ライフサイエンスコーパス: myocardial infarct

1 were the predominant source of IL-10 in the myocardial infarct.

2 d by Marlex mesh placed over the anticipated myocardial infarct.

3 d in myocytes in the viable border zone of a myocardial infarct.

4 te goal of regenerating heart tissue after a myocardial infarct.

5 fibrosis and vascular maturation in healing myocardial infarcts.

6 ed growth factor (PDGF) signaling in healing myocardial infarcts.

7 liability and accuracy in the measurement of myocardial infarcts.

8 is the main cause of coronary thrombosis and myocardial infarcts.

9 rates of arrhythmias in patients with healed myocardial infarcts.

10 nutes in persistently occluded or reperfused myocardial infarcts.

11 T were performed in six patients with healed myocardial infarcts.

12 lly provide new contractile tissue to repair myocardial infarcts.

13 Otherwise, myocarditis would commonly follow myocardial infarcts.

14 the beneficial effects of hMSCs in mice with myocardial infarcts.

15 ey after intravenous infusion into mice with myocardial infarcts.

16 ng leptin levels by 38%, resulted in smaller myocardial infarcts (27% reduction), and improved recove

17 ed circulating leptin levels by 41%, smaller myocardial infarcts (29% reduction), and greater recover

18 imary prevention trials include the European Myocardial Infarct Amiodarone Trial (EMIAT) and the Cana

19 ested a prospective hypothesis that European Myocardial Infarct Amiodarone Trial (EMIAT) patients wit

20 The European Myocardial Infarct Amiodarone Trial (EMIAT) was a random

21 ntrast-enhanced MR imaging for assessment of myocardial infarct and (b). cine MR imaging for assessme

22 eling during pathological conditions such as myocardial infarct and hypertension.

23 ugh its receptor ST2 protects the heart from myocardial infarct and hypertrophy in animal models but,

24 had great promise for treating ischemia for myocardial infarct and stroke, however clinical developm

25 many devastating clinical conditions such as myocardial infarct and stroke.

26 (18)F-FDG PET/MR scans of a canine model of myocardial infarct and was demonstrated in a human subje

27 ed cardiomyocytes to partially remuscularize myocardial infarcts and attenuate heart failure encourag

28 r CD36 is required for early phagocytosis of myocardial infarcts and induction of Nr4a1-dependent mec

29 wth factor (TGF-beta), is induced in healing myocardial infarcts and plays a role in suppressing the

30 er/cardiovascular diseases, type 2 diabetes, myocardial infarct, and atherosclerosis, respectively.

31 occlusive proximal coronary artery disease, myocardial infarcts, and early mortality.

32 ients (two left ventricular hypertrophy, two myocardial infarcts, and one without confirmed pathology

33 The mechanical properties of healing myocardial infarcts are an important determinant of LV f

34 Myocardial infarcts are routinely detected by nuclear im

35 SPECT and CMR detect transmural myocardial infarcts at similar rates.

36 to CA-125; the patient died as a result of a myocardial infarct before evidence of clinical progressi

37 served in the central necrotic zone of acute myocardial infarcts, but not in myocardium remote from t

38 Attempts to repair myocardial infarcts by transplanting cardiomyocytes or s

39 ith MRI, the complexity and heterogeneity of myocardial infarcts can be demonstrated.

40 determine whether the epicardial extent of a myocardial infarct could be defined during sinus rhythm.

41 To treat cardiac injuries created by myocardial infarcts, current approaches seek to add cell

42 We report that, in the presence of an acute myocardial infarct, cytokine-mediated translocation of B

43 ension was associated with increased risk of myocardial infarct death (HR, 2.15 [95% CI, 1.35-3.41]),

44 ial infarcts (HR, 1.75 [95% CI, 1.40-2.19]), myocardial infarct death (HR, 3.00 [95% CI, 1.98-4.55]),

45 eral of the agents to slow conduction in the myocardial infarcted dog hearts.

