ライフサイエンスコーパス: infarct

1 hyperintensities and small- and large-vessel infarcts).

2 d large cortical and non-lacunar subcortical infarcts).

3 y, metachromatic leukodystrophy and subacute infarct.

4 bed alignment of myofibroblast arrays in the infarct.

5 se-2 in ipsilateral cortex remote from clots/infarcts.

6 ute ischaemia and high sensitivity for small infarcts.

7 fractive error shifts, and nerve fiber layer infarcts.

8 .01), a high likelihood of adjacent cortical infarcts (5/7 versus 2/10, P < 0.06), and upregulation o

9 Of the 153 patients, 145 had prior infarct, 8 had hypertensive brain hemorrhage, and 164 ad

10 and randomisation, had brainstem or lacunar infarct, a substantial comorbid disease, an inability to

11 th an increased risk of incident subcortical infarcts (adjusted risk ratio, 2.54; 95% CI, 1.76-3.68)

12 cumulates within the thalamus ipsilateral to infarct after a delay with a focal distribution that is

13 global (LV ejection fraction) and regional (infarct and border zone) function.

14 und in cells that were mainly located in the infarct and border zones.

15 PET/MR scans of a canine model of myocardial infarct and was demonstrated in a human subject.

16 thalamus ipsilateral versus contralateral to infarct and we focused on the 95th percentile of R2* as

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

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

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

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

21 ges, thereby increasing PET signal in murine infarcts and both mouse and rabbit atherosclerotic plaqu

22 equired for early phagocytosis of myocardial infarcts and induction of Nr4a1-dependent mechanisms of

23 somal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a neurolog

24 frontal infarcts only and those with frontal infarcts and/or intracerebral haemorrhage were both sign

25 l MRI at 24 hours assessed the growth of the infarct, and the modified Rankin Scale (mRS) assessed fu

26 on and adverse remodeling in mice with large infarcts, and in ischemic cardiomyopathy, they improve L

27 se pathology or larger infarcts (ie, lacunar infarcts, and large cortical and non-lacunar subcortical

28 Early cortical infarcts are common in poor-grade patients after aneurys

29 n Cx43 (Connexin 43) was reduced in the peri-infarct area of wild-type compared with Mpo(-/-) mice.

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

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

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

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

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

35 was detected when moving from healthy toward infarcted area.

36 rganization of the collagenous matrix in the infarcted area.

37 sponse and infiltration of leukocytes to the infarcted area.

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

39 cularization group and in 10 patients in the infarct-artery-only group (1.4% vs. 1.7%) (hazard ratio,

40 ularization group and in 121 patients in the infarct-artery-only group that did not receive complete

41 lar pathologies (i.e. macro- and microscopic infarcts, atherosclerosis, arteriolar sclerosis, and cer

42 echanical conditions similar to those of the infarct border region; 2) direct stretch of CFBs mimicki

43 After MI, however, capillarization of the infarct border zone was impaired in KO mice, and the ani

44 g FVB/N mice with recombinant Emc10 enhanced infarct border-zone capillarization and exerted a sustai

45 Incident subcortical infarcts, cerebral microbleeds, and progression of white

46 red with those with normal BMI, amid similar infarct characteristics.

47 ectomy patients had a smaller median 24-hour infarct core of 17.3ml (IQR, 11.3-32.8) versus 24.3ml (I

48 blood flow (CBF) leads to cell death in the infarct core, but tissue surrounding the core has the po

49 pretreatment NIHSS score, target occlusion, infarct core, pretreatment alteplase), and the collatera

50 y (P < 0.01) and expression of GAP43 in peri-infarct cortex (P < 0.05).

51 d number of new cortical neurons in the peri-infarct cortex 65d after the insult.

52 corticospinal axons originating in the peri-infarct cortex.

53 axonal sprouting and plasticity, in the peri-infarct cortex.

54 In these areas, detrimental peri-infarct depolarizations (PIDs) contribute to secondary i

55 emic effects of haemorrhage as mechanisms of infarct development.

56 a requisite mechanism and clinical marker of infarct development.

57 n the Fazekas scale, embolic stroke pattern, infarct distribution and pertinent interaction terms, AF

58 , including regional myocardial dysfunction, infarct distribution, infarct size, myocardium at risk,

59 mic cores who remain at risk for significant infarct expansion and thus could still benefit from repe

60 nfarction (STEMI) victims remain at risk for infarct expansion, heart failure, reinfarction, repeat r

61 this study was to establish the origin(s) of infarct fibroblasts using lineage tracing and bone marro

62 study demonstrated that the vast majority of infarct fibroblasts were of epicardial origin and not de

63 so had more diabetes, dyslipidemia, smoking, infarcts from small-vessel disease, and "other definite"

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

65 95% CI 1.033-3.945], p = 0.040), and reduced infarct growth (p = 0.002).

