasorelaxation in chronically ischemic myocardium.

49 the mechanical or the electrical activity of ischemic myocardium.

50 ptake of a molecularly targeted agent in the ischemic myocardium.

51 reported to demonstrate increased uptake in ischemic myocardium.

52 sis that helps preserve the functionality of ischemic myocardium.

53 Cs) promote myocardial regeneration in adult ischemic myocardium.

54 al and function after transplantation in the ischemic myocardium.

55 scularization in patients with >10% to 12.5% ischemic myocardium.

56 may promote myocardial regeneration in adult ischemic myocardium.

57 , resulting in functional improvement of the ischemic myocardium.

58 (in vitro) and recruitment (in vivo) to the ischemic myocardium.

59 tyrosine nitration was detected in the post-ischemic myocardium.

60 nalyzed quantitative MPS measures of percent ischemic myocardium.

61 cally for restoration of blood supply to the ischemic myocardium.

62 programming strategy for preservation of the ischemic myocardium.

63 echocardiographic identification of recently ischemic myocardium.

64 l progenitor cell (EPC) transplantation into ischemic myocardium.

65 ohol has a direct cardioprotective effect on ischemic myocardium.

66 raftment and migration of BM-MSCs within the ischemic myocardium.

67 mmation, inhibit thrombosis, and protect the ischemic myocardium.

68 SPAMM %S was similar to sonomicrometry %S in ischemic myocardium (2 +/- 3 vs. 0 +/- 3 p = 0.067) but

69 Capillary density in ischemic myocardium 4 weeks after transplantation was si

70 on of complement during revascularization of ischemic myocardium accentuates myocardial dysfunction.

71 diated proteolytic processing of PKCalpha in ischemic myocardium activates PKC signaling in a recepto

72 upon prompt restoration of blood flow to the ischemic myocardium after an acute myocardial infarction

73 Capillary density at the border zone of ischemic myocardium also was significantly reduced in ER

74 In conclusion, in ischemic myocardium an NO donor inhibits glucose uptake

75 channels, myocardial damage, denervation of ischemic myocardium and a placebo effect.

76 Platelets can infiltrate ischemic myocardium and are increasingly recognized as c

77 70 kDa FAD-binding protein occur in the post-ischemic myocardium and are thought to be mediated by pe

78 eponderance of unsaturated acylcarnitines in ischemic myocardium and document the metabolic compartme

79 from a coronary event have less jeopardized ischemic myocardium and fewer recurrent cardiac events t

80 orphonuclear neutrophils, accumulates within ischemic myocardium and has been linked to adverse left

81 disease to precondition and thereby salvage ischemic myocardium and improve survival.

82 related to the increased ATP content in the ischemic myocardium and increased phosphorylation of PKA

83 Prolonged TCEC consistently occurs in ischemic myocardium and is apparently not affected by th

84 response through direct actions on both the ischemic myocardium and leukocytes.

85 usion territory before microembolization and ischemic myocardium and microinfarction after microembol

86 mined the genes that were upregulated in the ischemic myocardium and might be involved in EPC recruit

87 enous vasoactive substance, is released from ischemic myocardium and regulates coronary resistance.

88 ce angiogenesis and may accelerate repair of ischemic myocardium and skeletal muscle.

89 obilization of inflammatory monocytes to the ischemic myocardium and to adverse post-ischemic cardiac

90 ect of ESC-derived exosome for the repair of ischemic myocardium and whether c-kit(+) cardiac progeni

91 BG (ie, the reestablishment of blood flow to ischemic myocardium) and obscures key mechanisms, such a

92 patients treated medically, 46 had viable or ischemic myocardium, and 62 had scar only.