46 Human CDCs injected into the border zone of myocardial infarcts engrafted and migrated into the infa

47 In depolarized myocardial infarct epicardial border zones, the cardiac

48 In depolarized myocardial infarct epicardial border zones, the cardiac

49 o swine model (10 healthy and 5 with chronic myocardial infarct) for ventricular PFA, collecting intr

50 dult mongrel dogs (30-40 kg, 15 normal and 7 myocardial infarct group) were studied.

51 properties of collagen structure in healing myocardial infarcts have been characterized previously,

52 Myocardial infarcts heal by scar formation because there

53 Myocardial infarcts heal by scarring because myocardium

54 o examine whether MCP-1 critically regulates myocardial infarct healing, we studied the effects of MC

55 ogenesis, tumor progression, metastasis, and myocardial infarct healing.

56 eceptor blockers and aldosterone in the post-myocardial infarct heart failure patient.

57 In the present study, we quantify myocardial infarct heterogeneity by contrast-enhanced MR

58 eart disease (HR, 1.44 [95% CI, 1.24-1.68]), myocardial infarcts (HR, 1.75 [95% CI, 1.40-2.19]), myoc

59 us, redo, diabetes, ejection fraction, prior myocardial infarct, hyperlipidemia, or creatinine level.

60 were injected into the border zone of acute myocardial infarcts in immunodeficient mice.

61 f FASTSPECT imaging for measurement of acute myocardial infarcts in rat hearts.

62 e search terms "smoking ban" and "heart" or "myocardial infarct." Investigators supplied additional d

63 Ventricular tachycardia associated with myocardial infarct is a prominent cause of cardiac arres

64 es (MMP) and MMP inhibitors (TIMPs) within a myocardial infarct (MI) contributes to left ventricular

65 In our studies, we induced myocardial infarct (MI) in the immunocompromised NOD-SCI

66 utaneous coronary intervention (PCI) affects myocardial infarct (MI) size and left ventricular remode

67 of major adverse cardiovascular events than myocardial infarct (MI) size.

68 y may reduce ischemia-reperfusion injury and myocardial infarct (MI) size.

69 nregulation and reduce arrhythmia risk after myocardial infarct (MI).

70 s in approximately 12-week sham-operated and myocardial infarcted (MI) rats.

71 3 developed type 2 diabetes, and 15 suffered myocardial infarcts (MIs).

72 transplants exhibit long-term survival in a myocardial infarct model and contribute to long-term imp

73 farct size and improved function in a murine myocardial infarct model compared with WT-MSCs.

74 he potential to allow visualization of acute myocardial infarcts, MVO zones, and patchy microinfarcts

75 ys; the diagnoses in the other patients were myocardial infarct (n = 2), septicemia (n = 2), adult re

76 d resolved more slowly than those of typical myocardial infarct necrosis in nonimmunosuppressed patie

77 poxic episodes such as those associated with myocardial infarcts, obstructive sleep apneas, apneas of

78 Three had a recent myocardial infarct of an age less than the duration of u

79 id not affect exocytosis and inflammation in myocardial infarcts of eNOS knockout mice.

80 or MINOCA revealed the presence of a typical myocardial infarct on cardiac magnetic resonance imaging

81 were considered equivocal for assessment of myocardial infarct on the basis of fixed perfusion defec

82 major perioperative morbidity--specifically, myocardial infarct, perioperative hemorrhage, or portal

83 n three patients with no clinical history of myocardial infarct prior to imaging.

84 uced by approximately 30%, and the volume of myocardial infarcts produced by occlusion of the left an

85 In the myocardial infarct, R2* value increased from 41.0+/-12.0

86 Myocardial infarcted rats and aorto-caval fistulated rat

87 hu) mice, as well as the TREM2 signal in the myocardial infarct region.

88 To determine the role of FGF2 in myocardial infarct repair, we studied the evolution of l

89 etal muscle-derived myoendothelial cells for myocardial infarct repair.