66 polarizations (PIDs) contribute to secondary infarct growth and negatively affect stroke outcome.

67 included rates of vessel recanalization and infarct growth at 24 hours and occurrence of large paren

68 Infarct growth was explored in a similarly adjusted mult

69 up to 9 h after stroke onset did not reduce infarct growth.

70 fraction occurred in control mice with large infarcts (>/=25% LV).

71 umor progression, metastasis, and myocardial infarct healing.

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

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

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

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

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

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

78 decrease aberrant remodeling and fibrosis in infarcted heart tissue.

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

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

81 lation in vitro and transplantation into the infarcted heart.

82 nd ameliorated the cardiac phenotypes of the infarcted heart.

83 serve in regenerative medicine to repair the infarcted heart.

84 ident cardiac fibroblasts into iCMs in mouse infarct hearts.

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

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

87 5 leukocytes isolated from infarcted and non-infarcted hearts showed that MI provokes activation of a

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

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

90 ically indicate acute or hyperacute ischemic infarcts; however, they can also be due to hypercellular

91 ngles (NFTs), hippocampal sclerosis, lacunar infarcts, hyaline atherosclerosis, siderocalcinosis, and

92 t of Alzheimer's disease pathology or larger infarcts (ie, lacunar infarcts, and large cortical and n

93 The 6M-ME-ECTs implanted onto 1 week post-infarct immune tolerant rat hearts engrafted, displayed

94 bout post-stroke neurogenesis after cortical infarcts, important for the pharmacological modulation o

95 ng in the epicardium in suppressing the post-infarct inflammatory response through recruitment of Tre

96 To tackle this issue, 172 patients with an infarct initially sparing the thalamus were prospectivel

97 e.Thalamic alterations have been observed in infarcts initially sparing the thalamus but interrupting

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

99 ce suggested that activated DCs migrate from infarcts into pericardial AT via CCR7.

100 al nucleus was significantly associated with infarcts involving anterior areas (frontal P = 0.05, tem

101 ar nucleus was significantly associated with infarcts involving posterior areas (parietal P = 0.046,

102 capillary cerebral amyloid angiopathy, large infarcts, lacunar infarcts, microhaemorrhage, larger hae

103 r acute stroke, multiparous mice had smaller infarcts, less glial activation, and less behavioral imp

104 Alzheimer's disease pathology, macroscopic infarcts, Lewy bodies, TDP-43 pathology, and hippocampal

105 t interactions, fully abrogated metoprolol's infarct-limiting effects.

106 ution that is strongly linked to the initial infarct location (in relation with the pattern of connec

107 roup) were compared according to the initial infarct location in simple and multiple regression analy

108 fic thalamic nuclei depending on the initial infarct location; and (ii) such secondary alterations ca

109 s increased in 90% of patients with punctate infarcts (<1.5 mL) and in all patients admitted within t

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

111 Infarcted mice also had larger pericardial clusters and

112 myocardial cell administration in normal and infarcted mice.

113 In the noninfarcted region adjacent to the infarct, MICHF demonstrated substantially reduced work b

114 amyloid angiopathy, large infarcts, lacunar infarcts, microhaemorrhage, larger haemorrhage, fibrinoi

115 gion between head and forelimb areas of peri-infarct motor cortex.

116 raining at the ultrastructural level in peri-infarct motor cortex.

117 0 stimulated endothelial cell outgrowth from infarcted mouse heart explants via p38 MAPK-MK2.

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

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

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

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

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

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

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

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

126 In the infarcted myocardium, presence of sympathetic nerves and

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

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

129 Smad3 regulate repair and remodeling in the infarcted myocardium.

130 ast, alpha-smooth muscle actin expression by infarct myofibroblasts was not affected by Smad3 loss.

131 litates leukocyte infiltration and activates infarct myofibroblasts.