93 nto cardiac cells, concentrate in normal and ischemic myocardium, and act as a cardioprotector in viv

94 endothelial function, improved perfusion to ischemic myocardium, and an early reduction in cardiovas

95 Hibernating myocardium, ischemic myocardium, and scarred myocardium were associa

96 ly demonstrated the induction of IL-6 in the ischemic myocardium, and the current study addresses the

97 ionship of cellular K(+) and lactate loss in ischemic myocardium, and the role of extracellular pH an

98 Several of these pathways in the ischemic myocardium are intricately tied with the downst

99 Coagulation disorders and reperfusion of ischemic myocardium are major causes of morbidity and mo

100 Thus A1ARs in ischemic myocardium are presumably saturated by endogeno

101 engraftment and migration of BM-MSCs in the ischemic myocardium are unknown.

102 rdial blood flow and contractile function in ischemic myocardium are well matched, and there is no ev

103 o obtain prompt and effective reperfusion of ischemic myocardium as early as possible.

104 erventions must aim to improve blood flow to ischemic myocardium as much and as quickly as possible.

105 primary end point was > or = 5% reduction in ischemic myocardium at follow-up.

106 accurately depict the left ventricular (LV) ischemic myocardium at risk (T2-weighted hyperintense re

107 ein S-glutathionylation was enhanced in post-ischemic myocardium at the NQR 51-kDa subunit, but not a

108 ose NaNO(2) improves functional responses in ischemic myocardium but has no effect on normal regions.

109 vo produced a burst of neovascularization in ischemic myocardium but was followed by drug washout and

110 uch as SDF-1, and the migration of MPCs into ischemic myocardium, but not normal myocardium.

111 growth factor B) in revascularization of the ischemic myocardium, but the associated cardiac hypertro

112 y factor (MIF) exerts a protective effect on ischemic myocardium by activating AMP-activated protein

113 cle plasmid carrying HIF1 (MC-HIF1) into the ischemic myocardium can improve the survival of transpla

114 However, restoring blood flow to the ischemic myocardium can paradoxically induce injury by i

115 We determined by genome profiling whether ischemic myocardium can trigger a genetic program promot

116 though an effective approach in rescuing the ischemic myocardium, can itself trigger several adverse

117 Reperfusion of ischemic myocardium causes cardiomyocyte apoptosis in co

118 patients with TIMI scores </=2, 6.1% had >5% ischemic myocardium compared with 19.6% of patients with

119 induced eight times and of VEGF 20 times in ischemic myocardium compared with normal myocardium afte

120 In humans, T2 relaxation time in the ischemic myocardium declines significantly from early af

121 Viable or ischemic myocardium detected at dobutamine echocardiogra

122 d by direct injection of growth factors into ischemic myocardium during open-heart surgery.

123 osine provides significant protection of the ischemic myocardium during prolonged hypothermic ischemi

124 fatty acyl chain elongation was prominent in ischemic myocardium (e.g., following 20 min of ischemia,

125 mably because effective revascularization of ischemic myocardium, even without improvement in ventric

126 of cardiac death included age, % myocardium ischemic, % myocardium fixed, early revascularization, d

127 Reperfusion is mandatory to salvage ischemic myocardium from infarction, but reperfusion per

128 donors and S-nitrosating agents protect the ischemic myocardium from infarction, but the responsible

129 hesis that IC propranolol treatment protects ischemic myocardium from myocardial damage and reduces t

130 /R), TIMP4 mRNA and protein decreased in the ischemic myocardium from wild-type mice by 1 week post-I

131 T lymphocytes decreases apoptosis within the ischemic myocardium, hampers inflammatory response, limi

132 ) is crucial for measuring how much, if any, ischemic myocardium has been salvaged.

133 However, their role in the ischemic myocardium has not been well investigated.

134 cerevisiae to screen cDNA libraries from rat ischemic myocardium, human heart, and a prostate leiomyo

135 schemic cardiomyopathy, hibernating, but not ischemic, myocardium identifies which patients may accru

136 ow-derived macrophages and injected into the ischemic myocardium immediately following myocardial inf

137 The construct was then implanted onto ischemic myocardium in a rat model of acute myocardial i

138 D1 related to neutrophil infiltration in the ischemic myocardium in an infarct size-independent manne

139 macologic) have been reported to protect the ischemic myocardium in experimental animals; however, wi

140 arction, TREM-1 expression is upregulated in ischemic myocardium in mice and humans.