90 ajor adverse cardiac event (MACE), such as a myocardial infarct, revascularization, cardiac death, or

91 ulated in atherosclerotic plaques and at the myocardial infarct site.

92 tion of these induced endothelial cells into myocardial infarct sites after injury results in improve

93 -43%) in cardiomyocytes in vitro and reduced myocardial infarct size (-63%) after ischemia/reperfusio

94 ischemia, demonstrated significantly reduced myocardial infarct size (22.8+/-3.1%, mean+/-SEM) as com

95 ients demonstrated a 38% reduction in median myocardial infarct size (25th and 75th percentile) compa

96 rfusion and produced a profound reduction in myocardial infarct size (expressed as a percent of the a

97 ted whether PiCSO therapy can further reduce myocardial infarct size (IS) in patients undergoing pPCI

98 Myocardial infarct size (IS) was determined by tetrazoli

99 olysis in vitro, while in vivo, they reduced myocardial infarct size (IS).

100 IS, 28.5 +/- 4%) displayed a 54% decrease in myocardial infarct size (P < .001).

101 oning) proved highly efficacious in reducing myocardial infarct size (relative reduction, 86%, 39%, a

102 rs were independently associated with larger myocardial infarct size (total KBs, per 100 umol/L: B =

103 o ischemia-reperfusion significantly reduced myocardial infarct size after 20 min ischemia and 30 min

104 We also implicate Caspase3 in determining myocardial infarct size after ischemia-reperfusion injur

105 tl1 to mice resulted in a 66.0% reduction in myocardial infarct size after ischemia/reperfusion injur

106 ere reperfused and sacrificed 24 h later for myocardial infarct size analysis and cardiac tissue samp

107 Myocardial infarct size and apoptosis, production of per

108 veloped pressure and aortic flow and reduced myocardial infarct size and apoptotic cell death with lo

109 eatment with ACE inhibitors or ARBs on acute myocardial infarct size and arrhythmias are unknown.

110 pretreatment with captopril and losartan on myocardial infarct size and arrhythmias in a rat model o

111 tischemic ventricular dysfunction, increased myocardial infarct size and cardiomyocyte apoptosis comp

112 was to quantitate the relation between final myocardial infarct size and duration of symptoms before

113 Likewise, CTRP9-KO mice showed increased myocardial infarct size and elevated expression of infla

114 in 2 days, an effect associated with reduced myocardial infarct size and improved heart function.

115 bitor tyrphostin AG490 showed a reduction in myocardial infarct size and in number of cardiomyocytes

116 ppressed efferocytosis preceded increases in myocardial infarct size and led to delayed inflammation

117 Myocardial infarct size and left ventricular ejection fr

118 emonstrate for the first time in humans that myocardial infarct size and left ventricular function af

119 Unexpectedly, myocardial infarct size and neutrophil infiltration/acti

120 erebral infarct volume and edema, as well as myocardial infarct size and no-reflow in rat models of i

121 compare the effects of early and late PC on myocardial infarct size and postischemic dysfunction in

122 neutrophil adhesion protein CD18 could limit myocardial infarct size and preserve left ventricular fu

123 ion, the most effective therapy for reducing myocardial infarct size and preserving left ventricular

124 New approaches to limit myocardial infarct size and reduce progression to heart

125 ations into the effects of chronic uremia on myocardial infarct size and the protective effects of is

126 elays within this early time period on final myocardial infarct size are unknown.

127 The primary end point was myocardial infarct size as assessed by cardiac enzymes,

128 Primary endpoint was myocardial infarct size as assessed by cardiac magnetic

129 ardial injury and was associated with larger myocardial infarct size assessed at 6 months.