132 Patients with frontal infarcts only and those with frontal infarcts and/or int

133 heart function when delivered at the time of infarct or after ischaemic heart failure following myoca

134 maging showing a chronic stroke but no acute infarct or hemorrhage, no evidence of transient ischemic

135 1.4, 95% CI = 1.1-1.9), multiple old lacunar infarcts (OR = 1.9, 95% CI = 1.5-2.5), and moderate (OR

136 had a mismatch between clinical deficit and infarct, outcomes for disability at 90 days were better

137 escribed the relationship between strain and infarct pathologies, (2) assessed the relationship betwe

138 nships between left ventricular (LV) strain, infarct pathologies, and their associations with prognos

139 ered after the ischemic insult reduced brain infarct percentage and neurological deficit scores in C5

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

141 y CT Score [ASPECTS] >/=6) often demonstrate infarct progression significant enough to make them inel

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

143 mimicking the mechanical environment of the infarct region induces a synthetic phenotype with elevat

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

145 p62 indicated an impaired mitophagy in peri-infarct regions of LV in T2DM mice compared with control

146 rdiomyocytes and cardiac macrophages in peri-infarct regions of LV in T2DM mice.

147 of percutaneous coronary intervention in non-infarct-related arteries in patients with ST-segment ele

148 FFR-guided complete revascularization of non-infarct-related arteries in the acute setting resulted i

149 reperfusion immediately after opening of the infarct-related artery and before stent implantation.

150 dial infarction (TIMI) grade 0-1 flow in the infarct-related artery at arrival were randomized to con

151 al region immediately after reopening of the infarct-related artery may limit myocardial damage.

152 he risk among those who were treated for the infarct-related artery only.

153 ssel disease who underwent primary PCI of an infarct-related artery, the addition of FFR-guided compl

154 s) or to undergo no revascularization of non-infarct-related coronary arteries (590 patients).

155 to undergo complete revascularization of non-infarct-related coronary arteries guided by fractional f

156 The use of PCI in non-infarct-related coronary arteries remains controversial.

157 tervention (PCI) to restore blood flow in an infarct-related coronary artery improves outcomes.

158 disease who had undergone primary PCI of an infarct-related coronary artery in a 1:2 ratio to underg

159 as events in the group receiving PCI for an infarct-related coronary artery only.

160 y correlated with mortality in patients with infarct-related CS.

161 reserve-guided complete revascularization or infarct-related percutaneous coronary intervention only.

162 d in 2 patients (both in the group receiving infarct-related treatment only).

163 and regionally, suggests that CTT mitigates infarct risk in pediatric SCA by relieving cerebral meta

164 in the deep white matter, a location at high infarct risk in SCA (P < .001).

165 performance for detection of suspected acute infarct (SAI).

166 iffening, modeling the mechanical effects of infarct scar maturation, causes smooth muscle alpha-acti

167 in KO mice, and the animals developed larger infarct scars and more pronounced left ventricular remod

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

169 Haematoxylin and eosin staining of infarcts showed well demarcated zones of oedema and hypo

170 n residual motor cortex after motor cortical infarcts.SIGNIFICANCE STATEMENT Stroke is a leading caus

171 for LV ejection fraction </=47%, 1 point for infarct size >/=19%LV, and 2 points for microvascular ob

172 ivation cohort, LV ejection fraction </=47%, infarct size >/=19%LV, and microvascular obstruction >/=

173 simultaneous nonextensive infarct-size MVO (infarct size < 30% of LV mass and MVO < 2.5% of LV mass)

174 and was associated with significantly larger infarct size (56.5 versus 36.2 g), greater adverse LV re

175 /=24 mm, deferred stenting reduced the final infarct size (6% LV; IQR: 2% to 18% vs. 13% LV; IQR: 7%

176 Deferred stenting did not reduce final infarct size (9% left ventricle [LV]; interquartile rang

177 tify myocardial area at risk (AAR) and final infarct size (IS).

178 eft ventricular ejection fraction (LVEF) and infarct size (ISZ) are key predictors of long-term survi

179 transendocardial stem cell injection reduced infarct size (n=49, 9.4% reduction; 95% confidence inter

180 endent predictors of reverse remodeling were infarct size (odds ratio, 0.98; 95% confidence interval

181 in cardiomyopathy patients, and SNRK reduces infarct size after ischaemia/reperfusion.

182 in vivo, as evidenced by a 50% reduction of infarct size after ischemia/reperfusion versus wild type

183 Multivariable meta-regression revealed that infarct size and cardiac function were influenced indepe

184 ial ischemia/reperfusion injury with reduced infarct size and cardiomyocyte apoptosis.

185 o analyze whether these variables influenced infarct size and ejection fraction.

186 cardiac function in association with reduced infarct size and enhanced tissue repair (strengthened co

187 of MSC delivery influences the reduction in infarct size and improvement in left ventricular ejectio

188 e, rat, swine) which revealed a reduction in infarct size and improvement of LVEF in all animal model

189 m cell injection because of its reduction in infarct size and improvement of LVEF, which has importan

190 oronary artery occlusion exhibited increased infarct size and LV macrophage content after 24-48 h rep

191 Infarct size and LV mass decreased >/=30% in each group

192 Once infarct size and MVO were dichotomized by using univaria

193 tment before or after myocardial IRI reduced infarct size and Nlrp3 inflammasome activation in mice.