141 uction in number of neutrophils infiltrating ischemic myocardium in mice that were treated with rhADA

142 uclear cell (ABMMNC) injection into areas of ischemic myocardium in patients with end-stage ischemic

143 plications of these drugs for protecting the ischemic myocardium in patients.

144 be a novel approach to the protection of the ischemic myocardium in patients.

145 m involving hepatic cell mobilization to the ischemic myocardium in response to experimental myocardi

146 ater recruitment of bone marrow cells to the ischemic myocardium in the double-knockdown group.

147 getic profile, function, and recovery of the ischemic myocardium in the isolated blood-perfused rat h

148 occlusion, and after direct exposure of the ischemic myocardium in the presence of fixed occlusion t

149 n vitro and reduced their recruitment to the ischemic myocardium in vivo by 95%.

150 reduces macrophage infiltration to the post-ischemic myocardium in vivo.

151 c reticulum Ca2+ release channel activity in ischemic myocardium include an altered Ca2+ sensitivity

152 the protective effects of carvedilol on the ischemic myocardium include inhibition of apoptosis of c

153 ined regional low-flow ischemia in vivo, the ischemic myocardium increases its utilization of exogeno

154 nalysis of molecular mechanisms by which the ischemic myocardium initiates repair and remodeling indi

155 The selectivity for the ischemic myocardium is achieved by reduction of vasorela

156 Reperfusion of the ischemic myocardium is associated with a dramatic inflam

157 Ischemic myocardium is characterized by increased relian

158 ce of myocyte necrosis during reperfusion of ischemic myocardium is controversial.

159 tial for successful recovery, reperfusion of ischemic myocardium is inevitably associated with reperf

160 Echocardiographic identification of recently ischemic myocardium is possible using ultrasound contras

161 pecies (ROS) production after reperfusion of ischemic myocardium is sufficient to induce cell death.

162 Here, we show that ischemic myocardium is targeted, potentially opening a n

163 ion is essential in restoring circulation to ischemic myocardium, it also leads to irreversible event

164 Reperfusion of ischemic myocardium leads to a local burst of free radic

165 The timely reperfusion of ischemic myocardium limits infarction, but components of

166 oncerning the effect of high glycogen on the ischemic myocardium may thus be due to differences in th

167 When isolated from ischemic myocardium, mitochondria demonstrate increased

168 ery bypass grafting lies in the viability of ischemic myocardium, nuclear medicine studies and stress

169 e partially or completely eliminated in post-ischemic myocardium obtained from in vivo regional I/R h

170 man CD34- MNCs, or PBS was transplanted into ischemic myocardium of nude rats 10 minutes after ligati

171 l cell nuclei), but not significantly in the ischemic myocardium of parabiotic mice with hepatectomy

172 xpression of enhanced YFP, were found in the ischemic myocardium of parabiotic mice with intact liver

173 cells derived from transplanted cells in the ischemic myocardium of the hiMNC group.

174 naling and cyclooxygenase-2 increased in the ischemic myocardium of ticagrelor- versus clopidogrel-tr

175 er that provides metabolic protection to the ischemic myocardium, on the rise in [K+]e recorded by K-

176 denoviral vector encoding the VEGF gene into ischemic myocardium or limb can induce collateral blood

177 Prompt reperfusion of ischemic myocardium or myocardium that is in the process

178 improvements of function and/or perfusion of ischemic myocardium or skeletal muscle.

179 are due primarily to initial countershock of ischemic myocardium or to resultant postdefibrillation r

180 ignificantly reduced PMN accumulation in the ischemic myocardium (P<0.01).

181 lear-encoded genes that were up-regulated in ischemic myocardium participate in survival mechanisms (

182 but have significant amounts of viable, yet ischemic, myocardium, placing them at high risk for futu

183 , which are recruited in high numbers to the ischemic myocardium, promote these arrhythmias.