130 ocardial infarction, cardiac arrhythmia, and myocardial infarct size assessed by cardiac magnetic res

131 irus expressing miR-21 (Ad-miR-21) decreased myocardial infarct size by 29% at 24 h and decreased the

132 tosis by 48%, lipid peroxidation by 39%, and myocardial infarct size by 45%, and improved left ventri

133 myocardial ischemia/reperfusion, attenuated myocardial infarct size by 47%, and preserved left ventr

134 Simvastatin treatment attenuated myocardial infarct size by 58% in wild-type but not eNOS

135 In phase II, IB-MECA reduced myocardial infarct size by 61%; infarct size (tetrazoliu

136 e past 3 years that have attempted to reduce myocardial infarct size by administration of adjunctive

137 Limitation of myocardial infarct size by an earlier brief complete occ

138 led ischemic postconditioning (IPoC), reduce myocardial infarct size by approximately 40% in animal m

139 antibody given before reperfusion can limit myocardial infarct size by nearly 50% and preserve globa

140 Reduction of myocardial infarct size by remote ischemic preconditioni

141 We have shown that myocardial infarct size can be reduced by topical coolin

142 as to investigate the effects of DMI-4983 on myocardial infarct size caused by regional ischemia and

143 CPA; 100 microgram/kg) significantly reduced myocardial infarct size compared with control animals, a

144 striction without muscle stimulation reduced myocardial infarct size considerably.

145 Myocardial infarct size following 60 minutes coronary ar

146 decreased vascular inflammation and reduced myocardial infarct size following ischemia and reperfusi

147 histone deacetylase inhibitor, SAHA, reduces myocardial infarct size in a large animal model, even wh

148 adolescent period and male gender increased myocardial infarct size in a young rat model of ischemia

149 Inhibition of leukocyte adhesion can reduce myocardial infarct size in animals.

150 itional studies, rosuvastatin did not affect myocardial infarct size in eNOS-deficient mice compared

151 h mitochondrial division inhibitor-1 reduced myocardial infarct size in mice subject to coronary arte

152 nhibition of PYK2 activation by Na2S reduced myocardial infarct size in mice.

153 ecovery of cardiac function and reduction in myocardial infarct size in mouse heart response to I/R i

154 applied to the arm has been shown to reduce myocardial infarct size in patients with ST-elevation my

155 best compounds (11f) is also shown to reduce myocardial infarct size in rat.

156 14643) also cause a substantial reduction of myocardial infarct size in the rat.

157 2 and PGA1) cause a substantial reduction of myocardial infarct size in the rat.

158 e accurate means of noninvasively estimating myocardial infarct size in this canine model than two-di

159 endothelial cell adhesion molecules decrease myocardial infarct size in vivo.

160 tabolic fuel substrate utilisation increased myocardial infarct size in wild-type (WT), but not SIRT3

161 increases plasma IL-10 levels and decreases myocardial infarct size in wild-type mice but not in lit

162 Myocardial infarct size is a major determinant of left v

163 Myocardial infarct size is a major determinant of progno

164 Myocardial infarct size is a major determinant of progno

165 nversion time (TI) and their interactions on myocardial infarct size measurements to establish the fo

166 Our study assesses the effect on myocardial infarct size of preconditioning at a distance

167 months, the oxygen group had an increase in myocardial infarct size on cardiac magnetic resonance (n

168 oes not substantially or consistently reduce myocardial infarct size or neutrophil accumulation in do

169 erapy resulted in a significant reduction in myocardial infarct size per area at risk compared with s

170 ngioplasty, it has become possible to reduce myocardial infarct size through early reperfusion.

171 Myocardial infarct size was also reduced in FGF2 Tg hear

172 Myocardial infarct size was determined by triphenyltetra

173 Myocardial infarct size was increased in uremic animals,

174 Myocardial infarct size was increased, and coronary flow

175 Myocardial infarct size was measured through triphenylte

176 No difference of myocardial infarct size was observed between groups.

177 myocardial ischemia and 72 h of reperfusion, myocardial infarct size was reduced by 42% in the transg

178 Myocardial infarct size was reduced significantly, from

179 trin2 KO mice were subjected to in vivo I/R, myocardial infarct size was significantly greater in Ses

180 iac function was significantly improved, and myocardial infarct size was significantly reduced after

181 Myocardial infarct size was significantly smaller in gro

182 Myocardial infarct size was similar between study groups

183 owed that adjunctive therapy further reduced myocardial infarct size when coupled with reperfusion.