194 tion in mice resulted in marked reduction of infarct size and persistent recovery of cardiac function

195 st effective therapy for reducing myocardial infarct size and preserving left ventricular systolic fu

196 ate monocyte CD36 in the mitigation of early infarct size and transition to Mertk-dependent macrophag

197 yte-specific Smad3 loss did not affect acute infarct size but was associated with attenuated cardiomy

198 3 loss were not a result of effects on acute infarct size but were associated with unrestrained fibro

199 CMR-measured infarct size declined progressively after reperfusion in

200 citation to rats, ATTM significantly reduced infarct size following either myocardial or cerebral isc

201 ceptor (ADRB1) antagonist metoprolol reduces infarct size in acute myocardial infarction (AMI) patien

202 f PYK2 activation by Na2S reduced myocardial infarct size in mice.

203 l Infarction) examined the effects of NAC on infarct size in patients with ST-segment-elevation myoca

204 ous nitroglycerin is associated with reduced infarct size in patients with ST-segment-elevation myoca

205 Cexo but not Fbexo after reperfusion reduces infarct size in rat and pig models of myocardial infarct

206 phere-derived cells after reperfusion limits infarct size measured acutely, while providing long-term

207 dy, routine deferred stenting did not reduce infarct size or MVO and did not increase myocardial salv

208 tervention, with ongoing studies focusing on infarct size reduction using ancillary therapies.

209 m effects of adjunct cardioprotection beyond infarct size reduction, that is, on repair, remodeling,

210 ction in cardiac magnetic resonance-assessed infarct size relative to placebo (median, 11.0%; [interq

211 ept trials with surrogate end points such as infarct size to larger clinical outcome trials.

212 y PCI trials (total 2,632 patients) in which infarct size was assessed within 1 month after randomiza

213 Myocardial infarct size was increased, and coronary flow rate and +

214 Two days later, infarct size was quantified.

215 during ischemia/reperfusion insult, and the infarct size was reduced.

216 creased cardiac wound debridement, increased infarct size, and depressed cardiac function, newly impl

217 enyltetrazolium chloride staining determined infarct size, and fluorescence-activated cell sorting as

218 y end points included changes in LV volumes, infarct size, and major adverse cardiac events.

219 ded left ventricular (LV) ejection fraction, infarct size, and microvascular obstruction.

220 ge in left ventricular ejection fraction and infarct size, and the duration of time subjects was aliv

221 the middle cerebral artery markedly reduced infarct size, and this correlated with improved neurolog

222 nfarction, measurements of cardiac function, infarct size, apoptosis, both vascular and arteriole den

223 Acute myocardial infarct size, extent of microvascular obstruction, and I

224 AS-1 administration significantly decreased infarct size, improved cardiac function after myocardial

225 ntained their reparative properties, reduced infarct size, increased scar thickness, and attenuated L

226 myocardial infarction significantly improved infarct size, LV ejection fraction, and adverse LV remod

227 d myocardium of female WT mice and evaluated infarct size, MSC retention, inflammation, remodeling, a

228 the effect of deferred stent implantation on infarct size, myocardial salvage, and microvascular obst

229 yocardial dysfunction, infarct distribution, infarct size, myocardium at risk, microvascular obstruct

230 Despite no significant differences in infarct size, obese patients had significantly more impa

231 hin-1 preserved cardiac function and reduced infarct size, parallel to the persistence of the transpl

232 ols for assessing edema, myocardium at risk, infarct size, salvage, intramyocardial hemorrhage, and m

233 ssue composition (edema, myocardium at risk, infarct size, salvage, intramyocardial hemorrhage, and m

234 eover, Malat1 KO mice presented larger brain infarct size, worsened neurological scores, and reduced

235 enhanced endogenous fibrinolysis, to reduce infarct size.

236 atification by treatment window and baseline infarct size.

237 cardiac magnetic resonance imaging-assessed infarct size.

238 ng ischemia/reperfusion and showed a greater infarct size.

239 The primary endpoint was final infarct size.

240 d Na2S did not result in additive effects on infarct size.

241 nhancement (LGE) imaging overestimates acute infarct size.

242 as the presence of simultaneous nonextensive infarct-size MVO (infarct size < 30% of LV mass and MVO

243 nt to cleavage, showed significantly reduced infarct sizes and improved systolic function.