184 ion of miR-377 knockdown hCD34(+) cells into ischemic myocardium promoted their angiogenic ability, a

185 Exosome-mediated delivery of Shh to ischemic myocardium represents a major mechanism explain

186 Injection of apelin into the ischemic myocardium resulted in accelerated and increase

187 arrow-derived macrophages, injected into the ischemic myocardium, retained their anti-inflammatory ph

188 The transplantation of MITO cells to the ischemic myocardium showed a stronger transplantation ef

189 They activate the PKG/PLN pathway in the ischemic myocardium, suggesting that the combination of

190 On 24-h CMR, ischemic myocardium T2 times returned to normal values (

191 Thereafter, ischemic myocardium-T2 times in CMR performed on days 4

192 ver 20- and 4000-fold more selective for the ischemic myocardium than 2 and cromakalim (1), respectiv

193 rate was greater in patients with viable or ischemic myocardium than those with scar (43% vs. 8%, p

194 determine the effect of high glycogen on the ischemic myocardium, the glycogen content of Langendorff

195 In the ischemic myocardium, the MSC(HO-1) group had greater exp

196 that bone marrow stem cells (BMSCs) protect ischemic myocardium through paracrine effects that can b

197 ac function after their transplantation into ischemic myocardium through paracrine secretion of growt

198 faction and may impair the responsiveness of ischemic myocardium to proangiogenic factors.

199 rated backscatter (IBS), which is reduced in ischemic myocardium, to predict an occluded infarct-rela

200 which was administered as 6 injections into ischemic myocardium (total, 6.0 mL), or placebo (mock pr

201 Reperfusion of the ischemic myocardium triggers a complex inflammatory resp

202 In this pig model, moderately ischemic myocardium undergoes metabolic and structural a

203 s have shown improvement in perfusion of the ischemic myocardium using genes encoding angiogenic grow

204 F (phVEGF165) was injected directly into the ischemic myocardium via a mini left anterior thoracotomy

205 protein that mediates AMPK activation in the ischemic myocardium via an interaction with AMPK upstrea

206 contains subcellular organelles) within the ischemic myocardium was associated with a >135% increase

207 The area of ischemic myocardium was consequently reduced from 6.45+/

208 Mast cell degranulation in the ischemic myocardium was documented by demonstration of a

209 Percent ischemic myocardium was estimated from a 17-segment mode

210 Image contrast between normal and ischemic myocardium was excellent.

211 signal intensity index threshold to identify ischemic myocardium was first determined in a derivation

212 regression model, the presence of viable or ischemic myocardium was found to predict subsequent even

213 At follow-up, the reduction in ischemic myocardium was greater with PCI+OMT (-2.7%; 95%

214 7 weeks, cardiac function was measured, and ischemic myocardium was harvested for analysis of perfus

215 ctron transfer activity (ETA) of SQR in post-ischemic myocardium was significantly decreased by 41.5

216 In ischemic myocardium, we observed that tissue-resident ma

217 dification of the 70-kDa protein in the post-ischemic myocardium, we used the identified S-glutathion

218 ial BOLD responses (MBRs) between normal and ischemic myocardium were compared with mixed model analy

219 m aluminum garnet LMR to areas of viable but ischemic myocardium were followed clinically and underwe

220 Foci of ischemic myocardium were identified on LV EMM by preserv

221 intensity (SI) increase (PSIC) in remote and ischemic myocardium were made with repeated measurements

222 The functions of these vectors in ischemic myocardium were tested by injecting them into n

223 D34+ stem cells induce neovascularization in ischemic myocardium, which enhances perfusion and functi

224 Ischemic myocardium with reduced active force will lengt

225 terstitial edema early on reperfusion in the ischemic myocardium, with maximal content of neutrophils

226 echano-arrhythmogenesis has been reported in ischemic myocardium, with unclear underlying mechanisms.

227 itative techniques allowed identification of ischemic myocardium within 15 minutes of tracer administ

228 trium localized preferentially in previously ischemic myocardium within the first hour after reperfus

229 tors is an effective means of protecting the ischemic myocardium without hemodynamic changes.

230 r can be successfully achieved in normal and ischemic myocardium without significant morbidity or mor