184 ontinued interest in the concept of limiting myocardial infarct size with adjunctive agents administe

185 al tissue, mitigating redox stress, reducing myocardial infarct size, and preserving high-energy phos

186 n of the VEGFR2/VE-cadherin complex, reduced myocardial infarct size, and the extent of no-reflow in

187 Acute myocardial infarct size, extent of microvascular obstruc

188 r-to-balloon time, leading to a reduction in myocardial infarct size, hospital length of stay, and to

189 ent and severity of myocardial injury (i.e., myocardial infarct size, ischemic risk zone, and no-refl

190 accurately quantify myocardial injury sizes: myocardial infarct size, ischemic risk zone, and no-refl

191 eficient (APN-KO) mice resulted in increased myocardial infarct size, myocardial apoptosis and tumor

192 ltrasound targeted hs-MB destruction limited myocardial infarct size, preserved left ventricular func

193 one reductase gene (GSNOR(-/-)) have reduced myocardial infarct size, preserved ventricular systolic

194 the result of which is a marked reduction in myocardial infarct size, severity of stunning, or incide

195 de sustained ischemia lead to a reduction in myocardial infarct size.

196 terventions have been investigated to reduce myocardial infarct size.

197 R injury in humans, and reduces experimental myocardial infarct size.

198 episodes of VT and VF, as well as decreased myocardial infarct size.

199 peptide resulted in significant reduction of myocardial infarct size.

200 e as an adjunct to thrombolysis would reduce myocardial infarct size.

201 are predictors of ST-segment resolution and myocardial infarct size.

202 may attenuate reperfusion injury and reduce myocardial infarct size.

203 ioning may be useful means by which to limit myocardial infarct size.

204 tion, reactive oxygen species formation, and myocardial infarct size.

205 to increase plasma IL-10 levels and decrease myocardial infarct size.

206 rates that a probiotic supplement can reduce myocardial infarct size.

207 cNAc levels in vivo was sufficient to reduce myocardial infarct size.

208 Both myocardial infarct size/area at risk and O2(-) productio

209 Unexpectedly, however, the myocardial infarct size/area at risk was greater, despit

210 Myocardial infarct size/area at risk was reduced by 51.2

211 itric oxide synthase (iNOS) markedly reduces myocardial infarct size; this effect is associated with

212 hrombolytic therapy and who had thallium-201 myocardial infarct-size measurements performed several w

213 mia reperfusion injury (IRI) associated with myocardial infarct, stroke, and several other clinical c

214 wth factor (phVEGF165) in the border zone of myocardial infarct tissue in rat hearts were investigate

215 (99m)Tc-Glucarate marks acute myocardial infarct very early after occlusion and appear

216 One animal with a myocardial infarct was analyzed separately.

217 Myocardial infarct was induced by balloon occlusion of t

218 ogical conditions, extensive regeneration of myocardial infarcts was reported recently after direct s

219 Canine myocardial infarcts were created by coronary ligation.

220 Myocardial infarcts were created in Yorkshire pigs (n=6)

221 Fischer rats with one-week-old myocardial infarcts were injected with collagen or salin

222 ceptor (IGF-1R) in the stressed cells, large myocardial infarcts were produced in Fischer 344 rats at

223 iffusing capacity, and one patient died of a myocardial infarct while improving on therapy.

224 sustained VTs from six patients with healed myocardial infarcts who were undergoing arrhythmia surge

225 Noninvasive imaging of myocardial infarcts with 99mTc glucarate is possible wit