244 BK knockouts, exhibited significantly larger infarct sizes compared with their respective controls.

245 osis of dying cardiomyocytes and for smaller infarct sizes in female and male mice after permanent co

246 Infarct sizes of the conditional mutants were compared w

247 62 male Wistar-Hannover rats with a range of infarct sizes, plus 14 sham-operated rats, were examined

248 variability and lower ability for detecting infarct suggest that 2DST strain estimates may be less p

249 number after relevant pathological insults (infarcts), suggesting a similar expansion of cells that

250 Persisting T2 hyperintensity was defined as infarct T2 >2 SDs from remote T2 at 6 months.

251 n (MI), segments with a transmural extent of infarct (TEI) of </=50% are defined as being viable.

252 In the region remote to the infarct, the MINF rats exhibited preserved strain and in

253 often found far from the cavity or the peri-infarct tissue.

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

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

256 ranscriptional regulation pattern across the infarcted tissue.

257 ligation by mitigating adverse remodeling of infarcted tissue.

258 30 mg.kg(-1).day(-1)) in the supplied water (infarcted treated group, I + PY).

259 ponse following stroke while increasing peri-infarct vascularization compared to nonporous hydrogel c

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

261 Ability to discriminate infarcted versus noninfarcted segments by late gadoliniu

262 v/TM was more effective at reducing cerebral infarct volume and alleviated neurological deficits than

263 The total infarct volume and neurological deficits were significan

264 y more obvious (P < 0.01) reduction of brain infarct volume and neurological deficits.

265 Secondary endpoints were the change in infarct volume from baseline to day 30, and from 24 h to

266 The primary endpoint was the change in infarct volume from baseline to day 5 and was assessed i

267 is disproportionately severe relative to the infarct volume may benefit from late thrombectomy.

268 n increased brain hemorrhage transformation, infarct volume, and edema.

269 cerebral artery occlusion and evaluated for infarct volume, behavioral recovery, and inflammation.

270 with patient age, clinical stroke severity, infarct volume, brain volume, and cardiovascular risk fa

271 I led to decreased mortality rate, decreased infarct volume, improved functional outcome, reduced mic

272 oprotective effects, including reduced brain infarct volume, neuronal apoptosis, cerebral edema, and

273 P < 0.001) independently of age, gender and infarct volume, which was confirmed by voxel-based lesio

274 the severity of the clinical deficit and the infarct volume, with mismatch criteria defined according

275 tration and either clinical outcome or acute infarct volume.

276 s) revealed a significant reduction in final infarct volumes (mean [SD], 110 [65] vs 319 [147] mL; P

277 0-2, 25% vs 0%; P = .04), and smaller final infarct volumes (mean [SD], 87 [77] vs 242 [120] mL; P <

278 ular risk factors, clinical stroke severity, infarct volumes and brain volumes of patients with uncha

279 ion by antagonism of alpha4 integrin reduces infarct volumes and improves outcomes.

280 tween patient age, clinical stroke severity, infarct volumes as well as brain volumes and the differe

281 and determined clinical stroke severity and infarct volumes as well as total brain volume by neuroim

282 demonstrated significantly smaller cerebral infarct volumes compared with wild-type mice.

283 Infarct volumes were quantified by MRI after 48 hours.

284 with reduced leukocyte infiltration, smaller infarct volumes, and decreased neurological deficit.

285 ice displayed significantly reduced cerebral infarct volumes, developed significantly less neurologic

286 attractant protein 1 concentrations, whereas infarcts were associated with elevated tumor necrosis fa

287 Cerebral infarcts were associated with highest overall neuromarke

288 Embolic infarcts were defined as new foci of reduced diffusion a

289 Patients were excluded if infarcts were located in both the anterior and posterior

290 Infarcts were manually outlined and images were transfor

291 The infarcts were manually outlined and transformed into ste

292 c resonance imaging (MRI)-documented lacunar infarcts were randomly assigned in a factorial design to

293 Infarcts were significantly larger after blood clot infu

294 domen also showed a small peripheral splenic infarct, while CECT of the chest revealed bilateral mili

295 ents with residual iron had higher T2 in the infarct zone surrounding the residual iron when compared

296 mean change, 0.0+/-2.7 ms; P=0.837), whereas infarct zone T2 decreased (-9.5+/-6.4 ms; P<0.001).

297 rogeneity of electric conduction in the peri-infarct zone than wild-type mice.

298 iPSC-EVs preserved viable myocardium in the infarct zone, whereas reduction in apoptosis was signifi

299 ntricular mass and superior perfusion in the infarct zone.

300 er MI by reducing neovascularization in peri-infarct zones.